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The authors reported three cases, whose vertebral arteries had been injured by blunt trauma to the neck which was followed by cerebello-brainstem infarctions. Case 1: a 32-year-old man, who developed severe vertigo and nausea 7 days after a traffic accident. He showed neck pain and horizontal nystagmus on admission. Three days later, he became drowsy. CT scan of the head demonstrated right-side cerebellar infarction, and the angiography revealed an occlusion of the right vertebral artery at C4-5 level. After the removal of the right cerebellar hemisphere, he recovered neurologically and was discharged from the hospital, able to walk. Case 2: a 47-year-old man, who suddenly became comatose 6 hours after an accident. Plain CT demonstrated a highly dense basilar artery. Angiography revealed the occlusion of the left vertebral artery, and severe stenosis of the right vertebral artery. The basilar artery was not visualized. Anticoagulant therapy was started immediately. He survived, but he developed locked-in syndrome. Case 3: a 53-year-old man, who developed transient apnea after an injury. On admission, neurological examination showed horizontal nystagmus, weakness of his right upper limb, and sensory disturbance in the left side of the body. Neck traction was done for spinal C1 and C2 fractures. Twenty-one hours after the injury, he became comatose suddenly. The four-vessels angiography revealed the occlusion of both vertebral arteries. The basilar artery was visualized through the posterior communicating arteries. He died on the 6th day after the trauma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Blunt injury of the vertebral artery: report of three cases]. 259 54

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

A 46-year-old man developed sudden dysarthria and atactic gait and was noted to be unable to get up even on the bed about one year prior to his death. By following several days, he started to have scanning speech, nausea, trancal ataxia and dysmetria in succession. The cerebro-spinal fluid yielded moderate pleocytosis. There were no sensory disturbance, pathological reflexes and Romberg's sign. Half a year later, submandibular tumor was noted. The biopsy showed metastatic small cell undifferentiated carcinoma, presumably of pulmonary origin, and paraneoplastic cerebellar degeneration was suspected. He died of bronchopneumonia, superimposed on lung cancer on February 25 in 1979. The necropsy showed a large tumor in the right lung which was histologically verified small cell undifferentiated carcinoma (so-called oat-cell carcinoma). The cerebellum disclosed diffuse cortical atrophy, chiefly of Purkinje cell type. Moderate demyelination with reparative gliosis and foamy macrophages was seen in the white matter, which was considered secondary to cortical devastation. The morphometric study on Purkinje cell loss showed interesting distribution of the lesions. The severely affected portions were the central lobe and culmen in the vermis, and the ala lobuli centralis and quadrangular lobe in the hemisphere, respectively. The lingula was strikingly spared. The finding was compared with that of other cerebellar disease in reviewing the literature.
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PMID:[An autopsy case of carcinomatous subacute cerebellar degeneration--on distribution of cerebellar cortical lesions]. 609 6

Clinical features of cerebellar infarction in the territory of the superior cerebellar artery (SCA) were investigated in six male patients, ranging in age from 50 to 69 years. In all patients, there were MR images of infarction located in the area supplied by the SCA. The lesion was on the left-side in 2, right-side in 3 and bilateral (recurrent) in 1 patient. The onset of disease occurred with nausea, vomiting and floating sensation, with no overt brain stem signs other than symptoms of unilateral cerebellar ataxia and dysarthria. Five of the 6 patients had heart disease and cerebral angiography without definite evidence of SCA occlusion, strongly suggesting occlusion of the artery at its periphery due to cardiogenic embolism. A comparison of these 6 patients with those reported previously in Japan suggests that patients with SCA occlusion may be divided into two distinct subgroups: one manifesting diffuse brain stem signs in addition to cerebellar signs, and the other showing cerebellar signs as the only neurologic manifestation. In the former group, comprising the vast majority of patients, SCA occlusion occurred at the origin of the vessel due to a thrombus under a state of hypertension, diabetes mellitus or malignancy, producing signs of brain stem involvement, such as dissociating sensory disturbance and Horner's sign. While in the latter group, which included these 6 patients, paucity of brain stem signs, absence of definite cerebral angiographic evidence of SCA occlusion, and the presence of heart disease were distinguishing clinical features. Cardiogenic cerebral embolism was probably the underlying pathology in many of the cases and the functional prognosis was favorable.
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PMID:[Cerebellar infarction in the territory of the superior cerebellar artery, presenting a predominant cerebellar symptom--with special reference to its pathophysiology]. 761 47

