neurology exam

8/7/2019 neurology exam

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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 , claw hand )

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 andrhinorrhea, partial Horners. 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 approachSumatriptan 6mg subcut

Oral tablets(slower) VerapamilSumatriptan MethylsergideZolmitriptanRizatriptan

Ergotaminesumatriptin 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 headachethat is unresponsive to treatment. Trigeminal nerve surgery is carried out:

Gangliotomy or pre-ganglionic nerve- root section. These provide numbness tho pts still feel clusterheadache 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


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Sensations are described by delusional overtones. I feel lump on my skull, my bones are

rotting

Negative tests dont reassure pt

Willing undergo investigations.

Q3. Classification of hereditary neurological Dx

1) Single gene disorders

Autosomal dominant: Huntingtons disease

Autosomal recessive: cystic fibrosis

X linked traits: Duchennes syndrome

X-dominant: phosphate diabetes

2) Chromosome anomalies 3) multifactoral disorders

Structural cancerDeletion rheumatismMicrodeletion atherosclerosis

Duplication hypertensionInversionIso chromosome

TranslocationRing shaped

Numerical

Aneuploidy (Downs)Polyploidy4. PHM progressive her myopathy

Duchenne

Myasthenia5. Neurohereditry amyotrophies

ALS

Syringomyelosis

6. Pathology of extra pyramidal system

Q4. Spastic paralysisThis 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. Babinskis), 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 atrophyDiagnostic 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


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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 kernigs 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

Diagnostics1. 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- fractureRx 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.


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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 voiceStrengthless, 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 dont 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 airway2. 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. Completehemisection 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. jointposition 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 theischial tuberosity and the greater trochanter (femur). It innervates the hamstring mus of the thigh (semi

tendinous, membranous and biceps femoris)

Causes of damage:


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Hip dislocation

Penetrating injuries

Incorrect IM injections

Entrapment

Systemic causes( Diabetes mellitus, sarcoidosis)

Symptoms:Muscle weaknessLoss 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

Benedicts syndrome: paralysis of CN III; ipsilateral ptosis, divergence strabismus. Contralateral; atheoid,

intentional tremorQ11. 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.


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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 weaknessPain increases cardiac & resp mus involvement

Paralysis developsResp 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 balanceVentilation

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

Beckers dystrophyDejenrines dystrophy

Duchennes dystrophy:X-linked recessive disorder affecting boys

Clinical:

delayed motor dev

clumsiness( 3-5 yrs)

waddling gait(glutei mus involvement)

sway back posture

Gowers 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 anddeltoid may also be affected.

Investigation:

Musc enzyme creatine kinase

ECG

EMG

Musc biopsy

TxOrthopedic Tenotomy may prolong mobility


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Steroids

Intrauterine diagnosis+ abortion

Q13. Pallidar system and its lesion. Parkinsons 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. Italso 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 (Parkinsons Dx, paralysis agitans)

Akinesia: hypomimia, only eyes move; head doesnt, speech becums monotonous, body

is stiff, arms dont 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. Charkos neural amyotrophia & Hoffmans

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 & tizanidinePhysiotherapy

Riluzone

Hoffmans 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


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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 &

fasciculations of tongue

Spastic paralysis, without atrophy

Nystagmus, ptosis and facial paresis Forced laughter and crying

No gag reflex Oral automatism

Exaggerated gag reflex

NB: bilateral damage of CN XGONNER!!

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 progressive4. benign

Criteria:

2 or more lesionsMore than 1 attack

Pathogenesis:

Immune deficiency

Viruses

Genetic factors

It is multifactoralScattered lesionsdetermination 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


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Hyperreflexia

Extensor plantar response( Babinskis sign)

No abd reflexes

3. Sensory loss

Numbness, paraesthesia

Post column lesion: no position awareness

Llhermittes 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

1 & 1 INF Copolymer(binds to immune complexes and eliminates)

In case of 1 or 2 progressive

Cytostatics(anti tumor)

Corticosteroids

plasmapharesisSymptomatic

Spasticity: antispastics

Urinary : catheterization

Ataxia: 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


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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-rayCT scan

Myelograpy / MRI

Angiography

Lumber puncture is NEVER performed coz this can lead to herniation!!!!

