Understanding the Central Nervous System

 Introduction & neuro-anatomy  GBS
 Parkinsonism  MND
 Multiple sclerosis  M.G
 Stroke (CVA, intracranial hemorrhage )  Headache
 Epilepsy  Intracranial neoplasm and pressure
 Peripheral neuropathy  Meningitis & CSF examination
1- Central nervous system: - (brain, spinal cord).
2- Peripheral nervous system: - (nerves &nerve roots, B- ganglia.).
 When approaching a patient with a neurologic disorder always ask yourself:
1- Where is the lesion?  by history & examination .

2- What is the cause of the lesion?  Make D/D based on which part affect.
3- IS the lesion focal, multifocal or diffuse?  Specific investigation to make diagnosis
then proper treatment prescribed.
1- Anatomical classification
A- The Central Nervous System (CNS) is formed of 2 main parts:-
Intracranial :- 2 Cerebrum hemisphere (frontal, temporal, Parietal,

(BRAIN) occipital).
Brain Stem: - (midbrain, pons, medulla oblongata).
Cerebellum: - 2 hemisphere right & left. It coordinates
the movements of the same side of the body.
Basal ganglia (Caudate, lentiform, substantia nigra).
Intervertebral :- Spinal Cord :- 31 segments ( 8 cervical, 12 thoracic,
(SPINAL PART) 5 lumber, 5 sacral, 1 coxygeal) end by which called
conus medullaris
Cauda Equina.
It is formed of 2 cerebral hemispheres, connected to each other by the corpus callosum, and
to the upper part of the brain stem by the 2 cerebral peduncles.
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 The surface of each hemisphere is divided into 4 lobes:
1.Frontal lobe: - Ant to Central sulcus (Voluntary motor control).

2. Parietal: - Post to Central sulcus (somatic sensation).
3. Temporal: - below lateral sulcus (hearing).
4. Occipital: - Behind Parieto-occipital Sulcus (vision).
 The lobes are separated from each other by sulci (fissures):
The Central Sulcus separates the frontal from the parietal lobe.
The Parieto-occipital Sulcus separates the parietal from the occipital lobe.
The Lateral Sulcus (Sylvian fissure) separates the frontal & parietal lobes from the
temporal lobe.
It is formed of: Midbrain, Pons, Medulla.

The Motor nuclei of the Cranial Nerves are arranged in the Brain Stem as follows:
 Cr 3 & 4 in Midbrain.
 Cr 5, 6 & 7 in Pons.
 Cr 9, 10, 11 & 12 in Medulla.
Note: - Cr 1, 2 & 8 are Sensory nerves concerned special sensations, perceived in Special
areas of the cerebral Cortex.
Cr 1, 2 & 8 have no motor nuclei, in brain stem.
It lies behind the Brain Stem and occupies most of the posterior cranial fossa, consists of
central vermis anterior lobe, posterior lobe & folocculonodular lobe. It is concerned with
coordination of voluntary motor activity and maintenance of equilibrium.
 (extrapyramidal tract):- explained later on.
2)
 It lies in the spinal canal & ends at the lower border of the 1st lumbar vertebra.
 The lower most 3 segments of the spinal cord (S3, 4, 5) are known anatomically as the
conus medullaris while the above 4 segments (L4, 5, S1, 2) are known anatomically
as the epiconus.
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 It is formed of gray matter (cells) surrounded by white matter.
 In a transverse section the gray matter resembles the letter H (2 anterior & 2 posterior
horns).
 The white matter contains ascending and descending nerve fibers arranged into tracts.
 Cauda Equina: - it comprises roots of spinal nerves blow (L1) vertebra (some lumber
sacral & coccygeal nerves).
b- divided in to:-
1. Spinal nerves: - from spinal cord 31 pair.
2. Cranial nerves: - from brain stem 12 pair.
1- Motor function :- (movement & coordination) its responsibility of  (Cerebral

hemisphere, Spinal cord, Peripheral nerves, Cerebellum, Basal ganglia).
2- Sensory function: - its responsibility of  (Cerebral hemisphere, Spinal cord,
Peripheral nerves).
Note: - Cerebellum, Basal ganglia diseases not affect sensory.
3- Mentality: - mainly in frontal lobe of cerebral hemisphere.
1. The Pyramidal System (U.M.N.):

It originates in the motor area 30% & premotor area 30% & 40% from primary sensory area
then terminates at the anterior horn cells (AHC) of the different levels of the spinal cord. It
supplies the opposite side of the body.
Divided in to: -
a- cortico-spinal tract: The axons of these tracts descend in the depth of the cerebral
hemisphere in the corona radiata, to pass in the internal capsule (genu & ant lf3 of post.
limb) & continue their descent in the midbrain, pons & medulla.
In the lower medulla, 80% of the fibers decussate (cross) to descend in the white matter of
the opposite side of the spinal cord, while the remaining fibers descend directly in the white
matter of the same side.
b- cortico-bulbar tract: - the descending tract to pass in the internal capsule (genu)
then separate to supply the motor nuclei of the cranial nerves of both sides except the lower
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½ of the facial nucleus & the hypoglossal nucleus which are supplied only from the opposite
tract Opposite side.
2- The Lower Motor Neurone (L.M.N.)

It is formed of AHC & peripheral motor nerves (which transmit the motor impulses to the
voluntary muscles).
AHC: they are a special type of nerve cells situated in the anterior horns of the H shaped gray
matter of the spinal cord. They receive the voluntary motor impulse from Their axons exit from
the spinal cord as the anterior roots (spinal nerves) OR (the nerve emerge from AHC of spinal
cord called spinal nerves and nerve emerge from brain stem nuclei called cranial nerves and
both are (LMN)).
N.B.: The motor nuclei of the cranial nerves are similar in function to the AHC of spinal
nerves.
Thus, lesion of a cranial nerve nucleus, like lesion of an AHC, is a LMN lesion.
3- The Extrapyramidal (extra Pyramidal System) :-

It originates from centers situated at CNS mainly the Basal Ganglia.
It controls the opposite side of the body.
4- The Cerebellar System:

It is composed of the spino-cerebellum, cerebro-cerebllum & vestibule-cerebellum.
It coordinates the movements of the same side of the body.
Any voluntary muscle in our body need 2 nerve supply (UMN & LMN) TO contract so if one of
them is injured the result is weakness of that muscle.
UMN ( coticospinal tract) LMN ( AHC & Peripheral nerves ) spinal n.

Transmission of electrical impulse Transmission of electrical impulse from spinal
of voluntary movement from motor cord to motor end plate (neuromuscular
cortex to AHC. junction).
Inhibitor of muscle tone and reflex. Generation of muscle tone and reflex.
Muscle tone :- its slight continuous involuntary muscle contraction during rest (contraction
at rest), so can be measured by resistance of skeletal muscle during passive movement at joint
level.
Note :- the pyramidal tract especially the (UMN), & Extrapyramidal tract (basal ganglia)
have inhibitory effect on muscle tone, so if there lesion in one of them the hypertonia well
present either in form of spasticity in (UMNL) OR in form of rigidity in (basal ganglia lesion)
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spasticity Rigidity
indicate lesion in pyramidal system , Indicate lesion in extrapyramidal system, the
resistant is not constant throughout the resistant is constant throughout the passive
passive movement e.g. :- clasp knife movement e.g.:-lead pipe rigidity if with tremor
spasticity known as cogwheel rigidity.
deep & superficial.
Deep tendon reflexs: -

Its response between then stretching receptor in muscle tendon and (LMN) of that muscle
called reflex arch. So when there is (LMNL)  Hyporeflexia or Areflexia.
And the (UMN) inhibited this reflex, SO in (UMNL) there is Hypereflexia or exaggerated brisky
reflex.
Note: - the pure or primary extrapyramidal lesion not affecting the reflex.
In cerebellum lesion (degeneration) the reflex is pendular in response.
Upper limbs Lower limbs
Biceps (C5, C6) Knee (L3, L4).

Brachioradialis (C5, C6) Ankle (S1, S2).
Triceps (C7.C8)
Superficial reflexes: -
1- Plantar reflexes (L5, S1) its done.by applying blunt (a key) along the late. Border of
sole of foot toward the little toe the result could be:-
Normally: - planter flexion of toe.
Babinski sign: - if extension of big toe +/- fanning of other toes occur in D/D (UMNL,
Deep sleep, coma, anesthesia, and infant baby less than 1 year).
No response:-
Known as equivocal response occur in sensory loss or callus of skin (thick skin).
2- Hoffman reflex: - it is done by flickering the terminal phalanx of middle finger by

your thumb.
Normally: - no changes.
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Positive Hoffman (abnormally):- PT thumb flexion or adduction in response to examiner
flickering, positive in (UMNL).
Other superficial reflexes: - Abdominal reflex T9-T12 +ve normal present.
Cremastric reflex L1-L2  +ve normal present.
Anal reflex  S2, S3, S4  +ve normal present.
Note: - the superficial reflexes normally present but it’s may disappear OR reversed as in
(UMNL).
Finding (signs on examination) UMNL LMNL

Paralysis or paresis ,(weakness) Paralysis or weakness below the Paralysis or weakness at
level of the lesion. (Pyramidal the level of the lesion ,
distribution ) (segmental distribution )
Tone Hypertonia (spasticity) Hypotonia (flaccidity)
Deep reflexes Hyperreflexia Hyporeflexia
Clonus May be present. Indicate Absent.
severity of lesion if +ve
Pathological deep reflexes:-e.g May be present Absent.
patellar & adductor reflex
Superficial reflexes Lost May and may not.
Planter reflex (one of superficial + ve (Babinski):- . Dorsiflexion Plantar flexion of toes or no,
reflexes. of big toe ± fanning of other response say, equivocal
toes. response. (Never say -ve
Babinski).
Muscles wasting Mild wasting & if present it is Early & marked wasting due
late, due to disuse. to loss of muscle tone
Fasciculation’s Absent. May be present
Note: - any cause of upper motor neuron lesion start sudden onset can lead which called
spinal shock , its transient flaccidity ( Hypotonia ) , Hyporeflexia , may persist for 1 month
The longer duration of spinal cord poor prognostic .
Mixed lesion: - The finding of an extensor plantar response (Babinski sign) with an
absent ankle reflex suggests a mixed UMN and LMN lesion.
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Causes of mixed lesion :-
1. Vitamin B12 deficiency subacute combined degeneration.

2. Friedreich's Ataxia.
3. Diabetic amyotrophy , Amyotrophic lateral sclerosis.
4. Others: Syringimylia, , cervical myelopathy, and tabes dorsalis 3ry syphilis .
 Functions of the extrapyramidal system (basal ganglia)

1. Initiation of movement :- in lesion difficult initiation of walk and hyperkinesia
2. Coordination between agonists and antagonists during rest :- in lesion resting tremor
3. Postural righting reflex :- in lesion flextion posture tendency to fall in turning around
4. Inhibitory to tone :- in lesion hypertonia in form of rigidity .
 Signs of cerebellum lesion ( coordination )

Coordination between agonist and antagonist muscle done by the basal ganglia during rest if
damaged (static tremors) ,and by the cerebellum during active movement if
damaged(kinetic tremor) intentional tremor .
The lesion in cerebellum lead to motor ataxia at same side of lesion .
Other types of ataxia :-

1. motor ataxia :- cerebellum lesion
2. sensory ataxia :- posterior column sensation loss ( deep sensation )
3. vestibular ataxia :- labyrinthitis, cerebllopontine angle tumors
4. combined ataxia :- mixed lesions .
Cerebellar-ataxia Sensory Ataxia

cerebellar involvement Post column sensation (sense of movement &
sense of position)
Pt. cannot maintain balance even with eye (positive Romberg sign) With eye closure,
opened fall tend to be toward the affected site. balance is rapidly lost.
Reflexes are normal or pendular. Reflexes are usually absent or decreased
Wide based gait Stamping gait
sensation are normal Deep sensation are usually lost
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Face (eyes, mouth) Nystagmus horizontal, Speech is scanning dysarthria.
In the upper limbs  finger to nose tests (intentional tremor, dysmetria).

Alternating hand movements (Dys-diado-kinesia).
Rebound phenomena.
In the lower limbs  heel to shine test.
 Heel-toe test walk on strait line (tandem gait).

