• Vishnumurthy Shushrutha Hedna, Abhay Kumar, Bayard Miller, Sharathchandra Bidari, Arash Salardini, Michael F Waters, Maria Hella, Edward Valenstein, and Stephan Eisenschenk.
• Departments of Neurology and.
• J. Neurosurg.. 2014 Mar 1;120(3):624-7.

AbstractIntracranial hypotension (IH) has been a known entity in neurocritical care since 1938. Even though many cases are spontaneous, the incidence of intracranial hypotension in the neurocritical care setting is increasing by virtue of the increased number of neurosurgical interventions. Whether spontaneous or secondary in etiology, diagnosis of IH usually requires the presence of orthostatic symptoms, including headaches and nausea with low opening CSF pressure. However, typical clinical features in the appropriate clinical context and imaging, even with normal CSF pressure, can indicate IH. In the neurocritical care setting, challenges for accurate semiology include altered sensorium and reduced levels of responsiveness for which many etiologies may exist, including metabolic dysfunction, traumatic brain injury, IH, or nonconvulsive status epilepticus (NCSE). The authors describe 3 patients whose clinical picture and electroencephalography (EEG) findings initially suggested NCSE but who did not respond to treatment with antiepileptic drugs alone. Neuroimaging suggested IH, and subsequent treatment of IH successfully improved the patient's clinical status. To the authors' knowledge this paper is the first in the literature that reports a correlation of IH with electrographic findings similar to NCSE as cause and effect. The authors' hypothesis is that thalamocortical dysfunction causes EEG findings that appear to be similar to those in NCSE but that these conditions do not coexist. The EEG activity is not epileptogenic, and IH results in blocking network pathways producing thalamocortical dysfunction. The authors discuss the hypothesis and pathophysiology of these epileptiform changes in relation to IH.

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