Nervous System Examination: Anatomy and Functions

Nervous System Examination
Neuromuscular System Examination

Carey Francis Okinda, May/June 2012
Lesson 1: Preview of Anatomy and Physiology of the Nervous System
At the end of the lesson the learner will be able to: -
1) Outline the basic anatomy of the nervous system

2) Explain how the nervous system functions
1.0 INTRODUCTION
Neurological diseases contribute a major burden on health care resources. In examination of the nervous
system, neurological assessment seeks to delineate the patient’s disease in terms of both functional and
structural (anatomical) aspects. An elaborate and complete neurological examination calls for concentration
and cooperation of the patient. It is therefore important that the examination process is planned in relation to
the patient’s problem as exhibited by the information obtained during history taking.
The history in a patient with a nervous system disorder is a very important aspect of physical examination
as the historical information may in itself be diagnostic. For instance description of attacks of seizures or
convulsions and altered mental function in epilepsy, progression of degenerative disease and neoplasms,
ascending paralysis pattern in Gullein-Barry syndrome (GBS) and the description of the abruptness of
gradualness of hemiplegia in cerebrovascular accident (CVA) or stroke.
Neurological examination aims to confirm the extent of disability as described by the patient and assess the
presence or absence of factors relevant in the diagnostic context of the problem. Thus neck rigidity in a
patient with headache is consistent with meningitis and an extensor plantar response in a patient with
episodes of hemiparesis is suggestive of cerebral infarction.
The diagnosis in nervous system disorders can be physiological (e.g. right hemiplegia), anatomical (e.g. left
internal capsule lesion), pathological (e.g. internal carotid artery occlusion) and aetiological (e.g.
atherosclerosis). Neurological examination attempts to establish and explain patterns of functional
abnormality whose features depict lesions in the neuronal systems i.e. the nuclei and their interconnecting
pathways or with disease syndromes.
The features may be negative or positive expressions of dysfunction. For example, upper or lower motor
neuron lesions (UMNL or LMNL), patterns of sensory disorders or visual disturbances are negative
expressions while seizures in cerebral cortex and involuntary movements or tremors in basal ganglia
disease are positive aspects.
2.0 BASIC ANATOMY & PHYSIOLOGY
The nervous system is made up of the central nervous system (CNS), which includes the brain and spinal
cord (vertebral column) and the peripheral nervous system (PNS) that includes the cranial nerves arising
from the brain and spinal nerves originating from the spinal cord. The cranial nerves run between the brain
and the periphery while the spinal nerves (which leave and enter the vertebral column) and the sensory and
motor nerve endings (in the skin, the organs).
Carey Francis Okinda 1

Diagram 1.1: General Layout of Nervous System
Somatic Nervous System (SNS) Autonomic Nervous System (ANS)

CENTRAL NERVOUS SYSTEM
Somatic Integration Centres Autonomic Integration Centres

(CNS)
BRAIN
SPINAL
CORD
Sympathetic Division
Division (afferent)
Somatic Sensory
Division (afferent)
Visceral Sensory
Division (efferent)
Division (efferent)
1)
Parasympathetic
(PNS) Cranial Nerves & Peripheral
PERIPHERAL NERVOUS SYSTEM
Somatic Motor
(efferent)
Somatic Somatic Visceral Autonomic effectors
and Special Effectors receptors (cardiac and smooth
receptors (skeletal muscle, glands)
Nerves
muscles)
Stimulus Response Stimulus Response
2.1 Nerve Cells
The nervous system has two principal cells – the neurones, basic structural and functional units of the
system and neuroglia or glial (glia = glue) cells - supportive cells, aid in the function of neurones.
Neurons: Structure & Function

Neurons are specialized cells in the nervous that respond to chemical and physical stimuli, conduct
electrochemical impulses and release chemical regulators that are specific in function. These characteristics
enable the neurons perform functions such as perception of stimuli, learning, memory and control of
muscles and glands. Neurons vary in size and shape. Have three principal regions namely: the cell body,
the dendrites (processes) and the axon.
The Cell Body (Perikaryon)
Peri = around and karyon = nucleus meaning around the nucleus. This is the enlarged portion of the neuron
that contains the nucleus. It serves as a nutritional centre and has Nissl bodies that contain the rough
endoplasmic reticulum that is the site for protein synthesis. Cell bodies are clustered in the CNS to form
nuclei and in the PNS they cluster to form ganglia.
Dendrites (Dentron = tree branch)

Dendrites are thin-branched processes that extend from the cytoplasm of the cell body and serve as
receptor site that transmit impulses to the cell body.
Diagram 1.2: The Neurone
The Axon (Nerve Fibre)
The axon is a larger process that conducts impulses away from the cell body. It has two parts, the axon
hillock near the cell body) and axon collaterals (the side branches extending from the axon).
It transports proteins and other molecules faster than the simple diffusion through axoplasmic flow and
axonal transport. The axoplasmic flow is slow resulting from rhythmic waves of contraction pushing the
cytoplasm from the axon hillock to nerve endings. The axonal transport is rapid and bi-directional
(retrograde and orthograde). The retrograde movement is blamed for movement of herpes virus, rabies
virus and tetanus toxin from the nerve endings towards the cell body.
Classification of Neurons/Nerves
The classification of the neurons/nerves can be functional or structural.
Functional Classification
Neurons are classified according to function basing on the direction of conduction of impulses.
a) Sensory (afferent) neurons - these are the neurons that conduct impulses from sensory receptors to the
central nervous system.
b) Motor (efferent) neurons - conduct impulses out of the CNS to the effecter organs
c) Association neurons (interneurons) - are neurons located in the CNS and serve the associate or
integrative functions of the nervous system for example associating the right motor response for a
sensory stimulus.

Diagram 1.3: Relationship between sensory and motor fibres of PNS and CNS
Motor Neurons
There are two types of motor neurons: - the somatic motor neurons and autonomic motor neurons. The
somatic motor neurons provide reflex and voluntary control of skeletal muscles while the autonomic motor
neurons innervate involuntary effectors such as the smooth muscles, cardiac muscle and glands.
The cell bodies of autonomic nerves innervating these glands are located in the autonomic ganglia located
outside the CNS. The autonomic nerves have two subdivisions that are the sympathetic and
parasympathetic nerves. Autonomic motor neurones together with their central control centres form the
autonomic nervous system.
Structural Classification
Structural classification is based on the number of processes extending from the cell body. There are three
classes- bipolar neurons, multipolar neurons and pseudounipolar neurons.
The bipolar neuron has two processes at either ends of the cell body. They can be found in the retina of the
eyes. The multipolar neurons have several dendrites and one axon. These are the most common neurons
e.g. motor neurons.
The pseudounipolar neurons have a single short process that divides like a ―T‖ to form larger processes e.g.
sensory neurons – one end of the T receives stimuli and produces nerve impulses and the other end
delivers these stimuli to synapses within the brain or spinal cord.
Cell bodies of sensory nerves are located in the dorsal ganglia f the spinal cord and cranial nerves outside
the CNS.
Nerves
A nerve is a bundle of axons outside the central nervous system. Most nerves are composed of both motor
and sensory fibres (mixed nerves) however, others e.g. some cranial nerves that contain only sensory
processes for example those serving special senses of sight, hearing and smell.
2.2 Neuroglia
Neuroglia cells are supportive cells in the nervous system. Glial cells are about five times more abundant
that neurons. In addition, they have limited mitotic activity.

There are six types of glial cells: -
a) Schwan cells - cells that form myelin sheaths around peripheral nerve axons
b) Oligodendrocytes - form the myelin sheaths around axons of the CNS
c) Microglia - are phagocytic cells that migrate through the CNS and remove foreign or degenerated
material
d) Astrocytes - are cells that help regulate the external environment in the CNS
e) Ependyma - are cells lining the ventricles of the brain and central canal of the spinal cord.
f) Satellite cells – cells that support neuron cells bodies within the ganglia of the PNS.
2.3 The Central Nervous System (CNS)
The CNS consists of the brain and spinal cord. It receives input from sensory neurons and directs the
activity of motor neurons that innervate muscles and glands. Association neurons in the brain and spinal
cord associate appropriate motor responses with sensory stimuli maintaining homeostasis in the internal
environment and continued existence of the organism in a charging external environment.
The Brain
The brain constitutes about one-fiftieth of the body weight. The brain is divided into three main parts namely;
-
1. Fore brain or diencephalon (cerebrum)
2. Brain stem (mesencephalon/mid brain, pons and medulla)
3. Hind-brain (cerebellum).
Fore brain - Cerebrum
The cerebrum is the largest portion of the brain accounting for 80% of the telecephalon mass and occupies
the anterior and middle cranial fossa. The cerebral hemispheres extent throughout the length the length of
the skull from the fore head to the occiput above the anterior, middles cranial fossa and the tentorium
cerebelli. It is also called the diencephalon. It is divide by a deep cleft – the longitudinal cerebral fissure into
the right and left cerebral hemispheres. The two hemispheres are separated by falx cerebri penetrating the
hemispheres to the depth of the corpus callusum, which connects them. Each hemisphere contains one of
the lateral ventricles.
The under surfaces of the two hemispheres are joined by cerebral peduncles of the midbrain, anteriorly to
the structure of the floor of the third ventricle. The lateral surfaces of the brain are boldly convex in
conformity with the shape of the skull.
The cerebrum consists of an outer cerebral cortex (2-4 mm of grey matter) and an underlying white matter.
Its surface is folded into convolutions with the folds forming the gyri (gyrus) and the depressed zones
groves called sulci (sulcus). The lateral sulcus (fissure of Sylvius) separates the temporal lobe and frontal
lobe and the central sulcus (fissure of Rolando) passes over the medial surface of the hemispheres
separating the frontal and parietal lobes.
Each cerebral hemisphere is subdivided by deep sulci (fissures) into five lobes: - frontal, parietal,
temporal, and occipital (all visible from the surface) and the deep insula lobe.
Interior of the cerebral hemispheres
 The cerebral cortex is composed of nerve cells on the surface

 Cerebral lobes are connected by masses of nerve fibres or tracts that make up the white matter
 Afferent and efferent fibres link up different parts of the brain and spinal cord
 Nerve fibres in the cerebral hemispheres are of three main groups
a) Commissural fibres found gathered in the corpus callosum and radiate widely and symmetrically
through the white matter of the hemisphere joining the two hemispheres.
b) Association fibres extent from one gyrus to the next connecting different parts of the hemisphere
(confined to each hemisphere)
c) Projection fibres are both sensory (afferent) and motor (efferent) fibres joining the grey matter of the
hemisphere with the lower centres. The fibres laterally to the thalamus at the base of the
hemisphere and a head of the caudate nucleus where they are called internal capsule. Form the
internal capsule the fibres radiate upwards and outwards forming a curved fan to reach the cortex.
Internal capsule
The internal capsule consists of afferent fibres passing from the cortex cell bodies in the thalamus and
efferent fibres passing down from cell bodies in the cortex to the crus cerebri of the mid brain.
Anterior Limb
The anterior limb contains fronto-pontine fibres from cell bodies in the frontal lobe and pons below the
thalamus into the cerebral penducle.
Genu and posterior limb
These contain the cortico-spinal tracts (pyramidal tracts).
Corpus Callosum
Commences at the anterior commissure and terminates at the diencephalon and consist of a mass of
commissural fibres that extend from the cortex to the cerebrum between symmetrical parts of the
hemispheres.
Internal structures
The interior of the cerebrum has white matter with large masses of grey matter forming the basal ganglia
and cavities. The basal ganglia whose function is mainly motor, consists of corpus striatum complex.
The thalamus is a wedge shaped structure consisting of two masses of nerve cells and fibres lying in the
walls of both the third and lateral ventricles. It contains nuclei of sensory tracts from the skin, viscera and
organs of special senses.
The hypothalamus is composed of a number of nerve cells and is situated below and in front of the
thalamus immediately above the pituitary gland. It is linked to the posterior lobe of the pituitary gland by
nerves and to the anterior lobe by a complex system of blood vessels. These connections enable the gland
to control hormone production by the pituitary gland.
Functions of the cerebral hemispheres
1. Mental activities involved in memory, intelligence, sense of responsibility, thinking, reasoning, moral
sense and learning.
2. Sensory perception of pain, temperature, touch, sight, hearing, taste and smell.
3. Initiation and control of voluntary muscle action.

Functional areas of the cortex
Figure 1.4: Functional areas of the Brain
a) Motor area
 The motor area lies in the precentral gyrus and anterior wall of the central sulcus
 Initiates movement of various areas of the body
 The cells of the motor cortex send their axons down the pyramidal tracts
 The opposite half of the body is represented upside down along the motor cortex
 Blood supply is via the middle cerebral artery that supplies the area controlling structures of the
face, arm and trunk and the anterior cerebral artery covering the areas of the legs and perineum.
b) Sensory area
 Lies in the postcentral gyrus and the posterior wall of the central sulcus
 It corresponds to the motor area
 Plays a role in appreciation of kinaesthetic sensibility, touch, and temperature e.t.c.
c) Auditory area
 Lies within the upper part of the temporal lobe immediately below the anterior transverse temporal
gyrus (below the lateral sulcus). It lies near the posterior branch of the middle meningeal artery
 The middle cerebral artery supplies it.
d) Visual area
 The visual area lies on the medial surface of the occipital lobe behind the parieto-occipital sulcus
and includes the greater part of the occipital lobe.
 Each occipital cortex receives impulses from its own half of each retina i.e. it registers the opposite
visual filed.
e) Olfactory area (rhinencephalon)

 Lies deep within the temporal lobe
f) Taste area
 The taste area lies near the lower end of the postcentral gyrus

g) Speech area
 The speech area is situated in the lower part of the parietal lobe and extends into the temporal lobe.
 Perceives the spoken word
 There is a dominant area in the left hemisphere in right-handed people and vice versa.
The Limbic System
These are grey matter formations surrounding the corpus callosum and the diencephalon. The word ―limbic‖
means ―boarder‖. The hippocampus forms part of the limbic system. The main functions of the limbic
system are control of emotional behaviour and control of motivational drives that control the internal
conditions of the body e.g. body temperature, osmolality of body fluids, drive to eat and drink and control of
body weight.
Frontal Lobe
Forms the anterior portion of each cerebral hemisphere and it is separated from the parietal lobe by the
central sulcus. The precentral gyrus located in the frontal lobe just in front of the central sulcus is involved in
motor control.
Functions
1. Voluntary motor control of skeletal muscles

2. Personality development
3. Higher intellectual processes
a. Concentration
b. Planning
c. Decision making
4. Verbal communication
The Brain stem
The brain stem is the mass of nervous tissue connecting the cerebral hemispheres with the spinal cord. It is
an extension of the spinal cord upwards into the cranial cavity and consists of fibres and nerves. The brain
stem ha s three portions the mesencephalon (mid brain), the pons and medulla. The brain stem contains
motor and sensory nuclei that perform motor and sensory functions for the face and head regions. It
provides control functions for respiration, cardiovascular system, gastrointestinal functions, equilibrium, eye
movements and many stereotyped movements of the body. It serves as a command station for signals from
higher neural centres to initiate or modify specific control functions throughout the body.
Mesencephalon (Mid brain)
 The midbrain is the part of the brain stem that lies between the lower part of the cerebral hemisphere
(where it is connected with the internal capsule and thalamus) and the upper part of the pons. Most of
the mid brain lies in the posterior cranial fossa.
 The third and fourth cranial nerves leave the brain stem at the mid brain.
 Tracts of the mid brain consist of descending tracts in the crus (basis pendunculi) and ascending tracts
in the tegmentum.
 It is a relay station for fibres on their way to the thalamus.
 Blood supply is via the posterior cerebral artery while venous drainage is the cerebral veins, which drain
into the greater cerebral vein.

The Pons
 The pons is broad transverse mass that lies in front of the cerebellum below the mid brain and above
the medulla (separates the midbrain and the medulla).
 The fifth cranial nerve emerges from the brain at the pons
 The pons has the nuclei for the sixth cranial nerve, seventh cranial nerve and the pontine (sensory)
nucleus of the fifth cranial.
 Consists of ascending tracts (tegmentum) and descending tracts (crus cerebrei)
 Blood supply is via pontine branches of the basilar artery and venous drainage is through the inferior
petrosal sinuses and the basilar plexus.
Medulla
The medulla oblongata is the upward continuation of the spinal cord and lies in the cranium above the
foramen magnum. It is 2.5 cm long, pyramid shaped with the base upwards. The upper part is conical while
the lower part is cylindrical resembling the spinal cord. The upper part of the anterior surface is deeply
grooved in the midline and has a bold cylindrical convexity on the median groove called the pyramid
containing the pyramidal tracts that decussate at the lower part of the medulla. Attached to the medulla and
pons are the nuclei of the cranial nerve VI, VIII, nerve intermedius and VII. The medulla has rootlets for
cranial nerves IX, X, XI and XII.
The posterior surface of the medulla extends on the lower portion to the central canal and upper part
expands into the forth ventricle. The outer aspect of the medulla is composed of white matter, which is
passes between the brain and spinal cord, and the grey matter lies centrally.
The medulla consists of two distinct parts –n the closed part which adjoins the spinal cord and the open part
that forms part of the forth ventricle. The open part contains decussation of pyramids and has the spinal
nucleus for cranial nerve V. The open part has the nuclei for cranial nerves IX, X, XI and XII: special
impulses from the carotid sinus and carotid bodies are passed to the vital centres – the cardiac centre,
vasomotor centre, respiratory centre and reflexes centres for vomiting, coughing, sneezing and swallowing.
Blood supply
 Ventrally by vertebral and basilar arteries

 Laterally and dorsally by the posterior inferior cerebral arteries.
The medulla has special functions such as: -

 Decussation of pyramids
 Sensory decussation
 Cardiac centre control
 Respiratory centre controls
 Vaso motor centre controls
 Reflex centres
The Cerebellum (Hind brain)
The cerebellum lies posterior to the mid brain in the posterior cranial fossa. It consists of two hemispheres
joined in the midline by a narrow portion of the cerebella substance called the vermis. Grey matter forms
the surface of the cerebellum while the white matter lies deep.
The cerebellum consists of a small anterior lobe separated from two large posterior lobes by a primary
fissure and has three peduncles that connect each hemisphere to the three parts of the brain stem. The
superior penducle links to the mid brain, the middle penducle to the pons and the inferior peduncle to the
medulla. It has three morphological parts, which have distinct functions. The archaecerebellum has
vestibular connections responsible for equilibrium and control of fine movements, palaecerebellum found in
the anterior lobe has spinal connections (spino-cerebellar tracts) responsible for postural control
mechanisms and the neocerebellum located in the posterior lobes and forms the feedback circuits from the
basal ganglia and cerebral cortex required for control of muscular tone and accurate voluntary movements.
Connections of the cerebellum
There are three main connections: -
a) Superior peduncle with efferent fibres to the red nucleus, thalamus and cortex of the opposite side
(palaecerebellum)
b) Middle connection with afferent fibres from the pontine nuclei of the opposite side (neocerebellum)
c) The inferior connection that is mainly afferent (palaecerebellum and archaecerebellum) except for the
cerebello-vestibular tracts.
Blood supply
 The under surface is supplied by two arteries – the posterior inferior cerebral artery the largest branch
of the vertebral artery that is one of the most tortuous arteries and the anterior inferior cerebral artery a
branch from the basilar artery.
 The upper side is supplied by the superior cerebral artery which is branch of the basilar artery
Venous drainage
The superior and posterior surfaces drain into the straight and transverse sinuses while the inferior surface
drains into the inferior petrosal, sigmoid and occipital sinuses.
Function
The main unction of the cerebellum is coordination of voluntary muscular movement, posture, balance, and
equilibrium, which depends upon the integrity of the sensory pathways and the activity of the cerebellum
involving all the connections. The cerebellum receives afferent fibres from proprioceptor organs of the body
(labyrinths and muscles) via the dorsal and ventral spinocerebellar tracts. The principal causes of
incoordination are sensory loss and lesions of the cerebellar and its connections.
Symptoms of cerebellar lesion
 Muscular hypotonic due to loss of facilitatory influence of the cerebellum upon the stretch reflex.
 Static tremor following failure to maintain fixed posture
 Voluntary tremor
 Ataxia/incoordination
 Dysdiadochokinesis (inability to carry out alternating movements with rapidity and regularity)
 Nystagmus
Blood supply
 The brain receives 1/5th of the total cardiac output.

