NEURO ANATOMY OF BRAIN

INTRODUCTION
• CNS consists of brain and spinal cord. Brain is situated within the
caranial cavity and the spinal cord lies within the vertebral
column
• In the brain the grey matter is present arounf the periphery and
the white matter in the centre
• The brain is protected by the cranium (bony covering), the
meninges – dura mater, arachnoid mater and pia mater and the
CSF (arachnoid space)
PARTS OF THE BRAIN
• Fore brain – cerebrum + diencephalon
• Mid brain
• Hind brain – pos, medulla, cerebellum
CEREBRUM
• Longitudinal cerebral fissure – divides into two hemispheres
• Corpous collosum – joins the two hemispheres across the median
plane
• Each cerebral hemisphere consist of
Outer grey matter
Inner white matter
Basal ganglia
Lateral ventricle
• Each cerebral hemisphere has 3 poles
 Frotal pole
Temporal pole
Occipital pole
• Lobes of cerebral cortex
Frontal
Parietal
Temporal
Occipital
• Surfaces of cerebral cortex
Superolateral
Medial
Inferior
• Borders of cerebral cortex
Supromedial
Inferolateal
Medial orbital
Medial occipital
BASAL GANGLIA
Parts of the basal ganglia
Corpus straitum
Caudate nucleus
Lentiform nucleus
Claustram
Aygdaloid body
Caudate nucleus has a head, body and a tail
 Lentiform nucleus – lateral surface, medial surface, inferior
surface
Amygdaloid body – nuclear mass in the temporal lobe and is
continuous wth the tail of caudate nucleus
Claustrum – saucer shaped nucleus between the putamen and
insula
Functions:
• Corpus straitum regulates muscle tone and help in smoothening
voluntary movements
• It controls automatic movements and coordinated movements of
different parts of the body for emotional expression
INTERNAL CAPSULE
• Large band of fibres situated in the inferomedial part of cerebral
hemispheres
• In horizontal sections of brain it appears v shaped with its
concavity directed laterally
• It consists of fibrous going from and to the cerebral cortex
THALAMUS
• Large ovoid mss of grey matter above the mid brain
• Largest part of diencephalon
• Thalami on both sides are separated by the cavity of the 3rd
ventricle
HYPOTHALAMUS
• Most inferior part of diencephalon and contains several small
nuclei and tracts
• Mamillary bodies appear as rounded elevation on the base of the
brain in the region of interpenduncular fossa
METATHALAMUS
• Consists of two rounded medial and lateral geniculate bodies
which protrude from posterior inferior surface of thalamus
EPITHALAMUS
• Lies posterosuperior to thalamus
• Consists of pineal gland and habenular nuclei
SUBTHALAMUS
• Small area that lies between thalamus and midbrain
• It contains several nerve tracts and subthalamic nuclei which are
associated with basal ganglia
LIMBIC SYSTEM
• The limbic system is a complex set of structures that lies on both
sides of the thalamus, just under the cerebrum
• It includes the hypothalamus, the hippocampus, the amyglanda
and several other nearby areas
• It appears to the primarily responsible for our emotional life, and
has a lot to do with the formation of memories
• HIPPOCAMPUS – is concerned with long term memories
BRAINSTEM
Mid brain
• Connects forebrain with the hind brain
• Cavity is called cerebral aqueduct, connects third ventricle with
the fourth ventricle
Transverse section through midbrain
• Tectum is the part posterior to aqueduct
• Each half of the midbrain anterior to aqueduct is called cerebral
peduncle
• Each cerebral peduncle is divided into
a) CRUS CEREBRI – anteriorly
b) SUBSTANTIA NIGRA – middle
c) TEGMENTUM – posteriorly
• Medial and lateral geniculate bodies are situated in the posterior
aspect of midbrain
• Superior colliculus is connected to lateral geniculate body by
superior brachium, inferior colliculus is connected to medial
geniculate body by the inferior brachium
PONS
• Large middle part of brainstem
• Has two surfaces
a) Ventral
b) Dorsal
• Dorsal surface is hidden by the cerebellum, and forms the upper
half of the floor of fourth ventricle
VENTRAL SURFACE
• Ventral surface is convex towards both sides and is transversely
striated
• In the median plane it shows a vertical basilar sulcus which
lodges the basilar artery
• Laterally the surface is continuous with the idle cerebellar
peduncle
• Trigeminal nerve is attached to this surface at the junction of pons
with the peduncle
• Abduceent, facial and vestibulocolear nerve are attached to the
lower border
MEDULLA
• Lies in the anterior part of posterior cranial fossa extending down
to the foramen magnum
• Medulla is divided into the right and left halves by the anterior,
lateral and posterior regions by anterolateral and postolateral
sulci
• Anterior region is in the form of an elevation called the pyramid
• Upper part of the lateral region shows an oval elevation
• The rootlets of hypoglossal nerve emerge from the anterolateral
sulcus between the pyramid and the olive
• Rootlets of 9th and 10th and the cranial part of accessory nerve
emerges through the posterolateral fissure
• Upper part of the posterolateral region shows a V shaped
depression which is the lower part o the floor of fourth ventricle
 • Below the floor three elevations are seen: fasciculus racillis,
fasciculus cueatus and inferior cerebellar peduncle
• Upper ends of fasciculus grascillis and fasciculus cutenatus
expands to form the gracile and cuneate tubercles
• In the lower part of medulla there is another elevation called
tubercinerium produced by spinal nucleus of trigeminal nerve
• Medulla is divided into two parts, the lower closed with a central
canal, upper open part where central canal opens out to form the
fourth ventricle
CEREBELLUM
• Largest part of hind brain
• Grey matter is highly folded and the arrangement is called arbor
vitae
• Consists of two cerebellar hemispheres united to each other
through a median vermis
• Superior surface is convex, the two hemispheres are continous
• Inferior surface has a notch called vallecula that seperates the two
hemispheres
Each hemisphere is divided into three lobes
1.Anterior lobe – lies on the anterior part of superior surface
2.Middle lobe – largest
3.Flocculonodular lobe – smallest
• Middle lobe is limited in front by the fissure prima and by the
posterlateral fissure on the inferior surface
• Cerebellum is divded into numerous small parts by fissures
• Horizontal fissure – sperates superior surface from the inferior
 • Fissure prima – seperates anterior lobe from the middle lobe on
the superior surface
• Posterolateral fissure – seperates middle lobe from the
flocculonodular lobe on the inferior surface
VENTRICLES OF THE BRAIN
• Lateral ventricles – irregular cavities situated on each cerebral
hemisphere
• Each communicates with the third through an intraventricular
foramen
• Each lateral ventricle has – central part and three horns –
anterior, posterior and inferior
THIRD VENTRICLE
• median cleft between the two thalami
• developmentally it represents the cavity of the diencephalon
• posteriorly it communicates with thefourth ventricle through
cerebral aqueduct
FOURTH VENTRICLE
• last and lowest ventricle of cerebrum
• tent shaped
• its roof contains three apertures for the closely guarded release of
CSF into the sub arachnoid space
• dorsally on the lower par of the roof there is a median aperture
foramen of magendie
• on either sides iit communicates with the subarachnoid space
through lateral apertures foramina luchka
CSF PATHWAY
Lateral ventricles→ foramen of monro→ third ventricle→ cerebral
aqueduet→ fourth ventricle→ foramen of luschka and magendie
→subarachnoid space→ arachnoid villi →venous drainage system of
brain

