Successful treatment of co-occurring catatonia and obsessive-compulsive disorder with concurrent electroconvulsive therapy and benzodiazepine administration.

Catatonia, associated with a variety of medical and psychiatric conditions such as mood disorders and schizophrenia, is frequently treated with either benzodiazepines or with electroconvulsive therapy (ECT) in treatment-resistant cases. Simultaneous treatment with both is usually avoided. Here, we report a case of the use of the benzodiazepine antagonist flumazenil before ECT to facilitate the simultaneous use of lorazepam and ECT for the treatment of co-occurring catatonia and obsessive-compulsive disorder. Both catatonia and obsessive-compulsive disorder symptoms improved in the patient. Physicians should be aware of flumazenil as a clinical tool for use in treatment-resistant cases.

Ciliary neurotrophic factor improves nerve conduction and ameliorates regeneration deficits in diabetic rats.

Ciliary neurotrophic factor (CNTF) protein and bioactivity are reduced in the peripheral nerve of hyperglycemic rats with a cause related to metabolism of hexose sugars by aldose reductase. Here the efficacy of CNTF treatment against disorders of nerve function in hyperglycemic rats was investigated. CNTF treatment from the onset of 8 weeks of galactose feeding prevented nerve conduction slowing in a dose-dependent manner. Streptozotocin-induced diabetic rats were maintained for 4 weeks before CNTF treatment was initiated. Four weeks of CNTF treatment significantly improved nerve conduction compared with untreated diabetic rats and also normalized the recovery of toe spread after sciatic nerve crush. One week of CNTF treatment significantly improved the distance of sensory nerve regeneration achieved after nerve crush injury compared with untreated diabetic rats. CNTF was without effects on any parameter in nondiabetic rats. Eight weeks of diabetes did not impair macrophage recruitment 1 and 7 days after nerve crush; neither did intraneural injections of CNTF and CNTFRalpha enhance recruitment in diabetic or control rats. These observations point to the potential utility of CNTF in treating nerve dysfunction in experimental diabetes.