 Gait ataxia (wide based gait) patient tends to fall towards the side of the lesion.
 Romberg's test (+ve in sensory ataxia).
 Hypotonia, pendular reflex.
Note:- sensory and muscle power is not affected in isolated cerebellum lesion .
Sensations, in general are classified into:
I. SOMATIC SENSATIONS: are conducted to the CNS via "somatic nerves;" they include:
1. Superficial sensations:
Pain, Temperature, Touch.
2. Deep sensations (Proprioceptive):
Vibration sense, Joint sense (position), Muscle sense (tension & pressure).
3. Cortical sensations:
Tactile localization, 2 points discrimination, Stereognosis, Graphesthesia.
II. VISCERAL SENSATIONS: all sensations from internal viscera reaching the CNS via the
"autonomic nerves."
III. SPECIAL SENSATIONS: including vision, hearing, smell & taste reaching the CNS via the
"cranial nerves".
SOMATIC SENSATIONS :- (Ascending tracts)
1. All somatic sensations, whether superficial or deep pass through 3 order neurons from
receptors in the skin & deep structures to reach the cortical sensory area of the opposite
side.
2. The cell of the 1st order neuron is always in the posterior root ganglion.
3. The cell of the 3rd order neuron is always in the thalamus of the opposite side.
4. The 2nd order neuron varies according to the type of sensation.
Dorsal Columns tract (gracil & cuneat):- carry Position-Vibration & fine Touch.
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1st order neuron in dorsal root ganglia.
2nd order neurons in Medulla (here the fibers decussate to the opposite side of
the medulla).
.3rd order neurons are in the thalamus  internal capsule Post central gyrus (Sensory cortex)
spinothalamic tracts :-
lateral spinothalamic (carry pain & temperature ) :-

1st order neuron in dorsal root ganglia
2nd order neurons in the dorsal horn (here the fiber decussate to the opposite side of the
cord.
3rd order neurons are in the thalamus  internal capsule Post central gyrus (Sensory
cortex)
ventral :- ( carry crude touch ) :-

has the same pathway as pain & temp. but in the 2nd order neuron it ascends in the Ventral
Spinothalamic tract of the opposite side of the spinal cord
These are a mixture of superficial & deep sensations

arriving to the thalamus via the 1st & 2nd order neuron & conducted from the thalamus, via
the 3rd order neuron to the cortical sensory area in the parietal lobe.
 Tactile localization :- the ability to detect the site of touch in body and while closed both
eyes.
 2 points discrimination :- the ability to diffrenciate touch by on object or two while
closed of both eyes .
 Stereognosis :- identify the textures of objects .
 Graphesthesia :- ability to identify number written on hand .
Note :- cant test the cortical sensation in part which have lost the superficial and deep
sensation.
Look to examination sheet of neurological examination from page ( 9 to 11).
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Cerebral cortex & internal capsule  UMNL hemiplegic distribution

Above C5  Bilateral UMNL +sensory loss in all limbs
 If C3,C4,C5 all involved bilaterallydeath
C5 to T1 ( brachial plexus )  LMNL+sensory loss in upper limbs
 The lower limb may affect (UMNL).
T2 to T12/L1  Bilateral UMNL in legs
 Sensory level on trunk 1- t8-
umbilicus
 T10at umbilicus
 T11-t12below umbilicus
Below L1 (lumbosacral plexus ) cauda-equina  LMNL in lower limbs
DEFINITION: Paralysis of one side of the body due to pyramidal tract lesion at any point
from its origin in the cerebral cortex down to the 5th cervical segment (beginning of origin of
brachial plexus).
Causes of hemiplegia :- ( V, T, T, I, I).

1- Vascular :- most common cause ( thrombotic ,embolic , hemorrhagic )
2- Tumor Brain ( primary or metastatic) .
3- Trauma ( subdural hematoma , epidural hematoma, brain contusion ) .
4- Infection :-brain abscess ,subdural empyema , encephalitis , meningitis .
5- Inflammatory Demyelination :- multiple sclerosis ( demyelinating )
Clinical Picture:
Onset & Course:
 Acute onset & regressive course (vascular, infective & traumatic lesions).
 Gradual onset & progressive course (neoplastic lesions).
 Remittent & relapsing course (MS).
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Symptoms & Signs: Vary according to the onset:
1) Acute lesions : the clinical picture passes through 2 stages:
a. Stage of flaccidity: due to neuronal shock.
b. Stage of spasticity: this is the stage of established hemiplegia.
2) Gradual lesions : the hemiplegia passes directly to the stage of spasticity.
The lesion causing hemiplegia may occur at 3 main levels:

1- Hemispherical:- cortical hemiplegia, sub- cortical hemiplegia, capsular hemiplegia.
2- Brain stem (crossed hemiplegia):- midbrain hemiplegia, pons hemiplegia, medullary
hemiplegia.
3- Spinal cord: - involvement above level of brachial plexus (above C5), no cranial
involvement.
Cortical hemiplegia Sub- cortical Capsular hemiplegia

characterized by one or more of the It is indistinguishable Complete hemiplegia
following: from cortical associated with U.M.N.
1. Coma if the lesion is extensive. hemiplegia except 1. facial and hypoglossal
that the paralysis is paralysis on the opposite
2. Convulsions if the lesion is irritative.
more extensive side of the lesion.
3. Contralateral cortical sensory loss.
4. Aphasia if the. lesion is in the dominant
2. Hemi hypoesthesia on
hemisphere.
the opposite side of the
5.Homonymous hemianopia.
lesion.
6. Usually start (monoplegia) then 3. Hemianopia may occur.
hemiplegia especially in vascular lesions.
4. No convulsions,
If lesion is irrelative: - eyes fixed to aphasia or coma.
opposite side of lesion.
If lesion Is destructive: - eye look to
side of lesion.
So don’t depend on eye to localize of
lesion.
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Brain stem (crossed type):- The lesion is on one side of the brain stem resulting in the
picture of crossed.
Hemiplegia characterized by:

1. Hemiplegia on the opposite side of the lesion.
2. Cranial nerve paralysis of LMN nature on the same side of the lesion.
Note: - These why called crossed because the hemiplegia in side and the cranial nerves
involvement other side.
Midbrain hemiplegia Pons hemiplegia Medulla hemiplegia

 Cranial nerves (3, 4)  Cranial nerves 5, 6, 7  Cranial nerves (9, 10, 11, 12)
involvement.  pin point pupil (sympathetic  Pupil normal.
 Pupil dilated not reacting. lesion) eye fixed to opposite side.  Ataxic breathing (irregular).
 Neurogenic  Apneustic breathing (post
hyperventilation. inspiratory pause).
Weber's syndrome: Millard Gubler Syndrome: Avellis Syndrome:
1. Hemiplegia on the 1. Hemiplegia on the opposite side 5. Hemiplegia on the opposite
opposite side of the lesion. of the lesion. side of the lesion.
2. 3rd cranial nerve paralysis 2. 6 & 7 cranial N. paralysis on the 6. (9,11 & 10) cranial N paralysis
on same side of lesion. same side of lesion. on the same side of the lesion.
Note:-
Locked – in syndrome: - its bilateral upper brain stem infarction 2ry to basilar arterial
occlusion.(Quadriplegia with face involvement bilaterally).
Pseudo-bulbar palsy: - is bilateral impairment of the function of the (cranial nerves IX, X,
XI and XII) which control the muscles of eating, swallowing and-talking. It is the result of an
upper motor neuron lesion to the corticobulbar pathways in the pyramidal tract.
Bulbar palsy:- refers to bilateral impairment of function of the lower cranial nerves IX, X, XI
and XII, which occurs due to lower motor neuron lesion.
Note :- Pseudo-bulbar & bulbar its terms for nuclei in medulla oblongata , (Psudobulbar =
UMNL, bulbar = LMNL).
Bulbar palsy: - vascular, tumor (high brain stem), trauma, inflammatory (M.S),
degeneration (MND).
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Pseudo-bulbar Palsy:-
 inflammatory & infection:- Multiple sclerosis, Guillain-Barre syndrome, Poliomyelitis
 Vascular :- Medullary infarction.
 Degeneration: - Motor neuron disease, Syringo-bulbia.
 Tumor: - Brain-stem glioma.
Psudobulbar Bulbar
UMNL LMNL
Exaggerated jaw reflex Absent
Exaggerated of glabellar reflex Absent
No fasciculation of tongue Fasciculation may present
Spinal cord hemiplegia ( hemi cut in spinal cord ) :- The lesion is on one side of the
cord & is situated between C1 & C5 segments, it is caused by:- stab wound, disc prolapse,
M.S. or tumors resulting in the picture of Brown-Sequard syndrome characterized by:-
At the Level of the Lesion:
1. Ipsilateral localized LMNL of the muscles supplied by the affected segments.
2. Ipsilateral loss of all sensations in the area supplied by the dorsal roots of the affected
segments.
Below the Level of the Lesion:
1. Ipsilateral hemiplegia.
2. Ipsilateral deep sensory Joss.
3. Contralateral superficial sensory loss for pain & temperature.
Note :-
brown sequared syndrome :- its hemi cut in spinal cord IT may occur in ant level, so if
occur blow the T1 the PT will suffer of ipsilateral lower limb monplegia reather than hemiplegia
and other mentonied feature as before.
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Typical features of spinal cord lesions are :-
 Bilateral svmptoms and/or signs even if lesion unilateral.

 Impaitred. bladder & bowel control.
 ± Sensory level on the trunk.
 impaired of sexual function in male.
Note: Partial spinal cord lesions do not produce all these effects & they may be
difficult to distinguish from lesions at higher levels in the nervous system.
Causes of spinal cord lesion  DDx of Spastic paraplegia:
1. Trauma.
2. Tumor.
3. Vascular (Anterior spinal artery thrombosis).
4. Inflammation [Transvers Myelitis].
5. Spinal cord compression.
6. Degeneration  Friedrich's ataxia
 Vit B 12 deficiency
 cercical myelopathy , Syringomyelia , Diabetic myelopathy
Brown squared syndrome: - see before.

Transvers myelitis: - acute inflammation of spinal cord may occur at any level, unknown
etiology may follow viral infection, associated also with multiple sclerosis.
Treatment: - corticosteroid.
Syringimylia :- its dilatation of spinal canal, (Spared of posterior column sensation deep
sensation).
Sub-acute combined degeneration (vit-b12 deficiency)
Blood: - sign of anemia (macrocytic hyper-chromic) megaloblastic.
Neurologically :- (3-P)
Posterior column sensation loss (sensory ataxia).
peripheral neuropathy :- glove stock sensory loss
pyramidal lesion :-
 Spapstic paraplegia (UMNL) in both leg.
 Knee Hypereflexia.
 Absent ankle due to peripheral neuropathy.
Other neurological affection: - cerebellum ataxia, optic atrophy, dementia.
Its degenerate (UMNL) & (LMNL) so called combined.
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Conus Medullaris Syndrome (UMNL) Cauda Equina Syndrome (LMNL)

usually bilateral unilateral
Sudden and bilateral. Gradual and unilateral.
Knee jerks preserved but ankle jerks affected Both ankle and knee jerks affected
Urinary retention tend to present early in Urinary symptoms tend to present late in
course of disease. course of disease.
Typically symmetric, Hypereflexia. Asymmetric Areflexia paraplegia.
Localization of sensory loss:-
Site of lesion Presentation

peripheral neuropathy . Glove & stocking distribution.
nerve root lesion . Localized area in limbs or part in body.
complete transverse lesion in spinal cord All sensation at and below site of lesion.
Hemi cut in spinal cord (brown squared Ipsilateral posterior column loss.
syndrome). Contralateral spino-thalamic sensation loss.
Central canal dilatation (Syringiomylia). Affecting spino-thalamic tract bilaterally
Spear of posterior column.
Hemispherical ( capsular , thalamic ) Contralateral all sensation loss
hemihyposthesia or hemi-anesthesia.
Tremor , chorea , athetosis , Hemiballismus.
1- Tremor: - it’s rhythmic oscillating movement of limb or a part of a limb or head.
Types :- (resting, intentional, postural).
a- Resting =static tremor:- occur during rest , occur in Parkinson’s diseases of basal
ganglia which responsible for control between agonist &antagonist muscle during rest.
b- Intentional tremor = kinetic tremor:- occur during movement in cerebellar diseases

[cerebellum is responsible for coordination between agonists and antagonists during
movement].
c- Postural tremor:-occur when a part of the body fixed in position against gravity & the
type are (flapping tremor (Astrexis)), fine tremor).
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 Fine tremor: - Familial tremor (autosomal dominant) more in upper limbs.
Increase sympathetic:-
1- Anxiety.
2- Endocrine: - thyrotoxicosis, pheochromocytoma, hypoglycemia.
3- Drugs: - sympathomimetic (salbutamol), theophylline, lithium.
4- Habits :- caffeine, smoking.
 Flapping tremor (astrexis):- failure (renal, liver, respiratory type 2), phenytoin toxicity,
acute thalamic lesion usually unilateral.
2- Chorea:- rapid purposeless involuntary movement &occurs in proximal limbs more than
distal, suggest disease of basal ganglia (Caudate nucleus ).
3- Athetosis: - it sudden attacks of continues involuntary movement (snake like) in distal and
proximal limb suggest lesion in (lentiform nucleus).
4- Hemiballismus: - swinging movement in one side of the body usually lesion in

contralateral side of thalamus.
1- Hemiplegic gait (pyramidal gait):- due to (UMNL) affect one side of body.
The upper limb held in flexion and adduction & lower limb extension (streak like) with
circumduction at hip during walking.
2- Stepping gait: - occur in common peroneal nerve lesion (foot drop).
3- Stumping gait: - occur in sensory ataxia (deep sensation loss).
4- Motor ataxia (cerebellum):- broad based gait, drunken like gait.
5- Waddling gait: - occur in any proximal musculoskeletal abnormality in lower limbs.
6- Festinating gait (shuffling):- extrapyramidal lesion, (Parkinson’s disease).
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Dysphasia/Aphasia: A disturbance in the comprehension.
Or production of spoken or written language due to brain centers Lesion.
(1) Wernicke aphasia: fluent aphasia with poor comprehension and poor repetition.
Due to lesion in Wernicke's area located in the parietal and temporal lobes of the dominant
hemisphere usually due to CVA  MCA occlusion.
(2) Conduction aphasia: fluent aphasia with good comprehension and poor repetition.
(3) Broc’s aphasia: non-fluent aphasia with good comprehension and poor repetition.
Due to lesion in Boca’s area located in the frontal lobe of the dominant hemisphere
(4) Global.
Dysarthria :- poorly articulated speech, disturbance of speech due to a problem in the
muscles, the lesion not in centers of speech.
 Pyramidal tracts Lesion.
 Lesion Cranial nuclei concerned with articulation (5, 7, 10, 12) their nerves and the
muscles that supply.
Lesion in Cerebellum for the coordination of the muscles of speech. (Cerebellum ataxia).
Lesion in Extrapyramidal system for speech to be expressive. (Parkinson’s ).
Types of dysarthria:-
1- Slurred speech: - caused by Pseudo-bulbar palsy (12) or affecting cranial nerves (5, 7),
myasthenia gravis.
2- Staccato speech: - The speech is explosive with separation of syllables.
It occurs in cerebellar lesions as inhereditary ataxias, M.S...
3- Scanning speech (slurred staccato): also seen in cerebellar lesions.

