Examination of the Nervous System

Prof Dr. P. T. Thomas

 Has multiple functions

Reaches all over the body

CNS - brain and spinal cord

PNS - cranial nerves and

spinal nerves

Motor: pyramidal, extrapyramidal,

balancing, coordination
Sensory: two tracts
Autonomic

All the systems are interconnected

No system can function in

isolation
 Functions of the nervous system
• Cognitive functions: consciousness, awareness, insight,
memory, judgement, reasoning
• Speech: spoken (ability to express and understand) and
written (read and write) communication
• Motor: All voluntary movements need skeletal muscles to
contract with precision and speed
• Sensory: Sensations of touch, pain, position, vibration
• Special senses: smell, vision, taste, hearing, discriminative
touch
• Autonomic functions: control of internal organs, heartbeat
and respiration, BP, temperature regulation, sexual functions
 Patient’s complaints / symptoms
• LOC: brief- syncope, seizure; prolonged - coma
• Motor system: weakness, slowness, clumsiness,
involuntary movements
• Sensory system: numbness, tingling, paresthesia
• ANS: bloating abdomen, constipation, sweating (↑
or ↓), sphincter dysfunction, ED, BP fluctuation
• CN: anosmia, vision, diplopia, trigeminal neuralgia,
unable to close eye, drooling, loss of hearing,
dysphagia, nasal voice, nasal regurgitation,
drooping shoulder, dysarthria
 ELECTRICAL SYSTEM compared to MOTOR SYSTEM
Power station
Motor cortex
Generator
Cortico-nuclear
tracts
UMN From left
UMN Cranial and right
nerve
Nuclei M
Cortico-spinal
Transformer
tract from Muscles of
opposite Head and neck
Break anywhere cerebrum
will result in
Loss of function Ant.
horn
House cells

LMN
Skeletal
Light or muscles of trunk
Equipment M and limbs
at home
Two parents

Single parent
 Terms used
• Central nervous system (CNS): brain and spinal cord
• Peripheral nervous system (PNS): CN, spinal nerves
• Extrapyramidal, vestibular, cerebellar - systems
• Upper motor neuron (UMN): corticonuclear, corticospinal
• Lower motor neuron (LMN): cranial nerves and spinal nerves
• Neuromuscular junction - neurotransmitters
• Autonomic nervous system (ANS): sympathetic and parasympathetic
Physiology of the Extrapyramidal System
Basal ganglia circuits regulate the initiation, amplitude and speed of movements.
Diseases of the basal ganglia are collectively known as movement disorders. They
are characterized by motor deficits (bradykinesia, akinesia, loss of postural reflexes)
or abnormal activation of the motor system, resulting in rigidity, tremor, and
involuntary movements (chorea, athetosis, ballismus, and dystonia).
Several neurotransmitters are found within the basal ganglia,. Acetylcholine is
present in high concentrations within the corpus striatum. Acetylcholine acts as an
excitatory transmitter at medium-sized spiny striatal neurons that synthesize and
release the inhibitory neurotransmitter GABA and project to the globus pallidus.
Dopamine is synthesized by neurons of the substantia nigra, whose axons form
the nigrostriatal pathway that terminates in the corpus striatum. Dopamine released
by these fibers inhibits striatal GABAergic neurons. In Parkinson disease,
degeneration of nigral neurons leads to loss of dopaminergic inhibition and a relative
excess of cholinergic activity. This increases GABAergic output from the striatum and
contributes to the paucity of movement, a cardinal manifestation of the disease.
Anticholinergics and dopamine agonists tend to restore the normal balance of striatal
cholinergic and dopaminergic inputs and are effective in treatment.
 The autonomic nervous system (ANS)
ANS is the part of the nervous system that is responsible for
homeostasis. Except for skeletal muscle, which gets its innervation
from the somato-motor system, innervation to all other organs is
supplied by the ANS. Nerve terminals are located in smooth muscle
(e.g. blood vessels, the wall of the gastrointestinal tract, and urinary
bladder), cardiac muscle, and glands (e.g. sweat, salivary, tear glands).
Although survival is possible without ANS, the ability to adapt to
environmental stressors and other challenges is severely
compromised. The importance of understanding the functions of the
ANS is underscored by the fact that so many drugs used to treat a vast
array of diseases exert their actions on elements of the ANS. Also,
many neurologic diseases result directly from a loss of preganglionic
sympathetic neurons (e.g. multiple system atrophy and Shy–Drager
syndrome) and other common diseases (e.g. Parkinson disease and
diabetes) are associated with autonomic dysfunction.
From: Autonomic Nervous System
Ganong’s Review of Medical Physiology, 25e, 2016