Tx: A B C

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, Babinskis, 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, producingexcessive 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


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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. Strumpells 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 malformationsAbnorm 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 vasopathy6. 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 permin (norm= 50-55) neuronal death occurs. The region in which this occurs is called the ischemic

prenumbraAn 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


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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

ECGEEG

Tx and prophylaxis

1. risk factors

2. pharm therapy

3. surgeryGeneral measures

respiration

metabolism

cerebral autoregulation

rehabilitation

Medical therapy(a) anti aggregants

(b) anti coagulants

Surgery

Q24. Hereditary ataxias. Friedrichs ataxia

Dominantly inherited:

ACDAs:

Type 1 Type 2 Type 3

Mild ataxia Expressed ataxia Only ataxia

Opthalmoplegia Expressed retinopathy

Mild dementia DementiaOptic atrophy Extrapyramidal features

Spasticity

Recessively inherited:

1Louis-Barr syndrome characterized by cerebellar ataxia, multisystem disorders andocular, cutaneous teleangiectasia due to chromosome 11 gene defect.Purkinje and

granular cell loss occurs

2Friedrichs ataxia (chromosome 9 defect)


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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 Rombergs sign & ataxia

Pes cavus( Friedrichs foot)

Kyphosis/ scoliosis

Limb weakness

Abs of abd reflexes

No Babinskis sign

Abs of lower limb reflexes

dysathria

Diagnostic variants:

Marys spastic ataxia + spastic paraparesis

Strumpell- Lorraine syndromeQ25. Gait infringement. Ataxia diff diagnosis and clinic

1. Ataxic

Sensory

Cerebellar

2. Hemiplegic

3. Parkinsonian

4. steppage

5. myopathic

6. frontal lobe7. hysterical

8. cautious

9. choreic10. 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


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Friedrichs 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 Rombergs sign

Pes cavus( Friedrichs foot)

Kyphosis/ scoliosis

Limb weakness

Abs of abd reflexes

No Babinskis sign

Abs of lower limb reflexes

Autosomal dominant Cerebellar ataxia (ADCAs)

Idiopathic late onset ataxiaType 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

(mmH2O)

cells protein appearance

Normal 70-120 - 20-40 Clear

tumor incr incr Incr protein Clear

Abscess 600-700 incr Incr Clear then cloudy

Purulent

meningitis

250-700 Incr incr Yellowish

TB meningitis 200-450 Yellowish

Syphilis 200-300 Cloudy

Subdural

hematoma

Incr Norm Yellowish

SAH Incr RBCs Bloody

MS normal Lymphocytes Clear

Symptoms:

Hydrocephalus

1. Internal hypertensive2. Occlusive non communicating

3. Communicating internal

4. Pyocephalus


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5. Foramen monro obstruction

6. Norma pressure

7. Hypersecretion

8. Hypoliquorrhea

Liquorodynamic tests1) Queckenstedts test:

To determine degree of blockageLP 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 systemWilsons Dx (hepatolenticular degeneration)autosomal recessive.

Rare Autosomal Dx of Cu++ metabolism affecting the liver (it looks cirrhosed).

Cu accumulates in organs esp. on Decements 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 andurine.

Clinical pic:

Acute: Chronic:

Bradykinesia wing beating tremor

Behavioral changes dysarthria, dystonia, rigidity

Involuntary mvmnts chorea movements

Liver involvement psychosis

Kayser-fleisher ring- diagnostic featureDiagnosis:

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


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Pathway Sense

Spinothalamic pathway:

Receptor post horn lat nuc of thalamus

Pain & temp

Simple touch

Dorsal column pathway:(proprioception tofasciculus gracillis & cunateus)

Receptor fasc gacilis & cunateus latnuc of thalamus(the fibres cross in med obl)

Discriminating touchProprioception( conscious)

Dorsal spinocerebellar tracts:

ANT: receptor ant horn vermis

POST: post horn

Unconscious proprioception

Muscles, bones, ligaments

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 lobeSelective 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: cows milk

Clinic:General; fever, myalgia

Specific;

Memory loss

Olfactory hallucinations

Focal neurological signs

Confusion

Diagnostics:


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CSF tests;

WBC increase

Protein incr

Glucose decr

PCRTx:

Antiviral therapyAnticonvulsants

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:

CommunicatingThere 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 tumorsClinic:

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

communicatingChari 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. Somefibres 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.


