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1 Clinical features of upper motor neuron syndrome?

4 importent symtomes:
1. Motor deficit:
- totoal/ plagia: all movements in the partj of the body are absent.
- Partial/paresis: patient can make some movements but the are weak in that reagion.
o Monoparesis: only 1 limbis affected.
o Hemiparesis: arm&leg of 1 side affected
o Paraparesis: both legs&arms are affected
o Tetraparasis: both legs&arms are affected
2. Hypertony/regidity: Increased muscle tone, passive flexion/extension is defficult due to
increased tonicity.
3. Pathological reflexes:
Balbinski reflex
Hoffman reflex
Marinescu
4. Sinciesias: involuntary movements, which occur in affected limb when the normal limbs make
some movements.
2 Topographical diagnosis of hemiplegia: cortical hemiplagia, capsular hemiplagia,
hemiplegia in midbrain lesions, spinal hemiplegia?
- Cortical hemiplegia: the motor deficit is unequal may by largest in the face arms & little in the
legs, this is because the 4th area is supplied by 2 big arteries (middle & anterior cerebral artery.
- Capsular hemiplegia: the lesion is in the internal capsula, & has anterior limb, knee, & posterior
limb. If we have a lesion in the internal capsula there appears a hemiplegia which affects the
body part equally.
- Spinal hemiplegia: the lesion affects the anterior horn of spinal cord & appears a motor deficit
in the same side of the lesion.
- Brainstem lesion: appears alternated syndrome, paresis of one cranial N & in the contralateral
side we have motor deficit.
3 Paraplegia, tetraplegia, pseudobulbar syndrome?
The lesion in paralegia is in 2 places: spinal cord & pons.
Etiology: Tumor, Trauma, Vascular, Infections, Degenerative disease.
Tretraplegia: motor deficit of all 4 limbs. The lesion may be in spinal cord or in the pons, if it is
in pons patient is in coma.
Pseudobulbar syndrome: lesion of both geniculate tracts.
Symptomes:
Trouble of swallowing & phonation.
Emotional lability
Presence of pathological reflexes
4 The lower motor neuron syndrome: anatomy, clinical features?
The lower or peripheral motor neuron syndrome controls the automatic movements, tonic
movement, it is the center of all the tendon reflexes.
Symptoms of PMNS:
Motor deficit: all the muscles are equally affected and patient loose all voluntary reflex
movements in the affected part.
Hypotony: in the refion of deficit appears hypotony.
Atrophy: the contour of the muscle disappears.
Fasciculations: involuntary movements of one or small group of muscles.
Electromyography: representation of muscular contractions.
PMNS may be caused by:
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Leasion in the anterior horn of the spinal cord

Leasion in the anterior roots of the spinal cord
Leasion in the nervous plexus
Leasion in peripheral nerves
5 the topographical & the differential diagnosis of the lower motor neuron syndrome?
Pyramidal syndrome increased hypertony, increased reflexes & atrophy appears sooner.
Myasthena gravis: disease of neuromuscular junctions with unkown etiology, the
receptors that transmet the nervous impulses are diminished.
Motor deficit in dyskalemia: usually appears after eating sweet food.
Muscular disease: deficit is biggest in the proximal part of the limb & atrophy too is inten
proximal part. Tendon reflexes are normal.
6 Parkinson disease: definition & symptoms?
Definition: it is a degenerative disease with familjar autosomal dominant transmission. The
black substance is more affected due to unkown etiology & globus pallidus also affected.
Symptoms:
Akinesia: Patient has difficulty in starting the movements.
Face is like mask
Blinking is rare
Walk is made by short shuffling step, position like ?
Polylalia, slow thinking,
Hypertony: the whole body is flexed like a ? due to rigidity.
Pillow sing(+)
Tremor: involuntary movement which usually affect the finger, hands, head, & leg, it
appears during emotional stats & disappears during sleep. Salivation is excessive. Patient is
selfish, with increased irritability.
7 Prakinson disease: Treatment:
-Due to decreased levels of Dopamine , we give Dopamine substitutes like Dopamine agonists
and also we give Anti-cholinergic drugs to restore the balance b/w Dopamine and Acetylcholine
1.We start with Selegilin 2 tb / day ( 1tb = 5 mg ) or
Rasagilin (Azilect)1mg.
2.Viregit - 1 - 3tb / day ( 1 tb = 100 mg ) in increasing doses. Increases the Dopamine level.
3.Substitution of Dopamine: -L - Dopa + Decarboxylase.
Drugs - Sinemet , Nakom , Madopar. Dose - 750 mg / day for all drugs.
4.Bromocriptine - A Dopaminergic drug. Dose - 15 - 30 mg / day in increasing dose.
SURGICAL:
If a patient has increased Tremor than Akinasia, we make Sterotactic operation (electrode
inserted into the Thalamus ). Side effect - Hemiparesis occurs sometimes.
8 Acute chorea: anatomy,symptoms,investigations,treatment?
In acut chorea there appears the atrophy of the Neostriatium (caudate nucleus&putamen
nucleus)& frontal lobe.
Symptoms: Appears after weeks of Rheumatic disease.
1. Hypertony: Amplitude of passive movements is increased
2. Involuntary movements. It affects the fingers, shoulders, lips, and tongue, & appears during
active movements, they are rapid, illogic and are increased by emotions and disappear by sleep.
The involuntary movements affected the writing, speech, eating.
3. Psychic lability: increased depression, insomnia, trouble of attention.
Investigation:
- Streptococcal serology
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Hematologica,metabolic,endrinology
MRI-scan for brain
Treatment :1. Penicillin: Dose: 3 mil / day.

2. Cortisone: 1 mg / kg / day.
After 6 months we continue with Moldamine.
For involuntary movement, we give Majeptil or Haloperidol. Dose: 2-5 mg every day.
9 Chronic chorea:anatomy,symptoms,investigation,treatment?
In chronic chorea there appears the atrophy of the Neostriatium (caudate nucleus&putamen
nucleus)& frontal lobe. Chronic chorea is a degenerative disease.
Symptoms:
1. Hypotony.
2. Involuntary movements: all parts of the body is affected.
3. Psychic lability.(violence and depression )
4. Voice/ speech is affected. (Dysatria)
5. Face- grimace appears.
6. Walk: like a dance.
7. Writing is affected.
8. Dementia - it may appear later in the course of the disease.
9. EEG -course is slow.
10.GCT, PET-Atrophy of Caudate nucleus and anterior part of lateral Ventricles are big.
Treatment:
1. Reserpine: dose-5-10 mg / day.
2. Majeptil or Haloperidol dose- 5-15 mg / day.
Investigations:
MRI and CT scans in moderate-to-severe Huntington's disease show a loss of striatal volume
and increased size of the frontal horns of the lateral ventricles
If genetic testing is considered then extensive genetic counselling in a specialist unit is
required in view of the implications of an untreatable, familial, progressive, neurodegenerative
disease.
Testing for alternative causes of movement disorders (including SLE, antiphospholipid
antibody syndrome, thyroid disease and Wilson disease) and dementia.
10 Hepatolenticular degeneration(wilsons disease) Pathophysiology, clinical forms,
treatment?
Wilson's disease is a disease of copper toxicity. Absorbed dietary copper is bound mainly to
albumin in the portal circulation from which it is avidly extracted by hepatocytes. Hepatocellular
copper is subsequently used for cellular metabolic needs, incorporated into ceruloplasmin or
excreted into bile. The transport of hepatocellular copper to bile is thought to involve a vesicular
pathway (Golgi apparatus) that depends on ATP7B (copper transporting P-type ATPase)
function.4 The absence or diminished function of ATP7B results in a decrease in biliary copper
excretion, which is responsible for the hepatic accumulation of this metal in Wilson's disease.
Initially the copper is stored in the liver, when it accumulates beyond the cellular capacity for its
safe storage, hepatocellular injury may result. Toxic effects of excess copper include the
generation of free radicals, lipid
Treatment:
1. Diet - avoid liver, cabbage, pea and chocolate.
2. Cuprenil ( Penicillamine ) - 1 mg / day. 1 tab-250 mg.
Clinical forms :Neurological:
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1. Hypertony.
2. Involuntary movements (choleric / athetosis / myoclonic )
3. Tremor ( Intentional tremor as in Cerebellar diseases )
4.. Speech, Writing, Walk are affected.
5. Epileptic Seizures may appear (total / partial )
6. Psychic troubles
HEPATIC:
1. Cirrhosis.
2. LFT`s are positive.
11 Cerebellum:anatomy,physiology,etiology of cerebellum syndrome?
The cerebellum is placed in the posterior part of the brain, being separated from the Occipital
lobe by Tentorium & from the Brainstem by the 4th Ventricle. It has 2 hemispheres & a central
part called Vermis. Both Hemispheres & the Vermis are divided in many lobes. It is made up of
the gray matter (cortex) and white matter.
The cortex from gray matter has 3 layers: Granular layer, Purkinje Cell layer, Molecular layer.
The Cerebellum has 4 Cerebellar nuclei: Dentate, Fastigial, Emboliform, Globose nucleus.
The Cerebellum has 3 parts: Archaecerebellum, Palaecerebellum, Neocerebellum.
The Cerebellum has 3 Cerebellar Peduncles: Superior, Middle & Inferior.
The function of cerebellum is to ensures the co-ordination of movement, regulates the muscle
tone & equilibrium of the body.
Etiology of cerebellum syndrome:
1. Vascular disease: Ischemia & hemorrhage.
2. Tumor: Medulloblastoma in children
3. Trauma: Contusion & Hematoma.
4. Inflammatory: Encephalitis in Parotiditis or Mumps.
5. Intoxications: Drugs -Phenobarbitone. Alcohol intoxication.
6. Degenerative disease: Multiple Sclerosis.
7. Metabolic disease: Hartnup disease
8. Paraneoplastic cerebellar syndrome.
12 Semiology of cerebellum ataxia: troubles of muscular tone?
Ataxia: disturbance of co-ordination. The generalized ataxia with jerking movements of head,
arms, and legs, stiffening of the body, loss of balance, dizziness, blurred vision, dysarthria, &
diplopia.
These episodes may occur several times a month, may last seconds to minutes, & can be
precipitated by anxiety, emotional stress, fatigue, & sudden postural changes (kinesigenic
stimulation). Mild exercise, kinesigenic stimulation, and vestibular caloric stimulation may be
used to induce attacks.
13 Semiology of the Vestibular Syndrome: nystagmus, troubles of equilibrium?
Nystagmus: Involuntary movement of the eyes, rhythmic, bilateral & has 2 components:.
1. Rapid: is for correction.
2. Slow: shows the deviation of Vestibular lesion.
Nystagmus can be:
1. Horizontal. (Peripheral VS, Central VS in pons)
2. Vertical (Central VS in midbrain region)
3. Rotatory. (Central VS in medulla oblongata)
It can also appear in some intoxication (eq, alcohol), or in the paresis of CN III called paretic
Nystagmus. Bilateral nystagmus can appear in Amblyopia.
Troubles of equilibrium: Static Equlibrium troubles: evidentiated by Romberg`s test and of the
stretching of arms.
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14 The central & Peripheral Vestibular Syndrome symptoms?