Spinal cord anatomy

• The spinal cord is the long cylindrical lower part of the CNS
occupying the upper two thirds of the vertebral canal.
• It is continuous rostrally with the medulla oblongata at foramen
magnum and ends caudally as tapered conus medullaris, at the
level of lower border of first lumbar vertebra (L1).
• It gives origin to 31 pairs of spinal nerves. The region of origin of
a pair of spinal nerves is called spinal segment.
• The spinal cord has central grey and peripheral white matter.
• In transverse section the grey matter has an irregular H-shape,
and looking somewhat similar to a butterfly with two anterior
horns, two posterior horns and a grey commissure containing a
central canal.
• In the thoracic and upper two lumbar segments there are also
lateral horns because these segments of spinal cord are
associated with the autonomic nervous system.
• In three-dimensional view of grey matter of a spinal segment, the
horns appear as long vertical pillars hence now a days, they are
termed grey columns.
• However, the term ‘horn’ is still frequently used in texts on
physiology and medicine.
• In each half of the spinal cord, the white matter is divided into
anterior, lateral and posterior white columns or funiculi.
 • Each funiculus is subdivided into fasciculi or nerve tracts.
• The individual nerve fibres carrying action potentials to
(ascending) or from (descending) the brain are usually grouped
together to form fasciculi/tracts.
• The spinal cord is extremely important for the overall function of
the nervous system.
• It forms the communication link between the brain and the
peripheral nervous system below the head, integrating incoming
information and producing responses through reflex mechanisms.
• The spinal cord is the lower elongated part of the central nervous
system (CNS).
• It is cylindrical in shape, slightly flattened anteroposteriorly and
occupies the upper two-third of the vertebral canal.
• Spinal cord measures about 45 cm (18”) in adult male and 42 cm
in adult female, and weighs about 30 g.
• It extends as a downward continuation of medulla oblongata from
the upper border of the posterior arch of first cervical vertebra
(C1) to the lower border of the first lumbar vertebra (LI).
• Its lower tapering extremity is called conus medullaris.
• The apex of conus medullaris continues downwards as a thin,
thread-like filament called filum terminale.
• Spinal cord provides attachment to 31 pairs of spinal nerves which
connect it to the tissues of the trunk, girdles, limbs, and the
viscera.
• The spinal cord contains large number of ascending and
descending pathways, which serve as conduits for nervous
information, passing to and fro between different parts of the body
and the brain.
Functions of the spinal cord
• The execution of simple reflexes.
• The transmission of impulses to and from the brain
 Visual pathway
Origin of the Optic Nerve
• The fibers of the optic nerve are the axons of the cells in the
ganglionic layer of the retina.
• They converge on the optic disc and exit from the eye, about 3 or 4
mm to the nasal side of its center, as the optic nerve.
• The fibers of the optic nerve are myelinated,but the sheaths are
formed from oligodendrocytes rather than Schwann cells, since
the optic nerve is comparable to a tract within the central nervous
system.
• The optic nerve leaves the orbital cavity through the optic canal
and unites with the optic nerve of the opposite side to form the
optic chiasma.
Optic Chiasma
• The optic chiasma is situated at the junction of the anterior wall
and floor of the third ventricle.
• Its anterolateral angles are continuous with the optic nerves, and
the posterolateral angles are continuous with the optic tracts.
• In the chiasma, the fibers from the nasal (medial) half of each
retina, including the nasal half of the macula, 1 cross the midline
and enter the optic tract of the opposite side, while the fibers from
the temporal (lateral) half of each retina, including the temporal
half of the macula, pass posteriorly in the optic tract of the same
side.
Optic Tract
• The optic tract emerges from the optic chiasma and passes
posterolaterally around the cerebral peduncle.
• Most of the fibers now terminate by synapsing with nerve cells in
the lateral geniculate body, which is a small projection from the
posterior part of the thalamus.
 • A few of the fibers pass to the pretectal nucleus and the superior
colliculus of the midbrain and are concerned with light reflexes
Lateral Geniculate Body
• The lateral geniculate body is a small, oval swelling projecting
from the pulvinar of the thalamus.
• It consists of six layers of cells,on which synapse the axons of the
optic tract.
• The axons of the nerve cells within the geniculate body leave it to
form the optic radiation.
Optic Radiation
• The fibers of the optic radiation are the axons of the nerve cells of
the lateral geniculate body.
• The tract passes posteriorly through the retrolenticular part of the
internal capsule and terminates in the visual cortex (area 17),
which occupies the upper and lower lips of the calcarine sulcus on
the medial surface of the cerebral hemisphere.
• The visual association cortex (areas 18 and 19) is responsible for
recognition of objects and perception of color.
blood supply to brain and spinal cord
To brain and spinal cord (circle of willis) →sub arachnoid space
In the circle of willis
Anterior circulation
Posterior circulation
Anterior circulation
↓
Common carotid artery
↓ ↓
Internal carotid artery external carotid artery
↓ ↓
Brain face
↓ ↓
Anterior circulation posterior circulation
↓ ↓
Cerebral artery basilar artery
↓ ↓
Anterior and middle cerebral artery vertebral artery→posterior
cerebral artery
 Anterior circulation
↓
Origin: arch of aorta
↓
Ascending (common carotid artery)
↓
Enter into neck through common carotid artery
↓ ↓
Internal carotid artery external carotid artery
↓ ↓
Enter into cerebrum supply to face
↓ ↓
Anterior middle
Cerebral artery
↓ ↓ ↓ ↓
Rt lt rt lt
↓(superficial) ↓(deep)
Supply to frontal and paraital
Posterior circulation
Origin: arch of aorta
↓
Subclavian branch
↓ start
Vertebral artery
↓
Enter into base of the neck
↓
Passes through foramen magnum
↓
posterior cerebral artery
↓ ↓
Right left
(supply to temporal and occipital lobe)
BRANCHES OF CIRCLE OF VILLIS
Cerebral portion
Cranial portion → basilar artery
Cerebral portion
The combine of anterior cerebral artery and middle cerebral
artery
Opthalamic artery, it enters into the orbit
Optic canal
Optic nerve (lateral)
Posterior communicating artery, it passes above oculomotor nerve
Anterior cerebral artery it passes to the medial aspect of optic
nerve and also this is present opposite of anterior communicating
artery
Middle cerebral artery – largest branch in cerebral portion it
enter in cerebral sulcus
Cranial portion
Subclavian artery passes to the foramen
Vertebral artery
↓
Subclavian artery
↓passes to foramen transverse
6th cranial vertebra
↓
Enters skull
↓
 Foramen magnum
↓
Subarachnoid space
↓
2border
↓ ↓
Upper lower
↓ ↓
Medulla basilar artery
Posterior spinal artery
↓enters in (arises from artery)
Posterior spinal cord
Anterior spinal artery
↓enters in (arises in medulla)
Anterior/ posterior spinal cord
Meningeal branch
↓
Cranial bone
Postero inferior cerebral
↓
Largest branch
↓
 Supply to cerebellum and medulla oblongata
↓
Postero inferior cerebral artery
Basilar artery
↓
Pontine artery
↓
Labrynithen artery
Areas of the brain
Corpus straitum and internal capsule
Middle cerebral artery
Anterior cerebral artery
Thalamus
Posterior cerebral artery
Posterior communicating artery
basilar artery
midbrain
posterior cerebral artery
superior cerebral artery
basilar artery
pons
anterior cerebral artery
superior cerebral artery
inferior cerebral artery
medulla oblongata
vertebral artery
 anterior spinal artery
posterior spinal artery
cerebellum
superior cerebral artery
anterior cerebral artery
postero inferior cerebral artery
Veins of brain
external cerebral vein
internal cerebral vein
Blood supply and area of the spinal cord
3 small artery present – 2 posterospinal artery and 1 anterior
spinl artery
Posterior spinal artery
↓
It directly comes from vertebral artery
↓
Inside the skull it is connected in posteroinferior cerebral artery
Anterior spinal artery
↓
Inside the skull it was connected to vertebral artery
 BLOOD SUPPLY TO THE OPTIC PATHWAY
↓ ↓
Carotid arterial system vertebral arterial system
↓
Posterior communicating artery
Middle cerebral artery
Posterior cerebral artery
Optic lesions
It damage completely – complete lesion
Optic atrophy – muscle weak
Optic neuropathy – nerve weak\
Acute optic neuritis
Central serotoma
Central of eye is affected whether in right/ left side
It will damage partially – partial lesion
Pre – optic chiasma
Right eye get most affected
It cause damage to nasal cavity and right side (heianopia) in an
eye
Homonius – both eyes medial aspect get affected
Occipital lobe
It mostly affect the left side eye
Here also both – hemianopsia and homoninus are present
Optic tract and lateral geniculate body
Color blindness
 Cranial nerves
There are 12 pairs of cranial nerves
Olfactory nerves (sensory fiber)
Origin: It was origin in the olfactory nerve receptor cell, olfactory
bulb, olfactory tract, olfactory nerve fiber
Insertion and opening to the skull: opening in the plate of
ethmoid bone
Function: smell
Optic nerve
Origin: back of the eyeball, optic tract, thalamus, optic chiasma,
retina
Insertion and opening to the skull: optic canal
Function: vision
Occulomotor nerve
Origin: anterior surface of midbrain and also ciliary muscle and
ciliary ganglion, sphincter of the eye ball
Insertion and opening to the skull: superior orbital fissure
Function: rises upper eyelid, turns eyeball upward downward and
medially
Trochlear nerve
Origin: posterior surface of brain, posterosuperior oblique
muscle, superior orbital
Insertion and opening to the skull: superior orbital fissure
 Function: assisting in turning eyeball downward and laterally
Trigeminal nerve
Ophthalmic nerve
Origin: from anterior aspect of pons
Insertion and opening to the skull: superior orbital fissure
Function: skin of foreheaf movement, scalp, eyelids and nose
movement, musocus membrane of paranasal sinus and nasal
cavity
Maxillary nerve
Origin: anterior aspect of pons
Insertion and opening to the skull: foraen ovulae
Insertion: skin of face over jaw, teeth of the upper jaw, mucus
membrane of nose and maxillary sinus and palate
Mandibular nerve
Origin: anterior aspect of the pons
Insertion and opening to the skull: foramen roudum
Insertion: muscle of mastigation, anterior belly of diagnostic,
tensor tympani
Abducens nerve
Origin: medulla oblangata
Insertion and opening to the skull: superior orbital fissure
Function: lateral rectus muscle, eyeball movement laterally
Fascial nerve
Origin: medulla oblangata
 Insertion and opening to the skull: internal fascial canal and
stylomastoid foramen, all fascial muscle
Function: all fascial expression
Vestibulocochlear nerve
Origin: medulla oblangata
Insertion and opening to the skull: internal acoustic meatus
Function: vestibular division is for positioning the head
Glossopharyngeal nerve
Origin: medulla oblangata
Insertion and opening to the skull: jugular foramen
Function: swallowing, half of tounge and pharynx function
Vagus nerve
Origin: medulla oblangata
Insertion and opening to the skull: jugular foramen
Function: continuation of the 9th nerve and passes to the liver,
kidney, pancreas and great thoracic blood vessels
Accessory nerve
Origin: medulla oblangata
Insertion and opening to the skull: jugular foramen
Function: sternoclyoastoid and trapezius
Hypoglossal nerve
Origin: medulla oblangata
Insertion and opening to the skull: hypoglossal canal
 Function: muscle of tounge

