Neurocritical care
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Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) is a devastating complication, yet despite multiple lines of investigation an effective treatment remains lacking. Cytokine-mediated inflammation has been implicated as a causative factor in the development of posthemorrhagic vasospasm. In previous experiments using the rat femoral artery model of vasospasm, we demonstrated that elevated levels of the proinflammatory cytokine interleukin (IL)-6 are present after hemorrhage and that a polyclonal antibody against IL-6 is capable of attenuating experimental vasospasm. ⋯ These findings support the conclusion that inflammatory cytokines, in particular IL-6, play an important role in development of vasospasm in the rat femoral artery model. Furthermore, these results suggest that the inhibition of inflammatory cytokines may be an appropriate strategy for the treatment of vasospasm after SAH.
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Recent advances in continuous electroencephalogram (EEG) monitoring with digital EEG acquisition, storage, and quantitative analysis allow uninterrupted assessment of cerebral cortical activity in critically ill neurological-neurosurgical patients. Early recognition of worsening brain function can prove of vital importance as one can initiate measures aimed to prevent further brain damage. Although continuous EEG monitoring provides adequate spatial and temporal resolution and is able to continuously assess brain function in these critically ill patients, it requires a trained electroencephalographer to interpret the massive amounts of data generated. ⋯ This permits real-time viewing of several hours of EEG on a single page. Examples are presented from three patients, two with recurrent seizures and one with diagnosis of subarachnoid hemorrhage. These patients illustrate the ability of this novel method to detect important real-time physiological changes in brain function that could enable early interventions aimed to prevent irreversible brain damage.
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Case Reports
Delayed emergence from anesthesia associated with absent brainstem reflexes following suboccipital craniotomy.
One of the most feared complications after intracranial surgery is development of acute intracranial pathology, which may result in hypoperfusion and brain injury. Thus, early neurological assessment, performed in the operating room immediately after emergence from anesthesia, is a practice that may contribute to timely diagnosis of neurosurgical complications. Failure to awake after general anesthesia precludes conductance of neurological assessment. ⋯ Approximately 60 minutes after termination of surgery, the patient suddenly woke up. After the fact, we discovered that the neurosurgeon performed a generous field block with bupivacaine along the neck incision line. We presume that our patient's failure to awaken was caused by paralysis of brain-stem caused by migration of bupivacaine from the site of the injection.
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Levetiracetam is neuroprotective in murine models of closed head injury and subarachnoid hemorrhage.
Prophylactic treatment with antiepileptic drugs is common practice following subarachnoid hemorrhage (SAH) and traumatic brain injury. However, commonly used antiepileptic drugs have multiple drug interactions, require frequent monitoring of serum levels, and are associated with adverse effects that may prompt discontinuation. In the current study, we test the hypothesis that levetiracetam, an anticonvulsant with favorable interaction and adverse event profiles, is neuroprotective in clinically relevant models of SAH and closed head injury (CHI). ⋯ Levetiracetam is neuroprotective in clinically relevant animal models of SAH and CHI. Levetiracetam may be a therapeutic alternative to phenytoin following acute brain injury in the clinical setting when seizure prophylaxis is indicated.