1.

Deep sensation : Structure and symptoms of damage at various

level.sensory ataxia.Methods of examination.
Symptoms of damage
Gyrus postcentralis here is for sensory function-damage causing anaesthesia
of opposite site, irritation cause sensory problem.
Infraparietal sulcus-centre of body hym and image-damage cause unable to
recognize non-functioning part of body, e.g leg.
Upper part of g. supramarginalis (stereognosis)-damage cause unability to
recognize stuff by shape
Damage of lower part of g. supramarginalis- no plan, no idea, lose learnt
skills
Damage of gyrus angularis: Gertmann’s syndrome, impaired L-R orientation,
unable to calculate, disorder of reading, writing, and finger agnosia.
Includes  vibration sense, joint sense, muscles sense, nerve sense
Method of examination
(a)Rhomberg’s test -> swaying with eyes open – cerebellar ataxia
 Swaying with eyes closed – sensory ataxia
(b)Graphesthesia
©Stereognosis
(d)Double simultaneous stimulation
(e)Barosthesia
(f)textures

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2.Pathway of pain and temp sensations : structures,symptoms of damage
(a) in cerebral cortex (b) in internal capsule of spinal cord
The 1st order neuron: cells of posterior root ganglion and its axon. Axon is
divided into lateral and medial branch. Lateral branch form afferent sensory
nerve.
Medial branch enters spinal cord to ascend a few segments forming
Lissaeur’s tract, and relays in the cells of Substantia Gelatinosa of Rolandi
capping the posterior horn of gray matter.
The 2nd order neuron: cells of Substantia Gelatinosa of Rolandi and its
axon.The axon crosses to opposite side, ascends in Lateral Spinothalamic
Tract of the spinal cord then in the lateral lemniscus of the brain stem, to
relay in the thalamus.
The 3rd order neuron:starts in the cell of thalamus, its axon ascends to pass
through the posterior limb of internal capsule conducting the impulse to the
cortical sensory area in the parietal lobe.
3.Structure of pyramidal pathways,its function.Symptoms of damage at
diff lvls in cerebral cortex,internal capsule,brain stem,in cervical spinal
cord.
Symp: Interruption of the pyramidal tract at or below its cortical origin
causes impairment of movement in the opposite body-half, especially
severe in the arm and leg; characterized by muscular weakness, spasticity
and hyperreflexia, and a loss of discrete finger and hand movements.
Babinski's sign is associated with this condition of . a massive bundle of
fibers originating from pyramidal cells of various sizes in the fifth layer of the
precentral motor (area 4), the premotor area (area 6), and to a lesser extent
from the postcentral gyrus.
Structure n func – originates in motor area 4 and premotor area 6 and
terminates the ant horn cells of diff lvls of spinal cord.Supplies opposide side
of body.

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4.Physiological deep and superficial reflexes, reflex arches
Deep reflexes
- Upper limb  Biceps reflex (C5,C6),Brachioradialis
reflex(C5,C6),Triceps reflex(C6,C7),Supraspinatous (C3,C4) and finger
reflexes(C8,Th 1)
- Lower limb  Knee reflex (L2,L3,L4),Ankle reflex(S1,S2),Patellar
reflex(L2,L3,L4),Adductor reflex (L4)
Superficial reflexes
- Abdominal reflex(Th6-Th12),Cremaster reflexes (L1),Gluteal reflex
(L4,L5), Anal reflex(S3,S4,S5),Plantar reflex(S1,S2)

5.Differential diagnosis of central and peripheral paralysis

Central paresis- increase muscle tone,increase tendon reflex, have
pathological reflex
Peripheral paresis – atrophy,atonia,areflexia
6.Alternating crossing syndrome in lesions of brain stem,pons,in medulla
oblongata

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7.Cerebellum (func,structure,peduncles,symptoms of abnormalities in
cerebellum and methods of examination
Fxn: maintainence of equilibrium,muscle tone coordination and regulation
of fine,voluntary motor activity
Str:2 main parts;1.A midline central structure(vermis)
2.2 Lateral cerebellar hemisphere
Symp:1.Lesion of the archicerebellum/Disturbance of equi during walking or
standing.
2.Lesion of neocerebellum lead to incoordination of movement.
3.Lesion of paleocerebellum leads to disturbance of muscle
tone/hypotonia
Invs:2 main syndromes which is hyporeflexia and also
hyperthermia,standing and swaying,staggering gait,nystagmus and deviation
of body towards affected side.
8.Main types of ataxia:causes and differential diagnosis
Ataxia is incoordination of voluntary motor activity with or without
disequilibration in the absebnce of motor weakness
Types: cerebellar, sensory, vestibular, combined, hysterical.
Etiology: Hereditary/acquired (infective, vascular, toxic, neoplastic,
metabolic and demyelinating)/idiopathic
DD:Test for Cerebellar ataxia-1)finger to nose test 2)Finger to finger test
3)Adiadokokinesis and dysdiadokokinesis 4)Rebound
phenol.5)Buttoning,unbuttoning test 6)Heel to knee test 7)Walking test
along straight line

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9.Extrapyramidal system : func,structures and neurotransmitters.Main
symptoms of injury.Parkinsons syndrome :causes and clinical pic.
Fxn:
Regulation and integration of voluntary motor activity, regulation and
maintenance of muscle tone, regulation and maintenance of associative
movements.
Str: include all fibers that can influence the motor end plate activity and do
not pass in pyramidal tract. It is composed of different centres scattered at
different levels of neural axis and all are interconnected via one main cell
station (globus pallidus)
Muscle dystonia: prolonged muscle contraction causing abnormal posture or
repetitive movements due to many causes.
Parkinson’s syndrome
Etio: Paralysis agitans post-encephalitic and atherosclerosss, idiopathic,
symptomatic such as inflammatory, vascular, toxic, neoplastic and
traumatic.
c/pic: tremors,rigidity, loss of emotional and associative movement resulting
in immobile face (mask face), monotonous speech, loss of swinging of arm
during walking, oculogyricrisis,obesity diabetes insipidus,
sialorrhea,amenorrhea. Pyramidal signs.

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10.Symptoms of spinal cord lesion : post and lat columns,ant n post lat
horns,ant horns of gray matter
The lesion is on one side of the spinal cord, situated between C1&C5
segments, caused by stab wound, disc prolapsed, tumor resulting in the
picture of Brown-Sequard syndrome with characteristics:
a) At the level of lesion: Ipsilateral localized L.M.N.L of the muscle
supplied by affected segments; Ipsilateral loss of all sensation in area
supplied by dorsal roots of affected segments
b) Below the level of lesion: Ipsilateral hemiplegia, Ipsilateral deep
sensory loss, Contralateral superficial sensory loss for pain and
temperature, touch diminishes on both sides.

11.Symptoms of total transverse lesion of spinal cord at lvl of cervical

segments,cervical enlargement,thoracic segments of lumbar sacral
enlargement
Cauda equina consists of the collection of lumbo-sacral nerve roots in the
lower part of spinal canal, whose lesion cause motor weakness or paralysis
of one or both limbs, with painful onset and maybe of late manifestation.
Damage at the level below C3 can lead to paralysis of respiratory muscles,
respiratory problem.
Cervical enlargement (between C5-T1) where anterior horn of
cervicalsegment is invaded leading to peripheral paresis of arm, atrophy but
at leg having central paresis
Sensory damage below C5 causing urine incontinence
Thoracic enlargement at the level T5 retains normal function of arm, but
legs having spastic lower paraplegia, and urinary retention
Damage at T10:Normal upper limb reflex,decreased abdominal reflex.

