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Q1.

Flaccid paresis
Mech:
It occurs as a result of interruption of motor unit system along its course (ant horns or roots, plexus or
peripheral nerves.)
It is characterized by:
 Decreased overall strength
 Hypotonia/atony of muscle
 Hyporeflexia/ areflexia
 Neurogenic muscle deterioration
 Fasciculations of muscles
If damage is in the plexus or peripheral nerve, it is acc by sensory loss.
Diagnostical variants:
Radicular syndromes
Peripheral nerve lesion (Wrist drop <radial nerve>, claw hand <ulnar nerve>)
Plexus damage
Sp cord damage
Q2. Cluster headache
It is thus named because of its seasonal nature, is common in men and manifests as severe, stabbing,
periorbital pain, unilaterally. Accompanied by ipsilateral tearing, blood shot eyes, nasal congestion and
rhinorrhea, partial Horner’s. Unlike patients with migraine CH pts prefer to keep moving/pace.
It may either be episodic or chronic
Duration: 30mins-3hrs, esp. at night
Rx: divided into
Symptomatic Prophylactic

O2 mask steroids alternate approach


Sumatriptan 6mg subcut

Oral tablets(slower) Verapamil


Sumatriptan Methylsergide
Zolmitriptan
Rizatriptan
Ergotamine
sumatriptin nasal spray

In cases of chronic cluster headache (i.e. cycle of headache is more than 6mnths without remission);
Lithium is reported to be effective. Side effects include confusions, drowsiness, seizures, thirst and
rashes.
Combination therapy is also beneficiary. Surgical treatment is indicated in patients with cluster headache
that is unresponsive to treatment. Trigeminal nerve surgery is carried out:
Gangliotomy or pre-ganglionic nerve- root section. These provide numbness tho pts still feel cluster
headache sensations, pain is absent.

Psychogenic headache:
Unlike the name suggests, the patient is not psychotic. The symptoms are constant and localized in a
discrete area.
• Pain which can be pointed at by a finger
• Sensations are described by delusional overtones. “ I feel lump on my skull”, “ my bones are
rotting”
• Negative tests don’t reassure pt
• Willing undergo investigations.
Q3. Classification of hereditary neurological Dx
1) Single gene disorders
 Autosomal dominant: Huntington’s disease
 Autosomal recessive: cystic fibrosis
 X –linked traits: Duchenne’s syndrome
 X-dominant: phosphate diabetes
2) Chromosome anomalies 3) multifactoral disorders
 Structural cancer
Deletion rheumatism
Microdeletion atherosclerosis
Duplication hypertension
Inversion
Iso chromosome
Translocation
Ring shaped
 Numerical
Aneuploidy (Down’s)
Polyploidy
4. PHM progressive her myopathy
Duchenne
Myasthenia
5. Neurohereditry amyotrophies
ALS
Syringomyelosis
6. Pathology of extra pyramidal system
Q4. Spastic paralysis
This is evidence of involvement in damage of CNS structures (brain and sp cord) and occurs as result of
pyramidal tract lesion as well as extrapyramidal. Spastic palsies are characterized by presence of spastic
finger/toe signs (e.g. Babinski’s), absence of skin reflexes e.g. abdominal and cremasteric reflexes. If the
lesion is after the decussation there is ipsilateral hemiplegia and if the lesion is bilateral, tetraplegia.
Gen signs
 Decreased strength and loss of subtle mvmnt
 Hypertonia
 Hyperreflexia (Exaggerated proprioceptive reflexes)
 Decr or loss of extraproprioceptive reflexes
 Presence of pathological reflexes
 No degenerative atrophy
Diagnostic variants:
• Subcortical lesion: contralateral monoparesis of hand
• Internal capsule: spastic contralateral hemiplegia
• Peduncles: same as abv + Oculomotor paralysis
• Pons: contralateral hemiplegia + ipsilateral paralysis of trigeminal etc
• Pyramidal lesion: contralateral, flaccid hemiparesis
• Cervical: ipsilateral, spastic hemiplegia
• Thoracic: spastic, ipsilateral monoplegia of leg( if damage is bilateral paraplegia)
• Ant root: flaccid, ipsilateral plegia
• Alternating syndrome: if lesion involves decussation.
Q5. Meningococcal infection
Acute inflammation of subarachnoid space and meninges characterized by presence of PMN in CSF.
Infection may be direct (sinusitis) or indirect (blood)
Etiology
Neisseria meningitis
Mixed infections may occur after head injury, mastoiditis or after lumber puncture.
The blood brain barrier limits host defenses thus promoting bacterial multiplication. Purulent exudate
extends thru out subarachnoid space. The pia mater normally protects against brain abscess formation.
Vascular structures may also be affected producing vasculitis: arteritis, venous thromboembolitis=
infarction.
Clinical
TRIAD: Fever, headache, neck stiffness are the classical picture.
 Meningitic symptoms: severe fronto-occipital headache, stiff neck, photophobia
 Meningitic signs: +ve kernig’s symptom, neck stiffness
 Systemic signs: pupuric or petechial skin rash, high fever
 Neurological signs:
Impaired consciousness
Seizures (focal& generalized)
CN signs
Direct cochlear involvement (sensorineural deafness)
Focal neurological signs (hemiparesis, dysphasia, and hemianopia)
 Non neurological signs:
Inappropriate ADH
DIC
Arthritis
Endocarditis
Diagnostics
1. CT scan : to exclude intracranial mass
2. Lumber puncture
3. CSF exam
 Protein
 Decreased glucose levels
 Culture(gram –ve cocci)
 Color change (yellowish)
4. Blood analysis: neutrophillic leukocytosis
5. X-ray to detect source of infection e.g. Chest- pneumonia, Skull- fracture
Rx and prophylaxis
Once meningitis is suspected Rx is started IMMEDIATELY. ABiotics must penetrate BB- barrier.
Initial blind therapy: ampicillin/ penicillin G + cephalosporin (+ aminoglycoside in neonates)
Thereafter according to causative agent. Duration of Rx is 1wk
Remove any source of infection, and in the critically ill supportive therapy.
Q6. Myasthenia gravis, Myasthenia syndrome
This is a disorder in neuromuscular transmission resulting in fatigue of skeletal muscles esp. ocular,
oropharygeal and facial musc. When edrophonium Cl is introduced there is drastic muscle strength
increase
The forms: Neonatal, congenital, drug induced autoimmune forms.
Clinical features include:
 Class 1- only ocular muscles
 Class 2- mild generalized weakness
 Class 3- moderate generalized and mild to moderate ocular-bulbar weakness
 Class 4- severe gen and O-B weakness
 Class 5- myasthenic crisis( resp failure etc)
Diplopia & ptosis
Dysarthria, Dysphagia, jaw mus weakness + fatigue of palate musc= myasthenic voice
Strengthless, cannot walk.
Myasthenic syndrome: a disorder of neuromuscular jxn caused by AB dev against Ca++ channels.
It is characterized by
 Primary weakness of lower then upper limbs
 Fatigue but unlike M.G the ocular and bulbar mus are unaffected.
 Reduced tendon reflexes
 Atrophy of affected musc
 Cholinergic dysfunction (impotence, excessive sweating, and xerostomia).
 Anti cholinesterases don’t relieve muscle weakness.
Emergency cases (myasthenic crisis & cholinergic crisis)
Primary care includes:
 ID and treat primary cause e.g. infection, drug overdose.
 Improve ventilation(intubate, improve posture as required)
Specific Rx:
 Neostigmine(anticholinesterase) IV 8-12 mg/24hrs
 Atropine(to counteract cholinergic effects)
 Prednisolone 100mg daily
 Plasmapheresis or IVIG(immunoglobulin G, IV)
Management:
Main aim is to restore or maintain breathing:
1. clear airway
2. sit pt at 450
3. Give nasal O2, and intubate and ventilate for as long as required.
Q7. Brown-Sequard syndrome
Occurs in cases of partial/ unilateral lesion of the spinal cord, e.g. in cases of tumors. Complete
hemisection is rare.
 Motor deficit: dragging leg and in higher lesions (cervical) weakness of finger
mvmnts on side of lesion.
 Upper motor neuron signs (esp. in side of lesion): extensors of arms and flexors in
legs paralysis, increased reflexes, increased tone and extensor plantar response. i.e.
ipsilateral spastic paralysis below level of lesion
 Sensory deficit: numbness on side of lesion and contralateral dyaesthesia i.e. joint
position sense and touch localization is impaired ipsilaterally while pain and temp
sensation is impaired contralaterally.
Q8. Sciatic nerve neuropathy
It is formed by union of the common peroneal and tibial nerves. It passes through the greater sciatic
foramen and in the popliteal fossa splits to form its constituent nerves. The nerve descends btwn the
ischial tuberosity and the greater trochanter (femur). It innervates the hamstring mus of the thigh (semi
tendinous, membranous and biceps femoris)
Causes of damage:
 Hip dislocation
 Penetrating injuries
 Incorrect IM injections
 Entrapment
 Systemic causes( Diabetes mellitus, sarcoidosis)
Symptoms:
Muscle weakness
Loss of knee flexion
Distal foot and leg muscle weakness
Ankle reflex is absent
Sensory loss in outer leg.
Rx:
Treatment of primary cause
Physiotherapy
Knee brace
Q9.Modes of inheritance
Autosomal dominant:
Autosomal recessive:
Sex-linked:
Q10. Alternating paralysis in mesencephalon lesion
Mesencephalon (midbrain) consists of 4 parts:
 Tectum
 Tegmentum
 Sub nigra
 Cerebral peduncles
In case of lesion involving the decussation of pyramidal tracts an alternating spastic paralysis develops.
The fibres of the tracts cross at the decussation therefore, in case of a lesion half the fibres which crossed
innervate one side each, and one limb on each side is paralysed.
• Lesion of Oculomotor nerve: Opthalmoplegia
• Lesion of Trochlear nerve: strabismus(cross eyedness), downward Diplopia, Nystagmus,
Notangelic symptoms: choreic hyperkinesia, paralysis of extremities, disbalance, cerebellar distress.
Parino syndrome: vertical stare paresis, abs of convergence, two sided ptosis
Red nucleus: intentional hemi tremor, hemi hyperkinesia
Clod (inf red nuc): ptosis, divergence strabismus, ipsilateral midriasis, intentional hemi tremor,
hypomyotnia contralaterally
Fua (sup red nuc): same as red nuc.
Substantia nigra: hypermyotonia, akinetic rigidity contralaterally
Tegmentum: ipsilateral; ataxia, Claude- Bernard syndrome, tremor, myoclonia. Contralateral
hemanesthesia and colliculi reflex abs
Weber syndrome: flaccid paresis of CN III ipsilateral with hemiplegia contralateral side
Benedict’s syndrome: paralysis of CN III; ipsilateral ptosis, divergence strabismus. Contralateral; atheoid,
intentional tremor
Q11. Poliomyelitis
An acute viral infection affecting the ant horn cells of spinal cord and the motor nuclei of the brainstem
Etiology:
Polio virus, an RNA containing enterovirus. 3 strains exist (coxsackie and echovirus). Fecal oral
transmission, 5-35 days incubation period.
Clinical picture:
Stages
1. Preparalytic: fever, sweating, malaise, headache, GIT upset. This stage may improve or progress.
2. Severe headache, back and limb pain, mus tenderness, meningism, may improve or progress to
paralytic stage.
3. Paralytic:
Spinal form Brainstem form
Mus fasciculation pharyngeal, facial, laryngeal, lingual mus weakness
Pain increases cardiac & resp mus involvement
Paralysis develops
Resp mus involvement
Diagnosis:
Feces
Nasopharyngeal secretions
CSF examination (polymorphs and lymphocytes incr, protein elevated, norm glucose) + Clinical picture
are enuf to confirm diagnosis.
Serological tests and virus isolation for later confirmation.
Exclude:
 Acute meningitis (during meningial stage)
 Guillian- Barre syndrome( paralytic stage)
Rx and prophylaxis:
Bed rest with well monitored fluid balance
Ventilation
Physiotherapy and splints in case of limb deformities
Sabin and Salk vaccinations are available
Clinical forms:
1. sub-clinical + resultant immunity
2. mild+ resultant immunity
3. meningism without paralysis(pre paralytic+ ri)
4. meningism with paralysis( paralytic + ri)
Post-polio syndrome: years after og Dx; malaise, fatigue, myalgia
Q12. Progressive myopathies
Erb-Goldflam Dx
Becker’s dystrophy
Dejenrine’s dystrophy
Duchenne’s dystrophy:
X-linked recessive disorder affecting boys
Clinical:
 delayed motor dev
 clumsiness( 3-5 yrs)
 waddling gait(glutei mus involvement)
 sway back posture
 Gower’s sign(difficulty in rising, child “climbs up” himself to get up)
 Kyphosis in later stages(age 20)
Pseudohypertrophy usually occurs, with enlarged, rubbery hard gastrocnemius muscle, quadriceps and
deltoid may also be affected.
Investigation:
Musc enzyme creatine kinase
ECG
EMG
Musc biopsy
Tx
Orthopedic Tenotomy may prolong mobility
Steroids
Intrauterine diagnosis+ abortion
Q13. Pallidar system and its lesion. Parkinson’s Dx.
The pallidum is a gray structure that develops from the 3rd ventricle and is related to the subthalamic
nucleus. It is covered by the putamen laterally and together they are known as the lentiform nucleus. It
also forms part of the extrapyramidal system. Formerly it was known as the paleostriatum and acted as
the center of lowest order of the brain.
Lesion produces:
Hypokinesia-hypertonia syndrome (Parkinson’s Dx, paralysis agitans)
 Akinesia: hypomimia, only eyes move; head doesn’t, speech becums monotonous, body
is stiff, arms don’t swing when walking
 Rigor: cog wheel phenomenon upon attempts to relax limbs, head drop test (head falls
slowly back when raised). No pathological reflexes
 Tremor: pin rolling tremor that disappears with intention.
Types of tremor: parkinsonian, intention, posture/static, essential
Bilateral lesion is known to produce severe consciousness disorders and delirium or amentia.
Hyperkinesia-hypotonia syndrome
 Athetosis: slow, writhing, worm-like involuntary mvmnts. Grimacing and abnorm tongue
mvmnts, spasmodic outburst of laughing or crying
 Chorea: short, fast involuntary jerks in single muscles randomly. Characteristic decrease
in tone
 Spasmodic torticollis: tonic disorder of neck muscles= slow involuntary turning of head
 Torsion dystonia: extensive turning and twisting mvmnts of the trunk and proximities. Px
may not be able to stand or walk.
*Q14. Vascular encephalopathy
Q15. Progressive Dx of peripheral nerves. Charko’s neural amyotrophia & Hoffman’s
amyotrophia.
The cause of motor neuron disorder is unknown but it is linked with: ageing, viruses, toxins, mineral
deficiency, genes, and excitotoxins.
Clinical features:
 Frontal dementia
 Pseudobulbar palsy
 Progressive bulbar palsy(tongue has atrophy, fasciculations, looks wrinkled and wasted,
gag and jaw reflex are absent)
 Corticospinal involvement(brisk reflexes, incr tone)
 Progressive mus atrophy(weakness, atrophy and fasciculations=skeleton hand)
Ultimately resp mus become involved= death.
Rx is symptomatic:
Spasticity; balcofen & tizanidine
Physiotherapy
Riluzone
Hoffman’s infantile amyotrophia:
Autosomal recessive
Characterized by:
 Reduced fetal mvmnts during gestation
 Weakness and hypotonia at birth
 Hypotonic posture(arms and legs abducted and externally rotated)
 Contractures, wasting and fasciculations
 Death by 18 months
Q16.Bulbar and pseudobulbar paralysis
Bulbar Pseudobulbar