4- Monotonous speech: The speech is expressionless and monotonous. It occurs in
extrapyramidal lesions as Parkinsonism.
Dysphonia / aphonia: - hoarse or whispered speech this may be due to a local problem
affecting the vocal cords.
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Agnosia: Inability to recognize previously familiar objects despite normal vision, hearing &
touch.
Apraxia :- inability to perform complex movement in presecnce of normal muscle power

,sensory & cerebellum, central lesion (frontal lobe).
Astereognosis: - inability to recognize familiar object by touch, parietal lobe.
Agraphaesthesia: - inability to determine number drowns in hand, parietal lobe.
Micrographic: - pt written by very small letters or numbers (Parkinsonism).
Agraphia: - it’s a type of aphasia when pt. can’t write native language.
Frontal release sign: - its reappearance of primitive reflex seen in frontal lobe lesion or
Parkinsonism.
Ataxia: - inability to coordinate simple voluntary movement despite normal muscle power.
Headache: - Headache denotes pain or discomfort from the level of the brows back to the
sub occipital region.
Syncope: - sudden transient loss of consciousness 2ry to decrease cerebral perfusion and pt
can return to consciousness without medical intervention.
Coma: - gradual or acute alternation in level of consciousness and need medical care. Multiple
causes including metabolic.
Vertigo: - sense of movement in absent of real movement. (Ear problem).
Dizziness or dizzy spell: - sense of movement after standing (postural hypotension).
Page | 18
They result in disturbance of movement and posture without significant paralysis or sensory
impairment.
The term "movement disorders" is often used in basal ganglia disease.
1- Akinetic OR bradykinesia (Parkinsonism) in which there is decrease of movement often

associated by an increase in muscle tone rigidity +/- resting tremor.
2- Hyperkinesia’s or dyskinesia’s excessive abnormal involuntary movements.
1- Primary (idiopathic) known as Parkinson’s disease (no paralysis, sensory & reflexes not
affected).
2- secondary to the other causes, may associated with (abnormal in power, sensory &
reflexes):-
1. Trauma: - repeated trauma.
2. Tumor: - meningioma.
3. Infection: - encephalitis.
4. Vascular: - atherosclerosis.
5. Toxic: - co poisoning, cyanide poisoning.
6. Drugs (reserpine, lithium, metoclopramide, haloperidol, phenothiazine).
Page | 19
Progressive degeneration in dopaminergic neurons & receptors
Idiopathic Degeneration of substantia nigra  decrease dopamine in

the Basal ganglia (imbalance between acetylcholine & dopamine) ACH which becomes greater
than dopamine) lead to inhibition of motor cortex  bradykinesia.
Parkinson PT also have Lewy bodies which are cytoplasmic neuronal inclusion body (not
pathognomonic).
It is less common in cigarette smoker.
(bradykinesia, rigidity, and tremor).
of Parkinsonism usually starts unilaterally and gradual bilateral involvement is

characteristic.
Bradykinesia must present:-

 Mask face (expressionless).
 Decrease eye movements and delay to initiation of movement
especially in upward gaze.
 Voice becomes soft and monotonous [dysarthria].
 Drooling of Saliva: - due to dysphagia.
 Reduced arm swinging, Micrographia.
Gait: Festinating & Shuffling, Short stride.
Resting tremor: - early sign and start unilateral more observed in hand (pill-rolling) and
may occur in jaw tongue and lower limb.
The tremor decrease in movement or patient in stress.
Rigidity: - late sign it’s presented with hypertonia in limbs (flexors & extensor) all over the
rang of joint in passive movement (lead pipe rigidity & cogwheel rigidity = lead pipe +
tremor).
Flexor posture.
Postural instability (frequent falling down):- its late sign.
Page | 20
Patient may have greasy skin like patient of acromegaly.

1/3 of patient may develop dementia later in disease.
Reappearance of primitive reflex & exaggerated glabellar reflex it may occur.
Freezing phenomena: - inability to initiate movement as in starting walking.

Power, reflex, sensation, sphincters are normal in Parkinson disease and it may affect in
Parkinsonism.
The diagnosis is made clinically & there is no diagnostic test for Parkinson's disease.
Imaging (CT or MRI) may necessary to investigate patients to exclude other causes of
Parkinsonism if there are any unusual features as change in reflexes or sensation or power .or
If it’s staring symmetrical bilateral.
Treatment of underline cause if present. (TUC).

Note: - Patients presenting before the age of 50 are usually tested for Wilson's disease.
 Levodopa  improves bradykinesia and rigidity.
The initiation of levodopa therapy should be delayed until there is significant disability to
decrease long term side effect.
If levodopa (L-DOPA) given alone more than 90% of L-dopa decarboxylted to dopamine
(Cannot cross BBB) extracerbrally & only10% Reaches the CNS.
Therefore Levodopa is given with decarboxylase inhibitor (Carpidopa OR Benserazide).
Side effects of L-DOPA:-
1- Postural hypotension.
2- Nausea & vomiting  controlled by domperidone (dopamine antagonist, only peripherally
acting).
3- Hallucinations, depression & facial dyskinesia controlled by amantadine especially for
dyskinesia.
End-of-dose deterioration: - Worsening of disease occurs despite levodopa therapy after 3-
5 yrs. in up to 50% of pts.
Controlled by more frequent dosing or converting to a slow-release preparation.
On-Off phenomenon: Sever bradykinesia alternating with dyskinesia.
It’s difficult to treat but sub-cutaneous (apomorphine ) is helpful.
Page | 21
 Bromocripitine: - may be used single in early of disease or in combination in advanced

stage.
 Anticholinergic drug (Tri-hexyphenidyl OR Benzhexol)•

Effective to improvingTremor and Rigidity.
No effect on bradykinesia.
Should be avoided in elderly patients BECAUSE they cause confusion and hallucinations.
Other side-effects include: - dry mouth, blurred vision, difficulty with micturition,
constipation.
 Amantadine: - improving Bradykinesia and used also for dyskinesia which produced by L-
DOPA treatment in late of disease.
S/E: - livedo reticularis.
 Selegiline:- (MAO-B inhibitor)
Selegiline has a mild therapeutic effect but there is Evidence that it slows the progression of the
disease.
S/E (DYSKINESIA).
 COMT inhibitor  tolcapone and entacapone: - its potentiate the effect of L-DOPA, this
allow L-dopa dose to reduce and give less frequent.
S/E (DYSKINESIA, nausea, insomnia, hallucination).
 Surgery:
Stereotactic thalamotomy can be used to treat tremor.
Pallidotomy: - used to treat rigidity.
Brain stimulation: - by implantation of (brain pace maker) which send electrical impulse to
specific site of brain.
 its variable, but early onset carry poor prognosis & shorten in life
expectancy.
Pt. who develops the disease after 70 yrs has better.
Page | 22
The blood reaches the brain through two systems of blood vessels:
The carotid system. The vertebra-basilar system.

Each internal carotid artery enters the Each vertebral artery passes upwards through the
cranial cavity through the carotid foramen Vertebral foramina to enter the cranial cavity
and canal to the cavernous sinus where it Through the foramen magnum and runs upwards
lies lateral to the optic chiasma; The on Each side of the medulla. Both arteries meet
internal carotid artery then divides into its at the lower border of the pons to form one
two main terminal branches. midline single artery called basilar artery.
middle cerebral Anterior cerebral Basilar artery:-divides into its two terminal
(MCA) (ACA) Branches the posterior cerebral arteries.
Supply the lateral supplies the medial Each posterior cerebral artery supplies the whole
aspect of the aspect of the occipital lobe and the posterior part of the
anterior (3/5) of anterior 3/5 of the temporal Lobe (posterior 2/5 of the cerebral
the cerebral. cerebral hemisphere hemisphere) & brain stem.
Both anterior cerebral arteries are connected together by the anterior communicating artery.
Also, the internal carotid artery of each side is connected to the posterior cerebral artery of the
same side by the posterior communicating artery. In this way the circle of Willis is formed
where the two carotid arteries communicate with each other and with the vertebra-basilar
system.
Note :- each artery of this have cortical branches and capsular branch, also the occlusion or
stenosis of one of these artery its well compensated partially by communicating branches but if
the ischemia persist it well lead to manifestation according to which site of brain affected.
The lateral aspect of anterior 2/5 of cerebral hemisphere responsible for motor & sensory of
trunk & upper limb , so the ischemia of these part which 2ry to ( MCA or its branches )
occlusion or stenosis .well affect mainly upper limbs and trunk but not only ( b/c it well affect
the lower limb also due to pressure of edema).
The medial aspect of anterior 2/5 of cerebral hemisphere responsible for motor & sensory of
lower limb, so the ischemia of these part which 2ry to (ACA or its branches) occlusion or
stenosis. Well affect mainly lower limb but not only (b/c it well affect the upper limb also
due to pressure of edema.
Page | 23
Anterior Medial aspect  Mentality and 1. Contralateral hemiplegia

cerebral artery Of hemisphere inhibition of affecting L.L. > U.L.
(ACA) primitive reflexes. 2. Contralateral cortical sensory
 Motor & sensory of loss in the lower limb.
L.L. 3. Incontinence of urine.
 Cortical bladder 4. Mentality and personality
center. changes.
5. Forced grasp reflex reappear.
Middle cerebral Lateral aspect of Motor and sensory 1. Contralateral weakness and
artery hemisphere. of upper limb. sensory" loss In Upper limbs <
(MCA) Upper part of optic Legs.
radiation. 2. Contralateral Homonymous
In dominant Hemianopia.
hemisphere center 3. Dominant hemisphere 
of speaking. Aphasia.
In non-dominate 4. Non-dominant hemisphere 
area of regulate Apraxia.
complex movement.
Penetrating Internal capsule  Site of passage of 1.Contralateral complete motor &
branch motor fibers (UMN) sensory loss affecting the upper
(Lenticulo & sensory fibers of and lower limbs to the same
striate artery the other site of extent.
body. 2.Contralateral hemianopia may
 Site of passage of occur.
lower part of optic 3.No loss of consciousness or
radiation. aphasia.
Posterior Posterior 2/5 of Vision, memory, third 1- Contralateral homonymous
cerebral artery cerebral cranial nerve for eye hemianopia with macular
hemisphere movement sparing as the macula has
(Occipital/partial double blood supply.
Lobes) midbrain. 2- Visual agnosia , amnesia
3- Ipsilateral (CN-III)  diplopia
& ophthalmoplegia.
Basilar artery Pons & medulla  Cranial nerves  Vertigo + Nystagmus + Ataxia.
Decussating of cotico- Locked-in syndrome
spinal tract. (Quadriplegia + intact vertical
eye movements)
Page | 24
The branch of Cerebellum &  Coordination. Wallenberg's syndrome
Vertebral- Lateral medulla  Cranial nerves in (Lateral medullary syndrome) :-
artery medulla. 1. Ipsilateral ataxia.
(posterior  Sympathetic chain. 2. Ipsilateral Homer's.
inferior 3. Ipsilateral 5th, 9th, 10th, 11th,
cerebellar True bulbar palsy.
artery ) 4. Contralateral spinothalamic
sensory loss.
5. Vestibular disturbance.
Note: - posterior Colum and
pyramidal tract intact because it
lie in middle of medulla not
lateral.
Note: - other syndromes of brain stem discussed before in hemiplegia.
Cerebra Vascular Accident [CVA]
Sudden onset of' focal1neurologic deficit due to vascular disease (stroke).
Stroke: - Sudden onset of focal neurological deficit that lasts more than 24hrs.
Completed stroke means the deficit usually within 6 hours, deficit is not progressing.
in which the focal neurological deficit

worsen after initial presentation.
Minor stroke: - Patients recover without significant deficit, usually within a week it’s called
Reversible Ischemic Neurological Deficit (RIND).
Transient ischemic attack [TIA]:- Sudden onset of focal neurologic deficit
That is completely reversible within < 24 hrs. (Most TIA last' only for 5-15 min).
The attack is usually sudden. TIAs have a tendency to recur.
• Age: Old.
• Gender: - (male > female, except in the very young and very old).
th
Stroke: - 4 leading cause of death worldwide.
Stroke is the leading cause of neurologic Disability in adults.
Page | 25
1- Gender (male > female) 1. HTN, DM, Heart disease (HF,

b/c of endogenous estrogen in pre- AF, endocarditis)
menopause protective. 2. Hyperlipidemia, obesity.
2- Heredity :- positive family history 3. Smoking, excess alcohol, life
3- Previous vascular diseases. style .
4. Polycythemia, Oral contraceptives.
1- arterial embolism, arterial thrombosis.