A 40-year-old normotensive man suddenly developed diplopia, tinnitus and a burning sensation on the left side of his body while driving a motorcycle. He did not complain of headache, nausea or vomiting. Neurologic examination revealed left trochlear nerve palsy and impaired pinprick, temperature and joint position sensation of the left limbs. There was no ptosis or motor deficit. He had a mild bleeding diathesis due to alcoholic liver cirrhosis. Computerized tomography and magnetic resonance image of the brain disclosed hemorrhages in the right midbrain tectum and the left temporal lobe. After nine months of observation, there was nearly complete recovery of symptoms, except for mild residual diplopia. From a literature review, only nine case of midbrain tectal hemorrhage involving the inferior colliculus have been reported. These patients had a unique clinical presentation. Diplopia due to trochlear nerve palsy, either unilateral or bilateral, was present in all of the cases. Tinnitus and sensory disturbance contralateral to the lesion side were very common. Only three patients had risk factors for hemorrhage, including bleeding diathesis, hypertension and vascular anomalies. In the majority of patients, no underlying causes were detected. The outcome was favorable with conservative treatment.
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PMID:Midbrain hemorrhage presenting with trochlear nerve palsy. 1067 25

Functional dyspepsia is a symptom complex characterised by postprandial upper abdominal discomfort or pain, early satiety, nausea, vomiting, abdominal distension, bloating, and anorexia in the absence of organic disease. Gastrointestinal motor abnormalities, altered visceral sensation, and psychosocial factors have all been identified as major pathophysiological mechanisms. This perspective has now replaced the earlier view that the condition was the result of a sole motor or sensory disorder of the stomach. Future therapeutic strategies should be aimed at reducing nociception as well as enhancing the accommodation response.
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PMID:Pathophysiology of functional dyspepsia. 1207 69

We experienced a patient of CIDP who was twice complicated with aseptic meningitis following high-dose intravenous gammaglobulin therapy. The patient was a 29-year-old woman who first developed gait disturbance in September 1998. Neurological examination revealed muscle weakness and sensory disturbance in the distal parts of four extremities and decrease of deep tendon reflexes. Cerebrospinal fluid analysis revealed an elevated protein content and a normal cell count. Steroid therapy was effective in early stage, however, this effectiveness had been reduced gradually. She received high-dose intravenous gammaglobulin administrations in September 1999. On the fourth day after start of this therapy, she developed severe headache, nausea and nuchal rigidity without fever. Cerebrospinal fluid analysis revealed an increased cell count of mononuclear predominance and an elevated protein content. As bacterial culture remained negative and viral titers were not elevated, aseptic meningitis was diagnosed. The therapy was stopped, and thereafter her headache continued for 7 days. The muscle weakness and sensory disturbance were remarkably improved, but 9 months later, her symptoms became worse again. She received high-dose gammaglobulin administrations for 2 days in June 2000 and developed aseptic meningitis again. Over again, 9 months later, she received the same medication for only 1 day in March 2001 and she developed mild headache but not meningitis. Aseptic meningitis with CIDP following high-dose gammaglobulin therapy was rare, however, we should pay attention to this therapy in patients with CIDP and may prevent the occurrence of aseptic meningitis by reducing the total dose and shortening the administration periods of gammaglobulin.
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PMID:[A case of recurrent aseptic meningitis caused by high-dose intravenous gammaglobulin therapy for chronic inflammatory demyelinating polyneuropathy]. 1208 Jun 12