 Blood flow is regulated by baro-receptor reflexes and local auto-regulatory mechanisms
 The supporting glia ensure the accomplishment of metabolic requirements
 Transport of metabolites to and from the brain depends on active cellular transport mechanism, is
usually provided by the blood brain barrier (BBB).

2.4 The Spinal Cord
The spinal cord is the downward continuation of the brain stem. It is enveloped by the three meninges and
lies within the vertebral canal protected by the vertebral column. The spinal cord extends from the foramen
magnum where it is continuous with the medulla oblongata to the level of the first or second lumbar
vertebra.
The spinal cord is a cylinder somewhat flattened from the back to front and the lower end tapers into a cone.
On the ventral side it has a deep midline groove – the anterior median sulcus and a shallow sulcus on the
dorsal aspect. The spinal cord has two symmetrical enlargements, cervical enlargement at C3 – T1 and
lumbar enlargement at T9 – L1 that occupy the segments of the limb plexus corresponding to brachial
plexus (C5-T1) and lumbar-sacral plexus (L1-S3) respectively.
Spinal nerve roots
The anterior and posterior roots of the spinal nerves unite within the intervertebral foramina. The anterior
and posterior roots pass from then cord to their appropriate intervertebral foramina where each evaginates
the dura matter.
Blood supply
The spinal cord is supplied by the anterior and posterior spinal arteries, which descend from the level of the
foramen magnum. There are two posterior spinal arteries arising from the vertebral and posterior inferior
cerebral artery. The single anterior spinal artery is formed by the union of a branch from each of the
vertebral arteries and reinforced by segmental arteries and lies on the anterior median fissure.
Internal structure of the spinal cord
The spinal cord consists of a central mass of grey matter enclosed in a cylindrical mass of white matter and
is divided into two halves by the anterior median fissure and posterior median septum.
The grey matter

 The grey matter is a fluted column like a letter ―H‖ with two posterior, two anterior and two lateral
columns.
 The posterior columns contain nerve cells that are stimulated by sensory impulses from the periphery of
the body.
 Anterior column contain nerve cells of the lower motor neurone (LMN), which are stimulated by the axon
of the upper motor neurone (UMN) or cells of connector neurones that link the anterior and posterior
columns.
 The lateral columns contain connector cells of the sympathetic part of the autonomic nervous system
(ANS).
 The grey commissure connects the grey matter in the right and left halves of the cord.
The white matter

Contains three kinds of fibres- the ascending, descending and connecting (inter-segmental) fibres which are
arranged in three columns or tracts formed by sensory fibres ascending to the brain, motor fibres
descending from the brain and fibres of connector neurones respectively.
Posterior white columns

 Are occupied by the ascending fibres lying between posterior grey horn and posterior median septum.
 They convey sensations of cutaneous sensibility, temperature and proprioception impulses from the
joints, ligaments, tendons and muscles.
 The fibres from the lower parts of the body lie nearest to the midline
Anterior white columns
The anterior white columns lie between the anterior grey columns and the anterior median fissure and
contain uncrossed pyramidal fibres and the vestibulo-spinal fibres that are all descending fibres.
Lateral white columns
Contain both ascending and descending fibres and most of them are crossed.
Descending fibres
Descending fibres consist of crossed pyramidal tract (cortico-spinal tract), which lie posteriorly, and the
rubro-spinal, tecto-spinal and vestibulo-spinal.
Ascending fibres
The ascending fibres consist of spino-cerebellar tracts and the spino-thalamic fibres.
Projection Fibres
1. Afferent fibres
2. Efferent fibres
3. Ascending fibres
4. Descending fibres
Afferent fibres
The afferent fibres are conveyed to the cerebral cortex by three neurones. The first neurone lies in the
posterior root ganglion of the spinal cord, the second neurone lies in the grey matter of the spinal cord or
brain stem and the third neurone lies in the thalamus where it passes through the internal capsule to the
cortex.
Efferent impulses
These are impulse from the motor cortex, which are conveyed to the striated muscles by two neurones – the
upper motor neurone (UMN) and the lower motor neurone (LMN). The UMN decussate and pass into the
motor nuclei of the cranial nerves and anterior horn cell of the spinal cord, whence the UMN pass into the
motor nerves of the muscles concerned. The extra-pyramidal tracts are mediated by several neurones
whose cell bodies lie in the brain stem (tectum, red nucleus, vestibular nucleus) and are acted upon by the
basal ganglia and cerebral cortex.
Ascending tracts
These are all the incoming tracts destined for the cortex of the opposite cerebral hemisphere, cerebellum
and brain stem or spinal cord.
Descending tracts
Descending tracts are tracts that descend to the motor nuclei of the brain stem and spinal cord from the
cerebral cortex in two main systems – the pyramidal and extra-pyramidal systems.

Pyramidal tracts
 Pyramidal tracts pass directly to the cell bodies of the LMN.

 They run from the motor area (pre-central gyrus and front part of central sulcus) through the internal
capsule, midbrain and pons and into pyramids of the upper medulla.
 In the lower medulla most of the tracts decussate forming the crossed pyramidal tracts, which lie in the
posterior part of the lateral column of the white matter in the spinal cord. The uncrossed pyramidal
fibres descend in the anterior column of the white matter and cross the anterior white commissure to
synapse with anterior horn cells of the opposite side.
Extra-pyramidal tracts
 Extra pyramidal tracts are usually interrupted by several relays connections en route.
 They run from the frontal and temporal cortex through the internal capsule and relay at different levels.
 Most tracts synapse with the pontine nuclei and pass to the cerebellum from where the tracts pass to
the red, reticular, vestibular and olivary nuclei.
 Other fibres pass from the cortex to the basal ganglia into the red and reticular nuclei.
 From the brain stem the extra pyramidal tracts descend to synapse with the LMN.
 The tracts lie in the lateral column of the white matter of the spinal cord anterior to the crossed
pyramidal tracts.
The Motor System
The motor system comprises of the: -

1. Cerebellum
2. Corticospinal system (pyramidal system, upper motor neurone)
3. Extrapyramidal system
4. Lower motor neurones
The Cerebellum
 The cerebellum receives afferent fibres from the spinal cord, vestibular system, basal ganglia and the
cerebral cortex.
 It modulates movement via its connections with the thalamus, basal ganglia and the cerebral cortex.
 Features of cerebellar disease/lesion include: -
o Lack of coordination (adiadocokinesia)
o Incoordination (ataxia) that affects mainly the trunk with the patient encountering difficulty in sitting
up or standing. There is no or little effect on coordination in the limbs.
o Hypotonia
o Nystagmus
o Slurring speech
o Intention tremor
o Pendulous knee jerk.
 Cerebellar lesions are usually not associated with paralysis
 The lesions if unilateral they do show on the side of the lesion.
Spinocortical (pyramidal tract) system, Upper Motor Neurone
 Consists of the central pathways linking the pyramidal cells (in the motor cortex) with the motor
neurones the brain stem and spinal cord.
 The fibres arise from the motor area, which occupies the anterior aspect of the central sulcus (Rolandic
fissure) and adjacent precentral gyrus.

 There is localization of function in the motor area with different body parts of the opposite side of the
body being represented separately.
 Body parts performing highly skilled movements such as the fingers and thumb have the largest areas
of cortical representation
 Fibres of the corticospinal tract descents into the internal capsules occupying the anterior 2/3 of the
posterior limb and then into the cerebral pendulces in the midbrain
 The pyramidal tract is concerned with initiation of voluntary and skilled motor acts especially fine distal
movements.
 Lesions affecting the corticospinal fibres alone cause weakness of the contralateral side of the body
impairing fine and rapid distal movements of the digits, weakness of hip flexion and shoulder abduction.
 Hemiplegia and monoplegia results from extensive lesions involving the corticospinal tracts,
extrapyramidal tracts and subcortical structures.
 Lesions of the corticospinal tract also damage the neighbouring structures such as the extrapyramidal
nuclei and pathways.
 Signs of upper motor neurone lesion (UMNL)
o Weakness in corticospinal tract distribution, shoulder abduction, finger movements, hip flexion and
toe dorsiflexion.
o Little or no atrophy
o Spastic hypertonia
o Hyperreflexia
o Loss of superficial reflexes
o Extensor plantar response on opposite side of the lesion (Babinski’s sign)
 Controls complex volitional movements needing postural adjustments and fine movements.
The Lower motor neurone
 Controls muscular movement

 Consists of: -
o Anterior horn cells or homologous cells in the brain stem
o Efferent nerve fibres from the above cells
o Peripheral nerves to the muscles
o Muscles fibres innervated by these fibres and their terminal axonal branches
 Efferent nerves fibres pass through the anterior spinal nerve root
 The cardinal signs of LMNL include: -
o Weakness, flaccidity
o Decreased muscle tone (hypotonia)
o Absent tendon reflexes (loss of tendon reflexes)
o Muscle wasting – usually severe
o Fasciculation in affected muscles
o Flexor plantar response
o Superficial reflexes are normal
o Distribution of the weakness and wasting relates with the lesion in the spinal segment, nerve root
or peripheral nerve.
 The lower motor neurone facilitates initiation of voluntary movements, maintains the posture and muscle
tone. These activities have their initiation in the higher neural centres (cerebral cortex), which have to
be transmitted to the muscles only if the LMN is intact.
Extrapyramidal system
 Comprises of the parts of the nervous system concerned with movement and posture excluding the
motor cortex and the corticospinal pathways.
 The system includes the basal ganglia, substhalamic nuclei, substantia nigra and structures in the
midbrain.
 Has a complex connection with fibres from the thalamus and cerebral cortex
 There are no direct pathways with the spinal cord and basal ganglia
 It is connected indirectly with the lower motor neurones through pathways arising from the brainstem
such as the dentatorubrospinal, retinospinal and oliviospinal tracts.
 The functions are control of posture and initiation of movements especially involving change of posture
e.g. sitting, standing, walking, running and turning over while lying
 Features of extrapyramidal lesions
o Difficulty in initiating voluntary movements due to impaired orientation and balancing of reflexes
and altered tone
o Lead pipe or cog wheel rigidity
o Normal or increased reflexes
o Abnormal posture
o Involuntary movements/tremors
o Normal power
o Plantar response normal or extensor
1.5: The Peripheral Nervous System

Lesson 2: Neurological History
1) Take an appropriate neurological history
Examination of the Nervous system
The examination of the nervous system must be ―directed‖ to facilitate completion of the working diagnosis
and assessment of the extent of structural and functional derangement. Correct interpretation of signs of
diseases of the nervous system greatly depends on the examiner’s knowledge of physiology and anatomy.
Requirements
1. A tendon hammer (Patella hammer)

2. Tuning fork
3. Disposable sterolets or needles
4. Cotton wool
5. An ophthalmoscope
6. Test-tubes or small bottles
7. Snellen’s chart
History taking
History is of fundamental significance in diagnosing neurological disorders as it facilitates careful

understanding of the pertinent issues raised by the patient in a progressive step by step fashion coupled
with a matching logical interpretation that yields a formidable and clear picture of the natural history of the
disease via important clues to the nature of the illness.
The Complains
Disorders of the nervous system may present with a legion of complains of, which the important ones are
discussed below: -
1. Disturbances of memory
2. Disturbances of mood
3. Loss of consciousness
4. Delusions and hallucinations
5. Insomnia
6. Headache
7. Visual disturbance
8. Giddiness and vertigo (feeling of loss of balance with the impression that the surroundings are whirling
around)
9. Dizziness (subjective feeling of unsteadiness)
10. Tinnitus (a subjective awareness of noise in the absence of any external stimuli)
11. Deafness
12. Aural pain or discharge
13. Dysphagia (may be associated with bulbar or pseudobulbar palsy)
14. Weakness or paralysis of limbs
15. Tremors
16. Numbness, paraesthesia (pins and needles)
17. Loss of sensation
18. Disturbances of bladder and bowel function (frequency and incontinence are associated with bilateral
upper motor neurone lesions; incontinence may follow unilateral cerebrovascular accident; dementia is
associated with incontinence)
History of presenting illness
This demand for careful, logical and conclusive interview of the patient in order to establish the chronology
of events in neurological disorders. It is important to merge adequately all the associated scenarios.
Past Medical History
Past medical problems may be of importance in patients with neurological disease. The important areas to
consider include: -
 Trauma
o Can lead to subdural and extradural haematoma.
o Chronic subdural haematoma has a latent period of weeks to months compared to extradural
haematoma
o Head injury can be associated with pneumococcal meningitis and tetanus
 Cardiovascular system
o Hypertension
o Rheumatic heart disease
 Respiratory system
o For example in pneumonia as chronic hypoxia is associated with confusional states in the elderly
 Haematological disorders such as bleeding disorders

 Hepatocellular failure may present with confusion, drowsiness, seizures and features of encephalopathy
 Renal failure can be associated with depression, headache, drowsiness, and symptoms of peripheral
neuropathy, visual loss, seizures and coma.
 Joint and connective tissue disease can cause limitation of joint movement.
 Endocrine and metabolic disorders
o Diabetes mellitus
o Hypoglycaemia, hypocalcaemia and hyponatraemia are associated with seizures
o Hypothyroidism may occur with Carpo-tunnel syndrome, cerebella disease and dementia.
 Neoplastic diseases may metastasise

 Sexually transmitted diseases such as syphilis (Tabes dorsalis and general paralysis of the insane) and
HIV (encephalitis) are associated with neurological pathologies.
 Tuberculosis and leprosy
 Recent viral infection e.g. post-infective polyneuropathy such as Guillain Barre Syndrome (GBS)
Family, Social and Drug History
 Smoking is a risk factor in cerebrovascular disease

 Drugs
o Phenothiazines are associated with Parkinsonism
o Metoclopromide causes severe dystotic reactions
o Isoniazid leads to peripheral neuropathy
 Alcohol
 Dietary history
o Deficiency of thiamine, nicotinic acid, pyridoxine, vitamin B12 and folic acid
 Occupation – exposure to toxic substances e.g. lead
 Sexual history
 Travel
 Contact with tuberculosis, meningitis and polio.
 Family history of neurological disease
o Neurofibromatosis (von Recklinghausen’s disease – an autosomal dominant disorder in which
fibromas are derived from the sheaths of the peripheral nerves, nerve roots and cranial nerves)
o Huntington’s disease (an autosomal dormant disorder that presents with choreiform movements)
o Freidreich’s ataxia (results from degeneration of the spinocerebellar, corticospinal tracts and the
posterior columns)
General Scheme for examination
1. General Examination
a. Higher mental functions - appearance, behaviour, consciousness, delusions, emotional state,
gait, hallucinations, illusions, intelligence, memory, mood, orientation, presence of
hallucinations and delusions and speech
b. Examination of the skull
c. Signs of meningeal irritation
2. Cranial nerves
3. Motor system
a. Muscle bulk
b. Muscle tone
c. Muscle power
d. Reflexes - tendon reflexes and superficial reflexes
e. Coordination
f. Involuntary movement
4. Sensory system
a. Touch
b. Pain, deep pain
c. Vibration
d. Temperature
e. Position, proprioreception
f. Stereognosis

Lesson 3: General Examination – Higher Mental Functions
1) Perform general examination of the nervous system

2) Interpret findings on general examination of the nervous system
Higher mental functions
Evaluation of the metal state of a patient should be explored in relation to features suggestive of organic
disease of the brain through analysis of the patient’s personality, memory, education and abstructional
ability.
Appearance
 Generally assess
o State of the patient – apathy, disturbed patient, agitated patient or confusion
o Attention of the patient
o Interest in the surroundings
o Grooming – is the patient well groomed or unkempt.
o The hair and nails
Behaviour
 Any unusual behaviour should be noted
Communication
 Flow of the conversation

