Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Herpes simplex encephalitis (HSE) is commonly treated empirically with acyclovir without confirmatory brain biopsy. Three consecutive adults with molecularly verified mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome presented with, and were treated for, apparent HSE. MELAS syndrome in adults may present as an atypical, recurrent form of HSE and should be added to the list of neurologic diseases that can mimic HSE.
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PMID:MELAS syndrome masquerading as herpes simplex encephalitis. 825 41

There is paucity of data evaluating intracranial pressure (ICP) rise and its management in acute viral encephalitis (AVE). Noteworthy is the current prevalence of unselective and broad utilization of ICP lowering therapies in clinical practice. Trends in current management of ICP in AVE emanate from data extrapolated from results of studies done on cerebral malaria, bacterial meningitis, stroke, and brain trauma patients. In this article we review (1) clinical correlates of raised ICP, (2) pathology, (3) imaging data, (4) monitoring, and, (5) treatment, of raised ICP in AVE. ICP monitoring is a useful adjunct to management of raised ICP in adults, becoming especially important in Herpes encephalitis and encephalitis with status epilepticus. In children it substantially influences clinical management and continuous monitoring of mean blood pressure (MBP) and ICP can aid in early diagnosis and treatment when cerebral perfusion pressure (CPP) falls below critical levels. Current evidence suggests that the pathomechanisms that contribute to the development of raised intracranial pressure vary in viral encephalitides of different etiology, and different forms of cerebral edema result at different times in the course of the illness, thus creating a need for studies to investigate the usefulness of various edema-specific ICP lowering modalities in AVE.
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PMID:Raised intracranial pressure in acute viral encephalitis. 1937 1

Herpes simplex encephalitis (HSE) is the most frequent cause of sporadic fatal encephalitis in the Western world. Definitive diagnosis by viral PCR of cerebrospinal fluid (CSF) and treatment with aciclovir have improved the prognosis significantly. Nevertheless, the condition is rare and presents with non-specific symptoms that can easily be mistaken for systemic infection or non-infective encephalopathy. We report a case of HSE which was not recognised by four separate doctors, leading to substantial delay in diagnosis and treatment. Our patient presented with fever, headaches, altered behaviour and generalised bradykinesia. This was initially diagnosed as otitis interna (labyrinthitis) and, subsequently, an ischaemic stroke. There was a delay of 10 days in the initiation of aciclovir from symptom onset. MRI and CSF PCR confirmed herpes simplex virus type-1 (HSV-1) infection. The patient improved on aciclovir, but is disabled with word-finding difficulties and cognitive slowing.
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PMID:Diagnostic delay in a case of herpes simplex encephalitis. 2168 59

Herpes simplex encephalitis (HSE) still remains a serious illness with high morbidity and mortality. The characteristic presentation of HSE usually consists of fever, headache, and altered mental function. We present three patients with atypical features of HSE. First, a 48-year-old man with symptomatic posttraumatic epilepsy, who developed a gastrointestinal infection, seizures, and fever. After significant clinical improvement, the patient had fever again and developed a status epilepticus, which led to the diagnosis of HSE. Second, an 84-year-old woman with hyperactive delirium after levofloxacin intake. Cranial computed tomography (CCT) revealed hypodense temporal changes, prompting lumbar puncture and diagnosis of HSE. Third, a 51-year-old diabetic woman presented with fever and acute confusion. As CCT and cell count of cerebrospinal fluid (CSF) were normal, infection and hyperglycemia as initial diagnoses were postulated. Due to aphasic symptoms, the differential diagnosis of a stroke was taken into account. Thus a second lumbar puncture led to the correct diagnosis of HSE. These atypical presentations need a high grade of suspicion and a high willingness to reconsider the initial working diagnosis, in order to prevent a diagnostic delay.
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PMID:Pitfalls associated with the diagnosis of herpes simplex encephalitis. 2391 95