Cerebellum
INTRODUCTION
It is the dorsal part ad largest of the hind brain and it presents in
the cranial fossa
Behind the cerebellum, pons and medulla oblongata was present
4th ventricle seperates the cerebellum fro the pons and medulla
Occipital lobe and cerebellum are separated by tendorium
cerebella
CONNECTIONS
Inferior cerebellar pednucleus
Middle cerebellar pednucleus
Superior cerebellar pednucleus
EXTERNAL FEATURES
It presents in oval shape, the transverse measurement is greater
than anteroposterior measurement
Weight – 150g
Dividing area of two cerebellar hemisphere is vermis
Surfaces
Superior cerebellar surface
Inferior cerbellar surface
Superior
It is elevated in midline in superior aspect superior vermis is
present
Inferior
In this inferior vermis is present, in this surface one groove is
present called vallecullar
NOTCHES
Anterior cerebellar notch
It was wide, shallow and v shape
Posterior cerebellar notch
Deep and narrow
FISSURES AND SULCI
Horizontal fissure
Seperates the superior and inferior surface
Postrolateral fissure
Separate inferior surface
Primary fissure
It appears only at development, it is present in v shape
INTERNAL STRUCTURE OF CEREBELLUM
Layers –
Grey matter (external)
White matter (internal)
Under the grey matter two structure present
Cerebellar cortex
Cerebellar nuclei
Under white matter
Intra cerebellar fibres
Extra cerebellar fibres
Connects the cerebellum to the spinal cord
CEREBELLAR STRUCTURE
Tonsil
It is a small lobular present in inferior surface of cerebellum. In
this area, it was raised by maintain the intracranial pressure. In
that foramen magnum and subarachnoid space, CSF and circle of
willis was maintained by this structure
LOBES OF CEREBELLUM
Vestibular cerebellum
Spino cerebellum
Ponto cerebellum
BLOOD SUPPLY TO CEREBELLUM
Superior cerebellar artery and vein
Anterior cerebellar artery and vein
Posteroinferior cerebellar artery and vein
FUNCTIONS OF CEREBELLUM
Vestibulocerebellar lobe
Maintaining the equilibrium of the body
Spinocerebellar lobe
Regulates the muscels tone and posture
Pontocerebellar lobe
It maintains the co – ordination and voluntary movement

Pyramidal system
It is otherwise known as corticospinal tract. It is a decending tract
originated from pyramidal cells of motor cortex
This pathway is concentrated in skill movements specially at the
distal parts of limbs. It promotes the movements of flexors of leg
and extensors of arms

Extra pyramidal system

It is a center, modulate and regulate the pyramidal system (in –
direct control)
Centers
Cortical center
Subcortical center
Basal ganglia (where tract passes through)
Putamen
Caudate nucleus
 Globus pallidus
Interbrain
Subthalamic nucleus
Thalamus
Midbrain
Reticular nucleus
Substansia nigra
Superior colliculus
Hindbrain
Vestibular nucleus
Olivar nucleus
Pontine nuclei
Reticular nuclei
Cerebellar nuclei
FUNCTIONS OF PYRAMIDAL SYSTEM
It regulates muscle tone with the help of that is was maintain
posture and equilibrium
It controls automatic associate movements such as co – ordination
movements of arms and legs during walking
It control reflex muscular activity
CONNECTION B/W THE CEREBELLUM AND PYRAMIDAL
SYSTEM
Afferent pathway
 Efferent pathway
Afferent pathway
Cortex → pons → cerebellum →thalamus
Cortex → striatum →thalmus
Cortex → substansia nigra →thalamus
Cortex →pallidum → thalamus
Efferent pathway
Olivo spinalis tract
Supraspinalis tract
Vertibulospinalis tract
Tectospinalis tract
Reticulospinalis tract

Spinal tract
Ascending tract
Decending tract – pyramidal tract, extra pyramidal tract
Intersegmental tract
ASCENDING TRACT
The impulses/ information are passing through the spinal to
higher center
DECENDING TRACT
The impulses are passes higher centers to the spine
INTERSEGMENTAL TRACT
The result of spinal response is intersegmental tract
POSITION
Anterior
Posterior
Lateral
Anterior
Ascending tract
Anterior spino thalamic tract
Decending tract
Anterior Cortico spinal tract
Vestibule spinal tract
Tecto spinal tract
Media reticulospinal trac
Intersegmental tract
Anterior intersegmental tract
Lateral
Ascending tract
Posterior spino cerebellar tract
Anterior spinocerebellar tract
Lateral spino thalamic tract
Spinotectal tract
Dorsal lateral tract
Decending tract
Lateral corticospinal tract
 Rupra spinal tract
Lateral reticulospinal tract
Olingospinal tract
Descending automatic fibers
Intersegmental tract
Lateral intersegmental tract
Posterior
Ascending tract
Fasiculo gracillis
Decending tract
Septomarginal tract
Intersegmental tract
Posterior intersegmental tract
FUNCTION OF THE TRACT
Decending tract
Corticospinal tract
It involves both crossed and uncrossed types
Origin: from motor area of brain
Function: controls voluntary movements
( eg: right upperlimb moved – left lower limb move involuntary)→ we
can treat and cure the spinal injury
Rubrospinal tract
Crossed
Origin: red nucleus of mid brain
 Function: facilitated the flexor muscle tone
Reticulospinal tract
Medially it was uncrossed
Laterally both (crossed & uncrossed)
Origin: brain stem of reticular formation
Function: action on voluntary movements and muscle tone
Tectospinal tract
It is crossed tract
Origin: brain stem of reticular formation
Function: action on voluntary movements and muscle tone
Vestibulospinal tract
It is a uncrossed one
Origin: lateral vestibulonuclei of medulla oblongata
Function: controls the body equilibrium
Oligospinal tract
Mostly present in crossed manner
Origin: inferior olivary nucleus medulla oblongata
Function: forms the part of extra pyramidal system (lesions leads
to paraplegia)
Asecending tract
Anterior spial and lateral spinal tract
It is a crossed tract
Function: simple touch and pressure, pain and temperature
Faciculous gracilis
It is uncrossed one
It concentrated in the impulses of leg and lower part of trunk
Fasiculous cuneatus
It was uncrossed one
It concentrated in the impulses of upper part trunk and neck
(2) and (3) function: it give impulses to the muscles, tendon and joints
to the cerebral cortex – vibration sense and fine touch
Anterior spino cerebellar tract → crossed
Posterior spino cerebellar tract → uncrossed
Function: proprioceptive impulses from muscles, tendon and joints to
the cerebellum (maintain spine structures balance)
Spino tectal tract:
Function: it was useful for spino visual reflex
Spino olivery tract
It is crossed one
Function: proprioceptive impulses to the olivery muscles
Dorso lateral tract
Function: useful for pain and temperature
 Plexus
The network of axon is called as plexus. In that spinal nerves, 2 rami
are present
anterior rami
posterior rami
in that spinal cord the anterior rami and posterior rami is
connected in one network called plexus

cervical plexus
Root value:
Anterior rami of c2 – c4 also a contribution from c1
It consist of – muscular and cutaneous branch
In cervical plexus, anterior and posterior rami in 4 cervical
vertebra. It supplies to head, neck, superior part of shoulder and
chest