 Appropriateness of the conversation
 Is the patient silent, monosyllabic or talkative
 Content of speech
 Flight of ideas (rushing stream of ideas with some connection)
 Thought disorder (remarks with on logical connection)
 Perseveration (patient keeps repeating your questions)
 Aphasia
 Neologisms (strange words)
 Word salad (words stuck together oddly)
Consciousness
Consciousness is a state of normal cerebral activity in which the patient is aware of both self and
environment and responds to internal changes and external environmental changes. Sleep is a normal
variation in consciousness. Drowsiness, stupor
Coma
Coma is a state of altered cerebral activity/function. In a patient with coma, history is of great importance. It
is essential to discover the mode of onset whether is gradual or sudden. Coma can be divided into six
categories
1. Alert
2. Drowsy but response to verbal stimulation
3. Unconsciousness, no response to verbal commands but withdrawal response to pain
4. Unconscious with flexion of upper and lower limbs to pain (decorticate)
5. Unconscious with hyperextension of upper and lower limbs to pain (decerebrate)
6. Unconscious with no response.
The Glasgow coma scale is used to grade the conscious level numerically to assess deterioration or
improvement. The best score is 15 and the worst is 3
Glasgow Coma Scale (GCS)
Eye-opening Best Verbal response Best Motor response

Spontaneous 4 Oriented 5 Obeys commands 6
To speech 3 Confused 4 Localizes pain 5
To pain 2 Inappropriate 3 Normal withdrawal 4
None 1 Incomprehensive 2 Abnormal flexion 3
None 1 Abnormal extension 2
None 1
Causes of Coma
A. Metabolic
 Hypoglycaemia, diabetes mellitus, renal failure, hepatic failure, hypothermia, hypothyroidism,
cardio-respiratory failure, hypoxic encephalopathy
B. Drug over dosage - drugs, alcohol
C. Structural
 Diffuse
o Meningitis, encephalitis, cerebral malaria, head injury, sudarachnoid haemorrhage, epilepsy,
hypertensive encephalopathy
 Focal
o Supratentorial - cerebral haemorrhage, cerebral infarction with oedema, subdural haematoma,
extradural haematoma, tumours and cerebral abscess
o Subtentorial - cerebellar haemorrhage, pontine haemorrhage, brainstem infarction, tumour and
cerebellar abscess
Basic neurological examination in a patient with coma includes: -

1) Assess level of consciousness (Glasgow coma scale)
2) Look for signs of head injury – local bruising, fractures, penetrating wounds, bleeding from nose and
ears.
3) Splint the neck
4) Check for neck stiffness if no neck injury is present (causes of coma with neck stiffness include –
subarachnoid haemorrhage, meningitis, encephalitis, intracerebral haemorrhage and cerebral
malaria)
5) Examine the pupils
6) Examine ocular movements
7) Examine the limbs – posture, tone and movement
8) Reflexes and plantar response
9) Fundi

Delusions
 Are false beliefs that are overvalued and unshakable

 They can be delusions of persecution (paranoid delusions), grandeur or poverty (depressive delusions).
 There are also nihilistic delusions of love (erotomania), infidelity, influence (alienation) and reference.
 Denote psychiatric illness, organic psychoses (confusional states, dementia and alcohol and drug-
induced), organic illnesses (endocrine disorders, S.L.E), functional psychoses (schizophrenia,
depression, mania), psychogenic psychoses and hysteria.
Emotional state
 Observe if the patient has: - elation, euphoria, despair, depression and depersonalisation
 Inquire about the sleep pattern – insomnia or hypersomnia
 Ask about dreams
Illusions
 Are false perceptions of a real object and are common in psychiatric illnesses e.g. acute confusional
states.
Gait
Assessment of the patient’s gait is of great significance in examination of the nervous system because
alteration in the position of the patient during walking follows neurological disorders affecting the cerebrum,
extra-pyramidal system, cerebellum, spinal cord, posterior roots, peripheral nerves, muscle disorders, and
bonny deformities. It may also result from hysteria.
Gait Description Lesion/causes

Spastic gait  Patient walks on a narrow base dragging the feet along  Corticospinal lesions
and has difficulty in bending knees  Spinal cord disease
(pyramidal tracts)
 Paraplegia
Hemiplegic  Is a spastic type of gait involving one limb  Pyramidal lesions
gait  The patient leans towards the opposite healthy side
Scissors  There is medial rotation of the legs which cross each other  Cerebral lesions
gait while walking  Bilateral pyramidal
 Has excessive spasm or contracture of the adductor lesions
muscles
Shuffling  Patient walks with the head and body bend forwards  Parkinson’s disease
(Festinant) (flexion dystonia) (Prkinsonism)
 Makes quick, short shuffling steps as if trying to catch up
with gravity
 There is reduced or absent swinging movements of the
arms
 If patient is pushed forward (propulsion), backwards
(retropulsion) or sideways (lateropulsion), he/she is unable
to stop.
Stamping  Patient raises foot very suddenly and abnormally high,  Tabes dorsalis
gait jerks it forward and brings it to the ground with a stamp (posterior column
(sensory often with the heel landing first. lesions)
ataxia)  Situation is made worse with eyes closed

Gait Description Lesion/causes
Cerebellar  Patient walks on a broad and irregular base and keeps  Cerebellar lesions
ataxia then feet widely apart swinging the legs irregularly as a
(drunken or drunken person.
reeling gait)  In unilateral lesions, there is tendency of the patient to fall
towards the side of the lesions due to loss of muscle to on
the side
High  Patient raises foot to overcome foot drop and avoid tripping  Polyneuropathy
stepping over his toes. On landing the toes reach the ground first  Poliomyelitis
gait due to weak doriflexors  Common peroneal
 There is no ataxia nerve palsy
Waddling  Patient walks with a gait like that of the duck  Congenital dislocation
 Body is usually tilted backwards with increased lumbar of the hip
lordosis and the feet are planted widely apart.  Osteomalacia
 The body swings from side to side with each step taken  Myopathies
with the heels and toes being brought down simultaneously  Muscular dystrophy
 Has difficulty maintaining trunkal and pelvic posture.  Advanced pregnancy
Hysterical  Irregular bizarre type of gait that is altered form time to time 
gait and is exaggerated when the patient is being observed
Dancing  Jerky involuntary movement and patient walks on a wide 
gait base with the steps kept in an irregular fashion e.g. chorea
Hallucinations
 Are false impressions referred to special senses (hearing, seeing, smelling, taste)
 Evident in temporal lobe epilepsy (partial seizures), delirium tremens (associated with withdrawal from
alcohol), migraine, functional psychoses, grief reactions and hysteria
Intelligence
 Obtaining information based on educational and occupational history and assessment of general
knowledge can assess intelligence of a patient.
Memory
 Memory is a higher mental function concerned with the ability to grasp and retain new information. It
involves adequate processing of the input (visual, auditory, olfactory, sensory), registration and
appropriate recall. Memory may be from internalised experience. Loss of memory is termed amnesia.
Antegrade amnesia
 Is loss of recent memory of ideas or images

 Indicates the severity of organic brain disorders (but not necessarily permanent)
 Effected by the Limbic system that has a well-established connection with memory storage. The
hippocampus is responsible for initial retention while the mammillary bodies do the retrieval-scanning
process.
Causes
a) Gross dementia
b) Epileptic seizure
c) Head injury
d) Cerebrovascular disease
e) Dysphasia
f) Depression
g) Acute confusional states
h) Wernicke-Korsakoff syndrome
Retrograde amnesia
 Inability to recall past or remote events
Examination
 Immediate recall
o Ask patient to repeat back a series of numbers in the order given
o Or repeat a sentence said
o Recall six digits forwards and four digits backwards
 Recent memory (antegrade)

o Test orientation in person, time and space
o Tell the patient a short story and ask him/her to repeat it – about four times
o Recent current affairs
 Remote memory (retrograde)

o Forms part of permanent store of information in the brain
o Difficult to test
o Defects denote failure of retrieval
Orientation
 Assess the orientation of the patient in person, time and place by posing direct questions.
Speech
Speech formation is a cortical function with centres in the dominant hemisphere. The centres are situated in
form of a quadrilateral consisting of four areas – visual area (calcarine sulcus in the occipital lobe), auditory
area (superior temporal gyrus), and Broca’s area (3rd frontal convolution) and writing area (2 nd frontal
convolution).
The muscles of articulation are the larynx, palate, tongue and lips that are innervated by the cranial nerves.
Defects of speech may originate from cortical centres (aphasia) or in the peripheral motor mechanisms
(dysarthria). The defects include difficulties in articulation, fluency, verbal comprehension, naming, reading,
writing and repetitions.
Aphasia
 Disturbance in ability to sue language

 May be motor (loss of ability to express) or sensory (loss of ability to comprehend) or global (both
expressive and comprehensive aphasia)
 Receptive aphasia can be auditory (word deafness) or visual (word blindness)
 Reception and interpretation of speech depends on the function of vision and hearing.
 Lesions in front of the central sulcus (Rolantic fissure) are termed anterior aphasic syndromes affecting
articulation and fluency while those behind the sulcus are called posterior aphasic syndromes affecting
reading and writing.
Causes of Aphasia
a) Injury to speech centres

b) Thrombosis
c) Tumours
d) Abscess
e) Degeneration
Motor aphasia
 Inability to speak or write (dysgraphia)

 Patient may: -
o Find difficulty in constructing sentences
o Use wrong words
o Repeat words
o Have parapharasia (describe objects instead of naming)
Sensory aphasia
 May be auditory with inability to comprehend words heard or visual where there is inability to
understand the written words (agassia).
Examination
 Ask the patient to form written instructions
 Ask the patient to write, read and speak
 Test ability to comprehend other symbols e.g. mathematical or musical symbols
Global aphasia
 Both reception and comprehension centres are affected and the patient losses ability to understand.
Dysathria
Dysarthria is the defect articulation of speech due to incoordination of the peripheral mechanisms.
Stammering is a developmental disorder and lalling (―baby speech‖) is a congenital or infantile defect that
results in one speaking as a baby by dropping all difficult consonants. There are four types of dysarthria –
cerebellar dysarthria, pseudobulbar dysarthria, bulbar dysarthria and cortical dysarthria.
Cerebellar dysarthria
 The patient speaks slowly and deliberately scanning and emphasizing syllable by syllable with loss of
normal rhythm e.g. ―ar-til-ler-y‖ for artillery.
 It results from bilateral lesions of the cerebellar or its connections in the brain stem.
Pseudobulbar (spastic) dysarthria
 Results in slurring of individual syllables with loss of precision pronunciation as witnessed in alcoholic
intoxication e.g. ―conshishushon‖ for constitution.
 Results from bilateral lesions of the corticospinal fibres (upper motor neurone) supplying the muscles of
the face, larynx, tongue and respiration.
 Are supranuclear lesions above the brain stem nucleus

 Is a feature of pseudobulbar palsy together with brisk jaw jerk, dysphagia to liquids, bilateral Babinski’s
sign and aphonia.
Bulbar dysarthria
 Lower motor neurone lesion affecting speech musculature

 There is non-specific slurring of speech
 Bulbar palsy has dysphagia to solids and fluids are easily regurgitated back.
Cortical dysarthria
 Irregular hesitance in word production with difficult abstraction and voluntary movement of the lips and
tongue (orofacial apraxia) associated with aphonia.
Causes of dysarthria
a) Cerebellar lesions
b) Brain stem lesions
c) Pyramidal tract lesions
d) Cortical lesions
Examination
 Use nonsense syllables such as ― papapa‖ or ―tatata‖ (tests movement of lips and jaws), ―sasasa‖ (tests
the tip of the tongue) and‖ kakaka‖ (body of the tongue) by combing them e.g. ―patakapataka‖ or
―faxasafasaxa‖.
Dysphonia
Dysphonia is a disturbance of sound production, which leads to a hoarse or soft voice. It is mainly due to
local abnormalities of the larynx or problems with the recurrent laryngeal nerve.
Aphonia
Aphonia is loss of voice due to diseases of the larynx and vocal cords (bilateral adductor palsy).
Skull Examination
Signs of meningeal irritation
1) Neck stiffness/rigidity
 This is increased resistance to passive flexion of the neck

 There may be head retraction
 Examination
o Passively flex the head on the chest
o Flexion causes pain in the posterior part of the neck
o Movement is resisted by spasm in the extensor muscles of the neck
o Note the tightness of the neck muscles

2) Kerning’s sign
 Depends on traction of the inflamed meninges and spinal nerves

 Examination
o With the patient lying supine in bed
o Flex the hip fully
o Flex the knee joint at about 900
o Passively extend the patient’ knee on either side
o There is pain and spasm of the hamstrings and extension movement can not go beyond 90 0
Figure 3.1: Kerning’s sign
3) Brudzinski’s sign
 Depends on traction of the inflamed meninges and spinal nerves

 Examination
o Flex the patient’s head on the chest
o The patient draws up the lower limbs
Figure 3.2: Brudzinski’s sign

Lesson 4: Examination of the Cranial Nerves (I-VI)
1) Perform examination of the cranial nerves I - VI

2) Interpret findings on examination of the cranial nerves I - VI
1.0 Introduction
There are 12 pairs of cranial nerves that facilitate communication within the body. Of the 12 pairs, 2 pairs
arise from the neurone cell bodies located in the fore brain and ten pairs from the mid brain and brain stem.
Cranial nerves are designated by Roman numerals (which represent the order in which the nerves are
positioned from the front of the brain to the back) and names that indicate the structures innervated by the
specific nerves. The I and II cranial nerves arise from the fore brain and consist of more central nervous
tissue than peripheral nerve tissue. The III to XII cranial nerves arise from the brain stem to innervate facial,
cranial and cervical tissues.
Majority of the cranial nerves are mixed nerves containing both sensory and motor fibres. The cranial
nerves associated with special senses e.g. olfactory, auditory and optic nerves contain sensory fibres only.
The cell bodies of sensory neurones are located in the ganglia near the sensory organ and not in the brain.
Pathologies of cranial nerves can occur due to disease involvement of their intracranial or extracranial
courses and at the sites of origin in the brain and brains stem
Figure 4.1: Cranial Nerves

Figure 4.2: Functions of Cranial Nerves

Table 4.1: Pathway and Function of Cranial Nerves
No Name Motor / Origin Nuclei Function
sensory
I Olfactory nerve Purely Anterior olfactory nucleus Transmits the sense of smell; Located in
Sensory olfactory foramina of ethmoid
II Optic nerve Purely Lateral geniculate Transmits visual information to the

Sensory nucleus brain; Located in optic canal
III Oculomotor nerve Mainly Midbrain Oculomotor nucleus, Innervates levator palpebrae superioris,
Motor Edinger-Westphal superior rectus, medial rectus, inferior
nucleus rectus, and inferior oblique, which
collectively perform most eye
movements; Located in superior orbital
fissure
IV Trochlear nerve Mainly Midbrain Trochlear nucleus Innervates the superior oblique muscle,
Motor which depresses, rotates laterally
(around the optic axis), and intorts the
eyeball; Located in superior orbital
fissure
V Trigeminal nerve Both Pons Principal sensory Receives sensation from the face and
Sensory trigeminal nucleus, Spinal innervates the muscles of mastication;
and trigeminal nucleus, Located in superior orbital fissure
Motor Mesencephalic trigeminal (ophthalmic nerve - V1), foramen
nucleus, Trigeminal rotundum (maxillary nerve - V2), and
motor nucleus foramen ovale (mandibular nerve - V3)
VI Abducens nerve Mainly Posterior Abducens nucleus Innervates the lateral rectus, which
Motor margin abducts the eye; Located in superior
of Pons orbital fissure
VII Facial nerve Both Pons Facial nucleus, Solitary Provides motor innervation to the
Sensory (cerebell nucleus, Superior salivary muscles of facial expression and
and opontine nucleus stapedius, receives the special sense of
Motor angle) taste from the anterior 2/3 of the tongue,
above and provides secretomotor innervation
olive to the salivary glands (except parotid)
and the lacrimal gland; Located and
runs through internal acoustic canal to
facial canal and exits at stylomastoid
foramen
VIII Vestibulocochlear Purely Lateral Vestibular nuclei, Senses sound, rotation and gravity
nerve (or auditory- Sensory to CN VII Cochlear nuclei (essential for balance & movement);
vestibular nerve or (cerebell Located in internal acoustic canal
statoacustic nerve) opontine
angle)
IX Glossopharyngeal Both Medulla Nucleus ambiguus, Receives taste from the posterior 1/3 of
nerve Sensory Inferior salivary nucleus, the tongue, provides secretomotor
and Solitary nucleus innervation to the parotid gland, and
Motor provides motor innervation to the
stylopharyngeus (essential for tactile,
pain, and thermal sensation)[citation needed].
Some sensation is also relayed to the
brain from the palatine tonsils.
Sensation is relayed to opposite
thalamus and some hypothalamic
nuclei. Located in jugular foramen

No Name Motor / Origin Nuclei Function
sensory
X Vagus nerve Both Posterol Nucleus ambiguus, Supplies branchiomotor innervation to
Sensory ateral Dorsal motor vagal most laryngeal and pharyngeal muscles;
and sulcus of nucleus, Solitary nucleus provides parasympathetic fibers to
Motor Medulla nearly all thoracic and abdominal
viscera down to the splenic flexure; and
receives the special sense of taste from
the epiglottis. A major function: controls
muscles for voice and resonance and
the soft palate. Symptoms of damage:
dysphagia (swallowing problems).
Located in jugular foramen
XI Accessory nerve Mainly Cranial Nucleus ambiguus, Controls muscles of the neck and
(or cranial Motor and Spinal accessory nucleus overlaps with functions of the vagus.
accessory nerve or Spinal Examples of symptoms of damage:
spinal accessory Roots inability to shrug, weak head movement,
nerve) velopharyngeal insufficiency; Located in
jugular foramen
XII Hypoglossal nerve Mainly Medulla Hypoglossal nucleus Provides motor innervation to the
Motor muscles of the tongue and other glossal
muscles. Important for swallowing
(bolus formation) and speech
articulation. Located in hypoglossal
canal
2.0 The Olfactory Nerve (Cranial nerve I)
The olfactory nerve is a sensory nerve with olfactory nerve fibres arising from sensory cells in the olfactory
epithelium in the nasal cavity. It passes through the cribriform plate of the ethmoid bone into the cranial
cavity to reach the olfactory bulb (1st order neurones). The first order neurones synapse with the second
order neurones that transmit the impulses to the olfactory area of the cerebral cortex (the uncus and the
parahipocampal gyrus). The second order neurones travel in two directions with one group moving medially
and the other laterally through the temporal lobe (the reason for hallucinations of smell in temporal lobe
epilepsy).
Figure 4.2: Olfactory Nerve
.
Examination
Requirements
 3 small bottles containing pungent odours or common bedside substances e.g. soap, lemon peels,
pineapple
Testing/Examination
 Ask the patient to close the mouth and eyes

 Test each nostril separately while closing the opposite nostril by placing a finger over it.
 Present the bottles closer to the nostril of the patient and ask them to identify the substances on
inhalation.
 Do not use irritating substances such as ammonia and acetic acids because they will stimulate the
trigerminal nerve.
Interpretation
1. Hallucinations – e.g. the aura stage in temporal lobe epilepsy (TLE) and psychosis
2. Anosmia – loss of sensation of smell
Causes
a. Local conditions – coryza, polyps, atrophic rhinitis and sinusitis
b. Neurological conditions
i. Head injury – fractures of the anterior cranial fossa
ii. Tumours – frontal lobe
iii. Meningitis/TB meningitis
iv. Nerve disorders
c. Hysteria
3. Paranosmia – pleasant odour feels offensive and vice versa e.g. psychoneurosis.