Damage to nuclei or trunks of CN IX-XII Lesion of corticonuclear tracts of CNIX-XII


May be uni or bilateral Always BILATERAL
Dysphagia, dysarthria, dysphonia Same as bulbar
Paralysis is flaccid: with atrophy & Spastic paralysis, without atrophy
fasciculations of tongue
Nystagmus, ptosis and facial paresis Forced laughter and crying
No gag reflex Oral automatism
Exaggerated gag reflex
NB: bilateral damage of CN X…GONNER!!
Tests:
1. Oral automatism
• Irritate thenar= chin contraction
• Naso labial test gives kissing reflex
Q17. Multiple sclerosis
Classification by clinical course:
1. Relapsing- remitting
2. 2o progressive ( short remission)
3. 1o progressive
4. benign
Criteria:
2 or more lesions
More than 1 attack
Pathogenesis:
• Immune deficiency
• Viruses
• Genetic factors
It is multifactoral
Scattered lesions…determination of age of lesion:
Recent:
Late:
Astrocyte proliferation in area
Old:
Lesion is clearly demarcated + abs of all cells
Clinical:
Onset age 20-25yrs
Lethargy, headache, depression
1. Sensory disorder
 Neuritis( shift of central scotoma)
 Trigeminal neuralgia
 Pupillary escape
 Disturbances of ocular mvmnts: Nystagmus, Diplopia
Fundoscopy reveals atrophy of disk
2. Motor symptoms
 Mono and para paresis
Signs:
 Hypertonia
 Hyperreflexia
 Extensor plantar response( Babinski’s sign)
 No abd reflexes
3. Sensory loss
Numbness, paraesthesia
 Post column lesion: no position awareness
 Llhermitte’s sign: shock-like sensation in limbs upon neck flexion
 Spinothalamic lesion: dyaesthesia + contralateral pain &temp sense loss
Also;
Vertigo, ataxia, sphincter disturbance, personality changes, mental disorder
Rx:
Pathogenetic
During attack:
 methlyprednisolone (decr inflammation)500-1000mg/day, iv, 3-5dy
 Plasmapheresis
 Vascular therapy: anti aggregants & oxidants
In case of remission, to prevent attack
 β1 & α1 INF
 Copolymer(binds to immune complexes and eliminates)
In case of 1 or 2 progressive
• Cytostatics(anti tumor)
• Corticosteroids
• plasmapharesis
Symptomatic
 Spasticity: antispastics
 Urinary : catheterization
 Ataxia: β blockers
 Bowel:
 Pain: analgesics
 Paroxysmal: anticonvulsants
Q18. Traumatic intracranial Hematoma. Epidural and subdural hematoma. Diag& Tx
Intracranial hematoma is often a cause of secondary brain damage following head trauma, it may either be
extra or intradural. Brain damage is caused either directly or indirectly by tentorial or tonsillar herniation.
Extradural hematomas are usually as a result of tearing the middle meningeal vessels which then bleed
into the extradural space (esp. temporal, temporoparietal # or ruptured transverse or sagittal sinus)
Subdural hematomas are as a result of rupture of the bridging vessels from cortical surface to venous
sinuses.
Epidural hematoma: accumulation of blood in the potential space btwn dura and bone. It may be spinal
or intracranial and is caused by damage to mid meningeal artery.
Clinic:
1. Signs of trauma:
• disturbance of consciousness
• Bruises on face or head
• Physical hitting
2. progressive deterioration
• decreasing Glasgow scale
• focal neurological signs( epileptic seizures, opthalmoplegia, strabismus convergence, ptosis)
• contralateral central hemiparesis
• somatic changes( incr BP)
• ipsilateral papillary dilation
Spinal symptoms include weakness, numbness and incontinence (fecal and urinary)
Examination:
• In case of incr ICP, there will be bradycardia + hypertension
• Lacerations may be observed
• CSF otorrhea, rhinorrhea( napkin & handkerchief test)
• Hemotympanum
• Disturbed consciousness
• Facial palsy
Diagnosis:
CBC
Skull x-ray
CT scan
Myelograpy / MRI
Angiography
Lumber puncture is NEVER performed coz this can lead to herniation!!!!
Tx:
• ABC
• In case of high ICP give osmotic diuretics
• For coagulopathy give Vit K or protamine sulfate
• Surgery:
A horseshoe flap is made with burr holes to drain. This is done after CT scan
Subdural (burst lobe): this is caused by bleeding of damaged cortical arteries or underlying
parenchymal injury.
The hematoma and accompanying edema expand leading to incr ICP wch leads to decr cerebral
perfusion and global cerebral ischemia. The hematoma itself deforms and displaces the brain causing
either transtentorial or subfalcine herniation. If brain goes through the foramen magnum tonsillar
herniation occurs. It may be acute, sub acute, chronic
Clinic:
• Headache and confusion
• Weakness
• Seizures
• Incontinence
• Hemiparesis contralateral
• Gait disorders
• Papilledema, Babinski’s, dysphasia, stiff neck, hemianopia, dysarthria.
Diagnosis:
CT scan of head shows hyperdense, concave towards brain mass, unlimited by suture lines)
Tx:
Surgical: a question mark flap is made with subsequent evacuation including necrotized brain tissue.
Q19. Striatal system, kinds of hyperkinesias
The striatal system is the center of higher order among structures making up the extrapyramidal system.
The nigrostriatal fibres are dopiminergic while the strionigral fibres are GABA-nergic
Damage to the striatal system is characterized by a loss of neuronal system of higher order, producing
excessive excitation of neurons of the next lower system.
 Athetosis: Slow, writhing, worm-like involuntary mvmnts. Grimacing and abnorm
tongue mvmnts, spasmodic outburst of laughing or crying
 Chorea: Short, fast involuntary jerks in single muscles randomly. Characteristic decrease
in tone
 Spasmodic torticollis: Tonic disorder of neck muscles= slow involuntary turning of head
• Torsion dystonia: Extensive turning and twisting mvmnts of the trunk and proximities.
Px may not be able to stand or walk.
Q20. Hemorrhagic stroke, classification, diagnostics, Parenchymatous hemorrhage, etiology,
pathogenesis, diagnostics, Treatment, prophylaxis
Q21. Hereditary Dx with 1o defeat of pyramidal system. Strumpell’s spastic paraplegia.
This condition is called progressive spastic spinal paralysis; it commences in early childhood and
progresses slowly. Degeneration of the corticospinal tracts occurs leading to: initial complaints of
extreme heaviness of legs, followed by incr in weakness and eventually spastic paraparesis. This is acc by
spastic gait disorder, Hypertonia, Hyperreflexia. Spastic paraparesis of arms follows later.
Q22. Method of angiography. Radioanatomy of brain vascular system. Zone of blood supply of a.
cerebri media sinistra
 Intra arterial intro of contrast wit imaging by x ray film or by DSA(Digital subtraction
angiography)
 Intravenous DSA: under LA catheter is intro into femoral artery and guided up to carotid
or vertebral artery.
Carotid & vertebral angiography
Look out for:
Vessel occlusions, stenosis, plagues
Aneurysms
Arteriovenous malformations
Abnorm tumor circulation
Vessel displacement or compression
 The left middle cerebral artery passes through the Sylvain fissure and supplies the left
frontal and temporal lobe.
 The ant cerebral artery crosses corpus callosum supplies the medial part of frontal lobe
 Vertebral supplies sp cord, brain stem, cerebellum
 Basilar supplies brain stem, cerebellum
 Post cerebral supply parietal and frontal lobes
Q23. Ischemic stroke. Etiology, p/genesis, clinic, diagnosis, Tx, prophylaxis
Etiology
1. large artery stenosis(in pts with risk factors)
2. small vessel/ penetrating artery Dx.(lacunae)
3. cardioembolism
4. haemodynamic
5. non atherosclerotic vasopathy
6. hypercoagulation disorders
7. idiopathic
P/genesis
Permanent lack of blood flow to a focus, depriving of O2 & glucose. At a CBF level of 8-10ml/100g per
min (norm= 50-55) neuronal death occurs. The region in which this occurs is called the “ischemic
prenumbra”
An atherosclerotic plague forms sub intimally and comprises of intimal cells, smth musc cells, and
collagen and elastic fibres.
Hemorrhage with or without the plague may occur, causing stenosis or occlusion, sometimes the plague
itself may be emboli.
Clinic
 TIA
 Embolic strokes
 Headache & seizures
 Hypertension
 Pulsation of vessels
Neurologic signs:
 Hemianopia
 Opthalmoplegia
 Hemiataxia
 Hemiparesis
 Aphasia
Diagnosis
Blood test
CT/MRI
LP
Cerebral angiography
US
ECG
EEG
Tx and prophylaxis
1. risk factors
2. pharm therapy
3. surgery
General measures
 respiration
 metabolism
 cerebral autoregulation
 rehabilitation