a. Thrombosis: - Large, blood vessel Atherosclerosis, Vascolitis (giant cell arteritis).
b. Embolisms: - cardiogenic emboli responsible of 20% of strokes.
Causes: arrhythmias (AF), MI, cardiomyopathies, valve lesions.
Artery to artery [mainly from Carotid, artery due to atherosclerosis] and it accounts for
10% of strokes.
c. Hypertension: - lead to Small blood vessel obstruction due to intrinsic blood vessel
disease, this lead to infarction small infarctions called lacunar infarction. Responsible for
20% of strokes.
i.e. lacunar infarction :-These are small infarcts (0.5-1.5 cm in diameter) wedge shaped
produced by occlusion of the penetrating branches small size (B.V ) of the major cerebral
arteries and are mainly due to sustained hypertension especially in old diabetic patients the
manifestations if present depends on site of infarction ( internal capsule, thalamus, basal
ganglia and pons).
d. Hypotension: - decrease in cerebral perfusion usually transient and its leads to TIA.
2- (intra-cerebral or subarachnoid).
Cerebral tumors (bleeding inside the tumor)\ subdural hematomas\ Peripheral nerve
lesions \ brain abscess\ Todd's paresis (after epileptic seizure)\ Hypoglycemia\Encephalitis\
Focal seizures.
Page | 26
these are attacks of cerebral ischemia too brief to cause infarction and
usually lasting few minutes or hours (max 24 hours) from which the patient recovers
completely.
as causes of stroke but the Micro emboli arising from atheromatous plaques in the
large cerebral vessels (carotid or vertebra-basilar) or from the heart. This the commonest
cause for TIA.
It’s may occur secondary to decrease cerebral perfusion (cardiac arrhythmia,

hypotension, or stenosis).
A rare due to Subclavian stenosis proximal to the

Origin of the vertebral artery. During exercise of the arm there is peripheral Vasodilatation and
blood flows retrograde from the vertebral artery into the subclavian artery causing vertebro-
basilar ischemia.
its transient and mild depend on which circulation involved anterior
or posterior circulation, but the affection of the anterior circulation care poor prognosis than
posterior one.
Anterior circulation (cerebral manifestation) Posterior circulation (brain stem)

Amaurosis fugax (transient loss of vision) unilateral, Diplopia, vertigo, vomiting,
due to retinal artery occlusion. dysarthria, Ataxia, Hemi-sensory loss,
Aphasia \Hemiparesis\ Hemi-sensory loss\ Hemianopia Hemianopia visual loss, Loss of
visual loss consciousness (rare but more
common than ant).
Note: - All this manifestations are transient and disappear completely within 24 hrs.
The recurrent rate is 30% in five years and 1/3 in first year.
The risk of developing stroke is (5 time) after first attack of (TIA).
Medical:
1- Antiplatelet aggregating drugs: they reduce the incidence of strokes by about 50%.
2- Anticoagulant drugs are less effective in preventing strokes.
Note:-It’s given in high risk patient or in recurrent cases.
3- Treatment of any risk factor.
Page | 27
Etiology: - discussed earlier.

Risk factors: - as above.
Clinical picture:-
Blood pressure  or  .
Heart rate [irregularly irregular pulse  AF].
Bruit over the carotid artery on Auscultation' suggest carotid 'artery stenosis.
The neurological deficit depends on occluded artery see table before.
The most common stroke is caused by infarction in the internal capsule following
thromboembolism in a middle cerebral artery branch.
 There is a contralateral hemiplegia or hemiparesis, develops over seconds, minutes or hours

(occasionally longer).
Aphasia is usual when the dominant hemisphere is affected.
Weak limbs are at first flaccid and Areflexia or Hyporeflexia  spinal shock stage .
After a variable interval, usually several days, reflexes return, becoming exaggerated. An
extensor plantar response appears.
The initial test of choice Non-contrast CT scan of the head because is the most sensitive test
for detecting blood in the brain & it can differentiate between hemorrhagic and ischemic
stroke. (But-they-are-negative for ischemia within the first 48 hours after symptom onset)
Diffusion-weighted MRI is the most accurate test for detecting cerebral ischemia.
MRl is more sensitive than CT in detecting strokes of the brain stem & cerebellum.
In ischemic stroke (MRA) or CT angiography to detect degree of narrowing because the

stenosis > 70% indication for surgery endartrectomy, recently not recommended in
established stroke.
 Cardiac sources  Electrocardiogram (ECG) & Echocardiogram.

 Carotid disease  Carotid duplex.
A transthoracic or transoesophageal echocardiogram can helpful confirm the presence cardiac
source or to identify endocarditis, intra-cardiac thrombus.
 CBC: - polycythemia, thrombocytosis.
 ESR: - if increase suggest for Vascolitis and SLE.
 RBS: - may present with hyper or hypoglycemia.
 Lipid profile: - for hyperlipidemia.
Page | 28
Stabilize the patient, airway, and Antiplatelet therapy :- 1)Psychological therapy.

provide adequate oxygenation. Aspirin is the 1st-line Drug 2)Physiotherapy.
 NOP tell asses the conscious level for prevention of ischemic 3)Social rehabilitation.
and swallowing and gag reflex ( to stroke. 4)Skin care: - bed sore.
prevent aspiration pneumonia ) Dipyridamole' or' clapidogrel 5)Respiratory care: -
Thrombolytic:-Tissue plasminogen (t- may add to enhance aspiration pneumonia.
PA) activator is given to PT with antiplatelet therapy. 6)Nutritional care.
ischemic stroke if (CT scan shows no Antiplatelet agent risk of 7)Urination and
hemorrhage if PT presents, within in recurrence by (25% -35%) defecation care For
first 3 hours of symptoms onset. Rx the risk factor for (UTI).
atherosclerosis (HTN, DM,
Aspirin given:-within 48 hours
Hyperlipidemia Statins.
decrease early mortality and
recurrence.  Blood pressure :- don’t
Note: - Aspirin (300 mg daily) lower the blood pressure in
reduces the risk of early recurrence first week because its return
should be started immediately after an within normal level in first
ischemic stroke unless alteplase has days , and the early
been given, if alteplase started aspirin reduction can decrease the
given after 24hrs. cerebral perfusion and
 Blood pressure: - rapid reduction of increase the infarcted area
blood pressure decrease cerebral The necessary
perfusion and risk of brain edema. reduction of blood
pressure in case with (heart
Treat: - the hypoglycemia,
failure, renal failure, aortic
hyperglycemia especially if glucose
dissection, hypertensive
more 200mg/dl.
encephalopathy).
Treat: - hyperthermia if present by
acetaminophen.
Note:-Hyperglycemia and
hyperthermia may increase volume of
infarction.
Dexamethasone: - may give in large
stroke with edema.
Note: - Antiplatelet therapy are more effective than anticoagulant to prevent recurrent of
stroke.
Page | 29
They are not used in all case , since they are not result in better
out comes and may increase risk of hemorrhagic transformation, so it used in selective cases
as flowing indications:-
1. Stroke in evolution: - gradual progressive weakness (over days) denotes gradual &
progressive thrombus formation.
2.Recurrent T.I.A.s
3. Embolic especially in cardiac cases to prevent recurrent embolization.
4. Patient with cardiac problem as (arrhythmias, valve lesion or replacement).
1. Bed sore, DVT/PE, constipation  2ry to bed ridden.

2. Depression.
3. Aspiration pneumonia.
4. UTI: - prolonged catheterization.
5. Epilepsy.
Contraindications of thrombolytic:-
1. Sustained BP > 185/110 despite treatment.
2. Platelets <100,000.
3. Gastrointestinal or urinary tract hemorrhage in last 21 days.
4. Major surgery or trauma in last 14 days.
5. Neurosurgery, serious head trauma in last 3 months.
6. History of intracranial hemorrhage (any time).
7. Recent treatment with heparin or warfarin and activated partial thromboplastic time& INR
above normal.
Page | 30
Its include:-
1- Intra-cerebral hemorrhage  hemorrhagic stroke.
2- Subarachnoid hemorrhage (most important) hemorrhagic stroke.
3- Subdural and extradural hemorrhage  not considered as stroke.
Intra-cerebral hemorrhage
Causes Common site of bleeding
1- Rupture of micro-aneurysms commonest cause 1. Basal ganglia 60%.
(charcot-bouchard aneurysms). 2. Thalamic region 10%.
2- Others: - bleeding disorders, vasculitis anticoagulants, 3. Cerebellum 10%.
thrombolytic therapy, Cocaine, amphetamine. 4. Pons 10%.
3- HTN: - risk factor.
 Clinical picture :- depends on site of bleeding , its similar to ischemic stroke so make
difficulties in clinical history and examination to differentiated between ischemic and
hemorrhagic but CT- SCAN is helpful ( recent hemorrhage show hyperdense lesion & in
ischemia show hypodense lesion).
The following are suggestive of hemorrhagic stroke:-

1- Onset if occur in day time and during stress.
2- Known case of hypertension.
3- Moderate to severe headache and Alternation of level of consciousness (drowsiness to
coma), irregular respiration.
4- Neck stiffness
5- Hesitation of optic disc margin (hypertensive retinopathy).
Pontine hemorrhage: - characterized by deep coma total paralysis , pinpoint pupils ,

absent of conjugation eye movement.
 Investigation: - CT-scan highly diagnostic can determine (site, dimension of cerebral
hematoma & provide information about presence of edema and effect on ventricles & if
there shifts in brain structure (herniation).
 Treatment:-
1- Resuscitation as in ischemic CVA.
2- Put patient in 45 degree and give (I.V mannitol) to decrease cerebral edema.
3- Control of hypertension with gradual reduction.
Page | 31
4- Urgent neurosurgery to evacuation is May indication in deep coma  poor prognosis.
Note: - antiplatelet & anticoagulants are contraindication.
 Definition: - Flooding of the subarachnoid space with blood, (where intracranial vessels
present).
 Epidemiology: -
Age >20.
Sex:-women > men.
 Etiology: - the most common cause of (SAH) is rupture of
1. intracranial aneurysms which may cause by :-
A. Congenital (berry aneurysms) most common.
B. Atherosclerotic.
C. Mycotic (e.g. in S.B.E.).
2. Intracranial A-V malformation, OR Hemorrhage in brain tumors.
3. Blood diseases as: purpura, leukemia.
4. Severe hypertension as in eclampsia.
5. Head trauma.
6. Wrong administration of anticoagulants.
 Pathology: - subarachnoid hemorrhages, 85% are caused by saccular ('berry')

aneurysms found in the circle of Willis, (Positive Familial association).
The site of aneurysms:-

Anterior communicating anterior cerebral junction 29%.
Posterior communicating-internal carotid junction 28%.
Note: - rupture of aneurysm commonly participating by (Physical exertion, stress,

straining as constipation & severe cough and sexual excitement, bending forward)
Associated with adult polycystic kidney disease (APCKD) & congenital collagen defects, e.g.
Ehlers-Danlos syndrome.
Page | 32
 Clinical picture: - one of the following.
1- Typically presents with a sudden, severe headache (thunderclap) often occipital +
vomiting.
2- Signs of Meningism but non infective meningitis  photophobia, There may be neck
stiffness usually start after (3-12 hours).
3- May coma or epilepsy.
4- Focal hemisphere signs (hemiparesis, aphasia etc.) at onset if there is an associated

intracerebral hematoma.
5- A 3rd nerve palsy due to local pressure from an aneurysm of the posterior communicating
artery.
6- Subhyaloid hemorrhage by Fundoscopy.
 Investigation:-
1)CT scan without contrast initial study of choice.
2)lumbar puncture (LP) is indicated if the patient has negative CT scan& possible (SAH)
LP is most sensitive at 6- 12 hours after symptom red color (CSF) due to (RBC)
Xanthochromia (yellow-to-pink CSF) usually is seen by 12 hours after the onset of bleeding
it’s due to (RBC) hemolysis.
3)Angiography should be performed once SAH is confirmed.
4)Cardiac :- (ECG) may show ST segment depression and elevation later on.
 Treatment:-
1- Calcium channel blockers (Niphidipine) are given acutely to prevent spasm & ischemia.
2- With paracetamol and codeine for headache.
Don’t lowering blood pressure if present risk of ischemia.
Seizure prophylaxis. Treat  (ICP) if present.
• Call neurosurgery: treatment either. Open clipping or endovascular coiling.
 Prognosis: Immediate mortality about 30%. Re-bleed rate is about 40% in first 4 wks.
 Complications:-
1- Rebreeding. 2- Vasospasm &cerebral ischemia.
3- Seizers. 4- Hydrocephaly.
5-(ICP). 6- Glycosuria.
Page | 33
Seizure: - is any clinical event (somatic, psychic or Autonomic manifestations) caused by an

abnormal electrical discharge in the brain.
Epilepsy: - recurrent attacks of seizure.
Epilepsy is a disorder characterized by: - recurrent, transient attacks of somatic, psychic

or Autonomic clinical manifestations associated with E.E.G. changes and may be associated with
Disturbance of consciousness.
Mechanism:- Inhibitory synaptic activity between neurones failsThis produces high-voltage

spike.
 Common in children.
 Gender: - Female = male.
 Affected in 0.5 of population (so common disease).
1. Idiopathic epilepsy: i.e . no cause can be found. This is the commonest etiology.
 The family history is positive in some cases. It starts in the (5-25) years  USUALLY
primary generalized epilepsies.
patient not taking his treatment, genetic predisposing, sleep deprivation,

Physical and mental exhaustion.
-Flickering lights, including TV and computer screens (primary generalized epilepsies only)
Uncommonly: loud noises, music, reading, hot baths.
Note: - if first attacks occur in adult or more than 25yrs age suggest of 2ry cause.
2. Others: - a cause can be detected.
CVA (may occur in ischemic or [it may occur many years after the (1ry –secondary).
hemorrhagic stroke) trauma)
Hematomas,[Neurofibromatosi
s, tuberous sclerosis] .
Vascolitis  SLE.
Infection Metabolic & electrolytes disturbance Drugs & toxin
(Meningitis, Encephalitis, (Na, Na, Ca ,Mg) (Alcohol, CO, lead,

Abscess). Hypoglycemia, Organ Failure: - botulism, cyanide).
(respiratory Hypoxia, liver cell Drugs :- (overdose or
failure & Renal Failureuremia). withdrawal)
Page | 39
Note: - vitamin deficiency, antiepileptic drugs &high fevers especially in children.
Sun stroke, Water intoxication (over hydration) can cause epilepsy.
According to clinical and EEG characteristics.
Partial seizures: They start focally in one region Generalized seizures: They start in both
of the brain. cerebral hemispheres at the same time.
Simple Complex Absence (Petit Mal) seizures (Typical &
Atypical).
Simple partial Complex partial seizures (Grand Mal) fits Tonic-colnic seizures.
seizures where where consciousness is Tonic seizures. (part of grand mal)
consciousness is impaired.
maintained.
Partial seizure with secondary generalized Partial Colnic seizures. (part of grand mal)
seizures progressing to generalized tonic- colnic Myoclonic seizures.
convulsions. Atonic (Astatic) seizures.
A. Simple partial seizures: where there is no loss of consciousness.

