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Anhedonia, the impaired ability to experience pleasure, is a core feature of major depressive disorder, one of the most common comorbidities in epilepsy. It is also reported as a clinical feature independent of depression in a number of other neurological conditions. This study aimed to establish the prevalence of anhedonia in a sample of people with epilepsy, with and without a diagnosis of depression, and to examine the clinical and demographic characteristics of those who present with this symptom.A consecutive sample of 211 people (118 female, 93 male, mean age 38.09 years) completed the Snaith-Hamilton Pleasure Scale (SHAPS) to determine the presence of anhedonia and the Hospital Anxiety and Depression Scale to determine levels of anxiety and depression. The majority of patients had focal epilepsy (n = 165), and the remaining patients had generalized epilepsy (n = 22), or unclassified epilepsy (n = 24). Sixteen percent of the sample had a clinical diagnosis of depression at the time of the study.Over one in three of the sample (35%) reported significant anhedonia on the SHAPS. While these patients were more likely to have a diagnosis of depression (p 0.01), 30% of people without a diagnosis of depression also reported significant anhedonia. Difficulties gaining pleasure on 12 of the 14 items on the SHAPS were associated with cognitive difficulties, with those reporting an inability to feel pleasure on the item scoring significantly lower on tests of cognitive function than those who were able to gain pleasure. Of the three cognitive domains examined (overall intellectual ability, verbal memory, and processing speed), a poor memory had the strongest relationship; with lower memory function associated with an impaired ability to experience pleasure on 9 of the 14 items.While anhedonia is well recognized as a feature of depression, our data suggests that it can be present in up to a third of people with epilepsy who do not have a diagnosis of depression. Cognitive difficulties, particularly impaired memory function may mediate some features of anhedonia. The implications of these findings for the clinical management of anhedonia in people with epilepsy are discussed.

We describe a 33 year old man with a severe vasculitis causng a profound axonal neuropathy and brainstem syndrome. The atient became unresponsive and lost all movement and braintem reflexes. The EEG showed poorly reactive rhythms suggesting lobal cortical dysfunction. The clinical signs were compatible with rainstem death except that an irreversible cause had not been emonstrated. The patient was treated and subsequently made a ood recovery.

Background Type 1 episodic ataxia is a disorder characterised by paroxysmal cerebellar incoordination and interictal myokymia. It is caused by dominant negative mutations of KCNA1 , which encodes the presynaptic and axonal potassium channel subunit Kv1.1. Mutations in the disorder increase neuronal excitability and neurotransmitter release in neuronal cultures. Our hypothesis is that type 1 episodic ataxia prolongs the action potential at presynaptic terminals thus causing increased neurotransmitter release. We aimed to test this hypothesis in mouse models of type 1 episodic ataxia. Methods We used two mouse models, one with a knockout of the KCNA1 mutation ( KCNA1a –/–) and one with a knockin of the mutation KCNA1a (V408A/+). We used scanning ion conductance microscopy to acquire super-resolution images of very small synaptic boutons (∼1 μm diameter) in mouse hippocampal neuronal cultures and achieved direct electrophysiological recording from these boutons. We compared wild-type, KCNA1a –/–, and KCNA1a (V408A/+) mice. Action potentials were either elicited by injection of a depolarising current at the bouton or via a second pipette at the cell body. Findings Presynaptic action potential half width was larger in KCNA1a –/– mice than in their wild-type littermates when directly elicited at the bouton (mean 1·43 ms [SE 0·12] vs 0·86 [0·068]) and when elicited by depolarising the cell body (1·44 [0·089] vs 1·17 [0·055]), and was also larger in KCNA1a (V408A/+) mice (1·14 [0·063] vs 0·91 [0·065] and 1·38 [0·063] vs 1·11 [0·048], respectively). In separate prepulse experiments, wild-type mice showed an increase in bouton action potential half width when moving from hyperpolarising to depolarising subthreshold prepulse steps. KCNA1a –/– mice also showed increasing action potential half widths with the steps. However, in KCNA1a (V408A/+) mice this positive correlation was abolished. Interpretation A prolonged presynaptic action potential in type 1 episodic ataxia might cause the increase in neurotransmitter release. Progressive presynaptic depolarisation in KCNA1a (V408A/+) mice has no effect on Kv1.1 inactivation, which in turn might affect the digital-analogue facilitation of synaptic transmission in hippocampal synapses. Since Kv1.1 is abundantly expressed in cerebellar basket cells, it could lead to added inhibition of cerebellar Purkinje cells and ataxia. Funding Wellcome Trust.