Neurosurgery
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Biography Historical Article
Frederic Gibbs and his contributions to epilepsy surgery and electroencephalography.
Frederic Gibbs' (1903-1992) long research career was devoted to the understanding and treatment of epileptic phenomena and closely associated with the development of electroencephalography (EEG). After medical school, he joined the Harvard Neurological Unit at Boston City Hospital directed by Stanley Cobb. In the early 1930s, Gibbs developed a thermoelectric blood flow probe and, with William Lennox, proved in animals and humans that a seizure increases cerebral blood flow. ⋯ Gibbs convinced Percival Bailey to collaborate on patients with refractory temporal lobe psychomotor seizures without tumors. In 1947, the first nonlesional temporal lobe excisions based on EEG localization were performed in these patients, and, by 1948, anterior temporal lobectomy had become their procedure of choice. Gibbs and Lennox received the coveted Lasker Award among other honors as pioneers in establishing the modern era of epilepsy diagnosis and treatment.
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Coil instability possibly translating into higher delayed rebleeding rates remains a concern in the endovascular management of cerebral aneurysms. ⋯ The individualized approach resulted in complete occlusion of 114 aneurysms (89.7%), with neck remnants and residual aneurysms detectable in 11 (8.7%) and 2 (1.6%) cases, respectively. Treatment morbidity was 11.9%, without significant differences between surgical (15.6%) and endovascular (9.3%) patients (P = .09). Recurrences from coil compaction were safely treated by re-embolization, whereas recurrences from aneurysmal regrowth may best be managed surgically when technically feasible.
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Cerebral aneurysms (CAs) have a high prevalence in the general population and cause lethal subarachnoid hemorrhage. We recently demonstrated that chronic inflammation is an underlying pathogenesis of CA. However, we identified the negative involvement of angiotensin receptor signaling in the pathogenesis of CA. ⋯ Angiotensin-converting enzyme is not involved in the pathogenesis of CA formation. Imidapril suppresses CA formation in an ACE-independent and MMP-9-dependent manner.
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Nitric oxide (NO) depletion and periadventitial inflammation contribute to the pathogenesis of cerebral vasospasm. L-Citrulline increases L-arginine levels, thereby raising NO synthesis. Transgenic C57Bl6 mice with a haptoglobin (Hp) 2-2 genotype develop more severe vasospasm than wild-type (Hp 1-1) mice after subarachnoid hemorrhage (SAH). ⋯ L-Citrulline is safe; increases BA patency, neurobehavioral scores, and NOS expression in Hp 2-2 mice after SAH; and is a potential agent for treatment of vasospasm after SAH.