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Arteriovenous (AV) fistulas of cerebral and spinal arteries are characterized angiographically by an immediate AV transition without a capillary bed or "nidus" as occurs in AV malformations (AVM's). The clinical presentation, morphology, radiology, and treatment of 12 patients with cerebral AV fistulas and of 12 patients with spinal AV fistulas are reviewed. In the patients with cerebral lesions, headache and seizure disorders were the most common presentations followed by subarachnoid hemorrhage, cardiac failure, progressive neurological dysfunction, and incidental detection on prenatal ultrasound study. In patients with spinal AV fistulas, weakness and sensory disturbance in the lower extremities were the most frequent clinical presentations followed by back pain, disturbances of micturition, and grand mal seizure. The etiology of the symptom complex produced by AV fistulas in each of these locations differed, with venous hypertension being important in spinal cord lesions. Of the patients with cerebral lesions, nine had a single AV fistula, one had two fistulas, and two had multiple fistulas. An AVM was observed in five patients with fistulas (two large, three small). Nine patients exhibited extramedullary AV fistulas of the spine, of whom eight had a single fistula and one had three fistulas; three patients had intramedullary spinal AV fistulas. An arterial aneurysm was found in association with two fistulas, one cerebral and one spinal. Venous ectasias or varices, frequently exhibiting mural calcification, were observed to be prominent in all AV fistulas involving cerebral arteries and in two involving spinal arteries. The location and size of the venous complexes reflected the diameter of the fistula. In addition to conventional imaging techniques (cerebral angiography, computerized tomography, and magnetic resonance (MR) imaging), MR angiography was a helpful adjunct in the evaluation of fistulas. Treatment strategies employed for AV fistulas in both locations included open surgical and endovascular procedures, frequently used in combination. A satisfactory outcome was observed in all patients.
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PMID:Arteriovenous fistulas of the brain and the spinal cord. 827 Oct 12

Myelopathy is a rare central nervous system manifestation in systemic lupus erythematosus (SLE). We present a case of SLE, who developed motor paralytic bladder and various other neurological abnormalities. A 29-year-old female with SLE was admitted to our hospital because of complete dysuria without any troubles on defecation. Accelerated hypertension had been noticed 2 weeks before the admission. Physical examinations revealed that she had muscle weakness in right brachial biceps, bilateral carpal extensor and flexor, and flexor muscles of bilateral lower extremities. Slight sensory disturbance was present on her soles. Bilateral Chaddok and Babinski's signs were positive. Electromyographic studies including nerve conduction velocities of her limbs were normal, however, neurogenic discharges were observed in anal sphincter muscles. Cystometry demonstrated atonic bladder, but any pathological findings such as lupus cystitis and interstitial cystitis were not observed in the biopsied specimens from her bladder. Antibodies to single-stranded DNA, U1 RNP, Sm and SS-A/Ro were positive in her serum, and lupus anticoagulant and anticardiolipin antibodies (IgG) were also detected. In her cerebral spinal fluid (CSF), elevated protein level and albuminocytologic dissociation were recognized, while glucose level was low. Magnetic resonance imaging (MRI) study detected high signal intensities in the inner part of medulla oblongata and in the spinal cord at second lumbar spine level. After two courses of methyl-prednisolone pulse therapy, the patient's neurological symptoms including dysuria had completely recovered and abnormal findings previously observed on MRI had also disappeared. After 7 months of the episode, she became normotensive. The proteins and glucose levels in her CSF had gradually returned to normal. Among patients with SLE, correlations of antiphospholipid antibodies with myelitis/myelopathy or accelerated hypertension have been reported. Therefore, possible roles of antiphospholipid antibodies were considered in the pathogenesis of neurologic abnormalities observed in our patient. In addition, low glucose level in CSF might be a good indicator for the diagnosis of lupus-associated myelopathy.
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PMID:[A case of systemic lupus erythematosus with various central and peripheral neurological disorders presenting with motor paralytic bladder as a major manifestation]. 859 61

