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By the time that a patient with an acute neurologic injury is admitted to the neurocritical care unit, the primary damage has already occurred and the major focus of intervention shifts to that of preventing secondary injury. The brain accounts for only 2% of the body's mass, yet it utilizes 25% of the body's energy stores and receives 15-20% of the total cardiac output. It is exquisitely sensitive to even the briefest period of anoxia, with the latter frequently resulting in dire consequences.
Brain temperature plays a major role in modulating the effects of ischemia and anoxia. The potential life-saving effects of hypothermia have been evident ever since early people first noted that individuals who became immersed in ice-cold water and drowned were able to be revived with no apparent neurologic injury. Cold-water immersion was recognized as having life-preserving effects; however, the mechanisms by which this occurred remained largely unknown. Although early physicians such as Hippocrates understood that cold water or ice had tissue-preserving and anti-inflammatory effects, its application to preserving the brain tissue took severalcenturies of medical advancement to be realized.
Induced hypothermia was first used as a modern neurologic therapeutic tool by Dr. Temple Fay, who reported cooling 124 patients with severe head injury in the 1940s. This then led Bigelow et al. to use hypothermia as a neuroprotective agent during cardiac surgery that required cardiac arrest (CA), causing global cerebral ischemia.
Spontaneous dissection of the vertebral artery is uncommon.
We report a 49-year-old woman who presented with the rapidly progressing basilar artery syndrome who was given an intravenous dose of tissue plasminogen activator seven hours after the onset of first symptoms. Thirty minutes after the injection, a dramatic recovery of the patient's consciousness and neurological signs was noted.
To our knowledge, this is the first reported case of intravenous tissue plasminogen activator use in acute vertebral artery dissection.
Genetic factors may be important in the etiology of subarachnoid hemorrhage (SAH) and intracranial aneurysm (IA) formation. Several studies have reported the familial occurrence of SAH and IA, although in most cases asymptomatic family members were not studied with elective angiography. The examination of data from large sibships could provide important information about the frequency of IA occurrence in at-risk individuals and the mode of inheritance for familial SAH/1A.
We reviewed published case series of sibships with SAH and at least four siblings, in which at least one sibling underwent elective angiography. Data were collected on age-of-onset, clinical events, presence of hypertension, angiographic findings, and outcome. Patients were classified as “affected” if they had a SAH or if an IA was detected by elective angiography, and “unaffected” if they were asymptomatic and had a negative angiogram.
Seven case series with 52 individuals (26 men and 26 women) met our inclusion criteria. The sibships ranged from 6 to 13 members. Most of the siblings (32 of 52, 61%) were asymptomatic, 18 (35%) had a SAH, and 2 (4%) had focal symptoms but no SAH. Elective angiography of 34 siblings showed an IA in 11 (32%) and was negative in 23 (68%). The overall rate of affecteds (SAH or IA) was 56%.
Based on data from these sibships, angiography of asymptomatic at-risk siblings demonstrated an IA in almost one-third of cases. Familial SAH/IA segregated with a pattern that was consistent with an autosomal dominant trait in this selected series of sibships, although other factors could produce these findings.
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