Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of pituitary apoplexy causing pituitary hemorrhage with extension into the third ventricle is reported. The patient was a 73-year-old, obese female admitted with sudden onset of vomiting and impaired consciousness. Neurological examination revealed that she was stuporous, with marked neck stiffness and a dilated left pupil. A plain skull X-ray showed sellar enlargement and destruction of the dorsum sellae. Computed tomography demonstrated a high-density area in the third and lateral ventricles and a round, high-density mass in the suprasellar cistern. The patient died the next day. Autopsy revealed a large tumor in the sellar and suprasellar areas. The tumor and the hematoma within it compressed the floor of the third ventricle and passed through the lamina terminalis and the hypothalamic region. Histological examination disclosed a basophilic adenoma. The pituitary hemorrhage appeared to be the result of ischemia and necrosis within the pituitary adenoma caused by its acute expansion. The extension of the hematoma into the third ventricle was attributable to the large size of the tumor and its close adhesion to the floor of third ventricle.
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PMID:[Pituitary hemorrhage extending into the third ventricle. Case report]. 248 40

The authors report a case of brain abscess following cerebral infarction. A 73-year-old man was admitted to our clinic with symptoms of right hemiparesis and total aphasia. CT scan revealed abnormal low density area in the left fronto-temporo-parietal region. Cerebral angiography demonstrated occlusion of the left middle cerebral artery at the M1 portion. On the 16th hospital day, an episode of generalized seizure with high fever appeared, and intermittent high fever persisted thereafter. Two months after admission, CT scan revealed several cystic lesions with marked ring enhancement at the site of cerebral infarction, suggesting multiple abscesses. Aspirations of left frontal and parietal abscesses were accomplished and the cultures of the pus disclosed Proteus vulgaris. Due to progressive hydrocephalus, a ventriculoperitoneal shunt was constructed one month later. Repeated CT scans showed a gradual diminution of the abscesses. It is considered that the blood-brain barrier is broken and the local immunological system against bacteria may be weakened when the brain is damaged by ischemia. Brain abscess seems to be developed in such circumstances even under the influence of transient bacteremia which originates in other parts of the body. Therefore the possibility of cerebral abscess should be suspected if patients with cerebral infarction suffer from the symptoms such as fever, neck stiffness or disturbance of consciousness.
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PMID:[Brain abscess following cerebral infarction: a case report]. 267 75

Three cases of extracranial vertebral artery dissections with upper limb peripheral motor deficit (C5-C6) are reported. Six similar cases were also found in the literature. Central neurological symptoms occurred in five of these nine cases, suggesting the diagnosis of dissection. The peripheral motor or sensorial deficit was strictly isolated in the four other cases, simulating radicular neuralgia due to discopathy or foraminal compression. In case of dissections, a precise analysis of pain is helpful to guide diagnosis; sharp, unbearable, continuous and extended neck pain without nocturnal paroxysms and posterior neck stiffness is typical. Analgesics or anti-inflammatory drugs are ineffective. Peripheral motor deficit is more common than sensory deficit. Recovery was complete in this series. In most cases, the radiculopathy appears to be due to cervical root compression in its extraforaminal course due to the dissection hematoma and rarely to radicular ischemia.
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PMID:[Cervical deficit radiculopathy in 3 cases of vertebral artery dissection]. 989 90

Delayed cerebral ischemia as a result of cerebral vasospasm is the most common cause of death and disability after aneurysmal subarachnoid hemorrhage (SAH). It leads to death or permanent neurologic deficits in over 17-40% of SAH patients. The initial and main symptom of cerebral vasospasm is diffuse headache and may be accompanied with a slight increase in discomfort from neck stiffness and fever. The clinical diagnosis of cerebral vasospasm is made when the patient experiences an altered level of consciousness or a new focal neurologic deficit. There has been a great progress in identifying the patients at risk, putative mechanisms, and possible treatment options for cerebral vasospasm. However, the problem is by no means solved, mainly due to a limited understanding of the pathologic mechanisms of this complex disease. The iatrogenic factors that can increase the risk of cerebral vasospasm include prolongation of the subarachnoid clot by antifibrinolytic drugs, hypotension, inappropriate treatment of hyponatremia, hypovolemia, hyperthermia and increased intracranial pressure. Nimodipine has been shown to improve neurologic outcome and decrease the incidence of cerebral vasospasm. Triple H therapy is a treatment designed to augment cerebral blood flow for patient with cerebral vasospasm. Hypervolemic hypertension is induced with intravenous volume expansion with crystalloid or colloid to increase cardiac output and raise blood pressure. However, small randomized trials showed no clear benefit. Recently, balloon and chemical angioplasty with superselective intra-arterial injection of vasodilators has emerged as the primary intervention for treating medically refractory ischemia from cerebral vasospasm and in many centers is being used as a first-line treatment or even prophylactically. In addition, promising new treatments for cerebral vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia; however, all still need further clinical trials. Newly recognized mediators of cerebral vasospasm after SAH include endothelium-derived mediators, vascular smooth-muscle-derived mediators, proinflammatory mediators involved in blood-brain barrier disruption, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Moreover, observations in the laboratory have, in many circumstances, matched those of reported small series. Larger, prospective, randomized trials are needed to verify several hypotheses of molecular pathophysiology and clinical treatment regimens.
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PMID:Treatment of cerebral vasospasm after subarachnoid hemorrhage--a review. 1567 31

A 32-year-old woman developed a headache, seizures, and stupor on postpartum day 8. An initial diagnosis of possible encephalitis was made considering the presence of fever, neck stiffness, and abnormal CSF findings. MRI demonstrated hyperintense signals consistent with bilateral borderzone areas. MRA showed severe proximal narrowing of anterior, middle, and posterior cerebral arteries bilaterally. The patient recovered completely over 2 weeks, and repeated MRI and MRA scans were normal. Reversible vasoconstrictions have been known to occur during puerperium, and the clinical symptoms of our patient resembled such cases. Prior reports attributed these cases of postpartum angiopathy to capillary leakage and edema resulting in leukoencephalopathy. Our case suggests reversible borderzone ischemia as an additional pathological process.
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PMID:Postpartum angiopathy associated with reversible borderzone ischemia. 1827 36