Medical therapy
(a) anti aggregants
(b) anti coagulants
Surgery
Q24. Hereditary ataxias. Friedrich’s ataxia
Dominantly inherited:

ACDAs:
Type 1 Type 2 Type 3
Mild ataxia Expressed ataxia Only ataxia
Opthalmoplegia Expressed retinopathy
Mild dementia Dementia
Optic atrophy Extrapyramidal features
Spasticity
Recessively inherited:
• 1Louis-Barr syndrome characterized by cerebellar ataxia, multisystem disorders and
ocular, cutaneous teleangiectasia due to chromosome 11 gene defect.Purkinje and
granular cell loss occurs
2Friedrich’s ataxia (chromosome 9 defect)
Damage of spinocerebellar tracts, posterior funiculi and pyramidal tracts. Symptoms are caused by the
damage to various systems
Characterized by loss of:
• position sense
• discrimination
• stereognosis
Clinic:
• +ve Romberg’s sign & ataxia
• Pes cavus( Friedrich’s foot)
• Kyphosis/ scoliosis
• Limb weakness
• Abs of abd reflexes
• No Babinski’s sign
• Abs of lower limb reflexes
• dysathria
Diagnostic variants:
Mary’s spastic ataxia + spastic paraparesis
Strumpell- Lorraine syndrome
Q25. Gait infringement. Ataxia diff diagnosis and clinic
1. Ataxic
• Sensory
• Cerebellar
2. Hemiplegic
3. Parkinsonian
4. steppage
5. myopathic
6. frontal lobe
7. hysterical
8. cautious
9. choreic
10. dystonic
11. spastic
12. toe walking
Ataxia
Sensory ataxia:
Unconscious/ disturbed. No proprioception
+ve Romberg sign
Cerebellar ataxia:
Feet set wide apart when standing or walking.
Steps are jerky and unsure. Heel-to-toe walking is impossible.
-ve Romberg sign
Thalamic ataxia:
Contralateral ataxia with tendency to fall backwards or to opposite side of lesion
Spinal ataxia:
Ataxia and disequilibrium with Spasticity
Ataxia teleangiectasia:
(Louis Barr syndrome)
Progressive cerebellar ataxia with cutaneous and ocular teleangiectasia and immunodeficiency
Pts confined to wheel chair
Friedrich’s ataxia:
Damage of spinocerebellar tracts, posterior funiculi and pyramidal tracts, Symptoms are caused by the
damage to various systems
Characterized by loss of:
• position sense
• discrimination
• stereogenesis
Clinic:
• +ve Romberg’s sign
• Pes cavus( Friedrich’s foot)
• Kyphosis/ scoliosis
• Limb weakness
• Abs of abd reflexes
• No Babinski’s sign
• Abs of lower limb reflexes

Autosomal dominant Cerebellar ataxia (ADCAs)


Idiopathic late onset ataxia
Type 1
Type 2
Type 3
Intermittent ataxias
Q26. Normal CSF. Liquorodynamic tests
CSF is secreted by the choroids plexus (esp. of lateral ventricles); it enters subarachnoid space through
foramina lushka and magendie. Then it circulates up and around the brain and spinal cord.

Pressure cells protein appearance


(mmH2O)
Normal 70-120 - 20-40 Clear
tumor incr incr Incr protein Clear
Abscess 600-700 incr Incr Clear then cloudy
Purulent 250-700 Incr incr Yellowish
meningitis
TB meningitis 200-450 Yellowish
Syphilis 200-300 Cloudy
Subdural Incr Norm Yellowish
hematoma
SAH Incr RBCs Bloody
MS normal Lymphocytes Clear
Symptoms:
Hydrocephalus
1. Internal hypertensive
2. Occlusive non communicating
3. Communicating internal
4. Pyocephalus
5. Foramen monro obstruction
6. Norma pressure
7. Hypersecretion
8. Hypoliquorrhea
Liquorodynamic tests
1) Queckenstedt’s test:
To determine degree of blockage
LP is performed in lying position and CSF pressure by manometer.
If CSF column moves in synchrony with pulse; subarachnoid passage is free
Next apply pressure on abd (this engorges spinal veins hence incr CSF P), when abd P returns to norm,
CSF P rapidly falls to normal. If there is blockage the CSF P dsnt reach the manometer, if it rises slowly
then and incompletely drops, then thr is incomplete blockage.
2) Pneumoencephalography
3)CT, MRI ventriculography
4) Digital subtraction angiography
5) Bacteriological tests
6) Biochemical tests
Special tests
Q27. Hereditary Dx with 10 defect of extrapyramidal system
Wilson’s Dx (hepatolenticular degeneration)autosomal recessive.
Rare Autosomal Dx of Cu++ metabolism affecting the liver (it looks cirrhosed).
Cu accumulates in organs esp. on Decement’s membrane of the eye, nail bed and kidney.
Deficient ceruloplasmin wch normally binds to Cu, leads to incr of loosely bound Cu in all organs and
urine.
Clinical pic:
Acute: Chronic:
Bradykinesia wing beating tremor
Behavioral changes dysarthria, dystonia, rigidity
Involuntary mvmnts chorea movements
Liver involvement psychosis
Kayser-fleisher ring- diagnostic feature
Diagnosis:
Decr ceruloplasmin
Incr serum Cu
Incr urinary Cu
Liver biopsy
Tx:
Low Cu diet
Chelating agent (penicillinase)
Life long therapy
Q28. Sensory system. Anatomy, general characteristics and types of sensory deficit
This system connects the individual wit his environment, by relaying info from both external and internal
environment.
Receptors: specialized sensory organs that recognize stimuli and transmit it as impulses.
Types; exteroceptors, teleceptors (eyes, ears), proprioceptors, entero and visceroceptors.
RECEPTORS

Specialized visceral somatic


Pathway Sense
Spinothalamic pathway: Pain & temp
Receptor post horn lat nuc of Simple touch
thalamus
Dorsal column pathway:(proprioception to Discriminating touch
fasciculus gracillis & cunateus) Proprioception( conscious)
Receptor fasc gacilis & cunateus lat
nuc of thalamus(the fibres cross in med obl)
Dorsal spinocerebellar tracts: Unconscious proprioception
ANT: receptor ant horn vermis Muscles, bones, ligaments
POST: post horn

Types of sensory deficit:


• Paraesthesia
• Dyaesthesia
• Hyperesthesia
• Anesthesia
• Hypoesthesia
• Analgesia
• Hyperalgia
• Hypalgia
Primary sensory modalities include light touch, pin prick, joint position, and vibration
Complex ones include 2 point discrimination, graphesthesia.
• Agraphesthesia
• Abarognosis
• Asterognosis
Hemisensory loss: Bilateral sensory
Contralateral; complete cord lesion
Parietal lobe
Selective cortical lesion
Thalamic lesion
Pontine lesion
Medullary lesion
Spinothalamic tract lesion
Brown Sequard syndrome
Q29. Spring and summer vernal encephalitis
This is an acute viral infection causing neuronal damage with edema and inflammation.
Agent: Arbovirus
Vector: tick
Way of infection: cow’s milk
Clinic:
General; fever, myalgia
Specific;
Memory loss
Olfactory hallucinations
Focal neurological signs
Confusion
Diagnostics:
CSF tests;
WBC increase
Protein incr
Glucose decr
PCR
Tx:
Antiviral therapy
Anticonvulsants
ICP management
Attenuated viral vaccine (prophylaxis)
Q30. Myelosyringosis P/genesis, clinic, Tx.
This is a congenital pericental cavity of the cervical spine that may extend to the thoracic cord or to the
medulla.
P/genesis:
• Communicating
There exists communication with the central cord leading to hydrodynamic disorder of CSF pathways.
Usually ass. With congenital malformations (Chiarin malformation)
• Non communicating
There exists a cystic dilation of the cord. May be due to trauma, intramedullary tumors
Clinic:
Depends on the localization of cavitation.
1. Dissociated sensory loss at level of lesion acc by painless skin ulcers, scars, edema etc
2. Weakness and wasting of musc at level of lesion.
3. Pyramidal deficit & sphincter disturbances
4. Tendon reflexes depressed at level of lesion
5. Scoliosis
6. Cape-like sensory loss
7. syringobulbia (involvement of medulla)
Communicating is characterized by hydrocephalus, cerebellar ataxia, and sensory deficit in limbs
Non communicating has weakness, impaired sensation and Spasticity, Radicular pain.
Tx:
Depends on underlying cause.
1. Decompression of distended syrinx
2. Surgical (indicated in cases of mild deficits, sp cord enlargement, pain or spasticity
• communicating
Chari malformation: removal of post rim of foramen magnum, with subsequent drainage
Post traumatic: drainage, myelotomy
Q31 Visual analyzer, visual frustration, topical diagnosis
The optic nerve is made up of rods and cones; it passes thru
the optic foramen and unites with optic nerve from other side
to form the optic chiasma. They subsequently form the optic
tract which is made up of ipsilateral temporal and
contralateral nasal fibres due to the partial decussation. Some
fibres go straight to the lateral geniculate bodies while some
go to the superior colliculi. The axons of the cell bodies in
the LGB form the optic radiation. These end in the sulcus
calcarneus of the occipital lobe.
Visual impairment:
1. Macula( area of best vision coz of high cone concentration) fiber atrophy
 Impaired central vision only
2. peripheral nerve fiber atrophy
 impaired peripheral vision
3. Direct damage of optic nerve
 Ipsilateral central scotoma
 Contralateral papilledema
4. Centre of chiasma damage
 Bitemporal hemianopia
5. Damage to optic tract
 Homonymous hemianopia
6. destruction of areas 19 &18
 alexia
 agnosia
7. refractive defects
 presbyopia
 hypermetropia
 myopia
 astigmatism
Q32. Viral meningitis & meningioencephalitis, forms, etiology, clinics, diagnostics and Tx
Viral meningitis
Routine culture reveals no microbes hence it is called aseptic meningitis
Etiology
 enterovirus
 mumps virus
 herpes simplex virus(HS2V)
 EBV
Clinic
Prodromal phase meningial phase recovery (7-14 days)
Fever headache
Malaise photophobia
Sore throat drowsiness
Signs
Mild meningism, skin rashes, Cx (febrile seizures, ADH secretion)
Diagnostics:
CSF (lympho, mono)
PCR to detect viral DNA
Throat swab or stools
Serological tests
Tx
Symptomatic:
IV acyclovir (antiviral)
Meningioencephalitis
Virus may act directly via immune system. The viral infection causes neuronal damage w edema and
inflammation.
Common causative agents:
• EBV
• Varicella zoster
• Mumps
• Herpes simplex virus
Clinic:
General symptoms: fever, myalgia
1. EBV
• Meningism
• Cerebrum: coma, epilepsy, dysarthria,
• Mid brain: Oculomotor palsy
• Cerebellum: ataxia
• Brainstem: tetraparesis, Nystagmus
• Sp. cord: motor & sensory dysfxn
2. HSV1 &2
• HSV1: oral and labial rashes
• HSV2: genital and neonate infection
• Headache, decr consciousness, fever, seizures
• Inf frontal lobe & temp lobe: behavioral changes, hallucinations(gustatory & olfactory), cerebral
edema= central tentorial herniation
Diagnosis:
CT, MRI, CSF, EEG, PCR
Tx
Acyclovir 10-14 days
Q33. Huntington’s Dx
Chorea is involuntary, jerking mvmnts of limbs and axial mus groups and is difficult to stop.
HD is an autosomal dominant disorder which has its onset in middle ages with subsequent death within
10-12 yrs. It can be predicted by locus identification.
Clinic:
Chorea
Initial symptom, feeding and walking become impossible
Dementia
Behavioral disorders
Hypotonia
Primitive reflexes e.g. grasp, pout, palmomental reflex
Proximal extremities, trunk and facial musc affected such dat speaking& swallowing is difficult.
Diagnosis:
Family history
CT scan (atrophy of caudate nuc)
MRI
Tx
Phenothiazines
Haloperidol
In the initial stages
Q34. Defects in mimic musculature, Central & peripheral types, variants of facial nerve lesion
Anatomy:
The facial nerve is made up of motor fibres supplying musc of facial expression, visceral fibres, and
afferent fibres.
Motor nucleus is in the lower pons medial to the descending nucleus & tract of the 5th CN.
The nerve exists from the lateral aspect of the brainstem and enters the internal auditory meatus
Facial canal close to inner ear gives branches exits skull thru stylomastoid
process.
Visceral & afferent fibres arise and end in super salivary and solitary nuclei.
Central paralysis
Lesion of supranuclear fibres: contralateral paralysis of inf mimic musc may be combined with central
hemiplegia

