Post-epileptic seizure posttraumatic stress Disorder: A mediation analysis.

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). We used semi-structured interviews and validated psychometric scales (NDDIE for depression and GAD-7 for anxiety) to collect data on general psychiatric comorbidities. We also assessed epilepsy specific psychiatric symptoms (interictal and peri-ictal). We performed a mediation analysis through PROCESS for SPSS to evaluate the effect of history of past trauma and subjective ictal anxiety on PS-PTSD through interictal depression and anxiety symptoms. RESULTS: We enrolled 135 PWE, including 35 patients with PS-PTSD (29.5 %). Patients with PS-PTSD had significantly higher depression (12.87 vs 10; p = 0.005) and anxiety (7.74 vs 5.01; p = 0.027) scores and higher prevalence of peri-ictal psychiatric symptoms, compared to patients without PS-PTSD. The relationship between other past traumatic experiences and PS-PTSD was totally mediated by interictal depression and anxiety. We found a significant indirect effect of interictal anxiety symptoms on the path between subjective ictal anxiety and PS-PTSD. SIGNIFICANCE: Our results showed that patients with PS-PTSD have a more severe psychopathological profile (more peri ictal and inter ictal depressive and anxiety symptoms). Both inter ictal and subjective ictal anxiety appear to have a significant role in PS-PTSD.

When should we test patients with epilepsy for autoimmune antibodies? Results from a French retrospective single center study.

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. METHODS: In this retrospective single center study from the French Salpêtrière Hospital, data from 286 adult patients with epilepsy who received an autoantibody assay for the first time were analyzed. All patients were evaluated at our institution between January 2007 and December 2018 for assessment of new-onset epilepsy (n = 90) or established epilepsy (n = 196). We only analyzed patients that were screened for autoimmune antibodies. Demographic, clinical and neuroimaging measures were compared between patients with and without autoimmune encephalitis using Fisher's exact test for categorical variables and Welch's t test for continuous variables. Our primary goal was to identify significant factors that differentiated patients with and without autoimmune encephalitis. RESULTS: We identified 27 patients with autoimmune epilepsy (9.4% of the patients who had been tested for autoantibodies). The significant factors differentiating patients with and without autoimmune encephalitis were: (i) the existence of a new-onset focal epilepsy + (e.g., newly diagnosed epilepsy < 6 months associated with additional symptoms, mainly cognitive or psychiatric symptoms), (ii) the presence of faciobrachial dystonic seizures very suggestive of anti- Leucine-rich glioma inactivated 1 (LGI1) encephalitis, and (iii) the presence of magnetic resonance imaging (MRI) abnormalities suggestive of encephalitis. CONCLUSION: New-onset focal seizures combined with cognitive or psychiatric symptoms support the test for autoimmune antibodies. Further clinical already known red flags for an autoimmune origin are the presence of faciobrachial dystonic seizures and MRI signal changes consistent with encephalitis. On the other hand, isolated new-onset seizures and chronic epilepsy, even with associated symptoms, seem rarely linked to autoimmune encephalitis and should not lead to systematic testing.

Psychogenic non-epileptic seizure-status in patients admitted to the intensive care unit.

BACKGROUND: 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. RESULTS: Among 171 patients with PNES, we identified 25 patients (15%) who presented 39 episodes of PNES-status leading to ICU admission. Some 76% of the patients were women. The median age at the time of the PNES-status episode was 35 years. Half (48%) alleged a history of epilepsy, but epilepsy was confirmed in only 12%. A history of psychiatric disease was found in 68%. PNES were present in 85% of patients before PNES-status, and semiology of PNES and PNES-status was similar for 79% of the patients, including hyperkinetic movements in 95% of the episodes and suspected loss of consciousness in 87%. Benzodiazepines were administrated in 77% of the episodes, antiepileptic drugs in 87%, and antibiotherapy for a ICU-related infection in 15% of the episodes. Oral intubation was performed in 41% of the episodes. Blood tests showed normal levels of creatine phosphokinase and leucocytes in 90% and 95% of the episodes, respectively. No epileptic activity was found during per-event electroencephalography but interictal epileptic activity was found in 10% of the episodes. CONCLUSION: Hyperkinetic PNES-status should always be considered as a differential diagnosis of status epilepticus, with a high risk of iatrogenic consequences.

Neuronal injuries evidenced by transient cortical magnetic resonance enhancement in hemiplegic migraine: A case report.

BACKGROUND: Magnetic resonance imaging abnormalities in hemiplegic migraine have been described previously but were limited to a cortical thickening and biphasic alternation of hypoperfusion and hyperperfusion. Our report reveals possible blood-brain barrier disruption during migraine. CASE: We present the first demonstrated case of regressive diffuse hemispheric cortical enhancement in sporadic hemiplegic migraine, with histological correlation revealing neuronal lesions similar to ischemic lesions. This is probably due to the severity of the attack as indicated by the left hemiplegia and transient altered consciousness in our 43-year-old male patient. CONCLUSION: Cortical contrast enhancement on 3D T1 images may suggest migraine severity and be predictive of neuronal loss.

Severity of arterial defects in the retina correlates with the burden of intracerebral haemorrhage in COL4A1-related stroke.

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.G498V mutation. Mutant mice developed cerebral microhaemorrhages and macroscopic haemorrhages (macrohaemorrhages), the latter with reduced penetrance, mimicking the human disease. Microhaemorrhages that occurred in early postnatal life were associated with a transient, generalized increase in blood-brain barrier permeability at the level of capillaries. Macrohaemorrhages, which occurred later in life, originated from deep brain arteries with focal loss of smooth muscle cells. Similar smooth muscle cell loss was detected in retinal arteries, and a time-course analysis of arterial lesions showed that smooth muscle cells are recruited normally in arterial wall during development, but undergo progressive apoptosis-mediated degeneration. By assessing in parallel the extent of these retinal arterial lesions and the presence/absence of macrohaemorrhages, we found that the arterial lesion load in the retina is strongly correlated with the burden of macrohaemorrhages. We conclude that microhaemorrhages and macrohaemorrhages are driven by two distinct mechanisms. Moreover, smooth muscle cell degeneration is a critical factor underlying the partial penetrance of COL4A1-related macrohaemorrhages, and retinal imaging is a promising tool for identifying high-risk patients. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Paroxysmal Exercise-induced Dyskinesias Caused by GLUT1 Deficiency Syndrome.

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.