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The presence of positive antibody titres to Toxoplasma and Toxocara in an adult epileptic population has been examined in relation to other observations of aetiological importance. With Toxoplasma, and more particularly with Toxocara, a higher incidence of positive antibody titres was recorded than in nonepileptic populations. Comparison with previous studies in childhood epilepsy indicate that the incidence of positive titres increased with age throughout adult life. Despite attention to the age of onset of epilepsy, presumed aetiological factors, and electroencephalographic and clinical observations, no causal relationship between parasitic infection and the aetiology of epilepsy was established.

1. The intra-arterial blood pressure responses to Valsalva's manoeuvre and postural change were investigated as indices of cardiovascular reflex activity in seventeen Parkinsonian patients on maximally tolerated doses of L( -)-dopa (levodopa) and repeated in nine patients on levodopa with an extracerebral decarboxylase inhibitor, L-alpha methyldopahydrazine. The results were compared with control pretreatment responses.2. There was significant impairment of the pressor response to Valsalva's manoeuvre on levodopa, which returned to control values after the addition of L-alpha methyldopahydrazine.3. The systolic, diastolic and mean arterial pressures measured in a horizontal position during treatment with levodopa, with and without L-alpha methyldopahydrazine, were significantly lower than pretreatment values. 4. It is concluded that the impairment of baroreflex function by levodopa is mediated, at least in part, at the periphery. In contrast, mechanisms operating within the central nervous system contribute to the lowering of blood pressure recorded in the horizontal position in patients receiving levodopa.

1. Cardiovascular reflex activity has been studied in thirty Parkinsonian patients, none of who had received levodopa or sympatholytic drugs.2. Changes in blood pressure and pulse rate in response to Valsalva's manoeuvre and head-up tilt were investigated by intra-arterial recording.3. Cardiovascular reflexfunction deteriorated with advancing age, but there was no correlation with either the duration or the severity of the Parkinsonism.4. These results are discussed in relation to previous reports of hypotension in Parkinsonism.Numerous therapeutic successes and several important adverse reactions have followed the adoption of levodopa (t-dopa) as treatment for Parkinsonism. The frequent occurrence of orthostatic hypotension as a reversible, dose-dependent effect of levodopa therapy has led to a resurgence of interest in the mechanisms of blood-pressure control in these patients. It has been reported that the blood pressure is lower than normal in Parkinsonism irrespective of drug administration and there have been suggestions of a generalized defect of catecholamine metabolism (Barbeau, 1970). More recently it has been found that plasma renin activity is decreased (Barbeau, Gillo-Joffroy, Boucher, Nowaczynski & Genest, 1969;Michelakis & Robertson, 1970). Shy & Drager (1960) have described six patients who presented with autonomic dysfunction including orthostatic hypotension and subsequently developed some of the clinical features of Parkinsonism.To obtain further information on the control of blood pressure in Parkinsonian patients before administration of levodopa, we have studied the cardiovascular response to Valsalva's manoeuvre and to head-up tilt. MATERIALSPatients. Thirty patients were investigated, of these twenty-eight had idiopathic and two postencephalitic Parkinsonism. There were fifteen men and fifteen women, their ages ranging

There are no pharmacokinetic grounds for adjusting dosages of either ropinirole or L-dopa when given in combination.

In comparison with levodopa, 3‐0‐methyldopa (30MD) is inadequate treatment for Parkinsonism. Therapeutic concentrations of levodopa could not be detected in the blood of patients receiving 6 gm per day of 30MD for 10 weeks. It is concluded that 30MD is not demethylated to levodopa in appreciable quantities in man. A possible explanation is the inability of man to excrete 30MD in the bile and the consequent failure of the intestinal bacterial flora to bring ab out demethylation.

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