Legend:
Organization of sympathetic (left) and parasympathetic (right) nervous systems. Cholinergic nerves are shown in red and
noradrenergic nerves are shown in blue. Preganglionic nerves are solid lines; postganglionic nerves are dashed lines.

Date of download: 3/14/2016 Copyright © 2016 McGraw-Hill Education. All rights reserved.
 Examine/Assess the functions of NS

• Mental functions: COMIBED/BEDOMIC/MOBIDEC

• Speech: aphasia/dysphasia, dysarthria, dysphonia
• Special senses: smell, vision, hearing, taste, cortical-
discriminative touch (stereognosis, graphesthesia, 2-point discrimination)
• Motor functions of cranial nerves and limbs
• Sensory functions of cranial nerves and limbs
• Diagnosis: should state the site, nature and cause of
the lesion / risk factors
 Optic radiation traverses parietal and temporal lobes to reach occipital cortex.
Parietal and temporal lobe lesions also cause homonymous hemianopia.

Frontal lobe
Reasoning, problem-solving
Visual area
Language
Imagining, planning, inhibitions Comprehension
(modesty – civility) communication
Area 8 (frontal eye field)
situated in the frontal cortex
controls conjugate
eye movements

(pursuit or saccadic eye

movements)

Left area 8 lesion will cause eyes to

remain deviated to the left side
Doll’s eye movements unaffected
 Speech is an important function served by the dominant hemisphere

These areas are supplied State the hand preference

by the middle cerebral artery of neuro patients

Wernicke’s
Pars triangularis
Pars opercularis Sensory speech
Area 45 Area 44 Area 22

Broca’s motor speech area

 Type of Auditory
aphasia
Repetition Naming comprehension Manifest
Receptive aphasia
mild – moderate mild – severe defective fluent
Wernicke's paraphasic
Transcortical
sensory aphasia good mod – severe poor fluent

Conduction aphasi poor poor relatively good fluent

a

Anomic aphasia mild mod – severe mild fluent

Expressive aphasia
mod – severe mod – severe mild difficulty non-fluent
Broca's effortful, slow
Transcortical
motor aphasia good mild – severe mild non-fluent

Global aphasia poor poor poor non-fluent

Mixed
transcortical moderate poor poor non-fluent
aphasia
 Remember the homunculus

Internal
capsule
A large area of the cortex is dedicated to cranial nerves and hands
Corticobulbar/ corticonuclear tracts bilaterally innervate cranial nerve nuclei
From: Nervous System Disorders
Pathophysiology of Disease: An Introduction to Clinical Medicine, 7e, 2013

Legend:
Schematic illustration of upper motor neuron pathways. (Redrawn, with permission, from Ropper AH et al, eds.
Adams and Victor’s Principles of Neurology, 9th ed. McGraw-Hill, 2009.)