According to the site of the excitatory focus in the brain the fits may be:
Motor partial seizure Focal: There is a movement of part of a limb or of the whole limb.
which may be: Jacksonian: march course movement involving the muscles of
one side of the body.
It usually has a focal onset either in the thumb, angle of the mouth
or big toe depending on whether the wave of excitation in the
motor area spreads from above downwards or vice-versa.
Note: - More prolonged episodes may leave paresis of the
involved limb lasting for several hours after the seizure called
(Todd's palsy).
Sensory partial seizure General sensation: In the form of paraesthesias (due to irritation
which may be: of the cortical sensory Area) involving one limb (focal) or one half
of the body (Jacksonian).
Special sensation : Visual hallucinations (irritation of the visual
area
Olfactory hallucinations (irritation of the uncus in temporal lobe).
They usually include unpleasant disgusting smells.
Auditory hallucinations (irritation of the auditory sensory area).
Depersonalization, (dej a-vu) or (jamais-vu) phenomena
(irritation
of the temporal lobe).
Page | 40
B. Complex partial seizures: where there is disturbed consciousness.
The lesion usually is in the temporal lobe, episodes of altered consciousness without the patient
collapsing to the ground, The fit starts with an Aura which is followed by Absence, Automatism and
Amnesia.
Aura absence automatism amnesia
usually in the form of: the patient There may be champing of Amnesia for the
 Olfactory hallucinations appears staring teeth, smacking, and licking attack. (PT can’t
& (Deja-vu) or eyes and may of lips or Purposeless remember what is
(jamais- vu) not respond to movements of limbs. The happened during
phenomenon. Questions. patient may walk and leave attack.
 Emotion of fear or the room he may become
relation. violent if prevented.
1. It starts in childhood and improves at puberty.

2. They are a developmental abnormality of neuronal control, (not under line cause, not 2ry to
tumor).
The fit may be:
There is sudden loss of consciousness of short the loss of consciousness may be associated
duration (few seconds), with cessation of with:
motor activity or speech. There is a blank  High frequency (30 -100 attacks/day);
Expression on the face. the patient does not fall to the ground but
Note:- Children with typical absence attacks looks dazed and staring.
tend to develop generalized tonic-clonic  Sudden very brief jerky movements of the
seizures in adult life (known as primary head and or the upper limbs (myoclonic
generalized epilepsy) petitmal).
Important Notes: - Not preceded by aura & no postictal confusion

Each attack is accompanied by 3 Hz spike-and-wave EEG activity.
Fit may be precipitated by hyperventilation or photic stimulation.
Drug of choice: Valproate or Ethosuximide.
Page | 41
It is characterized by the presence of 3 stages:

Pre-ictal stage (aura): It Ictal stage (seizure): Sudden loss of Post-ictal stage
is a warning sign for a consciousness: lasting not more than 10 (sequelae):
coming attack. minutes
 It gives an idea about Tonic phase (10 seconds) with the The sequelae may
the site of onset of onset of coma, the body take a state with include: headache,
the attack. extension of the limbs, rolling of the sleepiness, confusion or
 The aura may be eyeballs upwards, cyanosis of the face Todd's paralysis.
somatic, psychic or (Due to cessation of respiration ), Todd's paralysis: - is
autonomic. clenching of the teeth with tongue-biting paralysis following an
and frothing from the mouth, retraction epileptic fit it does not
of the head to one side, and urinary last more than 24 hours
incontinence may occur. and is due to neuronal
-Clonic phase (1-2 minutes): the exhaustion.
whole muscles of the body contract & Note: - memory function
relax repeatedly & rapidly with abnormal may not be recovered for
respiration. some hours.
C
 There is a sudden, brief involuntary contraction of a muscle.
 It may occur in the muscles of the face, palate or extremities.
 For example Juvenile myoclonic epilepsy, it starts between 12-16 years of age.
D-
 They start in childhood.
 The attacks occur without warning and last few seconds.
 There is sudden loss of postural tone, and the child may fall to the ground.
 No loss of consciousness.
 Poor response to treatment.
D/D of epilepsy :- (syncope, psychogenic, migraine, CVA, TIA).
epilepsy syncope
Loss of conscious may gradual and Sudden transient loss of consciousness due to 
preceded by aura due to increase cerebral perfusion ( pt. may raging to conscious
abnormal electrical discharge from CNS without medical interventions) CVS problem.
Not related to posture & may Occur after rising from lying or sitting posture & not
associated with tonic clonic movement. associated with abnormal movement.
Cyanosis. Pallor skin.
Loss of conscious duration( > 5min) Loss of conscious just for seconds.
Urine incontinence no
Postictal (headache, confusion, fatigue, Not present pt. resume normal activity
Todd’s palsy)
Head trauma or tongue pitting No tongue pitting but head trauma may occur
Page | 42
Feature Generalized tonic- Psychogenic seizure

clonic seizure
Age of patient Any (past infancy) Usually older child or adult
events during an attack None (not remember) can recall detailed description
Tongue biting Frequent Rare
Urinary incontinence Frequent Rare
Injuries Common Rare
Abnormal neurologic signs May be present None
Postictal confusion Prominent Absent
EEG changes during seizure May Present Absent
Electroencephalography (EEG):- It should be performed after a first fit.

Help to determine the Type of epilepsy and guide therapy.
Inter-ictal recording are abnormal only in 50% of cases, so normal EEG doesn’t exclude
epilepsy.
EEG: - IS Poor Predictor of seizure recurrence.
Investigation to determined cause if present:-

Imaging (brain CT-scan or MRI):- indicted to defining or excluding a structural cause
(tumor)as in partial seizures which are resistant to therapy. But imaging it can never confirm a
diagnosis of epilepsy.
Indications for brain imaging in epilepsy

Epilepsy starts after the age of 20 years. Seizures have focal features on examination.
EEG shows a focal seizure source. Control of seizures is difficult or deteriorates.
Check blood glucose, urea, electrolytes, LFT, pulse oxymetry & ABG,FBC, ESR CRP.
LP (lumber puncture) if there is signs of Meningism.
Should be started if more than one seizure has occurred.

Not prescribed in first attack unless, pt. has:-
Abnormal neurological signs on examination OR presented firstly with status epileptics OR
have strong positive family history in this situations long term therapy is recommended.
Drug of choice in long term therapy according to type of epilepsy.
Page | 43
1)Start with single first-line drug with low dose & gradually increase to effective control of
seizures.
2)If the maximum dose of a first-line is achieved and sustained for at least 6 to 8 weeks
and seizures are still not controlled, a second line drug should be started while gradual
withdrawal of first line drug.
 If seizures recur during the period of tapering (withdrawal) of the first drug, the patient
should continue with combination therapy of both drugs.
3)Do not use more than two drugs in combination at same time
Note:-If above fails, consider structural or metabolic lesion or could be psychologically.
After complete seizure control (pt. free of seizure for 2-4 yrs) treatment may stopped
gradually over 6-12 months.
 Classical absence seizures, carries the best prognosis low recurrent rate.
 Primary generalized epilepsies & Seizures that begin in adult life, especially partial type,
have a marked liability to recur after drug withdrawal.
 Generalized seizures are more readily controlled than partial seizures.
 In overall the recurrence rate of seizures after drug withdrawal is about 40% & 90% of
recurrences occur within the first year.
Pt. can drive if he is free from all type of seizures for 1 yrs or seizures occur only during sleep
for 3 years (pt. also should not drive during withdrawal & 6 months thereafter)
AED (antiepileptic therapy )

Types of epilepsy Drug of choice
st
Line of therapy 1 line 2nd line 3rd line
Partial or partial with 2ry carbamazepine Sodium valproate OR Gabapentin Phenytoin
generalized Phenobarbital
Primary generalized (tonic- Sodium Carbamazepine OR Lamotrigine
clonic) or myoclonic or Atonic. valproate Clonazepammyoclonic type Clonazepam
Absence (petit-mal) Ethosuximide Sodium valproate Clobazam
Note:-
 Phenytoin and carbamazepine are not ideal agents for a young woman wishing to use oral
 Contraception, because the drugs induce liver enzymes (Carbamazepine is the safest drug
during pregnancy).
 Plasma level monitoring is used when using drug with narrow therapeutic index such as
(phenytoin).
Page | 44
50% seizure free without treatment.

20% seizure free but with continue treatment.
30% seizure persists in spite of treatment.
Carbamazepine Drowsiness, ataxia, nystagmus, diplopia,

hyponatremia, Rashes, thrombocytopenia.
Sodium valproate Hepatotoxic , ataxia , thrombocytopenia
Phenytoin CNS ( ataxia , diplopia , cerebellar degeneration ,
astrexis in toxicity).
Peripheral neuropathy , lymphadenopathy
Gum hyperplasia, hirsutism, induce liver ENZ (OCP
failure), Induce (SLE), folate deficiency.
 Suspected when a series of seizures occurs without the patient return to awareness between
attacks for > 30 minutes.
Note:-Status is never the presenting feature of idiopathic epilepsy (usually there is underline
cause).
1. Abrupt (sudden) withdrawal of anticonvulsant drugs.

2. Presence of a major structural lesion.
3. Acute metabolic disturbance (electrolyte disturbance, hypoglycemia)common causes.
Note: - electrophysiology’s confirmation of the seizures (EEG ) should be obtained early as
possible.
1- Call for Help Then Resuscitation (ABC) air way mouth gag to prevent tongue biting &
suction of frothy then delivery of oxygen.
2- Obtain Veins Line Draw Blood For Investigation And Administration Of (50ml
50% dextrose saline ,100mg thiamine & 0.4mg naloxone)
3- Send investigation to determined underline cause (urea, electrolytes, Ca+2 & Mg, LFT, FBC,
blood sugar, toxicology screen if indicated) PT with fever and leukocytosis with Meningism
 lumber puncture is indicated.
4- If seizure stop with any step of the following don’t give further anticonvulsant.
Page | 45
1st drug (diazepam or lorazepam)

Diazepam given I.V or rectally.
Lorazepam given I.V only.
Diazepam 10 mg
Repeated after 15 min Lorazepam 4mg
(Slow IV bolus)
Slow I.V at 2mg/min.
(Trial twice)

If seizures continues
Phenytoin or fosphenytoin.
IV infusion
With vital sign, ECG, ABG Phenytoin15mg/kg.
At rate of 50mg/min.
monitoring
Phenobarbital10 mg/kg.
Trial Once
At rate of 50-75mg/min.
I.V infusion

If seizures continues
Phenobarbital
I.V infusion
( trial twice )
repeated each 15min
If seizure continues 30-60 min

intubation and ventilation
With General Anesthesia
(propofol or thiopental or
midazolam or pentobarbital )
Page | 46
An inability to maintain repeated or sustained muscle contraction (fatigability).
It’s Autoimmune Disease characterized by the formation of Antibodies against the Acety
choline receptors at post synaptic membrane of the neuromuscular junction. ] it’s not LMNL
or muscular Disease[ .
Occur most common between 15-50 yrs.
More in female. Associated HALA B8-DR3 as SLE.
Course of Illness is usually Relapsing & Remission.
1)Emotional upset.
2)Febrile illness.
3)Pregnancy & Menstruation.
4)Exposure of extremes cold or Heat.
]weakness & fatigue which has Diurnal variation[  Symptoms more at end of day or after
exercise.
1) Ocular Ms. (ptosis, diplopia) most common presenting feature 90 % 80% of ocular
manifestation is Asymmetrical If bilaterally presents & may by unilateral in presentation.
2) Limbs involvement  U.L more than lower limbs.

Proximal muscle more than distal.
Upper limbs: - Shoulder  pt. note that need frequent Resting.

Lower limbs: - (pelvic girdles) if doing activity need elevation of arm above shoulders.
There difficult to climbing stairs.
Page | 45
 Note:-Limbs usually affected bilaterally symmetrically.
3) Pharyngeal Ms.:- Dysphagia.

4) Laryngeal Ms.:- Dysphagia l nosal voice.
5) Facial muscles (paresis)  Snarling Smile + Jaw hang.
Notes: - muscle wasting is very rare and late.
Nate: - Sensation & reflexes are normal.

 Mysthenic crisis: - its sever attack of MG with involvement of respiratory muscles requiring
intubation & ventilation.
Its occur in 20% of pts. and it is common cause of Death.
Note: - thymus  70% of pt. with Mg have lymphoid Hyperplasia in thymus.

