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 56-year-old man with rheumatoid arthritis developed emotional lability and myoclonic seizure in the left arm, followed by fever and generalized convulsion. Brain magnetic resonance imaging (MRI) revealed leptomeningeal lesions with abnormal enhancement. MRI lesions were localized predominantly in the right cerebral subarachnoid spaces. Electroencephalogram showed epileptogenic focus at the right frontal and central points. After administration of valproate sodium improved convulsion and myoclonus, single photon emission computed tomography (SPECT) using N-isopropyl-p-(123)I-iodoamphetamine was performed. Brain SPECT displayed hypoperfusion predominantly in the right cerebral hemisphere. Cerebrospinal fluid (CSF) disclosed mild pleocytosis and marked elevations of interleukin-6 levels. Repeated CSF analyses showed cytology of class I and negative results for infectious pathogens. Methylprednisolone pulse therapy (1 g for 3 days, iv) and subsequent prednisolone administration (daily 50 mg, po) ameliorated neurological symptoms dramatically. Prednisolone was tapered to 20 mg/day for 5 months. Leptomeningeal MRI lesions were attenuated gradually followed by restoration of cerebral hypoperfusion on SPECT. He was diagnosed as rheumatoid leptomeningitis (RLM). Although clinical features of RLM exhibited variable deficits of the central nervous system (CNS), MRI failed to detect the corresponding CNS lesions. We first highlighted neuroradiological changes of cerebral hypoperfusion and leptomeningeal lesions in RLM. These neuroimages of our patient supported that leptomeningeal inflammation and the adjacent cerebrocortical ischemia could cause encephalitis-like symptoms in RLM patients.
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PMID:Rheumatoid leptomeningitis: radiological alteration of cerebral hypoperfusion and subarachnoid lesions. 2082 56

A retrospective study to investigate the clinical epidemiological characteristics of vertigo was carried out on 187 patients with vertigo. A clinical history for each patient was recorded precisely about the attack, frequency, and development of vertigo, its duration, intensity, and the accompanied symptoms including the risk factors for cerebrovascular disease, etc. All the patients were subjected to physical examination with special attention to neurologic systems and Dix-Hallpike maneuver, computed tomography/computed tomography-angiography (CT/CTA) and MRI scan were performed when necessary. Majority of the patients in this study suffered with posterior circulation ischemia (59.89%) and benign paroxysmal positional vertigo (16.04%). Other ailments that affected these patients included migraine, Meniere's disease (1.6%), sudden hearing loss (1.07%), vestibular neuronitis, multiple sclerosis, acute viral encephalitis, meningioma, neurosis, posttraumatic vertigo, acute myocardial infarction (0.53%), and neurosis (14.97%). It appeared that in comparison to younger patients the elderly population is likely to be more susceptible to vertigo. Vertigo attacks patients with various diseases, which pre-dispose the patients to this disease. Presentation of vertigo can be clinically diagnosed in most cases of patients suffering from posterior circulation ischemia.
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PMID:A clinical epidemiological study in 187 patients with vertigo. 2097 71

Acute confusional migraine (ACM) is a rare migraine variant, affecting children and adolescents, as well as adults. Between 0.45 and 7.8% of children with migraine present with ACM, but the disorder may well be underdiagnosed. ACM is an exclusion diagnosis and some dangerous causes of confusion (e.g., epilepsy, ischemia, hemorrhagia, neoplasm, intoxication and encephalitis) should be ruled out. The confusional state often manifests with a wide diversity of cortical dysfunctions, such as speech difficulties, increased alertness, agitation and amnesia. Exact history taking, clinical examination, and laboratory, radiological and electroencephalographical findings lead the practitioner towards the diagnosis. Approximately half of the cases may be triggered by mild head trauma. Transient global amnesia is an important differential diagnosis, possibly caused by similar pathophysiological mechanisms. The exact pathomechanism remains unclear, with the common hypothesis comprising of the confusional state as a complex aura phenomenon, in which the cortical spreading depression wave reaches not only the occipital, but also the temporal, parietal and frontal cortex, as well as the brainstem and the hippocampi, leading to transient hypoperfusion and dysfunction of these brain areas.
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PMID:Acute confusional migraine: our knowledge to date. 2236 29