Peripheral paralysis
Viral infections, vascular disorders, otitis media, mastoiditis, petrous bone fracture may cause this,
leading to flaccid paresis of all mimic musc including forehead musc.

Post recovery, preserved fibres send new axons to the damaged portions leading to faulty innervation wch
may cause:
• Contracture
• Synkinesis
• Crocodile tears( paradoxical gustolacrimal reflex)
Variants of facial nerve lesion
1. contralateral supranuclear lesion: unilateral lower face with normal eye closure
2. ipsilateral nuclear lesion
3. bulbar/ pseudobulbar palsy
4. nuclear lesion: pons, internal auditory meatus, facial canal, peripheral nerve
lesions
Other disorders incl Bell’s palsy, Ramsey Hunt syndrome, hemifacial spasm
Ramsey Hunt syndrome:
Herpes zoster infection with characteristic zoster eruptions in the auditory meatus, it has sudden facial
weakness and pain. Sero sanguinous discharge is present from ear, as well as deafness (damage to CN
VIII)
Hemi facial spasm:
Esp. in mid aged females, characterized by unilateral clonic spasms of m orbicularis oculi. Also ipsilateral
clicking sound (os. Stapedius). Contractions are worsened by stress.
Q35. Hemorrhagic stroke, SAH
Etiology:
Cerebral aneurysms
Small thrombosed aneurysms
Hypertension
Clinic:
Headache
Disturbed consciousness
Nausea & vomiting
Meningeal signs
• neck stiffness
• +ve kernig’s
• coma
• epileptic seizures
• focal signs
• papilledema
• pyrexia
Diagnostics:
CT, LP, MRI, MRA, angiography
Tx:
Evacuation of clots ,endotracheal intubation, stabilize arterial pressure and cardiac rhythm
Medical tx- use triple “h” therapy i.e induce ( inorder to prevent vasospasm) hypertension,
hypervolemia, hemodilution. To maintain perfusion to cerebrum . use calcium blockers

Surgery of aneurysm 1-open craniotomy


2endovascular method
Prevent / reduce risk factors
Q36. Sexual chromatin, pathology
Se x chromosome is the 23rd pair of chromosomes
X- Trisomy
Female w no external disturbances
Decr reproductive capability
May be:
• 4X chromosomes: tetrasomy
• 5X chromosomes: pentasomy

Kleinfelters Dx
Genotype: 47XXY, 48XXXY, 49XXXXY
Or 47XYY, 48XYYY
Typically males
Clinic:
Onset at puberty
Hypogonadism
Sterility
Externally; tall, asthenic, gynecomastia, long limbs
Turner’s syndrome
Genotype: 45XO
Typically females
Clinic:
Short stature
Hypogonadism
Amenorrhea
Sterility
Poor secondary sexual characteristics
Webbed neck, cubitus valgus
Edema of legs
Coarctation of aorta
Q37. Olfactory system, lesion, topical diagnosis
Sup. Regio olfactoria+ nasal septum------bulbus olfactorius -------trigonum olfactorum---- ant perforated
sub------- temporal lobe fila olfactoria
1st neuron= bipolar olfactory cells
2nd neuron= mitral & tuft cells of bulb
3rd neuron= n. amygdaloideus

Lesion of olfaction:
1. Agenesis of olfactory tracts
2. Dx of upper olfactory mucosa
3. Fracture of lamina cribrosa causing tearing of fila olfactoria
4. Destruction of bulb by contusions e.g. falling on back of head
Anosmia (uni or bilateral) may be the only neurological sign of damage. Often patients do not realize
their loss of olfaction and instead complain of loss of taste.
Diff diag:
Impairment maybe temporary or permanent

Upper resp tract infection head injury


Drugs
Viral infections
Tumors
Endocrine Dx
Foster Kennedy syndrome: ips anosmia, optic atrophy, cont papilledema
Hallucinations may occur in cases of partial seizures & migraine
Q38. Ischemic Stroke, Clotting of post inf cerebral artery
Etiology
large artery stenosis(in pts with risk factors)
small vessel/ penetrating artery Dx.(lacunae)
cardioembolism
haemodynamic
non atherosclerotic vasopathy
hypercoagulation disorders
idiopathic
P/genesis
Permanent lack of blood flow to a focus, depriving of O2 & glucose. At a CBF level of 8-10ml/100g per
min (norm= 50-55) neuronal death occurs. The region in which this occurs is called the “ischemic
prenumbra”
An atherosclerotic plague forms sub intimally and comprises of intimal cells, smth musc cells, and
collagen and elastic fibres.
Hemorrhage with or without the plague may occur, causing stenosis or occlusion, sometimes the plague
itself may be emboli.
Clotting:
(Lateral medullary syndrome) on ipsilateral side:
1. cerebellum: ataxia, dysarthria, vertigo
2. brainstem: Horner’s syndrome, sensory loss( pain & temp, pharyngeal and laryngeal
paralysis)
Contralateral sensory loss of pain and temp in limbs & trunk
Q40. Transverse lesion of sp Cord
In the acute phase spinal shock develops:
(Lesion of upper cervical) comprising of resp insuf, quadriplegia, Neurogenic shock, loss of bladder and
rectal control, this is acc by ipsilateral Horner’s syndrome
Lesion of lower cervical cord leads to paralysis of intercostals= resp insuf
Upper thoracic: paraparesis, paralytic ileus (splanchic nerve dist)
Lower thoracic: abd intact, no resp disturbance, lumber & sacral = bladder& rectal retention
Epiconus: impaired mvmnts of hip joint, knee joint, foot & toe joints. No Achilles’ reflex, reflex bladder
& rectal emptying, priaprism, impotency, anhydrosis
Conus: (S3-C) flaccid paresis of bladder, incontinence of bladder, impotence, saddle anesthesia (S3-S5)
Cauda equina: sciatic Radicular pain, pain in bladder wch incr on tussis & sneezing, sensory dist to L3,
paresis of lower limbs, incontinence
Q41. Acute Polyneuropathy, Gullier Barre syndrome
Acute demyelinating neuropathy, of viral etiology
Clinic:
Sensory; paraesthesia, paresis
Weakness
Areflexia
Back pain (initial symptom)
Facial pain
Papilledema
Autonomic disorder (retention of urine, tachycardia)
Diagnostics
CSF, nerve conduction tests, ancillary tests, (exclude sp cord dx, myasthenia gravis)
Tx
Supportive
Plasmapheresis, IVIG
Q42. Classification of sp cord tumors
In adults: in kids:
Extradural
Metastasis metastasis
Myeloma lymphoma
Lymphoma
Neurofibroma
Extramedullary
Meningioma Dermoid
Schwanoma
Intramedullary
Astrocytoma astrocytoma

Extramedullary tumor:
Originate in area of post roots and produce Radicular pain as they grow.
Dorsomedial growth: press on post tracts, roots, and pyramidal tracts
Clinic:
Ipsilateral spastic paralysis with paraesthesia& defects in proprioception, coughing and sneezing incr pain
(rheumatic felt in distal limbs 1st)
• Tumor in foramen magnum= pain, para- and hyperesthesia
• Tumor in area of C2= paresis of SCM & trapezius (accessory nerve)
• Hour glass tumor: neurinoma in intervertebral foramen growing to the outside & sp cord.
Produces compression symptoms and later brown Sequard syndrome.
Hypoesthesia in corresponding dermatome
Bladder and rectal paralysis
Ventral growth: press on ant roots
Clinic:
Flaccid paresis of hands, spastic paralysis if pyramidal tracts r involved
Hyperesthesia if pressure is on ventrolateral funiculus
Incontinence of bladder and rectum

Intramedullary tumor: longitudinal growth


No Radicular pain, sensory disorders, bladder & rectum disorders
Atrophy of supplied mus
If tumor involves upper cervical thickening= signs of bulbar involvement
Q43. Research of eye ground
Fundus of eye seen with ophthalmoscope (aa Central retinal, cilio retinal, & v central retinal)
Clinical importance:
Neuritis of optic nerve
Brain tumor= atrophy of papilla
Incr ICP= stagnant optic disk
Disc found with great difficulty= papilledema
Disc flashes like white tennis ball= 1o disc atrophy
Variants of changes:
1. Papilledema:
Caused by raised ICP (mass lesions or CSF circulatory disturbance), cerebral edema, raised CSF protein,
metabolic disorders, malignant hypertension, and circulatory disturbance.
Incr venous caliber---disc margins start to blur, disc becums diffuse, swollen, and elevated
2. 2o optic atrophy: if pt survives papilledema---nerve head becums grey-white---decr visual acuity---decr
swelling--- gliosis (scarring)
3. 1o optic atrophy: after any toxic injury, occlusion of retinal artery
4. Other disorders: macular degeneration, emboli o retinal vessels, retinitis pigmentosa, centrous serous
retinopathy.
Unusual disc appearance: pre papillary arterial loops, embryonic defects (persistent hyaliod A, persistent
Bergmeisters papilla) colobomas of optic disc, drusen (dev abnormality)
Q44. Lumbar osteochondrosis
Radiculopathy with ass back and leg pain can occur at any level but affects mostly L4/L5 & L5/S1
Disc rupture is usually in postero lateral direction.
Compression symptoms:
Lateral disc protrusion
• Leg pain: severe, sharp, shooting pain radiating to cutaneous supply and musc supply aggravated
by coughing sneezing
• Paraesthesia
• Restricted spinal mvmnts + scoliosis
• +ve Lasegue’s sign
Severe pain may inhibit micturation
Central disc protrusion
Usually bilateral signs
• Leg pain: bilateral down thighs
• Paraesthesia
• Sphincter paralysis
Sensory loss: saddle anesthesia
Motor loss: foot drop
Reflex loss: ankle reflex
L5 radiculopathy S1 radiculopathy
Motor signs: foot weakness, wasting & foot drop wasting & weakness of plantar reflexes
Sensory loss: lateral calf and dorsum of foot lateral foot, sole
Tx
Rest, steroids, opiods, mus relaxants, heat, limit work
Surgery if: no response to Tx after 4 weeks, foot drop, other Dx
Types of surgery:
Lateral disc= microdiscectomy
Central disc= laminectomy
Post surgery avoid lifting
Q45. Prophylaxis of H. Dx
1. Initial referrals for evaluation and counseling (in cases of still births, fetal abnormalities)
2. Info gathering (pedigrees, past records, assessment, counseling)
3. Calculating genetic risks
4. Prenatal diagnosis (US, maternal serum screening, amniocentesis, Doppler analysis
5. Genetic counseling (old mum, recurrent sp abortions, consanguinity)
6. Genetic screening (ID of gene Dx and genetic predisposition)
Q46. Cerebellar Dx, ataxia
Anatomy: the cerebellum lies in the posterior fossa, posterior to the brainstem, separated form the
cerebrum by tentori cerebelli. It consists of 2 hemispheres & mid line structure- vermis, the cortex has 3
cell layers, efferent cells= purkinje cells, afferent= spinocerebellar tract
Damage:
Midline structures; truncal ataxia, -ve Romberg’s sign
Hemispheres; (produces ipsilateral signs) ataxia, dysmetria, dysdiadochokinesia, intentional tremor,
Nystagmus, scanning dysarthria, titubation, head tilt, involuntary mvmnts
Classification:
Degenerative, developmental, demyelinative, Neoplastic, paraneoplastic, infectious, metabolic, drug/
toxic & vascular