The Optic Nerve (Cranial Nerve II)
The optic nerve is considered to be a forward extension of the brain that carries visual impulses from the
retina to the lateral geniculate body acting as an afferent pathway for papillary reflexes (from the
occulomotor nerve).
Sensory fibres from the retina pass behind as optic nerve entering the cranial cavity through the optic
foramen. Nerve fibres from both sides (left and right eye) meet at the optic chiasma (is in close contact with
pituitary gland) where the medial (nasal) half of fibres from each retina representing the temporal field
decussate. The fibres from the outer (temporal) half representing the nasal field remain on the same side.
This results in formation of optic tracts containing fibres from the outer half of the retina from the same side
and inner half of the retina on the opposite side.
The optic tracts pass posteriorly to the lateral geniculate body on the same side from where optic radiations
emerge and pass through the posterior limb of the internal capsule into the calcarine cortex of the occipital
lobe.
Figure 4.4: Optic Nerve

Examination
Test for
1. Visual acuity
2. Visual field
3. Colour vision
4. Fundoscopic examination
Visual Acuity (V)
 Use the Snellen’s chart, which is constructed so that the top letter is visible to the normal eye at 60m
and at subsequent lines at 36m, 24m, 18m, 9m, 6m and 5m respectively.
 Examine each eye separately while blocking the other eye using the hand.
 The patient should be 6m away from the chart.
 Visual acuity (V) is recorded as d/D; where d is the distance at which the letters on the Snellen’s chart
are read by the patient (usually 6m) and D is the distance at which the letters should be read by the
normal eye. For example the visual acuity of normal eyes will be R6/6, L6/6.
 If the visual acuity is less than 1/60, it can be recorded after using: -
o Counting fingers (CF)
o Hand movements (MH)
o Perception of light (PL)
o No perception of light (No PL)
 Myopia (short sight) – use concave lens for correction
 Hypermetropia (hyperopia) – long sighted, use converging lens for correction
Visual field (VF)
This is the full extend of ones vision. The area of the retina and the margins of the orbit, nose and check
limit the visual field and. The extend of the visual field varies with stimuli used, that is, the field is larger to
larger objects or brightly illuminated objects than to smaller ones or dimly illuminated objects.
Figure 4.5: Visual Field
Examination
1. Confrontation
 Compares the patient’s visual filed with the examiner’s field
 Let the patient be 1m away from the examiner
 The eyes of the patient and those of the examiner should at the same level
 Look directly at the patient’s eyes as you instruct the patient
 Test both eyes at the same time (binocular) or separately (monocular)
 Test all the four directions – upwards, downwards and sideways.
Figure 4.6: Visual Field
2. Red pin test

 Outlines the central filed
3. Perimetry
 Mapping out of the visual filed using a perimeter
 Changes in the visual fields can be: -
Pathologies
1. Central scotoma – loss of vision in the centre of the field

2. Paracentral scotoma – seen in diseases of the choroids, retina, glaucoma, alcoholism and vitamin B12
deficiency.
3. Heminopia – loss of sight in one half of the visual field.
4. Homonymous heminopia – loss of sight in same half of both fields
5. Quadrantanopia – blindness in one quadrant of the visual filed
6. Super or inferior attitudinal heminopia – loss of sensations in the upper or lower halves respectively. It is
encountered in optic nerve damage (ischaemia and trauma) and occipital lesions (gives bilateral
lesions).
7. Bi-temporal – loss of vision in the temporal halves. Seen in lesions affecting the optic chiasma such as
tumours of the pituitary gland, inflammation and trauma.
8. Bi-nasal – affects the nasal fields and results from lesions of the optic fibres and open angle glaucoma.
9. Concentric constriction seen in papilloedema, cortical lesions, retinal disorders (retinitis) and hysteria.
Colour Vision
 Use the pseudo-isochromatic plate with multiple culoured dots outlining certain digits (ishihara).
 The common deficiencies include: -
o Red-green deficiency (an inherited sex-linked recessive condition)
o Blue-yellow deficiency
o Total colour blindness (rare)
o Acquired causes – vascular and optic nerve diseases

Fundoscopic Examination
 Use the ophthalmoscope to examine the fundus, optic disc and retinal blood vessels
 The abnormalities include: -
o Papilloedema
o Features of inflammation
o Demyelination
o Vascular disease
o Atrophy
o Haemorrhages
Third (Occulomotor), Fourth (Trochlear) and Sixth (Abducent)
The third, fourth and sixth cranial nerves innervate the external eye muscles (external ocular muscles) and
the pupil (third nerve only).
Eye movements
Eyes normally move symmetrically with the visual axes meeting at a point, which the eyes are directed (the
conjugate). The movement depends on the brain stem integration of the third, fourth and sixth cranial nerve
nuclei. The ocular movements seen are: - abduction, adduction, elevation, depression (cardinal movements
with the eyes in mid-gaze position), diagonal movements and rotary movements (internal rotation and
external rotation). Infranuclear (LMNL1) of the third, fourth and sixth cranial nerves affects individual
muscles/groups of muscle while supranuclear (UMNL2) causes paralysis of conjugate movements of the
eyes.
Principal Occular muscles

Muscle Innervation Function
1. Superior rectus Occulomotor Elevate the eye (with the eye in abduction)
2. Inferior rectus Occulomotor Depress the eye (with eye in abduction)
3. Lateral rectus Abducent Abduct the eye
4. Medial rectus Occulomotor Adduct the eye
5. Inferior oblique Occulomotor Depress the eye (with eye in adduction)
6. Superior oblique Trochlear Elevate the eye (with eye in adduction)
Disturbances of ocular movements
1. LMNL (infranuclear)
 Third nerve palsy, fourth nerve palsy, sixth nerve palsy
2. UMNL (supranuclear)
 Conjugate gaze palsies
 Lateral gaze palsy, upward gaze palsy, downward gaze palsy
 Internuclear
 Complex gaze palsy – convergence nystagmus
3. Cerebellar
 Nystagmus
4. Extrapyramidal
 Slowed and interrupted smooth pursuit movements
1 Lower motor neurone lesion

2 Upper motor neurone lesion
Occulomotor Nerve (CN III)
Anatomy
The third cranial nerve originates from the nuclei (in close relation to red nuclei, substancia nigra and
pyramidal pathways) in the midbrain. It runs anteriorly passing through the carvenous which is lateral to the
internal carotid artery and enters the orbit via the superior orbital fissure to supply the superior rectus (SR),
inferior rectus (IR), inferior oblique, medial rectus and the levator palpebrae supirioris. The third cranial
nerve has parasympathetic fibres that supply the sphincters of the pupils.
Figure 4.7: Occulomotor Nerve
Examination
 Patient stabilizes head looking directly ahead at the examiner

 Ask patient to move eyes only to follow an object in the examiner’s hand
 Move the object in different directions (always move back to the centre before executing the next
movement)
Figure 4.8: Examination of Oculomotor nerve
 Examine for the papillary response

o Reaction to light
 A partially dark room is preferable
 Patient holds both eyes open and fixes gaze straight ahead
 Examine each eye separately
 Approach with a pen light beam from the side and shine the light on the pupil
 Observe the response
o Accommodation
 Patient fixes gaze at an object directly ahead at a distance
 Hold an object at 10-12 cm from the patient’s nose
 Ask patient to adjust focus from the distant object to the near one
 Observe movement of the pupils
 Accommodation is lost in midbrain lesions, neurosyphilis, encephalitis and diabetes mellitus.
Pupil Examination
 Compare the size in bright and dark lighting
 Observe the shape and contour
 Check for mobility with the reaction to light and accommodation
Ocular nerve palsy
 Eye deviated downwards and outwards

 Ptosis
 Pupils are dilated and fixed
 Papillary abnormality
 Squint
 Diplopia
Trochlear Nerve (IV)
Is the smallest cranial nerve and it originates form a nuclei in the midbrain just below the third cranial nerve.
Its nucleus is adjacent to the aqueduct of Sylvia. The nerve leaves the brain on the posterior aspect and
runs through the cavernous sinus to the orbit via superior orbital fissure to supply the superior oblique
muscles.

Examination
 Ask patient to move eyes only to follow an object in the examiner’s hand as it is moved upwards
Trochlear nerve palsy

 Impaired downward movement
 Diplopia
 Squint (rare)
Abnormalities
Abnormality Description Associated Causes

features
1. Nystagmus  Involuntary rhythmical  Vertigo  Vestibular system lesions
oscillatory movements of  Vestibular-cerebella connection
the eye (brain stem)
 Can be horizontal, vertical,  Drugs (benzodiazepines,
rotary phenytoin, barbiturates)
 Are jerky movements
 Observe rate, rhythm and
amplitude
2. Ptosis  Downward and lateral  Dilated  Third nerve palsy
displacement of the eyes pupils
 Loss of
conjugate
3. Strabismus  Abnormal ocular  Dizziness  Ocular nerve palsy
(squint) movement where visual  Instability  Trochlear nerve palsy
axes do not meet at a point  Limited  Abducent nerve palsy
of fixation. movement
 Paralytic squint I due to  Diplopia
paralysis (weakness of  False
muscles). orientation
 Non-paralytic of field of
(concomitant) squint is due vision
to misalignment of axes
and not muscle weakness.

Abducent Nerve (VI)
Arises from the lower pons in the midbrain leaving the brain at the junction between the pons and medulla
and runs the longest intracranial path. It passes forwards and laterally lying over the temporal lobe to pierce
the dura at dorsum sella and enters the cavernous sinus passing on the lateral aspect into the orbit through
the superior orbital fissure to supply the lateral rectus muscles. The facial nerve loops around the abducent
nucleus.
Examination

 Ask patient to move eyes only to follow an object in the examiner’s hand as it is moved laterally
Abducent nerve palsy

 Impaired lateral movement
 Diplopia
 Squint
Trigerminal Nerve (V)
Fifth cranial nerve is a mixed nerve containing both motor and sensory fibres. It originates from the lateral
aspect of the inferior surface of the pons via two roots (a larger sensory root and a small motor root). The
two roots pas forwards in the posterior fossa into a cavity in the dura matter where the sensory root expands
forming the trigerminal (gasserian) ganglion that gives rise to three large nerve trunks; - 1st division
(ophthalmic), 2nd division (maxillary) and 3rd division (mandibular). The motor root fuses with the mandibular
branch/trunk.
The trigerminal nerve supplies sensation to nasal mucosa, hard and soft palate, anterior 1/3 of the tongue,
and the buccal mucosa. The motor part innervates the temporalis, masseter, medial and lateral pterygoids
and tensor veli palatini.
The sensory root divides at the pons and fibres conducting impulses for light touch and posture enter the
principal sensory nucleus in the pons, and those for pain and temperature pass downward into the spinal
cord reaching the cervical segments. The ophthalmic division enters the lowest part and the maxillary at the
highest.

Ophthalmic Division
 Supplies the conjunctiva, conjunctival surface of the lower eye lids, lacrimal glands, medial part of skin
of the nose, upper eye lids, fore head and scalp (up to the vertex region).
 Lesions of the ophthalmic division lead to: -
o Loss of cutaneous/corneal sensitivity
o Trophic changes in cornea (neuropathic keratitis)
o Abolition loss of corneal reflex
Maxillary Division
 Supplies
Examination
Examination involves sensory reflexes and motor functions.
Sensory
 Light touch – use a cotton wisp over the patient’s anterior scalp and paranasal areas
 Pain – use pin prick over the fore head and paranasal areas
 Thermal – use cold and hot water tubes
 Test each of the divisions separately
Reflexes
 Corneal reflex
o Twist a light wisp of cotton into a fine hair
o Ask patient to gaze into a distance or the ceiling
o Steady your hand by gently resting your little finger on the patient’s cheeks
o Lightly touch the lateral edge of the cornea at the conjunctival margin (never touch the central
cornea)
o The patient blinks if the reflex is present and compare the two sides
OR
o Lightly blow a puff of air into each cornea in turn
o The patient blinks
 Jaw jerk
o Place a finger horizontally across the chin
o Ask patient to open mouth and relax
o Tap the finger with a patellar hammer
o Response – movement of the jaw (can be difficult to elicit in normal people)
o Affected with lesions at the pons and brain stem (spinal tract/nucleus)
Motor
 Ask the patient to clench their teeth

 Observe the temporal and messeter muscles that should stand out
 Then palpate the muscles
 In paralysis the muscles on the affected side fail to become prominent and on patient opening the
mouth; the mouth deviates towards the paralysed side as the healthy lateral pterygoid muscles push it.

Lesson 5: Examination of the Cranial Nerves (VII - XII)
1) Perform examination of the cranial nerves VII - XII

2) Interpret findings on examination of the cranial nerves VII-XII
Facial Nerve (CN VII)
The facial nerve contains mainly motor fibres that supply muscles of facial expression. It is accompanied on
its course by sensory fibres subserving taste.
The sensory fibres reach the external acoustic meatus and some stimulate secretion of saliva an others
convey taste impulses from anterior 2/3 of the tongue.
The facial nerve originates in the ventral part of the pons and its fibres pass backwards to loop around the
nucleus of the sixth cranial nerve before turning forward to emerge from the lateral aspect of the lower
boarder of the pons and runs medial to the eighth cranial nerve. It crosses the posterior fossa to enter the
petrous portion of the temporal lobe and runs to exit the skull at the stylomastoid fossa.
Before emerging from the skull it gives off parasympathetic lacrimal fibres and expands to form geniculate
ganglion, which contains cells of taste of taste fibres of the chorda tympani that supply the anterior 2/3 of the
tongue.
Within the facial canal the facial nerve gives off a branch to the stadepius muscle and after emerging from
the stylomastoid foramen it gives branches to stylohyoid muscle, digastric and occipitofrontalis. It then runs
forward and within the parotid gland it divides into a number of branches that innervate muscles of facial
expression including the buccinator and platysma.
Examination
General inspection
 Inspect the face for symmetry both at rest and during conversation
 Note any asymmetry, unequal movements, facial weakness, drooping on one side of the face or mouth
unable to maintain position until instructed to relax, the eye is widely open than normal, less
pronounced nasolabial fold and the furrows of the brows are smoothed out.
Motor function
 Ask the patient to shut eyes as tightly as possible

o Observe the affected side
o Attempt to open the eye while the patient attempts to keep it closed
 Ask patient to frown or raise eye brows
 Ask the patient to show upper teeth or smile and the mouth will be drawn to the healthy side
 Ask patient to whistle – patient is unable
 Ask the patient to puff out the cheeks and tap with the finger on each inflated cheek in turn. Air can
escape on the weak or paralysed side.
 Bell’s phenomenon
o The eyeball rolls upwards during attempted forced eye closure in a normal phenomenon, which is
usually preserved in lower motor neurone lesion of facial nerve.
Taste
 Use the four basic tastes – sweet, sour, salt and bitter
 Examination
o Rinse the patient’s tongue
o Apply the solution to the surface of the protruded tongue with a small swab or spatula
o Ask the patient to indicate the perception
o Rinse the tongue after each test before introducing the next solution
o Apply the bitter test last
Lesions of the facial nerve
1. Upper motor neurone lesion (UMNL)

2. Lower motor neurone lesion (LMNL)
3. Bell’s palsy
UMNL
 Affects muscles of the lower part of the face as the occipitofrontalis and orbicularis occuli muscles are
bilaterally innervated from the cortex.
 Arises mainly from vascular lesions of the brain
 Paralysis is evident on the opposite side of the lesion
 Facial reflexes are increased
LMNL
 There is complete paralysis of the whole side of the face

 The face is smooth and free from wrinkles
 Because the stadepius muscle is paralysed sounds on the affected side of the facial palsy may seem
unusually louder (hyperacusis)
 Loss of taste over the anterior 2/3 of the tongue implies damage of the seventh nerve in the facial
canal

Bell’s palsy
The nerve is affected either at or after it has left the stylomastoid foramen or sometimes in its course
through the temporal lobe. It is accompanied by oedema of the facial nerve within the facial canal. It is
common in arterial hypertension and viral infections. Exposure ton cold triggers the situation. Physical
examination reveals paralysis of the upper and lower parts of the affected side of the face. The eye on the
affected side cannot close and on attempting to do so the eyeball rolls upwards – Bell’s sign.
Vestibulocochlear Nerve (CN VIII)
The eighth cranial nerve supplies the internal ear, which has two functions of hearing and equilibrium. The
cochlear, which is supplied by the cochlear portion, is responsible for hearing while the semicircular canals;
the utricle and the saccule, which are responsible for equilibrium, are supplied by the vestibular component.
The structures concerned with equilibrium are concerned with recognition of position the head in relation to
gravity and its movements in space. The two parts run together from the internal acoustic meatus to the
lateral aspect of the pons. The eighth nerve lies on the lateral side of the seventh cranial nerve in the
posterior fossa.

