Sepsis associated encephalopathy (SAE) is a common but poorly understood neurological complication of sepsis. It is characterized by diffuse brain dysfunction secondary to infection elsewhere in the body without overt CNS infection. The pathophysiology of SAE is complex and multifactorial including a number of intertwined mechanisms such as vascular damage, endothelial activation, breakdown of the blood brain barrier, altered brain signaling, brain inflammation, and apoptosis. Clinical presentation of SAE may range from mild symptoms such as malaise and concentration deficits to deep coma. The evaluation of cognitive dysfunction is made difficult by the absence of any specific investigations or biomarkers and the common use of sedation in critically ill patients. SAE thus remains diagnosis of exclusion which can only be made after ruling out other causes of altered mentation in a febrile, critically ill patient by appropriate investigations. In spite of high mortality rate, management of SAE is limited to treatment of the underlying infection and symptomatic treatment for delirium and seizures. It is important to be aware of this condition because SAE may present in early stages of sepsis, even before the diagnostic criteria for sepsis can be met. This review discusses the diagnostic approach to patients with SAE along with its epidemiology, pathophysiology, clinical presentation, and differential diagnosis.
The study is suggestive of the existence of impaired supraspinal/intracortical inhibitory circuits which may account for the hyperexcitability of the motor system being prominent in the morning among drug naïve patients with JME. In this study, increased activity of cortical inhibitory networks, as evidenced by prolonged cortical silent period existed among drug naïve JME patients, but was found to be significant only in female patients. This may explain the increased seizure susceptibility in this cohort, at this time of the day and an increased manifestation of JME in females.
A 22-year-old man, with a past history of generalized tonic-clonic seizures treated with phenobarbital, presented with spinocerebellar ataxia. The electrophysiological studies revealed a demyelinating motor-sensory neuropathy. The serum vitamin E level was low. Sural nerve biopsy revealed loss of large myelinated fibers with evidence of remyelination. Vitamin E supplementation led to clinical and electrophysiological recovery of sensory conduction and evoked potentials. Motor nerve conduction, however, showed only partial recovery. Vitamin E deficiency leading to a demyelinating neuropathy, as in the present case, suggests that the full spectrum of the disease entity is not fully defined.
JME is associated with poor sleep quality and altered architecture, irrespective of treatment status. REM sleep is significantly decreased in JME patients. Epileptiform discharges are frequent in lighter NREM sleep and EDI is higher in drug naïve patients. Although AEDs disrupt the NREM sleep, their use is associated with arousal stability in lighter stages of sleep and lower EDI, in particular with valproate.
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