Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of malignant neuroleptic syndrome in a 55 years old male diagnosed 3 years ago of alcoholic paranoid psychosis who was chronically treated with haloperidol, clothiapine, and phenobarbital. Twenty one days after neuroleptic drug withdrawal the patient was admitted to the recovery room because of hyperthermia (40.2 degrees C), left basal pneumonia, acute respiratory insufficiency, extrapyramidal rigidity, mutism, dysarthria, deep coma, hypotension, and tachycardia. Two days after he presented massive rhabdomyolysis, atrial flutter with hemodynamic deterioration which reverted to sinus rhythm and acute anterolateral and inferior myocardial infarction documented by enzyme rise and electrocardiographic alterations. Rhabdomyolysis and myocardial infarction were the precipitating factors of the renal insufficiency. A malignant neuroleptic syndrome was suspected and intravenous treatment with dantrolene sodium 1.5 mg/kg every 24 hours was initiated. Bromocriptine was not administered. The patient died 14 days after in the course of a sepsis and cardiogenic shock.
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PMID:[Malignant neuroleptic syndrome associated with myocardial infarction, acute renal insufficiency and rhabdomyolysis]. 168 57

A 54-year-old man received insertion of an acupuncture needle into the region extending from the posterior neck to the back on two occasions for the treatment of shoulder stiffness. Two weeks after the second acupuncture, he developed fever, dysarthria and mictionary disturbance, finally reaching the condition of tetraplegia. He was immediately admitted to an emergency room in our hospital, and was diagnosed as sepsis with DIC, ARDS, heart failure, renal failure, liver failure, and myelitis. After one month, he recovered with transverse myelopathy as a residual deficit. Neurological findings showed transverse myelopathy below the level of Th2 at that time. Cervical CT revealed an irregular low density at the periphery of the cervical vertebra from the C2 to C4 level. Cervical MRI revealed an irregular swelling of his spinal cord from the C2 to C7 level. We explained the mechanism of transverse myelopathy in this case as follows. After the acupuncture, he suffered a focal infection of the region of needle insertion, and then the infection expanded to the cervical vertebra, thus causing osteomyelitis, sepsis, and finally cervical myelitis. Direct injury of the spinal cord and nerve roots as a complication of acupuncture was previously reported, but indirect injury of the spinal cord due to myelitis had not been reported except our present case. Careful attentions should be paid to the complications of acupuncture.
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PMID:[A case of transverse myelopathy caused by acupuncture]. 178 54

A 60 year-old man was admitted to our hospital because of gait disturbance and dizziness. At 57 years of age, he noticed his walking unstable. After then, he had dizziness due to orthostatic hypotension, urinary difficulty, loss of livid, and forgetfulness. Neurological examination revealed he had severe orthostatic hypotension, cerebellar ataxia, dysarthria, hyperreflexia of four limbs, myoclonus of right leg, and atonic bladder. His brain CT showed cerebellar atrophy. Thereafter he had recurrent syncopic attacks. His gait disturbance progressed steadily, so he became bedridden. In his terminal stage, his limbs showed rigidity. About 3 years later he died of pneumonia and sepsis. At autopsy brain weighted 1,230 g. Glossly the putamens was bilaterally shrunken, the color of the substantia nigra and locus ceruleus became pale. Base of the pons and the cerebellum were atrophic. Microscopical examination confirmed the degeneration of striato-nigral and olivo-ponto-cerebellar systems without Lewy body. In the spinal cord there was depletion of neuronal cells in the intermediolateral nuclei and Onufrowitz nuclei. In addition to the conventional neuropathological staining methods, we performed the immunohistochemical studies using monoclonal antibody against synthetic peptide of beta protein which detected senile plaque of every stages with formic acid pretreatment, and compared to the modified Bielschowsky method and Congo red method. Our case showed many very primitive and primitive senile plaque in neocortices and hippocampal region. A few neurofibrally tangle were seen in hippocampus. We supposed our case might combine multiple system atrophy and Alzheimer' pathology.
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PMID:[An autopsy case of multiple system atrophy with many senile plaques]. 262 28

A case of multiple spontaneous intracerebral hematomas is presented. A 67-year-old man with 7 years history of hypertension had sudden clumsiness in his right hand and an hour later dysarthria appeared. A CT scan taken 3 hours after the onset revealed two well demarcated high density areas in the left putamen and in the parietal subcortex. A diagnosis of multiple intracerebral hematomas was made. On neurological examination he was midly stuporous (13 points of Glasgow Coma Scale). Dysarthria, right hemiparesis and right extensor plantar response were seen. CT scan of 6 hours later disclosed the same findings as the previous study. He recovered well and neurologically free in a few days. On the following CT scans both hematomas were isodense 2 weeks later, and ring-like enhancement effect was noted. CT scan showed normal appearance 7 weeks later. On MRI using 0.5 T unit t-1 and t-2 weighted spin echo images of these hematomas also showed the similar chronological changes. The history, these CT and MRI studies suggest that two hematomas of this case occurred almost simultaneously in one cerebral hemisphere. No causative factors such as blood dyscrasias, AVM, angioma, septicemia, malignancies or sinus thrombosis was identified. We consider that a hypertensive intracerebral hematoma of the putamen was followed by the parietal intracerebral hematoma within a few hours, although amyloid angiopathy was not completely excluded because no cerebral biopsy of the lesion was performed.
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PMID:[A case report of simultaneous multiple intracerebral hematomas]. 338 86