Date of download: 3/15/2016 Copyright © 2016 McGraw-Hill Education. All rights reserved.
 Corticobulbar/corticonuclear Tract
• Occupies genu of the internal capsule, middle three-fifths of
the crus cerebri in midbrain and tegmentum of pons
• Synapses on motor nuclei of CN III, IV, V, VI, VII, IX, X, XI, XII
• The motor nuclei of cranial nerves receive bilateral
corticobulbar input. Thus, unilateral corticobulbar tract lesions
usually produce weakness, but no serious effect on head &
neck muscles, except a few, such as:
• lower part of face, part of tongue & trapezius. They receive
UMN input only from the opposite motor cortex. This explains
why contralateral lower face is paralyzed along with contralateral limbs
in a cerebral lesion, tongue might deviate to weak side & shoulder
unable to shrug, while other cranial nerves escape with insignificant
functional deficit. Dysphagia is also not uncommon in cerebral strokes.
IMPORTANT INFO
Physiology: UMN are the final common pathway between cortical and subcortical structures,
such as the basal ganglia, in the planning, initiation, sequencing, and modulation of all voluntary
movements. UMN pathways can be interrupted in the cortex, subcortical white matter, internal
capsule, brainstem, or spinal cord. Unilateral UMN lesions spare muscles innervated by lower
motor neurons that receive bilateral cortical input, such as muscles of the eyes, jaw, upper face,
pharynx, larynx, neck, thorax, and abdomen. Unlike paralysis resulting from LMN lesions,
paralysis from UMN lesions is rarely complete for a prolonged period of time. Acute lesions,
particularly of the spinal cord, often cause flaccid paralysis and absence of spinal reflexes at all
segments below the lesion, known as spinal shock. After a few days to weeks, a state known as
spasticity appears, which is characterized by increased tone and hyperactive stretch reflexes. A
similar but less striking sequence of events can occur with acute cerebral lesions.
UMN lesions cause a characteristic pattern of limb weakness and change in tone. Antigravity
muscles of the limbs become more active relative to other muscles. The arms tend to assume a
flexed, pronated posture, and the legs become extended. In contrast, muscles that move the
limbs out of this posture (extensors of the arms and flexors of the legs) are preferentially
weakened. Tone is increased in antigravity muscles (flexors of the arms and extensors of the
legs), and if these muscles are stretched rapidly, they respond with an abrupt catch, followed by
a rapid increase and then a decline in resistance as passive movement continues. This sequence
constitutes the “clasp knife” phenomenon. Clonus—a series of involuntary muscle contractions
in response to passive stretch—may be present, especially with spinal cord lesions.
 Dysarthria 
• Dysarthria can result from any condition that damages motor control of
the structures necessary for speech production, including cerebellar or
basal ganglia disorders, and the specific characteristics of the
dysarthria may be useful in localization and differential diagnosis.
Dysarthria and dysphagia are prominent symptoms of lower motor
neuron lesions of cranial nerves IX and X. These symptoms tend to be
less prominent after unilateral central lesions because of bilateral
cortical input to the nucleus ambiguus.
• Bilateral central lesions often produce dramatic speech and swallowing
problems, however. This is known as pseudobulbar palsy because the
interruption of descending input to the brainstem simulates a lesion in
the brainstem itself (a "bulbar" lesion). The character of the dysarthria
is different in patients with upper and lower motor neuron lesions.
There is classically a strained, strangled character to the speech of the
former, while the latter sound breathy, hoarse, and hypernasal.
 Some facts about CN XI
• The motor nerves of cranial nerve XI that innervate the sternocleidomastoid and
trapezius muscles originate in the cervical spinal cord (at the C1-2 level for the
sternocleidomastoid and the C3-4 level for the trapezius). They ascend alongside the
spinal cord and enter the skull through the foramen magnum, and exit the skull
through the jugular foramen. The descending cortical input to the nuclei controlling
the trapezius originates almost exclusively in the contralateral cerebral hemisphere.
The cortical input to the nucleus for the sternocleidomastoid muscle comes from
both hemispheres, but predominantly the ipsilateral one. An additional confounding
feature is that the left sternocleidomastoid rotates the head to the right (and vice
versa).
• As a result, peripheral lesions produce weakness of the ipsilateral
sternocleidomastoid and trapezius muscles, resulting in weakness of shoulder
elevation on that side but impaired head rotation to the opposite side. Central lesions
produce weakness of the ipsilateral sternocleidomastoid but the contralateral
trapezius. When a central lesion is large enough to cause more extensive weakness
(ie, hemiparesis) there is weakness of shoulder elevation on the side of the
hemiparesis and weakness of head rotation toward the side of the hemiparesis
 Tongue weakness
• The hypoglossal nerve (CN XII) receives descending cortical
input from both hemispheres equally, except for fibers
destined for the genioglossus muscle that receive their cortical
input only from the contralateral hemisphere. There appears
to be variability in this pattern; unilateral central lesions
sometimes produce ipsilateral tongue weakness, more often
produce contralateral tongue weakness, and most often
produce no significant tongue weakness. Unilateral peripheral
lesions produce weakness of the ipsilateral tongue muscles
resulting in difficulty protruding the tongue to the opposite
side. Atrophy and fasciculations are often prominent with
peripheral lesions
 Discriminative Sensations

