Neurology

Question 1

causes of myopathy

Answer 1

1. Hereditary muscular dystrophy
2. Congenital myopahties
3. acquired (PACE PODS)
   Polymyositis or dermatomyositis
   Alcohol
   Carcinoma
   Endocrine( hypothyroidism, hyperthyroidism, Cushing’s syndrome, acromegaly, hypopituitarism)
   Periodic paralysis (hyperkalaemic or hypokalaemic or normakalaemic)
   Osteomalacia
   Drugs ( chloroquine, steroids)
   sarcoidosis

Question 2

causes of mononeuritis multiplex (refers to separate involvement of more than one peripheral or rarely cranial nerve, e.g. a common peroneal nerve palsy plus an axillary nerve palsy)

Answer 2

1. acute (usually vascular): a. diabetes mellitus, polyarteritis nodosa or connective tissue disease- SLE. rhematoid arthritis)
2. chronic: a. multiple compressive neuropathies, b. sarcoidosis, c. acromegaly, leprosy, carcinoma(rare), idiopathic

Question 3

causes of periphearl neuropathy

Answer 3

1. drugs and toxins: vincristine, phenytoin, amiodarone, cisplatinum, isoniazid
   2 Alcohol ( with or without vitsm b1 deficiency) amyloidosiis
2. Metabolic - diabetes, ureaemia, hypothyroidism, porphyria
3. Immune-mediated - Guillain-Barre syndrome
4. Tumour - lung carcinoma
5. Vitamin B12 or B1 deficiency
6. Idiopathic
7. connectiv etissue disease or vasculitis - SLE , polyarteritis nodosa
8. Hereditary
   (DAMIT BICH)

Question 4

common cause of a motor neuropathy

Answer 4

Guillain-Barre syndrome,
CIDP
drug (dapsone) /lead
porphyria

Question 5

common causes of sensory neuropathy

Answer 5

Diabetes
Alcohol
Drugs (hydralazine, isoniazid, metronidazole, chloroquine)
Infections (Lyme, HIV, 
Sarcoidosis
Vasculitis
Infiltration: Amyloidosis
Paraneoplastic
Kidney chronic disease (ureaemia)
T: hypothyroidism
Vitamn B12 deficiency

Question 6

cause of autonomic neuropathy

Answer 6

Guillain-Barre syndrome
Diabetes
Paraneoplastic 
Porphyria
HIV
Deposition (Amyloidosis)

Question 7

common causes of demyelinationg polyneuropathies

Answer 7

CIDP, multiple myeloma, MGUS, Poems, HIV, hereditory motor and sensory neuropathy, hereditary neuropathy with pressure palsy, multifocal motor neuropathy

Question 8

common cuases of mononeuritis multiplex

Answer 8

Diabetes, polyarteritis nodosa, Granulomatosis with polyangiitis, Rheumatoid arthritis, SLE, Sjogren’s syndrome, Sarcoidosis, amyloidosis, carcinoma

Question 9

causes of painful peripheral neuropathy

Answer 9

Diabetes mellitus
Alcohol
Vitamin B1 or B12 deficiency
CArcinoma
porphyria

Question 10

causes of proximal weakness

Answer 10

Myopahty, neuromuscular junction disease, Neurogenic (motor neurone disease, )

Question 11

Approach to cognitive impairment

Answer 11

ORA RLC
O rientation: year/season/month/day/date, country/state/city/hosptial/floor
R registration - window, basketball, tree
A attention- backwards from 100 by sevens, world
R recall
L language skill- repeat “west register street, naming two objects, obeying a three stage command, reading and writing a sentences
C construction copying two intersecting pentagons

Question 12

Antiepileptic agents for
partial or generalised tonic clonic seizure
absence, myoclonic seizure,
second line treatment

Answer 12

partial or generalised tonic -clonic seizures _ sodium valproate, carbamazepine, phenytoin
Absence seizure - ethosuximide, sodium valproate
Myoclonic seizure- sodium valproate, lamotrigine, topiramate
Second - line therapy for partial and generalised tonic clonic seizures - topiramate, gabapentin, lamotrigine, levetiracetam
combination should be considered only after two sequential monotherapy attmpts with two different agents have failed.
carbamazepine and phenytoin can cause interstitial nephritis, two can cause induction of the hepatic cytochrome P-450 enzyme system, while valproate casues an inhibition of the same.

Question 13

weakness : myopathy, neuromuscular junciton, lower motor neuron, , motor neuron

Answer 13

Upper: UL extension, LL flexion, non atrophy, no fac. inc.tone, inc. reflex, present babinski
LMN: distal ,segment wekness, severe atrophy, common fasci, dec. tone, dec. reflex, absent babinski
NJ: ocular, bulbar, proximal limb, non atrophy, non fasc, normal reflex, normal tone, absent babinski
Myopathy: proximal symm, mild atrophy, non fasc, nomrl or dec tone, normal or dec. reflex, absent babinski

Question 14

What is ‘pyramidal distribution’ and why

Answer 14

(ie. upper limb has greater flexor strength relative to extensor strength and the opposite is true in the lower limb).
With a corticospinal lesion, you get a spastic hard pyramidal paresis in the anterior muscles above T6 and posterior muscles below T6 ispilaterally.
The PMRF (pontomedullary reticular formation) inhibits ipsilateral anterior muscles above T6, and ipsilateral posterior muscles below T6.
Decreased FOF (freq. of firing) of the neurons in this pathway, like in functional deafferentation, pushes the central integrative state of involved alpha motoneurons toward facilitation.
This = increased tone in a pyramidal distribution
Extrapyramidal tract is inhibited and has lost its ability to perform its requisite inhibitory functions that modulate pyramidal influences.
Inhibit an inhibitory function = movement/spasticity