Nerves:
Hypoglossal nerve
Lesser and great occipital nerve
 Transverse cervical nerve
Ansa cervicalis – anterior and posterior root
Supraclavicular nerve
Hypoglossal nerve:
12th cranial nerve
Passes to the tounge
Arises from medulla oblongata and comes to c1 vertebra
Lesser and greater occipital nerve:
Small nerve present b/w 2nd and 3rd cervical vertebra. It passes to
the scalp and neck
Transverse cervical nerve
It is present in 2nd and 3rd cervical
Posterior border of SCM, near to external jugular vein
Ansa cervicalis
Present near to jugular vein
Present exactly on the carotid triangle other name – handle of
neck
Supraclavicular nerve
Descending nerve
Present in 3rd and 4th cervical
Passes to the posterior triangle of neck and also platysma
Muscular branch
Rectus captitis anterior
Rectus capitis lateralis
Longus colli
Inferior oblique
Longus capitis
Cutaneous branch
Lesser occipital nerve
Great auricular nerve
Transverse cervical nerve
Supraclavicular nerve

Brachial plexus
Anterior primary rami of spinal nerve c5 – c8 and t1
Roots: c5 – t1
Trucnks: upper, middle and lower
Cords and branches: lateral, medial and posterior
Branches: nerves to serratus anterior, nerves to rhomboid
Trunk: suprascapular nerve, subclavius nerve
Cords: lateral pectoral, musculocutaneous, lateral root of median,
medial pectoral, ulnar, median, upper subscapular, lattismus dorsi,
lower subscapular, axillary and radial
Axiallary nerve:
It is otherwise called as circumflex nerve. At the level of axilla
carries nerve fibers from c5 and c6
Median nerve:
Superficial and deep flexors in forearm, thenar and lumbrical
muscle and also give a sensation to the hand
Musculocutaneous nerve:
Biceps, brachialis, coracobrachialis continues to the elbow level
and sensation to the lateral forearm
Radial nerve:
Posterior portion of the upper limb, medial and lateral head of
triceps brachii in arm
Ulnar nerve:
Runs in the ulnar bone flexor carpi ulnaris, flexor digitorum
profundus and lumbricles

Lumbar plexus
Root value l1- l4
The plexus are supplies to the femoral and obturator nerves and
the muscle area of feoral and obturator
Femoral is the largest nerve which is started from the lumbar
plexus
Femoral nerve (lateral side)
It is present in the skin of upper thigh and inner leg
The muscle are extended to the knee
Obturator nerve:
Medial side of the thigh and also the motor function to the hip and
knee joints and abductor muscle and gracilis
Coccygeal plexus
Root value – s4 and s5
The plexus are passing to the small area of the coccygeal region
This plexus are affected rarely in the road traffic accident
It is affected, upto the healing process difficulty in sitting and
supine lying

Lumbosacral plexus
Root value: L4 to S4
Situated in the anterior to sacrum, supplied to the skin and
muscle motor and sensory function
The following nerve are present in sacral plexus
Sciatic nerve – tibial and fibular nerve
Gluteal nerve
Pudendal nerve
Sciatic nerve:
Root value: l4 to s3
2divisions: anterior and posterior
Started from hip joint, passes to the top of the leg, back of thigh,
piriformis, greater sciatic foramen and also the popliteal fossa
and long head of biceps femoris
2 branches: tibial and common peroneal nerve
Tibial nerve passes to the posterior compartment of leg to the foot
 Common peroneal nerve passes to the anterior, lateral
compartment of leg to foor
Gluteal nerve
Origin: pelvic
Root value: l4 and s1
Supplied to: the gluteus medius, minimus and maximus and also
piriformis
Pudendal nerve
Root value: s2 and s4
Function: main nerve to the perineum, carry sensation of both sex skin
and around the perineum, motor supply to the pelvic for male external
urethral sphincter, for female external and sphincter

Neurophysiology
MUSCLE TONE
DEFINITION
Muscle tone is defined as continuous and partial contraction of the
muscles with certain degree of vigor and tension. Muscle tone is
defined as the state of continuous and passive partial contraction of
muscle with certain vigor and tension. It is also called tonus. It is also
defined as resistance offered by the muscle to stretch.
MAINTENANCE OF MUSCLE TONE
In Skeletal Muscle
Maintenance of tone in skeletal muscle is neurogenic. It is due to
continuous discharge of impulses from gamma motor neurons in
anterior gray horn of spinal cord. The gamma motor neurons in spinal
cord are controlled by higher centers in brain
In Cardiac Muscle
In cardiac muscle, maintenance of tone is purely myogenic, i.e. the
muscles themselves control the tone. The tone is not under nervous
control in cardiac muscle.
In Smooth Muscle
In smooth muscle, tone is myogenic. It depends upon calcium level and
number of cross bridges.
Significance of Muscle Tone
Muscle tone plays an important role in maintenance of posture. Change
in muscle tone enables movement of different parts of the body. Muscle
tone is present in all the skeletal muscles. However, tone is more in
antigravity muscles such as extensors of lower limb, trunk muscles and
neck muscles.
Development of Muscle Tone
Gamma motor neurons and muscle spindle are responsible for the
development and maintenance of muscle tone. Muscle tone is purely a
reflex process. This reflex is a spinal segmental reflex. It is developed
by continual synchronous discharge of motor impulses from the gamma
motor neurons present in the anterior gray horn of the spinal cord.
Sequence of events
Impulses from the gamma motor neurons cause contraction of end
portions of intrafusal fibers (stimulus)
This stretches and activates the central portion of the intrafusal
fibers, which initiates the reflex action for development of muscle
tone by discharging the impulses
 Impulses from the central portion of intrafusal fibers pass through
primary sensory nerve fibers (afferent fibers) and reach the
anterior gray horn of spinal cord
These impulses stimulate the alpha motor neurons in anterior gray
horn (center)
Alpha motor neurons in turn, send impulses to extrafusal fibers of
the muscle through spinal nerve fibers (efferent fibers)
These impulses produce partial contraction of the muscle fibers
resulting in development of muscle tone (response).
When the frequency of discharge from gamma motor neurons
increases, the activity of muscle spindle is increased and muscle
tone also increases. Stimulation of gamma motor neurons
increases the muscle tone. Lesion in gamma motor neurons leads
to loss of tone in muscles.
Regulation of Muscle Tone
Though the muscle tone is developed by discharges from gamma
motor neurons, it is maintained continuously and regulated by
some supraspinal centers situated in different parts of brain. Some
of these centers increase the muscle tone by sending facilitatory
impulses while other centers decrease the muscle tone by
inhibitory impulses.
Supraspinal facilitatory centers
Supraspinal centers, which increase the muscle tone:
Motor area 4 in cerebral cortex
Cerebellum
Descending facilitatory reticular system
Red nucleus
Vestibular nucleus.
Supraspinal inhibitory centers
Supraspinal centers, which decrease the muscle tone:
Suppressor areas of cerebral cortex
Basal ganglia
 Descending inhibitory reticular system.
Role of motor area of cerebral cortex – coactivation
Motor area of cerebral cortex influences the activity of lower motor
neurons by sending motor impulses through the pyramidal tract fibers.
Motor impulses and → motor neurons simultaneously. This type of
simultaneous stimulation is called coactivation. It is also called α-γ
coactivation. Stimulation of α-motor neurons causes contraction of
extrafusal fibers. Stimulation of γ-motor neurons causes contraction of
intrafusal fibers, which leads to increase in muscle tone.
Role of cerebellum and basal ganglia
It is interesting to find that cerebellum and basal ganglia influence the
muscle tone without sending direct fibers to →motor neurons. These
parts of brain influence the muscle tone indirectly through brainstem
centers.
Role of brainstem centers
Brainstem centers which influence the →motor
Neurons are in reticular formation, red nucleus and vestibular nucleus.
These centers modulate the discharge from →motor neurons by
receiving signals from cerebral cortex, cerebellum and basal ganglia.
APPLIED PHYSIOLOGY – ABNORMALITIES OF MUSCLE TONE
Abnormalities of muscle tone are:
Hypertonia
Hypotonia
Myotonia.