Clinical features of the anterior inferior cerebellar artery (AICA) territory infarcts were investigated in ten patients, ranging in age from 38 to 76 years. In all patients, there were MR images of infarction located in the area supplied by the AICA. The lesion was on the left side in 6 patients and right side in 4. The lesion of brain stem including the middle cerebellar peduncle was found in 7 patients and that extended to the cerebellum was in 3 patients. The main ipsilateral neurological signs were the VII and VIII cranial nerves palsy and cerebellar ataxia. The V and VI cranial nerves palsy. Horner's syndrome, and dysphagia were also present. The main contralateral sign was superficial sensory disturbance, but no hemiplegia. The underlying pathology included chiefly hyperlipidemia, hypertension, and diabetes mellitus. Cerebral angiography was performed in 8 patients, most of which was observed severe arteriosclerosis suggesting poor hemodynamics in the vertebral and basilar arteries. The prognosis was relatively good, but the VII, VIII, and V cranial nerves palsy and contralateral superficial sensory disturbance remained as the sequelae. As mentioned above, there were various neurological findings and MR images in AICA territory infarcts. Especially there were some patients whose lesion extended to the upper medulla and neurological findings were similar to the Wallenberg syndrome. It is important that one investigates not only axial slices but also coronal slices of MR image to estimate the extension of AICA territory infarct.
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PMID:[Clinical features of anterior inferior cerebellar artery territory infarcts--a study of ten patients]. 904 27

Acute infarction confined to the territory of the white matter medullary arteries is a poorly characterised acute stroke subtype. 22 patients with infarction confined to this vascular territory on CT and/or MRI were identified from a series of 1,800 consecutive admissions to our stroke unit (1.2%) between August 1993 and March 1997. 19 patients had small infarcts (< 1.5 cm maximum diameter) and 3 large infarcts (> 1.5 cm). Small infarcts were associated with a history of smoking (69%), hypertension (58%), and hyperlipidaemia (37%), and less frequently with atrial fibrillation (21%). Significant (>50%) ipsilateral carotid stenosis (16%) was a less frequent finding in this group. Patients most commonly presented with weakness and/or sensory disturbance affecting mainly the upper limbs, but dysarthria, dysphasia, and ataxia were also seen. Large infarcts were infrequent in our series, but did not differ significantly from small infarcts with respect to clinical presentation or risk factor profiles (p > 0.05 for all comparisons). The majority of symptomatic patients with white matter medullary infarcts are associated with small (< 1.5 cm diameter) lesions and a risk factor profile consistent with small vessel disease. More data are required to elucidate the mechanism of larger (> 1.5 cm) infarcts. Because of the potential overlap between white matter medullary infarcts and internal watershed infarcts, suggested criteria for each are presented.
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PMID:White matter medullary infarcts: acute subcortical infarction in the centrum ovale. 971 27

We report a 40-year-old man with hypertension and diabetes mellitus, who had crossed oral-pedal sensory disturbance in lateral medullary infarction. He suddenly developed dysesthesia in the right mount and the left leg. His blood pressure was 150/90 mmHg. Neurological examination showed Horner's sign in the right eye and horizontal nystagmus. Sensory function revealed decreased temperature, hypalgesia and dysesthesia in the right mouth and the left leg. Vibratory and position sense were normal. T1- and T2-weighted images disclosed a low and high signal intensity area in the lateral portion of the right medulla oblongata, respectively. Brain and neck MRA using time-of-flight sequence revealed no obvious abnormal structures. We have diagnosed him as lateral medullary infarction. The unique topography of sensory dysfunction thought to be attributed to a far-lateral lesion in the medulla oblongata. Our patient suggests that lateral medullary infarction causes variable patterns of sensory disturbance. Thus, lateral medullary infarction should be warranted when we encounter patients with miscellaneous distribution of sensory impairment, such as crossed mouth-foot hypalgesia.
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PMID:[Sensory disturbance of crossed oral-pedal topography in a case of lateral medullary infarction]. 984 55

Clinical pictures of medial medullary syndrome are variable, depending upon the extent of the lesion. Facial palsy has rarely been observed even in medullary infarction. However, central-type facial palsy is usually found contralaterally to the infarct area at the level of the rostral medulla. In the present report, we discuss the pathogenesis of the neurological manifestations in a 57-year-old man with hypertension. The patient presented with mild left facial palsy of central type, right hemiparesis, paresthesia, with deep sensory disturbance of the right extremities. An MRI of the brain showed an infarction localized in the medial region of the left upper medulla. Although the exact course of the supranuclear facial pathways remains controversial, the ipsilateral central facial palsy in this patient is considered to have two possible causes: the interruption of aberrant fibers of the corticobulbar tract, which branch off and swing back at the level of the upper-middle medulla, or the disruption of recurrent ascending fibers from the contralateral pyramidal tract, through decussation.
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PMID:[Ipsilateral central-type facial palsy and contralateral hemiparesis associated with unilateral medial medullary infarction: a case report]. 991 22

