Summary: Purpose: Lamotrigine is an effective add-on therapy against a range of epileptic seizure types. Comparative studies with carbainaLepine (CBZ) as monotherapy in newly diagnosed epilepsy suggest similar efficacy. In this study, lamotrigine (LTG) and phenytoin (PHT) are compared.Methods: In a double-blind parallel-groups study. I X 1 patients with newly diagnosed untreated partial seizures or secondarily or primary generalised tonic-clonic seizures were randoniised to two treatment groups. One group (n = 86) received LTG titrated over 6 weeks from a starting dose of 100 mg/day. The other (ti = 95) received PHT titrated from 200 ing/tlay. Treatment continued for 5 4 8 weeks. K i~s i d t x ;The percentages of patients remaining on each treatment and seiLure frec during the last 24 and 40 weeks of the study, and times to first seizure after the first 6 weeks of treatment (dose-titration period). did not differ significantly between the treatment groups. These were measures of efficacy. Time to discontinuation, a composite index of effi safety, likewise did not distinguish between treatments. Adverse events led to discontinuation of 13 (IS%) patients from LTG and 18 ( 1 9%) from PHT. The adverse-event profile for LTG w.as dominated by skin rash (discontinuation of 10 (11.6%) patients compared with five (5.3%) from PHT] rather than central nervous system side effect sthenia, somnolence, and ataxia were each significantly inore frequent in the PHT group. The high rate of rash with LTG was probably due to the high starting dose and may be avoidable. A quality-of-life instrument. the SEALS inventory, favoured LTG. Patients taking PHT showed the biochemical changes expected of an eiizyrneinducing drug, whereas those taking LTG did not.Cotwlusiot~.~: LTG and PHT monotherapy were similarly effective against these seizure types in patients with newly diagnosed epilepsy. LTG was better tolerated, inore frequently causing rash. but with a lower incidence of central nervous system side effects.
Post-CEA seizure was associated with adverse outcome. Most were labile hypertensives with severe bilateral carotid/vertebral disease. MCAV changes suggested poor collateral recruitment, but no consistent pattern of early hyperperfusion emerged. It remains uncertain whether high MCAVs and severe hypertension after seizure onset are cause or effect. Clinicians treating these patients in acute medical units were generally unaware of the "post-CEA hyperperfusion syndrome" and tended to treat the hypertension less aggressively.
SUMMARY Serial serum prolactin and cortisol levels were measured in five patients after a grand mal seizure and in four volunteers with simulated seizures. Single levels were measured after a witnessed seizure in 26 patients and in a matched control group. Significant increase in both prolactin and cortisol levels occurred after seizures. The change in cortisol level may reflect a nonspecific stress response, but the increase in prolactin levels could not be accounted for on this basis, and probably indicates an alteration in hypothalamic neurotransmitter activity during the seizure. These findings may have clinical value in the diagnosis of epilepsy.Prolactin release from the anterior pituitary gland is thought to be controlled by release of neurotransmitter from the hypothalamus. Inhibition by dopamine' is important but noradrenaline2 and gamma aminobutyric acid (GABA)' may ailso inhibit prolactin release. The nature of the prolactin-releasing factor in mammals is uncertain, and the effect of 5-hydroxytryptamine (5-HT) on prolactin release in man is still unclear.46.Serum prolactin may, therefore, be considered as a peripheral marker of hypothalamic neurotransmitter activity. Many other factors are known to influence prolactin secretion, including stress7 and drugs.8 Electroconvulsive therapy has been shown to produce a marked rise in serum prolactin,9 and in a recent uncontrolled study a significant increase in prolactin levels was found 20 minutes after a grand mal convulsion.10 Paroxysmal discharges occur during grand mal seizures in major ascending and descending pathways concerned with consciousness and motor control, but involvement of the hypothalamus has not been studied. If a clearly defined rise in serum prolactin occurs after seizures this might have clinical applications in the assessment of patients with episodes of loss of consciousness of uncertain aetiology. As stress
Neuropsychiatric side effects often complicate anti-Parkinsonian therapy and pose a significant problem in the optimal management of idiopathic Parkinson's disease. Several publications report a relative lack of neuropsychiatric side effects in Parkinsonian patients treated with subcutaneous apomorphine. To investigate this further, we have used subcutaneous apomorphine to treat 12 non-demented IPD patients with previous oral drug-related neuropsychiatric problems. Treatment with apomorphine allowed alteration of anti-Parkinsonian medication and led to the abolition or reduction of neuropsychiatric complications in all patients. The mechanism remains unclear but may be due, in part, to a reduction in oral medication or a psychotropic action of apomorphine, possibly due to the piperidine moiety in its structure, or both.
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