Peripheral symptoms:
In the PVS, there appears the Star-like walking.
The patient draws a star-shaped pattern when asked to move a step forward and backward with
closed eyes.
The patient always falls on the same side of the lesion
The patient has Cochlear disturbances like diminished hearing or tinnitus
At Rombergs test, the patient falls on one side and
at Stretching test, the deviation is only on one side.
Central symptoms:
Disharmonious :- Patient deviates in all directions
15 Treatment of symptoms of central & peripheral vestibular syndromes?
Antibiotics
Cortisone
Vasodilators: Hydergine or Redergine 15dr/day
Papaverine 3tb/day ( 1 tb:4mg)
Symptomatic treatment:
Vertigo:
- Torecan: 3 tb / day ( 1 tb: 6,5 mg ) or 1-2 phials / day.
- Emetiral: 3 tb / day ( 1 tb: 5 mg )
Vegetative Troubles:
- Romargan: 3 tb / day ( 1 tb: 3 mg ).
16 Anatomical structure of sensitive function?
comprises 3 structures:
1.Receptors,
2.Sensitive Transmission Ways,
3.Cortical Sensitive Area.
1) Receptors: are typical structures specialized in the detection of different external and internal
stimuli.
Receptors for Tactile sensitivity:
-Meissner Corpuscles (placed in the papilla of the Chorium),
-Merkel Discs,
-Free Nerve Endings (the incircle the hair).
Receptors for Thermal sensitivity :
-Krausse for cold,
-Ruffini for warm.
Receptors for Pain sensitivity:
-Free Nerve Endings.
Receptors for Deep sensitivity:
-Golgi Organum (intendon),
-Vater Pacini Corpuscles in Aponeurosis and Periosteum,
-Neuromuscular Spindle.
2) Sensitive Transmission Ways:
For Thermal, Pain and Gross Tactile Sensitivity: Spinothalamic Tracts: anterior and lateral.
For Deep and Fine Tactile Sensitivity: Medial Lemniscus.
The sensitive transmission ways has 3 neurons:
The 1st neuron: is placed in spinal ganglion and in ganglion of cranial nerves. The structure of
sensitive fibers in different:-for deep sensitivity-the fibers are thick with much myeline and
resistance to compression and anoxia. For thermal and pain sensitivity- the fibers are thin.
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The 2nd neuron: is placed in the posterior horn of the spinal cord and in the sensitive nuclei of
cranial nerves for thermal, pain and gross tactile sensitivity. For deep sensitivity the 2nd neuron is
placed in Gall and Burdach nuclei in medulla oblongata. The axons of these nuclei make the
sensitive tract:- spinothalamic tract (anterior and lateral) and medial lemniscus.
The 3rd neuron: is placed in the ventro-posterior thalamic nuclei.
3) Cortical Sensitive Area:
Are in the opposite parietal lobe in areas: 3, 2, 1, 5 and 7.
Areas 3, 2, 1 are placed in the posterior central gyrus. Here is the sensitive homunculus with
head downward and leg upward (same as motor homunculus). The representation of different
parts of the body is different after their importance in sensitivity. Representation of hands,
fingers and lips is larger than for the trunk.
Area 5 and 7 represents integrative sensitivity, which is a complex sensitivity that joins together
the superficial and deep sensitivity.
The integrative sensitivities are:
1. Stereognosia: ability to recognize the object by touching. Disorders is called Asterognosia.
2. Dermolexia: ability to recognize the number or letters written on the skin with eyes closed.
Disorders- adermolexia.
3. Topognosia: ability to recognize top of the place of touch.
4. Somatognosia: ability to recognize different parts of the body. Disorders- asomatognosia.
5. Nosognozia: ability to recognize the motor deficit. Disorders- anosognozia.
6. Nosodiaphoria: ability to recognize the disease. Disorders- anosodiaphoria.
17 Sensibility(sensivity) dissociation: syringomielic dissociation, tabetic dissociation .

The senditive peripheral nerve syndrome. The sensitive nervous plexus syndrome:
semiology ?
SYMPTOMS OF SYRINGOMYIELIA:
1.
syringomelic dissociation,
2.
symmetrical disorders of sensitivity in the hands, arms, fingers,
3.
subjective symptoms: burning pain in both arms,
4.
deep sensitivity is preserved,
5.
atrophy of the muscles,
6.
fasciculations,
7.
deep reflexes disappears,
8.
sometimes these cavities compress the pyramidal tract and lead to paraparesis with
Babinskis sign positive bilaterally.
Muscle weakness and wasting (atrophy)
Loss of reflexes
Loss of sensitivity to pain and temperature
Other signs and symptoms of syringomyelia may include:
Stiffness in your back, shoulders, arms and legs
Pain in your neck, arms and back
Bowel and bladder function problems
Muscle weakness and spasms in your legs
Facial pain or numbness
Spinal curvature (scoliosis)
Symptoms: TABES DORSALIS
1.
deep reflexes disappear,
2.
tabetic ataxia appears, accompanied by hypotony,
3.
Romberg test is positive,
4.
loss of vibratory and position sense in lumbosacral territory,
5.
disorders of control of sphincters may appear neurogenic bladder and impotence,
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6.
7.
8.
optic acuity is diminished, the visual field is limited,

anisocoria (irregularity of the pupils) can appear,
Argyll Robertson Pupil reflex appears- loss of light reflex with preservation of
convergence reflex,
9.
dysphoria and dyspnea may appear (CN X is affected),
10.
there may appear trophic disorders in the bones and joints. The patient may have
spontaneous fracture and arthropathy.
SENSITIVE PERIPHERAL NERVE SYNDROME-semiology
Comprises: subjective and objective symptoms.
Subjective: pain and paraesthesias (pins, needles, tickling).
Objective: anesthesia, hypoesthesia, hyperesthesia.
Mononeuropathy/ mononeuritis- if disorders of sensitivity in a single nerve.
Multineuropathy/ multineuritis- if disorders of sensitivity in many nerves.
Polyneuropathy/ polyneuritis- if disorders of sensitivity in all the nerves
SENSITIVE NERVOUS PLEXUS SYNDROME:- semiology
Pain
Loss of sensation
Muscle weakness
Paralysis of some or all of the muscles of the shoulder and upper limb
Some patients may experience avulsion pain (a burning, crushing type of pain) in the
distribution of the injured nerves.
18 The radicular sensitive syndrome, the brown seguard syndrome, the total spinal cord
sensitive syndrome, the sensitive syndrome of the anterior and lateral cordons of the spinal
cord(anterior & lateral spinothalamic tracts), and the sensitive syndrome of the posterior
cordon of spinal cord?
Sensitive Radicular Syndrome:
Appears when sensitive roots are affected. Typical distribution: in limbs- longitudinal and in
trunk- horizontal distribution.
Etiology:
1.
discopathy (disease of intra-vertibral disc)
2.
T.B
3.
cervical rib.
In the SRS, the pain is by activities (that intraspinal pressure as in coughing, sneezing) and
also by elongation maneuvers like in Laessec and Bonne (pain on external rotation means disease
of joint and pain on internal rotation mean nerve involvement). Another maneuver is Neriinability to pick up an object from ground without moving the legs.
Sensitive Spinal Syndrome:
Sensitivity disorders in contralateral side of the lesion because the sensitive tracts cross in the
spinal cord (SC).
In the posterior cordon disease of the SC, tabetic dissociation appears with loss of deep and
tactile sensitivity and preservation of the thermal and pain sensitivity.
When one half of the SC is affected we have Brown-Sequard Syndrome with the following
SYMPTOMS:
1.
disorders of pain and thermal sensitivity in contralateral side of the lesion.
2.
disorders of deep and tactile sensitivity in the same side of the lesion.
3.
pyramidal syndrome in the same side of lesion.
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a band of anesthesia for all sensitivity on the same side of the lesion.
When we have a complet/ complex SC transection we have following SYMPTOMS:

1.
anesthesia for all sensitivities under the transection.
2.
pyramidal syndrome must be tetraplegic or paraplegic.
3.
disorders of control of sphincters.
4.
trophic disorders.
5.
vegetative disorders.
Etiology of SSS:
1.Trauma of SC.
2.Myelitis of SC.
3.Abscess of SC.
4.T.B of SC.
5.Multiple Sclerosis.
6.Hematomyelia (after rupture of a vessel of SC).
Sensitive thalamic syndrome:
A lesion in the thalamus has the following SYMPTOMS:
1. disorders sensitivity in contralateral side of the body, predominant for deep sensitivity because
thermal and pain sensitivity have representation in both the thalamus.
2. painful sensation- develops in the region of sensory impairment. This sensation has a burning
unpleasent quality. If we touch the arm, patient feels severe pain in the arm and so is with
emotions. Usually the thalamic pain in refractory to analgesic drugs but sometimes does so the
sedative.
3. pyramidal syndrome in contralateral side.
4. lateral homonymous hemianospsia.
5. involuntary movements (choreic, athetoid, tremors).
6. Cerebellar Syndrome with ataxia, disorders of muscular tonus and of equilibrium.
19 Medibrain sensitive syndrome, the cortical sensitive syndrome, the cortical sensitive
syndrome?
Sensitive Brainstem Syndrome:
It can be of 2 types: When lesion affects medulla and the lower part of pons:- loss of pain and
thermal sensitivity on the face in the same side of lesion due to the fibers which travel in the
trigemino-thalamic tract initially descend on the brainstem in the same side before synapse.
Under this lesion when we have disorders of sensitivity in the contralateral trunk and limbs and
ipsilateral on face, it is called Alternan Sensitive Syndrome. If the lesion is located above the
nucleus of the trigeminal nerve, we have disorders in contralateral face, trunk and limbs.
Cortical Sensitive Syndrome:
CSS appears in lesions of parietal lobe- 3, 2, 1, 5 and 7. It has following symptoms:
1.
disorders of thermal, pain and gross tactile sensitivity in the contralateral side of the
lesion.
2.
disorders of integrative sensitivity:
atopognosia,
adermolexia,
astereognosia,
tactile in-attention (cant recognize touch with closed eyes when touched
bilaterally),
asomatognosia,
anosognosia,
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anosodiaphoria.
20 Examination of sensibility(sensivity): superficial, deep & integrative sensibility?

Examination of sensibility:
Tactile Sensitivity: patient must be undressed and asked to close the eyes. We touch the body of
the patient with two cotton balls and ask him to count the number of times touched.
Thermal sensitivity: we take two test tubes, one with cold water and other with hot water. The
difference between both test tubes should be of 50 degrees C. Patient with closed eyes, we touch
with test tubes on different arms and note the patient reaction. If he doesnt feel the difference
between the two test tubes, then we consider it a pathological condition.
Pain sensitivity: patient with closed eyes, we produce painful stimuli and observe the reaction.
Deep sensitivity: vibration and position sense.
Vibration sense: we place tuning fork on surface of bones and note the patient reaction.
21 Frontal lobe :anatomy,semiology
Anatomy:
It extends from Frontal Pole to the Rolando Sulcus (Central Sulcus ). Before this Sulcus
is the precental Gyrus. In this place is the Motor Area 4. The Frontal Lobe comprises in the
external surface of 3 horizontal gyri: Superior , Middle and Inferior Frontal Gyrus. Under the
Frontal Lobe are present 2 Olfactory Bulbs, which are involved in smell. The Frontal Lobe has
many areas, the most important are: - 4, 6, 8, 9, 10, 11, 12, 44, 45, 46, 47, 25. Area 4 is the motor
area placed in the Precentral gyrus and her are located the Betz Cells. These cells are the motor
neurons that give the origin of Pyramidal and Geniculate Tract. In this area is the Motor
Homunculus of the with head down and leg upward. The different parts of the body have
different representation depending on their motor importance, the fingers, hand and lips occupy
the largest region and smallest by the Trunk. Each part of body has contralateral hemispherical
representation.
Area 6 and 8 are Extrapyramidal areas and are the end of Cerebellar System. If we
stimulate these areas we obtain conjugate deviation of the eye and head and patient has troubles
of co-ordination.
In the lower part of the area 4 is the area 44 or Broca`s Area. Lesion of this area gives
Broca`s Aphasia (Expressive Aphasia).
CONNECTIONS:
1. Sensitive Cortex (placed in PARIETAL Lobe)
2. Area 19.
3. Thalamus.
4. Striated Nuclei.
5. Black Substance.
6. Motor nuclei of Brain Stem.
7. Motor nuclei of Spinal Cord.
8. Cerebellum.
BLOOD SUPPLY:
Frontal Lobe is supplied by 2 arteries:
1. Anterior Cerebral Artery - Supplies to the Superior and Inter -hemispheric part of Frontal
Lobe.
2. Middle Cerebral Artery - Supplies to the Inferior part of Frontal Lobe.
SEMIOLOGY:
1. Hemiplegia - appears in the lesion of the Areas 4 and 6.
2. Akinesia - may appear difficulty in initiation of the movements.
3. Vestibular troubles.
4. Cerebellar troubles(Dysmetria , Adiadocokinesia, and Ataxia).
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5. Expressive Aphasia (Broca`s Aphasia ).

