Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
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We reported a case of juvenile cerebral infarction following minor head injury. The patient, a 12-year-old girl, developed right hemiparesis and aphasia almost immediately after having fallen from about 1 meter height during the exercise class at school. CT and MRI study showed lacunar lesions bilaterally and almost symmetrically in the paraventricular deep white matter on both sides. A new stroke area, responsible for the symptoms, was recognized about 24 hours later on CT scan just next to the lacuna of the left side. Although angiography revealed a rare anomaly of the right side aortic arch, associated with subclavian steal phenomenon, presumably of congenital in nature, no abnormality was found in the intracranial vessels. She made a rapid recovery during her hospital stay and showed no more than a slight motor weakness in her right upper extremity on discharge. The literature was reviewed on the embryology of the aortic arch and brachiocephalic arteries. We speculate that the lacunar lesions found bilaterally are dilated large normal Virchow-Robin space, and the pathogenesis of the stroke in this patient was discussed.
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PMID:[A pediatric case of cerebral infarction following minor head injury presenting interesting neuroradiological findings]. 893 87

We reported a case of adult moyamoya disease showing acute deterioration in which a unilateral occlusive lesion progressed to bilateral involvement during a period of 49 months. A 54-year-old male suffered from progressive weakness in his right extremities and disturbance of speech. On admission, neurological examination demonstrated mild right hemiparesis with global aphasia. A computed tomography (CT) scan showed a strange low density area in the territory of the left ACA and frontal branches of the left MCA. Left carotid angiography showed stenosis of the ICA at the terminal portion, occlusion of the ACA and MCA at each origin, and basal moyamoya vessels. Right carotid angiography demonstrated no occlusive lesions except for the general narrowing of the right ACA, without moyamoya vessels. This case was classified as adult-onset "probable" moyamoya disease according to the diagnostic criteria of the Japan Cooperative Research Committee. Left superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis was performed. The patient showed gradual amelioration of neurological symptoms, and was discharged on foot with mild motor aphasia. However, 4 years later he complained of weakness in his left lower extremity. A second cerebral angiography, performed 49 months after the initial angiography demonstrated severe stenosis of the left ICA at the terminal portion progressing in the proximal direction with decreasing basal moyamoya vessels, while severe stenosis extended from the terminal portion of the right ICA to the M1 portion with newly developed moyamoya vessels in the right basal area. At this time, we considered that this case was a definite case of moyamoya disease. The second cerebral angiography was completed uneventfully. However, the patient then suddenly showed acute deterioration 5 hours after the angiography. Emergent cerebral angiography disclosed an occlusion of the right ICA at the terminal portion. Thereafter he showed acute deterioration in consciousness. A CT scan at the time revealed a huge low density area in the territory of the right ACA and MCA. We performed emergent external decompression, but he did not recover from the sequelae of cerebral infarction and died 3 days later. This rare case suggested the possibility of progression to bilateral involvement although it was a case of adult-onset "probable" moyamoya disease. We consider that acute ischemic deterioration should be kept in mind especially in aged cases of adult-onset moyamoya disease. Careful observation should be performed by the serial MR angiography in adults with "probable" moyamoya disease even though they are clinically asymptomatic.
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PMID:[A case of adult moyamoya disease showing fulminant clinical course associated with progression from unilateral to bilateral involvement]. 899 Apr 73

We report four cases of difficult defaecation and/or faecal incontinence revealing a neurologic disease. These anorectal symptoms were associated with urinary disorders, but urinary symptoms always appeared several years after anorectal complaints. Clinical neurologic examination immediately led us to suspect a neurologic aetiology in two patients with the following signs: perineal hypoesthesia, absence of voluntary anal contraction and anal reflexes in one subject (final diagnosis: L1 neurinoma), and in the other a weakness in both thighs with absent tendon reflexes in the four limbs (final diagnosis: amiodarone neuropathy). In the two other patients with multiple cerebral infarction or multiple system atrophy, the neurologic aetiology was suspected on the absence of anal voluntary contraction contrasting with a normal perineal anatomy, but the final diagnosis was made only two years later when orthostatic arterial hypotension occurred.
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PMID:Difficult defaecation and/or faecal incontinence as a presenting feature of neurologic disorders in four patients. 905 87

