PERIODIC PARALYSIS is a syndrome characterised by intermittent muscular weakness with flaccidity associated with changes in serum postassium.
(a) Hyperkalaemic as in uraemia, adrenal insufficiency, overdose of spironolactones, triamterene, injudicious potassium supplementation.
(b) Hypokalaemic as in Diuretic therapy, GI Loss, Hyperaldosteronism, K-loosing nephritis, thyrotoxicosis.
Periodic paralysis is usually inherited as an autosomal dominant trait. It is often familial.
This usually begins in late childhood or adolescent stage. The attack is precipitated by a large carbohydrate meal at night or exercise. There is fladccid paralysis of sudden onset of the extremities and trunk muscles often sparing the muscles of respiration and those supplied by cranial nerves. This usually lasts for a day or two and then spontaneously recovers. Serum potassium level is usually below 2.5-3 mEq per litre.Administration of potassium chloride produces remarkable improvement. Similar attack is seen after diuretic therapy or in cases of thyrotoxicosis.
Similar attack as above may occur after exercise. No sensory changes are seen. This is common in childhood and disappears after the age of 20 years. There is a defect in the sodium channel gene on the long arm of chromosome 17. The attack lasts for half an hour to two hours. Lidlay and Chvostek’s signs are present. Intravenous calcium gluconate or chloride, IV diuretics, IV glucose, IV glucose with Insulin may cause improvement. Acetazolamide or Chloro-thiazide when used daily may prevent recurrences. Similar attacks may be seen after spironolactone or Triamterene therapy. Serum K level is raised to 5-7 mEq per litre.
Here during attack the K level is normal and after Na administration the condition improves. Treatment is done with acetazolamide.
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