6. Epileptic Seizures may appear such as- Adversive seizures with deviation of the eyes and head in the opposite side of the lesion.
- Jacksonian Motor Seizures (Clonic movements in one half of body, patient is conscious)
- Grand Mal Seizures.
7. Grasp Syndrome may appear ( Patient grasps the reflex hammer when passed through the
palm , probably an expression of hypertony)
8. Vegetative troubles such as : hypertension , excessive sweating and increase of temperature
9. Appetite may increase.
10 Troubles of Sphincter control (Incontinence or gatism, impotence).
11. Constructive Apraxia, Walking Apraxia , bucal cavity`s Apraxia (Apraxia -ability to use an
object properly).
12. Psychic troubles (memory deficiency, indifference, of attention, change of behavior, mania,
stupid, jokes) occur due to lesion in Areas 9, 10, 11.
22 Parietal lobe: anatomy, semiology?
Anatomy:
The Parietal Lobe (P L) is delimited:
- Anteriorly -by Rrolando Sulcus,
- Posteriorly - by an imaginary Peroendicular Sulcus,
- Superiorly - by hemisphere border,
- Inferiorly -by Sylvius Sulcus.
Important Areas of PL are - 3, 2, 1, 5 , 7 , 39 , and 40.
Blood Supply - by Middle Cerebral Artery.
Connections:
1. Motor Cortex.
2. Area 44.
3. Thalamus ( Ventral posterior nucleus - center for all sensibilities )
4. Oculomotor Nuclei
Semilogy:
1. The Cortical Sensitive Syndrome is characterized by contralateral hypoesthesia for Superficial
and Deep Sensibilities, predominantly for Deep Sensibility because the Superficial Sensibility
has a double representation Troubles of Integrative Sensibility ( Atopognosia ,Adermolexia ,
Tactile in- attention, Asomatognosia, Anosognosia and Anosodiaphoria ). The troubles of
sensibility have a radicular distribution or can be -Cheiol oral.
2 Constructive Apraxia and Apraxia for dressing and undressing.
3. Troubles of vision:
- Lateral Homonymous Hemianopsia.
- Quadrant anopsia
- Loss of Optokinetic Nystagmus (appears when in a moving vehicle )
4. Troubles of reading (Alexia), troubles of writing (Agraphia), troubles of calculation
(Acalculia).
5. Trophicity troubles with contralateral muscular atrophy appear in the distal part of the limb.
6. Jacksonian Sensitive Epilepsy - patient feels paresthesia in face , arm and legs.
7. Troubles of taste when the lover part of the Postcentral Gyrus is affected.
8. Psychic troubles
When the non-dominant hemisphere is affected, the patient has some typical symptoms
such as Anosognosia ,Asomatognosia ,Constructive Apraxia , and Dressing Apraxia more
frequent. When the dominant hemisphere is affected ,then appears: Finger agnosia , Acalculia ,
Right-Left disorientation, Ataxia , Agraphia.
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23A Temporal lobe: anatomy, semiology?

Anatomy: The temporal lobe is delimited by the anterior pole in the anterior, by sylvius sulcus in the
superior partand by conventional line in the posterior part.
On the external part ,this lobe has 2 vertical sulci with 2 vertical temporal gyri ( HESHL gyri ) and
2 temporal horizontal sulci , superior and inferior which divides into 3 gyri ;
- Superior temporal gyrus.
- Middle temporal gyrus.
- Inferior temporal gyrus.
On the medial side on temporal lobe are 2 gyri:
- Uncus of hypocampus.
- Parahypocampus gyrus.
The inferior side of this lobe has 2 sulci ( hypocampus sulcus and collateral sulcus ) and 3 gyri;
-Parahypocampus gyrus.
- Middle occipito-temporal gyrus.
- Lateral occipito-temporel gyrus.
The important areas of temporal lobe are: 41, 42, 21, 22, 20, 43, 37, 38, 52.
The temporal lobe is supplied by middle cerebral artery and posterior cerebral artery.
SEMIOLOGY:
Damage to temporal lobe produces following troubles;
1.Auditive troubles;
-Hypoacusia appear in unilateral destructive lesion.
- Deafness appears in bilateral lesion.
- Tinnitus appears in irritative lesion of Heschl gyri.
- In the lesion of left temporal lobe , auditive agnosia may appear.
2. Equilibrium troubles s.a vertigo accompanied by nausea and vomiting occurs.Nystagmus may
be absent.
3. Receptive aphasia or WERNIKE aphasia occurs.
4. Troubles of smell; appear in the lesion of hypocampus uncus s.a.
Anosmia
Hypoosmia
Olfactive hallucinations
5. Troubles of taste appear in lesion of 43 area.
6. Lateral homonimous hemianopsia.
7. Temporal epilepsy has following symptoms:
a.
Motor disturbances s.a elementary movements like masticatory movements, swallowing
movements
and complex movements like unexpected travel of patient.
b.
psycho-sensorial hallucinations:
-auditive hallucinations (sounds, voices)
-vestibular hallucinations (vertigo)
-visual hallucinations (lights, images, faces)
-taste hallucinations.
c.
troubles of conscience:
-dream state
-Sensation of familiarity ( dj vu, dj conue)
-Sensation of alienation ( jamais vu, jamais conue)
d.
vegetative troubles:
-troubles of breathing
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-Heart pain
-Abdominal pain
-Hypertension
23B Occipital lobe, anatomy,semiology?
Anatomy: The O.L. is delimited to anterior part by posterior conventional sulcus and in
posterior part by O.pole.
The O.L. is crossed horizontally by the calcarine scisure (fissure) in 3 areas: 17, 18 and 19.
Area 17 is the end of visual pathway.
Area 18 and 19 surround area 17 and their importance lie in recognizing the shape and figures.
Damage of these areas give metamorphoses (change of size, shape and colour of object).
O.L. is supplied by posterior cerebral artery.
SEMIOLOGY:
1.
Troubles of visual field:
-Lateral homonymous hemianopsia
-Quadrantanopsia.
-Double homonymous hemianopsia with preservation of central vision
2.
Cortical cecity the exam of eye fundus is normal.
3.
Visual hallucinations may be simple (light) or complex (objects, faces, animals).
4.
Metamorphosis changes of shape and colour of objects.
5.
Visual agnosia the patient recognize the objects, images or faces and cannot localize
object in space.
Sometimes agnosia for written letters appear.
6.
BALINT syndrome incapacity to change the position of vision direction from an object to
another
object.
7.
Psychic troubles:
-memory deficits
-Amnesia
-Loss of topographic memory.
24 Aphasia, receptor or wernike aphasia, motor or broca aphasia: semiology, etiology?
Receptive aphasia (fluent): With receptive aphasia, the person can hear a voice or read the
print, but may not understand the meaning of the message. Oftentimes, someone with receptive
aphasia takes language literally. Their own speech may be disturbed because they do not
understand their own language.
Causes Aphasia
Aphasia is usually caused by a stroke or brain injury with damage to one or more parts of the
brain that deal with language. (According to the National Aphasia Association, about 25% to
40% of people who survive a stroke get aphasia.)
Aphasia may also be caused by a brain tumor, brain infection, or dementia such
as Alzheimer's disease. In some cases, aphasia is a symptom of epilepsy or other neurological
disorder.
Expressive aphasia (non-fluent ) broca:
With expressive aphasia, the person knows what he or she wants to say yet has difficulty
communicating it to others. It doesn't matter whether the person is trying to say or write what he
or she is trying to communicate.
Etiology: trauma to the brain, tumor, cerebral hemorrhage by extradural hematoma,
stroke.
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25 Glossopharyngeal nerve IX-N: anatomy, semiology?

This nerve arises from the lateral surface of the medulla by a series of smal roots which lie just
rostral to those of the vagus nerve. IX, X, XI nerves leave the skull together through the jugular
foramen and are then distributed peripherally. The ninth nerve has a sensory component with cell
bodies in the inferior (petrosal) ganglion (the central processes of which end in the nucleus
solitarius) and the smal superior ganglion (the central processes of which enter the spinal
trigeminal tract and nucleus). It also receives the nerve of Hering from the carotid body. The
somatic efferent fibers of the ninth nerve are derived from the nucleus ambiguous and the
visceral efferent (secretor) fibers, from the inferior salivary nucleus. These fibers contribute to
the motor innervation of the striated musculature of the pharynx and the glands in the pharyngeal
mucosa.
The sensory function: this nerve mediates sensory impulses from the facial tonsils, the posterior
wall of the pharynx, and part of the soft palate, and taste sensation from the posterior third of the
tongue.
The isolated lesion of IX is a rarity is affected due to tumors in the posterior fossa or an
aneurysm of the vertebral artery. The nerves are compressed as they pass through the jugular
foramen.
Clinical aspects in this situation:
Hoarseness
Some difficulty in swallowing
Deviation of the soft palate to the sound side
Anesthesia of the posterior wall of the pharynx
Weakness of the upper trapezius and sternocleidomastoid muscle
26 vagus X-N: anatomy, semiology?
This nerve has an extensive sensory and motor distribution. It has two ganglia: the jugular, which
contains the cell bodies of the somatic sensory nerves (which innervate the skin in the conch of
the ear); and the nodose, which contain cell bodies of the afferent fibers from the pharynx,
larynx, trachea, esophagus, and the thoracic and the abdominal viscera. The central processes of
these ganglia terminate in relation to the nucleus of the spinal trigeminal tract and the tractus
soliatrius, respectively. The motor fibers of the vagus are derived from two nuclei in the medulla,
the nucleus ambiguous and the dorsal motor nucleus. The former supplies somatic motor fibers
to the striated muscles of the larynx, pharynx, and palate; the latter supplies visceral motor fibers
to the heart and other thoracic and abdominal organs.
Complete interruption of the intracranial portion of one vagus nerve results in a characteristic
paralysis:
The soft palate droops on the ipsilateral side and does not rise in phonation
Deviation of the uvula to the normal side on phonation is an inconstant sign
Loss of gag reflex on the affected side
The voice is hoarse, often nasal
Loss of sensation at the auditory meatus and beak of the pinna
Complete bilateral paralysis is incompatible with life.
27 spinal accessory XI nerve :- anatomy, semiology :The spinal nerve originates in the lower aspect of the medulla and also in the first five or six
cervical segments of the spinal cord. It is a motor nerve innervating the sternocleido and
trapezius muscles.
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Cerebrovascular accidents and neck and head trauma are very common causes of spinal
accessory nerve malfunction. The muscles innervated may be weak unilaterally or bilaterally or
they may be atrophied or paralyzed.
28 Hypoglossal XII nerve: anatomy,semiology
It is a purely motor nerve, which supplies the somatic musculature of the tongue. It arises as a
series of rootlets which issue from the medulla between the pyramid and inferior olivary
complex. The nerve leaves the skull through the hypoglossal foramen and innervates the
genioglossus muscle, the styloglossus and hypoglossus.
Complete interruption of the nerve results in paralysis of one side of the tongue
The tongue curves slightly to the healthy side as it lies in the mouth, but on protrusion it
deviates to the affected side owing to the unopposed push of the healthy genioglossus muscle.
The denervated side becomes wrinkled and atrophied
Fasciculations and fibrillation can be seen.
29. Neuralgia the syndrome of the sensitive irritation, cervicobrachial neuralgia: symptoms
after the affected roots: C6, C7, C8.
One of the most common causes of neck, shoulder and arm pain is disc herniation in the lower
cervical region. The roots most commonly involved in cervical disc protrusion are the seventh
and the sixth. When the sixth cervical root is involved, the full syndrome is characterized by:
Pain at the trapezius ridge and tip of the shoulder, with radiation into the anterior upper part
of the arm, radial forearm, and often into the thumb; paresthesias and sensory impairment in the
same regions; tenderness in the area above the spine of the scapula and in the supraclavicular and
biceps region; weakness in flexion of the forearm; diminished to absent biceps and supinator
reflexes.
When the seventh cervical root is involved, the full syndrome is characterized by:
Pain is in the region of the shoulder blade, pectoral region and medial axilla, posterolateral
upper arm, dorsal forearm and elbow, index and middle fingers, or all the fingers; tenderness is
most pronounced in the medial aspect of the shoulder blade opposite the third to fourth thoracic
spinous processes, in the supraclavicular area and triceps region; paresthesias and sensory loss
are more evident in second and third digit or tips of all digit; weakness is found in extension of
the forearm and in the hand grip; the triceps reflex is diminished to absent, and the biceps and
supinator reflexes are preserved.
Compression of the eighth cervical root at C7-T1 may mimic an ulnar palsy. The pain is along
the medial side of the forearm and the sensory loss is in the distribution of the medial cutaneous
nerve of the forearm and ulnar nerve of the hand. The weakness involves the muscles supplied by
the ulnar nerve.
30. Sciatic neuralgia: etiology, symptoms.
Spondylosis
Spondylolisthesis
Vertebral fractures
Protusion of the lumbar intervertebral disc
The fully developed syndrome of prolapsed intervertebral lumbar disc consists of:
stiff, deformed spine
pain radiating into the thigh, calf and foot
some combination of paresthesia, weakness and reflex impairment.
Pain may be characteristically provoked by pressure over the L5 and S1 vertebral spines and
along the course of the sciatic nerve at the classic points of the Valleix (sciatic notch,
retrotrochanteric gutter, posterior surface of the thigh, head of the fibula).
Elongation of the nerve by straight-leg raising or flexing the leg at the hip and extending it at
the knee (Lasegue maneuver)
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With the patient standing, forward bending of the trunk will cause flexion of the knee on the
affected side (Neri sign).
31. Brachial plexus paresis: etiology, symptoms.
Brachial plexus is formed from the anterior and posterior divisions of cervical roots, 5, 6, 7, and
8, and the first thoracic nerve roots. The fifth and sixth cervical roots merge into the upper trunk,
the seventh root form the middle trunk and the eight cervical and first thoracic roots form the
lower trunk. Each trunk divides into an anterior and posterior division. The posterior divisions of
each trunk unite to form posterior cord of the plexus. The anterior divisions of lower trunk form
the medial cord.
Lesion of the whole plexus. The entire arm is paralyzed and hangs uselessly at the side; the
sensory loss is complete below a line extending from the shoulder downward and medially to the
middle third of the upper arm. Biceps, triceps, radial periostal, and finger reflexes are abolished.
The usual cause is vehicular trauma.
32. Radial nerve paresis: etiology, symptoms

