The incidence of post-operative seizures in patients with CSDH evacuated via burr holes was low. Prophylactic AEDs should not be routinely administered if no other risk factor for seizure exists. Demographic and clinical factors did not appear to influence post-operative seizures.
Intradural extramedullary spinal cavernous malformations (CMs) remain the least common variant of these lesions and can originate from the inner surface of the dura mater, the pial surface of the spinal cord, and the blood vessels in the spinal nerves. Root-based-only extramedullary CMs are very rare in the thoracic region with only four cases reported. We present a case of 56-year-old male with 1-year progression of lower extremities weakness. Magnetic resonance imaging demonstrated a hyperintense lesion in the upper thoracic region. Surgical exploration revealed a CM with origin in the second thoracic nerve root with gross total resection. Histopathological examination confirmed a CM. The patient had complete recovery of neurological function at 3 months interval. Intradural extramedullary CM is extremely rare entity that must be considered in the differential diagnosis of intradural extramedullary lesions. Surgical resection is the treatment of choice to prevent further neurological damage.
Background:Nimodipine is a calcium channel blocker indicated for the management of patients with aneurysmal subarachnoid hemorrhage (SAH). Oral nimodipine has rarely been implicated in the development of acute colonic pseudo-obstruction in patients treated for SAH. Nimodipine acts by inhibiting the transmembrane influx of calcium ions essential for the excitation-contraction coupling process of smooth muscle cells. We thought that its mechanism of action could predispose patients to develop acute colonic pseudo-obstruction (Ogilvie syndrome). The purpose of this study was to revise the existing literature concerning the association between acute colonic pseudo-obstruction and nimodipine use in patients with SAH.Methods:Two patients with aneurysmal SAH who received oral nimodipine and developed Ogilvie syndrome were discussed. All previously published cases of aneurysmal SAH associated with acute colonic pseudo-obstruction were reviewed. Conclusion:This report linking the oral use of nimodipine with Ogilvie syndrome may further support the association of this disease with nimodipine use during the treatment of patients with aneurysmal SAH.
Nimodipine is a calcium channel blocker used for the management of patients with aneurysmal subarachnoid hemorrhage. Oral nimodipine has been rarely implicated in the development of acute colonic pseudo-obstruction (Ogilvie syndrome) in patients treated for aneurysmal subarachnoid hemorrhage. Nimodipine inhibits the transmembrane influx of calcium ions which are essential for the excitationcontraction coupling process of smooth muscle cells. We thought this mechanism of action could predispose patients to develop Ogilvie syndrome. This report aimed to examine the existing literature concerning the potential association between Ogilvie syndrome and nimodipine in patients with aneurysmal subarachnoid hemorrhage. All published cases of aneurysmal subarachnoid hemorrhage associated with Ogilvie syndrome were reviewed. We presented two female patients with aneurysmal subarachnoid hemorrhage produced after a ruptured anterior communicating artery aneurysm who received oral nimodipine and developed Ogilvie syndrome. The patients developed Ogilvie syndrome four to six days after receiving oral nimodipine. These two cases may further support the potential association of Ogilvie syndrome with the use of oral nimodipine during the treatment of patients with aneurysmal subarachnoid hemorrhage.
Spontaneous cerebral dissections in children are rare and can be associated with the formation of pseudoaneurysms. The management of these pseudoaneurysms is controversial as they can be treated either by surgery or endovascular techniques. On rare occasions, they may spontaneously thrombose. We present a 12-year-old male without a history of trauma who developed an intracerebral hematoma secondary to a ruptured pseudoaneurysm of the middle cerebral artery that showed a rapid spontaneous complete thrombosis. Five days after his initial diagnostic cerebral digital subtraction angiogram, a follow-up study showed no evidence of the previously observed pseudoaneurysm. Two months later, a computed tomographic angiography of the brain showed no evidence of the pseudoaneurysm. Thrombosed pseudoaneurysms should be closely followed by neuroimaging studies as they may subsequently recanalize.
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