Epileptic Disorders最新文献

Cerebellar fit (CF) is characterized by paroxysmal head retroflexion and opisthotonus with preserved consciousness.^1-3 Here, we present a case of a 43-year-old male with cough syncope (CS) due to Chiari 1.5 malformation, who exhibited CF during hyperventilation (HV).⁴ EEG revealed a normal posterior dominant rhythm of 8–9 Hz. Approximately 150 s after initiating HV, the patient experienced truncal convulsion accompanied by opisthotonic posturing (Video 1). Notably, the patient retained his consciousness with open eyes. No electrographic seizure patterns were evident, the posterior dominant rhythm was preserved, and the electrocardiogram demonstrated normal sinus rhythm (Figure 1). He underwent a foramen magnum decompression and his CS and CF disappeared. As a mechanism, HV may induce dissociation between intracranial and spinal cord cerebrospinal fluid pressures, which further lower the cerebellum and compress the brainstem and cerebellum.^2-5 CF may be caused by the Guillain–Mollaret triangle disruption and CS by dysfunction of the brainstem reticular formation.^{6, 7}

This study was partially supported by JPJSBP 120217720 and by the Nakatani Foundation for Advancement of Measuring Technologies in Biomedical Engineering : Technology Exchange Program.

None of the authors have any conflicts of interest to declare.

Herein, we present the case of a 21-year-old man with a history of generalized tonic seizures since the age of 4 years. These seizures occurred either spontaneously or could be provoked by auditory stimuli such as the sounds of a vacuum cleaner or an electric shaver. Despite trials with 10 different anti-seizure medications, his seizures remained refractory. Interictal electroencephalography (EEG) revealed generalized epileptiform activity, whereas ictal EEG showed a generalized attenuation pattern. Magnetic resonance imaging revealed extensive chronic infarctions, predominantly in the bilateral cerebral watershed areas. At the age of 17, the patient underwent a one-stage complete callosotomy, which only achieved remission of auditory-provoked seizures. Based on this experience and published reports, we propose that the posterior corpus callosum, particularly the isthmus and anterior splenium, may be involved in seizures caused by unexpected sound stimuli.

Psychosis of epileptic origin can present a wide range of cognitive and affective symptoms and is often underrecognized. Usually occurring in the inter- and postictal phase, epileptic psychosis is mostly related to temporal lobe epilepsy. Here, we describe the clinical presentation and diagnostic workup including routine EEG recording and brain MRI of a 63-year-old woman expressing isolated nihilistic delusions comprising belief of being dead and denial of self-existence. EEG showed an ictal pattern fulfilling the Salzburg criteria of nonconvulsive status epilepticus and brain MRI revealed extensive peri-ictal hyperperfusion. Delusional symptoms and EEG abnormalities subsided after acute antiseizure treatment. Our case illustrates how nihilistic delusions can occur as a direct clinical correlate of seizure activity, thereby expanding the spectrum of ictal neuropsychiatric phenomena in temporal lobe epilepsy and highlighting the need to consider an epileptic origin in patients presenting with psychotic symptoms.

The diagnosis of epilepsy is associated with loss of predictability, which invariably results in the fear of when and if future seizures will occur. For a subset of patients with epilepsy (PWE), there may be a pathological persistent fear of seizure occurrence, resulting in limitations to daily activities through avoidant behaviors. Paradoxically, the research of anticipatory anxiety of seizures (AAS; also referred to as seizure phobia) has been practically nonexistent and, not surprisingly, this condition remains underrecognized by clinicians. The available data are derived from three small case series of patients followed in tertiary epilepsy centers. In this study, we review the available data on the reported clinical manifestations of AAS in PWE, and of the potential role of variables associated with it, such as personal and family psychosocial and psychiatric history and epilepsy-related variables. In addition, we review the need for the creation of screening tools to identify patients at risk of AAS and discuss potential treatment strategies, which could be considered as part of the comprehensive management for PWE.