The nerve may be compressed in the axilla, for example in crutch syndrome palsy, but
more frequently at a lower point, where the nerve winds around the humerus. Common types of
injury at this latter site are pressure palsies incurred during sleep and fractures.
It is susceptible to lead intoxication and is frequently involved as a part of a neuroalgic
amyotrophy.
A complete radial nerve lesion results in paralysis of the extension of the elbow, supination of the
forearm, extension of the wrist and fingers, and extension and abduction of the thumb. Sensation
is impaired over the posterior aspects of forearm and a smal area over the radial aspect of the
dorsum of the hand.
33. Median nerve paresis: etiology, symptoms.

The nerve may be injured in the axilla by dislocation of the shoulder and in any part of its
course by stab, gunshot, or other types of wounds. The wrist is the common site of external
injury. Compression of the nerve at the wrist (carpal tunnel syndrome) may be result of
occupational exposure to repeated trauma; infiltration of the transverse carpal ligament with
amyloid (in multiple myeloma); or thickening of connective tissue in rheumatoid arthritis,
acromegalyand hypothyroidism.
Incomplete lesions of the median nerve between the axilla and wrist may result in causalgia.
Complete interruption of the median nerve results an inability to pronate the forearm or flex
the hand in a radial direction, paralysis of flexion of the index finger and terminal phalanx of
the thumb, weakness of flexion of the remaining fingers, weakness of abduction and
opposition of the thumb and sensory impairment over the radial two-thirds of the palmary
aspect of the hand and the dorsum of the distal phalanges of the index and third fingers.
34. Ulnar nerve paresis: etiology, symptoms.

The common injury is at the elbow, by fracture or dislocation of the joint. Another site of
compression is just distal to the medial epicondyle.
Complete ulnar paralysis is manifested by a characteristic claw- hand deformity; this is the
result of wasting of the smal hand muscles, permitting hyperextension of the fingers at the
metacapophalangeal joints and flexion at the interphalangeal joints. The flexion deformity is
most pronounced in the fourth and fifth fingers, since the lumbrical muscles of the second and
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third fingers, supplied by the median nerve, counteract the deformity. Sensory loss occurs over
the fifth finger, the ulnar aspect of the fourth finger, and the ulnar border of the palm.
35. The external popliteal nerve paresis: etiology, symptoms.

Pressure or sleep palsy
Obstetrical stirrups
Habitual and prolonged crossing of legs wile seated
Tight knee boots
Compression being to that part of the nerve which pass over the head of the fibula.
It may be affected in diabetic neuropathy
Injured by fractures of the upper end of the fibula.
Affected: the dorsiflexion of the foot and toes
Sensory trouble from dorsum of the foot and lateral aspect of the lower half of the leg.
36. Polineuritis: etiology, symptoms.
ETIOLOGY:
Toxin exposure to arsenic, thallium, lead, copper, zinc, mercury
Drugs: nitrofurantoin, isoniazid, vincristine
Systemic illness: hypothyroidism, syphilis, amyloid, myeloma, leprosy, lupus. Sarcoid,
polyarteritis, pernicious anemia, porphyry
Idiopathic type
Diabetes
Alcoholism
SYMPTOMS:
Impairment of motor function
most often the muscles of the feet and legs are affected at first
atrophy of affected muscles proceeds slowly over several months
diminution or loss of tendon reflexes
fasciculation and cramps are not important findings
sensory loss is affected in the distal segments of the limbs, and more in the legs than the arms
all sensory modalities are impaired or lost
paresthesias and dyesthesias,
autonomic disorders: sexual impotence, weak bladder and bowel sphincters and overflow
incontinence, etc
37. Poliradiculoneuritis: etiology, symptoms.
Etiology:
Most of the evidence suggests that the clinical manifestations of this disorder are the result of
all cell-mediated immunologic reaction directed at peripheral nerve.
Symptoms:
Weakness, which evolves more or less symmetrically, over a period of several days or a week
or two.
Proximal as well as distal muscles of the limbs are involved, usually the lower extremity
before the upper
The weakness can progress to total motor paralysis with death from respiratory failure within
a few days.
Pain occur in about 1/3 of the cases
Paresthesias are frequent
Objective sensory loss occurs to a variable degree and in a few is barely detectable; when
present, deep sensibility tends to be more affected than superficial.
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Muscle atrophy does not occur

Hypotonia and reduced and then absent reflexes are consistent findings.
Facial diplegia occurring in about cases and other cranial palsies usually comes latter, after
arms are affected
Disturbance of autonomic function are common
CBF- several days form onset protein level begins to rise
38. Anatomy of the cerebral vascular system; the most important arteries and anastomoses.
The brain is supplied by 2 main large arteries;
- 2 internal carotids.
- 2 external carotids.
Both internal carotids belong to carotid arterial system and supply the 2/3 rd of cerebral
hemisphere 7 1/3 rd by cerebro-basilar system.
At level of C4 the camuri carotid divides into 2 arteries ;
-External carotid.
- internal carotid.
The internal carotid gives 4 terminal branches ;
- Anterior cerebral artery.
- Middle cerebral artery.
- Anterior choroidal artery.
- Posterior communicating artery.
Both vertebral arteries belong to vertebro-basilar system. The vertebral arteries arise from the
subclavian arteries and then enter the cranial cavity via foramen magnum and join at the upper
margin of medulla oblongata into basilar artery. This artery ascends on the ventral surface of pons
and mesencephalon and divides into terminal branches , the posterior cerebral arteries.
The vertebro-basilar system supplies;
- Upper part of spinalcord.
- Brainstem.
- O. Lobe.
- Cerebellum.
B /w the carotid system and vertebro-basilar system are many anastomosis. One of these is the
CIRCLE OF WILLIS placed at base of brain and is formed by :
- 2 anterior cerebral arteries joined by ant.communicating artery.
- Both internal carotids.
- Posterior communicating arteries.
- Posterior cerebral arteries.
The anterior , middle and posterior arteries communicate on external surface of brain via the
meningial arteries.
The internal carotid artery is in the communication with external carotid via ophthalmic artery.
39. Cerebral circulatory debit; physiology and pathophysiology.
It is the blood quantity which passes the brain every minute.It is 750 ml / min. The cerebral blood
circulatory speed is 8 sec.In every minute the blood crosses the brain in 7 times. The total cerebral
blood is 130-150 ml.
The cerebral deficit depends on:
- Arterial pressure.
- Vascular resistance.
The cerebral circulatory debit is normal when the arterial pressure varies b/w 70-170 mm
Hg.Under 70 mm Hg cerebral hypoxia appears.
The vascular resistance depends on:
- Heart debit output.
- Blood viscosity.
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- State of cerebral vessels.