Auditory fibres
The auditory fibres arise from the cochlear ganglion of the inner ears and enter the skull through the internal
auditory/acoustic meatus lying lateral to the seventh cranial nerve to enter the brainstem at the lower
boarder (cerebellar-pontine angle) to synapse with the ventral and dorsal cochlear nuclei. The second order
tracts after partial decussation ascend in the lateral lemnicscus and medial geniculate body terminating in
the superior temporal gyrus of the opposite cerebral hemisphere.
Vestibular fibres
Originate from the three semicircular canals, utricle and saccule. The fibres arise from the vestibular
ganglion and enter the internal auditory meatus to accompany the cochlear nerve to the upper medulla. It
terminates in a group of vestibular nuclei in the pons and medulla. Fibres from the medulla communicate
with the cerebellum. These fibres run upwards into the cortical centres in the posterior part of temporal
lobes and downwards in the vestibulospinal tracts communicating with the spinal cord to influence motor
activity for coordination of motor reflexes that maintain equilibrium. The vestibular nerve establishes
communication with the third, fourth and sixth cranial nerves.
Disturbances of the Cochlear system
 Deafness
 Abnormal auditory sensations - tinnitus, hyperacusis, recruitment and auditory hallucinations and
delusions
Deafness
Deafness is hearing loss
1. Conductive deafness
a. Congenital atresia of external meatus
b. Wax or foreign body in external meatus
c. Otitis media
d. Middle ear effusion
e. Trauma to the drum or osscicular chain
f. Otosclerosis
g. Chronic suppuration
h. Carcinoma of the middle ear
2. Sensorineural deafness
a. Genetic
b. Prenatal – rubella
c. Perinatal – hypoxia, jaundice
d. Trauma – noise, head injury, surgery
e. Infection – meningitis, measles, mumps, syphilis
f. Degenerative
g. Ototoxicity – aminoglycosides, diuretics, cytotoxics
h. Neoplasms
i. Idiopathic
Tinnitus
Tinnitus is persistent ―ringing in the ears‖. Patients usually describe the sounds as ―buzzing‖, ―hissing‖ or
―singing‖ sounds in the ear. It is a symptom of eighth nerve damage.
Causes
 Deafness
 Lesions of the internal ear
 Ischaemia of auditory apparatus secondary to anaemia
 Atheroma
 Postural hypotension
 High doses of quinine, salicylates, streptomycin
 Irritation of the eighth nerve
Hyperacusis
 Light sounds are heard with painful intensity

 Results from paralysis of stapedius muscle and facial nerve palsy
Recruitment
 Seen in sensorineurol deafness due to damage of cochlear e.g. in Meniere syndrome
Halluscinations/delusions
 Non-organic psychoses e.g. schizophrenia

 May occur in organic lesions
 Epileptic auras e.g. in temporal lobe epilepsy
Examination
 Instrument of examination is the tuning fork (C = 256). Tuning forks emit pure tones that enable
accurate information to be obtained in order to compare air-conducted hearing (AC) and bone-
conducted hearing (BC).
 Principles of tuning fork tests
o Tuning fork is used to test for vibration sensation in the skin
o In AC hearing sound traverses the outer and middle ear to reach the cochlear stimulating the
organ of Corti.
o In BC hearing sound traverses the skull bones to reach organ of Corti.
o Pathological conditions in the outer and middle ear reduce AC hearing but have no effect on BC
hearing (conductive deafness) while problems in inner ear or central pathways reduce both AC
and BC (perceptive deafness).
Tests
 Schwabach’s test
 Rinne’s test
 Weber’s test
Schwabach’s test
 Softy strike the tuning fork and place it on the patient’s mastoid
 Ask the patient to indicate when the sound becomes inaudible
 Then examiner should place the tuning fork on his/her mastoid
 If he/she can still hear the sound, then the patient’s BC is reduced (perceptive deafness)
Rinne’s test
 Compares AC to BC
 Softy strike the tuning fork and place it on the patient’s mastoid
 Ask the patient if the sound is audible and let him/her indicate to you when the sound becomes
inaudible.
 When the sound is inaudible place the tuning fork at the external auditory meatus
 Ask the patient if the sound is audible.
 In conductive deafness BC is normal and is greater than AC
 In perceptive deafness BC and AC will be impaired. If it is unilateral deafness, both AC and BC will be
increased in the normal ear. Air conducted sounds are heard twice as long as BC sound (that AC>BC)
that is positive result. If BC lasts as long as or longer than AC sounds (that is BC> AC) this is a negative
result – sign of conductive deafness.
 Air conducted sounds are heard twice as long as BC sound (that AC>BC) that is positive result. If BC
lasts as long as or longer than AC sounds (that is BC> AC) this is a negative result – sign of conductive
deafness.
Weber’s test
 Softly strike the tuning fork and place it in the midline of the skull
 Sound reaches both ears by bone conduction (bilaterally equal)
 Assess BC by testing lateralization of sound

 In conductive deafness, sound lateralizes poorly. If patient has unilateral perceptive deafness sound is
lateralized to the normal ear.
Disturbances of Vestibular system
 Vertigo
 Nystagmus
Vertigo
Vertigo is the unconsciousness of disordered orientation of the body in space. Patients describe it as
―dizziness‖, ―giddiness‖ or unsteadiness. In vertigo, external objects seem to be going round the patient.
Postural vertigo is associated with change of position.
Causes of Vertigo
1. Sudden onset e.g. acute viral labyrinthitis (vestibular neuritis)

2. With focal features – brainstem ischaemia (transient ischaemic attacks TIA), multiple sclerosis,
migraine, temporal lobe epilepsy
3. Trauma
4. Motion – motion sickness
5. Drugs – gentamycin, salicylates, quinine, antihypertensives
6. Infection of the middle ear
7. Systemic disorders – postural hypotension, syncope, cardiac dysrthymia
8. Carotid sinus hypersensitivity
9. Anxiety and panic attacks
10. Hyperventilation syndrome
Nystagmus
Is uncontrollable pendular movement of the eyes due to disturbance of visual function, disturbance of
labyrinth function and disturbance of central nervous system involvement of the visual pathways.
Tests
 Eye movements – check for nystagmus

 Hallipike’s manoeuvre – positional testing

o Ask patient to sit on the couch
o Ask the patient to turn the head 45o to the left or right.
o Suddenly lower the patient 30o below the horizontal
o Ask patient to describe what he/she is feeling
o Repeat for the other side.
 Fistula test
o Compress the tragus into the external meatus or insufflate air into the ear
 Romberg’s sign
o Ask the patient to stand with the feet together and stretch out the arms
o The patient should initially be allowed to open the eyes and later close them
o Observe the patient’s stability
o Patient with lesions of the posterior column of the spinal cord will sway or even falls
o Unilateral labyrinth dysfunction patient sways to the side of the lesion
o A patient with central dysfunction sways to both sides.
 Gait
o Ask the patient to walk with the eyes open
o Patients with unilateral vestibular pathology veer towards the affected side
o Patients with central pathology stagger a few steps in one direction veering to the other side.
Glossopharyngeal (CN IX)
Arises form a series of radicles from the posterior lateral sulcus of the medulla between the fibres of the
vagus and accessory nerves. It crosses the posterior fossa and leaves the brain on the lateral aspect to
emerge through the anterior compartment of the jugular foramen to supply motor f fibres to stylopharygeus
muscle that elevates the upper pharynx and sensory fibres to posterior 1/3 of the tongue, tonsils, pharynx
and taste fibres in the region. It carries impulses for chemo and baroreceptors and conveys
parasympathetic fibres to parotid gland. Plays a role are secretion of saliva.

Examination
 Sensory – test sensation on posterior 1/3 of the tongue

 Motor – palatal reflex/gag reflex
o Tickle the back of the pharynx and note reflex contraction and elevation
 Lesions of the nerve cause loss of taste (ageusia)
The Vagus Nerve (CN X)
 The vagus nerve contains both sensory and motor fibres

 Sensory fibres carry sensibility to part of the external ear and efferent impulses from the pharynx and
larynx and thoracic and abdominal viscera.
 Vagus nerve has two types of motor fibres – those innervating the thoracic and abdominal viscera via
parasympathetic ganglia and those that are an elongation of the grey matter and are situated deep in
the medulla.
 Its fibres are distributed through glossopharyngeal, vagus and accessory nerves to the supply the
muscles of the palate, pharynx and larynx.
 Vagus nerve leaves the medulla in series with the roots of the glossopharyngeal nerve (above) and the
accessory nerve below.
 Leaves the skull at the jugular foramen together with the accessory nerve and passes down the neck in
the carotid sheath entering the thorax where the right and left branches differ.
 It lies on the posterior surface of the root of lung and pass through the oesophageal opening of the
diaphragm to enter the abdomen.
 In the neck it gives off branches of the recurrent laryngeal nerve.
 The terminal branches of the recurrent laryngeal nerve innervate all the muscles of the larynx except
the cricothyroid, which is supplied by the external branch of the vagus nerve.
 The internal laryngeal branch is the principal sensory nerve of the larynx.

Examination
 Motor functions of the vagus

o Place the patient facing the light with the mouth open and introduce a tongue depressor.
o Note any difficult in deglutition or speaking. Note pronunciation of words ―eng― for ―egg‖, ―rum‖ for
―rub‖.
o Note difficult in swallowing and regurgitation of fluids.
o Note appearance of the soft palate and pharynx
o Watch the movements of the palate during phonation
o Ask the patient to phonate (say ―ah‖) and observe whether both sides of the soft palate are
elevated and note the symmetry
o Test palatal reflex by touching the soft palate on either side with a wooden spatula and observe
the response, which should be elevation of the soft palate in the midline.
o Test pharyngeal reflex (―gag‖ reflex) by tickling each side of the pharynx with a wooden spatula
and note movement
Lesions of the Vagus nerve
 Nuclear lesions can occur in posterior inferior cerebellar thrombosis, medullary tumours, motor neurone
disease and poliomyelitis. They are associated with paralysis of the soft palate, pharynx and larynx.
 Lesions in the posterior fossa occur at its emergence at from the medulla and its exit from the skull
(jugular foramen). Affects neighbouring cranial nerves – ninth, eleventh and twelfth. Commonly caused
by tumours.
 Lesions of the recurrent laryngeal nerve. The left branch runs a longer cause hence its highly
susceptible to damage.
o In thorax it can be compressed by – aortic aneurysm, mediastinal masses, enlarged mediastinal
glands (due to neoplastic metastasis).
o In the neck – trauma, pressure of enlarged deep cervical glands (malignant or inflammatory),
enlarged thyroid, carcinoma of the oesophagus
o Lesions of recurrent laryngeal nerve may cause total paralysis of the larynx, paralysis of abduction
of the vocal cord on the affected side.
The Accessory Nerve (CN XI)
Accessory nerve a pure motor nerve that arises from the medulla and spinal cord. The accessory portion
arises from cells in the lower part of the nucleus ambiguous and the spinal portion from cells in the anterior
horn cells of the grey matter of the 1 st to 5th cervical segments.
The spinal rootlets unite to form a trunk that ascends in the spinal canal to the foramen magnum where it
joins the accessory part to form a common single trunk that leaves the skull through the jugular foramen in
the same compartment with the vagus nerve. The accessory fibres join the vagus to supply the pharynx;
larynx and the spinal portions enter the neck to supply the trapezius and sternocleidomastoid muscles.
Examination
 Instruct patient to shrug shoulders upwards against examiner’s resistance (tests trapizius)
 Ask patient to turn the head to the side against the examiner’s resistance, repeat for the opposite side
(tests sternocleidomastoid muscles)
 Lesions
o Paralysis of the sternocleidomastoid muscles – the neck and head will be in an abnormal
position, weak rotation of the head
o Paralysis of trepizius – the shoulders are lowered on the affected side, scapulae become
rotated downward and outward, slight winging of the scapulae.
Hypoglossal Nerve (CN XII)
Hypoglossal nerve is a motor nerve of the tongue originating in the hypoglossal nucleus of the lower part of
the medulla emerging between the pyramid and olive and runs a short course across the posterior fossa
passing through the hypoglossal canal to leave the skull. In the neck it passes downwards and forwards
turning medially to reach the tongue.
Examination
 Ask patient to protrude the tongue and note if the tongue is in midline or deviated
 Ask patient to move the tongue from side to side
 Ask patient to close mouth and push out the cheeks with the tip of the tongue
 Check for any wasting, fasciculations, furring, tremors, involuntary movements
 Lesions may be in medulla/hypoglossal canal, tumours and motor neurone disease (bulbar palsy)

Lesson 6: Examination of the Motor System
1) Perform examination of the motor system

2) Interpret findings on examination of the motor system
1.0 INTRODUCTION
The motor system comprises examination of: -
a) The bulk of muscles (muscles bulk)

b) Movement and strength of muscles (muscle power)
c) Tone of the muscles (muscle tone)
d) Reflexes
e) Coordination
f) Involuntary movements
g) The gait
The voluntary activity of the motor system depends on the integrity of various parts of the nervous system.
Initiation of voluntary movements occurs at the motor cortex (precentral convolutions of the cerebral cortex)
and the impulses are carried along the pyramidal tracts (corticospinal tract, the upper motor neurone). The
pyramidal tracts pass through the internal capsule, mid brain, the pons and medulla. At the junction of the
medulla and spinal cord, the fibres partially decussate and descend down terminating in the internuncial
neurones in the grey matter of the spinal cord where they synapse with the anterior horn cells.
As the pyramidal tract passes through the brain stem, it gives fibres to the motor nuclei of the cranial nerves
with a second ray of fibres originating from motor nuclei of the brain stem as cranial nerves and from the
anterior horn cells of the spinal as peripheral nerves (lower motor neurones) that terminate in the muscles.
An intact sensory system is necessary for reflex movements.
The integrity of the motor function relies on the motor cortex, pyramidal tract, brain stem, mid brain, pons,
medulla, spinal cord, peripheral and cranial nerves
2.0 EXAMINATION
2.1. Muscle Bulk
Muscle bulk refers to the size of the muscles and it is primarily assessed clinically by inspection and
palpation of the muscles. The muscle bulk can be affected in various disorders of the neuromuscular
system.Abnormalities of the muscles bulk are atrophy or wasting, contractures and hypertrophy.
Symmetry is important, with consideration given to handedness and overall body habitus. Generalized
wasting or cachexia should be noted and may reflect systemic disease, including neoplasia. Some areas
can be adequately evaluated by inspection alone, such as the thenar and hypothenar regions or the
shoulder contour. Some areas, like the thigh, leg, arm and forearm, may be better evaluated by
measurement. These measurements can also permit assessment over time.
Severe atrophy strongly suggests denervation of a muscle (such as with LMN lesions). This usually begins
at least a week after acute injury and gets progressively worse with time (unless reinnervation takes place).
Atrophy due to LMN damage must be distinguished from that which occurs secondary to disuse. However,
there is usually a clear substrate for disuse (bed rest, cast, etc.) and there is little overall change in strength.
Unfortunately, patients who have limited functional reserve (such as those with prior neural disease or the
elderly) can be severely affected by disuse and deconditioning.
Muscle wasting or atrophy
 The muscles are smaller, softer and flabbier than the normal muscle when they are contracted
 When atrophy is accompanied by fibrosis the muscle feels hard and inelastic (e.g. muscular dystrophy
poliomyelitis). The muscles shorten and cannot easily be stretched passively (contractures).
Assessment of muscle wasting
1. Comparison of contralateral muscle groups

2. Taking measurements – take the circumference of the limbs at identical positions from a fixed bonny
point
3. Palpation
4. Qualitative
i. CT Scan – shows atrophy
ii. EMG - electromyography
iii. Ultrasound studies
Interpretation
Muscle wasting can be symmetrical or asymmetrical and localized or generalized.
Generalized wasting
 Malignancy
 Diabetes mellitus
 Chronic debilitating infections e.g. tuberculosis and HIV/AIDS
 Thyrotoxicosis
Localized wasting
 Injury or disease of joint (disuse)

o Arthritis of carpophalangeal joints leads to wasting of the interossei muscles
o Arthritis of first metacarpophalangeal joint causes wasting of the thenar muscles
 Myopathy (primary disease of muscles)
 Diseases of anterior horn cell (AHC) that is the motor neurone disease
 Poliomyelitis
 Syringomyelia
 Nerve disease (peripheral neuropathy).
Wasting of muscles due to neuromuscular disease may exhibit a characteristic distribution in the early
stages for example myopathy affects proximal muscles, motor neurone disease – distal muscles and
diabetes mellitus – extensor digitorum brevis and cauda equina (glutei). Wasting of small muscles of the
hand due to involvement of the nerve segment C8-11 is caused by lesions at different levels such as: -
1. Anterior horn cell (AHC) – motor neurone disease, poliomyelitis and syringomyelia
2. Anterior roots of spinal cord – cervical spondylosis, patchy meningitis and tumours
3. Brachial plexus – injury, cervical rib and bronchogenic carcinoma
4. Peripheral nerve – ulnar nerve injury
5. Others – rheumatoid arthritis

Hypertrophy
Hypertrophy occurs in response to continued excessive workloads e.g. occupational, athletic training or in
certain myotonic disorders.
2.2. Muscle tone
Muscle tone is the state of constant degree of tension in muscles at rest. It is s sort of reflex dependent on
the spinal reflex arc. Afferent fibres from primary and secondary endings of muscle spindles enter the spinal
cord and synapse with efferent fibres, which pass to the muscles. Muscle tone enables the joints maintain
the posture.
Muscle tone is regulated by pyramidal and extra pyramidal tracts with the movements being coordinated by
the cerebellum and the related tracts. An increase in muscle tone is called hypertonia while a reduction is
termed hypotonia.
Examination
 Handling limbs and moving them passively through the full range of flexion and extension at their
various joints assess tone.
 Encourage the patient to be fully relaxed during the examination
 Normally there is a slight degree of resistance during movement
 Nervousness, cold and pain may interfere with the examination process
Hypertonia
 Is increased muscle tone which can be described as spasticity or rigidity

 Hypertonia is spastic in pyramidal lesions and rigid in extrapyramidal ones.
Spasticity
 Occurs when the tone is more in one group of muscles (the agonists) compared to the antagonists
 Spasticity is stretch sensitive and velocity dependent
 Hypertonia due to corticospinal system lesion (upper motor neurone lesion, UMNL) is called spasticity
which describes a state of increased tone of ―clasp-knife‖ type where resistance to passive movement
increases initially and as the movement is continued the resistance falls away suddenly giving way like
opening up the blade of a pen-knife.
 Spasticity due to brain stem or cerebral lesion has a characteristic distribution where the upper limbs
are held in flexion and the lower limbs in extension with the feet in plantar flexion (physiological
extension).
Rigidity
 Rigidity is hypertonia resulting from lesions at the basal ganglia (extrapyramidal) leading an increase in
tone and resistance in all groups of muscles (both agonists and antagonists).
 There are two types namely lead-pipe rigidity and cog wheel rigidity.
 In lead-pipe rigidity, the resistance feels uniform throughout the full range of passive movement
 For cogwheel rigidity the resistance has less uniform (jerky) diminishing resistance resulting in jerky
steps. It is regularly or irregularly variable. It is enhanced by asking the patient to contrast another
muscle e.g. clench a fist on the opposite side (Jendrassink’s manoeuvre).

