RESUMO
OBJECTIVE: The epileptic baboon provides an animal model for juvenile myoclonic epilepsy (JME), demonstrating spontaneous generalized tonic-clonic seizures (GTCS) in addition to generalized myoclonic, absence and multifocal seizures. While photoconvulsive responses have been described in this model, spontaneous GTCS have not been characterized. METHODS: In this study, we characterized 46 seizures in 7 epileptic baboons (5 females, 12 ± 3 years old) by video recording. While housed in single cages, the baboons were monitored for a median of 2 (range 1-10) weeks, with high-resolution, infrared-capable camera systems. Each GTCS was evaluated for evidence of preconvulsive ictal symptoms, focal convulsive behaviors, duration of the preconvulsive and convulsive periods, postictal immobility, and recovery of an upright posture. The circadian pattern of GTCS was also for each baboon. RESULTS: More than half of GTCS occurred in sleep, beginning from an upright position in all but one tethered baboon. Focal semiological findings were noted in 19 (41%) GTCS, and these included preconvulsive focal ictal motor behaviors as well as lateralized motor activity during the convulsions. The convulsive portion lasted 47 ± 10 seconds, whereas the entire seizure lasted 54 ± 21 seconds. Postictally, the baboons remained immobile for a median latency of 40 (range 14-347) seconds, recovering an upright posture after 173 (range 71-1980) seconds. GTCS demonstrated circadian patterns in all but one baboon, with 34 (74%) all seizures occurring between 1-9 am. SIGNIFICANCE: GTCS in the baboon revealed intersubject variability, but semiology remained stereotyped in a given baboon. Similar to GTCS in people with JME, focal symptoms were also observed in epileptic baboons. The postictal recovery period, characterized by postictal immobility and myoclonus as well as time to recumbency, also varied among baboons.
RESUMO
Neuropsychiatric sequelae have been reported in 15%-45% of survivors of carbon monoxide (CO) poisoning. Hyperbaric oxygen (HBO2) therapy reduces the incidence of cognitive and neurological a dysfunction. The efficacy of providing HBO2 beyond the first one to two days after initial insult is unknown. However, some evidence exists for the benefit of this treatment. We report on treating a patient 14 months after CO injury, who responded with markedly improved neurologic status. A 27-year-old scholar was found comatose due to CO poisoning (carboxyhemoglobin = 31.7%). He received five acute HBO2 treatments. After discharge, he developed chorea, Parkinsonism, dystonia, memory loss, slowed processing speed and verbal fluency, leaving him disabled. After the patient reached a clinical plateau, HBO2 was tried again at 90 minutes at 2.4 ATA plus air breaks. Neuropsychological testing was performed at baseline and after each 20 HBO2 cycles, five of which were performed during the period from 14-22 months after CO exposure. After the first 20 treatments, Parkinsonism and dystonia improved. After 40 sessions, further improvements were seen on mental speed, verbal fluency, and fine motor movements. The outcome following 100 treatments was that the patient regained independence, including the ability to drive and to become gainfully employed. Our case calls into question the concept that HBO2 therapy has no role during the chronic phase of CO brain injury. Randomized clinical trials should be considered to evaluate the therapeutic efficacy of HBO2 in patients with neurological sequelae following CO injury.
