Neurologic complications of lightning injuries.

Over the past ten years, we have cared for 13 patients who suffered serious neurologic complications after being struck by lightning. The spectrum of neurologic lesions includes the entire neuraxis from the cerebral hemispheres to the peripheral nerves. We describe these various neurologic disorders with regard to the site of the lesion, severity of the deficit, and the outcome. Damage to the nervous system can be a serious problem for patients struck by lightning. Fatalities are associated with hypoxic encephalopathy in patients who suffered cardiac arrests. Patients with spinal cord lesions are likely to have permanent sequelae and paralysis. New technology for detecting lightning with wideband magnetic direction finders is useful in establishing lightning-flash densities in each state. Florida and the Gulf Coast states have the highest densities. Colorado and the Rocky Mountain states have the next highest.

Dynamic F waves in neurogenic claudication.

Serial F waves were elicited before and after ambulation in 2 patients with neurogenic claudication. In both patients dynamic changes in F wave parameters consisting of either unelicitability or increased latencies occurred postexercise. The time course of these changes and their subsequent rapid reversibility over 15 minutes suggest ischemic-induced conduction block and slowing in proximal motor axons. These physiological changes may account for some of the dynamic neurological symptoms of this disorder. Moreover, F wave exercise testing may provide corroborative information for the diagnosis of neurogenic claudication.

Behavioral effects of chronic phencyclidine administration in rats.

The development of tolerance to phencyclidine (PCP) was examined in rats using behavioral rating scales with simultaneous measurements of locomotor activity, stereotyped behaviors, and ataxia. Significant tolerance to the stereotyped behaviors and ataxia induced by 5 or 10 mg/kg PCP was found on day 5 of chronic drug treatment. Because ataxia interferes with PCP-induced locomotor activity (Sturgeon et al. 1979), tolerance to PCP-induced ataxia produced an increase in locomotor activity on day 5. Tolerance to the ataxia, but not to the stereotyped behaviors induced by PCP, was more prominent after day 15 of PCP administration than after day 5. Administration of PCP for 15 days resulted in significant decrease in locomotor activity for the 5 mg/kg group but not for the 10 mg/kg group. These results suggest that behavioral tolerance, rather than supersensitivity, develops after chronic PCP administration. The effects of PCP returned to baseline over a 14-day withdrawal period for rats treated with 5 mg/kg PCP for 15 days. Rats treated with 10 mg/kg PCP for 15 days still had not returned to baseline when tested 28 days after cessation of PCP treatment.

Effects of lithium on behaviour induced by phencyclidine and amphetamine in rats.

d-Amphetamine and phencyclidine (PCP) have both been reported to produce manic-like sequela in humans, effects that are reportedly antagonized by lithium. To test the hypothesis that the acute effects of these drugs in rats may serve as models of mania, the behaviors induced by d-amphetamine (3 mg/kg) or PCP (5 mg/kg) were quantified on behavioral rating scales subsequent to chronic dietary pretreatment with lithium carbonate or control diet. On day 14 of pretreatment, PCP-induced stereotyped behaviors and ataxia were potentiated in rats receiving lithium (plasma levels 1.0 +/- 0.23 mEq/l). PCP-induced locomotor activity was not affected by lithium pretreatment. Stereotypies and locomotion induced by d-amphetamine were also not significantly affected by lithium pretreatment. These results suggest that neither PCP nor amphetamine administered acutely to rats will be useful models to explore the manic-like symptoms produced by these drugs in humans.

A comparison of the effects of neuroleptics on phencyclidine-induced behaviors in the rat.

The dose-response effects of neuroleptic pretreatment on phencyclidine (PCP; 3 or 5 mg/kg)-induced locomotor activity, stereotyped behaviors and ataxia were quantified in groups of male rats using rating scales recently developed in this laboratory. Three butyrophenone neuroleptics consistently produced dose-dependent antagonism of the behavioral effects of PCP administration. Fluphenazine antagonized the behavioral effects produced by 3 mg/kg PCP but not those produced by 5 mg/kg PCP. Each of the other neuroleptics examined (chlorpromazine, thioridazine, mesoridazine, triflupromazine, cis-flupenthixol) had no consistent antagonistic effect or actually enhanced one or more of the behavioral effects of PCP. Some neuroleptics slightly reduced PCP locomotion or stereotypies at high doses, but these effects were probably a non-specific consequence of the synergistic ataxia-producing properties of these drugs. In a second set of experiments, atropine sulfate pretreatment increased PCP-induced locomotor activity and stereotyped behaviors but had no effect on ataxia; pretreatment with physostigmine produced opposite effects. Combined pretreatment with haloperidol and atropine sulfate significantly reduced only haloperidol antagonism of PCP-induced ataxia, thus suggesting that non-dopoaminergic effects of neuroleptics may interfere with their ability to antagonize PCP.