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12.Pathways and segmental apparatus of spinal cord in cross section :
post,mid and lat parts of greay matter of spinal cord
Occipital lobe is the centre of visual, agnosia. Due to lesion, patien is unable
to describe or name the object shown (but s/he can smell or touch the
object), and patient has homonymous hemianopia (half of visual field
damage).
13.Optic nerve : func,structure and symptoms of damage
The receptors for vision are the cones(for day vision)&rods(for night
vision)of the retina, contains nasal&temporal fibres.
Concentric diminution of field vision: caused by glaucoma, retinal
abnormalities.
Central scotomata or loss of central vision due to demyelination of optic
nerve
Total unilateral visual loss-due to lesion of optic nerve
Bitemporal hemianopia: lesion affects centre of optic chiasm
Binasal hemianopia: due to bilateral lesions affecting uncrossed optic fibers
Homonymous hemianopia: lesion affecting optic tract
Homonymous quadrantanopia: loss of upper or lower homonymous
quadrants of visual fields due to lesion of temporal lobe/parietal lobe.
14.Oculomotor nerve : func,structure and symptoms of injury
Oc.n-it supplies all the extrinsic muscles of the eye, except the lateral rectus
and superior oblique;supply extraocular muscle(elevation of upper eyelid)
and intraocular muscle(constrictor papillae muscle of the iris and ciliary
muscle of lens).Lesion-External ophtalmoplegia(ptosis due to paralysis of
levator palpebrae muscle,diplopia on passive elevation of eyelid,divergent
paralytic squint).Internal ophtalmoplegia(ipsilateral dilated fixed
pupil;mydriasis ,affection of the light reflex)

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15.Trochlear and abducent nerve : func,structure,signs of damage
Troch.n.- supplies the superior oblique muscle of the eye; its origin is in the
midbrain below the cerebral aqueduct.
F(x)-turns eyes inwards and outwards
Lesion-diplopia when look downwards,limitation of movement of the
affected eye on looking in&downwards.
Abducent n,- a small motor nerve supplying the lateral rectus muscle of the
eye; its origin is in the dorsal part of the tegmentum of the pons just below
the surface of the rhomboid fossa,
F(x)-moves eyes outwards(laterally)
Lesion-Diplopia when look outwards,limitation of movement of affected eye
on loking outwards
16.Accessory nerve ; func,symptoms of damage
Acc.n-arises by two sets of roots: cranial, emerging from the side of the
medulla, and spinal, emerging from the ventrolateral part of the first five
cervical segments of the spinal cord; these roots unite to form the accessory
nerve trunk, which divides into two branches, internal and external;
Lesion-ipsilateral paralysis of the sternomastoid and trapezius m.

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17.Trigerminal nerve ; func,structure,symptoms of diff diagnosis of lesions
of nuclei and branches of trigerminal nerve
the chief sensory nerve of the face and the motor nerve of the muscles of
mastication; its nuclei are in the mesencephalon and in the pons extending
down into the cervical portion of the spinal cord; it emerges by two roots,
sensory and motor, from the lateral portion of the surface of the pons, and
enters a cavity of the dura mater, the trigeminal cave, at the apex of the
petrous portion of the temporal bone, where the sensory root expands to
form the trigeminal ganglion; from there the three divisions (ophthalmic,
maxillary, and mandibular nerves) arise.
Lesion-1)Sensory affection a)Peripheral lesion-loss of sens. on the same side
of face b)Central lesion-ipsilateral dissociated sensory loss of face 2)Motor
affection-weakness of mastication muscle on the same side of the
lesion,deviation of jaw to affected side 3)Reflex affection-ipsilateral loss of
corneal and conjunctival reflexes,ipsilateral loss of palatal reflex,exaggerated
jaw reflex

18.Hypoglossal nerve : func, clinical pic in lesion of this nerve. Jacksons

syndrome
Hypog.n-purely motor nerve which supplies the intrinsic tounge
muscle.arises from an oblong nucleus in the medulla and emerges by several
root filaments between the pyramid and the olive; it passes through the
hypoglossal canal, then courses downward and forward to supply the
intrinsic and four of five extrinsic muscles of the tongue.
Lesion-deviation of tounge to the opposite/to the side of
lesion(unilateral),spastic tounge;inability to protrude toungue(bilateral)
Jackson’s syndrome – 1. Hemiplegia on the opposite side of the lesion.
2. 6th and 7th cranial nerve paralysis on the same side of lesion.
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19.Glossopharyngeal and vagus nerve : func, symptoms of damage, Bulbar
syndrome
Gloss.n-mixed nerve carrying motor(stylopharyngeus,pharynx
constrictiors),sensory(general sensations from post.tounge 1/3 of
tounge,pharynx and tonsil,taste sensation from post.1./3 of
tounge),autonomic fibres(parasymp.fibres to parotid gland).Lesion-
ipsilateral loss of taste and general sensation from post 1/3 of
tounge,ipsilateral loss of pharyngeal reflex and hard to swallow.Vagus n.-
Mixed nerve carrying motor(soft palate,pharynx,larynx),sensory fibres(skin
over ext.auditory meatus,thoracic and abdominal viscera),autonomic
fibres(parasympathetic fibres to the heart,GIT and bronchial tree.Lesion-
Palato-pharyngeo-laryngeal paralysis resulting in True Bulbar
palsy,tachycardia,constipation,disorder of swallowing. Bulbar syndrome is
characterized by one side damage of bulbar nuclei of the nerves
(glossopharyngeal/facial nerve) with signs such as dystonisa,dysarthria and
dysphagia,decreased jaw jerk, displacement of soft palate cannot speak and
eat normally.
20. Bulbar and Pseudobulbar palsy :causes, clinical pic, diff diagnosis
Bulbar syndrome is characterized by one side damage of bulbar nuclei of the
nerves (glossopharyngeal/facial nerve) with signs such as
dystonisa,dysarthria and dysphagia,decreased jaw jerk, displacement of soft
palate cannot speak and eat normally.
Pseudobulbar syndrome is characterised by bilateral upper motor neuron
damage of both cortico-nuclear tract, with these signs: dysarthria, dystonia,
dysphagia, and increased jaw reflex, child-like behavior such as involuntary
cry or laugh.

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21.Cognitive functions : causes of disturbances
-refers to the general ability to organize,process and recall
informations.Cognitive impairment occurs in host of
chemical,metabolic,infectious disease that exert an impact on the
brain.When an area of the brain that determines cognitive func is
damaged,by excessive use of drugs,by alcohol or from physical trauma.

22.Higher cortical functions.

