Treatment for periodic paralysis

Sansone, Valeria; Links, Thera P.; Meola, Giovanni; Rose, MR

doi:10.1002/14651858.cd005045

Cited by 4 publications

(3 citation statements)

References 45 publications

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“…Side effects may include nephrolithiasis, nausea, anorexia, depression, mood instability, drowsiness, confusion, altered taste of carbonated beverages, vision impairment, rash, hepatic dysfunction, and paresthesias. 16,40 Liver function and complete blood count should be monitored with use of acetazolamide.…”

Section: Specific Pharmacologic Treatments Of the Nondystrophic Myotomentioning

confidence: 99%

The Nondystrophic Myotonias

Heatwole

Moxley

2007

Neurotherapeutics

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Summary:The nondystrophic myotonias are a heterogeneous set of rare diseases that demonstrate clinical myotonia, electrical myotonia, or both. These disorders are distinguished from myotonic dystrophy type 1 (DM-1), the more recently described proximal myotonic myopathy/myotonic dystrophy type 2 (PROMM/DM-2), and proximal myotonic dystrophy (a variant of DM-2) by characteristic clinical features, lack of abnormal nucleotide repeat expansions in the DM-1 and DM-2 genes, lack of cataracts and endocrine disturbances, and absence of significant histopathology in the muscle biopsy. The present article reviews each of the nondystrophic myotonias by exploring the unique clinical features, electrodiagnostic findings, diagnostic criteria, gene mutations, and response to pharmacologic therapy. These diseases are divided into those with chloride channel dysfunction (the myotonia congenita disorders) and those with sodium channel dysfunction (paramyotonia congenita, potassium-aggravated myotonia, and hyperkalemic periodic paralysis with myotonia). The variants that occur in each of these conditions are commented on. The differentiating features of the nondystrophic myotonias are summarized, and their predominant clinical, electrodiagnostic, and genetic characteristics are tabulated. For a comprehensive review of pertinent research and studies with application to diagnosis and treatment of individuals with nondystrophic myotonic disorders, the present article is best read in the context of other articles in this issue, especially those on ion channel physiology (Cannon) and pharmacology (Conte-Camerino), and on hyperkalemic periodic paralysis (Lehmann-Horn).

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Section: Specific Pharmacologic Treatments Of the Nondystrophic Myotomentioning

confidence: 99%

The Nondystrophic Myotonias

Heatwole

Moxley

2007

Neurotherapeutics

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“…In most patients with familial, periodic, or thyrotoxic periodic paralysis, there is one of a variety of identifiable genetic mutations affecting the function of the ion channels of skeletal muscles (1,2). These mutations alter the sensitivity of the channels so that excessive amounts of potassium enter the muscle cell in response to one of a variety of agents such as insulin, thyroid hormone plus insulin, or thyroid hormone plus adrenalin (3)(4)(5).…”

Section: Discussionmentioning

confidence: 99%

Pot Paresis: Marijuana and a case of Hypokalemic Periodic Paralysis

Feldman

Sarah

2009

The Journal of Emergency Medicine

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“…Acute attacks are often precipitated by rest after exercise, stress, or a high carbohydrate meal [1]. HypoPP may be familial with autosomal dominant inheritance or may be acquired in patients with thyrotoxicosis; it has been estimated that the risk of developing the disease is 8% in hyperthyroid Japanese men [3].…”

Section: Introductionmentioning

confidence: 99%

Hypokalemic periodic paralysis: a case series, review of the literature and update of management

Alkaabi¹,

Mushtaq

Al-Maskari

et al. 2010

European Journal of Emergency Medicine

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The objective of this study was to present a case series of patients with hypokalemic periodic paralysis. We described all patients with diagnosis of hypokalemic periodic paralysis admitted to the Al Ain Hospital (UAE) during the year 2006. Seventeen patients, all males and mostly Asians, were presented to the Al Ain Hospital over a 12-month period. The majority were admitted during the summer months. Four were thyrotoxic. All of the 17 patients received oral potassium supplements and recovered well without any major complications. In conclusion, clinicians should have a high index of suspicion, especially among Asians presenting with flaccid paralysis and hypokalemia. The main steps in the management include exclusion of other causes of hypokalemia, potassium replacement, hydration and close monitoring of the cardiac rhythm and serum potassium levels. When possible, the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis.

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Treatment for periodic paralysis

Cited by 4 publications

References 45 publications

The Nondystrophic Myotonias

The Nondystrophic Myotonias

Pot Paresis: Marijuana and a case of Hypokalemic Periodic Paralysis

Hypokalemic periodic paralysis: a case series, review of the literature and update of management

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