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:
