Antiepileptic drugs (AEDs) are effective against seizures, but their use is often limited by adverse effects, among them psychiatric and behavioral ones including aggressive behavior (AB). Knowledge of the incidence, risk factors, and the underlying mechanisms of AB induced by AEDs may help to facilitate management and reduce the risk of such side effects. The exact incidence of AB as an adverse effect of AEDs is difficult to estimate, but frequencies up to 16% have been reported. Primarily, levetiracetam (LEV), perampanel (PER), and topiramate (TPM), which have diverse mechanisms of action, have been associated with AB. Currently, there is no evidence for a specific pharmacological mechanism solely explaining the increased incidence of AB with LEV, PER, and TPM. Serotonin (5-HT) and GABA, and particularly glutamate (via the AMPA receptor), seem to play key roles. Other mechanisms involve hormones, epigenetics, and “alternative psychosis” and related phenomena. Increased individual susceptibility due to an underlying neurological and/or a mental health disorder may further explain why people with epilepsy are at an increased risk of AB when using AEDs. Remarkably, AB may occur with a delay of weeks or months after start of treatment. Information to patients, relatives, and caregivers, as well as sufficient clinical follow-up, is crucial, and there is a need for further research to understand the complex relationship between AED mechanisms of action and the induction/worsening of AB.
Research on omega-3 polyunsaturated fatty acids (n-3 PUFAs) has grown exponentially since researchers from Denmark visited Greenland in 1970 to study why the cardiovascular mortality among the Inuit population was considerably lower than in the Western countries. 6 The researchers related their findings to the diet of the Inuit, which consisted mainly of fish and meat from seals, whales, sea birds, and fur-bearing animals. These foods contain large amounts of n-3 PUFAs. 6 In the following decades, the health effects of n-3 PUFAs were studied extensively, covering almost all medical conditions, including
Our results suggest a risk of verbal memory deterioration after the use of depth electrodes along the longitudinal axis of the hippocampus. Until this issue is further investigated, caution regarding depth electrodes in the language-dominant hemisphere hippocampus seems advisable.
IntroductionIt is hypothesized that cerebral hypoperfusion promotes the development of Alzheimer pathology. We therefore studied whether longstanding cerebral hypoperfusion is associated with Alzheimer pathology in nondemented humans.MethodsCerebral blood flow and amyloid β (18F-Flutemetamol) positron emission tomography retention were assessed in eleven patients with unilateral occlusion of precerebral arteries resulting in chronic and uneven hypoperfusion. A subset of patients underwent tau (18F-AV-1451) positron emission tomography.ResultsThe blood flow was significantly reduced on the affected side of the brain in patients with unilateral occlusion of the internal carotid artery or stenosis of the middle cerebral artery. However, the cortical uptake of 18F-Flutemetamol or 18F-AV-1451 was not altered.DiscussionOur results suggest that longstanding cerebral hypoperfusion in humans does not result in accumulation of amyloid β fibrils or tau aggregates.
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