A-38-year-old man suddenly developed nausea, vomiting and vertigo during chiropractic neck manipulation. This was followed by right hemiplegia, right deep sensory disturbance and left hypoglossal nerve palsy, consistent with the medial medullary infarction (Dejerine syndrome). The MRI revealed infarction at left medial part of the medulla. The vertebral angiogram and MRA showed marked narrowing of the left vertebral artery. X-rays of the cervical spine showed no spondylosis, dislocation nor osteolysis of the odontoid process. The serological studies, including lupus anticoagulant, protein C, and protein S gave normal results. Although vascular accidents involving the brain stem after chiropractic neck manipulation have been reported since Pratt-Thomas and Berger, previous reports are still rare. In them lateral medullary infarction (Wallenberg syndrome) is probably the most common case. On the other hand, medial medullary syndrome (Dejerine syndrome) is absolutely rare. To our knowledge, the only one report has been made by Watanabe and his colleagues before our present case. The mechanism was suggested that rotation and tilting of the neck stretches and compresses the vertebral artery at the cervical joint causing injury to the vessel, with an intimal tearing, dissection, and pseudoaneurysm formation. Consequently, the present case may be caused by injury to the left vertebral artery with an intimal tearing during neck manipulation sufficient to cause disection and subsequent infarction of the brain stem.
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PMID:[The medial medullary infarction (Dejerine syndrome) following chiropractic neck manipulation]. 1268 91

A 68-year-old man presented with right eye pain and vertigo. Thereafter, he gradually leaned rightward, then laid down. He felt nausea and vomited. His right upper eyelid drooped and he felt dysethesia of the right hand. On neurological examination, ptosis of his right eye with slightly miotic right pupil, paresis of the right soft palate and hoarseness were noted. Arm deviation test demonstrated rightward deviation. He presented sensory ataxia of the right upper and lower extremities: finger nose test showed mild dysmetria of the right upper extremity, heel knee test demonstrated dysmetria of right lower extremity and these findings worsened when he closed his eyes. He showed mild bending of his bilateral ring and little fingers when he did rapid alternative movement. He leaned rightward when he sat and closed his eyes. Position sense of his right upper and lower extremities was decreased and sometimes he could not answer correctly when asked on which direction his finger pointed. Pinprick sensation was mildly decreased on the left side not including the face. Touch and vibration sense were normal. SEP findings on upper and lower extremity stimulation were normal. MRI of the brain showed T2 high intensity and partially T1 low intensity lesion at the right medulla (Figure). MR angiography showed no apparent lesion of major arteries such as dissection of the vertebral arteries. He complained and presented with hiccup initially. On MRI, the lesion was thought to involve the spinothalamic tract, medial lemniscus and inferior olivary nucleus. Ambiguus nucleus was in the lesion and solitary nucleus near the lesion. There is no report that seems to describe clinical features of a lesion like that in this case. Intermediate medullary infarction may present dissociated sensory disturbance like Brown-Sequard syndrome and position sensory disturbance without disturbance of vibration sense.
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PMID:[Intermediate medullary infarction: a case report]. 1609 22

The therapeutic efficacy and adverse reactions were compared between 14 patients who received TJ therapy using paclitaxel (PTX) and carboplatin (CBDCA) and 39 who received CAP therapy using cyclophosphamide (CPA), doxorubicin (DXR) and cisplatin (CDDP) as postoperative chemotherapy for cancer of the uterine body. In TJ therapy, PTX (175 mg/m(2)) and CBDCA (AUC 5) were administered on Day 1 (every 3 weeks), while in CAP therapy, CPA (500 mg/m(2)), DXR (40 mg/m(2)) and CDDP (50 mg/m(2)) were administered on Day 1 (every 4 weeks). Grade 3 or more severe hematotoxicity included leukocytopenia (incidence in the TJ and CAP groups: 71.4% and 64.1%, respectively), neutropenia (100%, 87.1%), thrombocytopenia (0%, 12.8%), and anemia (0%, 20.5%). No significant differences were noted between the two groups. Grade 3 or severe non-hematologic toxicities included nausea (0%, 15.4%) and vomiting (0%, 12.8%) with significantly higher incidence in the CAP therapy group (p=0.0000736, p=0.000736), peripheral sensory disturbance (7.1%, 0%) and arthralgia (7.1%, 0%) with significantly higher incidence in the TJ therapy group (p=0.00129, p=0.00000538). The survival rate and disease-free survival rate showed no significant differences between the two groups. TJ therapy is thought to be as effective as CAP therapy, and can be safely conducted, although precautions are required regarding arthralgia and neuropathy.
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PMID:[Adjuvant chemotherapy of paclitaxel plus carboplatin in uterine corpus cancer--comparison with cisplatin, adriamycin plus cyclophosphamide]. 1683 85


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