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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), cerebraledema= central tentorial herniation

Diagnosis:

CT, MRI, CSF, EEG, PCR

TxAcyclovir 10-14 days

Q33. Huntingtons 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:

ChoreaInitial symptom, feeding and walking become impossible

DementiaBehavioral disordersHypotonia

Primitive reflexes e.g. grasp, pout, palmomental reflexProximal extremities, trunk and facial musc affected such dat speaking& swallowing is difficult.

Diagnosis:Family history

CT scan (atrophy of caudate nuc)

MRITx

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.


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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 centralhemiplegia

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 lesion3. bulbar/ pseudobulbar palsy

4. nuclear lesion: pons, internal auditory meatus, facial canal, peripheral nerve

lesionsOther disorders incl Bells 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 kernigs

coma

epileptic seizures

focal signs

papilledema

pyrexia

Diagnostics:


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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 craniotomy2endovascular 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 DxGenotype: 47XXY, 48XXXY, 49XXXXY

Or 47XYY, 48XYYY

Typically males

Clinic:Onset at puberty

Hypogonadism

Sterility

Externally; tall, asthenic, gynecomastia, long limbs

Turners 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 cells2nd neuron= mitral & tuft cells of bulb

3rd neuron= n. amygdaloideus

Lesion of olfaction:

1. Agenesis of olfactory tracts

2. Dx of upper olfactory mucosa3. Fracture of lamina cribrosa causing tearing of fila olfactoria

4. Destruction of bulb by contusions e.g. falling on back of head


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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 disordersidiopathic

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 plagueitself may be emboli.

Clotting:

(Lateral medullary syndrome) on ipsilateral side:

1. cerebellum: ataxia, dysarthria, vertigo

2. brainstem: Horners syndrome, sensory loss( pain & temp, pharyngeal and laryngealparalysis)

Contralateral sensory loss of pain and temp in limbs & trunk

Q40. Transverse lesion of sp Cord

In the acute phasespinal shockdevelops:(Lesion of upper cervical) comprising of resp insuf, quadriplegia, Neurogenic shock, loss of bladder and

rectal control, this is acc by ipsilateral Horners syndrome

Lesion oflower cervical cordleads to paralysis of intercostals= resp insufUpper 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


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Acute demyelinating neuropathy, of viral etiology

Clinic:

Sensory; paraesthesia, paresis

Weakness

AreflexiaBack pain (initial symptom)

Facial painPapilledema

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 lymphomaLymphoma

Neurofibroma

Extramedullary

Meningioma DermoidSchwanoma

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 funiculusIncontinence of bladder and rectum

Intramedullary tumor: longitudinal growth

No Radicular pain, sensory disorders, bladder & rectum disordersAtrophy of supplied mus

If tumor involves upper cervical thickening= signs of bulbar involvement

Q43. Research of eye ground


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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 diskDisc found with great difficulty= papilledema

Disc flashes like white tennis ball= 1o disc atrophyVariants 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 Lasegues sign

Severe pain may inhibit micturation

Central disc protrusionUsually 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= laminectomyPost surgery avoid lifting

Q45. Prophylaxis of H. Dx

1. Initial referrals for evaluation and counseling (in cases of still births, fetal abnormalities)


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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 thecerebrum 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 Rombergs 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, chemotherapyAstrocytoma: common in children (if brainstem not involved OP),

Extrinsic;

Acoustic Schwanoma :(nerve sheath tumors)cerebellopontine angle lesions, bilateral chrct for NF2, theyr benign, damage CN VIII

Tx: translabyrinthine & middle fossa approachDermoid cysts: rare, embryogenic cysts. They adhere closely so cant 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:

Horners 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

BrainstemMid fossa

Cervical Cord

int carotid artery

ant roots of C8- T1

Congenital familial Horners 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)


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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 testsTx

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

MyelographyMRI

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 + SAH2. 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

DiagnosticsCT

TxSymptomatic

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)


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2. Vagus disorders

Palatal weakness: uni/ bilateral

Pharyngeal weakness: uni/ bilateral

Laryngeal weakness

3. Accessory disordersUnilateral paralysis of SCM (cant turn to opp side); bilateral (cant 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-XICallet-Sicard syndrome: extra cranial lesion involving CN IX-XIIVillarets syndrome: retropharyngeal space lesion involving CN IX-XII & Horners 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 weaknessDiagnosis:

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, Downs 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 chromosomeremains highly condensed and stains darkly during interphase = Barr bodies)Centromere constricted area of metaphase chromosomeTelomere DNA sequence at ends of chromosomesClassification

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

Downs syndrome:

Trisomy 21 affects both males and femalesClinic:

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: Alzheimers 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


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PSNS nuclei (Perlias) -between the autonomicINNERVATION:

Motor= mm recti sup, inf, medial, m. inf orbicularisAutonomic= m. sphincter pupillae, m. ciliare

Longitudinal fascicle:

Constitutes a collection of various fiber systems connecting nuclei abducens, Trochlear and OculomotorIt 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 reflexesSuperficial reflexesThese 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 reflexesDTR (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 normalDiff diag

MS

Tx

Steroids in acute phaseCyclophosphamide

Q61. Intracranial Hypertensive syndrome

Incr in brain-water content, incr in CBF, CSF or expanding mass = incr ICP


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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 gliaInterstitial: 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

SedativesSteroids

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 fingerWeak 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


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Rheumatoid arthritis

Osteomyelitis

Tx

Steroids

Muscle relaxants (500mg, PO/ 6 hrs)Physiotherapy

RestSoft 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: analgesicSurgery:

Nerve block, root section

Q64. Lesion of right internal capsule

Contralateral spastic hemiplegiaContralateral 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

ExcitotoxinsGenetic predisposition

Toxins

Minerals

Forms

I. Cervical: spastic paresis in legs, flaccid in arms, dysphagia

II.Bulbar: dysarthria, tongue fasciculations, pyramidal symptomsIII.Pseudobulbar form: Dysphagia, pathological laughing and crying, frontal dementia, l.m.n lesionsymptoms

IV.Lumbar form: flaccid paresis in legs, with atrophy & fasciculations

Clinic:@ Onset: asymmetric weakness & wasting of extremities

Bulbar & pseudobulbar featuresFrontal dementia

Pseudobulbar palsy:

Weak musc of mastication & facial expression

Incr gag& jaw jerk reflex

Drooling speech

Dysphagia

Immobile pointy tongue


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Progressive bulbar palsy:

Atrophy & fasciculation in mus supplied

Wasted tongue

No jaw & gag reflex

Corticospinal involvement:

Hypertonia

HyperreflexiaAnt 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- physiotherapyResp 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 dumbellClinic:

Ass with multiple neurofibromatosis

Caf au lait spots

Root painCompression symptoms may follow

Diagnostics:

MRI, CT

Oblique X-ray: foraminal enlargement

TXComplete removal, sacrificial coz other nerves compensate for lost ones

Q67. Lesion of frontal lobe


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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

TxExtensive contusion w edema= focal mass lesion: surgery

A, B, C

Elevate head & give barbiturates and furosemide

Cx

Post traumatic epilepsyIntracranial 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 therapy5. 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


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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 onlyBells 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)

Bells 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)

EmboliMech:


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CBF< 20-30ml/100g/min = neurological symptoms.

If flow is restored during critical period= OK

1. haemodynamic mech: reduced flow thru vessel2. embolic mech: from aortic arch, heart

Clinic:

Carotid artery (anterior)

Hemiparesis, hemi sensory loss, dysphasia, one eye blindnessVertebro- basilar (posterior)

Loss of consciousness, bilateral limb sensory dysfxn, vertigo, tinnitus, Diplopia

Tx

Anti platelet/ coagulant drugs

BP controlCarotid endarterectomy

Prophylaxis

Decr risk factors

Counseling

Q72. Progressive hereditary Erbs 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)

Avellis syndrome:

Ipsilateral flaccid hemi paresis of tongue, vocal cords, soft palate; contralateral hemiplegia

Jacksons syndrome:Ipsilateral flaccid of tongue; contralateral spastic paralysisWallenberg syndrome:

Ipsilateral unilateral paresis of tongue vocal cords, soft palate, Dysphagia, Horners syndrome, ataxiaContralateral anesthesiaSchmidts syndrome:

Ipsilateral paresis of vocal cord, SCM & trapezoid muscles

Contralateral spastic hemiparesisBabinsky:

Ipsilateral cer ataxia, Nystagmus, Horners synd, hyperthermiaContralateral 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 tractsQ74. Lesion of brain in case of flu, diphtheria & botulism