BLADDER CONTROL
Anatomy and physiology of the bladder
Bladder divided into
Detrusor (aka as “body” or “dome” of bladder)- consists of
smooth muscle
 ◦ Base-trigone and bladder neck, intimately connected to pelvic
floor.
Bladder outlet-two urethral sphincters
Internal (smooth muscle) sphincter-bladder neck and proximal
urethra
External (striated muscle) sphincter-membranous urethra.
Females-Less complex urinary sphincter
Mechanism
Regulation of micturition
Cortical control areas
In frontal and cingulate gyri as well as subcortical areas
Provide inhibitory influence on micturition at level of pons
Excitatory influence on external urinary sphincter.
Allows voluntary control of micturition
Normal bladder evacuation can be delayed until appropriate
time and place to void are chosen.
Pontine micturition center (PMC, Barrington’s nucleus or M-
region)
Locus ceruleus, pontomesencephalic gray matter, nucleus
tegmentolateralis dorsalis.
Essential for coordination of micturition.
Modulates opposing effects of parasympathetic and sympathetic
nervous systems on lower urinary tract.
In bladder emptying stage, PMC sends excitatory influence -
>sacral spinal cord ->detrusor contraction
Simultaneously sends inhibitory influence-> thoracolumbar cord-
>internal urinary sphincter relaxation.
In bladder storage phase, PMC inhibition->sacral spinal cord
supression-> detrusor relaxation
Simultaneously sends excitatory influence- >thoracolumbar cord-
>internal urethral sphincter contraction.
 Ascending sensory information reaches periaqueductal gray
(PAG) matter-> hypothalamus and thalamus-> anterior cingulate
cortex, insula, prefrontal cortex.
Inhibits PAG, which itself has excitatory input to PMC.
Hypothalamus has excitatory influence on PAG.
Conscious decision to void, prefrontal cortex inhibition of PAG
interrupted
Simultaneously hypothalamus stimulates PAG.
Result excitation of PMC.
Spinal neurons regulating micturition
Dorsal commissure, superficial dorsal horn, parasympathetic
nucleus.
Interneurons send rostral projections
Regulate spinal segmental reflexes.
Glutamate-> excitatory transmitter
Glycine and γ-aminobutyric acid (GABA)-> inhibitory
neurotransmitters
Bladder emptying phase
Supraspinal centers’ inhibitory outflow to PMC suppressed
↓↓thoracic sympathetic outflow
↑↑sacral parasympathetic outflow
↓↓pudendal nerve
Detrusor smooth muscle contraction, bladder neck smooth muscle
relaxation, external urinary sphincter relaxation.
Bladder filling stage
Supraspinal center inhibits PMC
↑↑thoracolumbar sympathetic outflow
↓↓sacral parasympathetic outflow to lower urinary tract.
 ↑↑ pudendal nerve.
Detrusor smooth muscle relaxation, bladder neck smooth muscle
contraction, external urinary sphincter contraction.

PAIN AND ITS MANAGEMENT

DEFINITION:
It is an unpleasant sensory and emotional experience arising from
actual or potential tissue damage
Pain is subjective, protective, and it is modified by the
development, behavior and personality

EFFECTS OF PAIN:
Increased heart rate
Diapheresis
High blood glucose
Dilated pupil
Decreased GI motility
Increased muscle tension
high RR

PAIN RECEPTORS:
Nociceptors ( pain receptors) are free nerve endings in the skin
that only responds to intense, potentially damaging stimuli
(mechanical, thermal, chemical)
Joints, skeletal muscle, fascia, cornea also have nociceptors.
Large internal organs doesn't contain free nerve endings.

PAIN PRODUCING SUBSTANCE :

Histamine, bradykinin, cetylcholine, serotonin, substance p,
prostaglandins
PAIN REDUCING SUBSTANCE:
Endorphin
Encephalin

PAIN FIBRES:
There are two fibres transmitting pain. They are,
A delta fibres- fast conducting, myelinated
C fibres - slow conducting , demylinated
PHYSIOLOGY OF PAIN:
Transduction
Transmission
Modulation
Perception

THEORIES OF PAIN:
1. GATE CONTROL THEORY:
Proposed by Melzach and wall in 1965 Stimulation of large diameter
fibres inhibits transmission of pain thus closing the gate
2. SPECIFIC THEORY
One of the earliest pain theory Proposed by Descartes (17th) and
Muller 1840 Pain is purely an afferent experience
3. PATTERN THEORY:
proposed by Goldschneider in 1896 Pattern of stimulation of nerve
endings determines whether the brain would intrepret stimuli as pain
attributes sensation of pain to pattern ( frequency and intensity)

TYPES OF PAIN:
Based on
Duration
Location
Intensity
Etiology
BASED ON:
Duration
1. Acute
2. Chronic
ACUTE PAIN:
Usually of recent onset and commonly associated with specific
injury lasting from seconds to 6 months.
It is protective, identifiable cause, and has limited tissue damage.
Resolves with or without treatment by treating the underlying
cause
CHRONIC PAIN
Constant or intermittent pain that persists beyond the expected
healing time and seldom attributed to a specific cause or injury.
Lasts for 6 months or longer.
Eg. Peripheral neuropathy, arthritic pain, headache
BASED ON LOCATION:
This is based on the site at which the pain is located.
Headache
Back pain
Joint pain
Stomach pain
Referred pain
Pain of internal organs in felt on some where else in the body
where there is same nerve root supply.
Eg. Cardiac pain is felt on left shoulder.
BASED ON INTENSITY :
Mild:
Pain scale reading from 1 to 3
Moderate :
Pain scale reading from 4 to 6
Severe:
Pain scale reading from 7 to 10
BASED ON ETIOLOGY :
Nociceptive pain
Somatic pain
Visceral pain
Neuropathic pain
Peripheral
Neuropathic pain
Central
NOCICEPTIVE PAIN :
1. Somatic pain
Originates from skin, muscle, bone or connective tissue.
Sharp sensation of paper cut or sprained ankle pain are common
example
2. Visceral pain
These are arises from the activation of nociceptors of thoracic
pelvic abdominal organs Characterised by cramping
,throbbing,pressing or aching Eg. Labour pain, angina
NEUROPATHIC PAIN:
1. Peripheral Neuropathic pain.
Due to damage to peripheral nervous system
Eg. Phantom limb pain
2. Central Neuropathic pain
Results from malfunctioning nerves from the central nervous
system.
Eg. Spinal cord injury, Post stroke pain
PAIN ASSESSMENT
PAIN MEASUREMENT :
Visual analog scale (VAS)
Verbal rating scale
Numerical rating scale
wong-baker faces pain rating scale.
PAIN MANAGEMENT
NON PHARMACOLOGICAL
PHARMACOLOGICAL
NON PHARMACOLOGICAL
Superficial heating
CRYOTHERAPY
EXERCISE
TENS
ACUPUNCTURE
ACUPRESSURE
PLACEBO THERAPY
CUTANEOUS STIMULATION
MASSAGE
MANIPULATION
MOBILIZATION
TRACTION
PHARMACOLOGICAL :
Non opioids
NSAIDS
Salicylates
COX-2 inhibitors
Acetaminophen
Celecoxib
Steroids
Opioids
Morphin
Dilaudid
Demerol
Fentanyl
Dolophyne
Analgesic adjuvants
 Benzodiazipines
Tricyclic antidepressants
ROUTES:
Oral
Rectal
Transdermal patch
Intravenous
Intramuscular
Subcutaneous
Intra spinal ( epidural or subarachnoid)

