BODY COMPOSITION IN HYPOKALEMIC FAMILIAL PERIODIC PARALYSIS *

Familial Periodic Paralysis is a rare disease entity probably first described in 1882 by Shakhnowitsch.' The role of potassium in this condition was not appreciated until in 1938 when Aitken et a1.2 related a lowering of serum potassium concentration to the attacks of paralysis. A voluminous literature on periodic paralysis has accumulated since then and recently, it has come to be recognized that there are three conditions in which transitory muscular paralysis may be associated with disturbed electrolyte metabolism. These include classical hypokalemic periodic p a r a l y ~ i s ~ , ~ , ~ as considered in the present communication, a form of hyperkalemic familial periodic paralysis known as adynamia episodica hereditariaaj7 and finally, a form of normokalemic periodic paralysis in which sodium ingestion acts to alleviate attacks.8 Other sporadic forms of periodic paralysis relating to aberrations in potassium metabolism have been described; however, these do not fit the classical description of this disease. Although the literature on periodic paralysis has been extensive, studies of tissue composition and of whole body composition have been

[1]  D. Poskanzer,et al.  Periodic paralysis with response to spironolactone. , 1961, Lancet.

[2]  D. Poskanzer,et al.  A third type of periodic paralysis, with normokalemia and favourable response to sodium chloride. , 1961, The American journal of medicine.

[3]  A. George The metabolic basis of inherited disease , 1961 .

[4]  P. Rowley,et al.  Studies in familial periodic paralysis , 1961 .

[5]  C. E. Miller,et al.  Exchangeable potassium as a parameter of body composition. , 1960, Metabolism: clinical and experimental.

[6]  P. Rowley,et al.  The effect of sodium loading and depletion on muscular strength and aldosterone excretion in familial periodic paralysis. , 1960, The American journal of medicine.

[7]  H. Werbin,et al.  Rapid Sensitive Method for Determining H3-Water in Body Fluids by Liquid Scintillation Spectrometry.∗ , 1959, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[8]  R. J. Johns,et al.  Potassium movement in patients with familial periodic paralysis: relationship to the defect in muscle function. , 1957, The American journal of medicine.

[9]  I. Gamstorp Adynamia Episodica Hereditaria , 1956, Acta genetica et statistica medica.

[10]  D. Streeten,et al.  Dependence of attacks of periodic paralysis upon retention of sodium; and failure to induce either paralysis or sequestration of potassium when dietary sodium is restricted. , 1957, Transactions of the Association of American Physicians.

[11]  I. Gamstorp,et al.  Adynamia episodica hereditaria: a disease clinically resembling familial periodic paralysis but characterized by increasing serum potassium during the paralytic attacks. , 1957, The American journal of medicine.

[12]  B. McArdle Familial periodic paralysis. , 1956, British medical bulletin.

[13]  E. Vastola,et al.  Intracellular Water and Potassium in Periodic Paralysis , 1956, Neurology.

[14]  J. Manery Water and electrolyte metabolism. , 1954, Physiological reviews.

[15]  P. Talso,et al.  The metabolism of water and electrolytes in congestive heart failure. II. The distribution of water and electrolytes in skeletal muscle in edematous patients with congestive heart failure before and after treatment. , 1953, The Journal of laboratory and clinical medicine.

[16]  P. Talso,et al.  The metabolism of water and electrolytes in congestive heart failure. I. The electrolyte and water content of normal human skeletal muscle. , 1953, The Journal of laboratory and clinical medicine.

[17]  P. Merton,et al.  The behaviour of radio-potassium in man. , 1952, The Journal of physiology.

[18]  M. R. Ball,et al.  The measurement of exchangeable potassium in man by isotope dilution. , 1950, The Journal of clinical investigation.

[19]  H. T. John,et al.  Periodic Paralysis, a Clinical Syndrome. , 1942 .