DIPTHERIAInfection with C.diphteriae affecting upper resp tract, skin

3 stages:

After 2-3 weeksPalate weakness after throat infection or Focal weakness of musc closest to cutaneous infection

After 4-5 weeks

Pupillary response impairment


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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 velocityTx

Horse diphtheria antitoxinABiotics

Supportive therapy

BOTULISMToxin 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

DysphagiaDifficulty in resp

Limb weakness is last

Muscarinic effects; xerostomia, blurry vision, paralytic ileus & postural hypotension

TxHospitalization

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 effectsCompression 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


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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 withsteroids 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 craniotomy3. 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 calledfocal epilepsy.Partial/ local/focal epilepsy

A. Simple partial seizures

Sensory

MotorB. 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, trunkJacksonian motor seizure: involuntary mvmnt from one musc group to another (march)

Mvmnt is clonic, after seizure affected limbs are weak

Todds 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 presentwith 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: dj 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


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Pt then sleeps cant 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 yearsSurgery:

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

ClinicPulsating tinnitus

Prominent facial veins

Pulsatile exopthalamus

Edema of periorbitPapilledema

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:

Brocas 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 fluencyComprehension

Assess spontaneous speech, writing, reading


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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 cant link i.e. dsnt see relation

Total: severe includes wernickes, brocas area

Agnosia:Loss of comprehension of auditory, visual other sensations tho sensory sphere is intact

Auditory, colour, finger, optic, tactile, time

Antons syndrome: when one is no longer aware of opposite side cant 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) cant carry out task when asked to but otherwise can perform it

Ideational (frontal lobe Dx) cant 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 proteinTx

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)


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Paratonia:

Rigidity when limb is moved rapidly but normal when moved slowly (frontal lobe or diffused cerebral

Dx)

Q84.Brain abscess

Maybe:Extradural

SubduralCerebral

Cerebral abscessHematogenous 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 epilepsyInternal 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 paresisThoracic: 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 bysleep with vomiting and nausea.

Without aura: headache acc by tensionMech: either neuronal or vascular

Types:

Basilar: bilateral visual symptoms, dysarthria, unconsciousness, vertigo

Hemiplegic: unilateral paralysis, often mistaken for strokeOpthalmoplegic: extra ocular nerve palsies

Sometimes may be acc by coma: migraine comaEnhancing factors: Diet (tyramines), hormones, stress, fatigue

Diagnosis:

Clinical history

Tx

Avoid risk factors

- Blockers

5HT2 blockers

Anticonvulsants, antidepressants


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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 localizationFalcine, convexity, olfactory groove, supra sellar, sphenoid wing, post fossa, tentorial

By histologySyncytial, transitional, fibroblastic, angioblastic

Clinic

Epilepsy, headache, vomiting, papilledema, foot weakness, homonymous hemianopia, memory and visual

impairment,Foster- Kennedy syndrome (optic atrophy+ papilledema), ptosis, facial painDiag

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, zygomaticusFor. Rotundum

n. mandibularis: supplies masticatory musclesFor 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

Charlins syndrome: severe pain in inner corner of eye, pain in root of nose, lacrimation and nasalsecretion ipsilaterally. (Irritation of ciliary ganglion)

Gradenigos syndrome: pain in area of frontal branch, with abducens paresis

Bing- Hortons: pain during sleep ass with reddening of ipsilateral face, lacrimation, nasal secretion and

Horners syndromeCarotid 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 comaFever CN paresis

Lethargy meningismVasculitis

Seizures, chorea, myoclonus, dementia may occur.

Diag

General exam (anemia, leukocytosis)

Chest X-ray

Tuberculin skin test


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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 andprediction 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 sleepCatalepsy: 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 somniaDiag:

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 impotence3. 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. Parkinsons Dx

An extrapyramidal disorder

Etiology:Idiopathic, encephalitis lethargia, 20 Parkinsons 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 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


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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

doesnt 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 tranquilizersQ95. 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

Tinels sign: percussion of nerve at the wrist produces incr paraesthesia

TxTreat 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


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May be idiopathic or symptomatic (encephalitis, Wilsons Dx)

Abnorm posture of head trunk and limbs

Normal during sleep

Diagnostics:

EMGTx

L- DopaCarbamazepine

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 Wernickes

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

neurology exam

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