1. We examined 156 patients 33 years after CO poisoning occurred at the Miike Mikawa Mine, Fukuoka, Japan. The subjects were classified according to age as follows: between 55 and 59 years (n = 14), 60 and 69 years (n = 62), 70 and 79 years (n = 60), and 80 and 87 years (n = 18). The mean age was 69.2 years old. Concerning the duration of coma that occurred soon after the accident, 64 remained comatose from 0 to 6 hours, 46 from 6 to 12 hours and 46 from 12 to 48 hours. 2. Subjective symptoms were observed in 96.8% of the patients. Among them, forgetfulness was noted in 89.7%, followed by irritability in 66.7%, headache in 59.6%, insomnia in 55.8%, limb pain in 46.8%, dull head feeling in 42.9% and dizziness in 36.5%. 3. Intellectual disturbances were observed in 68.6% of the patients, including impression disturbance in 58.3%, memory disturbance in 51.9%, calculation disturbance in 63.5%, thinking disturbance in 61.5% and disorientation in 14.1%. 4. Apathy and disorder of volition and interest which were found in 72.4% were included in personality change because all symptoms persisted for many years. Personality change was classified as follows: weakness of emotion and will (hypobulia) in 54.4%, infantilism in 35.2%, hyperactive, talkactive and lack of inhibition in 18.5%, lack of self-possession and unstable temper in 9.6%, depression in 15.3%, neurosis in 7.6% and schizophrenic state in 2.5%. Among these symptoms of personality change, weakness of emotion and will and infantilism were conspicuous among the patients who remained in a coma for more than 6 hours soon after the accident but showed no relationship with age. 5. Neurological symptoms that were found in 48.7% of the patients were classified as sensory disturbance in 25.6%, peripheral nerve symptoms in 16.0%, pyramidal symptoms in 14.1%, ataxia and cranial nerve symptoms in 7.1%, paroxysmal symptoms in 6.4% and focal symptoms in 4.5%, extrapyramidal symptoms in 21.8% (Parkinsonism in 4.5%, tremor in 10.9% and muscle rigidity in 16.0%) and vegetative symptoms in 37.2%. 6. At the time of investigation, 5 CO poisoning patients were classified as serious cases (3.2%), 20 as comparatively serious (12.8%) medium-degree cases, 28 as comparatively mild (17.9%) medium-degree cases, 37 as comparatively serious (23.7%) mild cases, 42 as comparatively mild (26.9%) mild cases, 24 (15.4%) as having symptoms which were not problematic, and 24 (15.4%) as having symptoms that markedly worsened due to complication. 7. A total of 138 (88.4%) cases had complications were classified as follows: 78 cases (50.0%) of hypertension, 62 cases (39.7%) of cerebral infarction, 24 cases (15.4%) of cardiac disturbance, 21 cases (13.5%) of diabetes mellitus, 14 cases (9.0%) of hepatic disturbance and six cases of silicosis (3.8%). 8. Cranial MRI was carried out for 129 cases (82.7%). Of the abnormal findings identified, cerebral atrophy accounted for 72.0% (93 cases), including moderate and severe cases in 47.2% (61 cases), pallidum lesion for 37.9% (49 cases), lacunar infarction (including cerebral infarction) for 52.7% (68 cases), and hippocampal atrophy for 18.6% (24 cases). Many cases of cerebral atrophy and hippocampal atrophy were observed in patients who remained in the initial coma for more than 12 hours and were 80 years of age or old. The cases of pallidum lesion were observed in patients who remained in the initial coma for more than 6 hours, and no relationship with age was found. The other findings, cerebral atrophy and lacunar infarction showed a slight relationship with age. 9. Among the moderate and serious cases of intellectual disturbance, cerebral atrophy constituted to 62.5%, lacunar infarction 68.7% and pallidum lesion 50.0%. Among the moderate and serious cases of personality change, cerebral atrophy constituted 78.5%, lacunar infarction 35.0% and pallidum lesion 50.0%. Moreover, among extrapyramidal symptoms, pallidum lesion constituted 58.6%, cerebral atrophy 55.1% and lacun
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PMID:[Long-term follow-up study on sequelae of carbon monoxide poisoning; serial investigation 33 years after poisoning]. 1050 96

