Isolated ocular myopathy and celiac disease in childhood.

Neurologic deficits complicating celiac disease are well-described in adults. Here we report a 12-year-old girl in whom isolated ocular myopathy was the presenting feature of biopsy-proven celiac disease; the process was apparently reversed by a gluten-free diet and vitamin supplementation.

Naloxone causes urinary urgency.

We present 2 cases in which naloxone, the opioid antagonist, produced urinary urgency. The mechanism of action and possible therapeutic applications are discussed.

Tourette syndrome: successful treatment with clonidine and oxycodone.

A 15-year-old boy with Tourette's syndrome exhibited severe involuntary self-mutilatory behavior. While clonidine effectively controlled the motor and phonic tics, it failed to ameliorate the self-mutilatory behavior. Administration of oxycodone (50 mg/day) combined with clonidine produced a dramatic reduction in the frequency and severity of the self-mutilatory acts within 12 h. This report indicates that disturbances in the functional interplay between the noradrenergic and opiatergic systems may be important in the pathophysiology of Tourette's syndrome.

Pineal melatonin in schizophrenia: a review and hypothesis.

It has long been suggested that abnormal functions of the pineal gland may be implicated in the pathophysiology of schizophrenia. We present evidence proposing that diminished melatonin secretion may be associated with the pathophysiology of a subgroup of schizophrenic patients characterized by cerebral atrophy and ventricular enlargement, negative symptoms, impaired cognitive and psychosexual development, onset at pubescence, poor response to neuroleptic medication, and possible increased risk of extrapyramidal symptoms. This view holds that a subnormal plasma melatonin level may be a marker of a subgroup of schizophrenia and may also denote a specific genetic susceptibility.

Pain management after lower extremity amputation.

Phantom pain may occur in up to 85% of patients after limb amputation. Although the pathophysiology of postamputation phantom pain is not well understood, it seems to be produced by a complex multifactorial interaction between the peripheral, sympathetic, and central nervous systems. The theoretical aspects of this are reviewed. Management of phantom limb pain may be both medical and surgical. Among the pharmacological agents proved effective against phantom pain are beta-blockers, tricyclic antidepressants, and anticonvulsants. Surgical management includes peripheral nerve stimulation, thermocontrolled coagulation of the spinal cord, spinal cord stimulation, transcutaneous nerve stimulation, and stereotactic deep brain stimulation.

Parkinsonism due to subdural hematoma. Case report.

The authors describe the case of a 38-year-old woman who presented with parkinsonian syndrome associated with chronic subdural hematoma. Gradual disappearance of the symptomatology followed removal of the hematoma. Chronic subdural hematoma may in rare instances cause a parkinsonian syndrome, probably by a pressure effect on basal ganglia structures or by altering the function of neurotransmitters.

The endogenous opioid system in neurological disorders of the basal ganglia.

The endogenous opioid peptides have for some time been implicated in the regulation of motor behavior in animals. Recently, however, there is increased evidence to suggest a role for these peptides in the control of human motor functions as well as in the pathophysiology of abnormal movement disorders. Degeneration of opioid peptide-containing neurons in the basal ganglia has been demonstrated in Parkinson's disease and Huntington's chorea, but the clinical significance of these findings is largely unknown. On the other hand, there is evidence that excessive opioid activity may be important in the pathophysiology of some movement disorders such as tardive dyskinesia, progressive supra-nuclear palsy, and a subgroup of Tourette's patients. These findings indicate that diseases of the basal ganglia are possibly associated with alterations in opioid peptide activity, and that these alterations may be useful in designing experimental therapeutic strategies in these conditions.

The effects of L-tryptophan on haloperidol-induced movement disorder in the rat.

An animal model of haloperidol-induced tardive dyskinesia was studied in relation to the dietary manipulation of tryptophan and its effect on the movement disorder. This study showed a significant negative behavioral response to the neuroleptic drug, haloperidol. Increased dietary tryptophan (1.0 vs. 0.3%) significantly reduced the frequency of drug-induced head movements. Brain serotonin levels were elevated by the drug treatment. Brain serotonin levels correlated significantly with the behavioral response. Contrary to expectation, brain dopamine levels did not correlate with the behavioral response. These findings suggest a possible serotonergic involvement in neuroleptic-induced tardive dyskinesia and an amelioration of the disorder through tryptophan supplementation.

Persistent tardive dyskinesia and neuroleptic effects on glucose tolerance.

The relations of persistent tardive dyskinesia (TD) to glucose tolerance and family history of type 2 diabetes mellitus (FH-NIDDM) were examined in 22 schizophrenic patients. All patients underwent a standard oral glucose tolerance test (GTT) while receiving haloperidol, and 15 patients also underwent a GTT when drug free. Fasting blood glucose (FBS) was significantly higher in the TD group than in the non-TD group in the medicated condition, but not in the drug-free state. TD and non-TD groups did not differ significantly in postload glucose levels either in the drug-free or in the medicated condition. However, relative to the drug-free state, haloperidol-treated TD patients showed decreased glucose tolerance while non-TD patients showed increased glucose tolerance. Seven (32%) of the 22 patients had an FH-NIDDM. A positive FH-NIDDM was significantly associated with the presence of TD and with higher drug-free FBS. A possible role of melatonin in mediating the TD-augmenting effects of FH-NIDDM and the neuroleptic-induced decrease in glucose tolerance has been proposed.

Controlled clinical trial of cannabidiol in Huntington's disease.

Based on encouraging preliminary findings, cannabidiol (CBD), a major nonpsychotropic constituent of Cannabis, was evaluated for symptomatic efficacy and safety in 15 neuroleptic-free patients with Huntington's Disease (HD). The effects of oral CBD (10 mg/kg/day for 6 weeks) and placebo (sesame oil for 6 weeks) were ascertained weekly under a double-blind, randomized cross-over design. A comparison of the effects of CBD and placebo on chorea severity and other therapeutic outcome variables, and on a Cannabis side effect inventory, clinical lab tests and other safety outcome variables, indicated no significant (p greater than 0.05) or clinically important differences. Correspondingly, plasma levels of CBD were assayed by GC/MS, and the weekly levels (mean range of 5.9 to 11.2 ng/ml) did not differ significantly over the 6 weeks of CBD administration. In summary, CBD, at an average daily dose of about 700 mg/day for 6 weeks, was neither symptomatically effective nor toxic, relative to placebo, in neuroleptic-free patients with HD.