Septic encephalopathy describes a diffuse cerebral dysfunction in association with sepsis. It is the most common cause of altered brain function in the intensive care unit setting but other causes have to be excluded. Alterations in the level of consciousness occur early and are common. Epileptic seizures may occur but asymmetric neurological findings are not typical. The pathophysiology of septic encephalopathy is diverse and not fully elucidated; however, perfusion abnormalities play an important role. Neuropathological findings are diffuse, widespread and often show features of ischemia and non-bacterial inflammation. Diagnostic procedures should exclude frequent differential diagnoses, such as stroke, meningitis or encephalitis. Cerebral computed tomography (CT) is usually unremarkable but magnetic resonance imaging (MRI) may reveal vasogenic edema in terms of a posterior reversible encephalopathy syndrome. Septic encephalopathy requires an adequate therapy of the sepsis syndrome but a specific therapy is not yet available.
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PMID:[Septic encephalopathy]. 2276 21

Hemolytic uremic syndrome is a multisystem disorder that is caused by infection with Shiga-toxin-producing Escherichia coli. HUS affects mainly children and is rare among adults. This retrospective case series analyzes clinical signs and MR imaging findings of 11 adult patients with HUS associated nervous system involvement during the epidemic EHEC outbreak in northern Europe with its epicenter in Hamburg in May 2011. The most prevalent imaging finding was symmetric pointy vasogenic edema of the brain stem in the acute and subacute phases of the disease (n = 5). One patient exhibited additional symmetric mesiotemporal signal changes mimicking limbic encephalitis. Two patients developed subcortical patchy lesions, and 4 subjects did not present with any signal changes. Remarkably, territorial ischemia, signs of hemorrhage, or blood-brain barrier disruption have not been detected. While brain stem lesions were transient and normalized with clinical recovery, supratentorial lesions did not resolve completely at 2-month follow-up examination.
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PMID:Central nervous system involvement in adults with epidemic hemolytic uremic syndrome. 2330 13

A 72-year-old man with varicella zoster virus (VZV) encephalitis complicated by an ischemic stroke in the right internal capsule, possibly due to secondary small-vessel vasculopathy, is described in this case report. The focus of this article is on the electroencephalogram (EEG) description of varicella zoster encephalitis and secondary vasculopathy because EEG descriptions are scarce in the literature and detailed descriptions are lacking. In this patient's EEG, right temporal theta waves were found in combination with a mild slowing of the background rhythm to 7.5 to 8 Hz in the acute stage with an amplitude asymmetry (right temporal lobe amplitudes were significantly higher compared with the left side). The theta waves were thought to originate from the ischemic lacunar stroke, the slowing of the background rhythm from early encephalitis, and the amplitude asymmetry was presumed to be of physiologic origin. A follow-up EEG 6 days after initiation of treatment with acyclovir showed a normal symmetrical background rhythm of 8 to 8.5 Hz, wherein the theta waves were significantly reduced in abundance, and the amplitude asymmetry was unchanged. In conclusion, the EEG may localize focal abnormalities possibly due to cortical or lacunar ischemia, which could be explained by early small and/or large vessel vasculopathy in patients with suspected VZV encephalitis.
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PMID:Ischemic Stroke as a Complication of Varicella Zoster Encephalitis: A Case Report With Detailed EEG Discussion. 2429 59