MUSCLE CONTRACTION
Contractility is the response of the muscle to a stimulus.
Contraction is defined as the internal events of muscle with change in
either length or tension of the muscle fibers.
TYPES OF CONTRACTION
Muscular contraction is classified into two types based on change in the
length of muscle fibers or tension of the muscle:
Isotonic contraction
Isometric contraction.
1. Isotonic Contraction
Isotonic contraction is the type of muscular contraction in which the
tension remains the same and the length of the muscle fiber is altered
(iso = same: tonic = tension).
Example: Simple flexion of arm, where shortening of muscle fibers
occurs but the tension does not change.
2. Isometric Contraction
Isometric contraction is the type of muscular contraction in which the
length of muscle fibers remains the same and the tension is increased.
Example: Pulling any heavy object when muscles become stiff and
strained with increased tension but the length does not change.
CONTRACTION TIME – RED MUSCLE AND PALE MUSCLE
Contraction time or total twitch period varies from species to species. It
is less in homeothermic animals than in poikilothermic animals. In the
same animal, it varies in different groups of muscles.
Based on contraction time, the skeletal muscles are classified into two
types:
Red muscles
Pale muscles.
Similarly, depending upon contraction time and myosin ATPase activity
the muscle fibers are also divided into two types:
Type I fibers or slow fibers or slow twitch fibers, which have small
diameter.
Type II fibers or fast fibers or fast twitch fibers, which have large
diameter.
Most of the skeletal muscles in human beings contain both the types of
fibers.
Red Muscles
Muscles, which contain large quantity of myoglobin are called red
muscles.
These muscles are also called slow muscles or slow twitch
muscles. Red muscles have large number of type I fibers.
The contraction time is longer in this type of muscles. Example:
Back muscles and gastrocnemius muscles.
Pale Muscles
Muscles, which contain less quantity of myoglobin are called pale
muscles or white muscles.
These muscles are also called fast muscles or fast twitch muscles.
Pale muscles have large number of type II fibers. Contraction time
is shorter in this type of muscles.
Examples: Hand muscles and ocular muscles.
 FACTORS AFFECTING FORCE OF CONTRACTION
Force of contraction of the skeletal muscle is affected by the following
factors:
Strength of stimulus
Number of stimulus
Temperature
Load.
1. Effect of Strength of Stimulus
When the muscle is stimulated by stimuli with different strength (voltage
of current), the force of contraction also differs.
Types of strength of stimulus
Strength of stimulus is of five types:
Subminimal or subliminal stimulus: It is less than minimal
strength and does not produce any response in the muscle if
applied once
Minimal stimulus, threshold stimulus or luminal stimulus: It is
the least strength of stimulus at which minimum force of
contraction is produced.
Submaximal stimulus: It is more than minimal and less than
maximal strength of stimulus. It produces more force of
contraction than minimal stimulus.
Maximal stimulus: It produces almost the maximum force of
contraction.
Supramaximal stimulus: It produces the maximum force of
contraction. Beyond this, the force of contraction cannot be
increased.
2. Effect of Number of Stimulus
Contractility of the muscle varies, depending upon the number of
stimuli.
If a single stimulus is applied, muscle contracts once (simple
muscle twitch).
 Two or more than two (multiple) stimuli produce two different
effects.
3. Effect of Variations in Temperature
If the temperature of muscle is altered, the force of contraction is also
affected
Warm temperature
At warm temperature of about 40°C, the force of muscle contraction
increases and all the periods are shortened because of the following
reasons:
Excitability of muscle increases
Chemical processes involved in muscular contraction are
accelerated
Viscosity of muscle decreases.
Cold temperature
At cold temperature of about 10°C, the force of contraction decreases
and all the periods are prolonged because of the following reasons:
Excitability of muscle decreases
Chemical processes are slowed or delayed
Viscosity of the muscle increases.
High or hot temperature – Heat rigor
At high temperature above 60°C, the muscle develops heat rigor.
Rigor refers to shortening and stiffening of muscle fibers.
Heat rigor is the rigor that occurs due to increased temperature. It
is an irreversible phenomenon.
Cause of heat rigor is the coagulation of muscle proteins, actin
and myosin.
4. Effect of Load
Load acting on muscle is of two types:
After load
Free load.
After load
After load is the load, that acts on the muscle after the beginning of
muscular contraction. Example of after load is lifting any object from
the ground. The load acts on muscles of arm only after lifting the object
off the ground, i.e. only after beginning of the muscular contraction.
Free load
Free load is the load, which acts on the muscle freely, even before the
onset of contraction of the muscle. It is otherwise called fore load.
Example of free load is filling water from a tap by holding the bucket in
hand.
Congenital childhood disorders
CEREBRAL PALSY
DEFINITION
Cerebral Palsy (CP) is a group of permanent disorder of the
development of movement and posture, causing activity limitation.
Cerebral palsy (CP) is a motor disorder, the condition involves
disturbances of sensation, perception, communication, cognition
and behavior, secondary musculoskeletal problems and epilepsy.
CAUSES
Maternal
Diabetes/hyperthyroidism
Exposure to radiation/toxins
Malnutrition
Cognitive impairment/seizures
Infections
Incompetent cervix
Bleeding
Polyhydramnios
Genetic abnormalities
 Previous child with development disabilities
Previous premature birth
Medication use (e.g, thyroid, estrogen, progesterone)
Severe proteinuria
Gestational
Chromosomes abnormalities
Genetic syndrome
Teratogen
Rh incompatibility infections
Congenital malformations
Fetal development abnormalities
Problems in placenta Functioning
Inflammatory response
Labour and delivery
Premature delivery
Prolonged rupture of membranes
Fetal heart rate depression
Abnormal presentation
Long labour
Preeclampsia
Asphyxia
Perinatal
Prematurity and associated problems
Sepsis and/ or central nervous system infections
Seizure
Intraventricular hemorrrhage
Periventicular hemorrhage
Meconium aspiration
Number of days on mechanical ventilation
Persistent pulmonary hypertension
Intrauterine growth restriction
Low birth weight
Postnatal/Childhood
Brain injury
Meningitis or encephalitis
Toxins
Traumatic brain injury
Infections
Stroke
CLASSIFICATION
Because of the wide variability in presentation and types of cerebral
palsy, there is no universally accepted classification scheme.
Spastic
Athetoid
Choreiform
Rigid
Ataxic
Hypotonic
Mixed
1) Spastic (Pyramidal)
characterized by persistent primitive reflexes, positive babinski
reflex, ankle
clonus, exaggerated stretch reflex, eventual development of
contractures.
Type of spastic cerebral palsy:
Hemiplegia: motor dysfunction on one side of the body, upper
extremity more affected than lower.
Diplegia: all extremities affected, but lower extremities more
effected than upper.
Tetraplegia (quadriplegia): all four extremities involved.
Triplegia: involving three extremities.
Monoplegia: involving only one extremities..
Paraplegia: pure cerebral paraplegia of lower extremities.
2) Dyskinetic (Nonspecific, extrapyramidal)
Athetoid: chorea (involuntary, irregular, jerking movements),
characterized by slow, wormlike, writhing movements that usually
involve the extremities, trunk, neck, facial muscle and tongue
Dystonic: slow, twisting movements of the trunk or extremities,
abnormal posture
Involvement of the pharyngeal and oral muscle causing drooling
and dysarthria (imperfect speech articulation)
3) Ataxic (Nonspastic, extrapyramidal)
Wide-based gait
Rapid, repetitive movement performed poorly
Disintegration of movements of the upper extremities when the
child reaches for objects
4) Choreiform:
Continual purposeless movements of wrists,fingers,toes and
ankles
5) Rigid:
Most hypertonic form
Cogwheel or leadpipe rigidity
6) Ataxic:
Very rare
Injury to developing cerebellum
Disturbance of coordinated movement viz. walking
Characterized by weakness, in-coordination, a wide based gait,
and trouble with fine and rapid movements.
7) Hypotonic:
Passing stage in spastic or ataxic cerebral palsy
8) Mixed:
Signs of pyramidal and extrapyramidal deficits
CLINICAL MANIFESTATIONS
1. Physical signs
poor head control after 3 months of age
stiff or rigid arms or legs
pushing away or arching back
floppy or limp body posture
cannot sit up without support by 8 months
uses only one side of the body, or only the arms to crawl
clenched hands after 3 months
leg scissoring
seizures
sensory impairment (hearing, vision)
after 6 months of age, persistent tongue thrusting
2. Behavioral signs
Extreme irritability or crying
Feeding difficulties
Little interest surrounding
Excessive slepping

