Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptomatic common carotid artery occlusion (CCAO) is rare. We studied 17 patients with ischemic cerebrovascular symptoms and unilateral CCAO on angiography to help clarify clinical and radiologic features. Mean age was 62 years; 65% were women. Predominant symptoms and signs included visual-ipsilateral monocular or retrochiasmal symptoms (88%), motor weakness (88%), sensory disturbance (59%), dizziness/lightheadedness (53%), and syncope (24%). Dysarthria, headache, or involuntary limb shaking occurred less frequently. Positionally related symptoms occurred in approximately two-thirds of the patients. TIAs were often multiple and preceded a stroke or occurred without subsequent stroke in 82%. Hemispheric TIAs contralateral to the CCAO occurred in 41%. Ten patients (59%) suffered stroke, seven (70%) of which were ipsilateral to the CCAO. Vascular risk factors included cigarette use (76%), hypertension (71%), diabetes mellitus (41%), and hyperlipidemia (41%); 82% had two or more risk factors. Known cardiac disease was present in 59%. CCAO was present at the origin of the vessel in most patients. Most had atherosclerotic narrowing of multiple extracranial large vessels. During follow-up, none of the patients had a spontaneous second infarct; five had TIAs, including two with amaurosis fugax, all in the CCAO territory. More restricted external carotid collaterals may, in part, explain the higher frequency of ipsilateral stroke and contralateral TIAs than reported for internal carotid occlusion.
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PMID:Common carotid artery occlusion. 279 68

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

We report clinicopathological features of a Japanese family with hereditary motor and sensory neuropathy associated with cerebellar atrophy (HMSNCA). Four affected members from a single generation were examined. They shared common clinical features, including insidious onset in teenage, slowly progressive cerebellar ataxia, amyotrophy, sensory disturbance, and dementia. In addition, all the patients showed hypoalbuminemia and hyperlipidemia and a marked atrophy of the cerebellum on magnetic resonance images. Autopsy of the proband revealed a severe loss of Purkinje cells, degeneration of posterior columns and spinocerebellar tracts of the spinal cord, and a marked loss of myelinated and unmyelinated fibers in the peripheral nerves. We consider that HMSNCA is a distinct form of hereditary multisystem neuronal degeneration.
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PMID:Hereditary motor and sensory neuropathy associated with cerebellar atrophy (HMSNCA): clinical and neuropathological features of a Japanese family. 966 74

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

A 52-year-old man with diabetes mellitus, hyperlipidemia and smoking habit, experienced transient ischemic attacks (TIAs) with symptoms of left orbital pain, left blepharoptosis and hoarseness lasting for five minutes on March 10, 1997. Subsequently, the same symptoms repeated once or twice daily. On March 28, he had dysphagia, numbness and disturbance of pain and temperature sensation (segmental dissociated sensory disturbance) on the right side of the body above the level of the Th10, the right upper limb and face. The deficits persisted for more than 24 hours. Angiographic studies revealed an occlusion of the left vertebral artery immediately after branching of the posterior inferior cerebellar artery. MRI demonstrated a hyperintense lesion on MRI T2 weighted image in the left lateral medulla. About three months after the completed stroke, he had six episodes of TIAs of left Horner's sign and hoarseness. To our knowledge, this is the rare case that had frequent TIAs presenting the Wallenberg syndrome before and after the onset of lateral medullary infarction. We speculate that the TIAs resulted from microembolism from the proximal end of occluted left vertebral artery and failure of the microcirculation in and around the lateral portion of the medulla oblongata.
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PMID:[A case with frequent episodes of transient ischemic attack presenting the Wallenberg syndrome before and after the onset of brain infarction]. 1042 53

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

We report 6 patients with Cheiro-oral syndrome (COS), with special reference to clinical features and responsible lesions. The time intervals from the onset of symptoms to arrival in our department were less than 24 hours in 3 patients, 2 days in 2, and 5 days in 1. All patients had subjective sensory disturbance involving the unilateral hand and ipsilateral perioral regions, and 4 patients presented with objective sensory disturbance. The body parts of tingling sensation tended to be larger than those of superficial sensory disturbance. Three patients developed motor disturbance including hemiparesis with or without ataxia, clumsiness of fine finger movements, and dysarthria. Magnetic resonance imaging revealed fresh infarctions around the thalamus, including lacunar infarctions in 5 patients and branch atheromatous disease in 1 patient. The lesion sites responsible for COS were ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei in the thalamus in 4 patients, thalamic pulvinar nucleus and medial geniculate body in 1, thalamic ventroposterior region-internal capsule-corona radiata in 1. Three patients had asymptomatic brain infarctions. Risk factors were hyperlipidemia, hypertension, diabetes mellitus, smoking, arteriosclerosis of the carotid artery, and polycythemia. In the convalescent stage, 5 patients suffered from residual sensory-motor disturbance, whereas 1 patient recovered from COS. COS has been attributed mainly to small infarctions in the thalamic ventroposterior nuclei. However, it is suggested that damage to ascending sensory fibers projecting to the thalamic VPL and VPM nuclei can cause COS. Because initial symptoms of COS are apt to be overlooked, early diagnosis and treatment are necessary to avoid residual sensory-motor disturbance.
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PMID:[A clinicoanatomical study of thalamic cheiro-oral syndrome]. 1652 19

Transient neurological attacks (TNAs) are attacks with temporary (< 24 h) neurological symptoms, and reported in 1975. Ischemic cerebral infarction often occurres after transient neurological symptoms which are not sometimes involved in transient ischemic attack (TIA) criteria. The purpose of this study was to clarity transient neurological symptoms before the onset of ischemic stroke. Consecutive acute stroke and TIA patients within 7 days of onset between July 2011 and December 2012 were studied. Questionnaire survey of transient neurological symptoms was done and we investigated the history of transient neurological symptoms and divided the patients into three groups, TIA group (history of TIA), TNAs group (history of TNAs), and no past history group. We compared clinical characteristics, the rate of posterior circulation lesions, and number of attacks among three groups. 184 patients (male 112 patients, mean 73 years old) were enrolled into the present study. TNAs group had 13 (7%) patients, and TIA had 20 (11%). Neurological symptoms of TNAs group were 5 (38%) transient dizziness, 3 (23%) disturbance of consciousness, 2 (23%) weakness of legs, 1 (8%) sensory disturbance of legs, 1 (8%) gait disturbance, and 1 (8%) sensory disturbance of lips. Five (38%) TNAs group had multiple attacks. In 33 transient neurological symptom patients, 17 (52%) patients did not have hospital visit, and 7 (21%) patient did not have antiplatelet and anticoagulant drug. TNAs group more frequently had hyperlipidemia, diabetes mellitus, and posterior circulation lesions among three groups. 20% posterior circulation lesion patients had TNAs history, and posterior circulation might be examined in TNAs patients.
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PMID:[Importance of transient neurological attacks (TNAs)]. 2499 Aug 31