Sphingosine-1-phosphate is a lipid mediator that has been implicated in protection from acute kidney injury (AKI) by activation of the sphingosine-1-phosphate 1 receptor (S1P1R). The research team of H. Thomas Lee demonstrates that mice with induced deletion of S1P1R on endothelial cells experience increased ischemia-induced AKI. These findings have important translational implications. Indeed, S1P1R agonists have been used for the treatment of patients suffering from autoimmune encephalitis. Endothelial S1P1R signaling could be targeted for AKI prevention in surgical patients.
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PMID:Sphingosine-1-phosphate receptor signaling during acute kidney injury: the tissue is the issue. 2402 42

Encephalitis continues to be one of the most dreaded diagnoses because a high rate of morbidity and mortality are accepted even before starting the treatment. Most encephalitis cases occur in rural areas due to poor environmental sanitation, high-vector density, shortage of protected water supplies and lack of health education. Vaccination, environmental sanitation, vector control, health education and attention to prompt diagnosis and treatment in rural hospitals are the four essential pillars for reducing case fatality rate (CFR) of encephalitis. Frequently, virulence of the virus, immunological state of the host, unavailability of antiviral drugs and lack of enough tertiary care hospitals (TCH) are not responsible for the high CFR. Basic supportive care is not being practiced meticulously in Primary and Secondary Care Hospitals (PSCH), and their services are not being utilized fully. Main causes of high mortality and morbidity rates are hypoxia and ischemia of brain and other organs precipitated by preventable, controllable or treatable complications due to lack of basic medical and nursing care during transport to the TCH. Undiagnosed Rickettsial infections are suspected to be partly responsible for the high CFR in some areas. Improving rural hospitals and their ambulance services are the most economical way to reduce CFR. "Treatment facilities must be made available at places where cases occur." The best way to reduce CFR of encephalitis in developing and underdeveloped countries is to increase and improve PSCH and sensitize politicians, administrators, medical/nursing professionals and more importantly to impress and convince the public to utilize them.
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PMID:Who's failure? encephalitis kills! 2511 19

The pathogenesis of disease progression in drug-refractory epilepsy is poorly understood. We report the case of a young woman with a four-year history of epilepsy that progressed rapidly as evidenced by the development of progressive focal cortical atrophy. She underwent biopsy that showed perinatal ischemia and a prominent inflammatory response, including T-cell infiltration and microglial activation. There was no consensus reached on the final diagnosis although the hypothesis of dual pathology (adult variant of Rasmussen's encephalitis and perinatal stroke) was considered. The possible role of inflammation in the progression of epilepsy caused by a "static" lesion (perinatal stroke) is discussed.
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PMID:Young woman with a four-year history of epilepsy and progressive focal cortical atrophy - What is the diagnosis? 2566 79

The CA1 (cornu ammonis) region of hippocampus is selectively vulnerable to a variety of metabolic and cytotoxic insults, which is mirrored in a delayed neuronal death of CA1 neurons. The basis and mechanisms of this regional susceptibility of CA1 neurons are poorly understood, and the correlates in human diseases affecting the hippocampus are not clear. Adopting a translational approach, the lesion evolution, temporal course, pattern of diffusion changes, and damage in hippocampal CA1 in acute neurologic disorders were studied using high-resolution magnetic resonance imaging. In patients with hippocampal ischemia (n=50), limbic encephalitis (n=30), after status epilepticus (n=17), and transient global amnesia (n=53), the CA1 region was selectively affected compared with other CA regions of the hippocampus. CA1 neurons exhibited a maximum decrease of apparent diffusion coefficient (ADC) 48 to 72 hours after the insult, irrespective of the nature of the insult. Hypoxic-ischemic insults led to a significant lower ADC suggesting that the ischemic insult results in a stronger impairment of cellular metabolism. The evolution of diffusion changes show that CA1 diffusion lesions mirror the delayed time course of the pathophysiologic cascade typically observed in animal models. Studying the imaging correlates of hippocampal damage in humans provides valuable insight into the pathophysiology and neurobiology of the hippocampus.
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PMID:Selective neuronal vulnerability of human hippocampal CA1 neurons: lesion evolution, temporal course, and pattern of hippocampal damage in diffusion-weighted MR imaging. 2608 14


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