Objective: Previous studies investigated the varying prevalence of post-epileptic seizure posttraumatic stress disorder (PS-PTSD). The current study aimed first to compare the profiles of patients with and without PS-PTSD and, second, to study the interaction between other past traumatic experiences, subjective ictal anxiety, psychiatric comorbidities, and PS-PTSD in people with epilepsy (PWE).
Methods: We conducted an observational study, investigating past traumatic experiences and PS-PTSD through standardized scales (CTQ-28, LEC-5 and PCL-5).
Background And Purpose: Seizures represent a core symptom of autoimmune encephalitides with specific therapeutic issues. To date, patients with new-onset seizures or established epilepsy are not systematically tested for autoimmune antibodies. We aimed to identify clinical and paraclinical criterion that could help to select patients requiring additional autoimmune antibodies serum and cerebrospinal fluid (CSF) detection.
View Article and Find Full Text PDFBackground: Psychogenic non-epileptic seizure-status (PNES-status), defined by psychogenic non-epileptic seizures (PNES) over 30 min, are often misdiagnosed as status epilepticus. We aimed to describe the features of patients who experienced PNES-status, admitted to an intensive care unit (ICU).
Methods: We screened the patients hospitalized in our epilepsy unit during a 4-year period, with a diagnosis of PNES-status and ICU admission.
Mutations in the α1 (COL4A1) or α2 (COL4A2) chains of collagen type IV, a major component of the vascular basement membrane, cause intracerebral haemorrhages with variable expressivity and reduced penetrance by mechanisms that remain poorly understood. Here we sought to investigate the cellular mechanisms of COL4A1-related intracerebral haemorrhage and identify a marker for haemorrhage risk stratification. A combination of histological, immunohistochemical, and electron microscopy analyses were used to analyse the brain parenchyma, cerebrovasculature, and retinal vessels of mice expressing the disease-causing COL4A1 p.
View Article and Find Full Text PDFTremor Other Hyperkinet Mov (N Y)
June 2016
Background: Glucose transporter type 1 deficiency syndrome is due to de novo mutations in the SLC2A1 gene encoding the glucose transporter type 1.
Phenomenology Shown: Paroxysmal motor manifestations induced by exercise or fasting may be the main manifestations of glucose transporter type 1 deficiency syndrome.
Educational Value: Proper identification of the paroxysmal events and early diagnosis is important since the disease is potentially treatable.