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Query: UMLS:C0027497 (nausea)
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We report a rare case of disproportionately large communicating fourth ventricle (DLCFV) combined with syringomyelia and Chiari malformation. The case was a 27-year-old male who underwent ventriculoperitoneal (V-P) shunt on the right side for hydrocephalus caused by traumatic intracerebral and intraventricular hemorrhage. One month later, he became somnolent with posterior fossa symptoms (nausea, vomiting and nystagmus). CT scan demonstrated enlarged fourth ventricle, which was diagnosed as DLCFV because the ventriculogram revealed patency of the aqueduct. One and half month later a second V-P shunt was made on the left side to increase the shunt flow. He became ambulatory with a cane, although the fourth ventricle remained moderately dilated on CT scan. Two months after the additional V-P shunt, he slipped and hit the occiput and immediately became tetraparetic. The patient was treated conservatively under the diagnosis of central spinal cord injury. The MRI taken 2 months after the accident revealed Chiari malformation (type 1), syringomyelia and a dilated fourth ventricle which was compressing the brainstem. After the fourth ventriculoperitoneal (FV-P) shunt, the tetraparesis transiently improved but then again worsened. On the CT scan the syrinx did non change in size, while the size of the fourth ventricle became normal. After syringoperitoneal (S-P) shunt the patient showed a moderate improvement of tetraparesis. Unfortunately he suffered appendicitis complicated with peritonitis and all the shunts were immediately changed to external drainage. However, the patient developed meningitis and became paraplegic. The motor function of the upper extremities slightly improved by aspiration of fluid via the external drainage system from the syrinx.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of disproportionately large communicating fourth ventricle (DLCFV) combined with syringomyelia and Chiari malformation]. 202 74

Hematomas of the basal ganglia in head injury have long been recognized by pathologists with an interest in head injury but their mechanism has not been revealed clearly. We report two cases of bilateral traumatic hemorrhage in the basal ganglia. Case #1, a 17-year-old male was admitted to our hospital immediately after a traffic accident. Neurological examination revealed that the patient was comatose and had right hemiparesis. CT scan showed bilateral hemorrhage of the basal ganglia and subarachnoid hemorrhage in the perimesencephalic cistern. MRI showed high signal intensity areas in the bilateral basal ganglia, perimesencephalic cistern, cerebral white matter and corpus callosum. The patient was diagnosed as having diffuse axonal injury coinciding with bilateral hemorrhage of the basal ganglia. Stereotactic aspiration for the hematoma of the left basal ganglia was carried out. Case #2, a 75-year-old male was admitted immediately after falling from the roof of his house. Neurological examination revealed no neurological deficit except for headache and nausea. CT scan on the day of injury revealed no abnormality. But CT scan 12 hours following the injury showed bilateral hemorrhage of the basal ganglia. Blood pressure of the patient was within normal range and he was diagnosed as having traumatic bilateral intracerebral hematoma. Conservative treatment was carried out and the patient was discharged 7 days after injury with no neurological deficit. The mechanism of traumatic hemorrhage of the basal ganglia has not been clear. In case #1, diffuse axonal injury (DAI) may have played an important role in the bilateral hemorrhage. But in case #2, non-DAI factor such as vasoparalysis syndrome may have existed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral traumatic hemorrhage in the basal ganglia: report of two cases]. 204 52

A rare case of the dural AVM mainly around the left petrosal sinus was reported. A 64 years old man was admitted just after the sudden onset of severe headache and nausea. The CT scan revealed subarachnoid hemorrhage in the left ambient cisterns. A small hematoma was also found in the left cerebellar peduncle. External carotid angiogram showed a dural AVM which nidus was located adjacent to the left superior petrosal sinus. Its feeding arteries were as follows; the middle meningeal artery, the artery of foramen rotundum, the accessory meningeal artery, the dural branch of occipital artery and the ascending pharyngeal artery. The voluminous petrosal vein and the dilated cortical veins were identified as drainers and, the portion of the latter appeared as "varix" embedded in the pons, which was clearly delineated by MRI. In the venous phase, stenotic straight sinus and residual Falcine sinus were illustrated. Superselective embolization of the feeding arteries was employed followed by the direct clippings of draining vein. Postoperative course was uneventful. The present case should be classified into the tentorial dural AVM. Only 26 cases of this rarely encountered entity was reported in the literature. Based on both the present and the previously reported cases, the clinical features, treatment and pathogenesis of this disease were briefly discussed.
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PMID:[Superior petrosal sinus dural arteriovenous malformation with varix indenting brain stem--report of a case and review of the literature]. 205 25

