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Therapeutic Options to Enhance Poststroke Recovery in Aged Humans
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Aurel Popa-Wagner, Dumbrava Danut, Roxana Surugiu, Eugen Petcu, Daniela-Gabriela Glavan, Denissa-Greta Olaru, Raluca Sandu Elena
Early after MCAO in rats, several EEG abnormalities were identified including nonconvulsive seizures, periodic epileptiform discharges, and intermittent rhythmic delta activity [102]. From 7 to 14 days after MCAO, we did not find evidence of abnormalities in the background EEG, although we did not carry out high density recordings to explore changes localized to the affected hemisphere. We did find, however, a persistent alteration in the sleep cycles post MCAO, particularly those related to their circadian rhythm. This is not entirely new. Few previous studies reported various sleep alterations occurring during the first weeks following experimental MCAO in rodents [103,104]. Intriguingly, one of these studies reported altered circadian variability of sleep patterns [104] similar to postischemic impairment of other circadian rhythms reported in stroke patients [105] and experimental models [106]. The observed increase in wakefulness during the nocturnal period after MCAO did not seem to recover from 7 to 14 days after stroke. This indicated that the impairment reflected a persistent injury, rather than a transient functional perturbation. Although post MCAO sleep changes were reportedly a poor indicator of infarct size [104], it is tempting to speculate that the sleep impairment reflected impaired cognitive functioning, which becomes especially relevant during the nocturnal period when rats are more active. Nevertheless, our data suggest that H2S hypothermia did not prevent the occurrence of post MCAO circadian sleep impairment.
Clinical Neurophysiology
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
Nevertheless, some patterns, when present, are helpful in pointing towards a broad aetiological category. Triphasic waves are frequently associated with metabolic encephalopathies such as hepatic encephalopathy (Figure 5.25), uraemia, electrolyte abnormalities, anoxia and lithium intoxication. Generalized periodic complexes are seen in Creutzfeldt–Jacob disease (CJD) (Figure 5.26), subacute spongiform panencephalitis (SSPE) and severe anoxia. Bitemporal periodic lateralized epileptiform discharges (PLEDs) in the appropriated clinical context would raise the possibility of herpes simplex encephalitis (HSVE) (Figure 5.27). However, if the patient has received early treatment with acyclovir, the EEG may show less specific temporal, frontal or generalized slowing. PLEDs are not specific for aetiology, and may also be seen in association with other acute or subacute destructive lesions (including cerebral infarcts) (Figure 5.28), again emphasizing the importance of the clinical context when interpreting EEG findings. Frontal intermittent rhythmic delta activity (FIRDA) was initially described in association with deep midline lesions, raised intracranial pressure, or subcortical dysfunction, but is now recognized as being much less specific and is more often found as a non-specific finding in diffuse encephalopathies.
Status epilepticus after C-4 ingestion: using liquid chromatography to quantify toxicity
Published in Clinical Toxicology, 2019
Robert Garcia, Amir Karimian, Chase Donaldson, Kerry Preston, Shawna Scully
The patient was started on empiric antibiotic therapy. However, lumbar puncture was performed, and CSF studies were negative for evidence of infection. CT and MRI imaging revealed normal brain anatomy. Electroencephalogram (EEG) was performed 12 hours after admission and showed persistent epileptiform activity. A central sharp wave was seen every 1–2 minutes. A midazolam drip was started at a rate of 1 mg/hr. The next morning, repeat EEG showed frontal intermittent rhythmic delta activity (FIRDA) along with intermittent breakthrough central sharp waves (Figure 1). Midazolam was switched to lacosamide and levetiracetam. The propofol was titrated off over the next 24 hours, without recurrence of seizure activity. 48 hours after admission, the patient was extubated.