Q48.Tumors of post cranial fossa


Intrinsic;
Metastasis: can cause CSF blockage & hydrocephalus (signs of incr ICP)
Cerebellar ataxia, Nystagmus. Tx= Op+ radiotherapy, ventriculoperitoneal shunt for hydrocephalus
Hemangioblastoma: cerebellar signs, signs of CSF obstruction, SAH Tx= OP
Medulloblastoma: MALIGNANT!!! Ataxia Tx= op, radiotherapy, chemotherapy
Astrocytoma: common in children (if brainstem not involved OP),

Extrinsic;
Acoustic Schwanoma :( nerve sheath tumors) cerebellopontine angle lesions, bilateral chrct for NF2, they
r benign, damage CN VIII
Tx: translabyrinthine & middle fossa approach
Dermoid cysts: rare, embryogenic cysts. They adhere closely so can’t be removed, evacuation can be
done & steroids) clinic: Depressed corneal reflexes, chemical meningitis (rupture of cholesterol into SA
space)
Q49. Pupillary accommodation
Ciliary contract, rectus contract, pupillary constriction
Aniso conia
Pupil constriction is characteristic of:
Horner’s syndrome:
Ipsilateral mild ptosis, miosis, sweating disturbance depends on site of lesion: if lesion is on proximal site
of fibres btwn int carotid= ipsilateral.
Levels of lesions: break my car I arrest
Brainstem
Mid fossa
Cervical Cord
int carotid artery
ant roots of C8- T1
Congenital familial Horner’s syndrome: loss of iris pigmentation
Preganglionic & post ganglionic lesions differentiation
In preganglionic: Intra ocular cocaine, receptors take up cocaine= dilation (in norm they take up adrenalin
and constrict)
In post ganglionic there r no receptors
Argyle Robertson (ass with syphilis)
Irregular, small pupils unresponsive to light, but can accommodate. May result from mid brain Dx,
diabetic neuropathy. Also motor nuc of Oculomotor is affected.
Diagnosis:
Underlying syphilis
Serological tests
Tx
Para-sympato-mimetic drugs: carbacol, opiates
Q50. Transversal myelitis
Rare, occurs in ass in EBV, small pox, viral infections
Clinic:
Fever, back and limb pain (b4 paralysis)
Paralysis is first flaccid then spastic (after 1-2 wks)
Bladder disturbance
Diagnosis:
LP
Check for underlying cause
Myelography
MRI
Tx
Supportive
Steroids
Q51. Brain – arterial aneurysm
Unusual swelling or dilation of vessels wch may rupture.
Shapes: saccular, fusiform, and mycotic
1. Saccular may be found in
Ant cerebral & communicans: leg weak, incontinence, confusion
Medial cerebral artery: hemiparesis hemiplegia dysphasia
Post inf cerebellar artery & basilar: asymptomatic
In case of rupture severe headache + SAH
2. Mycotic may be traumatic or vascular (carotid, vertebral, basilar)
3. Fusiform maybe atherosclerotic on basilar & int carotid: neuralgia
They rupture easily and cause carotid cavernous fistula (ipsilateral exopthalamus synchronous with pulse,
swelling eyelid paralysis of eye muscles
Aneurysm of intra cranial carotid affects optic chiasma, tract & nerve- visual field disturbance
Post comu artery- Oculomotor palsy
If aneurysm bursts:
SAH, incr ICP, headache, confusion, nausea, neck stiffness
If blood penetrates tissues= intra cerebral hematoma
Diagnostics
CT
Tx
Symptomatic
Surgery: clip neck of aneurysm
Q52. Caudal cranial nerves syndromes
Glossopharyngeal nerve (caused by: med or nerve root lesions norm ass with X-XI lesions= jugular-
foramen syndrome)
1. Glossopharyngeal neuralgia
Short, sharp pain (identical to tic douloreux) affects post pharynx & tonsillar area irradiates to ear, incr by
swallowing. Stimulation of vagus= bradycardia & syncope (Carbamazepine for relief)
2. Vagus disorders
Palatal weakness: uni/ bilateral
Pharyngeal weakness: uni/ bilateral
Laryngeal weakness
3. Accessory disorders
Unilateral paralysis of SCM (can’t turn to opp side); bilateral (can’t hold up head)
Trapezius paralysis (hanging shoulder & caudo lateral scapula)
4. Hypoglossal disorders
Lesion leads to atrophy & deviation of tongue to weak side
Jugular- foramen syndrome: lesion of CN IX-XI
Callet-Sicard syndrome: extra cranial lesion involving CN IX-XII
Villaret’s syndrome: retropharyngeal space lesion involving CN IX-XII & Horner’s syndrome
Q53. Intramedullary tumors
Not common, e.g. astrocytoma
Clinics:
Segmental pain
Loss of pain & temp at level of lesion (interruption of decussation)
Sensory loss
Tumor expansion: involve ant horn cells= l.m.n weakness, Corticospinal tract inv=u.m.n weakness
Diagnosis:
X-ray shows widening of interpedicular distance, Myelography confirms lesion, MRI differentiates from
syringomyelias
Tx: exploratory laminectomy, needle biopsy, aspiration, after OP; radiotherapy
Q54. Structure and classification of chromosomes, Down’s syndrome
Each chromosome contains a single DNA molecule organized into several orders of packaging =
metaphase chromosome.
Chromatin: DNA protein complex made up of histones (5 types), 8 histones = nucleosome. Nucleosomes
are tightly packed together to form a 30nm wide fiber (can be seen under electron microscope)
Special features
Euchromatin has high density coding regions or genes
Heterochromatin devoid or inactive genes maybe constitutive and facultative (inactive X chromosome
remains highly condensed and stains darkly during interphase = Barr bodies)
Centromere constricted area of metaphase chromosome
Telomere DNA sequence at ends of chromosomes
Classification
Normal karyotype = 23 pairs of chromosomes (22 homologous autosomes and 1 sex)
Chromosomes may be metacentric, submentacentric and acrocentric satellites
Bands: Starting at centromere each arm is divided into one or more regions

Down’s syndrome:
Trisomy 21 affects both males and females
Clinic:
Typical Mongolian face (moon face, small mouth, large tongue, close skewed eyes)
Males sterile but females fertile
Prenatal: nuchal thickening, duodenal stenosis and short femur
Infancy: flat nasal bridge, Brush Field spots, flat occiput
Childhood - adulthood: mental retardation, autoimmune disorders, hearing loss, short
Old age: Alzheimer’s pre-senile dementia.
Q55.Oculomotor nerves, Post longitudinal fascicle, lesion of Oculomotor
Motor nuclei- front part of periaqueductal gray matter
Autonomic (Edinger- Westphal) nuclei- poorly myelinated periaqueductal gray matter
PSNS nuclei (Perlia’s) - between the autonomic
INNERVATION:
Motor= mm recti sup, inf, medial, m. inf orbicularis
Autonomic= m. sphincter pupillae, m. ciliare

Longitudinal fascicle:
Constitutes a collection of various fiber systems connecting nuclei abducens, Trochlear and Oculomotor
It passes thru sp cord, pons & mid brain and carries impulses from the vestibular system.
Particulate lesion causes displacement of eye globe in horizontal (divergent strabismus) and vertical
planes (one eye medial and downward; on side of lesion the other is lateral and upward)
Also Nystagmus maybe present.
Lesions:
Complete lesion produces
Ptosis, dilated unresponsive pupil and fixed eye
Partial lesions produce only part f the syndrome e.g. opthalmoplegia
If all mus are paralysed= peripheral nerve damage
If only one mus= lesion in nucleus of Oculomotor nerve

Q58. Superficial and deep reflexes


Superficial reflexes
These are cutaneous reflexes caused by light irritation of skin or of areas that depend on spinal cord as a
motor center (abd, cremaster, scapula, gluteal, plantar).palatal pupilary conjuctival
Deep reflexes
DTR (deep tendon reflex) is an autonomic motor response to stimulation of the stretch receptors in
subcut tissues around joints and tendons (biceps, patellar, Achilles’, triceps).

Hyperactive reflexes occur in cases of hyperthyroidism, spastic disorders, pre-eclampsia; hyporeactive


reflexes occur in cases of hypothyroidism, drug intoxication, and flaccid neuromuscular disorders.
Q59. Post-vaccinal encephalitis, encephalomyelitis
Acute immune demyelinating disorder
Clinic
• After resolution of viral infection fever, nausea, vomiting.
• Meningeal signs: photophobia, neck stiffness
• Drowsiness
• Multifocal neuro signs: CNS involvement
• Myoclonic mvmnts
• Optic neuritis
Diagnosis
No test is available
EEG
MRI-small foci perivascular
CSF-mononuclear cells
CT is normal
Diff diag
MS
Tx
Steroids in acute phase
Cyclophosphamide
Q61. Intracranial Hypertensive syndrome
Incr in brain-water content, incr in CBF, CSF or expanding mass = incr ICP
Mech:
Cerebral edema may dev around an intrinsic brain lesion e.g. tumor, abscess or in relation to trauma or
ischemia. Edema may by:
Vasogenic: xs fluid thru damaged vessel wall to extra cellular space esp. in white matter
Cytotoxic: fluid intracellular i.e. neurons and glia
Interstitial: in case of obstructive hydrocephalus CSF is forced thru to the extra cellular space
Factors affecting cerebral vasculature: chemo & auto regulation

Clinic:
If CBF is maintained, ICP may show symptoms but not neuronal damage.
Headache, vomiting, papilledema, vomiting, brainshift

Diff diag:
Brain abscess, trauma, tumor, shift, MS, hematoma, meningitis, migraine

