Neurologist
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Case Reports
Internal carotid artery dissection heralded by an oculomotor nerve palsy: case report and literature review.
Acute oculomotor nerve (CN III) palsies are commonly attributed to microvascular disease or compressive lesions and aneurysms, but may rarely be associated with ischemic large vessel disease. We report a case of an extracranial internal carotid artery (ICA) dissection heralded by CN III palsy with review of the relevant literature. ⋯ Acute oculomotor nerve palsies with pupillary involvement warrant thorough investigation. When routine work-up fails to elucidate an etiology, extracranial carotid pathology should be considered.
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Review Case Reports
Risk of development of medication overuse headache with nonsteroidal anti-inflammatory drug therapy for migraine: a critically appraised topic.
The development of medication overuse headache (MOH) is associated with frequent use of analgesics, especially opiates, for treatment of primary headache disorders, particularly migraine. Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat migraine. ⋯ Acute NSAID therapy is associated with progression to MOH in migraineurs with a high baseline migraine frequency but may be protective in patients with low baseline headache frequency. However, a causal role for NSAIDs in progression from episodic to chronic headache has not been established.
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Brain death criteria have been based on 3 cardinal features throughout history: coma, brainstem areflexia, and apnea, and thus have undergone little change. In 1995, the American Academy of Neurology (AAN) detailed these criteria in a step-by-step fashion that included meeting prerequisites, performing the clinical examination, performing ancillary testing, and documentation. ⋯ Ultimately, their data supported the utility of the 1995 criteria and warned against the use of new technologies before proper validation. This review briefly tells the story of brain death criteria, making mention of the steps outlined by the AAN in 1995 and discussing the recent evidence released by the Quality Standards Subcommittee in the new 2010 Practice Parameter Update.
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Therapeutic hypothermia is now commonly used to improve neurologic outcomes in eligible patients after cardiac arrest. The physiologic effects of cooling and pharmacologic effects of sedatives and neuromuscular blocking agents can affect the clinical exam and neurophysiologic findings. This can lead to uncertainty in neurologic prognostication. In this article, we review data on assessing prognosis in patients treated with therapeutic hypothermia. ⋯ The American Academy of Neurology practice parameters for assessing prognosis after cardiac arrest may not be accurate for patients treated with therapeutic hypothermia. Application of these guidelines may lead to overly pessimistic prognostication and premature withdrawal of care. If uncertainty exists regarding the prognosis in a given patient after cardiac arrest, additional time should be allowed to pass, as patients may ultimately recover with good neurologic outcome.
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Case Reports
Nonconvulsive status epilepticus related to posterior reversible leukoencephalopathy syndrome induced by cetuximab.
Reversible posterior leukoencephalopathy syndrome (PRES) is a relatively uniform clinical and neuroradiologic manifestation of central nervous system toxicity. The clinical features are headache, altered mental status, and visual disturbances. PRES is often associated with arterial hypertension but it is most usually related to drug toxicity. In fact, it has been related to immunosupressants, cytotoxic, and new antineoplastic-targeted therapies such as sorafenib, sunitinib, bevacizumab, bortezomib, rituximab, and etanercept. ⋯ This case emphasizes that in any patient receiving treatment with anti-epidermal growth factor receptor agents and showing a compatible clinical syndrome, PRES should be suspected. We also review the clinical and neuroradiologic features of PRES, discuss its' pathogenesis, and highlight the importance of rapid recognition and withdrawal of the causative agent.