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)

We report on two children with bilateral thalamic astrocytomas. The first patient developed psychomotor regression at the age of 20 months followed by rapidly progressive ataxia, intention tremor, slurred speech, and bouts of drowsiness. Magnetic resonance imaging (MRI) of the brain showed swelling and high signal intensity in both thalami accompanied by supratentorial hydrocephalus. The second patient presented with progressive cerebellar ataxia, headache, and vomiting at the age of 11 years. MRI of the brain revealed symmetrical, hyperintense and sharply delineated swelling of both thalami. Additional lesions were seen in the cerebellum and the right temporal lobe. In both cases proton magnetic resonance spectroscopy (MRS) of the lesions showed a striking decrease of the neuronal marker N-acetylaspartate, an increase of choline-containing compounds, and a minimal lactate peak. Stereotactic biopsies from the thalamus of the first patient and from a cerebellar lesion of the second patient finally revealed glial tumors, namely a diffuse astrocytoma of World Health Organization (WHO) grade II in the first patient and an anaplastic astrocytoma of WHO grade III in the second patient. We conclude that the clinical manifestations and MRI patterns of bilateral thalamic astrocytomas are very similar to those of encephalitis and neurometabolic disorders and should therefore be included in the differential diagnosis of these encephalopathies.
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PMID:Diagnostic difficulties in childhood bilateral thalamic astrocytomas. 1257 91

A 69-year-old man was referred to our department because of acute onset nausea, vomiting, dysphagia, dysarthria and gait disturbance. He had a 50-day-history of amebic dysentery and had been treated with 1,500 mg metronidazole per day. Neurological examination revealed dysphagia, ataxic speech, ataxia of the left extremities and the trunk, and hyperactive deep tendon reflexes in all extremities. Sensory impairment of all modalities was apparent in a glove and stocking pattern, with mild paresthesia. Brain MRI showed T2 high signal lesions in the bilateral cerebellar dentate nuclei, more markedly on the left. On brain SPECT, obvious low blood perfusion was observed in the left cerebellar hemisphere. These findings well explained the ataxia of the left limbs. One month after discontinuing metronidazole, the cerebellar ataxia, dysphagia and MRI abnormalities completely cleared. Therefore, central nervous system damage induced by metronidazole is considered reversible. In spite of the presence of the MRI lesion in the right dentate nucleus, the patient had no ataxia of the right extremities and there was no hypoperfusion in the right cerebellar hemisphere. Thus, metronidazole does not appear to have a direct neurotoxic effect on the central nervous system. On the other hand, nerve conduction studies showed axonal polyneuropathy, which was not improved one month after cessation of the drug; thus metronidazole seems to exert more damage on peripheral nerves.
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PMID:[MRI and SPECT findings in a case of metronidazole-induced reversible acute cerebellar ataxia]. 1596 Jan 79

We investigated the clinical features of 15 patients with multiple isolated ischemic lesions in the cerebellum. The main initial symptoms were vertigo and nausea/vomiting in 8 patients each, and headache in 6 patients. Dysarthria and cerebellar ataxia of the limbs and trunk were observed in 14 patients. The ischemic lesions were in the posterior inferior cerebellar artery (PICA) plus superior cerebellar artery (SCA) territories in 4 patients (27%), and PICA plus SCA plus anterior inferior cerebellar artery (AICA) territories in 3 patients (20%). Infarcts were in the AICA plus SCA territories in 2 patients (13%), PICA only in 2 patients (13%), and SCA only in 4 patients (27%). Hemorrhagic lesions were observed in the ischemic area in 2 patients (13%). Vascular lesions included occlusive lesions of the vertebral arteries in 9 patients (60%), but no abnormalities of the vertebrobasilar arterial system were observed in 6 patients (40%). The functional prognosis was good in most cases. The underlying mechanism was atherothrombotic, including arteriogenic embolism in 9 patients (60%) and cardiogenic embolism in 3 patients (20%). An embolic mechanism was considered in all cases, but in some cases an accurate pathogenesis of the cerebellar infarction was obscure.
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PMID:Multiple cerebellar infarcts: clinical and pathophysiologic features. 1790 25

We present a case of a 4-year-old previously healthy child who had a possible first-time seizure at home, and upon a second Emergency Department evaluation was found to have gross cerebellar ataxia suggestive of acute stroke. Initial computed tomography scan and metabolic work-up were unrevealing. Subsequent neuroimaging demonstrated stroke in the left medulla and cerebellum secondary to left vertebral artery dissection. Cervical artery dissection may cause up to 20% of strokes in childhood and adolescence. Unlike typical adult presentations, antecedent or concurrent head and neck pain occurs less often in pediatric dissections. Symptoms of posterior circulation ischemia resulting from vertebral artery dissection may include vertigo, vomiting, ataxia, dysarthria, and seizure. Willingness to utilize newer, non-invasive imaging modalities may lead to earlier recognition of cervical artery dissection when patients have prodromal symptoms or episodes of transient ischemia. Vertebral artery dissection should be included in the differential diagnosis when evaluating children with first time seizure, headache, or neck pain.
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PMID:A preschool-age child with first-time seizure and ataxia. 1797 66

