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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute viral and other infectious causes of encephalitis usually produce fever, headache, stiff neck and alterations in consciousness, focal neurologic signs and seizures. A large number of viral and nonviral agents can cause encephalitis. Arthropod-borne viruses peak in summer, the tick-borne infections occur in early summer, enterovirus infections in later summer and mumps in the winter and spring.
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PMID:[Viral encephalitis]. 269 65

During 1959-1987, 126 patients in Aland Islands and main Finland had serologically verified infections with the virus of tick-borne encephalitis (Kumlinge disease). The most useful test for specific virological diagnosis was haemagglutination inhibition-IgM (HI-IgM). Most cases were from Aland Islands and nearby south-western main Finland. Two of the infections were imported. There were three laboratory infections and two transfusion infections. The disease occurred mainly from July to September. Detailed hospital records of 108 of the patients could be obtained. Ninety-five per cent of the patients had headaches, 82% had lymphocytosis of the cerebrospinal fluid, and 81% had high fever. Forty-four per cent had a confirmed biphasic course of disease. Seventeen per cent were severely ill. There were no deaths. The sequels were psychic irritability and fatigue for up to 1 year. There were eight cases of paresis, two of which became permanent.
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PMID:Tick-borne viral encephalitis in Finland. The clinical features of Kumlinge disease during 1959-1987. 270 99

We observed and recorded clinical and laboratory data from 54 children with fever and a maculo-papular rash admitted to Soroka Medical Center, Beersheva, Israel suffering from serologically confirmed rickettsial spotted fever. The rash generally began on the palms and soles and extended centripetally to the torso. Other clinical findings included myalgia, headache, hepatomegaly, and splenomegaly. None had a "tache noire". A left shift in the white cells, leucopenia, thrombocytopenia, hyponatraemia and impaired liver function tests were common laboratory abnormalities. All recovered following oral doxycycline therapy. Serious sequelae such as myocarditis, encephalitis, and disseminated intravascular coagulation, as reported in Rocky Mountain spotted fever, did not occur.
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PMID:Israeli rickettsial spotted fever in children. A review of 54 cases. 288 43

A 10-year-old boy had gait and speech disturbances 17 days after the initial symptoms of a fever, headache and cough. Four days later he was admitted to a hospital with mild disturbances of gait, speech, writing, visual acuity, left facial nerve, nystagmus and consciousness. Impairments of cranial nerves (II, III and VII), pyramidal sign and cerebellar sign were noticed. EEG showed generalized slow waves. Auditory brain stem response showed prolongation of the interval between I and V waves and poor differentiation between them. Brain CT could not find any abnormalities. Brain stem encephalitis was diagnosed. Clinical signs and symptoms continued for two weeks when steroid therapy was started and it was effective to improve the disease. He was discharged from the hospital without sequelae. Herpes simplex virus (HSV) type 1 was detected from cells in CSF on admission by fluorescence antibody method. HSV antibody titers in sera changed from 1/8 to 1/64 during three months by complement fixation test. Specific IgG and IgA by enzyme linked immunosorbent assay (ELISA) was high in CSF. Specific antibody in CSF/total antibody in CSF: specific antibody in serum/total antibody in serum for IgG and IgA classes were more than 1. Reports of mild type of HSV brain stem encephalitis seemed to be rare. Our case which was followed for several months carefully would be important to discuss.
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PMID:[A mild form of brain stem encephalitis due to herpes simplex virus]. 301 73

A post-mortem examined case of herpetic brainstem encephalitis is presented. Clinically, the patient had cephalalgia followed by ataxia, drowsiness and multiple palsies of some cranial nerves, developing into death in eight days. The pathologic examination of the brain showed necrotizing encephalitis in multiple foci limited to the brainstem, more distinctly in the pons and medulla oblongata. The technique of immunoperoxidase revealed rare glial cells with intranuclear immunoreactivity for herpes antigen. Rare viral particles with the morphological characteristics of the herpesvirus were identified in the nuclei of neurons in 10% formol fixed material. This is the second reported case of herpetic brainstem encephalitis confirmed by post-mortem examination. The pathway used by the virus to reach the central nervous system and its posterior dissemination to the oral cavity, the orbitofrontal region and the temporal lobes as well as to the brainstem, after a period of latency and reactivation, are discussed.
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PMID:[Herpetic brain stem encephalitis: report of an autopsied case with immunohistochemical and electron microscopy studies]. 303 59

