Lesions of basal ganglia due to disulfiram neurotoxicity.

Three cases of disulfiram induced Parkinsonism and frontal lobe-like syndrome associated with bilateral lesions of the lentiform nuclei on CT scan are reported. Symptoms developed either after an acute high dose of disulfiram (one case) or after several days to weeks of disulfiram treatment (two cases) and persisted over several years in two patients. These observations suggest that basal ganglia are one of the major targets of disulfiram neurotoxicity. The mechanisms of the lesions of basal ganglia may involve carbon disulfide toxicity.     

Dystonia and akinesia due to pallidoputaminal lesions after disulfiram intoxication

A case with segmental cranial plus crural dystonia of delayed onset and akinesia after acute intoxication with disulfiram is presented. Computed tomography showed bilateral pallidal lesions, whereas on magnetic resonance imaging additional small lesions of the putamen could be detected. Long-term observation with progression and a change of symptoms over a period of 10 years after the intoxication is demonstrated on videotape. Although other central side effects after intoxication with disulfiram are well known, movement disorders are uncommon. Carbon disulfide, a disulfiram metabolite, may be important in the etiopathogenesis.     

Downbeat nystagmus due to anticonvulsant toxicity

Isolated downbeat nystagmus was observed in 2 patients on multiple anticonvulsant regimens. The nystagmus disappeared when phenytoin dosage was reduced. Electrooculographic analysis revealed impaired downward tracking, supporting the concept of “pursuit” nystagmus.     

Profound behavioral toxicity due to tricyclic antidepressants

The incidence of tricyclic antidepressant-induced behavioral toxicity appears to be fairly high in elderly patients but has rarely been reported in the young. We present a case of significant behavioral side effects in a young woman secondary to elevated plasma levels of imipramine and desipramine, masquerading as an agitated psychotic depression.     

Permanent neurological deficits due to lithium toxicity

Two patients exhibited permanent neurological deficits following relatively uncomplicated episodes of lithium intoxication. Lithium toxicity alone appears to result in a fairly consistent combination of neurological findings, including deficits in recent memory, limb and truncal ataxia, and choreoathetosis or parkinsonism. The potential role of early hemodialysis in preventing these permanent deficits is discussed.     

Permanent neurological sequelae due to lithium toxicity

Lithium intoxication is well known to produce acute and chronic symptoms but development of permanent neurological deficit is a rarity. Six cases of manic depressive psychosis who developed neurological sequelae following treatment with lithium carbonate are described. There were multiple lesions in the central nervous system. However, the main brunt was borne by cerebellum. The serum lithium levels of five patients were within therapeutic range. The value of identifying the precipitating factors, early diagnosis and prompt intervention in the prevention of persistent neurological dysfunction is emphasized.     

A Creutzfeldt-Jakob like syndrome due to lithium toxicity.

Two patients with lithium toxicity presented with a neurological syndrome suggesting a diagnosis of Creutzfeldt-Jakob disease. In both cases, the initial EEG was consistent with this diagnosis. Neither patient had permanent neurological sequelae and the EEG returned to normal. A careful drug history should be taken in any patient who presents with a rapidly progressive dementia even when the EEG supports a diagnosis of Creutzfeldt-Jakob disease.     

Retinal ganglion cell toxicity due to oxcarbazepine and valproic acid treatment in rat

PurposeTo evaluate and to compare the possible toxic effects of oxcarbazepine (OXC) and valproic acid (VPA) on retinal ganglion cells (RGCs) in rat.MethodsForty female Wistar rats (21–24 days old and weighted between 44.6 and 57.3 g) were divided equally into 4 experimental groups which were applied tap water (group 1), 300 mg/(kg day) VPA (group 2), 100 mg/(kg day) OXC (group 3), and both VPA and OXC (group 4) via gavage for 90 days. Enucleation was performed for histopathologic analysis. RGCs were counted under the light microscopic examination.ResultsRGC numbers in OXC and combined OXC-VPA groups were found to be lower than those of control group. On the other hand RGC number was comparable with those of control group in VPA group.ConclusionOXC seems to be toxic to RGCs at 100 mg/kg dose when it is been given as a monotherapy or combined with VPA. Single VPA treatment has no effect on RGC number.