When the vascular resistance increases, the cerebral debit decreases.
The cerebral debit is regulated by:
- Neurogen mechanism.
- Metabolic mechanism
- Miogen mechanism.
Neurogen Mechanism:
The cerebral vessels upto 20 microns have innervation with is capable of hemodynamic effects.
The internal carotid and vertebro-basilar artery have sympathetic innervation. Stimulation of
sympathetic cervical nerves produces vasoconstriction effects with decrease of cerebral debit in the
ipsilateral hemisphere.
Metabolic Mechanism:
The cerebral vessels are sensible to chemical blood composition especially to O2 and CO2
concentrations. When CO2 increases vasodilatation of vessels appears and cerebral debit
increases.
If the O2 concentration increases vasoconstriction of vessels and cerebral debit decreases.
Miogen Mechanism:
The walls of vessels have smooth muscles which contribute to regulation of cerebral debit----walls
have to be normal.
40. Cerebral ischemia: Etiology, physiology, anatomopathogy (morphopatholgy), clinical
features.
Brain ischemia, also known as cerebral ischemia, is a condition in which there is insufficient
blood flow to the brain to meet metabolic demand This leads to poor oxygen supply or cerebral
hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke.[2] It is a subtype of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.
Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis.
There are two types of ischemia: focal ischemia, which is confined to a specific region of the
brain; and global ischemia, which encompasses wide areas of brain tissue.
The main symptoms involve impairments in vision, body movement, and speaking. The causes
of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain
ischemia can include unconsciousness, blindness, problems with coordination, and weakness in
the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest,
and irreversible brain damage.
Causes:
Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle
cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries,
blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects
have a higher predisposition to brain ischemia in comparison their healthy counterparts.
Sickle cell anemia may cause brain ischemia associated with the irregularly shaped blood cells.
Sickle shaped blood cells clot more easily than normal blood cells, impeding blood flow to the
brain.
Compression of blood vessels may also lead to brain ischemia, by blocking the arteries that carry
oxygen to the brain. Tumors are one cause of blood vessel compression.
Ventricular tachycardia represents a series of irregular heartbeats that may cause the heart to
completely shut down resulting in cessation of oxygen flow. Further, irregular heartbeats may
result in formation of blood clots, thus leading to oxygen deprivation to all organs.
Blockage of arteries due to plaque buildup may also result in ischemia. Even a small amount of
plaque build up can result in the narrowing of passageways, causing that area to become more
prone to blood clots.[citation needed] Large blood clots can also cause ischemia by blocking blood flow.
A heart attack can also cause brain ischemia due to the correlation that exists between heart
attack and low blood pressure. Extremely low blood pressure usually represents the inadequate
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oxygenation of tissues. Untreated heart attacks may slow blood flow enough that blood may start
to clot and prevent the flow of blood to the brain or other major organs. Extremely low blood
pressure can also result from drug overdose and reactions to drugs. Therefore, brain ischemia can
result from events other than heart attacks.
Congenital heart defects may also cause brain ischemia due to the lack of appropriate artery
formation and connection. People with congenital heart defects may also be prone to blood clots.
Other pathological events that may result in brain ischemia include cardiorespiratory arrest,
stroke, and severe irreversible brain damage.
Recently, Moyamoya disease has also been identified as a potential cause for brain ischemia.
Moyamoya disease is an extremely rare cerebrovascular condition that limits blood circulation to
the brain, consequently leading to oxygen deprivation.
Pathophysiology
During brain ischemia, the brain cannot perform aerobic metabolism due to the loss of oxygen
and substrate. The brain is not able to switch to anaerobic metabolism and because it does not
have any long term energy stored the levels of adenosine triphosphate (ATP) drop rapidly and
approach zero within 4 minutes. In the absence of biochemical energy, cells begin to lose the
ability to maintain electrochemical gradients. Consequently, there is a massive influx of calcium
into the cytosol, a massive release of glutamate from synaptic vesicles, lipolysis, calpain
activation, and the arrest of protein synthesis.[14] Additionally, removal of metabolic wastes is
slowed. The interruption of blood flow to the brain for ten seconds results in the immediate loss
of consciousness. The interruption of blood flow for twenty seconds results in the stopping of
electrical activity. An area called a penumbra, may result, wherein neurons do not receive enough
blood to communicate, however do receive sufficient oxygenation to avoid cell death for a short
period of time.
Symptoms
The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen
deprivation. Ischemia within the arteries branching from the internal carotid artery may result in
symptoms such as blindness in one eye, weakness in one arm or leg, or weakness in one entire
side of the body. Ischemia within the arteries branching from the vertebral arteries in the back of
the brain may result in symptoms such as dizziness, vertigo, double vision, or weakness on both
sides of the body[citation needed]. Other symptoms include difficulty speaking, slurred speech, and the
loss of coordination.[9] The symptoms of brain ischemia range from mild to severe. Further,
symptoms can last from a few seconds to a few minutes or extended periods of time. If the brain
becomes damaged irreversibly and infarction occurs, the symptoms may be permanent.
Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness,
brain damage or death, mediated by the ischemic cascade.
Multiple cerebral ischemic events may lead to subcortical ischemic depression, also known as
vascular depression. This condition is most commonly seen in elderly depressed patients. [citation
needed]
Late onset depression is increasingly seen as a distinct sub-type of depression, and can be
detected with an MR
41. The transient ischemic attack in carotidian system and vertebrobasilar system:
semiology, differential diagnosis.
Symptoms of transient ischemic attacks in the CAROTIDIAN system are:
a. Hemiparesis.
b. Transient cecity in one eye.
c. Lateral homonymous hemianopsia.
d. Aphasia.
e. Headache.
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f. Confusion.
Symptoms of transient ischemic attacks in the VERTEBRO-BASILAR system are:
a. Vertigo accompanied by:
Dyplopia.
Facial paresis.
Disarthria (trouble of speech).
Lateral homonymous hemianopsia.
Deafness.
Tinnitus.
Troubles of swallowing.
Hiccup.
Ataxia (troubles of coordination).

b. Alternate hemiparesis ( in right and then on left )
DIFERENTIAL DIAGNOSIS OF TRANSIENT ISCHEMIC ATTACKS:
1.
Jacksonian Epileptic Seizures; the evolution of epileptic seizures is performed step by
step. In the transient ischemic attack , one half of body is suddenly affected.
2.
Hypoglycemia; agitation and excessive sweating appear and laboratory tests are
positive. Administer 30% glucose solution, in 5 minutes the crisis disappears.
3.
Peripheral Vertigo; appears in ear diseases (labryntitis, otitis) and is associated with
hypoacusia and pain in ear.
Tumors; evaluation is progressive and worse. CT and EEG can be to used to differentiate them. In
tumor, the tomography reveals the tumoral process. On EEG, disturbances appear.
42. Internal carotid artery: anatomy, clinical, aspects.
Move the cursor along the course of the internal carotid artery and its branches to identify individual segments.
Begins at the bifurcation of the Common Carotid Artery (level of C4).

Terminal branches: Anterior Cerebral and Middle Cerebral Arteries.
Four segments: cervical, petrous, cavernous, and supraclinoid
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Move the cursor along the course of the internal carotid artery to identify individual segments.
The internal carotid artery is major paired artery, one on each side of the head and neck, in
human anatomy. They arise from the common carotid arteries where these bifurcate into the
internal and external carotid artery; the internal carotid artery supplies the brain, while the
external carotid nourishes other portions of the head, such as face, scalp, skull, and meninges.
The segments of the internal carotid artery are as follows:
Cervical segment, or C1, identical to the commonly used Cervical portion
Petrous segment, or C2
Lacerum segment, or C3
o C2 and C3 compose the commonly termed Petrous portion
Cavernous segment, or C4, almost identical to the commonly used Cavernous portion
Clinoid segment, or C5. This segment is not identified in some earlier classifications,
and lies between the commonly used Cavernous portion and Cerebral or Supraclinoid
portion
Ophthalmic, or supraclinoid segment, or C6
Communicating, or terminal segment, or C7
C6 and C7 together constitute the commonly used Cerebral or Supraclinoid portion
Mnemonic for Branches in Skull: Please Let Children Consume Our Candy
first letter for each branch in order.
1.
2.
3.
4.
5.
6.
7.
1.
2.
3.
4.
5.
6.
43. Anterior cerebral artery; anatomy, clinical aspects.

The ACA is one of the terminal branches of ICA. This artery has an interhemispheric tract. It
joins the opposite ACA via the anterior communicating artery. Then this artery goes around the
corpus calosum and deep and superficial branches.
The deep branches go to ;
Head of caudate nucleus.
Anterior part (pyramidal tract) and the knee of internal capsule (geniculate tract).
The superficial branches give the following arteries;
Orbital artery for orbital cavity and anterior face of frontal lobe.
The internal frontal artery for the 1st frontal gyrus and for the ascendant gyrus.
The internal PARIETAL artery for the paracentral and quadrangle gyrus
The terminal branches (pericalosum) for the corpus calosum.
Clinical Symptoms Of Total Anterior Cerebral Syndrome:
Contralateral crural hemiplegia.
Hemianesthesia.
Grasp syndrome.
Gatism (trouble of control of sphincter)
Akinesia.
Troubles of behaviour 9apathy, indifference).
Epilepsy (motor jacksonian, grand mal).
Clinical Symptoms Of Partial Anterior Cerebral Syndrome:
When the deep branches are affected, the symptoms are;
Contralateral hemiplegia.
Troubles of swallowing.
Troubles of phonation.
Paresis of tongue.
Dysarthria.
Vegetative troubles.
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When the bilateral anterior cerebral artery is affected, appear;

Paraplegia.
Troubles of sphincters.
Troubles of sensibility.
Akinetic mutism (no limb movements but only eyes).
44. Middle cerebral artery: Anatomy, clinical aspects.
It is one of terminal branches of ICA. It follows the course of sylvius. It gives the deep and
superficial branches.
The deep branches go to:
Putamen nucleus.
Caudate nucleus
Internal capsule.
Thalamus.
The superficial branches are:
ROLANDO sulcus artery.
Inferior parietal artery.
Temporal arteries (middle 7 posterior 0.
Artery of rounded fold.
CLINICAL ASPECTS:
When deep branches are affected, aymptoms are:
1.
Contralateral equal motor deficit (cause of affectation of pyramidal tract).
2.
Troubles of sensibility.
3.
When the superficial branches are affected, the symptoms are:
1.
Contralateral motor deficit is bigger in face and arms (cause of map of body)
2.
Hemianesthesia.
3.
4.
Expressive aphasia (BROCA [area 44] aphasia).
5.
Apraxia for dressing.
6.
Agraphia.
7.
Alexia
8.
Acalculia.
9.
Hemidepersonalization.
10.
Trophic troubles ( of body trophicity).
1.
2.
3.
4.
45. Vertebral and basilar arteries: anatomy and clinical syndromes.

VERTEBRAL ARTERIES
These have origin in subclavian arteries. The VA enters the cranial cavity via foramen magnum
and combines at upper margin of medulla oblongata into basilar artery.
In the extracranial tract, it gives branches to:
Muscles of neck
Cervical vertebral bone
Meninges
Spinal cord
In the intracranial tract, it gives branches to:
Cerebellum as inferior cerebellum artery.
Spinal cord (ant. and post).
SYMPTOMS of VA Ischemia:
Thrombosis of one VA does not have clinical symptoms cause of opposite VA takes over the
control.
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Symptoms appear when both arteries are affected.

When the inferior cerebellum artery is affected, appear the lateral syndrome of medulla
oblongata-WALLEN BURG SYNDROME.
THE BASILAR ARTERY
Gives the following branches to:
Midbrain.
Cerebellum (middle and superior cerebellum artery).
Inferior part of temporal lobe and occipital lobe.
Thalamus.
Caudate nucleus.
Corpus calosum.
Ischemia of BA is rare but severe. The SYMPTOMS are:
1.
Tetraplegia.
2.
Alternate symptoms ( ipsilateral cranial neve paresis and contralateral motor
deficit WEBER syndrome ; paresis of 7th nerve and pyramidal region contralaterally
MILLARD GUBLER syndrome (in pons).
3.
Troubles of sensibility in face or in contralateral of body.
4.
Cerebellum troubles (ataxia, equilibrium troubles, dismetria).
5.
Drop attacks (transient loss of muscular tonus) due to reticulate substance
in pons.
6.
Involuntary movements.
7.
Paresis of cranial nerves.
8.
Akinetic mutism.
9.
Trouble of conscience (coma, somnolence).
10.
Cortical cecity.
11.
Visual hallucinations.
12.
Visual agnosia.
13.
Psychic troubles.
46. Cerebral hemorrhage: etiology, pathophysiology, anatomopathology, clinical aspects.

