Electrophysiological studies on ciguatera poisoning in man (Part II)

Cameron, J.; Flowers, Andrew E.; Capra, Mike

doi:10.1016/0022-510x(91)90022-y

Cited by 76 publications

(38 citation statements)

References 11 publications

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“…Although abnormalities of transient Na ϩ conductances, as indicated by prolongation of the absolute and relative refractory period, have been reported with acute ciguatera poisoning, 3 there have been no studies that have assessed transient Na ϩ channel function in chronic ciguatera poisoning, at least to our knowledge. In the present series, the findings of normal refractoriness and RRP argue against persistent abnormalities of transient Na ϩ conductances as the underlying mechanism of chronic ciguatera sensitization.…”

Section: Discussionmentioning

confidence: 98%

“…7 In acute ciguatera poisoning, activation of voltage-sensitive Na ϩ channels results in prolongation of the relative refractory period and an increase in supernormality. 3 Consequently, the aim of the present study was to investigate axonal excitability and particularly Na ϩ channel function in patients with chronic sensitization symptoms following ciguatera poisoning.…”

mentioning

confidence: 99%

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Normal axonal ion channel function in large peripheral nerve fibers following chronic ciguatera sensitization

Vucic¹,

Kiernan²

2007

Muscle and Nerve

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Although the acute clinical effects of ciguatera poisoning, due to ingestion of ciguatoxin, are mediated by activation of transient Na+ channels, the mechanisms underlying ciguatera sensitization remain undefined. Axonal excitability studies were performed by stimulating the median motor and sensory nerves in two patients with ciguatera sensitization. Excitability parameters were all within normal limits, thereby arguing against dysfunction of axonal membrane ion channels in large-diameter fibers in ciguatera sensitization.

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Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

Normal axonal ion channel function in large peripheral nerve fibers following chronic ciguatera sensitization

Vucic¹,

Kiernan²

2007

Muscle and Nerve

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“…Nerve conduction studies may be abnormal 38. In experimental animals neurophysiological studies have demonstrated slowing of both mixed and motor nerve conduction velocities with reduction of depolarisation amplitudes 38…”

Section: Differential Diagnosismentioning

confidence: 99%

Neurology of ciguatera

Pearn

2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

203

171

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Ciguatera is a widespread ichthyosarcotoxaemia with dramatic and clinically important neurological features. This severe form of fish poisoning may present with either acute or chronic intoxication syndromes and constitutes a global health problem. Ciguatera poisoning is little known in temperate countries as a potentially global problem associated with human ingestion of large carnivorous fish that harbour the bioaccumulated ciguatoxins of the photosynthetic dinoflagellate Gambierdiscus toxicus. This neurotoxin is stored in the viscera of fish that have eaten the dinoflagellate and concentrated it upwards throughout the food chain towards progressively larger species, including humans. Ciguatoxin accumulates in all fish tissues, especially the liver and viscera, of "at risk" species. Both Pacific (P-CTX-1) and Caribbean (C-CTX-1) ciguatoxins are heat stable polyether toxins and pose a health risk at concentrations above 0.1 ppb. The presenting signs of ciguatera are primarily neurotoxic in more than 80% of cases. Such include the pathognomonic features of postingestion paraesthesiae, dysaesthesiae, and heightened nociperception. Other sensory abnormalities include the subjective features of metallic taste, pruritus, arthralgia, myalgia, and dental pain. Cerebellar dysfunction, sometimes diphasic, and weakness due to both neuropathy and polymyositis may be encountered. Autonomic dysfunction leads to hypotension, bradycardia, and hypersalivation in severe cases. Ciguatoxins are potent, lipophilic sodium channel activator toxins which bind to the voltage sensitive (site 5) sodium channel on the cell membranes of all excitable tissues. Treatment depends on early diagnosis and the early administration of intravenous mannitol. The early identification of the neurological features in sentinel patients has the potential to reduce the number of secondary cases in cluster outbreaks.

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“…With neurophysiologic testing, significant slowing of sensory and motor nerve conduction velocities, and F wave latencies has been demonstrated [27,29,30]. This observation may be related to nodal swelling and internodal length and volume increase, all of which have been confirmed with in vitro CTX exposure [28,31].…”

Section: Ciguateramentioning

confidence: 93%