Causes of hypertonia
a) Upper motor neurone lesion (UMNL)

b) Brain stem lesions
c) Extrapyramidal disease e.g. Parkinsonisms
d) Catatonia
e) Dementia
f) Confused states
g) Hysteria
Hypotonia
 There is little or no resistance to passive movements of the limb when handles or shaken.
 The unsupported part flops about inertly.
 Hypotonic muscles are abnormally soft and flabby to palpation (flaccidity) and the range of movement at
the joint is increased.
Causes
a) Lower motor neurone lesion (LMNL) e.g. poliomyelitis

b) Lesions of afferent sensory pathways e.g. Tabes dorsalis
c) Peripheral nerve lesions – polyneuropathy
d) Cerebella disorders
e) Myoneural joint disorders – myasthenia gravis
f) Muscle disorders (myopathy)
g) Chorea
h) Sleep
i) Drugs (sedatives).
2.3. Muscle Power
 Muscle power is the strength of the muscles

 Watching the patient walk, stand up from lying and sitting positions, dressing and undressing or lightly
jumping or hopping can assess muscle power easily and reliably.
 The muscles can be assessed in groups or individually by comparing with the examiner’s own strength.
Grading of Muscle power (function) by Medical Research Council Scale
Grade 0 Complete paralysis

Grade 1 A flicker of contraction only
Grade 2 Power detectable only when gravity is excluded by appropriate postural adjustment
Grade 3 The limb can be held against the force of gravity but not against the examiner’s resistance
Grade 4 There is some degree of weakness (fair or moderate strength)
Grade 5 Normal power
Examination
 The patient performing certain manoeuvres against resistance offered by the examiner tests muscle
power.
 Observe the muscle and feel the muscle
The Upper limbs
1. Abductor pollicis longus – supplied by median nerve, C6, C7 (damaged in carpal tunnel syndrome)
 Patient abducts the thumb in a plane at right angle to index finger
2. Opponens pollicis
 Patient to touch the tip of the little finger with the point of the thumb
3. First dorsal interosseous (ulnar nerve)

 Patient abducts the index finger
4. Interossei (C8, T1) and lumbricals (C8, T1)

 Flexion of metacarpophalangeal joints
 Extension of distal interphalangeal joints
 Interossei abduct and adduct fingers
 Paralysis e.g. ulnar nerve palsy ―Claw-hand‖ deformity.
5. Flexors of the fingers

 Ask patient to squeeze your fingers (index and middle fingers)
6. Extensors of the wrist (radial nerve)

 Ask patient to make a fist
 Try to forcefully flex the wrist against patient’s effort
 Ask patient to grasp something firmly
 Paralysis – radial nerve palsy wrist drop
7. Flexors of the wrist

 Patient to squeeze examiner’s fingers
 Let patient make a fist and try to overcome wrist flexion
8. Brachioradialis (C5)
 Patients arm midway between prone and supine
 Ask patient bend forearm while you oppose the movement by grasping the hand
 The muscle stands out prominently at the upper part
9. Biceps (C5)
 Patient forearm in full supination
 Patient to bend forearm
10. Triceps (C7)

 Patient to stretch out the forearm
11. Supraspinatus (C5)

 Lift the arm straight at right angle to the side
 Offer resistance during the after the first 30 degrees (remaining 60 degrees)
12. Deltoid
 Lift the arm (abduct) straight at right angle to the side
 Offer resistance during the first 30 degrees
 Abduct the arm forwards and backwards
13. Infraspinatus (C5)

 Push the arm backwards with the elbow held by the side and flexed at a right angle
14. Pectorals
 Patient stretches the arms out in front
 Let them clasp their hands together as the examiner tries to hold the apart
The Trunk
1. Serratus anterior
 Patient unable to elevate the arm above a right angle
 Ask patient to push against the wall with the hands while the arm is lifted forwards
 The scapula is ―winged‖ when the muscle is paralysed (scapula projects out)
2. Latissimus dorsi
 Patient clasps the hands behind their backs
 Ask them to move the arms upwards and downwards
3. Babinski’s ―rising up sign‖

 Inability to sit up in bed from supine position without the aid of the arms
 Paralysis of anterior abdominal muscle leads to displacement of the umbilicus when patient
attempts sitting up
 In spastic paralysis the affected leg rises first (not seen in hysteria)- Babinski’s sign
4. Beevor’s sign
 Umbilicus moves upwards in lower segment paralysis
 Umbilicus is pulled downwards in upper segment paralysis
5. Erector spinae
 Ask patient to lie prone and try to extend the head by extending the neck and back
The Lower limb
1. Extensors of the hip

 Extend the knee
 Lift patient’s foot off the bed
 Ask patient to push it downwards against your resistance
2. Flexors of the thigh (Iliopsoas, L3)

 Raise the extended leg from the bed while in supine position against resistance
3. Abductors of the thigh (L3)

 Abduct the limb
 Ask patient to bring it back to the midline against resistance
4. Adductors of the thigh (gluteus medius and minimis, L4)

 Bring patient’s legs together in the
 Ask patient to separate (adduct) them against resistance
5. Rotators of the thigh (L4)

 Extend the lower limb
 Ask patient to roll it outwards or inwards (moving the foot laterally or medially)
6. Extensors of the knee (Quadriceps femoris, L4)

 Bend up the knee
 Press your hand against the shin
 Ask patient to straighten the limb
7. Flexors of the knee (Hamstrings, L5)

 Raise a leg up from the bed
 Support the thigh with your left hand
 Hold the ankle with your right hand
 Ask patient to bend (flex) the knee against your resistance
8. Plantar flexors (depression) of the foot (gastrocnemius, L5, S1)

 Depress the foot against resistance
9. Dorsi flexors (elevation) of the foot

 Elevate the foot against resistance
10. Eversion and inversion of the foot (Peronei and tibialis posterior, L5, S1)
 Ask the patient to turn the plantar, flexed foot outwards and inwards.
11. Intrinsic muscles of the foot result in a ―claw foot‖ deformity in weakness or paralysis of the interossei
2.4. Reflexes
A reflex is an involuntary motor response to a stimulus that is dependent on the integrity of a sensory
receptor, an afferent pathway (in peripheral or cranial nerve centre in the spinal cord, brain stem or
midbrain) an efferent path (peripheral or cranial nerve) and an effector in the muscle. It is an immediate
motor or sensory response to an afferent sensory impulse. Reflexes are classified into three types –
superficial (skin) reflexes, deep (tendon) reflexes and the organic (visceral) reflexes.
Superficial reflexes
Superficial reflexes are elicitated by stimulating an area of the skin (scratching) or mucous membranes
(touching).
1. Glabellar reflex
2. Corneal reflex
3. Conjunctival reflex
4. Palatal reflex
5. Ciliospinal reflex
6. Grasp reflex
7. Abdominal reflex
8. Cremasteric reflex
9. Plantar response reflex
a. Babinski’s sign
b. Oppenheim’s sign
c. Gordon’s sign
d. Gonda’s sign
e. Chaddock’s sign
f. Schaefer’s sign
g. Rossolimo’s sign
h. Stranksy’s sign

Tendon reflexes
These are reflexes elicitated by striking a tendon and so stretching it resulting in a synchronous volley of
impulses from the sensory endings in the stretched muscle causing brief contraction of the muscles. It
tests the integrity of the afferent and efferent pathways and the function of the anterior horn cells of the
spoinal cord.
It is advisable to polish your skill of examining reflexes by: -
 Putting the patient at ease

 Ensuring the warmth and comfort of the patient
 Using the same types of tendon hammer
 Standardizing your technique (use same method always)
 Reassuring the patient
 Repeating the test several time to habitualize the skill
Tendon reflexes can be graded as:
Grade 0 Absent
Grade 1 Present (as a normal ankle jerk)
Grade 2 Brisk (as a normal knee jerk)
Grade 3 Very brisk
Grade 4 Clonus
1. Jaw jerk
2. Hoffmann’s sign
3. Biceps jerk
4. Triceps jerk
5. Radial (Supinator) jerk
6. Knee jerk
7. Ankle jerk
8. Test for ankle and knee clonus
Table Principal Tendon reflexes
Reflex Mode of elicitation Response Spinal Peripheral nerve

segment
Biceps jerk A blow upon the biceps Flexion of the Cervical 5-6 Musculocuteneous
tendon elbow
Triceps jerk A blow upon the triceps Extension of the Cervical 6-7 Radial
tendon elbow
Supinator or A blow upon the styloid Flexion of the Cervical 5-6 Radial
radial jerk process of the radius elbow
Flexor A blow upon the palmar Flexion of the Cervical 7-8 Median and ulnar
finger jerk surface of the semi-flexed fingers and thumb
fingers
Knee jerk A blow upon the Extension of the Lumbar 2-4 Femoral
quadriceps tendon knee
Ankle jerk A blow upon the tendon Plantar flexion of Sacral 1-2 Sciatic
calcaneus the ankle
Jaw jerk
 Ask the patient to relax the jaw and allow the mouth to hand open loosely
 Place a finger on the lower jaw and strike it with a hammer
 Observe the response. A brisk response suggests a lesion of the pyramidal tracts
Hoffmann’s sign
 Indicates increased tendon reflex activity in finger flexors

 Flex the distal phalanx of the middle finger and then abruptly release it
 Observe the response in the index finger and the thumb
 Is positive if the thumb and index finger flex with a flicking motion.
Biceps jerk
 Place your thumb on the biceps tendon and strike your

thumb with the reflex hammer and observing the arm
movement
 Repeat and compare with the other arm
 The brachioradialis reflex is observed by striking the
brachioradialis tendon directly with the hammer when
the patient's arm is resting
 Strike the tendon roughly 3 inches above the wrist
 Note the reflex supination. Repeat and compare to the
other arm.
 The biceps and brachioradialis reflexes are mediated by
the C5 and C6 nerve roots.
Triceps jerk
 Flex the elbow to a right angle
 holding the patient's arm with your other hand(support
the arm at the elbow joint
 Strike the triceps tendon just proximal to the point of the
elbow (use the base of the hammer)
 Observe the response
 Repeat and compare to the other arm.
 Result is contraction of the triceps causing extension at
the elbow
 The triceps reflex is mediated by the C6 and C7 nerve
roots, predominantly by C7.
Radial (supinator) jerk
 Flex the elbow to a right angle

 Place the forearm midway between pronation and supination
 Tap on the styloid process of the radius with a percussion hammer
 Observe the response
 Result if contraction of the branchioradialis causing flexion at the elbow and partial supination of the
forearm.

Knee jerk
 With the lower leg hanging freely off the edge of

the bench, the knee jerk is tested by striking the
quadriceps tendon directly with the reflex
hammer.
 Repeat and compare to the other leg.
 The knee jerk reflex is mediated by the L3 and L4
nerve roots, mainly L4.
 Insult to the cerebellum may lead to pendular
reflexes.
 Pendular reflexes are not brisk but involve less
damping of the limb movement than is usually
observed when a deep tendon reflex is elicited.
 Patients with cerebellar injury may have a knee
jerk that swings forwards and backwards several
times.
 A normal or brisk knee jerk would have little more
than one swing forward and one back.
 Pendular reflexes are best observed when the
patient's lower legs are allowed to hang and
swing freelly off the end of an examining table.
Ankle jerk
 The ankle reflex is elicited by holding the relaxed foot

with one hand and striking the Achilles tendon with the
hammer and noting plantar flexion.
 Compare to the other foot.
 The ankle jerk reflex is mediated by the S1 nerve root.

2.5. Coordination
Coordination facilitates smooth employment, interaction and cooperation of separate muscles or group
of muscle to accomplish a definite motor act. If coordination is imperfect (ataxia) performance of the
motor act is difficult or impossible to accomplish. Coordination involves various factors like the afferent
impulses from muscles/joint reception, cerebellar and muscle tone. Vision or sight aids in coordination
as the ataxia becomes more apparent when vision is eliminated (eyes closed).
Examination
The upper limbs
Evaluate the motor function by:
a) Ask the patient to touch use of alternating hands

 With arms stretched outward instruct the patient to us the index fingers to touch the nose rapidly
with the eyes closed
 Alternate the left and right hand
b) Rapid rhythmic alternating movement of fingers

 Ask patient to touch each finger to thumb in a rapid sequence
 Test each hand separately
c) Rapid alternate movements of the hands by alternately using the palmar and dorsal surfaces of the
hand
d) Ask the patient to draw a large circle in the air with the forefinger. The circle should be drawn
smoothly and accurately
e) Rapid movement of patient’s finger between his/her nose and the examiner’s finger.
 Ask patient to rapidly move the index finger back and forth between patient’s nose and
examiner’s finger.
 Test one hand at a time

The lower limbs
a) Ask patient to ―tandem walk‖ along a straight line and observe for the steadiness or unsteadiness
b) Heel-to-knee test
 With the patient lying in bed
 Ask patient to lift up one leg in the air and place the heel of this leg on the opposite knee and
slide the heel down the shin towards the ankle
 Patient’s eyes should be open
c) Ask the patient to draw a large circle in the air with the toe. The circle should be drawn smoothly
and accurately.
d) Romberg’s sign
 Tests loss of position sense (sensory ataxia) in the legs
 Ask patient to stand with feet placed together
 Ask patient to close the eyes
 Romberg’s sign is present if the patient sways or even falls when the eyes are closed e.g. tabes
dorsalis, sensory neuropathy.
e) One foot balancing test

 Ask the patient to close eyes and stand on one foot for at least 5 seconds

 Repeat for the opposite foot
Involuntary movements

Movement Description Testing Causes
Athetosis Writhing movement Inspection Degenerative disease of the basal ganglia
pronounced in distal
muscles
Can unilateral or
generalized
Esterifies An irregular abrupt, brief Inspection Hepatic failure, metabolic disorders – uraemia,
loss of posture seen in poisoning with hypnotic drugs and respiratory failure
outstretched hands and
tongue
Chorea Brief, involuntary, irregular, Inspection Inherited presenile dementia (Huntington’s chorea),
non-repetitive and rheumatic fever (Syndenham’s chorea), drugs
purposeless movements of (phenothiazudes), old age (senile chorea), systemic
a group of muscles diseases e.g. thyrotoxicosis and systemic lupus
occurring in a disorderly erythematosus and rarely in pregnancy (chorea
fashion in the face, limbs gravidarum)
and sometimes all over the
body
Cramp Is a form of muscle spasm Inspection Can occur in calf muscles in normal people, chronic or
where there is progressive neurogenic muscle weakness, and
hypercontraction of metabolic disorders e.g. hyponatraemia (heat stroke).
muscles fibres
Dyskinesia
Dystonia Abnormally maintained Inspection Parkinson’s disease (flexion dystonia) and hemiplegia
posture associated with (hemiplegic dystonia).
plastic rigidity
Myoclonus Rapid, irregular jerky Inspection Epilepsy, degenerative disorders of the cerebellum,
movements of a group of encephalitis.
muscles in a limb or whole
body in response to
extraneous stimuli e.g.
sudden loud noise
Epileptic
seizures
Myokymia Persistent twitchy and Inspection Fatigue, anxiety, facial nerve palsy.
rhythmical movement of the
periorbital muscles
Tetany Spasms of muscles in the Inspection, Hypokacalcaemia
distal parts of the limbs. Trousseau’s Alkalosis
The fingers and thumbs are sign
stiffly adducted and the Chovstek’s
hand partially flexed at the sign
metacarpophalangeal joints
(carpopedal spasm)
Tics
Torticolis Jerky or maintained Inspection
(wry neck) rotational and abducted
posture of the neck
Tremor Regular or irregular to and Anxiety, Essential tremor, Physiological tremor,
fro oscillatory distal Hysteria, Thyrotoxicosis, Parkinson’s disease, Hepatic
movements. failure (flapping tremors), Renal failure, Respiratory
failure, Heavy metal poisoning e.g. mercury,
manganese, thallium

Lesson 7: Examination of the Sensory System
1) Perform examination of the sensory system

2) Interpret findings on examination of the sensory system
Introduction
The sensory system comprises of the following modalities: -
1. Tactile sensibility - light touch, pressure, tactile localization and discrimination

2. Position sense - proprioception
3. Stereognosis – recognition of the size, shape, weight and form of objects
4. Vibration
5. Pain
6. Temperature
Examination
Technique
 Begin testing sensation with touch and position
 Use a pin or wisp of cotton
 Examine areas with impaired sensation first
 Mark out the borders from the abnormal to normal
 Ask patient to close the eyes when examining
Tactile sensibility (light touch)
 Use a wisp of cotton or tip of your index finger and lightly touch each designated area
 Ask patient to indicator whether the touch is felt; where and how it is felt
 Do not use a recognizable pattern
 Sensation may be: -

o Abolished or reduced (hypaesthesia)
o Misperceived as painful
o Irritating or tingling sensation (hyperaesthesia)
o Mislocalized

 Two-point discrimination
o Touch selected parts of the body with blunt objects
o Ask patient to state if one or two objects are used (or if one or two points were touched)
o Discrimination distances are: - finger tips 2.8 mm, palms 8 – 12 mm, chest/forearm 40 mm,
back 40 – 70 mm, upper arm/thigh 75 mm.
Pain
 Tested using pin or applying pressure

 Absence of sensibility to pain – analgesia
 Partial loss – hypalgesia
 Exaggerated sensibility – hpyeralgesia e.g. spinal cord disease (tabes dorsalis), parietal and
thalamic lesions.
Superficial Pain
 Use a pin in each designated area Ask patient to indicator whether pain is felt and where it is felt
 Do not use a recognizable pattern
 Two-point discrimination (useful in posterior column lesions, partial cortical lesions, carpal tunnel
syndrome)
o Touch selected parts of the body with sharp objects
o Ask patient to state if one or two objects are used (or if one or two points were touched)