It is a blood collection due to rupture of blood vessels or due to erythrodiapedesis (frequent),
inside brain (cerebral hemorrhage) or inside the subarachnoid space (subarachnoid hemorrhage).
CH accounts for about 10-20% of all acute strokes. Male patients of 50 years are predominant.
By TOPOGRAPHY, 2/3 of cases of CH are situated in the striated nuclei.
CAUSES OF CH:
Arteriosclerosis.
HT.
Rupture of vascular malformation (aneurysms, angiomas).
Cranial traumas.
Blood dyscrasias (hemophilia, leukemia, thrombocytopenia, hepatic insufficiency,
treatment with anticoagulants)
Arteritis (collagen disease, syphilis, viral infections, TB.)
Cerbral hemorrhage inside the tumoral process in brain.
CH after the epileptical seizures.
CAUSES OF SAH:
Intoxication with alcohol.
Meningitis-encephalitis.
Collagenosis.
Rupture of vascular malformatios.
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PATHOPHYSIOLOGY:
The walls of BVs suffer a hyaline degeneration cause of HT. The elastic tissue is destroyedand
microscopic aneurysms appear, predominantly in the striated nuclei and in white matter of
brain.The rupture of microscopic aneurysm give the CH.
SYMPTOMS:
The onset of CH is abrupt, with severe headache and coma.
Hours or days before the CH, the patient may have:
Headache.
Vomiting.
Paresthesia.
Vertigo.
Usually the CH appears in the middle of days after muscular or sexual effort, after cough or
sneezing.
The examination of patient reveals:
Coma.
Troubles of breathing.
Reddish color of face.
Neck rigidity.
Deviation of eyes and head on the opposite side of motor deficit.
Anizocoria.
Bilateral babinski sign.
Vegetative troubles (increased temperature, increased pupil size, increased BP.)
Digestive hemorrhage may appear when hypothalamus is affected.
The eye fundus revels papilloedema and small hemorrhages in retina.
In lumbar puncture, in 80% case, the CSF is red.In 20% is clear. Sometimes the blood appears in
CSF only on mocroscopic examination.
47. Subarachnoid hemorrhage: etiology, clinical features.
(MOTOR DEFICIT IS ABSENT)
The frequency is 3-8 % of all acute strokes. The onset is brisk with severe headaches, vomiting ,
photophobia, troubles of conscience 7 increase of temperature > 38.
SYMPTOMS:
The examination of the patient with SAH reveals:
Neck rigidity.
Seizures of general hypertony.
KERNIG and BRUDZINSKY tests are + ve.
Focal neurological signs are absent.
Babinski sign.
The sp cord is red. The eye fundus in 30% of cases reveals papilloedema and small hemorrhage
of retina.
The immediate prognosis is good.
The distant prognosis is not good because the SAH can relapse.
48. Cerebral venous thrombosis; thrombosis of cavernous sinus, thrombosis of lateral sinus,
thrombosis of longitudinal superior sinus: semiology, treatment.
Thrombosis Of Cavernous Sinus:

Headache
Supraorbital pain
Exophthalmia
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Edema of eyelids
Fever
Neck rigidity
Paresis of following nerves 3,4,5,6
Epileptic seizures
Thrombosis Of Lateral Sinus

Pain in mastoid bone
Edema of mastoid
Contraction of sternocleidomastoid and trapezium muscles
Paresis of following nerves 9,10,11 (when the Thrombotic process affects the jugular
vein) and paresis of 5,6,7 (when affect the petrous sinus)
High intracranial pressure
Thrombosis Of Longitudinal Superior Sinus

Paraplegia
Troubles of control sphincters
Epileptic seizures
Psychic disturbances (confusion, agitation )
High intracranial pressure
49. Treatment of vascular ischemia; treatment of transient ischemic attacks, treatments of

constituted ischemic attacks.
Treatment of vascular Dementia: The aim of the management is the prevention of further
cerebrovascular lesions. This includes administering antiplatelet drugs and controlling major
vascular risk factors (hypertension, hypercholesterolemia, smoking and diabetes mellitus to
mention a few).
The general management of dementia includes referral to community services, judgment and
decision-making regarding legal and ethical issues (e.g., driving, capacity, advance directives),
and consideration of caregiver stress.
Cholinesterase inhibitors such as galantamine have shown to be helpful in various randomized
controlled trials. However their use is not licensed yet for this indication.
Behavioral and affective symptoms are particularly important in this patient group and deserve
special consideration. These problems, if they develop, tend to be resistant to conventional
psychopharmacological treatment and in many cases lead to hospital admission and placement in
permanent care.
Treatment of Transient ischemic attack
The mainstay of treatment following acute recovery from a TIA depends on the underlying
cause. It is not always immediately possible to tell the difference between a CVA (stroke) and a
TIA. Most patients who are diagnosed at a hospital's emergency department as having suffered
from a TIA will be discharged home and advised to contact their primary physician to organize
further investigations. A TIA can be considered as the last warning. The reason for the condition
should be immediately examined by imaging of the brain. Occasionally, none of these tests will
determine the cause, but the symptoms show that the stroke did occur. In 2012, Monmouth
Medical Center created a TIA Rapid Evaluation Center that provides timely, comprehensive
evaluations on an outpatient basis of stable patients who have experienced a recent ministroke.
To reduce risk of recurrence, it is strongly advised that patients undergo lifestyle changes
including quitting smoking, losing weight, eating more fruits and vegetables and exercising
regularly.
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Surgery
If the TIA affects an area supplied by the carotid arteries, an ultrasound (TCD) scan may
demonstrate carotid stenosis. For people with a greater than 70% stenosis within the carotid
artery, removal of atherosclerotic plaque by surgery, specifically a carotid endarterectomy, may
be recommended. The blood vessel is opened up and the plaque is removed. The carotid may be
replaced with a vessel retrieved from the lower leg or foot. The procedure is not technically
difficult but carries the potential complication of inducing a stroke. A stroke can occur during
surgery or after the procedure. The chance of a stroke ranges from 14 percent.
Some patients may also be given modified-release dipyridamole or clopidogrel.
Medication
The use of anti-coagulant medications, heparin and warfarin, or anti-platelet medications such as
aspirin may be warranted. Antiplatelet drugs prevent platelets from agglutinating or sticking to
each other, hence the term "blood thinner." The initial treatment is aspirin, second line is
clopidogrel (PLAVIX), third line is ticlopidine. If TIA is recurrent after aspirin treatment, the
combination of aspirin and dipyridamole is needed (Aggrenox).
Thinning the blood helps to ensure that small particles do not form and travel to the brain. These
drugs require frequent monitoring. These drugs also have side effects such as easy bruising and
bleeding from mild trauma.
An electrocardiogram (ECG) may show atrial fibrillation, a common cause of TIAs, or other
arrhythmias that may cause embolisation to the brain. An echocardiogram is useful in detecting
thrombus within the heart chambers. Such patients benefit from anticoagulation.
50. Treatment of cerebral hemorrhage.

Hemostatic drugs s.a.
Adrenostasin 3p/d i.m.
Venostat 2p/d i.m.
Etamsilat 3p/d i.m.
Antialgic drugs s.a.
Paracetamol
Algocalmin
Antiedematousdrugs s.a.
Glucose
Manitol
For nausea and vomiting:
Metclopramide 1-2p/d.
Cerucal 1-2 p/d.
Torecan 1-3 tb/d
Surgical treatment is indicated in rupture of vascular malformations. It is
contraindicated in coma and old persons.
51. Muscular dystrophies: clinical features, etiology.
Etiology:
Hereditary disease
The central issue is how an abnormal gene induces a degeneration of muscle fibers
Biochemical studies has revealed the following abnormalities: decreased glycolitic enzymes,
increase serum CK, aldolase, LDH, SGOT and SGPT
A number of biochemical and biophysical studies have implicated an abnormality of the
muscle surface membrane in the genesis of muscular dystrophy.
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CLINICAL FEATURES:
Duchenne
age of onset: infancy or early childhood
pattern of muscular involvement: pelvifemural
special features: hypertrophy-pdeudohypertrophy, cardiac involvement, mental
retardation
CK level: high
Inheritance: X-linked recessive
Becker
age of onset: childhood, adolescence or early adulthood
pattern of muscular involvement: pelvifemural
special features: cardiac involvement, mentation normal
CK level: moderate
Emery-Dreifuss
age of onset: childhood, adolescence
pattern of muscular involvement: humeroperoneal
special features: contractures posterior neck and biceps muscle
CK level: moderate
Landouzy-Dejerine
age of onset: late childhood, adolescence
pattern of muscular involvement: facioscapulohumeral
special features: cardiac normal, mentation normal
CK level: slight to moderate
Inheritance: dominant
Limb girdle
age of onset: childhood, adolescence, sometimes adulthood
pattern of muscular involvement: pectoral or pelvic both
special features: cardiac normal, mentation normal
Inheritance: variable recessive or dominant
Myotonic Steinert
age of onset: infancy, childhood, adulthood
pattern of muscular involvement: ocular, facial, sternomastoid, forearm, peroneal
special features: testicular atrophy
CK level: slight to normal
Congenital:
age of onset: birth, infancy
pattern of muscular involvement: pectoral and pelvic girdles, or diffuse
special features: mentation retardation, artrogryposis
Inheritance: dominant or recessive
52. Duchenne's hypertrophic form: positive diagnosis, differential diagnosis, treatment.
Positive diagnosis:
In young children appear an indisposition to walk or run, increasing dificulty in
walking, running and climbing stairs, became ever-more obvious as time passes
The iliopsoas, quadriceps and gluteal muscles are the first to be affected
Weakness of abdominal and paravertebral muscles accounts for the lordotic posture
and protuberant abdomen
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To rise from sitting position patients first flex their trunk at the hips, put their hands
on the knees, and push their trunk upward by working the hands up the thighs (Gowers sign)
the tendon reflexes are lost as muscle fibers disappear
ecg: prominent R waves in the right precordial leads
death is the usual results from respiratory weakness and pulmonary infections, and
sometimes cardiac decompensation
Differential diagnosis:
- acquired myopaties: polimiositis, thyroid, steroid associated, alcoholic
another types of muscle dystrophies ( limb girdle, myotonic dystrophies, etc)
myasthenia gravis
Treatment:
there is no specific treatment

vitamins, steroids, aminoacids, have all proved to be ineffective
they must avoid prolonged rest bed
obesity should be avoid
detection of carries, by measuring CK, and sex determination of the fetus, the
examination of amniotic fluid, are the basis for genetic counseling.
53. Myotonic Dystrophy: anatomopathology, clinical features.
age of onset: infancy, childhood, adulthood
pattern of muscular involvement: ocular, facial, sternomastoid, forearm, peroneal
special features: testicular atrophy
CK level: slight to normal
The phenomenon of myotonia expresses in prolonged contraction of certain muscles
following brief percussion or electrical stimulation, and in delay of relaxation after strong
voluntary contraction
Myotonia may precede weakness by several years.
Appear frontal alopecia
Testicular atrophy
Ginecomastia
54. Familial or hypokalemic period paralysis and hyperkalemic periodic paralysis: clinical
manifestation, laboratory findings, treatment.
Familial or Hypokaliemic periodic paralysis:
the onset is in late childhood or adolescence
usually the patient awakens to discover a mild or severe weakness of the limbs
diurnal attacks occur especially after a nap following a large meal
the distribution of the paralyses varies, limbs are affected earlier and often more
severely than trunk muscles and proximal muscles are possibly more susceptible than distal one.
Laboratory findings:
reduction in serum K level(< 1,8 meq/l)
Treatment:
daily administration of 5 to 10 g of KCL orally in aqueous solution prevents attacks

a low carbohydrate, low-salt, high-K diet
Hiperkaliemic periodic paralysis:
onset is usually in infancy and childhood
the attacks of weakness occur when the patient is resting in a chair, about 20 to 30
min after exercise
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the paresis begins in the legs, thighs, and lower back and spread to the forearms and
shoulders
an attack would actually be induced by administration of potassium salt.
55. Polymyositis: clinical features, EMG, treatment.

