Current neurology and neuroscience reports
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Brain injury is a dynamic process marked by an initial damaging insult followed by a cascade of physical, electrical, and metabolic changes capable of resulting in further patient disability. These subclinical changes should be detected at a time when therapeutic intervention is most efficacious and preemptive. ⋯ Intracranial pressure, continuous electroencephalography, brain tissue oxygen, cerebral microdialysis, cerebral blood flow, and jugular oximetry monitoring have been utilized to direct treatment of the critical ill neurologic and neurosurgical patient. Optimization of monitoring technique and protocol is an ongoing effort of intensivists in the field of neurocritical care.
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Sodium and fluid management in the brain injured patient directly impacts cerebral edema and cerebral perfusion pressure. Sodium is a major determinant of neuronal size and therefore hyponatremia is aggressively avoided, as hypoosmolar states result in cerebral edema. ⋯ Knowledge of normal homeostatic and brain regulatory volume mechanisms is necessary to avoid inducing further neuronal or systemic injury while trying to correct sodium and fluid disorders in brain injured patients. Osmotherapy is a common part of managing cerebral edema in neurocritical care units, but more studies are needed to establish practice guidelines.
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In the past 15 years, the increased availability and use of continuous electroencephalography (cEEG) in critically ill patients has substantially changed our understanding of the injured brain. We have become increasingly aware that electrographic seizures in this population may have only subtle or no clinical signs and that cEEG greatly increases the likelihood of detecting these seizures. This review highlights the rationale behind using cEEG rather than routine EEG for detection of nonconvulsive seizures and nonconvulsive status epilepticus in critically ill patients and defines which patients are at greatest risk. It also describes other applications of cEEG in the intensive care unit and how it may play an important role in monitoring brain function.
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Curr Neurol Neurosci Rep · Jun 2012
ReviewPapilledema: are we any nearer to a consensus on pathogenesis and treatment?
Papilledema is a term generally reserved (at least in the English language use of the term) by neuro-ophthalmologists for optic disc edema due to increased intracranial pressure. The etiology for the intracranial hypertension may be known (e.g., brain tumor, meningitis, cerebral venous sinus thrombosis) or may be idiopathic (idiopathic intracranial hypertension [IIH]). ⋯ The current initial management of papilledema in IIH includes weight loss and medical therapy (e.g., acetazolamide or furosemide). Patients who fail, are intolerant to, or noncompliant with maximum tolerated medical therapy might require optic nerve sheath fenestration or cerebrospinal fluid diversion (i.e., shunting) procedures.
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Curr Neurol Neurosci Rep · Apr 2012
Case Reports Meta AnalysisREM sleep behavior disorder and REM sleep without atonia as an early manifestation of degenerative neurological disease.
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by repeated episodes of dream enactment behavior and REM sleep without atonia (RSWA) during polysomnography recording. RSWA is characterized by increased phasic or tonic muscle activity seen on polysomnographic electromyogram channels. RSWA is a requisite diagnostic feature of RBD, but may also be seen in patients without clinical symptoms or signs of dream enactment as an incidental finding in neurologically normal individuals, especially in patients receiving antidepressant therapy. ⋯ Patients with idiopathic RBD often later develop other neurological features including parkinsonism, orthostatic hypotension, anosmia, or cognitive impairment. RSWA without clinical symptoms as well as clinically overt RBD also often occurs concomitantly with the α-synucleinopathy family of neurodegenerative disorders, which includes idiopathic Parkinson disease, Lewy body dementia, and multiple system atrophy. This review article considers the epidemiology of RBD, clinical and polysomnographic diagnostic standards for both RBD and RSWA, previously reported associations of RSWA and RBD with neurodegenerative disorders and other potential causes, the pathophysiology of which brain structures and networks mediate dysregulation of REM sleep muscle atonia, and considerations for the effective and safe management of RBD.