Pressure pain
 Examined by squeezing a distal muscle or the Achilles tendon

 Lost in tabes dorsalis
Stereognosia

 Place small familiar object e.g. coins, pencil, pen knife, scissors in the patient’s hand
 Ask patient to identify it.
 Occurs with posterior column lesions.
 Absence is referred to as asteriognosia
Graphesthesia

 Use a blunt instrument to draw a number or letter on patient’s hand, back
 Ask patient to identify it or distinguish the numbers or letters
Vibration
 Use a tuning- fork (128 Hz – lower C)

 Ask the patient to describe what she or he is feeling when a vibrating tuning fork is placed on a bony
area of the wrist, ankle and sternum

 Lost in tabes dorsalis, peripheral neuropathies and posterior column disorders e.g. peripheral
neuritis, nutritional neuropathy and Friedrich’s ataxia
Proprioception (Position)
 Recognition of movements in joints

 Ask patent to look away or shield eyes
 Explain how you will move a finger (or toe or elbow)
 Ask the patient to identify the direction of movement
Kinaesthetic sensation
 With patient’s eyes closed

 Grasp the finger and move its position
 Ask the patient to describe how the position has changed
Temperature
 Use test tubes containing cold and warm water or use the cold metallic part of the stethoscope or
tuning fork

Lesson 6: Investigations and Therapeutic Procedures in Nervous System Disease
1) Investigate disorders of the nervous system

2) Perform therapeutic procedures
3) Interpret findings of investigations
Investigations in Nervous System Disorders
1. Lumbar Puncture – Cerebro-spinal fluid (CSF)

a. Pressure
b. Macroscopic examination
c. Gram stain
d. ZN stain
e. Culture and sensitivity
2. Blood tests
3. Radiological
a. Skull X-rays
b. Spinal X-rays
c. Computerized tomography - CT scan
d. Magnetic resonance imaging (MRI)
e. Electro-encephalogram (EEG)
f. EMG
g. Myelogram
4. Biopsy
1.0 NORMAL CSF AND LUMBAR PUNCTURE

Appearance Crystal clear, colourless
Pressure 100 – 180 mm of water with patient in recumbent position
Cell content 5 cell/mm3, mononuclear cells only, no polymorphonuclear cells
Protein 0.1 – 0.5 gm/L
Glucose 2/3 – ½ of blood glucose
IgG < 15% of total CSF protein
CSF Pressure
It is usually at 130 mmH20 (normal range 70 – 180 mmH20). The CSF has a high specific gravity of 1.005, which
is vital as it enables the CSF draw in water, and prevents the brain from moving into the CSF. The CSF pressure
is determined by rate of production, rate of absorption and specific gravity, increased production and decreased
absorption increases CSF pressure. Pressure can also be increased in meningitis and hydrocephalus.
Reduced CSF pressure

1. Dehydration
2. Spinal subarachnoid block
3. Following previous LP
4. CSF leaks
5. Poor technique where the needle is not inserted in the subarachnoid space.

Increased CSF pressure
1. Brain oedema
2. Intracranial mass or lesions – tumours, space occupying lesions (S.O.L)
3. Infections e.g. meningitis
4. Acute stroke
5. Congestive cardiac failure (CCF)
6. Cerebral venous occlusions
7. Benign intracranial hypertension
Colour
The normal colour is clear and colourless water like fluid. The abnormalities of colour can be yellow colouration,
turbidity and blood stained CSF. Yellow colour (xanthochromia) is pathological picture seen in old haemorrhage,
jaundice and excess protein levels while turbidity is due to the presence of white blood cells as a result of
infection e.g. in meningococcal meningitis or following subarachnoid haemorrhage (gets clear on standing for
some time). Blood stained CSF is due to injury (is initially pink and streaky becoming clear in subsequent bottles)
or subarachnoid haemorrhage (the blood and CSF is uniformly mixed).
Cell content (Cytology)
The normal cell content consists of 0-5 cells/micro litre. Polymorphonuclear CSF has > 75% polymorphs and
lymphocytic CSF has >98% lymphocytes e.g. in viral and syphilitic infections. Pleocytosis is when there is a
mixed picture of the CSF exhibiting both compositions. Bacterial meningitis shows PMNL pleocytosis and TB
meningitis reveals lymphocytic or pleomorphic pictures.
Chemical content
This is mainly sugar and proteins. The chemical constitution of CSF resembles that of plasma except for low
protein content. The CSF sugar is ½ blood sugar levels (3.3 – 4.4 mmol/L).
Sugar content
The sugar content is normal in neoplastic meningitis, multiple sclerosis and viral meningitis and reduced in
bacterial infections and tuberculous meningitis.
Protein content
The protein content of CSF is 0.1-0.5 gm/L. The protein content is slightly raised in meningitis, inflammatory
polyneuritis (Gullein Barre Syndrome, GBS), myxoedema and diabetic neuropathy. It is markedly increased in
obstruction/blockage of theca in cases of spinal cord tumours (Froin’s syndrome), cerebral tumours and
peripheral neuropathy. The proteins are reduced in CSF leaks due to previous LP or traumatic dural leaks.
Chloride
Is reduced in meningitis
Immunoglobulins
Increased immunoglobulins indicate an inflammatory response as a result of increase in endothelial cell

permeability. The Ig’s are increased in bacterial, viral, fungal and spirochaetal infections. It is important in the
diagnosis of multiple sclerosis, demyelinating disease and CNS vasculitis.
LUMBAR PUNCTURE
Lumbar puncture is a procedure used for obtaining samples of cerebro-spinal fluid (CSF) by penetrating the
lumbar meninges below L3/L4 or L4/L5 interspaces. The CSF is secreted by cells of the choroids plexus and

absorbed via the arachnoid villi into the dural sinuses and spinal sinuses. The CSF gives information in terms of
CSF pressure, colour, cell content (cytology), chemical content and the Wassermann reaction.
Indications
1. Diagnostic
a. Diagnosis of meningitis/encephalitis
b. Diagnosis of suspected subarachnoid haemorrhage
c. Diagnosis of miscellaneous conditions e.g. multiple sclerosis, neurosyphilis, sarcoidosis and certain
polyneuropathies.
d. Measurement of CSF pressure e.g. in idiopathic intracranial hypertension
e. Myelography
2. Therapeutic
a. Intrathecal injection of contrast media and drugs such as methotraxate as in Burkitts lymphoma and
Acute lymphocytic leukaemia (ALL)
b. Removal of CSF therapeutically in idiopathic intracranial hypertension
3. Administration of spinal anaesthesia
Contraindications of LP
1. Sepsis of the skin overlying the spinal cord (local infection)

2. Increased intracranial pressure
3. Intracranial hypertension
4. Anticoagulant therapy and uncontrolled bleeding diathesis
5. Spinal column deformities
6. Lack of patient cooperation
7. Uncorrected anaemia and heart disease (resultant hypotension may worsen the condition)
Requirements
A clean trolley arranged as follows
1. Top shelf
a. A sterile lumbar puncture pack containing
 Small hand towel, 1 sterile gown, Pair of gloves, 2 Draping towels , 2 Galipots, 2 Kidney dishes, 1
Sponge holding forceps, A long hollow lumbar puncture needle (Quincke needle)with a stylet
gauge 20 or 22, Sterile needle gauge 21 (for adults) and gauge 23 (for children), Syringe 5 cc ,
Bowl containing cotton wool and gauze swabs,
b. Spinal manometer
2. Bottom shelf
 Local anaesthetic, Antiseptic solution e.g. Hibitane , Receiver for used swabs , Decontaminant in
receiver for used instruments, Strapping , Scissors , 3 sterile specimen bottles, Extra sterile needles
(gauge 21 and 23), Extra syringes (5 cc) , 3 masks, Mackintosh/draw sheet
 Prepared medicines (if lumbar puncture is for administration of medicines and spinal anaesthesia)
Pre-Procedure Patient Education
1. Assess the indications for the procedure

2. Explain the major steps of the procedure, positioning and post-procedure care
3. Inform the patient of possible complications (e.g. bleeding, persistent headache and infection) and their
treatment
4. Obtain informed consent
5. Examine the fundi (fundoscopy) to exclude increased intracranial pressure

Lumbar puncture technique
1. Requirements – a long hollow needle (LP needle), a sterile LP tray and 3 sterile stoppered bottles
2. Examine the fundi to exclude increased intracranial pressure. Increased intracranial pressure presents a risk
of transtentorial or tonsilar herniation of the brain.
3. Ask the patient to lie on the left side aspect with the spine fully flexed with the back on the edge of the couch.
The trunk should be flexed with the knees and chin as approximate as possible.
4. Locate 3rd and 4th lumbar spines (the 4th lumbar spine lies in the transverse plane of the iliac crests)
5. Clean and drape the patient
6. Apply local anaesthesia
7. Use a disposable needle (8 cm length) with a withdrawable stylet
8. Put the needle firmly through the skin and press it steadily forwards and slightly towards the patient’s head
9. When the needle is felt to enter the spinal cavity withdraw the stylet and the CSF will drip slightly from the
needle.
10. Collect the CSF in three bottles
11. Allow patient to rest for the first 8 – 24 hours
Diagram: Lumbar Puncture Sites and Technique

NOTE
1. Insertion of the needle bevel-up minimizes dural trauma
2. A traumatic ―bloody tap‖ occurs when spinal venous plexus is penetrated. Often the fluid will clear as
succeeding tubes are filled. Spin down the first tube: if red blood cells have been in the spinal fluid for
sometime (for example, subarachnoid haemorrhage), xanthochroma will present in the supernatant fluid. If
the fluid is clear after it is spun down, the tap was only traumatic.
3. In some cases, conscious sedation is helpful in reducing patient anxiety and allowing maximal spinal flexion.
Difficulties and Complications with LP procedure
Obtaining a dry tap with failure to obtain CSF which can be due to incorrect puncture (incorrect position of the
patient or needle) or complete block to CSF flow (Do MRI to confirm this occurrence).
Problems with LP (complications)

 Brain herniation, Worsen spinal cord compression, Headache (due to low CSF pressure), Subdarachnoid
bleeding, Diplopia, Backache
3.0 ULTRASOUND
While the patient's history and physical examination are the building blocks of making a medical
diagnosis, the ability to peer inside the body can be a powerful tool thus theultrasound is an imaging
technique that provides that ability to medical practitioners.
What is an ultrasound?
Ultrasound produces sound waves that are beamed into the body causing return echoes that are
recorded to "visualize" structures beneath the skin. The ability to measure different echoes reflected
from a variety of tissues allows a shadow picture to be constructed. The technology is especially
accurate at seeing the interface between solid and fluid filled spaces
What is ultrasonography?
Ultrasonography is body imaging using ultrasound in medical diagnosis. A skilled ultrasound technician
is able to see inside the body using ultrasonography to answer questions that may be asked by the
medical practitioner caring for the patient. Usually, a radiologist will oversee the ultrasound test and
report on the results, but other types of physicians may use ultrasound as a diagnostic tool. For
example, obstetricians use ultrasound to assess the foetus during pregnancy. Surgeons and emergency
physicians use ultrasound at the bedside to assess abdominal pain or other concerns.
A transducer, or probe, is used to project and receive the sound waves and the return signals. A gel is
wiped onto the patient's skin so that the sound waves are not distorted as they cross through the skin.
Using their understanding of human anatomy and the machine, the technician can evaluate specific
structures and try to answer the question asked by the patient's physician. This may take a fair amount
of time and require the probe to be repositioned and pointed in different directions. As well, the
technician may need to vary the amount of pressure used to push the probe into the skin. The goal will
be to "paint" a shadow picture of the inner organ that the health care practitioner has asked to be
visualized.
The physics of sound can place limits on the test. The quality of the picture depends on many factors.
 Sound waves cannot penetrate deeply, and an obese patient may be imaged poorly.
 Ultrasound does poorly when gas is present between the probe and the target organ. Should the
intestine be distended with bowel gas, organs behind it may not be easily seen. Similarly,
ultrasound works poorly in the chest, where the lungs are filled with air.
 Ultrasound does not penetrate bone easily.
 The accuracy of the test is very much operator dependent meaning that the key to a good test is the
ultrasound technician.
Ultrasound can be enhanced by using Doppler technology which can measure whether an object is
moving towards or away from the probe. This can allow the technician to measure blood flow in organs
such as the heart or liver, or within specific blood vessels.
Uses
1) Diagnostic uses
a. Obstetrics
 Assessing the progression of pregnancy
 Diagnose growths or tumors of the ovary, uterus, Fallopian tubes.
b. Cardiology
 Echocardiography (echocardiography (echo=sound + cardio=heart + graphy=study)
 Evaluates the heart, the heart's valve function, and blood flow through them. It also
evaluates the heart wall motion and the amount of blood the heart pumps with each
stroke.
 Echocardiography can be performed in two ways: trans-thoracic: the probe is place
on chest wall to obtain images, and trans-esophageal: where the probe is placed
through the mouth into the oesophagus.
 Visualize the heart chambers to detect blood clots in conditions such as atrial fibrillation
(an irregular heart rhythm)
 Help diagnose endocarditis (an infection of the heart valves) by visualizing
"vegetations" (an infected mass) on the valves themselves
 Can detect abnormal fluid collections (pericardial effusions)
 Diagnose and monitor pulmonary artery hypertension.
c. Blood vessels
 Can detect blood clots in veins (superficial or deep venous thrombosis) or artery
blockage (stenosis) and dilatation (aneurysms)
 Carotid ultrasound is performed in patients with transient ischemic attacks (TIAs) or
strokes to determine whether the major arteries in the neck are blocked causing the
decreased blood supply to the brain.
 Detect aneurysm,
 Veins can also be evaluated by ultrasound and it is a common test to assess whether
swelling in a leg is due to a blood clot, deep vein thrombosis (DVT) or another cause.
d. Abdominal structures
 Evaluate most of the solid structures in the abdominal cavity. This includes the liver,
gallbladder, pancreas, kidneys, bladder, prostate, testicles, uterus, and ovaries.
 Screen for gallstones or an infected gallbladder
 Ultrasound is the test of choice to diagnose testicular torsion.
 Pelvic ultrasound is used in gynaecology to help assess non-pregnancy related issues
like lower abdominal pain, ovarian cysts, uterine fibroids, uterine growths, and
endometriosis.
e. The neck
 The thyroid gland can be imaged using ultrasound looking for nodules, growths, or
tumours.

f. Knee joint
 Ultrasound can be used to detect bulging of fluid from a swollen knee joint into the back
of the knee, called a Baker's cyst.
2) Screening uses
 Ultrasound may be used to screen for blood vessel diseases.
3) Therapeutic uses
a. Ultrasound may be used to help physicians guide needles into the body.
b. In situations where an intravenous line is required but it is difficult to find a vein, ultrasound
guidance may be used to identify larger veins in the neck, chest wall, or groin.
c. Ultrasound may be used to guide a needle into a cavity that needs to be drained (for example,
an abscess) or a mass that needs to be biopsied, where a small bit of tissue is removed for
analysis.
3.1.1 Risks
There are no known risks to ultrasound, and as technology has improved, the machines have become
smaller, portable and available for use at the patient's bedside.
4.0 MRI (Magnetic Resonance Imaging)
An MRI (or magnetic resonance imaging) scan is a radiology technique that uses magnetism, radio
waves, and a computer to produce images of body structures. The MRI scanner is a tube surrounded by
a giant circular magnet. The patient is placed on a moveable bed that is inserted into the magnet. The
magnet creates a strong magnetic field that aligns the protons of hydrogen atoms, which are then
exposed to a beam of radio waves. This spins the various protons of the body, and they produce a faint
signal that is detected by the receiver portion of the MRI scanner. The receiver information is processed
by a computer, and an image is produced. The image and resolution produced by MRI is quite detailed
and can detect tiny changes of structures within the body. For some procedures, contrast agents, such
as gadolinium, are used to increase the accuracy of the images.

