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Serious neurological manifestations of ciguatera: is the delay unusually long?
  1. GILLES ANGIBAUD,
  2. SABINE RAMBAUD
  1. Department of Neurology, Gaston Bourret Hospital, BP J5, 98849 Noumea, New Caledonia, South Pacific
  1. Dr Gilles Angibaud, Department of Neurology, Gaston Bourret Hospital, BP J5, 98849 Noumea, New Caledonia, South Pacific. Telephone and fax 00687 25 67 45.

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Ciguatera poisoning is the commonest fish food poisoning encountered in tropical islands, especially in the Pacific.1 The disease is usually benign, with gastrointestinal and cutaneous manifestations which resolve spontaneously within a few hours. However, serious forms of this fish poisoning, with cardiovascular and neurological disorders, have been described.1-3 The ciguatoxins involved in ciguatera disturbances are competitive inhibitors of the brevetoxins and have a common binding site on neuronal voltage dependent sodium channels.4 Even if their action remains partially understood a prolonged axonal sodium channel activation, by contrast with other fish toxins (tetrodotoxin for instance), is now described as the main mechanism by most authors.4

We present the results of the retrospective analysis of ciguatera cases admitted to Gaston Bourret hospital (Nouméa, New Caledonia, South Pacific) between January 1991 and December 1995. Fifty six cases were reviewed (19 female and 37 male patients, mean age 37 (SD 15), range 2–62).

Diagnosis of ciguatera was made on clinical grounds—that is, history of fish eating and suggestive clinical manifestations. Two groups were established. In the first, patients had only common signs of ciguatera poisoning including gastrointestinal (nausea, vomiting, abdominal pain, diarrhoea) and cutaneous symptoms (pruritus, itching sensations). Patients with the usual neurological complaints of ciguatera (paraesthesia, muscle pain) were included in this group (“common” group). In the other (“neurological” group) patients had infrequent or severe neurological features—namely, vertigo, ataxia, progressive muscular weakness or sensory loss (polyneuritis), visual blurring, and stupor or confusion. The delay between the consumption of fish and the onset of ciguatera was known in 43 patients (seven of 10 in the “neurological” group and 36 of 46 in the “common” group). There was a significant difference in delay between the groups (46.9 (SD 59) hours in the”neurological” group and 4.8 (SD 5.2) hours in the “common” group (p=0.0084, Mann-Whitney test)). Age, sex, number of previous episodes of ciguatera, and type of fish were not significantly different between the groups (χ2 test).

To our knowledge, this longer delay in serious neurological cases of ciguatera has never been statistically documented, although Allsopet al reported a long delay between the first manifestations of ciguatera and the onset of neurological signs.2 Further prospective studies are needed to assess this putative characteristic of “neurological ciguatera”. Ciguatoxins act on axonal sodium channels and elicit a prolonged activation. By this action, intracellular water and sodium influx could increase and induce neuronal oedema.4 In vitro ciguatoxins can provoke a nodal swelling and also a large increase in internodal length and volume.4 Changes in membrane sodium current induced by ciguatoxins have been linked to these swelling effects. Slowing of nerve conduction could be explained by both changes (nodal swelling and prolonged activation). In Guillain-Barré syndrome, internodal length is increased early in the disease and in experimental allergic neuritis the earliest pathological signs are breakdown of the blood-nerve barrier, oedema, and infiltration of activated lymphocytes. Also, we postulate that water and uptake of sodium induced by ciguatoxins could provoke secondary disturbances in nerve fibres, which would explain the long delay in “neurological ciguatera”. A striking oedema of the adaxonal Schwann cell cytoplasm has already been reported in vivo. In this report, the axon was shown to be compressed by adaxonal oedema.2 Raised endoneurial fluid pressure induced by oedema might reduce nerve blood flow. Direct compressive effects or endoneurial fluid pressure could both induce nerve blood supply deficiency. Further nerve (axonal?) disturbances could be due to the ischaemic effects of oedema. In this hypothesis, neuronal oedema would have to be managed as a neurological emergency.5Mannitol is known to be effective in the treatment of ciguatera,4 and its mode of action could be to suppress nodal swelling and sodium channel activation induced by ciguatoxins.

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