Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 10-year old child was admitted for vomiting and a high grade fever. He had been previously immunized twice against tuberculosis. A cerebellar syndrome appeared, and the brain CT scan showed an intracerebellar mass. Disseminated lesions were detected on abdominal (splenic abscess) and thoracic (mediastinal lymph nodes) CT scans. The bone scintigraphy also showed multiple localisations. A craniotomy was performed that revealed a cerebellar tuberculoma which was completely removed. The child received an antituberculous treatment over 18 months and is currently well with a 5 year follow-up.
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PMID:[Multifocal tuberculosis with cerebellar tuberculoma]. 133 63

A 55 year-old man complained of headaches, dizziness and vomiting. Neurological examination only showed a cerebellar syndrome. CT scan revealed two hyperdense round areas in the right frontal lobe and cerebellar vermis consistent with metastases and a lung carcinoma was diagnosed. Two months later he presented with typical right hemichorea. A second CT scan showed another hypodense lesion with slight contrast enhancement in the left subthalamic region. He died 6 months after clinical onset. Post mortem examination showed an adenocarcinoma of the right lung with liver metastases. Neuropathological examination revealed four intraparenchymatous metastases one of which involved the left subthalamic nucleus. Hemichorea secondary to metastatic neoplasm of the corpus Luysii is uncommon; only 6 cases have been reported previously; five of them had a post mortem examination of the brain. In three cases a CT scan was available and had demonstrated the site and nature of the lesion.
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PMID:[Hemiballismus and metastasis to the Luys' body. An anatomo-clinical case]. 378 60

A 30-year-old woman, who, since the age of 20, had epileptic seizures, was hospitalized in 1972 because of frontal headaches, nausea, and vomiting. Clinical examination revealed a right cerebellar syndrome; gamma-encephalogram showed a focus of subtentorial hyperactivity; iodoventriculography showed a deformation of the aqueduct. At surgery, a posterior fossa tumor implanted on the dura mater and tentorium of the right cerebellar fossa was enucleated. The histologic features were those of giant lymph node hyperplasia. Postoperative craniospinal radiotherapy was administered. Ten years later the patient was in good health and neurogically normal.
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PMID:Intracranial lesion resembling giant lymph node hyperplasia. 663 84

A 38-year-old homosexual male with AIDS suffered four neurological episodes including headaches, confusion, visual impairment, memory disturbances, and dysarthria which resolved spontaneously in a few days. He was admitted to hospital during a fifth episode. Neurological examination revealed a cerebellar syndrome. General examination was normal. CD4 count was 90. CSF contained two WBCs/mm(3) and 12.30 mg/dL protein. MRI revealed diffuse ill defined increased signal on T2-weighted images in the white matter. His condition worsened rapidly with vomiting and he died 1 month after admission. Neuropathological examination revealed diffuse brain oedema with ventricular compression, central diencephalic herniation and bilateral tonsilar herniation in the absence of a focal lesion. Microscopical examination revealed predominant involvement of the white matter with diffuse myelin pallor and massive perivascular dilatation containing an exudate expressing serum proteins and occasional macrophages. The same exudate was also diffuse in the leptomeninges. Parenchymal damage predominated around the perivascular spaces and included loosening of tissue, axonal damage with spheroids and reactive astrocytosis. There was no evidence of productive HIV encephalitis, no multinucleated giant cells; p24 immunostaining and RT-PCR for HIV genome were negative. There was neither significant inflammation nor microglial activation. In this illustrative case, the relapsing course of the neurological signs, the diffuse topography of the blood-brain barrier breakdown and the absence of local cause make it likely that the diffuse leak and axonal damage could be related to circulating factors.
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PMID:Acute, relapsing brain oedema with diffuse blood-brain barrier alteration and axonal damage in the acquired immunodeficiency syndrome. 971 86

We report on a 35 year old female with a 26 day history of an intermittent cerebellar syndrome (dysarthria, ataxia of extremities, gait and trunk, nystagmus), mild meningism, cephalgia, recurrent emesis and nausea. Symptoms developed after typically chickenpox exanthema. Examination of the liquor showed mild pleocytosis, elevated protein and increased albumin quotient. Virus was not found by EIA or PCR. There were elevated levels of IgM- and IgG-antibodies to VZV. The EEG showed mild general changes, compatible with an encephalitis. Neuroradiological examinations were unremarkful. The neurological deficits partly regressed in the follow-up of two months. To the best of our knowledge we are the first that describe the paradox of an intermittent cerebellar syndrome after infection with chickenpox without detection of the virus in the liquor. This phenomenon can be related to the unusual combination of cerebellar ataxia and the later occurrence of mild encephalitis.
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PMID:[Cerebellar syndrome after varicella infection without virus identification in cerebrospinal fluid--an important differential ataxia diagnosis]. 1059 44

Meningioma is an uncommon tumor of childhood. In this group, supra tentorial forms predominate. We report the case of a 14 years old boy without any past medical history. He presented headaches, vomiting and cerebellar syndrome. CT scan shows cerebellar tumor, enhanced by contrast and surrounded by edema, looking like tuberculoma. After fail of tuberculosis treatment, the boy is operated by suboccipital approach. Histology and immuno histochemical examination show fibroblastic meningioma. Even if it is rare, meningioma can occur in childhood, without neurofibromatosis disease. It can present many points of likeness with tuberculoma and therefore biopsy is mandatory before tuberculosis drugs giving.
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PMID:[Child cerebellar meningioma. A case report]. 1578 23