aralyses of widespread distribution and subacute evolution are attributable to a wider
spectrum of disease:
1.
infective (trichinosis, toxoplasmosis, viral infections, sarcoidosis)
2.
idiopathic polymyositis
-
1.
2.
3.
-
CLINICAL FEATURES:
a febrile illness or begin infection may precede the muscle weakness
patient becames aware of a painless weakness of the proximal limb muscles
the muscle are usually not tender, and atrophy and reduction in tendon reflexes are
not so pronounced
EMG: typical ,,myopathic pattern, many abnormaly brief action potentials of low
voltage and, in addition, numerous fibrillation potentials and salvos of pseudomyotonic activity
Treatment:
Prednisone, 60 mg per day
acetylsalicylic acid 0,6 every 4 h
physiotherapy
56. Myasthenia Gravis: Pathophysiology, anatomopathology, clinical aspects.
the autoimmune disturbance affecting the neuromuscular junction localized to the
skeletal muscle endplates
the changes in the postsynaptic membranes (endplates) are thought to result from the
presence of humoral antibodies that bind to the nicotinic acetylcholine receptors, thus reducing
the number of available receptor site for acetylcholine
there is no sign of central or peripheral nervous system involvement
the most frequently affected muscles are those that control eye movements, chewing,
swallowing, speech, breathing and head control
80% of mg patients have cellular changes in the thymus gland
thymectomy increases the rate of remission among the patient with MG
- onset: is usually insidious and progresses slowly
- weakness of muscles
- extraocular muscle involvement: diplopia
inability to chew or swallow
weakness of voice
breathing difficulties
difficulty in holding the head up
Objective assessment data:
ptosis
difficulty in smiling
nasal and dysarthric speech
57. Myasthenia Gravis: Positive diagnosis, differential diagnosis, treatment.
Diagnosis is determined by history, clinical manifestations and observing the individual-s
response to neostigmine or edrophonium. Each of these anticholinesterase drugs causes a
dramatic improvement in muscle strength in the MG patient.
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Differential diagnosis:
neurasthenic patients
other myopathies
oftalmoplegia of thyreoxicosis
Treatment:
anticholinesterase drugs: neostigmine (oral dose ranges from 7,5 to 45 mg every 2 to

6 h). the dose of pyridostigmine is twice that of neostigmine.
Thymectomy
Corticosteroids: dose of 40 to 45 mg/ day.
Plasmapheresis and immunosuppression
58. Median bulbar syndrome: etiology, clinical aspects.
(occlusion of vertebral artery or branch of vertebral or lower basilar artery)
on the side of the lesion:
Paralysis with atrophy of half the tongue
On the side opposite the lesion:
Paralysis of arm and leg sparing face
Impaired tactile and proprioceptive sense over half the body
59. Wallenberg syndrome: Etiology, Clinical aspects.
Site: Tegmentum of the medulla.
Cranial nerve involved: SPINAL V, IX, X, XI.
Tracts and nuclei involved: Lateral spinothalamic tract, descending pupilodilatator fibers,
spinocerebellar and olivocerebellar tracts.
Signs: Ipsilateral V,IX,X,XI palsy, Horner syndrome and cerebellar ataxia. Contralateral, loss of
pain and temperature sense.
Usual cause: Occlusion of vertebral or posterior-inferior cerebellar artery.
On the side of the lesion:
Pain, numbness, impaired sensation over half face
Ataxia of limbs
Vertigo, nausea, vomiting
Nystagmus, diplopia
Horner syndrome (miosis, ptosis, decrease sweating)
Dysfagia, hoarsness, paralysis of vocal cord, diminished gag reflex
Numbness of ipsilateral arm, trunk or leg
On side opposite lesion: Impaired pain and thermal sense over half the body, sometimes face
60. Median pontine syndrome: etiology, clinical aspects.

Medial inferior pontine syndrome (occlusion of paramedian branch of basilar artery)
On the side of the lesion
Paralysis of conjugate gaze to side of lesion
Nystagmus
Ataxia of limbs and gait
Diplopia on lateral gaze
On the side opposite the lesion
Paralysis of face, arm and leg
Impaired tactile and proprioceptive sense over half of the body
Medial midpontine syndrome (occlusion of paramedian branch of midbasilar artery)
On side opposite lesion
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Deviation of the eyes

Impaired tactile and proprioceptive sense over half of the body
Medial superior pontine syndrome (occlusion of paramedian branch of upper basilar artery)
Cerebellar ataxia
Internuclear ophtalmoplegia
Rythmic myoclonus of palate, pharynx,etc
Rarely impaired tactile and proprioceptive sense over half of the body.
61. Lateral pontine syndrome; etiology, clinical aspects.
Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery):
Horizontal and vertical nystagmus, vertigo, nausea, vomiting
Facial paralysis
Paralysis of conjugate gaze to side of lesion
Deafness, tinnitus
Impaired sensation over face
Impaired pain and thermal sense over half the body (may include face)
Lateral midpontine syndrome (short circumferential artery)
Ataxia of limbs
Paralysis of muscle of mastication
Impaired sensation over side of face
Lateral superior pontine syndrome (occlusion of anterior superior cerebellar artery):
Paralysis of conjugate gaze (ipsilateral)
Horizontal nystagmus
Skew deviation
Miosis, ptosis, decreased sweating over face (Horner syndrome)
Impaired pain and thermal sense on face, limbs and trunk
Impaired touch, vibration, and position sense, more in leg than arm
Millard Gubler syndrome and Raymond- Foville syndrome:
Site: base of pons
Cranial nerve involved: VII and often VI
Tracts and nuclei involved: corticospinal tract
Signs: facial and abducens palsy with contralateral hemiplegia; sometimes gaze palsy to side of
lesion
Usual cause: softening; tumor.
62. Mesencephalic syndromes: clinical features.
Weber syndrome:
Site: base of midbrain
Cranial nerve involved: III
Tracts and nuclei involved: corticospinal tract
Signs: oculomotor palsy with crossed hemiplegia
Usual cause: vascular occlusion; tumor; aneurysm
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Claude syndrome:
Site: tegmentum of midbrain
Tracts and nuclei involved: red nucleus and brachium conjunctivum
Signs: oculomotor palsy with contralateral cerebellar ataxia and tremor
Usual cause: vascular occlusion; tumor; aneurysm.
Benedikt syndrome:
Site: tegmentum of midbrain
Tracts and nuclei involved: red nucleus and brachium conjunctivum, corticospinal tract
Signs: oculomotor palsy with contralateral cerebellar ataxia and tremor and corticospinal signs
Usual cause: softening; tumor; tuberculoma, hemorrhage
Parinaud syndrome:
Site: dorsal of midbrain
Tracts and nuclei involved: supranuclear mechanism for upward gaze and other structures in
periapqueductal gray matter
Signs: paralysis of upward gaze and accommodation fixed pupils
Usual cause: pinealoma, hydrocephalus and other lesion of dorsal midbrain
63. Multiple sclerosis: etiology and symptoms
Most likely MS occurs as a result of some combination of genetic, environmental and infectious
factors, and possibly other factors like vascular problems.
Symptoms of MS usually appear in episodic acute periods of worsening (called relapses,
exacerbations, bouts, attacks, or "flare-ups"), in a gradually progressive deterioration of
neurologic function, or in a combination of both. Multiple sclerosis relapses are often
unpredictable, occurring without warning and without obvious inciting factors with a rate rarely
above one and a half per year. Some attacks, however, are preceded by common triggers.
Relapses occur more frequently during spring and summer. Viral infections such as the common
cold, influenza, or gastroenteritis increase the risk of relapse. Stress may also trigger an attack.
Pregnancy affects the susceptibility to relapse, with a lower relapse rate at each trimester of
gestation. During the first few months after delivery, however, the risk of relapse is increased.
Overall, pregnancy does not seem to influence long-term disability. Many potential triggers have
been examined and found not to influence MS relapse rates. There is no evidence that
vaccination and breast feeding, physical trauma, or Uhthoff's phenomenon are relapse triggers.
64. Multiple sclerosis: differential diagnosis, treatment.

Differential DIAGNOSIS:
Myelitis.
Tumors of s.cord.
Vitamin B12 def.
Tumors of sella turcia.
Strokes in territory of basilar artery.
Inflammatory disorders (SLE,polyarteritis nodosa).
Vasculitis.
TREATMENT:
Prednisone ( 50mg /d ).
ACTH (50-100 i. u/d i.m. for 2-3 wks).
Imuran (2 mg/ kg/d ).
Symptomatic treatment:
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spasticity: mydocalm tb(50mg ) 3 times/d , Chlorozoxazone tb (250mg ) 3 times/d,

diazepam, GABA derivative baclofen (10-100mg p.o, usually in the evening), tizanidine (1220mg p.o daily), gapapentin (300-400mg daily), spasticity of individual muscles can be treated
locally by i.m injection with botulinum A toxin or if its necessary, adductor tenotomy.
pain antialgics like algocalmin
trophicity vitamin B1, B6, B12, - ip/d for days.
urinary dysfunction: emepronium bromide, 200mg p.o. tid or qid.
fatigue: amantadine 100mg p.o, modafinil or tolderodine 2mg p.o.
other manifestations:-paroxysmal phenomena, including trigeminal neuralgia, tonic
brainstem seizures, episodic pains and dysarthria, and ocular ataxia can be treated with :
carbamazepine, oxcarbazepine, gabapentin; intention tremor: it may respond to isoniazid.
65. Etiology of secondary epilepsy.

The etiology can be one of the following.
1.
Infectious disease, of the mother during pregnancy, such as Toxoplasmosis and Rubella.
2.
Cerebellar trauma.
3.
Neuroinfections, such as meningioencephalitis.
4.
Metabolic disturbances, such as hypoglycaemia, uraemia, diabetes, etc.
5.
Alcohol intoxication.
6.
Tumours of the brain, such as meningiomas.
7.
Strokes.
8.
Cerebellar thrombophlebitis.
9.
Cerebellar abscess.
10.
Degenerative disease.
11.
Hypertensive encephalopathy.
66. International classification of epileptic seizures.
33
1. Partial (focal, localized) seizures

1.1 Simple partial seizures (without alteration of consciousness)
1.1.1
with motor signs
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focal motor without jacksonian march
focal motor with jacksonian march
versive
postural
phonatory (vocalization without interruption of speech)
1.1.2
with somatosensory or specific sensory symptoms (elementary
hallucinations)
somatosensory
visual
auditory
olfactory
gustatory
vertiginous
1.1.3
with autonomic symptoms or signs
epigastric sensations
pallor
sweating
blushing
gooseflesh
papillary dilatation
1.1.4
with mental symptoms and/or disturbances of higher cerebral
function (almost always involving alteration of consciousness, generally
seen in complex partial epilepsy)
dysphasia
dysmnesia
cognitive
affective (anxiety)
illusions
structured hallucinations
1.2 Complex partial seizures (with disturbance of consciousness,
sometimes beginning with simple manifestations only)
1.2.1 simple partial onset, followed by disturbance of consciousness with
simple partial features, followed by disturbance of consciousness with
automatisms
1.2.2 disturbance of consciousness at onset
Isolated disturbance of consciousness
automatisms
1.3 Partial seizures with secondary development of generalized tonic-clonic
(GTC) seizures (=GTC seizures with partial or focal onset; partial seizures
with secondary generalization)
1.3.1 simple partial seizures with secondary generalization
1.3.2 complex partial seizures with secondary generalization
1.3.3 simple partial seizures that develop into complex partial seizures and
then become generalized
2. Generalized seizures
2.1 Absence seizures
Only disturbance of consciousness
With automatisms
With mild clonic component
With atonic component
With tonic component
With autonomic component
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2.2 Atypical absences
Alterated muscle tone may be more prominent
On- and offset often gradual
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67. Partial epileptic seizures:

