pregabalin and Epilepsy--Temporal-Lobe

New-onset paroxysmal events in patients over 60 years of age are often diagnostically challenging owing to atypical presentation. Recurrent falls and transient states of confusion are especially common in the elderly population, yet their causes often remain undiagnosed due to concomitant cognitive deficits and motor impairments. We present an elderly patient with newly occurring 'blackouts' without obvious triggers and transient states of confusion for which he was amnestic. All neurological exams including brain MRI scan and routine electroencephalography (EEG) were normal. Long-term ECG monitoring using an event recorder captured an asystole during a habitual episode, leading to the diagnosis of syncope and pacemaker implantation. A subsequent video EEG monitoring performed due to ongoing unexplained confusional states revealed both bradycardia and long-lasting confusional states to be caused by unrecognised temporal lobe seizures. Ictal video EEG monitoring may play a crucial role in establishing a diagnosis of atypical temporal lobe seizures in the elderly.

Topics: Accidental Falls; Amnesia; Anticonvulsants; Confusion; Electroencephalography; Epilepsy, Temporal Lobe; Heart Arrest; Humans; Male; Middle Aged; Monitoring, Physiologic; Pacemaker, Artificial; Pregabalin; Recurrence; Syncope; Treatment Outcome; Video Recording

Mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is a common epilepsy syndrome that is often poorly controlled by antiepileptic drug (AED) treatment. Comparative AED effectiveness studies in this condition are lacking. We report retention, efficacy, and tolerability in a cohort of patients with MTLE-HS.. Clinical data were collected from a European database of patients with epilepsy. We estimated retention, 12-month seizure freedom, and adverse drug reaction (ADR) rates for the 10 most commonly used AEDs in patients with MTLE-HS.. Seven hundred sixty-seven patients with a total of 3,249 AED trials were included. The highest 12-month retention rates were observed with carbamazepine (85.9%), valproate (85%), and clobazam (79%). Twelve-month seizure freedom rates varied from 1.2% for gabapentin and vigabatrin to 11% for carbamazepine. Response rates were highest for AEDs that were prescribed as initial treatment and lowest for AEDs that were used in a third or higher instance. ADRs were reported in 47.6% of patients, with the highest rates observed with oxcarbazepine (35.7%), topiramate (30.9%), and pregabalin (27.4%), and the lowest rates with clobazam (6.5%), gabapentin (8.9%), and lamotrigine (16.6%). The most commonly reported ADRs were lethargy and drowsiness, dizziness, vertigo and ataxia, and blurred vision and diplopia.. Our results did not demonstrate any clear advantage of newer versus older AEDs. Our results provide useful insights into AED retention, efficacy, and ADR rates in patients with MTLE-HS.

Topics: Adolescent; Adult; Aged; Amines; Anticonvulsants; Ataxia; Benzodiazepines; Carbamazepine; Clobazam; Cyclohexanecarboxylic Acids; Databases, Factual; Diplopia; Dizziness; Epilepsy, Temporal Lobe; Female; Fructose; Gabapentin; gamma-Aminobutyric Acid; Hippocampus; Humans; Lamotrigine; Lethargy; Male; Middle Aged; Oxcarbazepine; Pregabalin; Retrospective Studies; Sclerosis; Topiramate; Treatment Outcome; Triazines; Valproic Acid; Vertigo; Vigabatrin; Vision Disorders; Young Adult

To determine whether a pharmacologic treatment could delay or prevent the epileptogenesis induced by status epilepticus (SE) through the protection of some brain areas, we studied the effects of the long-term exposure to pregabalin (PGB) on neuronal damage and epileptogenesis induced by lithium-pilocarpine SE.. SE was induced in adult and 21-day-old (P21) rats. At 20 min after pilocarpine, rats received 50 mg/kg PGB (pilo-preg) or saline (pilo-saline). PGB treatment was given daily at the dose of 50 mg/kg for 7 days after SE and at 10 mg/kg from day 8 until killing. Neuronal damage was assessed in hippocampus and piriform and entorhinal cortices in brain sections stained with thionine and obtained from adult and P21 animals killed 6 days after SE. The number of glial fibrillary acidic protein (GFAP)-reactive astrocytes was tested by immunohistochemistry in sections adjacent to those used for cell counting. The latency to spontaneous seizures was controlled by visual observation and EEG recording.. PGB induced neuroprotection in layer II of piriform cortex and layers III-IV of ventral entorhinal cortex of adult rats, whereas no hippocampal region was protected. In P21 rats, damage was limited to the hilus and similar in pilo-preg and pilo-saline animals. The number of GFAP-positive astrocytes was higher in pilocarpine- than in saline-treated rats. It was decreased in pilo-preg compared with pilo-saline rats in layer II of the piriform cortex. Adult pilo-preg rats became epileptic after a longer latency (39 days) than did pilo-saline rats (22 days).. These data underline the antiepileptogenic consequences of long-term PGB treatment, possibly mediated by the protection of piriform and entorhinal cortices in the lithium-pilocarpine model of epilepsy.

Topics: Animals; Anticonvulsants; Astrocytes; Brain; Cell Death; Cerebral Cortex; Convulsants; Electroencephalography; Entorhinal Cortex; Epilepsy, Temporal Lobe; gamma-Aminobutyric Acid; Glial Fibrillary Acidic Protein; Hippocampus; Immunoenzyme Techniques; Lithium; Neuroprotective Agents; Parahippocampal Gyrus; Pilocarpine; Pregabalin; Rats; Rats, Sprague-Dawley; Status Epilepticus