23.Frontal lobe damage symptoms
24.Focal symptoms of temporal lobe damage
25.Focal symptoms of irritation and destruction of occipital lobe
26.Parietal lobe focal symptoms damage. All dis questions have same
answers in the 3 pages

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13
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27.Gnosia,praxia : main concepts, localizations of centres.Agnosia.Apraxia
Gnosia: Ability to recognize,one comprehend meaning of various stimuli
Praxia : Able to perform movements
Localizations : Supramarginal gyrus of dominant hemisphere,fibres
connecting the supramarginal gyrus to motor area of dominant
hemisphere/ant part of corpus callosum.
Agnosia-Impairment of ability to recognize, or comprehend the meaning of,
various sensory stimuli, not attributable to disorders of the primary
receptors or general intellect; agnosias are receptive defects caused by
lesions in various portions of the cerebrum
Apraxia-inability to perform compound voluntary mtor activity in the
absence of paralysis,sensory loss of incoordination

28.Localization of speech func in cerebral cortex of brain.Types of

aphasia.Characteristics of motor aphasia.
Aphasia is difficulty or inability of speech in the absence of lesion of sense
organs or mental defects.
Type: I. Sensory or perceptive aphasia: 1) Visual:
-Visual agnosia-see but not recognize object, lesion at area 18 and 19,
-Alexia due tolesion in are 39 (word blindness)
2) Auditory: Auditory agnosia: lesion at area 22 (hear sound but deosn’t
recognize)

II. Motor or executive aphasia

1) Verbal aphasia-lesion at Broca’s area (can’t express ideas in words)
2) Agraphia-lesion in Exner’s area (cannot express idea in writing)

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III. Jargon’s aphasia: due to defect of association- Lesion at associative area,
speak meaningless words.
Localization of speech function :
-sensory : 1)visual(area 17,18,19) 2)auditory(area 41,42,22)
-motor : 1)broca’s area 2)exner ‘s area
-Associative(area 37)
29.Speech disorders:localization of speech func, types of
aphasia,characteristics of sensory aphasia,pathogenesis,clinical
pic,method of investigations.Diff diagnosis with subarachnoid hemorrhage
and meningitis.Treatment
Aphasia is difficulty or inability of speech in the absence of lesion of sense
organs or mental defects.
Type: I. Sensory or perceptive aphasia: 1) Visual:
-Visual agnosia-see but not recognize object, lesion at area 18 and 19,
-Alexia due tolesion in are 39 (word blindness)
2) Auditory: Auditory agnosia: lesion at area 22 (hear sound but deosn’t
recognize)

II. Motor or executive aphasia

1) Verbal aphasia-lesion at Broca’s area (can’t express ideas in words)
2) Agraphia-lesion in Exner’s area (cannot express idea in writing)

III. Jargon’s aphasia: due to defect of association- Lesion at associative area,

speak meaningless words.
Localization of speech function :

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-sensory : 1)visual(area 17,18,19) 2)auditory(area 41,42,22)
-motor : 1)broca’s area 2)exner ‘s area
-Associative(area 37)
Clinical pic –(1)aphasia,(2)dysarthria(slurred speech in pyramidal and LMN
lesion of speech muscle,Monotonous speech in Parkinsonism)
Method of examination
(1)Observe during history taking and comments
(2)Check for aphasia and dysarthria

30.Lumbar puncture:indication,contraindication,techniques ,complication.

Changes in CSF(dissociative syndrome)
Indication: CSF evaluation, CSF drainage (leakage hydrocephalus),
intracranial pressure measurement, wnd intrathecal drug administration.
C/indicationcellulitis at puncture site, non-communicating hydrocephalus,
intracranial mass, coagulopathy, complete spinal block above tap-site,
Tethered-cord syndrome.
Procedure:
Patient on lateral or sitting position,cover region with drape, 1mL lidocaine
injected s.c. till wheal appears, then inject 3 mL of Lidocaine at wheel site
(for deep anaesthesia)Needle is into 2nd bone meeting (resistance is felt)
Stylet is removed, and CSF is observed. Evaluate CSF. Replace stylet, w-draw
needle. Gauze applied.
Complication: tonsillar herniation, n-root injury, spinal headache,
aortic/arterial puncture.

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31.Chronic brain ischemia.Causes,mechanism of development, the criteria
for diagnosis,basic principles of treatment and prevention.
Chronic brain ischemia – progressive slow with time and age of pt.
Causes-
Dyslipidemia,Smoking,Atherosclerosis,Tumors,Vasculitis,Thrombosis,
Embolism,Hypertension,Alcoholism
Criteria of diagnosis –
Stage 1- beginning of disease, slight headache, dizziness, bad mood, bad
sleep, disturbed emotion, intentional tremor, numbness in extremities,
minor sensory disturbances.
Stage 2- severe headache,dizziness,discoordination in movement, numbness
in extremities, bad mood, pyramidal tract movement damage, deep
physiological reflex-hyperreflexia, bulbosyndrome
Stage 3- almost no complaints,severe neurological deficit and depression,
atrophy of brain, leukaryosis, diffuse ischemic change of brain,Bulbo and
pseudobulbo syndrome
Treatment – warfarin,anticoagulant,antiplatelets, admit to hospital within 1 st
hour

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32.Risk factors of disorders of cerebral circulation.TIA:def, classification,
differentiate TIA in carotid and vertebrobasilar system. Diagnosis and
treatment. Prevention.
Risk factors – Hypertension, Congestive heart failure, coronary heart
disease, atrial fibrillation, Blood disease, prior stroke, DM, sickle cell disease,
migraine, retinal emboli,infection, tumours, life style
(age,alcohol,smoking,contraceptive pills,genetic factors)
TIA –
Def: acute loss of focal cerebral/ocular function with symptoms lasting less
than 24 hrs.
Classification : (1) carotid (2)vertebrobasillar
Prevention – stop smoking, stress relief, exercise, healthy life style
Differentiate TIA in carotid and vertebrobasillar -
-Carotid : hemiparesis,aphasia,transient loss of vision in one eyes only.
-Vertebrobasilar:vertigo,dysphagia,ataxia and drop attacks,bilateral or
alternating weakness
Treatment :- 1)drugs( aspirin,antiplatelet-antiaggregating drugs,
anticoagulants,IV tPA within 3hrs of onset), 2)Surgical(endaterectomy,
angioplasty)

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33.Classification of cerebrovascular disease. Causes,mechanism of dev,
acute stroke syndrome.Stroke patient care. Primary and secondary
prevention
Def: CVD includes all disorders where it can transient / permanent affected
where involvement of more than one vascular cerebral circulation is
involved.
Causes : atherosclerosis,rupture,hypertension,ischemic heart disease,
hypoperfusion,embolism,hyperlipidemia
Classification : 1) hemorrhagic -1)Intracerebellar , 2)Subarachnoid
2)infarction – 1) cardiogenic embolism 2) CVD 3) other
Acute stroke syndrome also known as ischemic stroke.
Primary prevention – eliminate/control risk factor, education of patient
regarding risk factor reduction and signs and symptoms of acute stroke and
mild stroke,aspirin(30-325mg/day), dipyridamole,Sulfinpyrazone
Secondary prevention – Aspirin( 325-975 mg/day),Ticlopidine,
Anticoagulants(warfarin)
Treatment: CTscan, MRI,Ultrasound,Heparin 5000 IU , Pharmacological
therapy (recombinant tissure plasminogen activation,r-
tPA,heparin,LMWH,ANCROD)
Diagnosis: Correct for hypovolemia,treat fever, keep hypoglycemia
/hyperglycemia in control