Primary sensory cortex provides awareness of somatosensory

information and the ability to make sensory discriminations.
Touch, pain, temperature, and vibration sense are considered
the primary modalities of sensation and are relatively preserved
in patients with damage to sensory cortex or its projections from
the thalamus. In contrast, complex tasks that require integration
of multiple somatosensory stimuli and of somatosensory stimuli
with auditory or visual information are impaired. These include
the ability to distinguish two points from one on the skin (two-
point discrimination), localize tactile stimuli, perceive the
position of body parts, recognize letters/ numbers drawn on the
skin (graphesthesia), and identify objects by their shape, size,
and texture (stereognosis). Sensory inattention / extinction
 Cerebellum Physiology
The cerebellum is responsible for the coordination of muscle groups,
control of stance and gait, and regulation of muscle tone. Rather than
causing paralysis, damage to the cerebellum interferes with the
performance of motor tasks. The major manifestation of cerebellar
disease is ataxia, in which simple movements are delayed in onset
and their rates of acceleration and deceleration are decreased,
resulting in intention tremor and dysmetria (“overshooting”). Lesions
of the cerebellar hemispheres affect the limbs, producing limb ataxia,
whereas midline lesions affect axial muscles, causing truncal and gait
ataxia and disorders of eye movement. Cerebellar lesions are often
associated with hypotonia as a result of depression of activity of
alpha and gamma motor neurons. If a lesion of the cerebellum or
cerebellar peduncles is unilateral, the signs of limb ataxia appear on
the same side as the lesion. However, if the lesion lies beyond the
decussation of efferent cerebellar fibers in the midbrain, the clinical
signs are on the side opposite the lesion (ataxic hemiparesis).
 GLASGOW COMA SCALE
EYE OPENING BEST MOTOR RESPONSE BEST VERBAL RESPONSE
Spontaneous - 4 Obeys verbal command – 6 Oriented conversation – 5
To verbal command – 3 Localizes painful stimuli - 5 Disoriented conversation - 4
To pain – 2 Flexion withdrawal from Inappropriate words – 3
painful stimuli – 4
None - 1 Decorticate response to Incomprehensible words – 2
painful stimuli – 3
Decerebrate response to None - 1
painful stimuli – 2
None - 1

15 points: normal; 3 – 14 points: abnormal

 Neuroaxis
• Cortical level: One-third from axons of Betz cells in area
4; one-third from area 6; one-third from areas 3,1,2, 5
and 7
• Subcortical level: Corona radiata & Internal capsule
• Internal capsule: Anterior two-thirds of posterior limb
• Midbrain: Middle three-fifths of crus cerebri
• Pons: dispersed longitudinal bundles at the tegmentum
• Medulla: reunite to form pyramids ventrally
• Pyramidal decussation (Great motor decussation): 80%
to 90% cross the midline
• Corticospinal tracts – peripheral nerves – NM junction
 Examination of cranial nerves
• Assess the integrity of the 12 pairs of cranial
nerves
• Important to mention the side
 CN I Olfactory nerve: smell
Anatomy
-nerve fibers terminates in
olfactory bulb
-2nd order fibers run in olfactory
tract  terminate in primary
olfactory cortex of uncus in
temporal lobe.
Anosmia
- Loss of sense of smell, and food flavour
- Preserve elementary tastes: salt, sour,
sweet and bitter – carried by VII and IX
Causes
Head trauma
Tumour of olfactory groove (e.g. meningioma,
frontal glioma)
Temporarily lost after URTI / nasal blocked