Lhermitte-Duclos disease (LDD) is a rare cerebellar disorder characterized by diffuse or focal enlargement of cerebellar folia. Clinical manifestations are usually related to a mass effect and secondary obstructive hydrocephalus. Increased intracranial pressure symptoms and cerebellar symptoms are the most frequent patient complaints. We describe the case of a patient with LDD who developed secondary obstructive hydrocephalus. A 68-year-old woman was brought to the emergency room for sudden vertigo following several bouts of vomiting and headache. There were no external signs of trauma, serious illness or infection. On admission, the patient was alert and had no neurological deficits. Brain computed tomography (CT) and magnetic resonance imaging (MRI) showed hydrocephalus and a cerebellar mass in the right cerebellar hemisphere compressing the fourth ventricle. Suboccipital craniotomy and subtotal removal of the mass was performed. Pathological study of the surgical specimen showed abnormal ganglionic neurons and an enlarged molecular layer compatible with dysplastic gangliocytoma. Cytoreduction can achieve improvement in symptoms caused by mass effect, but postoperative swelling may aggravate obstructive hydrocephalus. Therefore, if symptoms still remain after removal of the mass, an additional shunting procedure may be needed as a further management option.
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PMID:Lhermitte-Duclos disease presenting with hydrocephalus. 2211 44

Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction due to a systemic response to infection. We report the case of a 4-year-old girl with fever and vomiting for 48h, brought to the university hospital of Grenoble because of vigilance disorders, loss of verbal fluency, and a cerebellar syndrome. She had a biological infectious syndrome. Infectious encephalitis was suggested first, but the cerebral scan and the lumbar punction were normal. Magnetic resonance imaging (MRI) showed a diffuse brain edema with extended involvement of cortical and basal ganglia. The electroencephalogram was globally slow. The infectious syndrome was explained by perforated appendicitis with peritonitis, treated by surgery and antibiotic therapy. Other infectious explorations were negative. No metabolic or autoimmune diseases were found. Hence, our final diagnosis was sepsis-associated encephalopathy. After 1 year of follow-up care, her clinical exam, MRI, and EEG were normal. Sepsis-associated encephalopathy has been increasingly described in the adult population, but until today only three pediatric cases have been published. It is diagnosed when the patient has a severe infectious syndrome associated with neurologic symptoms, mostly vigilance or consciousness disorders, no signs of shock, and only when other potential reasons have been ruled out. The MRI shows non-specific diffuse lesions with vasogenic edema on the subcortical substance or on the basal ganglia and the thalami. The electroencephalogram is slowed down on the whole. The main differential diagnoses are infectious encephalitis, acute disseminated encephalomyelitis, and cerebral vasculitis. Posterior reversible encephalopathy syndrome is an MRI diagnosis that presents characteristics similar to SAE. In the future, it could be discovered that it is the same physiopathology. At the moment, we only treat the symptoms and the causative infection. Most of the time, patients have neurologic sequelae that affect their verbal fluency. It can persist from a few months up to 6yrs. Although quite slow, the neurologic progression is good. The mechanisms are studied and there are hopes for specific treatments. The main explanation seems to be immune with alterations of the blood-brain barrier. Cytokines and activated leukocytes may attack the cerebral substance.
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PMID:[A child with sepsis-associated encephalopathy]. 2395 25

Paraneoplastic neurologic syndromes (PNS) can be the first manifestations of occult malignancies. If left untreated, PNS often lead to significant morbidity and mortality. Anti-Ri (anti-neuronal nuclear antibody type 2 [ANNA-2]) autoantibodies are commonly associated with breast and small cell lung cancers. Cases of anti-Ri paraneoplastic cerebellar degeneration are reported, but few describe severe nausea and coexisting limbic encephalitis as the major presenting features. We report a 75-year-old woman with medically-intractable emesis, encephalopathy, diplopia, vertigo, and gait ataxia for 3 months. Examination revealed rotary nystagmus, ocular skew deviation, limb dysmetria, and gait ataxia. After two courses of intravenous immunoglobulin, there was minimal improvement. Anti-Ri antibodies were positive in serum only. CT scan identified a 2.0 cm left lung mass, and histopathology revealed large cell neuroendocrine carcinoma with admixed adenocarcinoma non-small cell lung carcinoma (NCSLC). Though the patient achieved nearly complete clinical recovery after tumor resection, anti-Ri levels remained high at 20 months post-resection. To our knowledge this is the first report of a paraneoplastic brainstem cerebellar syndrome with coexisting limbic encephalitis involving anti-Ri positivity and associated mixed neuroendocrine/NSCLC of the lung with marked improvement after tumor resection.
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PMID:Anti-Ri-associated paraneoplastic brainstem cerebellar syndrome with coexisting limbic encephalitis in a patient with mixed large cell neuroendocrine lung carcinoma. 2544 85

BACKGROUND Dengue-associated neurological manifestations have recently been on the rise. Cerebellar syndrome complicating dengue fever has rarely been reported in the literature. We present a case report of dengue-associated cerebellar syndrome and performed a literature review to draw attention to this rare neurological complication. CASE REPORT A 60-year-old man presented with 4 days of fever, myalgia, arthralgia, headaches, and warning symptoms (persistent diarrhea and vomiting). He was admitted with serologically-confirmed dengue fever. He had been well until day 8 of illness, when he developed cerebellar signs and symptoms. The temporal relationship with the recent dengue fever suggested that he had dengue cerebellitis. He recovered well, with no neurological sequelae upon our clinic visit. CONCLUSIONS Dengue cerebellitis is a rare but recognized manifestation, which should be considered in patients from endemic areas of dengue fever who develop cerebellar syndrome.
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PMID:Dengue Cerebellitis: A Case Report and Literature Review. 3003 9


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