Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a 35-year-old male patient with Reye's syndrome, who showed temporarily lesions of claustrum, striatum, hippocampus and amygdala on CT, MRI and PET scan. He was previously healthy and affected upper respiratory infection. After taking 4 tablets of aspirin (335 mg x 4), he developed severe headache and status epileptics. The cerebrospinal fluid showed normal cell count and protein. The serum GOT and GPT elevated to 499 IU/l and 221 IU/l respectively. The parainfluenza virus type I titer was 32 times on admission and increased up to 128 times two weeks later. In spite of the anticonvulsant, status epileptics lasted for about one month and he needed mechanical ventilation. On 13-18 days of illness, abnormal lesions appeared in bilateral claustrum and striatum on CT and MRI. On 49 days of illness, abnormal lesions appeared in bilateral hippocampus and amygdala. All these lesions changed into normal on MRI on 111 days of illness. The 18F-FDG PET study on 80 days of illness revealed high uptake on striatum, hippocampus and amygdala bilaterally and changed into normal on 130 days of illness. He has improved markedly but showed long-standing abnormal signs of limbic dementia. We suggested this patient could be suffered from post infectious encephalitis in limbic system after Reye's syndrome.
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PMID:[An adult patient of Reye's syndrome--the possible background mechanism of lesions in claustrum, striatum and limbic system and limbic dementia]. 1061 54

Japanese encephalitis (JE) is an infectious encephalitis prevalent in Asia. It usually presents with fever, headache, convulsions and extrapyramidal symptoms. Limbic system involvement and hypothermia though common in autoimmune encephalitis have never been reported in JE. We report a case of an 18-year-old girl with no previous comorbidities who presented to us with a history of fever and headache for 1 week duration. She developed bilateral lateral rectus palsy and asymmetric flaccid weakness of all four limbs, after 2 days of admission, which was followed by altered sensorium and intermittent hypothermia. Neuroimaging revealed longitudinal myelitis extending from pons till the L1 level along with bilateral thalamic hemorrhage in brain. Cerebrospinal fluid (CSF) was positive for IgM antibody to JE virus. She was treated with supportive measures, but she developed intractable hypothermia and seizures and succumbed to illness after 2 weeks of admission.
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PMID:Hypothermia due to limbic system involvement and longitudinal myelitis in a case of Japanese encephalitis: a case report from India. 2844 26

Early recognition and prompt specific treatment are crucial factors influencing the outcome of patients with acute encephalitis. The aim of this study was to determine the main causes of acute encephalitis in our population and to find predictors that may lead to specific diagnosis. Adult patients admitted to our hospital with suspected diagnosis of encephalitis in the period 2006-2013 were included. One hundred and five medical records were analyzed. Eighty-two patients with infectious encephalitis were identified (78% of total cases), 53 (65%) men and 29 (35%) women, mean age 47.8 years. The most common microorganisms identified were: HSV-1 (11%), VZV (10%), HSV-2 (5%) and EBV (5%). Twenty-three patients (22% of the series) had non-infectious encephalitis. Headache (p < 0.0001) and fever (p = 0.008) were more frequent in encephalitis of infectious origin. Protein levels and white blood cell counts in the cerebrospinal fluid were significantly higher in patients affected by infectious encephalitis than in those affected by noninfectious encephalitis (OR 95% CI 12.3 [2.9-51.7] and OR 95% CI 7.4 [2-27], respectively). Identifying specific causal agents of acute encephalitis remains a major challenge. Cerebrospinal fluid markers, as well as specific clinical findings, may however contribute to initial differentiation between infectious and noninfectious causes.
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PMID:Clinical and cerebrospinal fluid findings contribute to the early differentiation between infectious and noninfectious encephalitis. 2864 79

Background: The differential diagnosis of autoimmune and infectious encephalitis is notoriously difficult. For this study, we compare the presenting clinical symptoms and paraclinical test results of autoimmune and infectious encephalitis patients. A clinical algorithm for the diagnosis of autoimmune encephalitis has recently been published. We test these Graus criteria on our cohort for diagnostic sensitivity and specificity within the first week of presentation. Methods: We included all patients seen at our department within a 10-year-period who were diagnosed with encephalitis. The discharge diagnoses served as the reference standard for testing the clinical algorithm for two conditions: use of all the clinical information available on a patient during the first week of hospital admission assuming undefined autoantibody status and microbiological test results (C1) vs. consideration of all the information available on a patient, including the results of serological and microbiological testing (C2). Results: Eighty-four patients (33 autoimmune, 51 infectious encephalitis) were included in the study. Fifty-one (17 autoimmune, 34 infectious) had a definite clinical diagnosis. The two groups differed significantly for the presence of headache, fever, epileptic seizures, and CSF cell-count at presentation. Application of the clinical algorithm resulted in a low sensitivity (58%) and very low specificity (8%) for the diagnosis of possible autoimmune encephalitis. The latter increased considerably in the subgroups of probable and definite autoimmune encephalitis. Whereas the sensitivity of the individual diagnostic categories was clearly time-dependent, the specificity rested foremost on the knowledge of the results of microbiological testing. Anti-CASPR2- and -LGI1-associated autoimmune encephalitis and tick-borne virus encephalitis presented particular diagnostic pitfalls. Conclusions: We define clinical symptoms and paraclinical test results which prove valuable for the differentiation between infectious and autoimmune encephalitis. Sensitivity and specificity of the clinical algorithm clearly depended on the amount of time passed after hospital admission and knowledge of microbiological test results. Accepting this limitation for the acute setting, the algorithm remains a valuable diagnostic aid for antibody-negative autoimmune encephalitis or in resource-poor settings. The initiation of immune therapy however should not be delayed if an autoimmune etiology is considered likely, even if the diagnostic criteria of the algorithm are not (yet) fulfilled.
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PMID:Evaluation of Clinical and Paraclinical Findings for the Differential Diagnosis of Autoimmune and Infectious Encephalitis. 2995 Oct 31

This is the first reported case of familial voltage-gated potassium channel (VGKC) autoimmune encephalitis. The symptoms of autoimmune encephalitis can mimic infectious encephalitis with headache, fatigue, and neuropsychiatric symptoms. Autoimmunity is emerging as a distinct cause of encephalitis in the children. Prompt recognition, diagnosis, and treatment are important to prevent brain damage. Two brothers presented two years apart with different symptoms. The explanation for their distinct symptoms lies in the multifactorial development of autoimmunity. The presentation of autoimmune encephalitis can depend on the offending antibodies. The most common are antibodies against the N-methyl-D-aspartic acid (NMDA) receptor and the VGKC complex. Antibodies to the VGKC complex are divided into three different groups depending on their antigenic target: leucine-rich glioma-inactivated protein 1 (LGI1), contactin-associated protein-like 2 (CASPR2), or neither. Anti-VGKC antibodies in children are associated with neuroinflammation and encephalitis. Autoimmunity to LGI1 and CASPR2 antigens is associated with distinct human leukocyte antigen (HLA) alleles. Different HLA isotypes are involved in antigen processing and presentation and can lead to a genetic predisposition to autoimmunity. VGKC autoimmune encephalitis can present with memory changes, psychiatric symptoms, and motor abnormalities. Both brothers presented with these symptoms in their own unique way. Efficient diagnosis and immunosuppression helped improve their outcomes.
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PMID:A Tale of Two Brothers: Familial Voltage-Gated Potassium Channel Autoimmune Encephalitis. 3269 18