The effects of puffer fish poisoning on peripheral nerve were investigated in 4 of 9 patients (7 adults and 2 children) treated at the Prince of Wales Hospital, Sydney, Australia. The patients had consumed soup made from 30 puffer fish. They experienced numbness of the lips approximately one hour later, and the numbness spread to the tongue, throat, and then hands and feet. Symptoms progressed rapidly, the gait became ataxic, and the reflexes were normal or depressed. Full recovery occurred within one week. The urine of each patient tested positive for tetrodotoxin. Excitability measurements of sensory and motor nerves showed that, compared with controls, axons were of higher threshold, compound muscle and sensory action potentials were reduced in amplitude, latency was prolonged, and strength-duration time constant was reduced. Threshold electrotonus of motor axons showed less threshold decline than normal on depolarization and greater threshold increase on hyperpolarization. The changes in excitability were reproduced in a mathematical model by reducing sodium permeabilities by a factor of 2. [1]

COMMENT. The neurotoxic effects of puffer-fish poisoning are due to tetrodotoxin blockade of Na⁺ channels. In an editorial, Kaji R and Nodera H, Tokushima University, Japan [2] discuss the differentiation of puffer fish poisoning and Guillain-Barre syndrome (GBS) with reference to persistent sodium channels. GBS occurs in a demyelinative form (acute inflammatory demyelinating polyneuropathy [AIDP]) and the axonal form (acute motor axonal neuropathy [AMAN]). In AMAN, anti-GMl antibodies may bind specifically to motor nerves and interfere with axonal sodium channels. Nerve excitability changes in AMAN are different from those in puffer fish poisoning, sensory fibers are spared, and a neurotoxin is not involved. Inflammatory mediators in AMAN are the likely explanation for reduced excitability of axons through sodium channels.