15% of pts. (Mainly late onset) have local Invasive lymphoma.
 Mg associated with other Autoimmune Disease :-

]Thyroid (Graves), DM I, RA, SLE[ Screening for these in History & Examination.
1- Tensilon test: - I.V edrophonium bromide  Improvement in muscle power after 30

sec. and persistent for 2-3 min it’s Diagnostic.
2-Serum Antibody:-
A-Acetyl-choline receptor Antibody(AChRA):- Specific
+ve in 50% of pt with pure ocular involvement.

+ve in 80% of pt with Generalized MG.
B- Anti-skeletal muscles Antibody(Anti musk-Abs):-
Found in case with -ve (Ach-R-Ab) with prominent ocular involvement.
3- EMG :- Electromyography:-
Shows detrimental response in muscle Action potential which evoked by repetitive

stimulation.
4- Chest CT scan & x-ray  for Assessment of thymus.

5- Screening of other Autoimmune especially Thyroid disease.
Page | 46
1- Anti-cholinesterase (pyridostigmine ) gives orally. D.O.C to III symptoms.
2- If unsuccessful Consider Immune Suppressive Drug (Glucocorticoids) It initial

immune suppressive of Choice, but take 1-3 months to show effect of improvement.
3- If Steroids fails  Azathioprine is added.
Note:-
Plasmopheresis & I.V immunoglobulin are used in Mysthenic Crisis.
4-Thymectomy:-
Should be done any Antibody +ve pts. 45 not confined to extra-ocular manifestation.
Its improve prognosis even if thymoma is not present
Its increase Remission rates after thymectomy done.
  Ach activity in Receptors.

  Immunological Reaction.
1- Drugs induce M6  Should be Avoid in MG pts as:-
 D-pencilamine  use in RA.

 Aminoglycoside gentamycin.
 Propranolol.
 Ciprofloxacin.
 Quinone.
The Ach-R-Ab & symptoms disappear with discontinuation of Drug.
2-Eaton-Lambrt-myasthenic Syndrome:-
As Its para-neoplastic syndrome of Small cell carcinoma of the lung it due to Antibodies against
Ca+ channels presynaptic membrane % EM6 Shows increasing (incrementally) Response in
Repetitive stimulation.
3- Botulism.
4- Organophesphrous poisoning.
5- Muscular Dystrophies.
Page | 47
Definition:-Its group of diseases of unknown etiology, that characterized by degenerative of

a gradual onset and progressive course, affecting the motor system only (systemic disease). It
may affect the U.M.N., or the L.M.N. or both Sensory are normal.
Etiology: - unknown but positive family history & viral infection, trauma, toxins may have
rule.
Pathology: - it may affect AHC in spinal cord (LMNL) or motor nuclei in brain stem (LMNL)
or motor cortex (UMNL), or all tree sites.
Clinical picture:-
Signs and symptoms: this depends on whether the U.M.N. or the L.M.N. or both (Mixed) are
affected, its depends on which type of motor neuron disease.
As this is a systemic disease: - the Signs and symptoms Are usually bilateral but start
unilateral then progress to be bilaterally.
Different form in presentation of motor neuron disease:-

1- Amyotrophic lateral sclerosis: - combination of UMNL &LMNL.(most important one).
2- Spinal (progressive) muscular atrophies: - Predominantly spinal motor neurons
affected (disease of childhood) only LMNL.
3- Progressive bulbar palsy: - lower cranial nerve nuclei and their supra-nuclear
connections are affected. Combination of UMNL & LMNL of cranial nerves (Pseudo-
bulbar & bulbar).
Amyotrophic lateral sclerosis

 Affecting both AHC of spinal cord &motor nucleus of cranial nerves in brain stem  (LMNL).
 Affecting pyramidal neurons of motor cortex (UMNL).
 It’s affecting male > female usually > 50 year.
 May have positive family history 5% of cases (AD).
Onset and Course: gradual onset and progressive course.
Clinical Picture :-
1- UMNLweakness, wasting, fasciculation, (May predominant), wasting (hand atrophy in
distal more than proximal.
2- LUMNL Hypereflexia, hypertonia, Hoffmann& Babinski signs.
3- Brain stem (bulbar or Pseudo-bulbar) dysphagia (aspiration), dysarthria, tongue
wasting & fasciculation.
Page | 50
Spinal (progressive) muscular Progressive bulbar palsy
atrophies(LMNL)
 Weakness and wasting of distal limb Early involvement of tongue, palate and
muscles at first (start distally). pharyngeal muscles
 Fasciculation in muscles.  Dysarthria/dysphagia.
 Tendon reflexes may be absent.  Wasting and fasciculation of tongue.
 This form of MND is more common in women.
Important note:-
 No sensory loss (sensory tract and nuclei are spared).
 No extra ocular muscle involvement b/c cranial nerves (3, 4, and 6) spared.
 No urinary bladder or bowel disturbance (their motor nuclei of ANS spared).
 No intellectual impairment in most cases.
 Cerebellum &basal ganglia not affected.
Investigation: - no specific test (diagnosis clinically)
1- EMG: - help to confirm denervation (fibrillation) & also fasciculation.

2- Nerve conduction study is normal (motor and sensory).
3- CSF: - usually normal but may show elevated protein.
4- Imaging (CT-scan or MRI) may need to rule out focal or structural spinal or cerebral
disease.
Management: - no cure treatment only supportive and control symptoms.
1- Psychological & physiotherapy are important.

2- Riluzole (antiglutamate ) has recently been shown to have a small effect in prolonging
life expectancy.
3- Avoid fatigue and exhaustion.
Prognosis: - poor especially (amyotrophic lateral sclerosis) starting with bulbar onset.
Death within 3-5 years of onset of disease in bulbar onset disease survival is 1.5 yrs.
Younger onset have poor prognosis.
Page | 51
Peripheral nerves: -
1- Motor nerves (spinal nerves & cranial nerves).
2- Sensory nerves.
3- Autonomic nerves.
Note: - Peripheral nerves myleineted by Schwann cells but central nerves mylinated by
oligidendrocyte.
This group of diseases affecting peripheral nerves (motor, sensory & autonomic), its share
same manifestation, predominant manifestations depends on which type of nerve is more
affected.
1- Mononeuropathy:- single nerve is involved usually due to trauma or entrapment

initially appears to be a single nerve lesion but may later develops into multiple nerve
lesions.
2- Mononeuritis multiplex: - (Non traumatic) more than one nerve in different area of
body usually due to DM, vasculitis or immune mediated or infection as (leprosy,
HIV or Lyme disease), the involvement is asymmetrical.
3- Polyneuropathy: - (non-traumatic) generalized symmetrical involvement of

peripheral nerves, distal and progressive gradually to proximal. May affect (sensory,
motor, autonomic nerves), have several etiology (SEE NEXT).
Manifestations of peripheral neuropathy

Motor manifestations :- Signs of (LMNL) affecting ( Hypotonia, Hyporeflexia, wasting)
1- L.L > U.L.
2- Distal more than proximal  loss of ankle reflex before knee.
3- Weakness in extensor more than flexor in both upper and lower
limbs  wrist& foot drop (stepping gait).
The cranial nerves may be affected specially Cr III, VI, VII and X.
Page | 52
Sensory manifestations All type of sensation may affected but :-
1- Distal more than proximal  glove& stock sensory loss.
2- Pt. may have sensory ataxia + stumping gait loss of deep
sensation.
3- Paraesthesias & numbness or burning sensation.
Autonomic if affected may found :-
manifestations 1- Skin :- (loss of hair, brittle nails and trophic ulcers).
2- Postural hypotension, sweating, cardiac rhythm, and
gastrointestinal, bladder and sexual dysfunctions may present.
Note:-All peripheral neuropathy have same manifestations but in guillian barre syndrome
have some difference in which the muscle affected in lower limbs is more in proximal than
distal.
Hereditary familial Charcot –Marie – tooth ( peroneal muscle atrophy)

Inflammatory & immune Acute guillian barre syndrome & chronic CIPD
mediated Vasculitis, RA, SLE, SJOGREN syndrome.
Infection HIV, leprosy, diphetria, Lyme disease.

Neoplasms Blood (lymphoma, myeloma) CA lung, carcinoid syndrome.
Endocrine diseases DM , hypothyroidism , acromegaly
Systemic diseases/ Chronic renal failure (CRF), liver cirrhosis, porphyria,
metabolic amyloidosis.
Vitamin deficiency Thiamine (B1), niacin (B3), pyridoxine (B6). Cyanocobalamin
(B12), folic acid (B9).
Toxin Alcohol, lead poisoning, arsenic, mercury.
Drugs CVS: - Amiodarone, Statins, Hydralazine.
Chemotherapy: - Cisplatin, Thalidomide, Vincristine.
Antibiotic:-Chloramphenicol, Isoniazid, Ethambutol, Metronidazole.
Other: Gold, Pyridoxine, Colchicine, Phenytoin.
Page | 53
acute severe polyneuropathy due to autoimmune destruction of myelin sheet in

peripheral nerves characterizes by ascending involvement.
Most common cause of (acute generalized flaccid paralysis).
Age: - Any age. Sex: - female>male.
etiology unknown but, 70% of cases an autoimmune which

develop in 1-4 weeks after infected diarrhea (campylobacter jejune) or (URTI) by mycoplasma.
AB that attacks the organisms but in same time attacks the myelin sheets of peripheral nerves
lead to destruction.
Note: - other infection as (influenza, CMV, HBV, HIV) may have a rule but not common.
Clinical pictures: - Ascending flaccid paralysis.
(Its rapid progression of symptoms occurs within hours to days).
Motor manifestation: - There is acute severe weakness or paralysis starting in the L.L. and
ascending 'to involve the trunk and respiratory muscles, followed by the U.L. muscles.
Its differs to other types of polyneuropathy, the weakness is proximal more than distal.
In spite of the severe degree of paralysis, wasting is not present early in the disease.
Respiratory muscle involvement seen in 20% of cases and need mechanical ventilation.
Cranial nerves involvement especially (3, 7, 10, 9 and 12) may present.
Bilateral facial involvement found in 40% of cases.
Miller fisher syndrome: - triad of (ophthalmoplegia + ataxia + Areflexia).

Sensory manifestation: - Sensory impairment may occur resulting in stock and glove start in
toes and progressive upward as hypoesthesia, paraesthesias or tingling and deep sensory loss.
Note: - Early in the disease there is tenderness of the calves even before start of weakness of
motor symptoms.
Page | 54
Autonomic manifestation: - tachycardia, bradycardia, dysrhythmias, fluctuations in blood
pressure & postural hypotension. Urinary retention and sexual dysfunction may be noted.
Diagnosis is based on (clinical picture Ascending flaccid paralysis with Areflexia in absent of
fever) + CSF changes.
 CSF examination show elevated in protein level only (no  in cell count)
 The changes in CSF occur after 48hrs of onset of symptoms.
 It’s normal in 10%of cases and may normal in first 10 days in some cases.
EMG: - Nerve conduction study (electrophysiological) its show demyelination in peripheral

nerves.
Rare show affection in axons but if present carry poor prognosis.
Note: - EMG normal in early of disease the changes found after week or more from symptoms.
 To determined cause: - serology (AB of CMV), stool analysis, CXR.

 To determined complication: - measure the vital capacity of lung.
D/D of Guillian barre syndrome

Infection Toxin Spinal cord lesions
Poliomyelitis.  Acute porphyria.  Cord compression.
Diphetria.  Lead poisoning.  Transvers myelitis.
Cause of death: - respiratory failure, aspiration pneumonia, arrhythmia.
 Admission to ICU: - respiratory and cardiac monitoring 50% need ventilation.

 Assessment for swallowing to prevent aspiration pneumonia may need nasogastric
feeding.
 As early as possible High dose of I.V immunoglobulin OR plasmapheresis in sever
case, both improve prognosis.
 Glucocorticoids are not effective.
Page | 55
80% to 85% of cases are recovered completely within 3-6 months and < 5%
dies.
Poor prognostic feature are:-

Prolonged mechanical ventilation, campylobacter jejuni preceding, old age, rapid deterioration
of case.
Chronic inflammatory demyelinating polyneuropathy:
Its same as GBS but its chronic and gradual progression and recovery and respond to
glucocorticoid therapy .
Charcot Marie tooth disease :- hereditary disorder (AD) affecting peripheral nerves
mainly motor and peroneal nerve ( involvement of muscles blow knee) wasting of leg muscles
and foot muscle may have foot drop and associated with (pes cavus) as well as friedreichs
ataxia.
Page | 56
Headache: - Headache denotes pain or discomfit from the level of the brows back to the
Sub-occipital region.
The structures sensitive to the pain are (The tissue covering the cranium, The Dural and
cerebral arteries. The intracranial venous sinuses, the meninges, specially the basal meninges)
but the brain parenchyma, are insensitive to pain.
Note: - the nerves that responsible to convey the pain are (5, 9 cranial nerves) & upper three
cervical segments.
1. Primary A. Migraine
B. cluster headache
C. tension headache
2. secondary Serious :- A-meningitis B - tumors
C -subarachnoid hemorrhage D -Giant cell arteritis
E -glaucoma
A+B+C (headache of raised intracranial pressure)
Non-serious :- sinusitis , conjunctivitis , URTI ……etc.