A 44-year-old right-handed Caucasian male was initialy diagnosed in 2007 with dermatomyositis (DM) and in 2009 with systemic lupus erythematosus (SLE) (overlap syndrome). He was treated with Methylprednisolone and Hydroxychloroquine. He interrupted the treatment in the last three years. The patient presented with fever (39.8 degrees C), left zoster ophthalmicus, headache and psychomotor agitation. The cerebral CT scan showed left hemispheric hypodense lesions. Herpetic encephalitis was suspected. The patient was referred to the Institute of Infectious Diseases. The patient's neurological status worsened, he presented spastic tetraparesis and aphasia. DW-MRI, ADC, DS and AngioMRI were done, the patient proved to have an ischemic stroke due to acute thrombosis of the left internal carotid artery and multiple watershed infarctions. An infectious pathology, including HSV-1, was excluded by PLEX ID performed from CSF. Acyclovir, anti vitamin K, steroidal intravenous pulse therapy was started. The patient was referred after two weeks to the Department of Neurology. Mild inflammatory syndrome, tests for anti-double stain DNA (dsDNA), anti-Sm, anti-SSA, IgM and IgG anti-cardiolipin antibodies and lupus anticoagulant were positive. He was currently treated with Methylprednisolone (48 mg/d), anti vitamin K, statin, symptomatics. The outcome was favorable, with good laboratory response. Overlap syndrome may be associated with a significant increase in the risk of stroke. Our case presented without clinically susceptible symptoms of stroke but found to have stroke after neurological assessment associated with overlap syndrome (DM and SLE).
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PMID:Ischemic strokes in a young patient with dermatomyositis, systemic lupus erythematosus and secondary antiphospholipid syndrome mimicking herpetic encephalitis. 2550 61

Herpes simplex encephalitis is an acute/subacute illness that causes both general and focal signs of cerebral dysfunction with fever, headache, and confusion as cardinal features. Recurrent herpes simplex meningitis, also known as Mollaret's meningitis, is another manifestation of central nervous system herpetic infection with recurrent episodes of fever, headache, and nuchal rigidity associated with cerebrospinal fluid (CSF) evidence of active herpes simplex infection. Bell's palsy is yet another manifestation of a herpes virus infection in at least some reported cases documented by CSF analysis. We report a case of a 70-year-old male who presented with acute transcortical motor aphasia initiating a stroke work-up that was negative. Physical examination revealed genital vesicles, and the CSF was consistent with active herpes simplex infection.
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PMID:Recurrent Transcortical Motor Aphasia-Another CNS Infectious Syndrome Associated with Herpes Virus Infection. 2695 55

The central nervous system can respond to threat via the induction of an inflammatory response. Under normal circumstances this response is tightly controlled, however uncontrolled neuroinflammation is a hallmark of many neurological disorders. MicroRNAs are small non-coding RNA molecules that are important for regulating many cellular processes. The ability of microRNAs to modulate inflammatory signaling is an area of ongoing research, which has gained much attention in recent years. MicroRNAs may either promote or restrict inflammatory signaling, and either exacerbate or ameliorate the pathological consequences of excessive neuroinflammation. The aim of this review is to summarize the mode of regulation for several important and well-studied microRNAs in the context of neuroinflammation, including miR-155, miR-146a, miR-124, miR-21 and let-7. Furthermore, the pathological consequences of miRNA deregulation during disorders that feature neuroinflammation are discussed, including Multiple Sclerosis, Alzheimer's disease, Parkinson's disease, Prion diseases, Japanese encephalitis, Herpes encephalitis, ischemic stroke and traumatic brain injury. There has also been considerable interest in the use of altered microRNA signatures as biomarkers for these disorders. The ability to modulate microRNA expression may even serve as the basis for future therapeutic strategies to help treat pathological neuroinflammation.
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PMID:MicroRNAs in Neuroinflammation: Implications in Disease Pathogenesis, Biomarker Discovery and Therapeutic Applications. 3102 30