Treatment of Parkinson's disease with levodopa combined with L-alpha-methyldopahydrazine, an inhibitor of extracerebral DOPA decarboxylase.

Thirty patients with Parkinson's disease were treated for four weeks with levodopa combined with an inhibitor of extracerebral dopa decarboxylase, L-alpha-methyldopahydrazine (MK 486). The therapeutic results were compared with the effects of treatment of a group of 40 patients with levodopa alone. Patients treated with the combined therapy improved more rapidly, had less nausea and vomiting, and required a much smaller dose of levodopa than patients treated with levodopa by itself.

Clinical and electroencephalographic assessment of diazepam in liver disease.

The effects of 5 mg of diazepam intravenously were assessed in 23 patients with liver disease, 10 of whom had clinical evidence either in the past or at the time of study of hepatic encephalopathy. Transient drowsiness occurred in all patients, but prolonged deterioration in conscious level was not observed. Serial electroencephalographic recordings showed the development of activity at faster frequencies, similar to that found in normal subjects, a change which is different from that usually observed in cirrhotic patients after administration of chlorpromazine and morphine when slow-wave activity is increased.

Livedo reticularis during amantadine treatment.

Livedo reticularis is a common side effect of treatment with amantadine for Parkinson's disease. Investigation of 40 such patients suggests that the livedo is a physiological response provoked by depletion of catecholamine stores in peripheral nerve terminals.

L-dopa and amantadine hydrochloride in extra-pyramidal disorders.

L-Dopa and amantadine hydrochloride were separately given to patients with diverse extra-pyramidal disorders including progressive supranuclear palsy; porto-systemic encephalopathy; oculogyric crises; drug-induced Parkinsonism; Huntington's chorea, hemiballismus; spasmodic torticollis, familial tremor; and athetosis. Akinesia and rigidity were improved in the first two conditions and simultaneously there was improvement in disordered eye movement. Amantadine provoked an exacerbation in spasmodic torticollis and familial tremor.

Myasthenia gravis in the dog.

An account is given of four cases of myasthenia gravis in the dog. All animals showed fatigue, and considerably reduced tolerance to exercise. Recovery followed rest or treatment with neostigmine.

Peripheral nerve and root lesions developing as a result of haematoma formation during anticoagulant treatment.

Three further cases of peripheral nerve and root lesions occurring during anticoagulant therapy are described. The literature is briefly reviewed.