Diagnosis
Test each nostril separately; use familiar items

MRI -reveals abnormalities in the olfactory bulbs

and tracts and in the inferior frontal lobes in
patients with post-traumatic olfactory
dysfunction
 R L Visual Pathway
Acuity of vision
Colour vision
Visual field
Blind spots
Pupil reflexes
Fundoscopy
SNELLEN CHART – Acuity of vision
   SNELLEN’S CHART AMERICAN CHART
IN METERS IN FEET
1 6/60 20/200

2 6/36 20/100

3 6/24 20/70

4 6/18 20/50

5 6/12 20/40

6 6/9 20/30

7 6/6 20/20

If vision poorer than 6/60 try finger counting – hand movement –

perception of light
Amsler Grid: Test for Macular Degeneration
or Other Vision Problems

Scotoma
L R
PEARLA
EWN have input from both sides

Convergence centre stimulation

results in accommodation reflex

Compression = surgical
lesion = only pupil affected

Ischaemia of nerve trunk

core = medical lesion –
pupil-sparing III nerve palsy
From: Nervous System Disorders
Pathophysiology of Disease: An Introduction to Clinical Medicine, 7e, 2013

Legend:

Extraocular muscles subserving the six cardinal positions of gaze. The eye is adducted by the medial rectus
and abducted by the lateral rectus. The adducted eye is elevated by the inferior oblique and depressed by the
superior oblique; the abducted eye is elevated by the superior rectus and depressed by the inferior rectus.
(Redrawn, with permission, from Greenberg DA et al, eds. Clinical Neurology, 8th ed. McGraw-Hill, 2012.)

Date of download: 3/16/2016 Copyright © 2016 McGraw-Hill Education. All rights reserved.
 Gaze palsy
•  An eye movement abnormality in which the two eyes move
conjugately but have limited movement in one direction is
called a gaze palsy. It is due to malfunction of one of the "gaze
centers" (cortical and brainstem regions responsible for
conjugate gaze) or to interruption of the pathways leading
from them. When the lesion is in a brainstem gaze center, the
neurons there cannot be activated either voluntarily or by
reflex (such as the oculocephalic reflex or "doll's eyes
response"). This is called a nuclear gaze palsy. When the lesion
is in a cortical gaze center (AREA 8), only voluntary gaze is
impaired; reflexes can still activate the brainstem neurons
responsible for gaze. This is called a supranuclear gaze palsy.

UpToDate
 Internuclear ophthalmoplegia
• An internuclear ophthalmoplegia or INO is
produced by a lesion in the medial
longitudinal fasciculus (MLF). This pathway
connects the sixth nerve nucleus on one side
up to the third nerve nucleus on the other,
allowing for conjugate horizontal gaze. A
lesion in the MLF is manifest by impaired
adduction on the affected side accompanied
by nystagmus in the other, abducting eye.
 Nystagmus
• Rhythmic oscillation of eyes
• Pendular nystagmus and jerk nystagmus (slow first phase and fast
corrective phase
• May be horizontal, vertical or rotary (torsional)
• Congenital and acquired
• Central and peripheral
• Peripheral: unidirectional with fast phase opposite the lesion; worse
when looking away from lesion side
• Central may be unidirectional, horizontal, vertical or torsional; fast
component is toward the side of gaze
• Downbeat nystagmus
• Upbeat nystagmus
From: Nervous System Disorders
Pathophysiology of Disease: An Introduction to Clinical Medicine, 7e, 2013

Superior tarsus
Inferior tarsus
Orbitalis:
Sympathetic
innervation

Legend:
Oculosympathetic pathways. This three-neuron pathway projects from the hypothalamus to the intermediolateral column of
the spinal cord, then to the superior cervical (sympathetic) ganglion, and finally to the pupil, the smooth muscle of the eyelids, and
the sweat glands of the forehead and face. Interruption of these pathways results in Horner syndrome. (Redrawn, with
permission, from Greenberg DA et al, eds. Clinical Neurology, 5th ed. McGraw-Hill, 2002.)

Date of download: 3/15/2016 Copyright © 2016 McGraw-Hill Education. All rights reserved.
HORNER’S SYNDROME
Case of Myasthenia gravis with muscle fatigue: before and after tensilon/edrophonium
Hypertropia of the right eye

Right CN IV paralysis
 Parks three-step test
1. Determine which eye is hypertropic in
primary position

Left eye hypertropia

 Parks three-step test
2. Determine whether the left hypertropia is
greater in right gaze or left gaze.

