Effect of gabapentin on sleep patterns disturbed by epilepsy.

For a long time, numerous sleep alterations induced by nocturnal epilepsy have been described. Such alterations include sleep fragmentation, decrement of sleep efficiency, increment of the wake time after sleep onset (WASO), increment of light sleep, and decrement of sleep depth. On the other hand, gabapentin (GBP), an antiepileptic drug analog of γ-aminobutyric acid (GABA) used as adjunctive and eventually, as a monotherapeutic treatment, induces a significant improvement in patients with both focal and secondarily generalized partial seizures. In experimental epilepsy models, this drug protects against pentylenetetrazol (PTZ)-induced convulsions. In consideration of such GBP properties, the aim of this work was to investigate its efficacy to protect against sleep disturbances provoked by convulsive seizures induced by the administration of PTZ. Nine-hour (9-hour) polygraphic studies were carried out in chronically implanted male adult Wistar rats separated into 4 different groups of 6 individuals. Control recordings in each group were done after saline administration. One group received a SC Subcutaneous (SC) injection of 50 mg/kg of PTZ alone while the other three groups were injected with either 15, 30, or 60 mg/kg IP Intraperitoneal (IP) of GBP 30 min prior to PTZ (50 mg/kg SC) administration. Animals displayed the whole range of electrophysiological and behavioral manifestations of the disease during the epileptic episodes induced by PTZ administration, and the states of vigilance were significantly altered. Insomnia occurred immediately after PTZ injection preceding the appearance of the first epileptic symptoms. Thus, both slow wave sleep (SWS) and rapid eye movement sleep (REM sleep) were completely inhibited during a relatively long period of time. The disturbing effects of epilepsy on sleep decreased when animals were under GBP treatment. Improvement of sleep was dependent on the administered dose of this antiepileptic drug.

Sleep characteristics in the quail Coturnix coturnix.

UNLABELLED: As mammals, birds exhibit two sleep phases, slow wave sleep (SWS) and REM (Rapid Eye Movement) sleep characterized by presenting different electrophysiological patterns of brain activity. During SWS a high amplitude slow wave pattern in brain activity is observed. This activity is substituted by a low amplitude fast frequency pattern during REM sleep. Common quail (Coturnix coturnix) is an animal model that has provided information related to different physiological mechanisms present in man. There are reports related to its electrophysiological brain activity, however the sleep characteristics that have been described are not. The objectives of this study is describing the sleep characteristics throughout the nychthemeral cycle of the common quail and consider this bird species as an avian model to analyze the regulatory mechanisms of sleep. Experiments were carried out in implanted exemplars of C. coturnix. Under general anesthesia induced by ether inhalation, stainless steel electrodes were placed to register brain activity from the anterior and posterior areas during 24 continuous hours throughout the sleep-wake cycle. Ocular and motor activities were visually monitored. Quail showed four electrophysiologically and behaviorally different states of vigilance: wakefulness (53.28%), drowsiness (14.27%), slow wave sleep (30.47%) and REM sleep (1.98%). The animals presented 202 REM sleep episodes throughout the nychthemeral cycle. Sleep distribution was polyphasic; however sleep amount was significantly greater during the period corresponding to the night. The number of nocturnal REM sleep episodes was significantly greater than that of diurnal one. CONCLUSION: The quail C. coturnix shows a polyphasic distribution of sleep; however the amount of this state of vigilance is significantly greater during the nocturnal period.

Effect of oxcarbazepine on sleep architecture.

The most common side effects following administration of antiepileptic drugs involve alterations in sleep architecture and varying degrees of daytime sleepiness. Oxcarbazepine is a drug that is approved as monotherapy for the treatment of partial seizures and generalized tonic-clonic seizures. However, there is no information about its effects on sleep pattern organization; therefore, the objective of this work was to analyze such effects. Animals (Wistar rats) exhibited three different behavioral and electrophysiological states of vigilance: wakefulness, slow wave sleep (SWS), and rapid eye movement (REM) sleep. Oral treatment with oxcarbazepine (100 mg/kg) produced an increment in total sleep time throughout the recording period. This increment involved both SWS and REM sleep. Mean duration of the REM sleep phase was not affected. In contrast, the frequency of this sleep phase increased significantly across the 10-hour period. REM sleep latency shortened significantly. Results obtained in this work indicate that oxcarbazepine's acute effects point to hypnotic properties.

Effect of oxcarbazepine pretreatment on convulsive activity and brain damage induced by kainic acid administration in rats.

Temporal lobe epilepsy is one of the most common types of epilepsy. Progress in the understanding and treatment of this type of epilepsy would be greatly facilitated by the availability of an animal model, which reproduced the behavioral and electrographic features of this condition. In this context, kainic acid (KA, 2-carboxy-3-carboxymethyl-4-isopropenylpyrrolidine) administration causes a syndrome characterized by an acute status epilepticus and subsequent brain damage similar to that in temporal lobe epilepsy of humans. The aim of the present study was to investigate whether oxcarbazepine (10,11-dihydro-10-oxo-5 H -dibenz(b,f)azepine-5-carboxamide), an antiepileptic drug, protects against both epileptic activity and brain damage induced by KA administration. Chronically implanted adult male Wistar rats were polygraphically recorded during 10 continuous hours under 4 different conditions: a) control, b) after KA administration alone, c) after KA administration in oxcarbazepine pretreated animals and d) after the administration of oxcarbazepine alone. Animals treated with KA alone presented behavioral and electrophysiological convulsive activity as well as brain damage. Latency of seizure installation was lengthened significantly and convulsive activity was slightly reduced, however, brain damage was still present in oxcarbazepine pretreated animals. Administration of oxcarbazepine alone induced a hypnotic behavior and brain damage was also present.