Uses
1) An MRI scan can be used as an extremely accurate method of disease detection throughout the
body. In the head, trauma to the brain can be seen as bleeding or swelling. Other abnormalities
often found include brain aneurysms, stroke, tumours of the brain, as well as tumours or
inflammation of the spine.
2) Neurosurgeons use an MRI in defining brain anatomy and evaluating the integrity of the spinal cord
after trauma, problems associated with the vertebrae or intervertebral discs of the spine.
3) Evaluate the structure of the heart and aorta, where it can detect aneurysms or tears.
4) It provides valuable information on glands and organs within the abdomen, and accurate information
about the structure of the joints, soft tissues, and bones of the body
Risks
An MRI scan is a painless radiology technique that has the advantage of avoiding x-ray radiation
exposure. There are no known side effects of an MRI scan. The benefits of an MRI scan relate to its
precise accuracy in detecting structural abnormalities of the body.
Patients who have any metallic materials within the body must notify their physician prior to the
examination or inform the MRI staff. Metallic chips, materials, surgical clips, or foreign material (artificial
joints, metallic bone plates, or prosthetic devices, etc.) can significantly distort the images obtained by
the MRI scanner. Patients who have heart pacemakers, metal implants, or metal chips or clips in or
around the eyeballs cannot be scanned with an MRI because of the risk that the magnet may move the
metal in these areas. Similarly, patients with artificial heart valves, metallic ear implants, bullet
fragments, and chemotherapy or insulin pumps should not have MRI scanning.
Results
After the MRI scanning is completed, the computer generates visual images of the area of the body that
was scanned. These images can be transferred to film (hard copy). A radiologist is a physician who is
specially trained to interpret images of the body. The interpretation is transmitted in the form of a report
to the practitioner who requested the MRI scan. The practitioner can then discuss the results with the
patient and/or family.
Pictures of an MRI of the spine
This patient had a herniated disc between vertebrae L4 and L5. The resulting surgery was a discectomy

5.0 COMPUTERISED TOMOGRAPHY (CT)/ COMPUTERIZE AXIAL TOMOGRAPHY (CAT) SCAN
A computed tomography (CT) scan is a non-invasive imaging method that uses x-rays to create cross-
sectional pictures of the body. It combines special x-ray equipment with sophisticated computers to
produce multiple images or pictures of the inside of the body. These cross-sectional images of the area
being studied can then be examined on a computer monitor, printed or transferred to a CD. CT scans of
internal organs, bones, soft tissue and blood vessels provide greater clarity and reveal more details than
regular x-ray exams. CT scanning provides more detailed information on head injuries, stroke, brain
tumours and other brain diseases than regular radiographs (x-rays)
Scanner Equipment
The CT scanner is typically a large, box-like machine with a hole, or short tunnel, in the centre. The
patient lies on a narrow examination table that slides into and out of this tunnel. Rotating around you,
the x-ray tube and electronic x-ray detectors are located opposite each other in a ring, called a gantry.
The computer workstation that processes the imaging information is located in a separate control room,
where the technologist operates the scanner and monitors your examination.
Operation
 CT scanning works very much like other x-ray examinations

 X-rays are a form of radiation like light or radio waves that can be directed at the body
 Different body parts absorb the x-rays in varying degrees.
 In a conventional x-ray exam, a small amount of radiation is aimed at and passes through the body
recording an image on photographic film or a special image recording plate. Bones appear white on
the x-ray; soft tissue, such as organs like the heart or liver, shows up in shades of gray and air
appears black.
 With CT scanning, numerous x-ray beams and a set of electronic x-ray detectors rotate around you,
measuring the amount of radiation being absorbed throughout your body. At the same time, the
examination table is moving through the scanner, so that the x-ray beam follows a spiral path. A
special computer program processes this large volume of data to create two-dimensional cross-
sectional images of your body, which are then displayed on a monitor.
 Refinements in detector technology allow new CT scanners to obtain multiple slices in a single
rotation. These scanners, called multislice CT or multidetector CT, allow thinner slices to be
obtained in a shorter period of time, resulting in more detail and additional view capabilities.
 Modern CT scanners are so fast that they can scan through large sections of the body in just a few
seconds, and even faster in small children. Such speed is beneficial for all patients but especially
children, the elderly and critically ill.
 For children, the CT scanner technique will be adjusted to their size and the area of interest to
reduce the radiation dose.
 For some CT exams, a contrast material is used to enhance visibility in the area of the body being
studied.
Uses
CT scanning of the head is typically used to detect:
1) Bleeding, brain injury and skull fractures in patients with head injuries
2) Bleeding caused by a ruptured or leaking aneurysm in a patient with a sudden severe headache
3) A blood clot or bleeding within the brain shortly after a patient exhibits symptoms of a stroke
4) A stroke (with a new technique called Perfusion CT)
5) Brain tumours

6) Enlarged brain cavities (ventricles) in patients with hydrocephalus
7) Diseases or malformations of the skull.
CT scanning is also performed to:
1) Evaluate the extent of bone and soft tissue damage in patients with facial trauma, and planning
surgical reconstruction
2) Diagnose diseases of the temporal bone on the side of the skull, which may be causing hearing
problems.
3) Determine whether inflammation or other changes are present in the para-nasal sinuses
4) Plan radiation therapy for cancer of the brain or other tissues
5) Guide the passage of a needle used to obtain a tissue sample (biopsy) from the brain
6) Assess aneurysms or arteriovenous malformations through a technique called CT angiography
NOTE:
 Women should always inform their physician and the CT technologist if there is any possibility that
they are pregnant.
Advantages
 Painless, non-invasive and accurate

 A major advantage of CT is its ability to image bone, soft tissue and blood vessels all at the same
time
 Provides very detailed images of many types of tissue as well as the lungs, bones, and blood
vessels
 Fast and simple; in emergency cases, they can reveal internal injuries and bleeding quickly enough
to help save lives
 Cost-effective imaging tool for a wide range of clinical problems
 Less sensitive to patient movement than MRI
 CT can be performed if you have an implanted medical device of any kind, unlike MRI
 May eliminate the need for exploratory surgery and surgical biopsy
 No radiation remains in a patient's body after a CT examination
 X-rays used in CT scans usually have no immediate side effects
Risks
 There is always a slight chance of cancer from excessive exposure to radiation

 Women should always inform their physician and x-ray or CT technologist if there is any possibility
that they are pregnant, Not recommended for pregnant women unless medically necessary because
of potential risk to the baby
 The risk of serious allergic reaction to contrast materials that contain iodine is extremely rare, and
radiology departments are well-equipped to deal with them.
NOTE:
 Because children are more sensitive to radiation, they should have a CT exam only if it is essential
for making a diagnosis and should not have repeated CT exams unless absolutely necessary. CT
scans in children should always be done with low-dose technique.
Cranial CT scan - Overview
A cranial computed tomography (CT) scan uses many x-rays to create pictures of the head, including
the skull, brain, eye sockets, and sinuses. A cranial CT scan is recommended to help diagnose or
monitor the following conditions:
1) Birth (congenital) defect of the head or brain
2) Brain infection
3) Brain tumour
4) Build-up of fluid inside the skull (hydrocephalus)
5) Craniosynostosis
6) Injury (trauma) to the head and face
7) Stroke or bleeding in the brain
A cranial CT may also be done to look for the cause of:
1) Changes in thinking or behaviour

2) Fainting
3) Headache, when certain other signs or symptoms are present
4) Hearing loss (in some patients)
5) Symptoms of damage to part of the brain, such as vision problems, muscle weakness, numbness
and tingling, hearing loss, speaking difficulties, or swallowing problems
6.0 SKULL AND SPINAL X-RAYS
They can be able to show: -

 Fractures of the skull vault or bone
 Skull and spinal lesions e.g. metastasis, osteomyelitis, Paget’s disease, abnormal skull foramen and
fibrous dysplasia
 Enlargement or destruction of the pituitary fossa e.g. inn situations of intrasellar tumours and
increased intracranial pressure
 Intracranial calcification e.g. tuberculoma, wall of an aneurysm and oligodendroglioma
 Lateral shift of calcified pineal (is used in CT imaging to recognize midline shift)
7.0 IMAGING IN SKULL FRACTURES
The skull is formed by the fusion of several flat bones held together by the cranial sutures. Each of the
flat bones consists of a thick outer table, the spongy diploe, and a thinner inner table. The inner table is
lined by a thick, fibrous, adherent dura mater. A shallow subdural space lies between the inner surface
of the dura and the thin arachnoid mater that covers the surface of the brain. See depictions of the skull
in the images below.
A skull fracture is a break in the skull bone and generally occurs as a result of direct impact. The skull is
deformed by localized impact, which may damage the cranial contents even when the skull does not
fracture. If the force and deformation is excessive, the skull fractures at or near the site of impact.
Skull fractures may occur with no associated neurologic damage, and conversely, fatal injury to
membranes, blood vessels, and brain may occur without overlying fracture. However, skull fractures
may be associated with intracranial haemorrhage, which may create an intracranial space-occupying
lesion. In addition, cerebral oedema associated with skull fractures is a common and frequently fatal
complication of head injury and may develop within minutes or hours of injury. Cerebral oedema may
accompany diffuse axonal injury or a space-occupying lesion, such as an intracranial hematoma. In
children, brain swelling may be the only identifiable feature of head injury. Severe brain oedema or a
large intracranial haemorrhage may cause downward brain displacement and coning, which is usually
fatal.

Anatomy
Skull thickness is not uniform, and therefore, the impact of forces required to cause a fracture depends
on the site of the impact. The skull is thick at the glabella, the external occipital protuberance, the
mastoid processes, and the external angular process. The skull vault is comparatively thinner than the
base of the skull. The skull vault is composed of cancellous bone, the diploë, which is sandwiched
between the inner and outer tables and consists of the lamina externa (1.5 mm) and the lamina interna
(0.5 mm). The diploë does not form where the skull is covered with muscles, leaving the vault thin and
prone to fracture.
Skull fractures are more easily sustained at the thin squamous temporal and parietal bones, the
sphenoid sinus, the foramen magnum, the petrous temporal ridge, and the inner parts of the sphenoid
wings at the skull base. The middle cranial fossa forms the thinnest part of the skull and thus represents
the weakest part, which is further weakened by the presence of multiple foramina. Other sites at risk for
fracture are the cribriform plate, the roof of orbits in the anterior cranial fossa, and the areas between
the mastoid and dural sinuses in the posterior cranial fossa.
Linear skull fractures
Linear fractures, the most common, involve a break in the bone but no displacement, and generally no
intervention is required. The fracture involves the entire thickness of the skull.
Depressed skull fractures
A fracture is clinically significant and requires elevation when a fragment of bone is depressed deeper
than the adjacent inner table. Depressed fractures may be closed or compound (open). Compound
fractures may be exposed when they are associated with a skin laceration or when the fracture extends
into the paranasal sinuses and the middle-ear structures. Depressed fractures may require surgery to
correct the deformity. Most depressed fractures involve the frontoparietal region, because the bones in
this area are relatively thin and because this part of the head is particularly prone to an assailant's
attack.
Diastatic skull fractures
Diastatic fractures occur along the suture lines and usually affect new-borns and infants in whom suture
fusion has not yet happened. In this type of fracture, the normal suture lines are widened (see the
images below).
Basilar skull fractures
 Most serious and involve a linear break in the bone at the base of the skull
 Most occur at 2 specific anatomic locations—namely, the temporal region and the occipital condylar
region
 Are often associated with dural tears, of which cerebrospinal fluid (CSF) rhinorrhea and otorrhea are
known complications. Such patients usually require close observation in the hospital.
Ping-pong skull fractures
 Is similar to a greenstick fracture of the long bones in children

 Occurs in the first few months of life and is usually caused by a fall when the skull hits the edge of a
hard blunt object, such as a table

 The skull appears deformed, with a shallow trench on the surface of the skull. The ping-pong skull
fracture was first described in a newborn whose head was impinging against the mother's sacral
promontory during uterine contractions. The use of forceps also may cause this injury to the skull,
but this mechanism is rare.
Birth fractures
 Caput succedaneum commonly occurs after vaginal delivery and is related to a serosanguineous
effusion, which appears as a soft-tissue swelling over the presenting part of the skull. Caput
succedaneum is a benign process that generally resolves within 2 weeks and usually does not
require any form of imaging. However, a cephalohematoma may develop after an instrumental
delivery and represents a subperiosteal hematoma.
 In contrast to a caput succedaneum, a cephalohematoma is limited by suture lines. In addition, a
cephalohematoma may be visible on a plain radiograph as a subperiosteal elevation. Birth skull
fractures may occur as a complication of forceps or vacuum extraction.
 Most are simple parietal linear fractures, but occasionally, they are more complex or depressed. In
some cases, associated extradural hematoma,subdural hematoma, or axonal injury is observed.
Growing skull fractures
In children, most skull fractures heal rapidly, with no long-term sequelae. However, in a small minority of
children, a fracture may remain un-united and enlarge to form a growing skull fracture. Most growing
skull fractures are located in the calvarium, but rare sites are the basiocciput and the orbital roof. Most
cases occur after falls, motor vehicle accidents, and child abuse. Cases related to difficult vacuum
extraction and corrective surgery for craniosynostosis have also been described.
Magnetic resonance imaging (MRI) is preferred to CT scanning for depicting dural tears early after the
head injury and allows timely surgical intervention and prevention of growth of the fracture. Cranial
Doppler ultrasonographic studies have also been used to achieve an early diagnosis.
Scalp injuries
The scalp may be injured with or without a breach in its surface. Lacerations are particularly common,
as the scalp is readily crushed and split against the underlying bone. Most scalp lacerations are linear
because of the convexity of the skull. When injured, the scalp often becomes markedly oedematous,
and hematoma formation is common above or below the galeal layer.
Missile wounds
Missiles can be subdivided into (1) low-velocity bullets, such as those used in air rifles, nail guns, stun
guns (used for animal slaughter), handguns, shotguns, and shrapnel, and (2) high-velocity bullets, such
as metal-jacket bullets fired from military weapons. Low-velocity and high-velocity bullet wounds are
shown in the images below.
Missiles produce brain injury by causing laceration and crushing, cavitation, and shock waves. The
injuries to the skull range from a graze to an entry wound and sometimes an exit hole (penetrating) or a
depressed fracture, with results ranging from focal haemorrhage to extensive neuronal damage.
Differentiating between penetrating and perforating skull wounds is important because of their different
prognostic implications. A poor postsurgical outcome occurs in 50% of patients treated for perforating
wounds, as compared with 20% of those with penetrating wounds. Additional examples of missile
wounds are shown below.

A missile injury through the frontal bone associated with an intracerebral hematoma/infarction along the
missile tract. Scan of a missile injury through the frontal bone associated with an intracerebral
hematoma/infarction along the missile tract.
Stab wounds
 Penetrating skull stab wounds are uncommon

 Stab wounds are caused by knives, nails, spikes, forks, scissors, and other sharp objects. Skull
penetration most commonly occurs in the thinnest parts of the skull, such as the orbital surfaces and
the squamous portion of the temporal bone. Injury to the brain usually occurs in the path of the
penetrating stab wound
 Unlike missile injuries, stab wounds have no concentric zone of coagulative necrosis caused by
dissipated energy, and unlike motor vehicle accidents, stab wounds cause no diffuse, shearing
brain injury.
 May cause an intracranial hematoma or infarct. Cerebral damage caused by stabbing is largely
restricted to the wound tract
 Stab wounds occasionally produce a narrow, elongated defect (a slot fracture); this injury is
diagnostic when identified. However, in some cases in which skull penetration is proven, no
radiologic abnormality is identified
 A stab wound to the temporal fossa is most likely to cause major neurologic injury because of the
thinness of the squamous temporal bone and because of the short distance to the brainstem and
blood vessels.
 The type of skull fracture sustained and the underlying brain injury depends on the variation in skull
thickness and on the strength and angle of the impact. A stab wound nearly perpendicular to the
skull may cause bone fragments to travel along the same trajectory as that of the penetrating object,
it may shatter the skull in an irregular pattern, or it may produce linear fractures that radiate away
from the entry site. Tangential stab wounds result in complex single defects, with both internal and
external bevelling of the skull and varying degrees of neurologic injury.
Non- accidental trauma
 Most fractures in children are a result of falls and bicycle accidents, but skull fractures in infants may
originate from neglect, falls, or abuse.
Extradural haemorrhage
 The temporal bone is usually the thinnest part of the skull and a fracture at this site may tear the
middle meningeal artery as it passes upward within a groove between the inner skull table and the
dura
 A blow to the temporal bone may result in a tear of the temporal artery without a fracture (15%). An
arterial bleed from a middle meningeal artery accumulates, forming a hematoma between the inner
skull table and stripped dura; this is called an extradural haemorrhage, which acts as a space-
occupying lesion. This accumulation can be immediate or delayed.
Subdural haemorrhage
 More common than an epidural haemorrhages especially common in the elderly, children, and
individuals with alcoholism
 Not usually associated with skull fractures but may occur after sudden jarring or rotation of the
head, a blow to the head, or a fall, trauma to the head may be trivial

 Movement of the brain relative to the dura, often associated with widened CSF spaces, causes
shears and tears of the small veins that bridge the gap between the dura and the cortical surface of
the brain
 Blood from torn vessels accumulates over several hours and usually tracks extensively as a thin film
over the surface of the brain. A small, self-limiting subdural haemorrhage may remain asymptomatic
and be an incidental finding.
Subarachnoid haemorrhage
 Subarachnoid haemorrhages may occur as a result of a ruptured intracranial arterial aneurysm or

trauma
 Traumatic subarachnoid haemorrhage is usually associated with brain contusion or laceration. In
rare cases, this type of haemorrhage is due to a direct blow to the side of the neck, which ruptures
the vertebral artery as it enters the cranial cavity.
Intracerebral haemorrhage
 May occur as a result of a ruptured atheromatous intracerebral arteriole, vasculitis, ruptured

intracranial arterial aneurysm, or trauma.
 Traumatic intracerebral haemorrhage is usually due to extension of haemorrhage from surface
contusions deep into the substance of the brain. Traumatic intracerebral haemorrhage may also be
the result of rupture of small blood vessels deep within the brain due to shearing stress.

Nervous System Examination: Anatomy and Functions

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Nervous System Examination: Anatomy and Functions

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Nervous System Examination

Neuromuscular System Examination

Lesson 1: Preview of Anatomy and Physiology of the Nervous System

At the end of the lesson the learner will be able to: -

1) Outline the basic anatomy of the nervous system

Carey Francis Okinda 1

Somatic Nervous System (SNS) Autonomic Nervous System (ANS)

Somatic Integration Centres Autonomic Integration Centres

Stimulus Response Stimulus Response

2.1 Nerve Cells

Neurons: Structure & Function

The Cell Body (Perikaryon)

Dendrites (Dentron = tree branch)

The Axon (Nerve Fibre)

The classification of the neurons/nerves can be functional or structural.

Carey Francis Okinda 3

Carey Francis Okinda 4

2.3 The Central Nervous System (CNS)

Fore brain - Cerebrum

Interior of the cerebral hemispheres

 The cerebral cortex is composed of nerve cells on the surface

Genu and posterior limb

These contain the cortico-spinal tracts (pyramidal tracts).

Functions of the cerebral hemispheres

Carey Francis Okinda 6

Figure 1.4: Functional areas of the Brain

e) Olfactory area (rhinencephalon)

Carey Francis Okinda 7

The Limbic System

1. Voluntary motor control of skeletal muscles

The Brain stem

Mesencephalon (Mid brain)

Carey Francis Okinda 8

 Ventrally by vertebral and basilar arteries

The medulla has special functions such as: -

The Cerebellum (Hind brain)

Connections of the cerebellum

There are three main connections: -

Symptoms of cerebellar lesion

 The brain receives 1/5th of the total cardiac output.

Carey Francis Okinda 10

Spinal nerve roots

Internal structure of the spinal cord

The grey matter

The white matter

Posterior white columns

Anterior white columns

Carey Francis Okinda 12

 Pyramidal tracts pass directly to the cell bodies of the LMN.

The Motor System

The motor system comprises of the: -

Spinocortical (pyramidal tract) system, Upper Motor Neurone

Carey Francis Okinda 13

The Lower motor neurone

 Controls muscular movement

1.5: The Peripheral Nervous System

Carey Francis Okinda 15

Lesson 2: Neurological History

At the end of the lesson the learner will be able to: -

1) Take an appropriate neurological history

Examination of the Nervous system

1. A tendon hammer (Patella hammer)