Thyrotoxic Hypokalemic Periodic Paralysis: Report of Four Cases in Black American Males1

Kilpatrick, Robin E.; Seiler-Smith, Susan; Levine, Steven N.

doi:10.1089/thy.1994.4.441

Cited by 33 publications

(20 citation statements)

References 27 publications

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“…However, although we cannot be certain that our observations would be borne out in a larger study, the differences in the normal range for CK in this ethnic group compared with non-African-Caribbeans suggests that there may indeed be some ethnic differences in muscle physiology, and until further studies are done, we suggest that caution be exercised when interpreting mildly abnormal decrements in the long exercise test in African-Caribbean individuals. Although uncommon, periodic paralysis has been described in this population17,18. We did not find increments during the long or short exercise tests to be helpful diagnostically.…”

Section: Discussioncontrasting

confidence: 52%

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Refined exercise testing can aid dna‐based diagnosis in muscle channelopathies

Tan

Matthews

Barber

et al. 2011

Annals of Neurology

121

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Objective-To improve the accuracy of genotype prediction and guide genetic testing in patients with muscle channelopathies we applied and refined specialised electrophysiological exercise test parameters.Methods-We studied 56 genetically confirmed patients and 65 controls using needle electromyography, the long exercise test, and short exercise tests at room temperature, after cooling, and rewarming.Results-Concordant amplitude-and-area decrements were more reliable than amplitude-only measurements when interpreting patterns of change during the short exercise tests. Concordant amplitude-and-area pattern I and pattern II decrements of >20% were 100% specific for PMC and MC respectively. When decrements at room temperature and after cooling were <20%, a repeat short exercise test after rewarming was useful in patients with myotonia congenita. Area measurements and rewarming distinguished true temperature sensitivity from amplitude reduction due to cold-induced slowing of muscle fibre conduction. In patients with negative short exercise tests, symptomatic eye closure myotonia predicted sodium channel myotonia over myotonia congenita. Distinctive 'tornado-shaped' neuromyotonia-like discharges may be seen in patients with paramyotonia congenita. In the long exercise test, area decrements from pre-exercise baseline were more sensitive than amplitude decrements-from-maximum-CMAP in patients with Andersen-Tawil syndrome. Possible ethnic differences in the normative data of the long exercise test argue for the use of appropriate ethnically-matched controls.Interpretation-Concordant CMAP amplitude-and-area decrements of >20% allow more reliable interpretation of the short exercise tests and aid accurate DNA-based diagnosis. In patients

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Section: Discussioncontrasting

confidence: 52%

“…Although uncommon, periodic paralysis has been described in this population. 17,18 We did not find increments during the long or short exercise tests to be helpful diagnostically.…”

Section: Annals Of Neurologymentioning

confidence: 62%

Refined exercise testing can aid dna‐based diagnosis in muscle channelopathies

Tan

Matthews

Barber

et al. 2011

Annals of Neurology

121

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“…Although the incidence of TPP is relatively high in the Asian population, TPP is no longer confined to certain geographic areas due to globalization and immigration (7). In addition, TPP has been increasingly reported in many other ethnic groups (8,9). The neuromuscular presentations of TPP and non-TPP are often indistinguishable.…”

mentioning

confidence: 99%

Early diagnosis of thyrotoxic periodic paralysis: Spot urine calcium to phosphate ratio*

Lin¹,

Chu²,

Cheng³

et al. 2006

Critical Care Medicine

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“…Orientals make up to 90% of all cases reported in the literature 8-10. It has also been reported in Caucasians,11 native American Indians,12 Blacks13 and Aborigines 14. TPP is predominantly a disease of males, the male:female ratio being 20:1 8…”

Section: Thyrotoxic Periodic Paralysismentioning

confidence: 81%

Hypokalaemic paralysis

Ahlawat

Sachdev

1999

Postgraduate Medical Journal

128

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SummaryAcute systemic weakness is a common complaint in the emergency department and has a wide diVerential diagnosis that includes neurologic, metabolic, and infectious aetiologies (box 1). Acute hypokalaemic paralysis, a clinical syndrome characterised by acute systemic weakness and low serum potassium, is a rare but treatable cause of acute weakness. Therefore, it is imperative for physicians, particularly those working in acute care settings, to be aware of this condition. Hypokalaemia is caused by a variety of disorders (box 2),while acute weakness has been reported with some but not all the causes of hypokalaemia (box 3).The most prominent clinical features of hypokalaemia or potassium depletion are neuromuscular, although other systems, such as cardiovascular and gastrointestinal, may also be aVected. Some patients complain of muscular weakness, especially of the lower extremities, while marked and generalised weakness of skeletal muscles is common with more severe potassium depletion. Very severe hypokalaemia may lead to virtually total paralysis including respiratory, bulbar and cranial musculature. Deaths from respiratory failure and arrhythmia have been reported. On physical examination, in addition to decreased motor power, the patient may demonstrate decreased or absent tendon reflexes. The sensations and level of consciousness are generally unaVected.The cardinal laboratory manifestation is a serum potassium of less than 3.5 mmol/l during an attack, although it is usually much lower. Abnormalities in electrocardiogram (ECG) are common. The typical changes include flattening and inversion of T waves, appearance of U waves and ST segment sagging. ECG changes are, however, not well correlated with the severity of the disturbances in potassium metabolism. Symptomatology results from the increased ratio between intra-and extracellular potassium concentrations, which modifies membrane polarization and thereby alters the function of excitable tissues such as nerve and muscle. Diagnosis of hypokalaemic paralysis should be considered in any patient presenting with a sudden onset, areflexic, pure motor weakness involving one or more limbs, without alteration in the level of consciousness or sphincter function, and laboratory evidence of hypokalaemia.Hypokalaemic paralysis results from either alteration in transcellular distribution of potassium or actual potassium depletion from renal or extrarenal losses. Most cases are due to a transcellular shift of potassium and the diVerential diagnosis includes familial periodic paralysis, thyrotoxic periodic paralysis, and barium poisoning. Familial periodic paralysis (FPP)All primary periodic paralyses have some features in common; they are all treatable and muscular weakness is reversible. Diagnosis is based upon patient history and confirmed by evaluation of serum potassium during attacks and by evaluating the response of muscle power to provocative testing with glucose, insulin, potassium, and cold.Familial hypokalaemic periodic paralysis occurs as an autosomal do...

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Thyrotoxic Hypokalemic Periodic Paralysis: Report of Four Cases in Black American Males1

Cited by 33 publications

References 27 publications

Refined exercise testing can aid dna‐based diagnosis in muscle channelopathies

Refined exercise testing can aid dna‐based diagnosis in muscle channelopathies

Early diagnosis of thyrotoxic periodic paralysis: Spot urine calcium to phosphate ratio*

Hypokalaemic paralysis

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