A 17-year-old boy who had mitochondrial encephalomyopathy with focal deficiency of cytochrome c oxidase (CCO) activity is described. He experienced 3 episodes of muscle weakness, fatigability, nausea, vomiting and concomitant increase of serum creatine kinase activity, at the age of 13, 15 and 17 years. During interval there was no muscle weakness and the serum creatine kinase activity was within normal range. Increased levels of lactic acid and pyruvic acid were observed in the blood and cerebrospinal fluid. After an aerobic exercise test, lactic acid and pyruvic acid in the blood increased to an abnormally high level, and the arterial blood became acidic (pH 7.297). On EEG, occasional intermittent irregular theta activities were observed in the anterior region, but there were no abnormalities on CT and MRI in the central nervous system. In the biopsied muscle, ragged-red fibers comprised 20% on modified Gomori-trichrome staining and a number of fibers with no CCO activity were scattered throughout. The CCO activity in the mitochondria isolated from the biopsied muscle was reduced to 49.2 nmol/min/mg protein (normal range 144.7-355.8), while other mitochondrial enzyme activities in the electron transport system were normal. From these data, the patient was considered to have a unique form of mitochondrial encephalomyopathy. By the administration of a large amount of coenzyme Q10, episodes of muscle weakness and nausea, and an increase of lactic acid and pyruvic acid in the blood after aerobic exercise test were no longer observed.
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PMID:[Mitochondrial encephalomyopathy (focal cytochrome c oxidase deficiency) with transient episodes of muscle weakness and elevation of serum creatine kinase activity]. 216 88

We reported a 51-year-old male with ischemic disturbance of right inner ear resembling Meniere's disease. The patient had a sudden-onset episode of vertigo, right severe hearing disturbance, nausea, vomiting and gait disturbance. Two days after, he had hypersomnia, vertical gaze palsy, double vision, left Horner's sign, and sensory disturbance of pain and temperature of right half body involving face. Brain MRI disclosed high intensity area in T2-weighted image and proton density in bilateral paramedian thalamo-mesencephalic region and right cerebellum (area of the anterior inferior cerebellar artery). Cerebral angiography showed 90% or more stenosis of the right vertebral artery, 50% stenosis of the left vertebral artery before the posterior inferior cerebellar artery (PICA), and 60% stenosis of distal portion of the basilar artery. Furthermore, stem portion of the posterior cerebral artery, and the right anterior cerebellar artery and the left vertebral artery after the PICA were absent or occluded. Right deafness was evaluated to be Jerger type II, namely disturbance of inner ear. Caloric tests showed no response, and right auditory brainstem response showed no waves. Main cause of this vertigo and right deafness was considered to be disturbance of inner ear due to ischemia of right labyrinthine artery, though this patient was not a typical case of the anterior cerebellar artery syndrome. Ischemic disturbances of inner ear have been reported only in patients with the anterior cerebellar artery syndrome, therefore this patient who had only acute ischemic disturbance of inner ear and did not have disturbance of caudo-lateral portion of the pons was considered to be very rare.
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PMID:[A case of ischemic disturbance of inner ear]. 259 43

We reported a 41-year-old male with paramedian thalamic and midbrain infarcts due to cerebral embolism from bilateral pulmonary arterio-venous fistula and primary medullary hemorrhage. The patient had an episode of sudden onset consciousness disturbance with left Weber's syndrome (right hemiplegia and left oculomotor palsy) and vertical gaze palsy at age of 23. He noticed numbness in the left hand and the left half body under clavicular when he had got up in a morning at age 41. He had headache and left tinnitus on second and third days, and on the 3rd and 4th days, he experienced nausea. He had severe hiccup persisting from the 6th to the 13th days. The 23rd days he was admitted to our hospital. He showed dysesthesia and paresthesia in left half body under clavicular, dysesthesia in left hand and vertical gaze palsy and convergence disturbance. MRI performed on the 18th and 24th days, disclosed hyperdense mass in T1 and T2-weighted images in dorsal site of medulla, but the 70th days MRI showed no abnormal lesions. Therefore we diagnosed the high intensity mass as primary medullary hemorrhage. Cerebral angiography showed no abnormal vasculature. Many members of his family had history of sever nasal bleeding. He had skin hemangioma and mucosal hemangioma in esophagus, stomach, colon and rectum, and bilateral pulmonary arterio-venous fistula which had been operated at age 39. His mother also had skin hemangioma and pulmonary arterio-venous fistula. Therefore this family was diagnosed Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia). MRI also disclosed multiple cerebral infarctions in bilateral thalamus, left cerebral peduncle and left cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Rendu-Osler-Weber syndrome presented paramedian thalamic and midbrain infarcts and primary medullary hemorrhage: a case report]. 269 33

A rare case with the episodes of vertebrobasilar TIAs which were caused by carotid ulcerative lesion and by persistence of proatlantal intersegmental artery is reported. This 69-year-old man was admitted on 14th Feb. 1985 with complaints of three attacks of vertigo, diplopia, nausea, vomiting and dysequilibrium lasting about 1 hour. His past history and family history were unremarkable. On admission, physical and neurological examinations revealed nothing particular, except bilateral carotid bruits. On the right side, innocent low pitched bruit was detected, however on the left side, carotid bruit was high pitched and was regarded as pathological. Blood pressure was 180/80 mmHg. Pulse rate was 66/min and cardiac arrhythmia was not detected by EKG. He also had no history of cardiac arrhythmia as mentioned above. CT scans and MRI showed only mild brain atrophy and no brain stem nor cerebellar lesions. Left carotid angiogram revealed ulcerative lesion of the common carotid bifurcation which was compatible with high pitched bruit. And at the level of the C2 vertebra, persistent proatlantal intersegmental artery originated from the left internal carotid artery which, after running upward, joined to the horizontal portion of the left vertebral artery above the atlas. Internal carotid and the vertebrobasilar vasculature beyond the proatlantal intersegmental artery were normal except slight irregularity of carotid siphon. Right carotid and vertebral angiograms revealed no abnormality and basilar artery was opacified clearly again via right vertebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of transient cerebral ischemia of the vertebrobasilar system caused by carotid ulcerative lesion and persistent proatlantal intersegmental artery: a case report]. 360 Sep 93