WOOG : Worse On Opposite Gaze

 Parks three-step test
3. Determine whether the left hypertropia is
greater with right head tilt or left head tilt
(Bielschowsky head tilt test)

BOOT : Better On Opposite Tilt (NORMAL SIDE)

The trigeminal nerve (cranial nerve V)
Downloaded from: StudentConsult (on 13 July 2009 04:28 AM)
© 2005 Elsevier
Check sensations near the midline on either side. Check for sharp as well as fine touch.
Check temporalis and masseter – clenching teeth, and pterygoids opening jaw against resistance




Dermatomes of the head and neck

Downloaded from: StudentConsult (on 13 July 2009 04:28 AM)
© 2005 Elsevier
 FACIAL NERVE
UMN innervation of UMN innervation of
Lower facial muscles Upper facial
muscles
R cortex L cortex R cortex L cortex

R 7th CN L 7th CN R 7th CN L 7th CN

nucleus nucleus nucleus nucleus
 L lower facial muscles L upper facial muscles still
paralyzed in right function in right cerebral lesion
cerebral lesion
R cerebral L cortex R cortex L cortex
lesion lesion

R 7th CN L 7th CN R 7th CN L 7th CN

nucleus nucleus nucleus nucleus
Facial Nerve: test lifting of eyebrows, eye closure,
mouth closure + puffing cheek, grin

Platisma

Downloaded from: StudentConsult (on 13 July 2009 04:28 AM)

© 2005 Elsevier
 Facial paralysis

Unilateral
Bilateral
UMN Lesion LMN lesion/Bell’s palsy
- Mainly affects -Weakness (ipsilateral) of
lower part of all facial muscles -Rare (<1%) – LMN type
the face opposite - Unable to close eye - bilateral weakness is less
side. Pulled to - No corneal reflex obvious than unilateral
normal side - Hyperacusis – stapedius weakness (no facial
- Features : paralysis asymmetry). GBS / AIDP
- Eyebrow & eye - Loss of taste sensation
closure spared: ant 2/3 tongue – chorda
blinking present tympani

76
 Vestibulocochlear nerve - VIII
• Body balancing system
• Dysfunction will cause vertigo, vomiting, loss of balance
• Hearing tested by rubbing of fingers
• Rinne’s test and Weber’s test, if hearing ↓
• Positive Rinne’s test – normal – air conduction is better
than bone conduction
• Weber’s test: lateralizes to blocked side – in conduction
deafness, and to normal side in nerve deafness
 IX Glossopharyngeal, X Vagus
• Supplies muscles of deglutition, vocal cords, soft
palate: closes nasopharynx, while swallowing and
speaking
• Uvula will be pulled to normal side
• Nasal intonation of voice, nasal regurgitation,
hoarseness of voice, bovine cough, dysphagia
• Sensory to pharynx & posterior part of tongue
• Gag reflex: afferent IX and efferent X
• Sense of taste to posterior 1/3 of tongue
Glossopharyngeal and Vagus

Arching of the palate, ignore the uvula

Gag reflex - touch both sides

Swallowing test

Any nasal regurgitation ?

Any nasal intonation of voice ?

Any hoarseness of voice ?

 Denervation Atrophy of the Tongue after Hypoglossal-Nerve Injury
Wasted and wrinkled right half of tongue with deviation to right side
Result of right hypoglossal nerve paralysis (LMN) outside brainstem

Junquera L, Gallego L. N Engl J Med 2012;367:156-156.