Note: - giant cell arteritis see rheumatology sheet.
Definition: - benign condition characterized by recurrent intense throbbing headache (usually

unilateral) associated with (nausea & vomiting). It may be preceded by visual, sensory,
and/or motor manifestations.
Epidemiology: - more in female.
Onset around puberty and at the menopause (+ve family history).
Precipitating factors
alcohol , week end (relaxation time) certain food (chocolate & cheese) or hunger
irregular sleep pattern Noise and irritating lights.
oral contraceptive pills With onset of hypertension.
Mechanism of migraine:-
Aura phase: - due to vasoconstriction of cerebral blood vessels .serotonin theory & hypoxic
theory with (CA uptake)
Headache phase: - due to reactivation vasodilatation of cerebral blood vessels (throbbing

headache), nitric oxide may have rule.
Page | 57
Clinical types of migraine
Classic migraine: Aura: immediately before the attack of headache.
1. Visual disturbances as scotomata flash of light, zig-zags or
hemianopia.
2. Motor or sensory manifestations: - weakness, aphasia or
parasthesia.
The manifestations of the aura are present on the opposite side of the
coming Headache.
Headache:
It occurs in periodic and recurrent attacks. It starts in the temple or
around the eye and spreads to involve the whole side of the head (hemi
cranial). It is throbbing, increases with bright light, excitement and
passes away with sleep in dark room.
It lasts for several hours (4 to 72) and associated with nausea,
vomiting, pallor and coldness of The face with engorged pulsatile
superficial temporal arteries, and may be followed by polyuria.
2. Common The headache is not preceded by an aura as the vasoconstrictive phase is
migraine:- without not severe. This is the most frequent type of migraine (80% of cases).
aura
3- migraine Aura without headache (just focal transient neurological symptoms).
equivalent
4- complicated Migraine with sever neurological deficits (aura) that persist(hours or
migraine day) after the resolution of pain , and it’s have different forms as
(Ophthalmologic migraine, Facial migraine, Hemiplegic migraine)
5- Basilar artery Migraine with brain stem symptoms as (vertigo, ataxia diplopia,
migraine dysarthria…etc.).
This is followed by severe occipital headache and vomiting similar as
(SAH).
It occurs in young females and is often related to menses.
Management:-
1- Avoid triggers (chocolate , cheeses ….etc)
2- Treatment of acute episodes :-
NSAID + metoclopramide or domperidone (dopamine antagonist) antiemetic.
Sumatriptan (serotonin agonist)
Ergotamine but should be avoid  easily lead to dependence.
Prophylactic treatment: - initiated when pts. have acute migraine headaches more than
three times per month. And drugs include:-
Propranolol or Timolol / Na- Valproate / verapamil (CA blocker)
Methyscrgide (serotonin antagonist) / Amitriptyline (TCA )
Pizotifen (antihistamine).
Note: prophylactic drugs take 2 to 6 wks. To become effective.
Page | 58
Epidemiology:-
 Less common than migraine.
 Common in middle age male than female.
Description of attacks:-
Begin without warning and are typically described as sever. Per-orbital & reach to intensity
within 5 minutes of onset and spreading gradually to the same side of the head and neck.
The headache is usually associated with conjunctival injection, lacrimation and rhinorrhea,
flushing and sweating of the face on the affected side. There is no nausea or vomiting as
seen in other forms of migraine & attacks last from 45 to 90.
The attacks are characterized by their regularity and occurrence in clusters (repeated 3 times
daily for 4- 8 weeks), the clusters are followed by long periods (up to 6 months or 1 year),
where the patients are completely free.
Treatment: - 100% oxygen and Sumatriptan, lithium therapy in severe cases.
Tension headache most common type of headache (Most Common Type )

Persistent daily headaches described as tight band-like headaches that occur bilaterally.
Headaches may be associated with tightness of the Posterior neck muscles (often radiates
forward from the occipital region)
 In contrast to migraine , the pain may continue for weeks or months without interruption,
but patient can usually continue normal activities.
The pain is less severe in the early part of the day and becomes more severe as the day
goes on
Note: - Local tenderness may be present over the skull but this tenderness not as from the
acute pain precipitated by skin contact in trigeminal neuralgia (tenderness here over temporal
area)
Treatment: relaxation and NSAIDs.
Headache 2ry to increase intracranial pressure:-

Present on waking (Worse in morning, +/- vomiting) and often improves as the patient
becomes upright (reducing the intracranial pressure)
Improves through the day
Worse bending forward OR cough and straining.
Nature: - Dull ache, often mild
May Relieved by analgesia.
Page | 59
Sudden Severe attacks of unilateral facial pain along one or more of the sensory branches of the
Trigeminal nerve, usually the mandibular or maxillary or both.
Epidemiology:-
It usually affects >50 yrs. if young think in M.S.
More commonly females.
Causes: - The exact cause is unknown (idiopathic) but there are certain as:-
1- Root compression by a tumors or blood vessels in the cerebella-pontine angle.
2- Trigeminal neuralgia is common in M.S., diabetes and in alcoholism.
3- Post herpetic neuralgia (herpes zoster infection) usually affecting ophthalmic division.
Precipitating factors of attacks:-

The attacks are precipitated by movements of the jaw as laughing, brushing of the teeth,
mastication ... etc.
Attacks description:-
Facial pain (electrical pain or stabbing) lasting seconds to 1-2 min between attacks patient free
from symptoms.
Note: - tenderness over temporal area may present.
Sensory & Motor examinations are normal even during attacks.
Treatment:
a)Medical:
 Carbamazepine if patient can’t tolerate it gives (gabapentin or phenytoin or
clonazepam).
b) surgical :- Injection of nerve or ganglion with alcohol or phenol provides relief for up to
One year.
Page | 60
Vascular: - Intracerebral hemorrhage, Subarachnoid hemorrhage (discussed earlier)

Tumors: - 1ry or 2ry the secondary are more common than primary tumors.
Trauma :-( epidural & subdural hematoma).
Infection: - meningitis, brain abscess.
Idiopathic: - benign intracranial hypertension (pseudo tumor cerebri).
General manifestations of increase intracranial pressure:-
1- Headache of increase (ICP), (see headache sheet).
2- Nausea & Vomiting ( usually morning & projectile)
3- Blurred vision  papilledema not always present.
4- Diplopia due to 6thor 3th cranial nerve involvement.
5-  Level of consciousness even coma.
6- Cushing triad (hypertension, bradycardia, cheyne stock respiration ) may
present due to effect on vasomotor center & brain stem.
Note: - in case of mass (space occupying lesion) there is my herniation brain structure &
dilatation ventricles of brain lead to herniation syndrome & false localizing signs.
Herniation:-
1- Subfalcine herniation: - medial cortex moves under the midline falx results in obstruction
of anterior cerebral artery of same side of mass  ipsilateral hemiparesis or even
hemiplegia.
2- Uncal herniation: - uncus displaced through tentorium lead to Compression on reticular
formation in in MB impairment of consciousness.
Compression of the 3rd nerve & its nucleus in the MB  Dilated fixed pupil.
3- Tonsillar herniation: tumors leads to herniation of the cerebellar tonsils into the foramen
magnum resulting in:
Compression of the medulla  respiratory irregularities & impairment of consciousness may
cardiorespiratory arrest.
Tonsillar impaction in the foramen magnum neck stiffness & head tilt.
False localizing signs: its false because the signs don’t pointing the site of mass
as:-
1- Ipsilateral hemiparesis
2- Ipsilateral (pupillary dilatation)
3- Involvement of 6th cranial nerve (unilateral or bilateral)
Note: - the pyramidal effect could be bilateral in huge mass so may found (bilateral
extensor planter response)
Page | 61
True localizing signs: - when the mass lead to irritation or destruction that present
clinically by neurological deficit according to the site of that mass, this signs my present
early stage of tumor as in case of brain stem tumors where are the neurological structures is
early affected, but may presented late as in frontal lobe tumors, which may be reach large
size before symptoms occur.
Note: - The manifestation here is depended on site of tumor for e.g. (seizure’s partial or
generalized, mentality disturbance motor or sensory affection, memory disturbance …….etc)
General Treatment of increase intracranial pressure:-

1. Elevate head of the bed.
2. Mannitol for edema.
3. Glucocorticoids-dexamethasone.
4. Oxygen.
5. Sedation (e.g., morphine, propofol or midazolam).
Definition: - is a condition of increased I.C.T. with no evidence of any intracranial

Mass or intracranial infection or hydrocephalus (i.e. no  CSF volume and No ventricular
dilatation). The term "benign" is used because there are no serious sequelae except visual
impairment.
Etiology: - idiopathic but may due to slight decrease in CSF reabsorption by arachnoid villi.
Epidemiology: - middle age obese female.
Association :- (important)
a) Diet: - (obesity, hyper or hypo-vitaminosis A ).
b) Endocrine: (pregnancy, menstrual irregularities, Addison’s disease)
c) Drugs: (tetracycline’s, steroid withdrawal, contraceptive pills, cimetidine, cyclosporine).
d) Hematological: • iron deficiency anemia. • Polycythemia.
Clinical feature:-
1. Headache is prominent while vomiting is minimal.
2. Blurring of vision due to papilledema with enlarged blind spot.
3. Transient attacks of loss of vision (Amaurosis fugax) not persist loss of vision.
4. Diplopia 2ry to 6th nerve palsy (false localizing sign) only false localized sign here.
5. Examination of the C.N.S. is normal & the patient looks well conscious.
Investigation: - (CT & MRI) of the brain shows

1- no mass and no dilatation of ventricles (may narrow ventricles)
2- CSF is normal except for increased pressure measured by lumber puncture.
Page | 62
The diagnosis by exclusion (modified dandy criteria):-
1- Symptoms of raised intracranial pressure.
th
2- No localizing signs except of Abducent nerve involvement (6 nerve ).
3- Patient is awake and alerts (conscious).
4- Normal (CT & MRI) NO EVEDINCE of masses or hydrocephaly with normal size ventricles.
5- No other explanation for intracranial hypertension.
Treatment:
Wight reduction & treatment of other association.
Acetazolamide no response  therapeutic Lumbar Puncture if failed (shunt).
Brain tumors are space-occupying lesions within the cranial cavity.

The majority are metastatic from malignancies outside the nervous system.
Metastases from extra-cranial primary tumors are usually located in the white matter of
brain.
Note:-Primary brain tumors Even when is malignant they do not metastasis outside the
nervous system.
Epidemiology: - cerebral tumors account for 2% of deaths at all ages in developed country.
Meningioma’s account for about (1/5) of intracranial tumors.
Note: - in general males more likely to

Classification of brain tumors
Primary brain tumors Secondary (metastatic ) from outside nervous
system 50%
Benign 15% Malignant 35% Tumors Metastases from :-
Astrocytoma (most Oligodendroglioma , 1- Bronchus.
common). 2- Breast.
Neurofibroma Ependymoma 3- Stomach.
Meningioma. Medulloblastoma 4- Prostate.
5- Kidney.
6- Invasion of the brain by nasopharyngeal
Craniopharyngioma.
tumors.
Classification of primary tumors according to site of origin:-
1. Tumors arising from the meninges : meningioma’s (arising from the arachnoid)
2. Tumors arising from the brain tissue: Glioma (astrocytoma, glioblastoma multiformis,
medulloblastoma).
3. Tumors of the blood vessels: Haemangioma, Haemangioblastoma.
4. Tumors of the cranial nerves: Acoustic neuroma of the 8th nerve.
5. Pituitary tumors:- They may present with (Hormonal Manifestations or Neurological
manifestations due to compression effect on optic chiasma or brain stem )
Page | 63
Suprasellar cranio-pharyngioma  produces lower quadrantic bitemporal hemianopia.
Intrasellar:
A- Acidophil adenoma gigantism or acromegaly.
B- Basophil adenoma (Cushing's syndrome).
C- chromophobe adenomas (hypopituitarism)
Note: - all Intra-sellar tumors produce upper quadrantic bitemporal hemianopia.
Clinical feature:-
a) General symptoms and signs of increased intracranial tension.(see above)
b) Specific symptoms and signs according to the site of the tumors (true localizing signs),
See above.
Note: - localized edema surrounding the tumors will cause a rapid progression of symptoms.
Any brain tumor can cause obstruction of (C.S.F) circulation lead to obstructive hydrocephaly.
Investigation:-
 CT or MRI of the head allows accurate localization of the tumors & effect of tumor on
brain structure.
 MRI is important in the investigation of tumors of the posterior fossa and brain stem.
 Plain skull X-rays are rarely of diagnostic value except in pituitary tumors.
 Chest radiography may provide evidence of primary pulmonary tumors.
Management:-
Medical (to Relief of raised intracranial Surgery is the mainstay of
pressure) as before. treatment
1. Elevate head of the bed. Meningioma and acoustic
2. Mannitol for edema. neuromas the best prognosis
3. Dexamethasone. (Meningioma can recur)
4. Oxygen.
5. Sedation (e.g., morphine, propofol or midazolam)
Dexamethasone & mannitol lower intracranial

pressure by resolving or preventing the reactive edema
around a tumor.
Radiotherapy and chemotherapy: - have a mild effect on cerebral metastases and

malignant gliomas in adults.
But their combination has greatly improved the prognosis in medulloblastoma in children .
Page | 64
This is a benign tumor of Schwann cells of the 8th cranial nerve, which may arise in isolation or
as part of NF2. (Neurofibromatosis type 2) Von Recklinghausen's disease.
Epidemiology: - third decade and is more frequent in females.

The tumor commonly on the vestibular division, this tumor makes up 80-90% of tumors at the
cerebello-pontine angle.
Other cerebello-pontine angle tumors rare as:-

(Meningioma, Cholesteatoma, Arachnoid cyst).
Clinical feature: - it presented with different neurological deficits according which

structure is damaged by direct pressure of tumor, at can affect in:-
1- Cranial nerves (5, 7, 8) Ipsilateral.
2- Cerebellum damage. Ipsilateral.
3- Contralateral hemiparesis (pyramidal tract compression in pons).
4- Other cranial nerves nuclei in medulla oblongata  Ipsilateral.
5- May lead to obstruction of (CSF) circulation  obstructive hydrocephalus.
Note: - Facial weakness is unusual at presentation, but facial palsy may follow surgical removal
of the tumor.
Investigations:-
MRI is the investigation of choice, CT being less useful in this region of the posterior fossa.
Management: - surgical removal, the prognosis is excellent.
Page | 65
 procedure to collect a sample of cerebrospinal fluid (CSF) for:-

1- Biochemical.
2- Microbiological & cytological analysis.
3- Treatment (therapeutic lumbar puncture) to relieve benign increased intracranial pressure&
give drugs as (methotrexate) in leukemia.
Using sterile precautions.