The development of new non-ionic magnetic resonance (MR) contrast media as gadodiamide injection increased the choice of paramagnetic contrast agents available in MR of the central nervous system (CNS). The purpose of our paper was to compare at the dose of 0.1 mmol/kg b.w. the safety of gadodiamide (Gd-DTPA-BMA) to gadopentetate dimeglumine (Gd-DTPA) and to gadoterate meglumine (Gd-DOTA) in two multicentric double-blind studies. A total of 551 patients were enrolled with 143 patients in the Gd-DTPA group, 132 patients in the Gd-DOTA group and 276 patients in the Gd-DTPA-BMA group. Safety was assessed by recording the adverse events up to 24 hours after the injection. One or more adverse events were recorded in 14% of the Gd-DTPA patients, in 15.1% of the Gd-DOTA patients and in 11.6% of the Gd-DTPA-BMA patients. These reactions were related to the contrast media in 9.1%, 13.6% and 8.7% of the cases respectively. Their intensity was defined as mild in 8.4% of the patients in the Gd-DTPA group, in 13.6% of the patients in the Gd-DOTA group and in 8.3% of the patients in the Gd-DTPA-BMA group. No severe reaction or death were recorded. An injection-site reaction (heat, coldness, pain) has been observed in 43% of the cases although an adverse event other than local reactions (headache, dizziness, nausea) has been noticed in 57% of the cases. No significant statistical difference was observed between the groups. Gadodiamide is a safe and effective contrast agent in MRI of the CNS in comparison with Gd-DTPA and Gd-DOTA currently in routine use.
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PMID:[Comparative studies of the tolerability of gadodiamide, dimeglumine gadopentetate and meglumine gadoterate in MRI tests of the central nervous system]. 747 75

Neurologic sequelae may occur months to years after cranial irradiation. The site of primary damage is probably the vascular endothelium. Over a 2.8-year period, four children with brain tumors, a mean of 11 years of age at diagnosis (range, 6.5 to 15.5 years), had new onset of severe intermittent unilateral headaches associated with nausea, episodic visual loss, hemiparesis, aphasia, or hemisensory loss. The headaches lasted 2 to 24 hours. All patients had previously received whole-brain (2,400 to 3,600 cGy) and additional local boost (1,800 to 3,100 cGy) cranial irradiation, as well as cisplatin-, lomustine-, and vincristine-containing chemotherapy regimens. Symptoms began 1.2 to 2.8 years after the diagnosis, when all had stable disease and were off treatment. MRI studies were unchanged, and CSF cytology, EEGs, echocardiograms, and magnetic resonance angiograms were normal in all. Cerebral angiograms, performed in three children, were normal but led to severe headaches and neurologic deficits (hemiparesis in one and visual loss in two) that resolved after 24 to 48 hours. Response to antimigraine and antiplatelet medications was variable. We conclude that (1) "complicated migraine-like episodes" may occur in children after cranial irradiation and chemotherapy as a sequela of therapy; (2) these headaches may not be the harbinger of impending strokes, severe intracranial vasculitis, or tumor recurrence; and (3) while cerebral angiography may be useful in differential diagnosis, it may cause transient worsening of symptoms.
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PMID:'Complicated migraine-like episodes' in children following cranial irradiation and chemotherapy. 747 78

A rare case of persistent primitive trigeminal artery variant (PTAV) with cerebellar ischemia is reported. A 23-year-old male complained of sudden dizziness and nausea after playing valley ball. CT scan and MRI on admission revealed no abnormal findings. Left carotid angiography demonstrated a PTAV anastomoting precavernous portion of left internal carotid artery to the left superior cerebellar artery. The 37 cases reported in literature were reviewed to characterise PTAV. Ninety-seven% of the cases arising from precavernous portion of internal carotid artery, and terminated in anterior inferior cerebellar artery in 73%, posterior inferior cerebellar artery in 13.5% and superior cerebellar artery in 13.5%. Approximately 22.2% of patients with PTAV have cerebral aneurysms. The hypotension or mechanical compression of PTAV on playing valley ball with poor vascular supply to the part of cerebellum possibly caused cerebellar ischemia in this case.
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PMID:[Persistent carotid-superior cerebellar artery anastomosis presenting with cerebellar ischemic attack: a case of persistent trigeminal artery variant]. 749 18


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