-simple partial seizures (motor Jacksonian seizures, adversive seizures, sensitive
Jacksonian seizures).
-complex partial seizures or temporal epilepsy(psychomotor seizures,
psychosensorial seizures, paoxistical troubles of evocation).
SIMPLE: The seizure may be Motor Jacksonian, Adversive or Sensitive Jacksonian.
a. Motor Jacksonian Seizures: The patient is awake and knows what is happening.
Briskly,one half of the body may have contractions.
b. Adversive Seizures: These appear in the region of the supplementary motor area. The
eye and the head of the patient are deviated and one arm is the raised position.
c. Sensitive Jacksonian Seizures: The onset is brisk, with paresthesia in half of the
body. The paresthesia begins in the face and then spreads downwards, going to the arms, and
then the legs.
COMPLEX: This is also known as Temporal Lobe Epilepsy. The lesion is in the temporal lobe
and this seizure may be a psychomotor seizure or a Psychosensorial seizure, or it can be a
paroxystical disorder of evacuation (dj vu deja come , Jamai vu or Jamai come).
a. Psychomotor Seizure: These are automatic movements and may be either simple or
complex.
- Simple: The patient presents movements of mastication, swallowing, dressing and
undressing, and wrapping the hands.
- Complex: The patient can move over a long distance. In this type of seizure, the
patient can be aggressive and violent.
b. Psychosensorial Seizure: This type of seizure causes hallucinations.
- Visual hallucinations: These may be simple or complex:
Simple: The patient can see different lights. The cause can be a temporal lobe abscess, tumor or
trauma.
Complex: The patient sees images and faces.
- Auditive hallucinations: This can be simple or complex
Simple - The patient hears sounds and voices.
Complex - The patient hears complete words.
- Gustatory hallucinations.
- Vestibular hallucination: - The patient complains about vertigo , nausea and equilibrium
disorders.
c. Paroxystical disorder of evacuation;- The patient may have a sensation of
familiarity (dj vu , or deja come ).
- Familiatity: He says he knows a place even if he has never been there.
- Alienation: The patient comes home and says that he does not recognise the place.
68. Grand Mall epilepsy and Petit Mall epilepsy or absence: symptoms and
electroencephalographic disturbance.
A. Grand mal Seizures
It is the classic and most characteristic form of epilepsy. Many patients report nonspecific
prodromal symptoms such as anxiety, irritability, a general feeling of not being well, difficulty
concentrating, preceding the seizure by minutes or hours. The seizure its sometimes
accompanied by a shout. There is generalized contraction of the muscles, with respiratory arrest,
cyanosis, rigidity, extension of the body. The tonic phase (10 seconds) is followed by a clonic
phase (2-5minutes). The patient remains amnestic and confused 10minutes or longer.
This is the most frequent type. It is a generalized discharge of the brain with loss of
consciousness and motor disturbances. Generalised seizures have their origin in the subcortical
structure of the brain. In it, both hemispheres are involved. Between each seizure, the EEG will
show sharp and slow waves with increased amplitude. This type of seizure can be divided into 5
stages:
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1. PRODROMAL STAGE: This is a couple of days to hours before the onset of the epilepsy. In it
the patient will complain of the following:
Headaches.
Depresion.
Irritability.
Anxiety.
2. Aura Stage: This is the stage immediately before the onset of the epileptic attack. About
50% of the patient will always feel the same symptoms before an attack.
An unpleasant odour.
Pain in the stomach.
An unpleasant taste.
Cinterating spot in his eye.
During the seizures, the patient suddenly loses his conscience and falls.
The seizure has 2 phases:
Tonic phase.
Clonic phases.
3. Tonic Stage: This is the stage during the epileptic attack. During the seizure , the patient
suddenly loses his consciousness and falls. He will have generalised tonic contractions of the
body. Because of the contraction of the respiratory muscles, the patient may cry. The head falls,
the legs remain in extension and slight internal rotation, while the arms are semiflexed and
slightly abducted. The jaw is closed and the tongue may be caught between the teeth. The eyes
may be open or closed, and may sometimes deviate to one side. The pupils are contracted and
miotic, and may be deviated because of the contraction of the abductor muscles. The patient may
also present incontinence of urine and faeces. Vegetative disorders, such as cyanosis, pallor of
the face, and salivation (with blood) may be present. This stage lasts for about 1 1 minutes.
The EEG will show discharges of sharp waves in all the derivations.
4. Clonic Stage: The patient has rapid and symmetric contractions of both arms and legs. The
head is jerking and the breathing is noisy. The corneal reflex and the papillary light reflex are
absent, while the tendon reflexes are decreased. The Babinski sign may be positive. This stage
lasts for approximately 40- 80 seconds. The EEG will show slow waves with high amplitude.
5. Postictal Stage: The patient is in deep coma, with generalised hypotony. The breathing is
noisy. Later on, the patient falls into a deep sleep, with regular breathing, after which, he
recovers consciousness, but is in a confused state of mind. He will complain of headaches,
pain in all the muscles, and amnesia of seizures. Sometimes, after the seizure, transitory
hemiparesis and ataxia may be present. The EEG will show the amplitude to decrease until it
reaches an isoelectric line. Then, it will slowly start to show the normal aspect.
In the clonic phase, slow waves with high amplitude appear.
In the postictal phase, the EEG course decreases down to a line (silentium) and then slow course
appears and slowly rises to normal. B/w seizures, on a normal course, sharp and slow waves
with high amplitude appears.
B. Petit mal Seizures

OR ABSENCE
It is a generalised seizure but without the convulsions. The patient loses his consciousness, but
does not fall, and he has fewer motor disturbances. The onset is usually in childhood, between
the ages of 1 and 13 years. It affects girls more often than boys. It usually lasts no more than a
few seconds, up to 1 minute. The onset may be induced by hyperventilation. The affected child
suddenly stops whatever activity he was engaged in, stares vacantly ahead for a period, and then
resumes activity as before. The patient presents automatic movements, such as blinking and
myoclonic jerks. The EEG shows sharp waves, with a typical frequency of 3 w/sec.
36
Neurology
dr.ddp321@gmail.com
69. Epilepsy: differential diagnosis.

1. Syncope: This is a brief loss of consciousness which appears only during the day. It is nonconvulsive and is usually due to hypotension or disturbances of the cardiac rhythm. The EEG is
normal.
2. Hysteria: This is a psychic disease, where the person falls in the presence of other people.
This appears after a conflict or fight. The patient has no urinary incontinence, cyanosis or
beating of the tongue, though he may have chronic movements. The EEG is normal. The
treatment for reviving the patient is to induce pain on him, such as beating him or a water
injection. The patient will cry with pain and open his eyes.
3. Vertiogo crisis: The patient falls but he is conscious. He may have nystagmus and vomiting
4. Transient Ischemic attacks: The onset is brisk, in half of the body. The patient has no
convulsions and usually has hypertension.
5. Narcolepsia: This is seen after encephalitis. This is a disease with a short crisis of sleep. The
patient falls asleep once or more during the day, but can be easily awoken.
70. Epilepsy: treatment, treatment of partial seizures, treatment of Grand Mall epilepsy,
treatment of Petit Mall epilepsy.
TREATMENT:
Identifiable causes of seizures should be eliminated whenever possible- a brain tumor or chronic
alcoholism.
Before treatment is begun, the physician must define the type of seizure that is present.
The patient should take the prescribed medication regularly in the dose indicated and keep a
protocol of any seizures that occur. Medication should be introduced at a low dose, which is
gradually increased to a typically effective dose. A change to a different medication should be
made only if the medication currently given was found ineffective or is not tolerated by the
patient.
GRAND MAL EPILEPSY:
1. Phenytoin (hidantoin): The dosage is 6-8 mg/kg BW/day, divided into 1-2 doses. A tablet has
100 mg, so an adult dose is about 2-4 tablets per day.
Secondary effects:
Atacsia.
Dysarthria.
Nystagmus.
Skin eruption.
Thrombocytopenia.
Hepatic troubles.
Gingival hyperplasia.
2. Primidona (dezoxiphenobarbital): The dosage is 5-30 mg/kg BW/day, divided into 1-2
doses. A tablet has 250 mg, so the adult dose will be 3 tablets per day.
3. Phenobarbital (Gardenal): The dosage is 2-5 mg/kg BW/day, divided into 1-2 doses. The
average dose for a child is 15mg, while that for an adult is 100 mg. The adult dose is about 1-3
tablets /day.
Secondary effects:
Vertigo.
Somnolence.
Psychic troubles.
Skin troubles.
Hepatic troubles.
Agranulocytosis.
4. Depakene (Valproic acid): The dosage is 25-30 mg /kg /day. The drug is available as 250
mg capsules.
37
Neurology
dr.ddp321@gmail.com
PETIT MAL:
1. Trepal: Also known as Trimetadion or Absentol. The dosage is 20 mg/kg/day. Each tablet
has 150 mg. Therefore, the adult dosage is 900- 1200 mg/day, or 6-8 tablets, divided into 2
doses.
2. Suxilep: The dosage is 20 mg/kg day. It is available in 250 mg tablets, so the adult dose is 38 tab/day.
3. Depakene (sodium valporate): Adult dosage is 900 mg/day ( 3 tab/day) a child dosage is
450 mg/day.
Each tablet is 300mg.
4. Clonazepam (rivotril): The dosage is 0,5 mg /kg/day. Each tablet contains 0,5 mg/2mg and
25 mg in phials. The adult dosage is 2-3 tab/day in 3 doses.
5. Ederen (acetazolamide): The dosage is 200-2000 mg/day. Each tablet has 250 mg. The
adult dosage is 1-10 tab. / day in 3-4 doses.
PARTIAL EPILEPSY:
1. Finlepsin (Carbamazepin): The dosage is 600-1200 mg/day. Each tablet has 200 mg. The
adult dosage is 3-6 tab./day.
2. Suxilep: as above.
3. Diazepam (valium): The dosage is 1mg /kg/day. Each tablet contains 2and10 mg , each phial,
10 mg.
The adult is 1-3 tab./day or 1-10 phials/day.
4. Clonazepam: as above.
5. Depakene: as above.
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Neurology

1 Clinical features of upper motor neuron syndrome?

Leasion in the anterior horn of the spinal cord

Treatment :1. Penicillin: Dose: 3 mil / day.

14 The central & Peripheral Vestibular Syndrome symptoms?

17 Sensibility(sensivity) dissociation: syringomielic dissociation, tabetic dissociation .

optic acuity is diminished, the visual field is limited,

When we have a complet/ complex SC transection we have following SYMPTOMS:

20 Examination of sensibility(sensivity): superficial, deep & integrative sensibility?

5. Expressive Aphasia (Broca`s Aphasia ).

23A Temporal lobe: anatomy, semiology?

25 Glossopharyngeal nerve IX-N: anatomy, semiology?

32. Radial nerve paresis: etiology, symptoms

33. Median nerve paresis: etiology, symptoms.

34. Ulnar nerve paresis: etiology, symptoms.

35. The external popliteal nerve paresis: etiology, symptoms.

Muscle atrophy does not occur

- State of cerebral vessels.

Disarthria (trouble of speech).

Lateral homonymous hemianopsia.

Ataxia (troubles of coordination).

Begins at the bifurcation of the Common Carotid Artery (level of C4).

43. Anterior cerebral artery; anatomy, clinical aspects.

When the bilateral anterior cerebral artery is affected, appear;

45. Vertebral and basilar arteries: anatomy and clinical syndromes.

Symptoms appear when both arteries are affected.

Cerebellum (middle and superior cerebellum artery).

Inferior part of temporal lobe and occipital lobe.

46. Cerebral hemorrhage: etiology, pathophysiology, anatomopathology, clinical aspects.

Thrombosis Of Cavernous Sinus:

Thrombosis Of Lateral Sinus

Thrombosis Of Longitudinal Superior Sinus

49. Treatment of vascular ischemia; treatment of transient ischemic attacks, treatments of

50. Treatment of cerebral hemorrhage.

there is no specific treatment

daily administration of 5 to 10 g of KCL orally in aqueous solution prevents attacks

an attack would actually be induced by administration of potassium salt.

55. Polymyositis: clinical features, EMG, treatment.

anticholinesterase drugs: neostigmine (oral dose ranges from 7,5 to 45 mg every 2 to

60. Median pontine syndrome: etiology, clinical aspects.

Deviation of the eyes

64. Multiple sclerosis: differential diagnosis, treatment.

spasticity: mydocalm tb(50mg ) 3 times/d , Chlorozoxazone tb (250mg ) 3 times/d,

65. Etiology of secondary epilepsy.

1. Partial (focal, localized) seizures

67. Partial epileptic seizures:

B. Petit mal Seizures

69. Epilepsy: differential diagnosis.

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