Tx
Remove expanding mass
ICP level > 30mmHg (norm= 0-10) requires Tx
Methods of decr ICP:
100ml, 20 % mannitol/ 15 mins a bolus
Controlled hyperventilation
CSF withdrawal
Sedatives
Steroids
Q62. Cervical osteochondrosis
Compression, shrinkage, saddle formation
Progressing atrophy of cervical disks and approximation of vertebrae
P/genesis:
Cervical Radicular syndrome is almost always a result of CO
Osteochondrosis of cervical column= C3-T1, the spaces btwn 5th & 6th as well as btwn 6th & 7th most often
involved.
These syndromes consist of Radicular irritation= paraesthesia & pain in segmental distribution, if more
severe; = Radicular sensory and motor loss ass w abnorm reflexes
Syndromology
C4- C5
Pain & numbness radiating to shoulder
Weakness of deltoid
C5- C6
Pain & numbness of top of neck, biceps, lateral arm, dorsal thumb & index
Weak biceps with decr reflex
Weak wrist flexion
C6- C7
Pain in top of neck, triceps, postero lateral arm to middle finger
Weak triceps, decr triceps reflex
C7- T1
Pain & numbness acr neck, arm, to small and ring fing
Wrist flexion and intrinsic arm musc r weak
Diff diag
MS
Trauma
Metastatic cancer of cervical spine
Rheumatoid arthritis
Osteomyelitis
Tx
Steroids
Muscle relaxants (500mg, PO/ 6 hrs)
Physiotherapy
Rest
Soft cervical collar
Microvascular decompression
Q63. Trigeminal neuralgia
Paroxysmal attacks of short, stabbing pain. Always unilateral
Etiology:
Root compression
Demyelination
Diagnosis
CT/MRI
Tx
Drug therapy: Carbamazepine
Pain: analgesic
Surgery:
Nerve block, root section
Q64. Lesion of right internal capsule
Contralateral spastic hemiplegia
Contralateral paralysis of facial and hypoglossal nerves (corticonuclear tracts)
A lesion causing rapid damage produces a contralateral paralysis dat is at first flaccid then it becums
spastic as the extrapyramidal tracts r damaged.
Q65. Lateral amyotrophic sclerosis (ALS)
Chronic progressive degenerating Dx involving motor neurons in sp cord and brain
Etiology
Viruses
Excitotoxins
Genetic predisposition
Toxins
Minerals
Forms
I. Cervical: spastic paresis in legs, flaccid in arms, dysphagia
II. Bulbar: dysarthria, tongue fasciculations, pyramidal symptoms
III. Pseudobulbar form: Dysphagia, pathological laughing and crying, frontal dementia, l.m.n lesion
symptoms
IV. Lumbar form: flaccid paresis in legs, with atrophy & fasciculations
Clinic:
@ Onset: asymmetric weakness & wasting of extremities
Bulbar & pseudobulbar features
Frontal dementia
Pseudobulbar palsy:
• Weak musc of mastication & facial expression
• Incr gag& jaw jerk reflex
• Drooling speech
• Dysphagia
• Immobile pointy tongue
Progressive bulbar palsy:
• Atrophy & fasciculation in mus supplied
• Wasted tongue
• No jaw & gag reflex
Corticospinal involvement:
• Hypertonia
• Hyperreflexia
Ant horn involvement (progressive muscular dystrophy):
• Atrophy, weakness, fasciculations
• ‘Skeleton hand’
• Resp musc failure is normally cause of death
Tx
Riluzone 100mg/day
Symptomatic:
Speech therapy
Nutrition
Drooling- amitryptilin
Musc weakness- physiotherapy
Resp failure mngmnt
Q66. Extramedullary tumors
Meningioma
Localization: thoracic region, intra dural
Clinic:
Esp. in elderly females
Ipsilateral paresis
Sensory disorders
Diagnostics:
MRI or CT Myelography
Surgery: complete removal tho recurrence is possible

Neurinoma
Localization:
Any level in post nerve roots, either within sp canal or in ‘dumbell’
Clinic:
Ass with multiple neurofibromatosis
Café au lait spots
Root pain
Compression symptoms may follow
Diagnostics:
MRI, CT
Oblique X-ray: foraminal enlargement
TX
Complete removal, sacrificial coz other nerves compensate for lost ones
Q67. Lesion of frontal lobe
Lesion leads to:
Defect in each area!!!
Q68. Brain contusion
May occur under or on opposite side of injury, it may be multiple and bilateral
Consciousness is only lost when bleeding into contusion (hematoma)
Clinic
Loss of consciousness, edema, seizures, focal neuro signs, blood into CSF (meningeal irritation &
hydrocephalus)
Diagnosis:
Gen exam:
Injury, basal skull fracture
Consciousness (eye opening, motor & verbal)
CT/MRI
Tx
Extensive contusion w edema= focal mass lesion: surgery
A, B, C
Elevate head & give barbiturates and furosemide
Cx
Post traumatic epilepsy
Intracranial hematoma
Post contusional encephalopathy
CSF leakage
Q69. Main principles of hereditary Dx Tx
1. Amelioration of clinical phenotype: symptomatic Tx and surgery
( correction of congenital anomalies)
2. Amelioration of metabolic abnormalities:
3. Replacement therapy e.g. hemophilia (replacement of factor VIII)
• IDDM insulin therapy
• Organ transplant
3. Modulation of gene expression
4. gene therapy: germ line therapy and somatic therapy
5. diet ethics e.g. galactosemia: removal of milk and diary products
Non specific
• special education
• symptomatic medication
• avoidance of environmental exposure
Surgical
• correction of anomalities e.g. cleft
• organ transplantation
• gene therapy
Q70. Facial nerve
This nerve has 2 subdivisions:
The larger (facial nerve proper) motor nerve that innervates mimic musc of face and the thinner (n.
intermedius) that has autonomic and somatic fibers.
Diagnostics of level of lesion:
Lesion may occur at many levels, there are several branches of the facial nerve along its path;
1. Before and at the internal acoustic porus (2 branches: n Facialis proper & intermedius)
Peripheral motor paralysis of mimic muscles+ hearing impairment/ deafness/ decr vestibular excitability

2. between internal acoustic porus and 1st branch (n. petrosus majoris)
PMP + impaired taste, lacrimation & salivation

3. after 1st branch till 2nd branch (n. Stapedius)


PMP + impaired taste, salivation & hyperacusis

4. after 2nd branch till chorda tympani


PMP impaired taste + salivation

5. below chorda tympani, after stylomastoid foramen


PMP only
Bells palsy:
Acute paralysis of face related to inflammation of facial nerve within canal or in stylomastoid foramen.
Usually unilateral, smtyms family history
Etiology:
Viral e.g. Varicella zoster, HSV
Overcooling
Idiopathic
Clinic:
• Pain ipsilaterally
• Weakness for 48hrs
• Taste impairment, hyperacusis, salivation
• Lacrimation is preserved
On attempts to close eyes, one eye dsnt close, instead it rotates upwards & out wards (as if it were closed)
“Bell’s phenomenon”
Tx
Protect eye when sleeping
Prednisolone to reduce inflammation
Antiviral therapy
Eye care to prevent drying
Massage
Physiotherapy
Q71. TIAs, causes mechanisms, clinic, Tx
These are episodes of focal neurological symptoms due to inadequate blood to the brain, with no residual
effects and resolution within 24hrs. imp precursors to cerebral stroke( infarction)
Causes:
• Underlying arthrosclerosis ( carotid, intracranial vessels, aorta)
• Emboli
Mech:
CBF< 20-30ml/100g/min = neurological symptoms.
If flow is restored during critical period= OK
1. haemodynamic mech: reduced flow thru vessel
2. embolic mech: from aortic arch, heart
Clinic:
Carotid artery (anterior)
Hemiparesis, hemi sensory loss, dysphasia, one eye blindness
Vertebro- basilar (posterior)
Loss of consciousness, bilateral limb sensory dysfxn, vertigo, tinnitus, Diplopia
Tx
Anti platelet/ coagulant drugs
BP control
Carotid endarterectomy
Prophylaxis
Decr risk factors
Counseling
Q72. Progressive hereditary Erb’s myopathy
Superior plexus paralysis due to avulsion of C5- C6 roots of the brachial plexus because of its vulnerability
to injury.
Example:
Shoulder injury in accidents motorcycle
During forceps birth
Clinic:
Loss of shoulder abduction & elbow flexion i.e. arms r limp and inflexible tho fxn remains intact
Paralysis of deltoid, brachial and biceps mus
Sensory loss in deltoid, radial aspects of forearm and hand
Q73.Alternating paralysis in medulla oblongata lesion
(CN IX, X, XI, XII nuclei)
Avelli’s syndrome:
Ipsilateral flaccid hemi paresis of tongue, vocal cords, soft palate; contralateral hemiplegia
Jackson’s syndrome:
Ipsilateral flaccid of tongue; contralateral spastic paralysis
Wallenberg syndrome:
Ipsilateral unilateral paresis of tongue vocal cords, soft palate, Dysphagia, Horner’s syndrome, ataxia
Contralateral anesthesia
Schmidt’s syndrome:
Ipsilateral paresis of vocal cord, SCM & trapezoid muscles
Contralateral spastic hemiparesis
Babinsky:
Ipsilateral cer ataxia, Nystagmus, Horner’s synd, hyperthermia
Contralateral spastic hemi paresis+ dissociated hemi anesthesia (only pain & temp r lost)
Bilateral lesion of CN IX-XII= bulbar palsy
Central paralysis of nuclei CN IX-XII= pseudobulbar palsy i.e. corticonuclear tracts
Q74. Lesion of brain in case of flu, diphtheria & botulism
DIPTHERIA
Infection with C.diphteriae affecting upper resp tract, skin
3 stages:
After 2-3 weeks
Palate weakness after throat infection or Focal weakness of musc closest to cutaneous infection
After 4-5 weeks
Pupillary response impairment
After 1-3 months
Gen sensorineuropathy
Weakness is asymmetrical esp. proximally, in severe cases resp paralysis occurs
Diagnosis:
Incr CSF protein, slowing of nerve conduction velocity
Tx
Horse diphtheria antitoxin
ABiotics
Supportive therapy
BOTULISM
Toxin of C. Botulinum can cause neuromuscular paralysis coz of inhibition of Ach release @ neuromus
jxns & autonomic synapses
Clinic:
Sudden weakness 12-72 hrs after ingestion of toxin:-
Ptosis
Diplopia
Facial weakness
Nasal speech
Dysphagia
Difficulty in resp
Limb weakness is last
Muscarinic effects; xerostomia, blurry vision, paralytic ileus & postural hypotension
Tx
Hospitalization
Ventilation, supportive care, Guanidine HCl
Q75&78 Adenomas
They arise from the ant portion of the gland and r usually benign
Classification:
• GH secreting
• Prolactinoma
• ACTH secreting
• TSH secreting
• FSH/ LH secreting
• Inactive
Clinic:
Local mass effects
Compression of adj structures, pituitary gland & cavernosus sinus
decr hormone output, pan hypopituitarism
incr intrasellar pressure
Headache
Visual field defect
Endocrine effects
• Hypersecretion
GH: acromegaly in adults & gigantism in kids
Prolactin: galactorrhea (in females), impotence (in men), amenorrhea, infertility
ACTH: Cushing Dx & syndrome
• Hyposecretion
GH: weight gain, loss of libido, fatigue
Gonadotropin: sterility, loss of libido, amenorrhea
ACTH: mus weakness & fatigue
TSH: 2o hypothyroidism
Prolactin: failure of lactation
Diagnosis:
Low pituitary hormone in presence of low target organ hormone
Cx: pituitary apoplexy= hemorrhage into tumor subst chrtrsd by severe headache, SAH; treat with
steroids or else death results.
Diagnosis:
If tumor is large; CT/MRI and skull X-ray
If tumor is small: CT/MRI
Tx
1. Drug therapy: bromocriptine, somatostatin analogues
2. Surgery
From below:
• Trans sphenoidal
• Trans ethmoidal
From abv:
• Trans frontal craniotomy
3. Radiotherapy
Q76. Focal epilepsy
An epileptic attack is a consequence of paroxysmal uncontrolled discharge of neurons within the CNS
Attacks which begin focally within one hemisphere are called focal epilepsy.
Partial/ local/focal epilepsy
A. Simple partial seizures
• Sensory
• Motor
B. Complex/ temporal/ psychomotor epilepsy
C. Partial seizures evolving to tonic/clonic convulsions
Simple motor: arise from frontal motor cortex with mvmnt in contralateral face, limbs, trunk
Jacksonian motor seizure: involuntary mvmnt from one musc group to another (march)
Mvmnt is clonic, after seizure affected limbs are weak
Todd’s paralysis: aversive seizures (head mvmnt pt is aware of)
Attacks progress to tonic/clonic with loss of consciousness
Simple sensory: arise from sensory cortex with paraesthesia in extremity and face. “March” is present
with limb weakness without involuntary movement.
Complex partial seizure/ psychomotor seizure/ temporal epilepsy:
Originate in the temporal lobe and r charac by complex aura and impaired consciousness
Visceral disturbance: taste, smell, hallucinations, tachy cardia
Memory disturbance: déjà vu, jamais vu, flash backs
Motor disturbance: fumbling, rubbing
Affective dist: displeasure, depression
Automatism: involuntary complicated mvmnts
Also confusion and head ache