Question 15

what are symptoms and signs in dominant parietal lobe

Answer 15

dysphasia,
acalculia, agraphia, left- right disorientation
finger agnosia
AALF

Question 16

what are symptoms and signs in non dominant parietal lobe

Answer 16

agraphaesthesia, sensory and visual inattention
dressing and contrucitonal apraxia
spatial neglect
lower quadrantic hemianopia
seizure

Question 17

Temproal lobe dysfunciton

Answer 17

memory loss
upper quadrantic hamianopia
dysphasia (receptive if dominant lobe)
seizure

Question 18

frontal lobe dysfunction

Answer 18

personality change
primitive reflexes: grasp, pout
optic nerve compression
gait apraxia
leg weakness
loss of micturition control
dysphasia (expressive), dysgraphia

Question 19

occipital lobe dysfunction

Answer 19

homonymous hemianopea

alexia (inability to read, word blindness)

Question 20

what are the causes of pseudobulbar palsy

Answer 20

Motor neurone diseae
Multiple sclerosis
bihemispheric vascular disease
brainstem tumour 
trauma

Question 21

What are the disorder of lower motor neurones (true bulbar palsy)

Answer 21

motor neurone diseae
brainstem vascular diseae
brainstem tumour
guillain barre syndorme
subacute menignitis
poliomyelitis
myastehnia graivs

Question 22

whach t are the common causes of cerebellar syndrome

Answer 22

demyelination - MS
alcoholic cerebellar degeneration
posterior fossa sapce occupying lesions
brainstem lesions
paraneoplastic cerebellar degeneration
drugs: 
friedreich's ataxia
arnold- chiari malformation

Question 23

Lateral medullary syndrome

Answer 23

ipsilateral horner’s syndrome
ipsilateral cerebellar signs
ipsilateral V, iX, X, and Xi nerve signs
contralateral spinothalamic signs (below the lesion)

“crosing “ of weakness or sensory disturbance is highly suggestive for a unilateral brainstem syndrome owing to crossing of corticospinal tract and spinothalamic sensory fibres causal to the mid-brainstems.

Question 24

treatment of MS

Answer 24

general: urinary spasm(baclofen), urgency(amitryptilline), tics(carbamazepine), intention tremor( propranolol, clonazepam)
immunomodulators: Interferon beta, glatiramer acetate, natalizumab, sphingolimod
managment of realpse:methylpred, ivig, plasmapharesis)

Question 25

what are signs of Left MCA Superficial Division infarction

Answer 25

Right face and arm upper-motor weakness due to damage to motor cortex, nonfluent (Broca’s) aphasia due to damage to Broca’s area. There may also be right face and arm cortical type sensory loss if the infarct involves the sensory cortex. Other deficits include a fluent (Wernicke’s) aphasia due to damage to Wernicke’s area.

Question 26

What are signs of Left MCA Lenticulostriate Branches

Answer 26

Right pure upper-motor hemiparesis due to damage to the basal ganglia (globus pallidus and striatum) and the genu of the internal capsule on the left side. Larger infarcts extending to the cortex may produce cortical deficits such as aphasia.

Question 27

What are signs of Right MCA Superficial Division

Answer 27

Left face and arm upper-motor weakness due to damage to motor cortex. Left hemineglect (variable) due to damage to non-dominant association areas. There may also be left face and arm cortical type sensory loss if the infarct involves the sensory cortex.

Question 28

Treatment of multiple sclerosis

Answer 28

General measures:
patient education and counselling
physiotherapy
occupational therapy
walking aids and orthoses
visual aids
Managemnt of acute attacks:
IV methyl prednisolone
plasma exchange
Prevention of relapses
interferon -beta(reduces the relapse rate by 33%, associated with 50-80% reduction in inflammatory activity on MRI, improve quality of life and cognitive function, adverse effects inlcude flu like symptoms, myalgia and fatigue, cau result in neutralizingn antibodies)
Glatirimer acetate (a synthetic polypeptide that competes with myelin basic protein, reduces the relapse rate by 35%, well otleratate)
Natalizumab: a monoclonal antibody targeting alfa 4 integrin on leucocytes, reduces the relapse rate by 67%, side effects, PML
symptomatic treatment:
spasticity: baclofen
depression: SSRIs, tricyclic antidepressants
fatigue: amantidine modafanil
Pain: carbamazepine, tricyclic antidepressants
bladder dsyfuncitons: self - intermittent catheterization, anti colinergic agents, alfa1 antagonists
sexual dysfunciton: counselling
erectile dysfunction: phosphodiesterase inhibitors sildenafil

Question 29

Medical treatment of MS approved?

Answer 29

interferon beta 1a or 1b
Glatiramer acetate
Natalizumab - monoclonal antibody against alpha 4 integrin(monthly infusion, risk of progressive multifocal leucoencephalopathy due to JC virus within the first 2 years of treatment)
Fingolomid: (sphingosine 1 - phosphate receptor modulators, sequesters lymphocytes in lymph nodes, preventing them from contributing to an autoimmune reaction)
BG12/Di Methyl Fumarate (may have a combination of anit-inlammatory and neuroprotective effects)
Teriflunomide (inhibitor of pyrimidine synthesis in T cells)
Alemtuzumab: monocolonal antibody - targets CD52, infusion over 5 days, annually for 2 years, side effects: infsuion reactions, infections, autoimmunity (20-30% develop thyroid disease)