We report an 8-year-old boy with left vertebral artery dissection featuring cerebellar ataxia in which congenital vertebral artery hypoplasia was suspected as a predisposing factor in the dissection. The patient suddenly suffered from vertigo and vomiting while swimming, and he was brought to our department. The initial brain Computed Tomography (CT) demonstrated no abnormalities, and his symptoms disappeared the next morning. However, one month after onset, brain Magnetic Resonance Imaging (MRI) revealed ischemic changes (infarction) in the left cerebellum. Transfemoral angiography showed complete occlusion at the C2 portion of the left vertebral artery, suggesting dissection and diffuse narrowing of the proximal segment of the occlusion site. Three-dimensional CT angiography also revealed diffuse narrowing of the left vertebral artery from the bifurcation of the subclavian artery. He has since been living daily life without any difficulties. The detailed etiology of cerebral artery dissection remains unknown, but arterial anomalies should be considered as a predisposing factor.
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PMID:An 8-year-old boy with vertebral artery dissection with cerebellar ataxia featuring suspected vertebral artery hypoplasia. 1876 94

A 15-year-old girl presented with a distal anterior inferior cerebellar artery (AICA) dissecting aneurysm manifesting as sudden onset of general tonic-clonic convulsion while singing a song. Physical and neurological examinations found headache, vomiting, right perceptive deafness, and right cerebellar ataxia. Cranial magnetic resonance imaging demonstrated a hemorrhagic mass in the brainstem region, and digital subtraction angiography revealed a fusiform dilatation of the anterior pontine segment of the right AICA. The diagnosis was dissecting aneurysm. Endovascular embolization was performed for aneurysm and parent artery occlusion using a Guglielmi detachable coil and 9 TruFill detachable coil systems, respectively, 2 weeks after occipital artery-AICA anastomosis. No ischemic complications were seen, and her neurological deficits completely recovered after the interventional therapy.
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PMID:Anterior inferior cerebellar artery dissecting aneurysm in a juvenile: case report. 1924 70

We report a 28-year-old male who presented with severe vertigo, vomiting, diplopia, clumsiness of right extremities. Physical examination revealed low reading of blood pressure in the left upper limb and evidence of mild left upper limb ischemia. On neurological examination he had right cerebellar ataxia. Computed tomography and magnetic resonance imaging, revealed an acute right cerebellar infarction in the anterior inferior cerebellar artery territory. Doppler ultrasono-graphy revealed an aneurysm of the left subclavian artery. The patient was tested positive for serology of syphilis.
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PMID:Left subclavian artery aneurysm secondary to syphilitic arteritis presenting with a right ischemic cerebellar infarction. 2013 37

Superficial siderosis (SS) of the central nervous system is a rare condition caused by chronic subarachnoid hemorrhage. Clinical manifestations typically include sensorineural hearing loss and cerebellar ataxia. Recurrent episodic encephalopathy in the setting of SS has not been reported. We describe a unique case of SS in a 67-year-old man with an 8-year history of episodic encephalopathy associated with headache and vomiting. The patient also had a history of progressive dementia, ataxia, and myelopathy. A diagnosis of superficial siderosis was made after magnetic resonance gradient-echo images showed diffuse hemosiderin staining over the cerebellum and cerebral convexities. No intracerebral source of hemorrhage was identified. The patient therefore underwent gadolinium-enhanced spinal MRI which suggested a possible vascular malformation. A therapeutic laminectomy subsequently confirmed an arteriovenous fistula which was resected. In SS, there are often long delays between symptom onset and definitive diagnosis. Early identification is facilitated by magnetic resonance imaging with gradient-echo sequences. When no source of hemorrhage is identified intracranially, then total spinal cord imaging is indicated to assess for an occult source of hemorrhage as occurred in our case.
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PMID:Episodic encephalopathy due to an occult spinal vascular malformation complicated by superficial siderosis. 1985 21

We report two patients with Marchiafava-Bignami disease (MBD). A 38-year-old male with chronic alcohol abuse developed acute onset cerebellar ataxia and altered sensorium. He was diagnosed to have acute form (Type II) of MBD. Magnetic resonance imaging (MRI) showed extensive lesions involving the corpus callosum in its entire extent and also bilateral corona radiata and centrum semiovale. Corpus callosum had heterogeneous signal changes with ring enhancement. Positron emission tomography scan demonstrated reduced cerebral glucose metabolism diffusely over both the cerebral hemispheres. The second patient was 55-year-old male with chronic alcohol intake developed acute onset vomiting followed by behavioral abnormalities and altered sensorium. MRI showed diffuse lesion involving entire corpus callosum with suggestion of necrosis. Both the patients subsequently recovered, the first patient is back to his previous occupation and the second patient could be rehabilitated with some lighter work in his previous work place. Functional brain imaging may help to understand the pathogenesis of acute MBD and possibly the behavioral manifestations.
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PMID:Marchiafava-Bignami disease: Two cases with magnetic resonance imaging and positron emission tomography scan findings. 1993 69

A 41-year-old man was admitted in June 2007 with a 1-month history of headache and cerebellar ataxia. At the age of 5 years, in May 1971, he had presented with headache, vomiting, and gait disturbance. Cerebral angiographical study demonstrated vascular shift caused by a mass lesion in the cerebellar vermis. He had immediately undergone partial removal. Histological diagnosis was medulloblastoma (MB). Postoperatively he received a total of 40 Gy radiation to the whole brain and 30.5 Gy to the spine without chemotherapy. He was again seen 35 years later with a radiation-induced glioblastoma (GB) that arose in the region of the original MB. The tumor was surgically removed, and he received radiotherapy and chemotherapy with ACNU, procarbazine, and vincristine. Postoperative irradiation reduced the size of the second tumor.
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PMID:Radiation-induced glioblastoma occurring 35 years after radiation therapy for medulloblastoma: case report. 2042 47


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