Partial seizures – tonic/clonic:


When focal seizures migrate to subcortical structures, excitation spread back to hemispheres =
tonic/clonic seizure
Tonic= 10 secs- no consciousness, fall to ground
Smiling frog with stretched legs, held breath
Clonic 1-2 mins
Violent shaking, eyes roll back, tachycardia
Pt then sleeps can’t b woken, once awake is confused.
Muscles ache, pt feels exerted, trauma from fall

Tx
Anticonvulsants (monotherapy)
Surgery
Withdrawal if pt is fit free >3 years
Surgery:
1. Temporal lobectomy
2. hemispherectomy
3. corpus callosal section
4. extra temporal cortical resection
5. selective amygdalo-hippocamectomy
Diff diag
Syncope, hypertensive crisis, panic attack
Q77. Carotid- Arterio anastomosis
A fistulous communication btwn the int carotid and the cavernous sinus may follow trauma, rupture of
small intra cavernous artery
Clinic
Pulsating tinnitus
Prominent facial veins
Pulsatile exopthalamus
Edema of periorbit
Papilledema
Opthalmoplegia
Diagnostics:
Angiography
Fundoscopy
Tx
1. fistule repair
• spontaneous closure
• trapping( ligation)
2. direct op repair
3. Embolisation
Q79. Aphasia, Apraxia, Agnosia
Aphasia:
Loss/impairment of language processing caused by brain damage
Cortical centers for language in dominant hemisphere:
Broca’s area
Temporal lobe receptive area
Parietal lobe receptive area
Etiology: Stroke, focal or diffuse lesions

Clinics:
Nonfluency, auditory incomprehension
Paraphasia (substituting correct words with incorrect ones)
Agraphia, anomia, alexia
Topical diagnosis:
Check content and fluency
Comprehension
Assess spontaneous speech, writing, reading
Motor aphasia: pt understands bt cant speak, is aware of defect
Sensory: not aware, cant understand, inadequate speech
Amnestic: pt understands can speak but forgets names of pple, obj, places etc
Semantic: can understand some words but can’t link i.e. dsnt see relation
Total: severe includes wernicke’s, broca’s area

Agnosia:
Loss of comprehension of auditory, visual other sensations tho sensory sphere is intact
Auditory, colour, finger, optic, tactile, time
Anton’s syndrome: when one is no longer aware of opposite side can’t feel paresis(visual agnosia)
In case of dominant parietal lobe lesion agnosia is of fingers.
Geographical agnosia –non dominant parietal lobe lesion
Finger agnosia-dominant parietal lobe lesion

Apraxia:
Inability to carry out skilled mvmnt despite full understanding of task and full motor power
Constructional (non dominant parietal lobe)
Dressing apraxia (non dom)
Gait apraxia (frontal lobe/ corpus callosum Dx)
Oculomotor (parieto- occipital lobe)
Ideamotor (dom hemisphere) can’t carry out task when asked to but otherwise can perform it
Ideational (frontal lobe Dx) can’t do sequence but can do each action separately
Q80. Early syphilitic meningitis
The initial event in neurosyphilis is meningitis.
Clinic:
Asymptomatic
Aseptic (fever, rash, malaise, neck stiffness)
Acute basal meningitis (hydrocephalus, CN palsies)
Diagnostics:
LP
CSF: leukocytosis, incr protein
Tx
If symptomatic give penicillin
If untreated:
Meningovascular, spinal, optic syphilis, gen paralysis
Tabes dorsalis
Syphilitic gummae
Q82. Muscle tone
It is the resistance of muscle to passive movement of the joint. It depends on degree of muscle contraction
and mechanical properties of muscle and connective tissue. Muscle contraction depends on anterior horn
cells.
Types of disturbance:
Hypertonia, Increased tone. Can be:
Spasticity: Affects different muscle groups to different extents. Resistance increases when passive
movement is initiated. Increased tone is velocity dependent (spasticity is caused by UMN lesion e.g.
stroke)
Rigidity: Increased resistance independent of direction (lead pipe and cog wheel). Rigidity indicates
extrapyramidal dysfunction – lesion of basal ganglia.
Hypotonia:
Excessive floppiness, reduced resistance and easily waved distal limb (involvement of LMN e.g. primary
muscle disorder cerebellar Dx)
Paratonia:
Rigidity when limb is moved rapidly but normal when moved slowly (frontal lobe or diffused cerebral
Dx)
Q84.Brain abscess
Maybe:
Extradural
Subdural
Cerebral
Cerebral abscess
Hematogenous spread from inflammatory Dx
Local spread may be direct (penetration) or indirect
Site depends on source:
Chronic otitis media (temporal lobe)
Mastoiditis
Compound #
Frontal sinusitis
Infected dental caries
Etiology: strep. Pneumonia, s. aureus, proteus, toxoplasma
Clinics:
Toxicity produces- pyrexia, malaise
Raised ICP
Focal signs
Neck stiffness (coz of tonsillar herniation or meningism)
Q85. Pyramidal tract lesion
Sub cortical lesion: contralateral monoparesis of hand/arm wth jacksonian epilepsy
Internal capsule: spastic contralateral hemiplegia & paresis of hypoglossal and facial nerves
Peduncle: alternating syndrome; ipsilateral occulomotor palsy and contralateral spastic hemiplegia
Pons: contralateral/ bilateral spastic hemiplegia & ipsi abducens and trigeminal palsy
Pyramidal lesion-flaccid contralateral hemiparesis
Cervical cord: spastic hemiplegia wc is ipsilateral
Ant horn: ipsilateral flaccid paresis
Thoracic: spastic ipsilateral monoplegia of leg (if bilateral= paraplegia)
Q86. Migraine
Common, familial disorder affecting females mostly; it is a unilateral, throbbing headache.
With aura: warning sign; visual, sensory or motor, with headache worsened by light, noise, relieved by
sleep with vomiting and nausea.
Without aura: headache acc by tension
Mech: either neuronal or vascular
Types:
Basilar: bilateral visual symptoms, dysarthria, unconsciousness, vertigo
Hemiplegic: unilateral paralysis, often mistaken for stroke
Opthalmoplegic: extra ocular nerve palsies
Sometimes may be acc by coma: migraine coma
Enhancing factors: Diet (tyramines), hormones, stress, fatigue
Diagnosis:
Clinical history
Tx
Avoid risk factors
β- Blockers
5HT2 blockers
Anticonvulsants, antidepressants
In case of acute attack: analgesics, Sumatriptan, ergotamine, methlyprednisolone
Q87. Brain Meningioma extrinsic tumourl
Slow growing and arise in subarachnoid granulations, esp. around venous sinuses. Usually benign
Class
By localization
Falcine, convexity, olfactory groove, supra sellar, sphenoid wing, post fossa, tentorial
By histology
Syncytial, transitional, fibroblastic, angioblastic
Clinic
Epilepsy, headache, vomiting, papilledema, foot weakness, homonymous hemianopia, memory and visual
impairment, Foster- Kennedy syndrome (optic atrophy+ papilledema), ptosis, facial pain
Diag
CT, MRI, angiography
Tx
Remove tumor, catheterization and embolization (to ease removal)
Q88. Trigeminal nerve
n. opthalmicus: nn. Frontalis, lacrimalis, naso cilliaris
Ganglion trigeminalis sup orb fissure
n. maxillaries: nn. Pterygopalatini, alveolaris sup, zygomaticus
For. Rotundum
n. mandibularis: supplies masticatory muscles
For ovale
Syndromes:
Neuralgia (tic douloreux): sharp, agonizing, pain in region of supply. Esp. when touched and trigged by
washing, brushing teeth etc
Symptomatic pain: in territory of one branch, pain. Coz of infected tooth, sinusitis, fractures etc
Charlin’s syndrome: severe pain in inner corner of eye, pain in root of nose, lacrimation and nasal
secretion ipsilaterally. (Irritation of ciliary ganglion)
Gradenigo’s syndrome: pain in area of frontal branch, with abducens paresis
Bing- Horton’s: pain during sleep ass with reddening of ipsilateral face, lacrimation, nasal secretion and
Horner’s syndrome
Carotid artery aneurysm
Other Dx (meningitis, cranial dx)
Trismus: strong tension, pt cant open mouth due to encephalitis, tetanus, rabies
Q89. TB meningitis
Etiology:
M.TB, Bovis
TBM is common result of TB infection of NS
After bacteremia, metastatic foci lodge in 1. Meninges 2. Cerebral/ spinal tissue 3. Choroid plexus
Rupture of encapsulated foci leads to spread of infection to SubA space
Clinic:
Stage 1 Stage 2 Stage 3
Non specific symptoms confusion coma
Fever CN paresis
Lethargy meningism
Vasculitis
Seizures, chorea, myoclonus, dementia may occur.
Diag
General exam (anemia, leukocytosis)
Chest X-ray
Tuberculin skin test
CT/MRI
Tx
Anti TB TX (Iso, Rif, Pyr)
Steroid therapy
Q90. Methods of clinical genetics
Genealogical: pattern of inheritance, expressivity& penetrance, probability or abnormal off spring
Statistical: frequency of dominant & recessive alleles, intensity of mutations, distribution of defects and
prediction of their appearance in future
Gemellary: relation btwn genetic and environmental factors in mutation
Cytological: investigation of structure of chromosomes & their possible mutations
Q91. Sleep, fxns & physiology, disturbances
Sleep is produced as a result of stimulation of sleep producing centers in the brain (RF& raphe nuc)
There are two stages: REM & non REM sleep

Fluctuating vitals stable vitals


Dreams, twitching, frm RF no dreams, no twitching, raphe nuc
Normal pattern comprises of: 60-90 mins non REM & 10-15 mins REM
Disturbance:
Narcolepsy: Irresistible desire to sleep
Catalepsy: sudden loss of postural tone
Sleep paralysis: paralysis upon awakening (2-3mins)
Hypnagogic hallucination: vivid dreams as pt fall asleep of while partially awake
Also: night terrors, night mares, sleep walking, sleep apnea, hypnic jerks, hyper & in somnia
Diag:
EMG & history
Tx: amphetamines
Q92. Diabetic neuropathy
NS damage is related to poor mngmnt of IDDM. Damage results from accumulation of sorbitol in axons
Variants& syndromes:
1. Poly neuropathy: distal weakness, sensory neuropathy (large: ataxic & small: painful anesthesia fiber)
2. Autonomic: pupil abnormalities, orthostatic hypotension, and impotence
3. Asymmetric: CN palsy without pain
4. Diabetic amyotrophy: pain & weakness esp. ant thigh, loss of knee reflex
Tx
Control of IDDM
Carbamazepine, antidepressants
Aldose inhibiting drugs
Manage autonomic neuropathy
Q93. Parkinson’s Dx
An extrapyramidal disorder
Etiology:
Idiopathic, encephalitis lethargia, 20 Parkinson’s Dx (drug induced/ toxic), ass with other Dx, familial
Mech:
Paleness of sub nigra& other brainstem structures coz of loss of neuromelanin (pigmentation cells). The
remaining cells contain Lewy bodies (with α synuclein).
Idiopathic is thought to be caused by imbalance in dopamine-Ach levels causing dopamine depletion. The
impaired motor fxn is coz of imbalance of inhibition and excitation.
Clinic:
Initially vague: aches and pains
TREMOR: pill rolling esp. in upper limbs at rest, improves w mvmnt and disappears when asleep
RIGIDITY: esp. in flexors, “cog wheel” tremor, and pt is in flexed position
BRADYKINESIA: mask like face, slow shuffling gait, dysarthria, dysphagia
Smtyms autonomic dist: postural hypotension
Tx
Anticholinergic drugs
Incr dopamine (L- dopa)
Dopamine agonists
Amantidine (for rigidity)
Human fetal medullary transplantation
Addnl: nausea, hypotension, confusion & dementia
Q94. Neurosis
This is an unpleasant, mal-adaptive psychological disorder that affects personality, mood & behavior. It
doesn’t affect daily activities.
Classification
• Anxiety neurosis: incr tension unrestricted to specific situations. Symptoms include; palpitations,
heart pain, dyspepsia, constriction of throat, tremors in extremities with sweating, clear
consciousness.
• Cardiac neurosis: neurasthenia (nervous exhaustion; back ache, lethargy, insomnia, musc pain,
depression, irritability, decr concentration)
• Compensation: belief that by continuing to be ill they will receive some form of compensation
• Compulsion: over powering impulse to perform certain activities repeatedly, hand washing,
touching, counting
• Expectation: anticipation of an event dat produces nervous symptoms
• Hysterical
• Obsessional: recurrent thoughts dominate the victims. E.g. reluctance to hand shakes for fear of
contamination
• War