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34.CVD:ischemic stroke.Reason and main types of ischemic
stroke,biochemical cascade.Main periods of stroke.First aid in develop of
stroke.
Classification: Acute and Subacute. Acute stage 1 hour – 3 hours ; Subacute
stage lasts 4-6 hours.
Degree of severity : Mild, Moderate and Severe(ultimately leading to death)
Main periods:most acute: first 3-5 days; acute: up till 3 weeks; rehabilitation
period: till 6 months;late rehabilitation period : more than 6 months
Treatment :-medical support (anticoagulants, aspirin, LMWH,
neuroprotection, thrombolysis)
35.The ischemic stroke : main causes and risk factors,pathogenesis, types.
Concept of therapeutic window. Emergency care for stroke. Results of
additional research methods. Identification of symptoms of focal brain
damage in comatose patient.
Def: abrupt and dramatic onset of focal neurologic symptom with
hemorrhage, deficit typically evolve more slowly and drowsiness is common.
Classification: Acute and Subacute. Acute stage 1 hour – 3 hours ; Subacute
stage lasts 4-6 hours.
Degree of severity : Mild, Moderate and Severe(ultimately leading to death)
Causes: Hypertension,rupture,IHD,embolism,atherosclerosis,hypoperfusion,
hyperlipidemia
Risk factors : Hypertension, IHD,Diabetes, smoking, atrial fibrillation,
peripheral ascular disease, previous TIA, cervical bruit, hyperlipidaemia,
increased hematocrit, oral contraceptive pill, cardiomyopathy.
Concept: to decrease adverse outcome, suggested rapid assessment of
brain attack like heart attack with tPA within 3-6 hours of onset of attack.
Investigation in coma pt : CTscan,MRI,Angiography images,Carotid
ultrasound
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Results of additional research methods:-
-Doppler ultrasonic imaging-map out image of moving column of blood in
vessel
- Digital subtraction angiography-visualize intracerebral vessel
-Cerebral angiography-show occlusion/stenosis in cerebral vascular
Tx: Treatment: medical support (osmotic therapy, thrombolysis, aspirin,
anticoagulants LMWH, neuroprotection)

36.Diff treatment of ischemic stroke in acute period,surgical treatment.

Primary and seconday prevention of stroke.
Treatment :1)Medical (supportive care,CTscan,r-tPA,Intraarterial
thrombolysis,heparin,LMWH,Ancrod,Aspirin.) 2)Surgical (endaterectomy,
angioplasty,stent placement)
Primary prevention – eliminate/control risk factor, education of patient
regarding risk factor reduction and signs and symptoms of acute stroke and
mild stroke,aspirin(30-325mg/day), dipyridamole,Sulfinpyrazone
Secondary prevention – Aspirin( 325-975 mg/day),Ticlopidine,
Anticoagulants(warfarin)
37.Ischemic stroke in vertebrobasillar system : clinical pic,diagnostic
method. Prevention of ischemic stroke- primary and secondary.
c/pic: facial paralysis, paralysis abduction of eye, paresis of conjugate gaze,
Horner’s syndrome, Ataxia, diminished pain and thermal sense over half
body,hemifacial sensory deficit.
Diagnostics: chest x-ray, ECG, CSR, FBC, Blood culture,platelet, electrolytes,
glucose level, ESR,lipid profile, Pt Ptt, serological test for syphilis, Brain MRI,CT,
Doppler US, MR angiography.

22
Primary prevention – eliminate/control risk factor, education of patient
regarding risk factor reduction and signs and symptoms of acute stroke and
mild stroke,aspirin(30-325mg/day), dipyridamole,Sulfinpyrazone
Secondary prevention – Aspirin( 325-975 mg/day),Ticlopidine,
Anticoagulants(warfarin)

38.Syndrome of hemorrhagic stroke : causes and risk factors,classification.

Clinical pic of intracerebral hemorrhage.Diagnosis and treatment.
Complication. Primary and secondary prevention.
Causes:Hypertension,Age,Cerebral amyloidosis,Coagulopathies,
Anticoagulant therapy, Intracranial aneurysm, vasculitis, atriovenous
malformation, intracranial neoplasm, head injury(trauma), tumor
Risk factors: gender(man more at risk),smoking,increase bp,family history of
stroke,increase blood cholesterol,DM,obesity, coronary artery disease,
drugs(oral contraceptive),alcohol,congenital heart defects
Classification: 1)Intracerebral hemorrhage 2)subarachnoid hemorrhage
Clinical pic: increase intracranial pressure,headache,pinpoint pupils
Diagnosis : CTscan,MRI,cerebral angiography,chest radiography, ECG,blood
tests.
Complication: increase ICP,herniation,cerebral edema, post stroke seizures
Treatment: surgery,maintain adequate oxygenation,if hypertension increase
mannitol given.

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39.Subarachnoid hemorrhage:etiology,mechanism of development of
clinical pic,complications.Diagnosis and treatment
Flooding of subarachnoid space with blood
Etio: head trauma, hemorrhage in a brain tumor, severe hypertension, blood
disease-purpura, wrong administration of anticoagulants, rupture of
intracranial angiomatous malformation, rupture of an intracranial aneurysm.
Clinical pic : Headache, neck stiffness, pain at the neck,lower back and limbs.
Nausea,vomiting and vertigo and fever
Diagnosis : CT scan, Lumbar puncture for csf exam, plain x-ray of skull,
angiography
Complication: Rebleeding,cerebral ischaemic infarction, hydrocephalus and
epilepsy.
Tx: Bed rest, analgesic and sedatives, antifibrinolytics, dehydrating measures
for brain, Lumbar puncture to relief headaches, treating the cause, and
surgical treatment by ligating of carotid artery
40.Emergency treatment of stroke patient in prehospital phase.Care for
stroke patient.
Emergency treatment in prehospital phase
-Do CTscan in nearest medical centre
-Check for unevenness in face, check weakness in one extremity,slurred
speech,take to hospital within(1-30mins)
-ask clinical symptoms
Care for stroke patient
-monitoring of vital signs,use mannitol if ICP increase,antihypertensive
agents,adjunctive therapies(supplemental oxygen,administer IV crystalloid
fluid to maintain volume,antiemetics if vomiting,calcium channel blockers,
antifibrinolytics,emergent ventricular drainage if necessary.

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41.Neuroprotective therapy in neurology.
Aim-prevent/slow disease progression and secondary injury by preventing
or slowing loss of neurons.
-neuroprotective therapy used in many CNS disorders include
stroke,neurodegenerative disease,traumatic brain injury and acute
management of neurotoxin consumption.
Common mechanism- increase lvl of oxidative stress ,mitochondrial
dysfunction,excitotoxicity,inflammatory changes, iron accumulation
42.Osteochondrosis:etiology,pathogenesis,classification of neurological
syndromes.Treatment of acute pain in neurological manifestation of
osteochondrosis.
Etiology: (1)Decompensation of trophic systems-disease of
GIT,liver,pancreas (homeostasis diseases) .(2)Local excessive load on spinal
segment( sacralization,lumbalization,narrow spinal canal)
Pathogenesis:-
1st stage : degenerative changes of pulp nuclei develop,destruction of
chondrocytes,pulp loose hydrophilous properties
2nd stage : degenerative changes in fibrous ring,fibrous ring break and cause
disk protrusion
3rd stage : changes in hyaline plates(subchondral sclerosis),hernia like
formation
Neurological syndrome classification
1).Reflex syndromes
2).compressive radicular syndromes
3).Compressive vascular-radicular syndromes (a) acute(transient,strokes) (b)
chronic ischemic myelopathy
Treatment :1.orthopedic,2.Medicines(analgesics,spasmolytics,non steroids)
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43.Causes and types of neurological syndromesof spinal osteochondrosis.
Treatment of pain,vertebrogenic syndrome.
Spinal osteochondrosis-degenerative lesion of cartilage-btwn vertebral disc
associated with reactive changes in neighbouring vertebraes,btwn vertebral
joints and connecting apparatus.
Causes- disease of git,liver,pancrease(homeostasis disease),sacralization,
lumbalization,narrow spinal canal,ages,genetic
Treatment- orthopedic,surgical,sanatorium,medicines(analgesics,
spasmolytics,non-steroids,myorelaxants,vit and biostimulants)
Vertebrogenous syndrome- limitation of mov in lumbarsacral part of spinal
cord and increase pain while mov. Protective training of long back muscles.
Painful paravertebral points,painful vertebral process, scoliosis, symptoms
of spinal cord instability.
44.Neurological syndromes of degenerative disc disease of lumbosacral
region. Reflex syndrome,compression syndromes. Concept of muscular
tonic syndromes and treatment.
Neurological syndrome classification
1).Reflex syndromes(a)lumbago(backache),(2)lumbalgia,(3)lumbar ischalgia
(muscular tonic,neuro dystrophic,autonomic vascular)
2).compressive radicular syndromes
3).Compressive vascular-radicular syndromes (a) acute(transient,strokes) (b)
chronic ischemic myelopathy
Reflex syndrome – occurs at irritation of diff receptors
Compression syndrome – occurs at compression and deformation of radix,
vessels and spinal cord.

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Concept of muscular tonic –clinical pic connected with secondary lesion of
nerves acc to compressive-ischemic type,type of tunnel syndrome result of
spasm and straining
Treatment- orthopedic,surgical,sanatorium,medicines(analgesics,
spasmolytics, non-steroids,myorelaxants,vit and biostimulants)
45.Neurological syndromes of degenerative disc diseases thoracic and
lumbar region.Clinical pic, diff diagnosis, treatment.
Lumbar spondylosis-1)motor manifestation-motor weakness/paralysis in 1
or both limbs,associated with hypotonia and hyporeflexia,affect the muscle
supplied by the affected root 2)sensory manifestation-painful
onset,radicular and to lower limbs,hypothesia/anaesthesia present,affects
superficial and deep sensations.3)autonomic manifestation-
sphincter(sensory atonic bladder,motor atonic bladder and autonomic
bladder) and vasomotor changes and trophic ulcers in L.L
Cervical spondylosis-1)manifestation of root compression,lateral prolapse
a)ant.root compression(localized LMN weakness or paralysis in muscles
supplied by compressed root.b)Post.root comp(pain and paresthesia at
onset,brachial neuralgia,hypothesia/anaesthesia 2)Manifestation of cord
compression,postero-lateral
a)Comp.of pyramidal tracts-weakness,paralysis with
hypertonia,hyperreflexia nelow level of comp. b)Comp.of spino thalamic
tracts-superficial sensory loss below comp.level c)comp.of post.column-
deep sensory loss(sensory ataxia below comp.level)
3)Manifestation of root and cord compression a)upper limb-combined signs
of LMN lesion(wasting muscles) and UMNL (hypertonia,hyperreflexia)
b)lower limb-weakness with signs of UMN lesion
46.Neurological syndromes and degenerative disc diseases in thoracic and
lumbar spine,etiopathogenesis,classification, clinical pic,diagnosis n
treatment in acute period.

27
47.Cervical intervertebral disc disease.Diagnosis and treatment in acute
period.
Cervical spondylosis-1)manifestation of root compression,lateral prolapse
a)ant.root compression(localized LMN weakness or paralysis in muscles
supplied by compressed root.b)Post.root comp(pain and paresthesia at
onset,brachial neuralgia,hypothesia/anaesthesia 2)Manifestation of cord
compression,postero-lateral
a)Comp.of pyramidal tracts-weakness,paralysis with
hypertonia,hyperreflexia nelow level of comp. b)Comp.of spino thalamic
tracts-superficial sensory loss below comp.level c)comp.of post.column-
deep sensory loss(sensory ataxia below comp.level)
3)Manifestation of root and cord compression a)upper limb-combined signs
of LMN lesion(wasting muscles) and UMNL (hypertonia,hyperreflexia)
b)lower limb-weakness with signs of UMN lesion
48.Reasons of dorsalgia(backpain).Complications of spinal osteochondrosis
and their prevention.the principles of treatment acute pain (lumbar
osteochondritis).
Dorsalgia- acute/chronic pain located in the post regions of the thorax ;
lumbosacralregion/adjacent region
Causes- spine disc herniation,degenerative disc disease/ isthmic
spondylolisthesis, osteoarthritis(degenerative joint disease),spinal stenosis,
trauma
Treatment- exercise,acupuncture,behavioral therapy, arch support,
intensive multidisciplinary treatment.
Prevention- avoid excessive exercise and spinal injuries, cartilage dietary
supplements containing chondroitin.
49.Neuritis of the median and ulnar nerve,brachial plexopathy:causes of
dev,major clinical pic,diagnosis.treatment option.

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50.Polyneuropathy syndrome : major clinical manifestation, causes of
dev,add objective diagnostic methods
Etiology: various causes: acquired or inherited.
Acquired-due to systemic disease
Inherited- such as some Charcot-Marie-Tooth disease, polyneuropathy with
optic atrophy, and hereditary neuropathy with liability to pressure palsies.
Idiopathic polyneuropaty is of unknown cause.
Classification of causes: Trauma/injury,Accident/sports-related injuries,
Systemic diseases
C/symptoms: Numbness, burning pain usually at the feet, tingling sensation,
elevated threshold to physical stimuli, decreased reflex such as ankle reflex.
Minimal motor signs.
Diagnosis: the patient has symmetrical, bilateral loss of sense for touch and
pain.
51.Gullain-Barre syndrome:causes n clinical manifestation.Diagnosis n
treatment.
Causes- allergic/autoimmune reaction secondary to a previous and non-
specific virus infection
Clinical pic – marked enlargement of calves,hyperlordosis,decrease tendon
reflex,normal sensation,pt unable to raise eyelids,lagophthalmus, ectropion-
dropping lower lid,inability to abduct left eye.
Diagnosis-(1)CSF-albuminocytologic dissociation, (2)NCS- delayed/absent F
waves,(3) Prognosis-CMAP amplitude,older age,rapid onset (4) antibiotics
Treatment- absolute rest in bed till heart rate reach below 100 bpm, care for
bulbar muscles( neostigmine,tube feeding,freq suction of secretions from
pharynx),care for resp muscle(freq suction to keep patent airway,
tracheostomy),corticosteroids,antibiotics(tetracycline),gamma-globulin n
plasmapharesis,physiotherapy
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52.Facial neuropathy.etiology.major clinical symptoms. Central facial
neuropathy.Treatment in acute phase of facial neuropathy.
Causes-lyme disease,HIV,tumor,sarcoidosis
Clinical symptoms- headache,feeling of tightness in facial area,difficulty
eating, impairment of taste,increase loudness of sound in one ear,sensitivity
to sound.
Treatment- anti-inflammatory drugs(steroids),antiviral drugs( acyclovir), eye
lubricating drops to protect eye if eye doesn’t close completely.
Central facial neuropathy- paralysis/paresis of lower half of one side of
face,results from damage to UMN of facial nerve.
53.Trigerminal neuralgia :causes,types,major clinical manifestations.
Opportunity for medical n surgical treatment.
Aetio-unknown,predisposing factors-root comp. by tumor or blood vessels
in cerebello-pontine angle,diabetes and alcoholism
Symp-severe, paroxysmal bursts of pain in one or more branches of the
trigeminal nerve; often induced by touching trigger points in or about the
mouth.
Affects mid.age,females more common.in between attacks,patient free.
T(x)-Medical-Carbamezepine,analgesics.Surgical-microvascular
decompression,section of affected sensory root,inject alcohol in nerve
ganglion
54.Clinical pic and treatment of facial neuropathy in acute period
Clinical symptoms- headache,feeling of tightness in facial area,difficulty
eating, impairment of taste,increase loudness of sound in one ear,sensitivity
to sound.
Treatment- anti-inflammatory drugs(steroids),antiviral drugs( acyclovir), eye
lubricating drops to protect eye if eye doesn’t close completely.

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55.Meningitis of brain and spinal cord.Meningeal syndrome,its clinical
pic.CSF fluid in health and in disease.
Csf analysis: for acute pyogenic or purulent meningitis, there is contained
mainly polymorph due to infection of meninges.
Subacute lymphocytic meningitis: csf contain mainly lymphocytes that is due
to infection by m/o not causing pus formation-viruses, bacteria and fungal.
Symptoms: acute onset with sudden chills, headache, vomiting, back ache,
blurring vision, stiff of neck and prostration.
In CSF examination: increased intracranial pressure, pus in CSF, cell
polymorphism, protein increase, chlorides decrease
56.Meningitis:etiology,pathogenesis,classification,main clinical pic of
meningitis.changes in csf.Clinical n pathological features n diagnosis of TB
meningitis
Etiology- Inflammation of meninges of brain due to viral or fungal or
bacterial infection or complication of lumbar drain placement or due to
intracerebral bleeding, or due to drug allergy, cancer and inflammation.
Classification – 1.acute pyogenic(purulent)meningitis (meningococci,
streptococci,pneumococci,hemophilus influenza), 2.Subacute lymphocytes
meningitis( virus,bacteria,fungi)
Csf analysis: for acute pyogenic or purulent meningitis, there is contained
mainly polymorph due to infection of meninges.
Subacute lymphocytic meningitis: csf contain mainly lymphocytes that is due
to infection by m/o not causing pus formation-viruses, bacteria and fungal.
Symptoms: acute onset with sudden chills, headache, vomiting, back ache,
blurring vision, stiff of neck and prostration.
In CSF examination: increased intracranial pressure, pus in CSF, cell
polymorphism, protein increase, chlorides decrease
Treatment- rifampicin,streptomycin,isonicotinic acid hydrazide
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57.Purulent meningitis:cerebral epidemic meningococcal meningitis
,secondary purulent meningitis,causes and underlying mech of dev,clinical
change in csf.principles of treatment.
Etiology-viral n bacterial infection mainly such as N.meningitis,virus
associated with mumps
Pathogenesis-Pathogenic agent enter the organism n infect the
brain,causing the inflammation of meninges of brain n CSF surrounding
brain n spinal cord.
Clinical pic- malaise,fever,headache,nausea,pleocytosis in CSF,vomiting,stiff
neck,irritable,drowsiness,photosensitive,delirium,seizure,coma
Fluid change- pus present in the CSF,change of colour green yellowish
Treatment-antibiotic treatment,interferon if applicable,surgery n lubar
drainage
58.The syndrome of meningeal irritation: causes n mech of dev, main
meningeal symptoms.analysis of normal CSF.
Csf analysis: for acute pyogenic or purulent meningitis, there is contained
mainly polymorph due to infection of meninges.
Subacute lymphocytic meningitis: csf contain mainly lymphocytes that is due
to infection by m/o not causing pus formation-viruses, bacteria and fungal.
Symptoms: acute onset with sudden chills, headache, vomiting, back ache,
blurring vision, stiff of neck and prostration.
In CSF examination: increased intracranial pressure, pus in CSF, cell
polymorphism, protein increase, chlorides decrease

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59.Viral encephalitis(herpes,influenza).Main clinical manifestation.lab n
add methods of studyof viral encephalitis.Main medication of treatment of
herpetic encephalitis
C/pic: fever, headache, mental states and behavioural changes with or
without focal signs localizing to temporal lobe. Seizures within 1 week of
initial symptoms, hemiparesis, dysphasic, papilledema (blurry vision and
postural changes)
Differential diagnosis: Use CT scan to confirm this.
Treatment: interferon, symptomatic treatment
60.Encephalitis:causes,classification,main syndrome.Diagnosis n treatment
of encephalitis.consequences of encephalitis.
Encephalitis is inflammation of brain substances, and if spinal cord is
involved-it is encephalomyelitis.
Etiology&Classification: Primary encephalitis caused by neurotrophicviruses
and pantropic viruses that attack CNS; Secondary encephalitis caused by
viruses, bacteria and parasites that incvade viscera outside brain but later
able to attack CNS.
C/symptoms: fever, headache, myalgia, dizziness, involves portions of the
temporal lobe and frontal lobes causing hemorrhagic necrosis,intranuclear
eosinophilic inclusion in neurons and glial cells
Dx: clinical symptoms and signs.
Tx: antiviral agent Acyclovir (Zovirax), support treatment

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61.Neurosyphilis: the pathogenesis of neurological symptoms.Clinical
forms.
It is due to affection of NS by T. pallidum which affect mainly meninges,
vessels and parenchyma. Mainly divided into Meningeal syphilis, Vascular
Syphilis, and Parenchymatous Syphilis.
Diagnose: Examination of CSF revealed increased pressure,lymphocytosis,
increase protein, decrease glucose. Penicillin is mainly by Penicillin G,
erythromycin, symptomatic treatment and physiotherapy
62.Secondary NeuroAIDS:causes n mech of dev,clinical variants,the
possibility of prevention and treatment
Etiology: 1)opportunistic infections(toxoplasma gondii,herpes
zoster,cryptogenic meningitis,neurosyphilis),2)tumor,3)drug related
complications
Clinical variant: acute and chronic HIV infection
Clinical features:Primary and Secondary effect of nervous system,condition
affecting CNS( CNS toxoplasmosis,primary CNS lymphoma,HIV
encephalopathy,Meningitis,Neurosyphilis,TB meningitis,Myelopathy) and
cond affecting PNS (distal sensory polyneuropathy,demyelinating
Polyneuropathy, mononeuritis multiplex, polyradiculopathy, myopathy)
Treatment- Highly active anti-retroviral drugs,painrelief(analgesics,anti-
epileptics),anti-inflammatory(corticosteroids,plasmopheresis),antidementia
drugs to relieve confusion and slow mental decline,antibiotics