We studied two autopsy cases of primary pituitary carcinoma. Case-1. A 45 year old female was admitted on Oct. 4 1978, with a complaint of right homonymous hemianopsia. And diagnosis was pituitary adenoma. Partial removal of pituitary tumor was performed on Oct. 23 1978. She died on Dec. 5 1978 due to bleeding of gastrointestinal tract. Autopsy disclosed a pituitary carcinoma invading the left hypothalamus, mamillary body, optic and V cranial nerves, and mid brain as well as sphenoid bone. No extracranial metastasis was noted. Case-2. A 44 year old female with a history of acromegaly for 6 years was admitted with a complaint of headache on May 8 1976. She was diagnosed as having pituitary adenoma. The subtotal removal of pituitary tumor was performed on May 21 1976 and followed by 4500 rad irradiation. At this time, pathological diagnosis was eosinophilic adenoma. Seven years later, she complained of progressive right hearing disturbance, dysarthria and ataxic gait 1983. The second subtotal removal of pituitary tumor was performed with a diagnosis of recurrence of pituitary adenoma on Oct. 7 1983. After the operation, she complicated sepsis and died on Jan. 14 1984. An autopsy disclosed a pituitary carcinoma from residual pituitary gland, continuously extending to the subarachnoid space of the pons, and invading right cerebello-pontine angle and cerebellum. The histological examination revealed pituitary carcinoma with high pleomorphism and glioblastoma multiform-like feature were within the tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two autopsy cases of primary pituitary carcinoma]. 341 67

We report a 54-year-old man with progressive generalized muscle atrophy and ophthalmoparesis in the terminal stage. He was well until 44 years of age (1982) when he noted weakness in his right hand and muscle atrophy; in May of 1985, he noted weakness in his left hand and in both legs. His weakness had become progressively worse, and he became unable to walk in November of 1985. He noted dysarthria one month later, and dysphagia in March of 1986. His difficulty in swallowing had also become worse; he regurgitated foods into the trachea in September of that year, and he developed a low grade fever on the same day. He was admitted to our service on September 24, 1987. On physical examination, general findings were unremarkable, except for low grade fever (37.3 degrees C). On neurologic examination, he was alert and mentally sound. He had normal vision and visual fields; ocular movements were normal. He had moderate weakness in facial muscles, dysarthria, dysphagia, and atrophy in his tongue. He had marked generalized muscle atrophy with fasciculation. He was unable to stand or walk. His muscle strength was not more than 1/6 in any part. The lower extremities were spastic. Deep reflexes were exaggerated in both lower extremities but were normal in upper extremities. Sensation was intact. Laboratory examination was unremarkable, and so was the cranial CT scan. He was treated with nasogastric feeding. He was able to communicate smoothly using his eyes, but a restriction in the vertical gaze was noted in February of 1989. The range of ocular movement was better in the oculocephalic reflex compared with his spontaneous vertical eye movements. In April of 1990, his horizontal gaze also had become slow, and he was complicated by bronchial asthma. He was treated with 20 mg/day of prednisolone; after the institution of prednisolone, his horizontal eye movement showed much improvement. In the terminal stage, he was able to move his eyes only very slowly; vertical gaze was impossible. His subsequent course was complicated by respiratory tract infection and septicemia, and he expired on July 15, 1992. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient had amyotrophic lateral sclerosis with oculomotor paresis. Post-mortem examination revealed spongy change involving the posterior column and the posterior spinocerebellar tract, in addition to severe degenerative change in the upper and the lower motoneurons, which were consistent with amyotrophic lateral sclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 54-year-old man with generalized muscle atrophy and oculomotor paresis]. 799 50

