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A case of CJD with PLD in the first EEG is reported. The PLD became bilateral in the next EEG. The subsequent EEGs showed shifting asymmetries. In this case, PSD reappeared after 5 months' absence. The PLD occasionally appeared over the hemisphere ipsilateral to the side of the myoclonic jerks. The clinical significance of the PLD and reappearance of PD, and the diagnostic importance of PLD are discussed.
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It has been suggested that the renal kallikrein-kinin system is dependent on mineralocorticoid activity. This hypothesis was studied in a patient with cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion. The 24-h urinary excretions of sodium, potassium, cortisol, active and inactive kallikrein, aldosterone, and prostaglandin E2 (PGE2) were studied during normal and excessive cortisol secretion and after bilateral adrenalectomy. Kallikrein, PGE2 and potassium rose during cortisol overproduction while aldosterone and sodium decreased. Kallikrein, PGE2 and potassium were positively related to cortisol excretion, whereas urinary aldosterone and sodium showed a negative relationship to cortisol. Kallikrein was inversely related to aldosterone. Excretion of inactive kallikrein followed closely the changes of active kallikrein. During cortisol excess, as in our patient, the mineralocorticoid activity of cortisol will exceed that of aldosterone. This suggests that the alterations in kallikrein, aldosterone and PGE2 during cortisol excess in the present study were due to the mineralocorticoid potency of the steroid.
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Hypokalaemic periodic paralysis is an autosomal, dominantly inherited disorder, characterised by attacks of partial or total muscle weakness and serum hypokalaemia. the mutations responsible are located in the CACNA1S gene (type 1) and in the SCN4A gene (type 2), and are all missense mutations where arginine is mostly replaced by histidine or sometimes glycine. The mutation has been localised in the voltage sensor of the transmembrane segment of calcium channel (type 1) and sodium channel (type 2) respectively. How muscle weakness develops is not known. Oral or intravenous administration of potassium is helpful in treating partial or complete attacks. Acetazolamide can reduce the frequency of attacks in type-1 hypokalaemic periodic paralysis.
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