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63.NeuroHIV:causes of dev.Clinical forms of primary and secondary
neuroHIV.Prevention of HIV infection.
Etiology – HIV causing immune dysfunctions that spread by hematogenic
way to CNS n PNS
Clinical forms:Acute and chronic HIV infection
Neuro pic: transient meningoencephalitis, myelopathy , peripheral
neuropathy, and dementia.
Tx: No real cure. Treatment with pyrimethamine and clindamycine or
sulfadiazine for 6 months.
Px: Avoid needle sharing, avoid unprotected sexual intercourse.
64.Vegetative dystonia syndrome:causes,types,clinical pics,vegetative
crisis, types n capabilities of their treatment
Causes- disorders of autonomic regulation,Parkinsonism’s disease
Vegetative crisis : paroxysmal non-epileptic nature of the state which appear
polymorphic vegetative disorders associated with the activation of central
vegetative structure
Types-Somatic,endocrine,neurological,psychiatric
Clinical pic – Heart palpitation, chills,sweating,headache,dizziness,nausea,
impaired func of intestine,irritability,variability in moods,fear and insomnia
Treatment :antidepressants,benzodiazepines,B-blockers,a-adrenergic
blockers

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65.Vegetative crisis,causes,types.Emergency care n prevention.
Vegetative crisis : paroxysmal non-epileptic nature of the state which appear
polymorphic vegetative disorders associated with the activation of central
vegetative structure
Types-Somatic,endocrine,neurological,psychiatric
Treatment :antidepressants,benzodiazepines,B-blockers,a-adrenergic
blockers
66.Syringomyelia:causes and neurological clinical symptoms
It is slowly enlarging of cervical cord , forming cleft-like cavity in the inner
portion of spinal cord, starts at cervical cord, destroy grey and white matter.
Syringomyelia is associated with Chiari type I malformations, spina bifida,
hydrocephalus and spinal cord tumors.
Symptoms: Wasting and weakness of small muscles of hand and forearm,
diminished tone and deep tendon reflexes, loss of pain and temperature
sensation.
67.Syringomyelia:aetiopathogenesis, morphology,clinical pic, basic
principles of treatment.
It is slowly enlarging of cervical cord , forming cleft-like cavity in the inner
portion of spinal cord, starts at cervical cord, destroy grey and white matter.
Syringomyelia is associated with Chiari type I malformations, spina bifida,
hydrocephalus and spinal cord tumors.
Symptoms: Wasting and weakness of small muscles of hand and forearm,
diminished tone and deep tendon reflexes, loss of pain and temperature
sensation.
Treatment: Surgically direct decompression and drainage

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68.Hereditary-degenerative disease of nervous syst:cerebellar ataxia of
Pierre Marie(causes n clinical manifestation)
Causes-autosomal dominant disease
Clinical pic –increase reflexes and muscle tone,eye movement disorders,
mental,memory and emotional disorders,gait disorders,disorders of
coordination,nystagmus,dysarthria
69.Hepatoventricular degeneration(Wilson’s disease):etiopathogenesis,
main clinical pic,Diagnosis n treatment
Hereditary disorder with copper accumulation in liver and CNS. Good
prognosis.Signs: liver disease, can even affect children; tremor, dysphagia,
dyskinesia, dysarthria, dystonia, purposeless movements.
Diagnosed by measuring copper level in serum, and treated by
penicillamine for lifelong treatment.
70.Inherited neurodegenerative diseases:family spastic
paralysis(Strumpel) :etiopathogenesis,mainclinical manifestations.
Causes: genetically recessive
Clinical pic:lower spastic paraplegia with increase muscle tone,high stretch
reflex,pathological reflex
71.Amylotrophic lateral sclerosis:etiopathogenesis,anatomy, clinical
course, prognosis
Fatal degenerative disorder of upper and lower motor neurons.
Etiology: mainly defect at gene (hereditary) or non-hereditary (unclear)
C/symptoms: muscle weakness, upper limb weakness more than lower
limb’s, dysarthria, slow speech rate, reduced voice quality, dysphagia,
muscle wasting and weakness, dyspnea, morning headache, sleep disorder
and respiratory failure can occur.
Duration: 3-4 years of survival rates Prognosis: Bad

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72.Parkinson’s disease:etiology,diagnosis criteria,clinical features of drug
therapy,neurostimulation therapy
Etio: Paralysis agitans post-encephalitic and atherosclerosss, idiopathic,
symptomatic such as inflammatory, vascular, toxic, neoplastic and
traumatic.
Dx: Assess the CPx
c/pic: tremors,rigidity, loss of emotional and associative movement resulting
in immobile face (mask face), monotonous speech, loss of swinging of arm
during walking, oculogyricrisis,obesity diabetes insipidus,
sialorrhea,amenorrhea. Pyramidal signs.
Treatment: anticholinergic drugs,L-dopa,L-dopa+Carbi-dopa,Dopamine
agonists and amantadine hydrochloride
Surgery-pallidectomy/thalamotomy
73.Hereditary neuromuscular disease:causes n classification,Amyotrophy
and its type.Neural amyotrophy of Charcot-Marie-Tooth syndrome:
etiopathogenesis,clinical features,diagnosis,treatment options
Classification
1)Progressive muscular dystrophy(Duschenne muscular dystrophy,Late
becker muscular dystrophy,Family visceral myopathy,Fasciopapulohumeral
muscular dystrophy Landuzi-Degerina,Scapulo peroneal form of
davidenkova)
2)Amytrophy(result of peripheral neuron lesion)- Spinal amyotrophy of
Werding-Hoffman,Paroxysmal amyotrophy of Kukelberg-Welander,Kennedy
amyotrophy,Charcot-Marie-Tooth disease,Hypertropic)
Charcot-Marie-Tooth syndrome
Clinical pic-(1)Demyelination of peripheral nerve(foot drop and stoppage
gait,StorkLeg deformity,scoliosis,high pedal arches/club feet,tremor),
(2)Neuronal loss of ant horn ceels n post nerve root ganglion neurons in

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lumbar n sacral segments(muscle weakness n wasting confined at
foot,Stockingand glove sensory impairment is minimal/absent)
(3)Ant horn cell involvement with secondary axonal loss n demyelination
of motor fibres
Diagnosis- lumbar punc(CSF protein content is elevated),nerve conduction
velocities ,nerve biopsy
Treatment – non specific, braces for correction of foot-drop n hand
deformities can b helped ambulatory by splinting/orthopedic procedures
74.Multiple sclerosis:clinical pic,diagnosis,treatment
Sympt:fatigue,motor weakness and spasticity,altered sensation such as
numbness,pins and needles,pain,trigeminal neuralgia,dysaesthesia,bladder
urge incontinence,inconstipation,visual defects on
exercise,diplopia,nystagmus,ataxia,dementia,vertigo,depression,rarely
euphoria
Dx:CSF evoke potentials,Ig G index Increase,MRI,antibodies to
myelin,MOG,NBP
Tx:interferon 1B and 1 alpha,methylprednisolone,palliation,spasticity

75.Multiple sclerosis:etiology,pathogenesis,clinical pic,diagnosis,treatment

Etio:Hereditary
Pathog: common demyelinating disorder of the central nervous system,
causing patches of sclerosis (plaques) in the brain and spinal cord
Sympt:fatigue,motor weakness and spasticity,altered sensation such as
numbness,pins and needles,pain,trigeminal neuralgia,dysaesthesia,bladder
urge incontinence,inconstipation,visual defects on
exercise,diplopia,nystagmus,ataxia,dementia,vertigo,depression,rarely
euphoria