 Remember cranial nerves?
• Which one is commonly affected in a cerebral
stroke?
• Which one is affected in Parkinson’s disease?
• Where is the lesion in Bell’s palsy?
• Tongue deviates to weak side or normal side?
• Jaw deviates to weak side or normal side?
• Face deviates to normal side or weak side?
• Uvula deviates to normal side or weak side?
• Which is the strongest cranial nerve muscle?
 EXAMINATION OF LIMBS
• What can you diagnose?
• Motor dysfunction – paralysis / paresis
• Extrapyramidal system dysfunction – slowness,
tremor, rigidity, abnormal movements
• Sensory dysfunction – which tract affected
• Cerebellar dysfunction - ataxia
• Proximal myopathy, muscular dystrophy
• Autonomic dysfunction: dryness of skin
 Pronator Drift

Pronator drift shows subtle weakness due to UMN lesion

Also test check reflex and look for piano movements

UMN lesions do not affect all muscles equally
Darcy P, Moughty AM. N Engl J Med 2013;369:e20.
 Upper Limb Myotomes
Joints Muscles Nerve roots
Shoulder Abductors, Lateral rotators
Adductors, Medial rotators C5, 6, 7, 8
Elbow Flexors C5, 6
Extensors C7, 8
Forearm Supinators C6
Pronators C7, 8
Wrist Flexors & Extensors C6, 7
Digits Long flexors & extensors C7, 8
Hand Intrinsic muscles C8, T1
 Lower Limb Myotomes
Joints Muscles Nerve roots
Hip Flexors, adductors L1, 2, 3
Medial rotators
Extensors, Abductors, L5, S1
Lateral rotators
Knee Extensors L3, 4
Flexors L5, S1
Ankle Dorsiflexors L4, 5
Plantar flexors S1, 2
Foot Invertors L4, 5
Evertors L5, S1
Pattern of weakness in UMN lesion
• Upper limb – adducted, medially rotated,
flexed at elbow and wrist
• Lower limb extended at hip and knee, plantar
flexed and laterally rotated and inverted
• This allows a stroke patient to walk with a
circumduction gait
 Neuro examination of limbs
• Posture of limbs, muscle bulk/wasting, fasciculation,
texture/consistency of the muscles
• Muscle tone, check each major joint separately
• Muscle power, check each joint separately, at least 2
movements for each joint
• Tendon reflexes
• Coordination
• Sensory: check dorsal column and spinothalamic tract
sensations & cortical/discriminatory sensations
 What is muscle tone?
• The resistance of a muscle to stretch due to stretch reflex is referred to as
muscle tone. Normal tone, especially of axial muscles, is required to keep
body posture.
• If the motor nerve to a muscle is severed (LMN lesion), the muscle offers no
resistance and is said to be flaccid.
• Hypotonia will also result from cerebellar lesion and acute stages of UMN
lesion.
• Hypertonia results when the resistance to stretch is high because of
hyperactive stretch reflexes. Two types: rigidity and spasticity
• Spasticity occurs in pyramidal tract lesion and rigidity in extrapyramidal
lesion.
• The sequence of stretch reflex and inverse stretch reflex in UMN lesion
produces the clasp-knife effect, which resembles the closing of a pocket
knife.
 Muscle tone
• Muscle tone is the resistance felt on passive movement of a joint –
caused by contraction of some muscle fibers
• The patient should be fully relaxed (not trying to help in the
movement)
• Know what is normal tone first by examining normal people
• Tone can be decreased – hypotonia, flaccidity
• Tone increased – hypertonia (spasticity and rigidity – lead-
pipe/plastic, and cogwheel)
• Spasticity occurs in UMN lesion and rigidity in extrapyramidal lesion
• Spasticity is velocity dependent stretch reflex, sudden ‘give’ and not
continuous. Rigidity is not velocity dependent
 How to examine a case of PD
• Neurological examination is same as in any other neuro
case: Observe for abnormal movements, posture, muscle
tone, power, reflexes, coordination, sensory system and gait
• In PD, resting tremor, mask-like face with poverty of
expressions and infrequent blinking can be observed
instantly
• Power, reflexes, coordination and sensory system will be
normal
• The cardinal signs, such as resting tremor, rigidity,
bradykinesia have to be demonstrated.
 Eliciting clonus
• Clonus occurs when a muscle is stretched suddenly
• Patellar clonus – quadriceps femoris, attached to
the patella - is stretched by pushing patella down
• Ankle clonus – calf muscles stretched on eversion
and dorsiflexion of foot
• Clonus can occur at wrist also, sometimes
• One or two movements can be normal. Sustained
clonus is pathological
 Muscle Power
• Compare left and right
• Test 2 movements for each major joint
• Use MRC grading scale for muscle power
– 0 = no movement
– 1 = only a flicker of movement seen
– 2 = able to move towards gravity
– 3 = able to move against gravity
– 4 = able to resist pressure to some extent
– 5 = full power, able to resist fully
• Ask the patient to perform the movement first (grade 3/5),
then apply pressure to look for 5/5 or 4/5
 Hoffmann’s sign
• Positive in UMN lesion with hyperreflexia
• Flicking the middle finger causes flexion of
thumb and other fingers
Tendon reflexes: spinal roots
involved