A retrospective clinical and pathological analysis has been performed of 24 cases of herpes simplex virus encephalitis (HSE) seen at the Institute of Neurological Sciences, Glasgow, between 1972 and 1985. All patients had been diagnosed on the basis of isolation of herpes simplex virus (HSV) from, and/or the demonstration of characteristic histological changes of acute necrotizing encephalitis (ANE) in brain biopsy and/or autopsy tissue. Clinical presentation on admission included a prodromal influenza-like illness (46%), sudden onset of headache and confusion (54%), meningism (38%), deep coma (42%), aphasia (54%) and focal neurological signs (79%). Seizures occurred in 46% of cases during the course of the illness. Of the 24 cases, 14 (58%) died and 10 (42%) survived. Intravenous acyclovir treatment was associated with the best prognosis. Cerebral biopsy of one temporal lobe was performed in 22 cases and in 19 of these a positive histological diagnosis of HSE could be made. HSV was isolated from 15 of the 19 (79%) biopsied cases in whom virus isolation was attempted. Only seven out of the 15 cases (47%) in which immunofluorescence assays for HSV antigens were performed were unequivocally positive. Herpes simplex virus was isolated in culture from all cases which were negative by immunofluorescence. Immunocytochemical analysis on tissue sections of five representative brain biopsies demonstrated the presence of HSV antigens in some astrocytes, neurons and macrophages especially within areas of inflammatory infiltration. In situ hybridization experiments with a cloned HSV DNA probe demonstrated viral RNA in astrocytes, neurons and macrophages in two human biopsies and mouse brains in areas broadly corresponding to the distribution of viral antigen labelling. The combined immunocytochemical and in situ hybridization procedure showed that many but not all of the cells containing viral RNA also contained HSV antigens, indicating a productive infection in these double-labelled cells.
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PMID:A clinico-pathological study of herpes simplex encephalitis. 320 Mar 68

The clinical features, investigative profiles and outcome of 46 patients with biopsy or autopsy-proven herpes simplex encephalitis admitted to the Institute of Neurological Sciences, Glasgow between 1962 and 1985 were analysed retrospectively. The protean presenting symptoms and signs included a history of a prodromal influenza-like illness (48 per cent), rapid onset of headache, clouding of consciousness and confusion (52 per cent), meningism (65 per cent), raised intracranial pressure (33 per cent), deep coma (35 per cent), mutism or aphasia (46 per cent), focal neurological signs (89 per cent), and seizures (61 per cent). When seizures occurred they were almost always focal. The electroencephalogram was the most useful diagnostic test being abnormal in all cases, the majority showing focal changes in one or other hemisphere. Of the neuroradiological procedures employed, computerized tomographic and isotope brain scanning most frequently demonstrated localizing abnormalities in one or both temporal and/or frontal lobes. Midline shift was seen in half the cases. The cerebrospinal fluid was abnormal in every case but was not diagnostic. Cerebral biopsy of one temporal lobe was performed in 40 cases and a positive diagnosis of acute necrotizing encephalitis was made in 37 of these. Herpes simplex virus was isolated from the brains of 29 of the 40 cases in which the procedure was attempted, but immunofluorescence assays for antigens to herpes simplex virus were only positive in 11 out of 25 cases. Serological assays showed a greater than four-fold rise in the anti-herpes simplex virus antibody titre in 13 out of 22 patients tested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A retrospective analysis of forty-six cases of herpes simplex encephalitis seen in Glasgow between 1962 and 1985. 325 5

