Neurology

Q. What are the causes of CVD (Stroke) in a young patient?

Answer:
 Mitral stenosis with atrial fibrillation (cerebral embolism from cardiac
source)
 Other cardiac cause—PFO, VSD, TOF
 Antiphospholipid syndrome
 SLE
 Hematological disease—sickle cell anemia, polycythemia rubra vera,
inherited deficiency of naturally occurring anti-coagulant (protein C,
protein S, antithrombin III, factor V Leiden). In all these conditions,
there is increased tendency of thrombosis.
 Vasculitis. Behcet’s disease
 Vascular malformation—AVM, berry aneurysm causing SAH
 Arterial dissection
 In female—oral contraceptive pill, eclampsia
 Homocystinuria
 Syphilis
 Premature atherosclerosis may occur in familial hyperlipidemia
 Rarely, migraine may cause cerebral infarction
 Drugs like amphetamine, cocaine.

Q. What are the causes of Transient Hemiplegia?

Q. What are the causes of Recurrent Hemiplegia?
Answer:
1. Transient Ischemic Attacks (TIAs) due to:
 Cerebral emboli: arising from:
 Ulcerated atherosclerotic plaques in carotid or vertebral arteries
 Mural thrombi in a diseased heart e.g. Atrial fibrillation
 Hyperviscosity: e.g. Polycythemia
 Vasculitis: e.g.
 Systemic Lupus Erythematosus(SLE)
 Poly arteritis nodosa (PAN)
2. Todd’s paralysis (post-epileptic)
3. Demyelinating Disease (Multiple sclerosis)
4. Hemiplegic migraine
5. Hysterical hemiplegia.
Q: Differences between different types of cerebrovascular disease (CVD)
Q: Differences between thrombosis, embolism, and hemorrhage
Q: Differences between thrombotic, embolic, and hemorrhagic Hemiplegia
Answer:
Q. What are the causes of Polyneuropathy?
Answer:
  Note: Common causes of Polyneuropathy:
 Diabetes mellitus
 Guillain-Barré syndrome
 Alcohol
 Leprosy
 Chronic renal failure
 Drugs like INH, vincristine
 Deficiency—vitamin B12, B1, nicotinic acid, B6.

Q: Causes of motor neuropathy?

Q: Causes of sensory neuropathy?
Q. What is the mechanism of neuropathy in Diabetes Mellitus (DM)?
Answer:
 Axonal degeneration
 Patchy or segmental demyelination
 Involvement of intraneural capillaries.
Q. What is the pathogenesis of diabetic neuropathy?
Answer:
1. Metabolic theory: Increased neuronal concentration of glucose results
in increased conversion of glucose to sorbitol. The resultant increase in
diacylglycerol, protein kinase C and Na-K ATPase activity causes
neuronal loss and demyelination.
2. Vascular theory: Increased aldose reductase activity causes
decreased NO that results in reduced blood flow in vasa nervorum.
3. Altered metabolism of fatty acid.
4. Nutritional: reduced concentration of nerve growth factor, vascular
endothelial growth factor and erythropoetin.
5. Oxidative stress.

Q. What are the causes of flaccid paraplegia?

Q. Discuss diagnosis of flaccid paraplegia?
Answer:
Q. How does the patient of Guillain-Barré Syndrome (GBS) usually present?
Answer:
 History of upper respiratory tract infection (URTI) or gastroenteritis
(viral or bacterial)
 After 1 to 3 weeks, weakness of lower limbs that ascends over several
weeks (ascending paralysis).
It may advance quickly, affecting all the limbs at once and can lead to
paralysis (quadriplegia)
 Respiratory paralysis in 20% case. Progressive respiratory involvement
and paralysis is the main problem
 Paresthesia and pain in back and limbs may occur
 Facial and bulbar weakness
 Autonomic dysfunction—change of blood pressure, tachycardia,
increased sweating, dysrhythmia may occur.

Q. What are the clinical findings in Guillain-Barré Syndrome (GBS)?

Answer:
 Flaccid paralysis involving lower limbs and may involve all 4 limbs
 Loss of all reflexes
 Bilateral facial palsy (in 50% cases, unilateral in 25% cases)
 Sensory loss—minimum or absent
 Sphincter involvement (rare).

Q. What investigations do you suggest in Guillain-Barré Syndrome (GBS)?

Answer:
 CSF analysis—typical finding is ‘albuminocytological dissociation’
(albumin may be very high, > 1000 mg %; lymphocytes are slightly
raised or normal, < 20/mm3. If lymphocyte is > 50, GBS is unlikely.
CSF protein may be normal in first 10 days)
 Antibodies to glycolipids of the myelin sheath: + ve in 70% of patients.
 Frequent monitoring of respiratory function tests (FVC, FEV1, PEFR)
 Arterial blood gas analysis (as respiratory failure may occur at any
time)
 Nerve conduction study (it shows slow conduction or conduction block.
Demyelinating neuropathy, usually found after 1 week)
 Investigation to identify CMV, mycoplasma or campylobacter should be
done
 Serum electrolyte.
 Note: Triad of acute symmetrical ascending paralysis of limbs,
areflexia and albumino: cytological dissociation in CSF is highly
suggestive of GBS.
Q. How to treat Guillain-Barré Syndrome (GBS)?
Answer:
 Ideally the patient should be treated in ICU and respiratory function
should be monitored regularly (vital capacity and arterial blood gases).
The patient may require artificial ventilation
 High dose intravenous gamma globulin should be given to all patients
(it reduces the duration and severity). Dose is 400 mg/kg/day for 5
days. It is helpful, if given within 14 days. Side effects of IV Ig: It may
precipitate angina or myocardial infarction. In congenital IgA deficiency,
it may cause allergic reaction
 Plasma exchange, if given within 14 days is equally effective in
reducing the severity and duration of GBS
 Steroid has no proven value (may worsen). Methylprednisolone with
immunoglobulin has no proven benefit
 Plasmapharesis may be required
 Physiotherapy is the mainstay of therapy
 Prevention of pressure sore and venous thrombosis
 Other symptomatic treatment.

Q: Causes of paraplegia (OCT 2011)

Q: 5 causes of spinal paraplegia (Kasr 2011)
Q: Classify and enumerate causes of paraplegia (Kasr 2009)
Answer: see book

Q. What are the most common causes of spastic paraplegia?

Answer: (7 T):
1. Trauma
2. Tuberculosis (Pott’s disease)
3. Tumor (meningioma, neurofibroma, lymphoma, leukemia, myeloma,
glioma)
4. Transverse myelitis
5. Tabes dorsalis
6. Twelve (B12 deficiency)
7. Thrombosis.
Q: Difference between UMNL and LMNL ( Kasr 2012 )

Answer: