Electroencephalographic monitoring during hypothermia after pediatric cardiac arrest.

BACKGROUND: Hypoxic ischemic brain injury secondary to pediatric cardiac arrest (CA) may result in acute symptomatic seizures. A high proportion of seizures may be nonconvulsive, so accurate diagnosis requires continuous EEG monitoring. We aimed to determine the safety and feasibility of long-term EEG monitoring, to describe electroencephalographic background and seizure characteristics, and to identify background features predictive of seizures in children undergoing therapeutic hypothermia (TH) after CA. METHODS: Nineteen children underwent TH after CA. Continuous EEG monitoring was performed during hypothermia (24 hours), rewarming (12-24 hours), and then an additional 24 hours of normothermia. The tolerability of these prolonged studies and the EEG background classification and seizure characteristics were described in a standardized manner. RESULTS: No complications of EEG monitoring were reported or observed. Electrographic seizures occurred in 47% (9/19), and 32% (6/19) developed status epilepticus. Seizures were nonconvulsive in 67% (6/9) and electrographically generalized in 78% (7/9). Seizures commenced during the late hypothermic or rewarming periods (8/9). Factors predictive of electrographic seizures were burst suppression or excessively discontinuous EEG background patterns, interictal epileptiform discharges, or an absence of the expected pharmacologically induced beta activity. Background features evolved over time. Patients with slowing and attenuation tended to improve, whereas those with burst suppression tended to worsen. CONCLUSIONS: EEG monitoring in children undergoing therapeutic hypothermia after cardiac arrest is safe and feasible. Electrographic seizures and status epilepticus are common in this setting but are often not detectable by clinical observation alone. The EEG background often evolves over time, with milder abnormalities improving and more severe abnormalities worsening.

Distribution of partial seizures during the sleep--wake cycle: differences by seizure onset site.

OBJECTIVE: To evaluate the effects of sleep on partial seizures arising from various brain regions. METHODS: The authors prospectively studied 133 patients with localization-related epilepsy undergoing video-EEG monitoring over a 2-year period. Seizure type, site of onset, sleep/wake state at onset, duration, and epilepsy syndrome diagnosis were recorded. Periorbital, chin EMG, and scalp/sphenoidal electrodes were used. A subset of 34 patients underwent all-night polysomnography with scoring of sleep stages. RESULTS: The authors analyzed 613 seizures in 133 patients. Forty-three percent (264 of 613) of all partial seizures began during sleep. Sleep seizures began during stages 1 (23%) and 2 (68%) but were rare in slow-wave sleep; no seizures occurred during REM sleep. Temporal lobe complex partial seizures were more likely to secondarily generalize during sleep (31%) than during wakefulness (15%), but frontal lobe seizures were less likely to secondarily generalize during sleep (10% versus 26%; p < 0.005). CONCLUSIONS: Partial-onset seizures occur frequently during NREM sleep, especially stage 2 sleep. Frontal lobe seizures are most likely to occur during sleep. Patients with temporal lobe seizures have intermediate sleep seizure rates, and patients with seizures arising from the occipital or parietal lobes have rare sleep-onset seizures. Sleep, particularly stage 2 sleep, promotes secondary generalization of temporal and occipitoparietal, but not frontal, seizures. These findings suggest that the hypersynchrony of sleep facilitates both initiation and propagation of partial seizures, and that effects of sleep depend in part on the location of the epileptic focus.

Type 1 protease resistant prion protein and valine homozygosity at codon 129 of PRNP identify a subtype of sporadic Creutzfeldt-Jakob disease.

A man was studied with sporadic Creutzfeldt-Jakob disease (sCJD) who had serial cortical syndromes evolving over 15 months without significant ataxia, prominent myoclonus, or periodic complexes on EEG examinations. This clinical phenotype correlated with a predominantly cortical and striatal distribution of lesions and accumulation of protease resistant prion protein with relative sparing of the brainstem or cerebellum. No amyloid plaques were seen and prion protein (PrP) immunohistochemistry only demonstrated very faint granular deposits in the cerebral cortex. Molecular analysis showed homozygosity for valine at codon 129 in the prion protein gene (PRNP) and protease resistant prion protein type 1 deposition. The comparison of molecular and clinicopathological features of the present case with those previously reported in sCJD, indicates that valine homozygosity at codon 129 and type 1 protease resistant prion protein are associated with a distinct phenotypic variant of sCJD. The data also support the view that the PRNP codon 129 polymorphism and the physicochemical properties of the protease resistant prion protein are major determinants of phenotypic variability in sCJD.