Herpes simplex encephalitis is the most common cause of sporadic encephalitis in the western world. Patients usually have altered levels of consciousness, altered levels of mentation, fever, headache, and personality changes. These may progress to hemiparesis and seizures. Exact diagnosis must be established by brain biopsy and identification of the virus in biopsy material. There is a great need for a noninvasive test that is positive early in the disease. Without antiviral treatment the mortality rate is greater than 70%, and many survivors have serious disabilities. Both adenine arabinoside and acyclovir decrease death and morbidity, but acyclovir is the preferred drug. With acyclovir about 40% of patients will survive with normal development or minor levels of impairment but more than half of the patients will die or suffer significant impairment. It is essential to treat early; patients who are young and have not reached coma or impaired consciousness may show 65% recovery and return to normal function. Development of new antiviral drugs or other types of therapies is desirable. Herpetic skin lesions are likely to be more confusing than diagnostic because other types of encephalitis with fever often precipitate recurrent herpes that is unrelated to the encephalitis.
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PMID:Antiviral treatment of a serious herpes simplex infection: encephalitis. 333 44

Cerebral aspergillosis is one of the most common mycotic infections in the central nervous system causing different clinical features such as brain abscess, granuloma, meningitis, and encephalitis. Cerebral aspergillosis, however, may lead to a cerebral vascular accident such as intracranial hemorrhage or cerebral infarction. In this report, we present two patients with cerebral aspergillosis accompanied by intracranial hemorrhage. A total of 124 reported cases of cerebral aspergillosis are reviewed to ascertain the pathogenesis of the associated vascular lesion. The first patient was a 9-year-old girl, who developed drowsiness with a headache during the medical treatment for acute myelocytic leukemia. CT disclosed subarachnoid and intraventricular hemorrhage. The autopsy revealed that the aspergillus arteritis was the cause of repeated hemorrhage. The second patient was a 15-year-old boy with allergic purpura and renal failure, who suddenly developed a stupor with convulsive seizure. CT disclosed an intracerebral hemorrhage in the right parieto-occipital area. The patient gradually deteriorated and died in spite of the surgical removal of the hematoma. The autopsy revealed that the hemorrhage was caused by the aspergillus arteritis. Cerebral aspergillosis has two routes of infection to the central nervous system: hematogenous dissemination from the distant site (usually the lung) and direct extension from the contiguous site (usually the paranasal sinuses or orbit). The primary mechanism of neuropathology is different between these two types. Primary cerebral arteritis is most often seen in patients with the former type, whereas primary basal meningitis occurs in the latter. The incidence of clinico-pathological features is different between hematogenous dissemination type and direct extension type.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral aspergillosis as a cerebral vascular accident]. 339 19

Lyme disease typically begins with a unique skin lesion, erythema chronicum migrans (ECM) (stage 1). Patients with this lesion may also have headache, meningeal irritation, mild encephalopathy, multiple annular secondary lesions, malar or urticarial rash, generalized lymphadenopathy and splenomegaly, migratory musculoskeletal pain, hepatitis, sore throat, non-productive cough, conjunctivitis, periorbital edema, or testicular swelling. After a few weeks to months (stage 2), about 15% of patients develop frank neurologic abnormalities, including meningitis, encephalitis, cranial neuritis (including bilateral facial palsy), motor or sensory radiculoneuritis, mononeuritis multiplex, or myelitis. At this time, about 8% of patients develop cardiac involvement--AV block, acute myopericarditis, cardiomegaly, or pancarditis. Throughout this stage, many patients continue to experience migratory musculoskeletal pain in joints, tendons, bursae, muscle, or bone. Months to years after disease onset (stage 3), about 60% of patients develop frank arthritis, which may be intermittent or chronic. Recently evidence suggests that Lyme disease may also be associated with chronic neurologic or skin involvement. Thus, Lyme disease occurs in stages with different clinical manifestations at each stage, but the course of the illness in each patient is highly variable.
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PMID:Clinical manifestations of Lyme disease. 355 39


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