Tx
Psychotherapy: cognitive, behavior therapy
Minor tranquilizers
Q95. Tunnel median nerve syndromes
C7- C8, lat median cords, supplies the palmar side of radial border of hand.
Causes
Entrapment under carpal ligament
E.g. rheumatoid arthritis, acromegaly, fluid retention, infiltration of ligaments
Symptoms
Pain esp. @ nite
Paraesthesia
Loss of sensory sensation
Mus wasting and weakness in thenar
Tinel’s sign: percussion of nerve at the wrist produces incr paraesthesia
Tx
Treat underlying cause
Diuretics
Surgery: division of ligament
Q96. Torsion dystonia
These are sustained abnormal postures produced by contraction of trunk & limb muscles.
TD has child hood onset, Autosomal dominant
Clinics
Extensive turning and twisting mvmnts of trunk and proximal extremities
May be idiopathic or symptomatic (encephalitis, Wilson’s Dx)
Abnorm posture of head trunk and limbs
Normal during sleep
Diagnostics:
EMG
Tx
L- Dopa
Carbamazepine
Anticholinergics
Stereotactic surgery:
Lesion in ventrolateral thalamus reduces dystonia in contralateral side
Q98. Neurological symptoms of alcoholism: neuropathy
Polyneuropathy is a common result of chronic alcoholism, it may occur alone or with Wernicke’s
encephalopathy etc Polyneuropathy is usually symmetrical, esp. in legs, methanol produces sudden
blindness.
Alcoholic neuropathy: sensorimotor neuropathy affects legs.
Mech: local compression of nerves during alcohol obtundation.
Radial compression in humerus spiral groove= wrist drop, peroneal nerve at head of fibula, ulnar nerve in
medial epicondyle; if deficit dsnt improve within 2mnths surgery or electrodiagnostic tx is indicated.
Clinic:
Progressive
Sensory symptoms: numbness, paraesthesia
Motor signs: foot drop, wrist drop, weakness
Diagnostics:
EMG: axonal damage
Incr liver enzymes
Tx
Stop OH, thiamine diet (100mg/day)
Q100. Subthalamic syndromes, panic attacks
The main structure: corpus luisi. Part of extrapyramidal system, in case of Corpus damage, there is
contralateral hemiballismus (pain attack)m
Borders: red nuc and sub nigra
1. lesion of all sensory pathways:
• Contralateral hemi anesthesia
2. lesion of trigeminal nuc & lat Spinothalamic tract
• Contralateral loss of pain & temp on face & body.
3. lesion of ant Spinothalamic tract& med leminiscus
• contralateral sensory loss with intact pain & temp
4. lesion of spino trigeminal nuc and tract & lat sp thalamic tract
• Loss of temp & pain on ipsilateral face contralateral body.
Q101. Tunnel syndrome of radial and ulnar nerves
Entrapment of a nerve in a tunnel where it passes:
Ulnar
Cubital or guyon’s tunnels
Causes:
Elbow trauma, repetitive mvmnt, and prolonged flexion
Clinical
(Cubital) claw hand
(Guyons)
In case of complete lesion dorsal and palmar sensory loss without fingers. In case of deep lesion motor
loss, in case of superficial only sensory loss.
Radial
Axillar groove
Post interosseous nerve
Sup sensory branch
Causes
(Axillar groove)
Bad use of crutches
Vigorous hand exercises
Clinic:
Weakness of muscles
Sensory loss on dorsal hand, thumb, index & mid finger
Wrist drop (no extension of hand & fingers)
PIN: same as abv
SSB: sensory loss in radial distribution
Q102. Neurofibromatosis
Dominant her Dx wch leads to multiple tumor formation in nerves.
Type 1(NF1)
Embryologic; overgrowth of mesoderm and ectoderm (meninges, skin, viscera, CNS, CVS)
Clinic:
Café au lait spots- demarcated edged spots wch grow with age
Scoliosis
Mental retardation & epilepsy
Neoplasia (intracranial, Intraspinal, peripheral nerves)
Lesch nodules
Mollusca fibrosa

NF2 (acoustic neuroma)


Tumors of CN VIII (vestibulocochlear)
Benign
Clinic
No café au lait
No scoliosis
Etc
Bilateral tumor of CN VIII (imbalance & deafness)
Diagnosis:
Family history
CT
MRI
Myelography (NF1)
Tx
Cosmetic surgery
Intraspinal: sacrificial removal of tumor
Q103. Disturbance of consciousness, cerebral comas; mech, diagnostics, diff diag, emergencies
Consciousness: a state of awareness of self and surroundings.
It may be: awareness, stupor, confusion, semi consciousness and deep coma.
By the Glasgow scale, coma is described as a state with absence of speech, eye opening and motor
response.
Mech: consciousness depends on intrxn of intact cerebral hemispheres with reticular activating system in
brainstem, mid brain, hypothalamus, and thalamus.
Damage may be:
Diffuse hemispheric (tumor, ischemia, renal- hepatic failure)
Bilateral thalamic involvement (astrocytoma)
Brainstem involvement (ischemia hemorrhage)
Supra tentorial mass (causing herniation)
Brainstem compression
Clinic:
1. Signs of trauma: basal skull fracture
Raccoon eyes, Battle’s sign, Hemotympanum, Rhinorrhea, otorrhea, Skull palpation
2. Blood pressure
3. Rectal temp and skin colour
4. Meningial signs
5. Optic fundus examination
Diagnostics:
CT, CSF, metabolic screen
Diff diag:
MS
Migraine
Trauma
Acute hypertensive crisis
Tx:
A, B, C
If etiology is unknown give 50ml glucose IV
NEVER introduce anything orally
Paraentral nutrition
Fluid/ electrolyte balance
Hemostasis
Monitor vitals
Q104. Brain dislocation, diagnostics and tactics
1. Tentorial herniation (lateral): this occurs in case of a unilateral expanding mass causing hern
niation
2. Tentorial herniation (central): occurs in cases of midline shift or diffuse swelling of cerebrum, it
leads to herniation thru the same hiatus
3. Midline shift (subfalcine) herniation: in case of a unilateral space occupying mass.
4. Tonsillar herniation: it is caused by sub tentorial expanding mass that leads to herniation of
cerebral tonsils thru foramen magnum causing brainstem and med obl involvement
Clinical:
LateralZ
Decr consciousness
Homonymous hemianopia (occlusion of post artery wch supplies occipital lobe)
Pupil dilation
Ptosis, impaired mvmnt
Limb weakness
Central
Diabetes insipidus (ADH associated)
Decr consciousness
Tonsillar
Resp impairment
Decr consciousness
Neck stiffness
Head tilt
Diagnostics:
CT
ICP monitoring

Tx
Remove mass
Decr ICP
Normalize blood gases
Q105. Epilepsy, attacks, status Tx
Successive tonic/clonic seizures with gaps in between, if consciousness does not return during gap=
status epilepticus. It is life threatening, and may be caused by: pregnancy, frontal lobe lesions, metabolic
disorders, head injury. Types: tonic/ clonic, absence seizures, status epilepticus, grand mall, petit mal
e.t.c.
Tx
GENERAL
Oxygen therapy- 10litres /min
IV infusion of 500ml 5%dextrose/0.9N saline
Prevent hyperthermia

Diazepam: short acting (5mg IV), decreases respiration


Phenytoin: long acting
5. Loading dose= 15mg/kg at rate of 50mg/min
6. maintenance= 500mg IV, PO daily
7. monitor ECG
PS thru out tx pt shud rcv initial anticonvulsant
Balance electrolytes
Anesthetics at non anesthetic doses may be used.
Q106.Alternating syndromes at Pons lesion
(My Friend Got Back Russian Girls)
1. Millar- Gubler: lesion of n. facialis (CN VII) & pyramidal fascicle
Ipsilateral flaccid paresis of face and body, contralateral hemi paresis
2. Foville: lesion of n facialis, pyramidal tracts & n. abducens
Ipsilateral flaccid paresis of face &body, convergent strabismus & contralateral hemi paresis
3. Gasperrini: lesion of n. abducens & facialis as well as cover of the pons
Flaccid paresis of face, audition, & contralateral hemi anesthesia
4. Brisso- sikara: lesion of pyramidal system n. facialis & its nucleus
Ipsilateral spastic paralysis of mimic musc, contralateral spastic hemiplegia
5. Raimon- sestan: lesion of median longitudinal fascicle and pyramidal tracts
Ipsilateral ataxia, choreatheoid hyperkinesia, contralateral spastic hemiplegia and hemi anesthesia
6. Graine: lesion of nucleus of n.trigeminis (CN V) and Spinothalamic tract
Ipsilateral sensory loss on face and contralateral hemi anesthesia on trunk and extremities
Q107. Acute cerebral hypertonic crisis (hypertensive encephalopathy)
It is caused by xs or malignant BP in cases of uncontrolled BP e. g. glomerulonephritis, pregnancy, and
pheocytochroma Mech: This is an acute, transient syndrome; Sudden severe cerebral hypertension

Spasm micro infarction


Incr BP forced ventilation petechial bleeding
Incr vascular
Permeability edema
In cerebral resistance Vessels
Clinic
Headache
Confusion
Coma
Papilledema
Proteinuria
Resp & cardiac failure
Diag
CT: wide spread white matter
MRI: incr brain H 2O content
Tx
Sudden improvement of high BP may lead to retinal damage, so decrease slowly (IV nitroprusside /
hydralazide)
Prophylaxis
Avoid risk factors, Regular check up
Q108. Spinal cord injury
Etiology
Violence, falls, injury i.e. trauma
Clinic
 Brown Sequard syndrome
 Cauda equina & conus medullaris syndromes
 Complete cord transection
 Ant horn syndrome
• Paralysis w loss of pain and temp below level of lesion
• Retention of proprioception
Central cord syndrome
• Arm & leg weakness
• Pain & temp are the most affected coz lat Spinothalamic tract crosses ventral to central
canal (Dissociated sensory loss in cape like distribution)
Diagnosis:
Motor weakness
Areflexia
Beevor sign:
Pt flexes neck to look at navel, and it moves upward.
Llhermitte’s sign
Diff diag:
Acute demyelinating polyradiculopathy ALS, MS, Cauda equina syndrome, Gullier Barre
Tx: Prevent bed sores, Catheterization, Splints.
Surgery: spinal fusion with plates on either side of spinous process abv and below affected vertebra

THE END!!!!!!!!!!!!!!