The development of central pontine myelinolysis (CPM) has rarely been reported in association with hemophagocytic syndromes (HPS). Here we report a unique case of Epstein-Barr Virus (EBV)-related HPS which was accompanied with CPM. A 72-year-old man who had no significant medical history was admitted to our hospital due to high fever and progressing dysphasia and dysarthria. Physical examination revealed anisocoria of the right pupil, fixed reaction to light, and paralysis of the left vagus nerves. Magnetic resonance imaging revealed low signal intensity on T1-weighted images and high signal intensity T2-weighted images in the patient's central midpontine lesion. Initial work-up showed anemia and thrombocytopenia with elevated levels of serum ferritin, lactate dehydrogenase, and soluble IL-2 receptor. Bone marrow aspiration revealed hemophagocytosis. The EBV genome was detected in the peripheral blood using the polymerase chain reaction method. He was diagnosed as having EBV-related HPS and CPM. Despite intensive treatment with methylpredonisolone, immunoglobulin, and etoposide, he died due to progressive disease and fungal septicemia. The etiology and relation between CPM and HPS are discussed.
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PMID:EBV associated hemophagocytic syndrome accompanied by central pontine myelinolysis. 1248 7

This report concerns two patients (female, 9 and 6 years) who were diagnosed with megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS). Although they exceeded the usual life expectancy of patients diagnosed with MMIHS because of total parenteral nutrition (TPN), they demonstrated progressive neurological deficits and showed histopathological features in the brain. Both patients were diagnosed with MMIHS in the neonatal period and were fed by TPN. The first patient developed visual and gait disturbances at the age of 7 years. Two months later, she developed dysarthria and muscular weakness, and could not maintain her posture. The level of serum selenium was extremely low. The second patient developed flexion and spasticity of the extremities followed by decorticate posture at the age of 3 years. Both patients died of sepsis. The brain weights of the two cases were 880 g and 715 g. In both cases, severe neuronal loss and gliosis were present in the medial convolutions of the occipital lobe, including the visual cortex. The postcentral gyrus and temporal transverse gyrus were also involved. In addition, extensive loss of Purkinje cells and granular neurons, and gliosis were observed in the cerebellum. We measured the selenium content of the brains and livers using the graphite furnace atomic absorption spectrometry method. Selenium was not detected in either brain, although the livers of both cases contained a low level of selenium. On immunohistochemical examination of the anti-oxidative enzymes, histiocyte-macrophage lineage cells in MMIHS cases, including microglia and Kupffer cells, showed only a weak reaction for glutathione peroxidase, of which selenium is an essential component. However, the cells in the control cases were strongly positive. In cases of MMIHS and methylmercury intoxication, the brain features similar lesions, in both their topographical and histopathological aspects. We considered that the brain lesions of the MMIHS patients mainly resulted from oxidative damage of the brain related to the low levels of glutathione peroxidase and other selenoproteins due to selenium deficiency.
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PMID:Encephalopathy in megacystis-microcolon-intestinal hypoperistalsis syndrome patients on long-term total parenteral nutrition possibly due to selenium deficiency. 1284 51

A 56-year-old woman with aortic regurgitation (AR) developd a high fever on April 25th, 2003, followed by the sudden onset of left hemiparesis and dysarthria on May 10th, 2003. MRI and MRA showed cerebral infarction due to occlusion of the right proximal portion of the middle cerebral artery. Streptococcus was isolated from arterial blood culture at the time of admission and cardiac examination such as echocardiography revealed active infective endocarditis. Cerebral angiography on the 31st day after the onset of symptoms demonstrated a fusiform-shaped aneurysm at the occluded M2 portion of the middle cerebral artery. Despite administration of antibiotics, a small subcortical hematoma was observed in the right temporal lobe surrounding the aneurysm on the 35th day. The direct surgery of aneurysmal trapping and resection was subsequently performed to prevent rebleeding. The sylvian fissure and perianeurysmal area were strongly adherent to granulation tissue and blood clot. After exposing the aneurysm, the dilated portion of the vessel was successfully trapped and resected. Other than residual left hemiparesis, the postoperative course was uneventful. Histological examination confirmed bacterial aneurysm due to bacterial embolization originating from infective endocarditis (IE). We report a rare case having a ruptured bacterial aneurysm of the middle cerebral arterial bifurcation requiring surgery following occlusion due to bacterial embolization after sepsis and meningitis due to infective endocarditis.
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PMID:[A surgically treated case with a ruptured bacterial aneurysm of the middle cerebral arterial bifurcation following occlusion]. 1528 88

We report a 70-year-old woman with sarcoidosis and multiple cranial nerve palsy. The patient suffered from dysarthria, dysphagia and weakness of the upper and lower extremities and died of sepsis. No abnormalities were noted in brain MRI. At autopsy, numerous epithelioid granulomas with Langhans giant cells were present in the bilateral lungs, including the hilar lymph nodes. The brain had a normal external appearance. Histologically, there were brainstem parenchymal lesions consisting of many microgranulomas, lymphocytic infiltration, activated microglias and astrocytosis. Perivascular lympocytic cuffing was also seen. Neither granulomas nor lymphocytic infiltration were seen in the leptomeninges. The present case was considered to be a peculiar type of neurosarcoidosis, that is, "sarcoid brainstem encephalitis".
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PMID:Disseminated intraparenchymal microgranulomas in the brainstem in central nervous system sarcoidosis. 1638 86


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