The patient is placed in the left lateral position with the knees and chin as close together as
possible.
Marked between (L3-L4), The (L4) spine usually lies on a line joining the iliac crests.
2% lidocaine is injected into the dermis.
The special needle is pushed through the skin in the midline .
When the needle is penetrating the dura mater, the stylet is withdrawn and a few drops of
CSF are allowed to escape.
Specimens of CSF are collected in (3) sterilized test-tubes and sent to the laboratory.
ask patient to lie flat after the procedure to avoid a subsequent headache, Analgesics
may be required for post-LP headaches OR may use veins blood patch prevent further (CSF)
escape and reduce the headache.
1- Spinal &epidural anesthesia.

2- Help in diagnosis of :-
• Infection (meningitis, encephalitis, myelitis).
• Inflammation (multiple sclerosis, GBS, bachects syndrome, sarcidosis , polyneuropathies ).
• SAH (sub-arachnoid hemorrhage).
3- Therapeutic as (leukemia, benign increase intracranial pressure).
4- measurement of CSF pressure.
1- Infection 2- Trauma 3- Bleeding 4- Post puncture headache
dr.saif darif | P a g e 66
5-tonsiler herniation if done with patient have mass intracranial .
1- Suspension of mass in brain or spinal 1- Uncooprative patient

cord or even brain abscess exclude by 2- Patient with papilledema without focal
C-T scan. neurological signs or mass in brain.
2- Papilledema in Fundoscopy + focal 3- Patient with previous lumber surgery or
neurological sign. lumber spine deformity
3- Infection over the needle entry site 4- patient with Hypotension
4- Bleeding tendency platelets < 40.000
or coagulopathy
5- Unconscious patient
Crystal clear, colorless
60-150 mm of H2O
< 5/mm3
No polymorphs or RBC.
Mononuclear cells only
0.2-0.4 g/L
⅔ to ½ of blood glucose
Absent
1. culture for organisms and sensitivity of antibiotics

2. Stain
• Gram satin.
• Ziehl Nielsen satin for (T.B).
• Indian ink for fungal infection
3. Cytology for  malignancy.
4. Electrophoresis for  multiple sclerosis (oligoclonal bands)
5. Serology for neurosyphilis.
6. PCR (polymerase chain reaction) for  viral (HIV) OR (T.B).
Definition: - It is the inflammation of the membranes covering the C.N.S., including the
dura, arachnoid & pia maters. Usually infective etiology, presents with combination of pyrexia,
headache and meningism.
Note: - Inflammation of the Dura mater is rare & Inflammation of the pia-arachnoid is more common.
 (Signs of meningeal irritation):-
1. Neck stiffness: Spasm of neck muscles on attempted flexion.
2. Kerning’s sign (with the hip joint flexed, extension at the knee causes spasm in the
hamstring muscles)
3. Brudzinski's sign (passive flexion of the neck causes flexion of the thighs and knees).
Commonest in pediatric age. But may occur at any age.

Gender: Males= Females.
Causes of meningitis:-
Infective (more common) important. Non infective
Viruses (most common) Entero-viruses (echo, Malignant disease
Coxsackie, polio), Mumps, Influenza, HSV, HZV, EBV.  Breast cancer.
 Bronchial cancer.
 Leukemia &Lymphoma
Bacteria  Streptococcus pneumonia (most Inflammatory disease may be
common bacterial cause in adult) associated with recurrent Sarcoidosis, SLE and Behçet’s
pneumonia. disease.
Homophiles influenza(associated otitis media,
URTI)
Neisseria meningitides (2nd most bacterial cause)
Staphylococcus aureus.
Streptococcus Group B common in pediatrics
Listeria monocytogenes more in pediatrics &
immune suppressive patient, HIV, DM, alcoholism,
pregnancy.
Gram-negative bacilli  pediatrics
Mycobacterium tuberculosis
Protozoa and parasites Toxoplasma ,Amoeba Inflammation by blood :- SAH.
Fungi  Candida , Histoplasma
1. Infection at any part in the body and reach to meninges either direct spread or through
blood stream (septicemia) e.g. Pneumonia, sinusitis, otitis-media, osteitis, brain abscess,
encephalitis, myelitis
2. Impaired immunity (Alcoholism,. Diabetes, HIV)
3. Splenectomy (especially capsulated organisms) H.influenza, pneumococcal, hepatitis B
virus.
4. Head trauma & neurosurgery.
any infection (FAHM) fever, headache, malaise, anorexia.

1. Headache of increase (ICP).
2. Photophobia + Blurring of the margins of the optic discs in Fundoscopy.
3. Constitutional symptoms (general symptoms): Fever, malaise, Anorexia, irritability
4. Pulse is usually rapid except if there is ( I.C.P) where it will be normal or slow.
5. Meningism: - Signs of meningeal irritation  noted before.
6. Signs of Neurological Deficits: impaired of consciousness, or coma, Convulsions,
Transient cranial nerve palsies due to exudation around the nerves. But other focal
neurological signs are rare.
Note:-
The presence of Purpuric Rash suggests of meningococcemia.
The severity& complication of this clinical picture are more in bacterial cause than viral
infection.
Most common and most common is (echo –virus) , Self-limiting no specific therapy.
Epidemiology: - Occur in children and young adult
Clinical picture: - Acute onset of clinical picture (see before).
Investigation: - CSF show excess of lymphocytes ay persistent even after recovery), but
glucose & protein levels are commonly normal.
Management: - no specific treatment (self-limiting).
Recovery occurs within days, and lymphocytosis may persist in the CSF.
Less common but high mortality.

Causes: - look to cause of meningitis above
Clinical picture: - see before.
Investigation: - In bacterial meningitis the CSF is cloudy (Turbid) the protein content is
significantly elevated and the glucose reduced.
Gram satin & culture may allow identification of the organism
Disease occurs in epidemics& spreads by droplet infection and is predisposed by overcrowding

(e.g., schools, soldiers).
Note:-Usually occurs in the pt. has previously had a Splenectomy.
Pathological: - The pia-arachnoid is congested and infiltrated with inflammatory cells.

With pus forms adhesions lead to obstruction to the flow of CSF leading to hydrocephalus, or
may damage the cranial nerves.
as before + sweating, joint pains and transient Purpuric rash, may presents
with complication as meningococcal septicemia (Cary poor prognosis if presented with
complication)
Complications:
1- Waterhouse-Freidreichson's syndrome.
2- Neurological: - Hydrocephalus. Deafens especially children with H.influenza ( by given
corticosteroid) other focal neurological lesions are rare.
3- Cardiac: - Pericarditis, Endocarditis.
4- Eye: -Conjunctivitis, Keratitis, Iridocyclitis.
5- Genitourinary: - Nephritis (renal failure), Epididymitis, Orchitis.
6- Joint: Purulent arthritis especially in the knee and shoulder.
Waterhouse-Freidreichson's syndrome: - is an acute fulminating meningococcal Septicemia

associated with (skin purpura (+/-) gangrene + adrenal hemorrhage (adrenal crisis) lead to
hypotension and coma) death may occur within 24 hrs. Due to disseminated intravascular
coagulopathy (DIC)
Treatment :- Corticosteroids along with blood transfusion, dopamine & heparin in suspected
D.I.C.
(presented with
complication or age of more than 60 years).
start treatment immediately, even before
Empirical (i.v) 3rd generation cephalosporin + vancomycin or rifampicin

-If meningococcal meningitis is suspected, the patient should be given parenteral benzyl
penicillin immediately.
Note:-
 Intravenous is better than intramuscular.
 The antibiotic may be modified after CSF examination.
Corticosteroids (dexamethasone):-
1- Should be given 20 minutes before antibiotic therapy to prevent adhesion and further
complication as (hydrocephaly)
2- Given for severe cases as Waterhouse-Freidreichson’s syndrome.
immunization and prophylaxis of contacts by given( rifampicin or ciprofloxacin)
Common in developing countries and common as a secondary infection in patients with AIDS.
Symptoms: - Headache, Vomiting, Low-grade fever, Depression, Confusion, Behavior changes

Signs: - Meningism (may be absent) Oculomotor palsies, Papilledema, Focal hemisphere
signs, Impaired conscious level.
see table, next.
Detection of the tubercle bacillus in a smear from the CSF may be difficult.
The CSF culture take up to 6 weeks, treatment must be started without waiting for confirmation.
Brain imaging may show hydrocephalus, or an intracranial tuberculoma
start as early as possible (early treatment improve outcome)
Anti TB + corticosteroid
curable and good if treatment is started early.

Tuberculous meningitis is fatal in a few weeks if untreated.
1- Obtain a CT to exclude to exclude subarachnoid Hge. Or an intracranial mass, before

lumbar punctures
2- Lumbar puncture for CSF examination is mandatory unless there are contra-indications.
CSF analysis
Bacterial Viral ~ TB meningitis
Appearance Turbid Clear Clear and (spider web) on
standing
Cells (per mm) > 2000 > 500 > 1000
Main cell type Neutrophil Lymphocyte Lymphocyte
Glucose Very low Normal Low
Protein (g/L) I  Normal or  
Other test Gram stain PCR. Ziehl-Neelsen stain

Bacterial antigen
3- Pyogenic Bacterial Organisms can be detected by Gram-stain or culture of C.S.F:-
Meningococci Gram (–ve) intra & extracellular cocci

Pneumococci Gram (+ve ) diplococci
Haemophilus Gram (–ve) bacilli

Understanding the Central Nervous System

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 Introduction & neuro-anatomy  GBS

2- Peripheral nervous system: - (nerves &nerve roots, B- ganglia.).

 When approaching a patient with a neurologic disorder always ask yourself:

1- Where is the lesion?  by history & examination .

A- The Central Nervous System (CNS) is formed of 2 main parts:-

Intracranial :- 2 Cerebrum hemisphere (frontal, temporal, Parietal,

1.Frontal lobe: - Ant to Central sulcus (Voluntary motor control).

It is formed of: Midbrain, Pons, Medulla.

Cr 1, 2 & 8 have no motor nuclei, in brain stem.

 (extrapyramidal tract):- explained later on.

1- Motor function :- (movement & coordination) its responsibility of  (Cerebral

Note: - Cerebellum, Basal ganglia diseases not affect sensory.

3- Mentality: - mainly in frontal lobe of cerebral hemisphere.

1. The Pyramidal System (U.M.N.):

2- The Lower Motor Neurone (L.M.N.)

3- The Extrapyramidal (extra Pyramidal System) :-

4- The Cerebellar System:

UMN ( coticospinal tract) LMN ( AHC & Peripheral nerves ) spinal n.

deep & superficial.

Deep tendon reflexs: -

Upper limbs Lower limbs

Biceps (C5, C6) Knee (L3, L4).

Normally: - planter flexion of toe.

2- Hoffman reflex: - it is done by flickering the terminal phalanx of middle finger by

Other superficial reflexes: - Abdominal reflex T9-T12 +ve normal present.

Cremastric reflex L1-L2  +ve normal present.

Anal reflex  S2, S3, S4  +ve normal present.

Finding (signs on examination) UMNL LMNL

The longer duration of spinal cord poor prognostic .

1. Vitamin B12 deficiency subacute combined degeneration.

 Functions of the extrapyramidal system (basal ganglia)

 Signs of cerebellum lesion ( coordination )

The lesion in cerebellum lead to motor ataxia at same side of lesion .

Other types of ataxia :-

Cerebellar-ataxia Sensory Ataxia

In the upper limbs  finger to nose tests (intentional tremor, dysmetria).

In the lower limbs  heel to shine test.

 Heel-toe test walk on strait line (tandem gait).

Sensations, in general are classified into:

SOMATIC SENSATIONS :- (Ascending tracts)

lateral spinothalamic (carry pain & temperature ) :-

ventral :- ( carry crude touch ) :-

These are a mixture of superficial & deep sensations

Look to examination sheet of neurological examination from page ( 9 to 11).

Cerebral cortex & internal capsule  UMNL hemiplegic distribution

Causes of hemiplegia :- ( V, T, T, I, I).

The lesion causing hemiplegia may occur at 3 main levels:

Cortical hemiplegia Sub- cortical Capsular hemiplegia

Hemiplegia characterized by:

Midbrain hemiplegia Pons hemiplegia Medulla hemiplegia

Typical features of spinal cord lesions are :-

 Bilateral svmptoms and/or signs even if lesion unilateral.

Brown squared syndrome: - see before.

Conus Medullaris Syndrome (UMNL) Cauda Equina Syndrome (LMNL)

Localization of sensory loss:-

Site of lesion Presentation

Tremor , chorea , athetosis , Hemiballismus.

1- Tremor: - it’s rhythmic oscillating movement of limb or a part of a limb or head.

Types :- (resting, intentional, postural).

b- Intentional tremor = kinetic tremor:- occur during movement in cerebellar diseases

4- Hemiballismus: - swinging movement in one side of the body usually lesion in

2- Stepping gait: - occur in common peroneal nerve lesion (foot drop).

3- Stumping gait: - occur in sensory ataxia (deep sensation loss).