DIAGNOSIS
Physical examination.
History taking.
Neurologic assessment .
Magnetic resonance imaging (MRI)
Ultrasound
Computerised tomography (CT)
Electroencephalogram (EEG.
Electromyogram (EMG)
Laboratory studies, to detect any blood clotting and screen for
genetic or metabolic problems.
Additional tests: Vision impairment, Hearing impairment, Speech
delays or impairments, Intellectual disabilities,
 Other developmental delays, Movement disorders
Gross motor function scale
I Has nearly normal gross motor function
II Walks independently, but has limitations with running and
jumping
III Uses assistive devices to walk and wheelchairfor long distances
IV Has ability to stand for transfers, but minimal walking ability;
depends on wheelchair for mobility
V Lacks head control, can’t sit independently, is dependent for all
aspects of care
TREATMENT
Medical
Therapy can help a person with cerebral palsy to enhance functional
abilities and therapy is chiefly symptomatic and preventive.
The broad aims of therapy are:
To establish locomotion, communication and self help.
To gain optimum appearance and integration of motor functions.
To correct associated defects as early and effectively.
To provide educational opportunities adapted to the individual
child’s needs and capabilities
To promote socialization experiences with other affected
unaffected children
The therapy treatment include:
1. Physical therapy
Physical therapy is directed toward good skeletal alignment for
child with spasticity, training, face involuntary motion and gait
training.
Physical therapy can help the child's strength, flexibility, balance,
motor development and mobility.
Physical therapy uses orthotic devices, such as braces, casting
and splints to support and improved walking.
2. Occupational therapy
3. Speech and language therapy
4. Recreation therapy
5. Pharmacological
The goal of drug therapy is to reduce the effects of cerebral palsy
and prevent complications:
Analgesic drug, to reduce intense pain or muscle spasm.
Botulinum toxin type A, used to reduce spasticity in targeted
muscle of the upper and lower extremities.
Inhaled nitrous / oral midazolam used for sedation
duringbotulinum toxin A injection.
Dantrolene sodium, baclofen, and diazepam to improving muscle
coordination and to muscle relaxation.
Anticonvulsants drug, to relieve or stop seizures
6. Surgical management
Surgery used to correct problems with bones and joints, by lengthening
any muscles and tendons that are too short and causing problems.
1. Orthopedic surgery
Orthopedic surgery may be required to correct contracture or
spastic deformities, to provide stability for an uncontrolled joint,
to address bone malalignment, and to provide balanced muscle
power.
Example for orthopedic surgery: tendon transfer, muscle
lengthening, and spinal deformities
2. Selective dorsal rhizotomy (SDR)
Selective dorsal rhizotomy (SDR) is a surgical procedure that can
help children with particularly severe muscle stiffness in their legs
to improve their walking.
The operation involves cutting some of the nerves in the lower
spinal column, which can help relieve leg stiffness.
3. Gastrostomy
Surgery may performed to improve feedings, correct
gastroesophageal reflux disease and correct associated dental
problems.
Hydrocephalous
INTRODUCTION
The term hydrocephalus is derived from the Greek words "hydro"
meaning water and "cephalus" meaning head.
As the name implies, it is a condition in which the primary
characteristic is excessive accumulation of fluid in the brain.
DEFINITION
Hydrocephalus is a condition caused by an imbalance in the
production and absorption of CSF in the ventricular system.
When production exceeds absorption, CSF accumulates, usually
under pressure, producing dilation of the ventricles.
Hydrocephalus is a build up of fluid inside the skull, leading to
brain swelling.
INCIDENCE:-
It is found in 1-3 of every 1000 born children in worldwide
TYPES
COMMUNICATING HYDROCEPHALUS
Communicating hydrocephalus is a condition that results when the
arachnoid villi are unable to adequately reabsorb CSF.
Intraventricular or subarachnoid hemorrhage
Infectious processes such as meningitis may also render the
arachnoid villi to be nonfunction.
May also be due to the overproduction of CSF. This is rare and is
usually associated with a choroid plexus papilloma or a choroid
plexus carcinoma
NON- COMMUNICATING HYDROCEPHALUS
Noncommunicating hydrocephalus is a condition that results when
the ventricular system does not communicate with the arachnoid
villi due to some obstruction in the normal pathways of CSF flow.
Consequently, CSF is produced in the ventricular system but
cannot flow to the arachnoid villa to be reabsorbed.
Such obstruction can occur when pathways are blocked by a
tumor, congenital abnormalities of the brain, cysts, inflammation
from infection, or any other condition that interferes with the
patency of these pathways.
CAUSES OF HYDROCEPHALUS
Congenital
Intrauterine infections →Mainly in ruballa, toxoplasmosis,
cytomegalovirus.
Congenital brain tumor
Intracranial hemorrhage.
Congenital malformation
Malformations of arachnoid villi
Acquired
Inflammation
Trauma
Neoplasm space occupying lesions like tuberculoma, subdural
hematoma or abscess, gliomas, ependymoma, astrocytoma,
choroid plexus papilloma, pseudotomor cerebri.
Chemical – hypervitaminosis ‘A’
Connective tissue disorder- Hurler syndrome, achondroplasia.
Degenerative atropy of brain
Arteriovenous malformations, ruptured aneurysm, cavernous sinus
thrombosis.
CLINICAL MANIFESTATIONS
IN INFANTS
Head grows at abnormal rate.
Anterior fontanel is tense, often bulging, & non pulsatile.
Scalp veins are dilated & markedly so when infant cries.
Macewen’s sign- with increase in intracranial volume, the bones
of the skull become thin & the sutures become palpably separated
to produce the cracked pot sound on the percussion of the skull.
Frontal bossing with depressed eyes.
Setting-sun sign- eyes rotated downward, in which sclera may be
visible above iris.
Feeds poorly
Pupils are sluggish, with unequal response to light
Changes in level of consciousness.
Opisthotonus position & lower extremity spasticity.
Cries when picked up & quiets when allowed to lie still.
If hydrocephalus is allowed to progress- there will be disruption in
the lower brainstem function as manifested by difficulty in feeding
& a shrill, brief, high-pitched cry. Eventually the skull becomes
enlarged, & the cortex is destroyed.
If the condition progress rapidly, the infant may display emesis,
somnolence, seizures & cardiopulmonary distress.
IN CHILDHOOD-
Headache on awakening with improvement following emesis or
upright posture.
Papilledema, strabismus.
Irritable & lethargic.
Apathetic, confused & often incoherent.
Bulging occiput, nystagmus, ataxia & cranial nerve palsies.
DIAGNOSIS
Routine daily head (occipitofrontal) circumference measurements.
Echoencephalography.
A head CT scan is one of the best tests for identifying
hydrocephalus.
Arteriography.
Brain scan using radioisotopes
Cranial ultrasound (an ultrasound of the brain)
Lumbar puncture and examination of the cerebrospinal fluid
(rarely done).
Skull x-rays.
TREATMENT
The treatment of hydrocephalus is directed toward –
Relief of the hydrocephalus,
Treatment of complications,
Management of problems related to the effect of the disorder on
psychomotor development. The treatment is, with few exceptions,
surgical.
MEDICAL MANAGEMENT
Management of hydrocephalus directed toward:-
Reducing intra cranial pressure
Prevention and Management of complication
ranaging problems caused by pathology
Medical Management include the use of osmotic diuretics and loop
diuretics to reduce CSF production .medical management is temporary
relief but main management is surgery
SURGICAL MANAGEMENT
A shunt is made up of radio plastic and has ventricular cathetar,
pressure valve, pumping chamber, and distal catheter that directs
the flow of CSF from the ventricles to other areas of body from
where it is absorbed.
Endoscopic Third Ventriculostomy
 Choroid plexectomy
Ventriculo-peritoneal shunt (V-P shunt).
Ventriculoatrial shunt
Ventriculopleural shunt
Ventriculogallbladder shunt.
PROGNOSIS
Prognosis depends on early diagnosis and prompt therapy.
With improved diagnostic and management techniques, the
prognosis is becoming considerably better.
Approximately two- thirds of patients will die at an early age if
they do not receive surgical treatment.
COMPLICATIONS
Seizure
Herniation of brain
Spontaneous arrest due to natural compensatory mechanisms,
persistent increased ICP and brain herniation.
Developmental delay
Depression.
SPINA BIFIDA
DEFINITION
Spina bifida is a developmental abnormality caused by a failure
of fusion of the vertebral arches and possibly the underlying
neural tube,characterised by the incomplete development of the
brain,spinal cord,meninges.(2,7)
Spina bifida is a primary neurological disorder.(7)
INCIDENCE
• Spina bifida cystica-1:300 live births.(7)
• Associated with hydrocephalus.
• More common in hispanics and caucasians.
• Worldwide incidence 400,000 per annum.
 • Folic acid use has reduced incidence by 70% in the past 20 yrs.
• Ireland
• 1979-32 per 10,000
• 1982-22 per 10,000(2)
• Site: 80% occur in the lumbosacral region
CAUSES
• Not known.
• Genetic, nutritional, and environmental factors play a role.
• Deficiency of folic acid.
RISK FACTORS
• Couples who already had an affected baby
• Obese women
• Diabetes
• Anti-seizure medicines
• Folic acid deficiency
• Mutation in methylenetetrahydrofolate reductase gene
CLASSIFICATION
• Spina bifida occulta
• Spina bifida cystica:
Meningocele
Myelomeningocele
Encephalocele
Spina bifida occulta
A bony deficit – present in 5 – 10% of the population and not
clinically significant. Those who have a lumbosacral cutaneous
abnormality have a high incidence of related underlying defects
Diastomatomyelia
Lipoma
 Dermoid cyst
The defects may cause symptoms of pain or neurological
impairment after many years
Spina bifida cystica
Mylomeningocele
The spinal cord and roots protrude through the bony defects and
lie within a cystic cavity, lined with meninges and/ or skin.
In most patients, the meningeal covering ruptures and the spinal
cord roots lie exposed to the air – myelodysplasia. Csf may leak
from the open lesion
Meningocele
Cystic csf filled cavity lined with meninges but devoid of neural
tissue. The cavity communicates with the spinal canal through the
bone defect.
Meningoceles occur far less frequently than myelomeningocele
they are rarely associated with the other congenital anomalies
DIAGNOSIS
(1) Blood tests
• Second trimester maternal serum alpha fetoprotein(MSAFP)
• Alpha-feto protein(AFP) is made naturally by the fetus and
placenta.
• But if abnormally high levels of this protein appear in the
mother’s bloodstream it may indicate that the fetus has a neural
tube defect.
• The MSAFP test, however, is not specific for spina bifida(positive
predictive value 2-4%).
(2) Ultrasound
• An advanced ultrasound can also detect signs of spina
bifida(sensitivity 96%,specificity 100%)
(3) Amniocentesis
• An analysis indicates the level of AFP present in the amniotic
fluid.
• A small amount of AFP is normally found in amniotic fluid.
• When an open neural tube defect is present , the amniotic fluid
contains an elevated amount of AFP because the skin surrounding
the baby’s spine is gone and AFP leaks into the amniotic sac.
(4)MRI
TREATMENT
• There is no cure for spina bifida.
• The nerve tissue that is damaged or lost cannot be repaired or
replaced.
• Treatment depends on the type and severity of the disorder.
• Children with the mild form need no treatment.
• Moderate to severe cases, surgical closure of back lesion within 6
months.
• There is no known cure for nerve damage caused by spina bifida.
• To prevent further damage of the nervous tissue and to prevent
infection , surgeon operate to close the opening on the back.
• The spinal cord and its nerve roots are placed back into the spinal
canal and covered with meninges.
• In addition , a shunt may be surgically installed to provide a
continuous drain for the excess
• CSF produced in the brain , as happens with hydrocephalus.
PREVENTION
• Folic acid reduces the risk of having a child with a neural tube
• defect,such as spina bifida.
• Dose-400micrograms daily.
 • Source-dark green vegetables,egg yolks,fruits like orange.
PROGNOSIS
Spina bifida is a:
• Static
• Nonprogressive defect.
• With worsening from secondary problems.
• The prognosis for a normal life span is generally good for a child
with good habits and a supportive family caregiver.
CEREBRO VASCULAR ACCIDENT
INTRODUCTION:
Cerebrovascular disorders” is any functional abnormality of the central
nervous system (CNS) that occurs when the normal blood supply to the
brain is disrupted. Stroke is the primary Cerebrovascular disorder in
the United States and in the world. stroke is still the third leading cause
of death.
ANATOMY & PHYSIOLOGY OF NERVOUS SYSTEM
The nervous system is divided into two parts:
Central nervous system
Peripheral nervous system
ARTERIES: Two internal carotid arteries, Two vertebral arteries
DEFINITION
A stroke, or Cerebrovascular accident (CVA), occurs when
blood supply to part of the brain is disrupted, causing brain cells to die.
Cerebrovascular accident or brain attack is sudden loss of
function resulting from disruption of blood supply to a part of the brain.
INCIDENCE
AGE: The percentage is higher for people age 65 and older. Of
those who survive, 50% to 70% will be functioning independent
and 15% to 30% will live with permanent disability.
SEX: Stroke is more common in men than in women.
RACE
African american have a higher incidence of strokes than whites.
This high incidence may be related to increase rate of
hypertension, diabetes mellitus and sickle cell anemia in african
americans.
African americans also have a higher incidence of smoking and
obesity than white, which are two other risk factors for stroke.
African american are twice as likely to die from a strokes as white.
COUNTRY
An estimated 700,000 person in the united states and 50,000 in
canada suffer a stroke annually.
Stroke is the third most commen cause of the death in the united
states and canada, behind cancer and heart disease.
In canada about 16,000 die from stroke each year, while in united
states there are over 160,000 deaths from strokes.
ETIOLOGY
Nonmodifiable risk factors :
Age : more than 65 yr
Gender : More in men than women
Race : African American
Family history : Heredity
Modifiable risk factors :
Hypertension
Heart disease
Smoking
 Excessive alcohol consumption
Obesity
Sleep apnea
Metabolic syndrome
Poor diet
Drug abuse and oral contraceptive
CAUSES:
Vessel wall embolus
Carotid artery most often the source
Related to thrombus formation distal to stenosis
Cardiac source
Mitral valve stenosis
Mitral valve prolapsed
Calcified mitral annulus
Ventricular aneurysm
Atrial or ventricular clot
Valvular vegetation
Atrial septal defect
Vascular sources
Intracranial artery thrombus (esp. African-Americans)
Aortic arch atherosclerotic Plaque
Transient hypotension with Carotid Stenosis
TYPES OF STROKE
Strokes are classified as ischemic or hemorrhagic based on the
underlying path physiologic findings.
1. Ischemic stroke
2. Thrombolytic stroke
3. Embolic stroke
Ischemic stroke: An ischemic stroke result from inadequate blood flow
to the brain from partial or complete occlusion of an artery. These
account for approximately 80% of all strokes. Ischemic stroke are
further divided into thrombotic and embolic.