Biceps jerk C 5, 6
Supinator jerk C 6
Triceps jerk C 7, 8
Knee jerk L 3, 4
Ankle jerk S 1, 2
If the tendon reflex shows no response

• Do reinforcement before declaring it absent

• Jendrasic maneuver: ask patient to clench
teeth or fist, then elicit the reflex again
• Grading: 0 = absent, 1 = present on
reinforcement, 2 = normal, 3 = hyperreflexia
 How to elicit tendon reflexes
• Needs practice
• Lift and drop the tendon hammer – don’t hit
• Start with a gentle stimulus, increase if needed
• Learn how to perform them from the right side
of the bed and in different postures of the
patient (lying, sitting)
 Plantar reflex
• Use a blunt object like a key, orange stick;
support it, do the action slowly and
deliberately. Use some pressure, and stop the
stimulus as soon as you see the response.
• If positive, it is called up-going plantar reflex
(Babinski sign)
• Normal plantar reflex is described as down-
going
 Abdominal reflex
• Umbilicus moves towards the stimulus in all
the four quadrants
• Abdominal reflex will be absent in UMN as
well as LMN lesions
 Upper motor Lower motor
neuron lesion neuron lesion

Wasting  ++
Fasciculations - ++
Tone Flaccid spastic Flaccid
Clonus ++ -
Power
Reflexes Or -
Plantar response Or -
Hoffman’s sign + -
 Features of cerebellar disease
• Signs are ipsilateral - DAANISH
• Dysmetria – unable to control the range, overshoot
• Ataxia – clumsy movements
• Adiadakokinesia / Dysdiadokokinesia- inability to perform rapid
alternating movements smoothly
• Nystagmus
• Intention tremor (not intentional)
• Speech – staccato speech - dysarthria
• Hypotonia, pendular knee jerk
• Broad-based gait
 Look for features of extrapyramidal system
disorder
• Look for tremor when the hands are resting
• PD tremor is described as pill-rolling, slow, resting;
disappears when the limb is used
• The tremor gets worse, when the patient is
stressed
• Test speed of movements – finger tapping, foot
tapping – look for asymmetry – slowness
• Rigidity; stooping posture, gait
• Asymmetry is typical in PD
 Sensory system examination
• Test both the tracts: spinothalamic and DCML
• At least one test for each tract
• Spinothalamic: pain, temperature, crude touch
• DCML – fine touch, proprioception (joint
position sense), vibration
• Discriminatory sensations: graphesthesia,
stereognosis and 2 point/touch discrimination
• Sensory loss can be total or dissociated
 Sensory system examination
• Dermatomal pattern sensory loss is possible in
spinal cord lesions
• Peripheral nerve distribution pattern sensory loss in
isolated nerve lesions
• Hemisensory loss (hemianaesthesia) is possible in
lesions in the brainstem, thalamus, internal capsule
• Dissociated sensory loss in spinal cord hemisection,
syringomyelia and lower medulla lesion
Dermatomes
Patterns of sensory loss possible
 Gait
• Test usual walking – observe arms swing,
slowness of movements, posture of upper limbs,
movements of lower limbs, turning around (en-
block turning in PD)
• Tandem walking (heel to toe), if needed
• Walking on tip toes, walking on heels, if needed
Common abnormalities: Hemiparetic gait, antalgic
shuffling gait, broad-based gait, high stepping,
stamping, waddling gait of proximal myopathy
• Romberg sign: positive in sensory ataxia