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Dx:CSF evoke potentials,Ig G index Increase,MRI,antibodies to
myelin,MOG,NBP
Tx:interferon 1B and 1 alpha,methylprednisolone,palliation,spasticity
76.Tension headache: causes n dev of basic principles of treatment
Causes-muscle contraction in head and neck region,stress,cold
temp,foods,alcohol,eye strain,dry eyes,fatigue,smoking,poor postures,sinus
infection
Treatment-
Ibuprofen/aspirin,indomethacin,ketorolac,naproxen,opiates,acetaminophen
Symptoms: dull head pain,pressure around forehead,tenderness around
forehead n scalp
77.Progressive muscular dystrophy:causes,classification.primary
progressive muscular dystrophy(Duschenne).Diagnosis n treatment.
Etiology: abnormal growth of muscle with wasting and weakening. Caused
by mutstion of dystrophin. Classification: Congenital MD, Distal MD,
Duchenne MD, Emery-Dreifuss MD, Facioscapulohumeral MD, Limb girdle
MD, Oculopharyngeal MD
1 progressive MD: weakness, m-hypertrophy, musculoskeletal, loss of
ambulation.
Dx: Serum Ck level is eleated (10X normal) and muscle biopsy
(hypercontracted muscle, no dystrophin)
Treatment: no cure, no effective drugs. Supportive: splint, physiothereapy,
orthopaedic surgey, braces

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78.Myasthenia gravis:etiology,pathogenesis,major clinical
manifestation,diagnosis,treatment
MG-neuromuscular disorder with characterized weakness and skeletal
muscle fatiguability.
Etiology: dec. no. of acetylcholine receptors at NM jxn and also autoimmune
attack against own NM jxn.
Pathogenesis: infection and systemic disorder and autoimmune attack
against own NM jxn, with dec. no. of acetylcholine receptors causing skeletal
muscle fatiguability, weakness.
C/pic: Weakness, skeletal muscle fatiguability, ptosis/diplopia, weakness at
chewing, palate, at swallowing, at facial –seen as “snarling smile”
79.Myasthenia and Cholinergic crises :cause of dev, diff diagnosis,
treatment
Myasthenia crisis -Exacerbation/worsening of myasthenia with respiratory
muscle impairment, and patients need artificial ventilation, appears due to
surgery/respiratory infection and has high risk to infection.Artificial
ventilation and thymectomy are indicated if thymoma is present.
Treatment- plasmapheresis,corticosteroids,haloperidolum at excitation
Cholinergic crisis- manifested by Excessive salivation, confusion, lacrimation,
pallor, miosis and collapse of the patient.
Treatment- atropinum

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80.Epilepsy.Epileptic syndrome.Classification.Basic principle of drug
treatment
Disorders characterized by recurrent transient attack of somatic
psychoautonomic clinical manifestation assoc. with EEG changes plus
disturbance of consciousness.
Etiology: idiopathic, symptomatic divided into local causes in the brain
(cong, traumatic, inflammatory, neoplastic and deg) and general causes with
2ndary effects on the brain (toxic, metabolic, endocrinal, cvs, nutritional,
physical, iatrogenic and hysterical)
Classif. Of attack: first partial seizures (elementary, complex symptom and
with secondary generalization); primary gen. seizure (can be absences, tonic
clonic, myoclonic jerk, atonic and akinetic)
Classification: local n general
Tx: moderate patient’s activity, avoid precipitating factors, stop alcohol
intake and ketogenic diet.
Specific: antiepileptic drugs-barbiturates, clonazepam, carbamazepine

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81.Epilepsy:def,causes,classification of epileptic seizures n epilepsies
diagnosis.treatment
Epilepsy is a disorder characterized by occurrence of atleast 2 unprovoked
seizures
Classification: local n general
Classif. Of attack: first partial seizures (elementary, complex symptom and
with secondary generalization); primary gen. seizure (can be absences, tonic
clonic, myoclonic jerk, atonic and akinetic)
Causes :brain damage from birth injuries,head injuries,stroke,brain
tumors,alcoholism,metabolic abnormalities,genetic cond present at birth,
idiopathic
Diagnosis: MRI,CTscan,EEG
Treatment : antiepileptic drugs,anticonvulsants
Surgery :ant temporal lobectomy,extratemporal resection,functional
hemispherotomy,corpus colostomy,Multiple subpial transaction
82.Nervous system in influence of extreme factors,overheating,
hypothermia,electrical shock
83.Neuroses:definition,causes,clinical forms
Def:is a class of functional mental disorders involving distress but neither
delusion nor hallucination
Causes – genetic factors
Clinical forms : anxiety neurosis,depressive neurosis,obsessive-
compulsion,somatization,compensation,post-traumatic stress disorder
84.Identifying symptoms of focal brain lesions in comatose pt
CT scan ,MRI,pupils,corneal reflex,examination of spine n skull,test for neck
stiffness,angiography,ultrasound.Monitoring of vital signs n lab tests

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85.Causes n mech of perinatal pathology
86.Brain concussion : clinical,morphological changes.diff diagnosis of
concussion n contusion of brain
Brain concussion- type of traumatic brain injury that is caused by blow to
head/body,a fall/another injury that jars/shakes the brain inside skull.
Clinical – passing out/forgetting what happened b4 injury
Morphological changes- bruises of brain
Diff btwn contusion n concussion
-contussion are localized,concussion are widespread
-contussion are macroscopic,concussion are microscopic
87.Bruising of brain: major clinical manifestations,diff diagnosis of
contusion n concussion in clinical symptoms n CTscan.
Clinical pic- headache,confusion,sleepiness,dizziness,loss of
consciousness,nausea n vomiting,seizures n diff in coordination n mov
Morphological change- edema,increase ICP,intracerebral
hemorrhage,subdural hematoma
Diff btwn contusion n concussion
-contussion are localized,concussion are widespread
-contussion are macroscopic,concussion are microscopic

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88.Migrain- etiology,pathogenesis,classification.clinical pic,treatment
Etio: hereditary, female:male=2:1, onset during puberty, more in urban
inhabitants (stress), more in obsessive perfectionist person, precipitated by
mental/physical exhaustion, menses or certain diet.
Pathogenesis: it is paroxysmal often familial disorder characterized by
unilateral intense throbbing headache associated with nausea and vomiting,
maybe preceded by visual sensory or motor sensation. Cerebral oligemia
leading to aura followed by cerebral and extracranial hyperemia leading to
headache.
Classification: idiopathic or acquired
c/pic: visual aura (visual for 20-30minute before unilateral throbbing
headache), aura with no headache, episodic headache (often pre-menstrual
severe headache)
tx: avoid precipitating factors (contraceptive, cheese, caffeine,
anxiety,alcohol, travel,exercise); corticosteroid, immunosuppressants, well-
balanced diet with Vits B, symptomatic treatment and physiotherapy.
89.Modern classification of closed head injury
Primary- direct trauma(epidural hematoma,subdural hematoma,
subarachnoid hemorrhage)
Secondary- hypotension,hypoxia,acidosis,edema
90.Hydrocephalus :reasons,types,diagnosis,treatment
Medial cond in which there is an abnormal accumulation of CSF in brain
Symptoms-headache,vomiting n nausea,pappilloedema,sleepiness,coma,
increase ICP, slow growth, urinary incontinence,muscle spasm,irritability
Type – communicating(non-obstructive) n non-communicating(obstructive)
Causes- congenital n acquire
Tx:surgical(cerebral shunts) n obstructive(endoscopy 3rd ventriculostomy)
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Good luck !!!
By darshni

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