Thrombotic stroke: A thrombotic stroke occurs from injury to a blood

vessels wall and formation of a blood clot. The lumen of the blood
vessel becomes narrowed and if it becomes occluded, infarction occur.
Thrombosis develops readily where atherosclerotic plaques have
already narrowed blood vessels. Thrombotic stroke, which is the result
of thrombosis or narrowed blood vessel, is the most common cause of
stroke. Two third of thrombotic strokes are associated with hypertension
or diabetes mellitus.

Embolic stroke: Another type of stroke may occur when a blood clot or
a piece of atherosclerotic plaque (cholesterol and calcium deposits on
the wall of the inside of the heart or artery) breaks loose, travels
through the bloodstream and lodges in an artery in the brain. When
blood flow stops, brain cells do not receive the oxygen and glucose they
require to function and a stroke occurs. This type of stroke is referred to
as an embolic stroke

CLINICAL MANIFESTATIONS
Visual Field Deficits :
Homonymous hemianopsia (loss of half of the visual field)
- Unaware of persons or objects on side of visual loss
- Neglect of one side of the body
- Difficulty judging distances
Loss of peripheral vision
- Difficulty seeing at night
- Unaware of objects or the borders of objects
- Diplopia
Motor Deficits
Hemiparesis
Weakness of the face, arm, and leg non the same side (due to a
lesion in the opposite hemisphere)
Hemiplegia
Paralysis of the face, arm, and leg on the same side (due to a
lesion in the opposite hemisphere)
Ataxia
Defective muscular co-ordination, unsteady gait Unable to keep
feet together; needs a broad base to stand
Dysarthria
Difficulty in forming words
Dysphagia
Difficulty in swallowing
Sensory Deficits
Paresthesia (occurs on the side opposite the lesion)
Numbness and tingling of Extremity
Verbal Deficits
Expressive aphasia
Unable to form words that are understandable; may be able to
speak in single-word responses
Receptive aphasia
Unable to comprehend the spoken word; can speak but may not
make sense
Global (mixed) aphasia
Combination of both receptive and expressive aphasia
Cognitive Deficits
• Short- and long-term memory loss
• Decreased attention span
• Impaired ability to concentrate
 • Poor abstract reasoning and altered judgement
Emotional Deficits
• Loss of self-control
• Emotional lability
• Decreased tolerance to stressful situations
• Depression
• Withdrawal
• Fear, hostility, and anger
• Feelings of isolation

ASSESSMENT AND DIAGNOSTIC FINDING

HEALTH HISTORY:
Past health history: Hypertension, previous stroke, aneurysm, cardiac
disease (including recent myocardial infraction), dysrhythmias, heart
failure, valvular disease, infective endocarditis, hyperlipidemia,
polycythemia, diabetes
Family history: Hypertension, diabetes, stroke, coronary artery
disease.
Medications: Use of oral contraceptives, use of antihypertensive and
anticoagulant therapy
Nutritional history: Anorexia, nausea, vomiting,dysphagia, altered
sensation of taste and smell
Cognitive perceptual history: Numbness, tingling of one side of body,
loss of memory, altered in speech, pain, headache, visual disturbance
PHYSICAL ASSESSMENT
• Glasgow coma scale
• NIH stroke scale
COGNITIVE FUNCTION :-
Orientation :
Speech :-aphasia & other problems
Fluent aphasia (motor/Borka’s) – inability to express self
Non-fluent aphasia ( sensory / wernicke’s) – inability to
understand the spoken language.
Global aphasia – inability to speak or understand spoken
language.
Other aphasia syndromes – amnesia, conduction.
Other alterations include :
• Confabulation – fluent , nonsensical speech
• Preservation – continuation of thought process with inability to
change rain of though without direction or repetition.
MOTOR FUNCTION :
• Voluntary movement
• Reflexive movement : Biceps, Triceps, Patellar, Achilles, Planter:

DIAGNOSTIC EVALUATION
Diagnosis of stroke, including extent of involvement
• CT, CTA (computer tomographic angiography)
• MRI, MRA (magnetic resonance angiography)
• SPECT (single photon emission computed tomography)
• PET ( Positron emission tomography )
• MRS (magnetic resonance spectroscopy)
• Xenon CT
• Electroencephalogram
• Cerebral angiography
• Cerebrospinal fluid analysis
Cerebral blood flow measures
• Cerebral angiography
• Digital subtraction angiography
• Doppler ultrasonography
• Transcranial Doppler
• Carotid duplex
• Carotid angiography
Cardiac assessment
• Electrocardiography
• Chest x-ray
• Cardiac enzymes
• Holter monitor
Additional studies
• Complete blood count
• Prothrombin time, activated partial thromboplastin time
• Electrolytes
• Blood glucose level
• Renal and hepatic studies
• Lipid profile
• Arterial blood gases analysis

MANAGEMENT :
MEDICAL MANAGEMENT :
1. Platelet-inhibiting medications : Aspirin, dipyridamole
[Persantine], clopidogrel [Plavix], and ticlopidine [Ticlid]).
 2. Thrombolytic therapy
3. Strains
4. Anti hypertensive drugs
5. Anti coagulant therapy
6. Osmotic diuretics
SURGICAL MANAGEMNT:
1. Carotid endarterectomy
2. Craniotomy
3. Carotid stenting
POST OPERATIVE COMPLICATIONS :
•Intraoperative embolization
•Postoperative internal artery occlusion
•Fluid and electrolyte disturbances