A 68-year-old right handed man with treated hypertension presented with acute-onset somnolence without hemiparesis, dysarthria or sensory disturbance. Although he became laconic and his verbal responses were only in short terms, his replies were accurate and judgmental. A cranial MRI in axial, coronal, and sagittal section revealed small hemorrhagic infarcts essentially limited to the bilateral capsular genua without involvement of the inferior thalamic peduncles. A 123I-IMP single photon emission CT disclosed remarkable hypoperfusion in the bilateral frontal cortex. After a week of somnolence, he gradually became wakeful, but was still abulic. Neuropsychological examinations revealed no memory disturbance. We consider that disconnection of the thalamo-frontal projection at the genua of the internal capsules caused somnolence, apathy, and abulia in our case. The hitherto reported cases of the genu infarcts that showed memory disturbance had the lesion involving both the inferior thalamic peduncle and its nearby mamillothalamic tract. In contrast, our case without memory disturbance had infarcts confined to the genua apparently sparing the two tracts, implicating that memory function may be preserved when such structures are intact.
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PMID:[A case of abulia without memory disturbance due to infarction of the bilateral genua of the internal capsules]. 1054 18

We report a patient with a dissecting aortic aneurysm associated with polymyalgia rheumatica (PMR). The patient is a 55-year-old Japanese man without a history of hypertension, diabetes mellitus and syphilis. He was admitted to an emergency hospital because of severe back pain, and was diagnosed as having a dissecting aneurysm of the descending aorta. After the admission, he began to notice severe muscle pain in his bilateral shoulder. Although his back pain gradually improved, his muscle pain progressively worsened, and his lower extremities were also involved. Then, he was introduced to our hospital. On neurological examination, he was alert and oriented. His cranial nerves were all intact. There was no muscle weakness nor sensory disturbance. Laboratory studies revealed that his erhythrocyte sedimentation rate was extremely high without elevation of the serum level of creatine phoshpokinase, rheumatoid factors and c-reactive protein. He was diagnosed as having PMR, and oral administration of prednisolone++ was started. Within several days, his muscle pain dramatically disappeared. As is known, there is a close relationship between PMR and temporal arteritis of giant cell arteritis. In general, PMR is a benign disease and responds well to steroid therapy, and prevalence of the giant cell arteritis is low in Japanese people. However, it should be kept in mind that the dissecting aneurysm is a relevant, severe complication of PMR because arteritis can be latently present in PMR.
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PMID:[The dissecting aortic aneurysm associated with polymyalgia rheumatica: a case report]. 1065 1

We reported a case of simultaneous medullary hemorrhage and hematomyelia. A 93-year-old woman, who had hypertension, was admitted to our hospital because of headache, numbness and weakness of the left extremities, and somnolence. On admission, weakness and disturbance of tactile sensations were observed in the left extremities. Magnetic resonance imaging showed medullary hemorrhage and hematomyelia and these two lesions were separated. Medullary hemorrhage was at the left dorsal paramedian area within mid-lower medulla oblongata, and hematomyelia was at the left side of the gray matter from medullo-cervical junction to upper cervical cord. Five days later from admission, weakness occurred in the right lower extremity and also in the upper extremity. This process suggested that the main lesion of tetraparesis was medullo-cervical junction. Review of 16 cases of medullary hemorrhage demonstrated that frequent neurological signs were palatal weakness, nystagmus, and disturbance of pain and temperature sense. But our case showed only disturbance of tactile sensations. Review of 19 cases of hematomyelia demonstrated that frequent neurological signs were sensory disturbance, paralysis and localized pain. Our case showed only paralysis. The cause of simultaneous hemorrhage was considered arteriovenous malformation or simultaneous multiple hypertensive hemorrhages.
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PMID:[A case of simultaneous medullary hemorrhage and hematomyelia]. 1065 65


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