A 34-year-old male with a history of angina pectoris suddenly developed weakness in the right upper and lower limbs, and consulted our hospital. Computed tomography (CT) and magnetic resonance imaging (MRI) suggested cerebral infarction. Cerebral angiography revealed stenosis at the M1 portion of the left middle cerebral artery. Hypertension, diabetes, tobacco or hyperlipidemia were not considered as risk factors for cerebral infarction. The lipoprotein (a) [Lp(a)] level was high. In the present case, medication with a nicotinic acid agent, niceritrol, for hyperlipoproteinemia and low density lipoprotein (LDL) apheresis were performed. Concerning family history, the patient's mother and younger sister had hyperlipoproteinemia. Recent studies have reported that increased Lp(a) levels are an independent risk factor even in cerebral infarction and coronary artery disease. Measurement of Lp(a) levels and treatment for increased Lp (a) levels may be important.
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PMID:[Juvenile cerebral infarction with familial hyperlipoproteinemia (a)--case report]. 916 61

Cardioembolic cerebral infarction is a subtype of stroke with a high mortality. The purpose of this study was to determine predictors of in-hospital mortality in 231 consecutive patients with cardioembolic stroke by means of a multivariate analysis. Three predictive models were constructed. A first model was based on demographic, anamnestic and clinical variables collected at the bedside examination (total 8 variables). A second model was based on clinical and neuroimaging variables (total 10 variables). A third model was based on the aforementioned clinical and neuroimaging variables and the presence of early recurrent embolism (total 11 variables). Deteriorated level of consciousness, limb weakness, presence of congestive heart failure, male gender, and age appeared to be independent prognostic factors of in-hospital mortality in the predictive model based on clinical variables and in the predictive model based on clinical and neuroimaging variables. In addition to these variables, early recurrent embolization was selected in the third predictive model. In the first two models, setting a cut-off point of 0.50 for predicting vital status at hospital discharge resulted in a sensitivity of 60%, a specificity of 89% and a total correct classification of 81%. The corresponding values of the third model were 62, 89 and 81%, respectively. These data may help clinicians to establish an early prognosis of this stroke subtype more accurately as well as to allocate patients with cardioembolic stroke in clinical trials correctly.
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PMID:Predictive clinical factors of in-hospital mortality in 231 consecutive patients with cardioembolic cerebral infarction. 964 75

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

Foix-Chavany-Marie syndrome (FCMS) is a syndrome that presents facio-pharyngo-glosso-masticatory diplegia with automatic voluntary dissociation. Its most common etiology is stroke in the regions of bilateral opercula. We described a 75-year-old woman with FCMS and crossed aphasia. She had cerebral infarction of left middle cerebral artery territory 23 years before. At that time she had transient right hemiparesis, but no aphasia. This time, she suddenly became mute and was brought to our hospital. Neurological examination revealed severe weakness in her bilateral lower face, pharynx, tongue, and sternocleidomastoideus. She had no weakness of limbs. Her listening comprehension was moderately disturbed and handwriting was paragraphic. Her emotional facial movement was maintained despite of disturbed volitional facial movement. CT scan disclosed fresh infarction at the right corona radiata and old infarction at the left middle cerebral artery territory. In this patient, lesions at the left operculum and right corona radiata with the preserved right operculum gave rise to FCMS. This implies following possibilities: 1) the corticobulbar tract and corticospinal tract run separately at the corona radiata, 2) volitional and emotional tracts of facial movement run separately at the corona radiata. It was demonstrated that FCMS is not always caused by bilateral operculum lesions. Our patient did not show aphasia after the first stroke including left language area, but became severely aphasic after the right corona radiata infarction. Simultaneous occurrence of FCMS and aphasia after corona radiata lesion suggested that the corticobulbar tract and a tract that conducts linguistic information are running adjacently in the corona radiata. Our case suggested that restricted corona radiata lesion may cause severe subcortical aphasia and in case of additional contralateral corticobulbar tract lesion, severe dysarthria may occur.
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PMID:[A case of Foix-Chavany-Marie syndrome and crossed aphasia after right corona radiata infarction with history of left hemispheric infarction]. 1020 73

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

Primary lymphoma of the thyroid gland is rare. The histopathology of most low-grade thyroid lymphomas is of a mucosa-associated lymphoid tissue (MALT) type. A typical feature of this type of lymphoma is a close lymphocyte-epithelium interaction. It tends to appear in patients with a history of autoimmune disease or chronic inflammatory disorders. A clinical picture of hypothyroidism may be present. Hyperthyroidism associated with thyroid lymphoma is also rare. Thyroid lymphoma could be misdiagnosed as lymphocytic thyroiditis or small cell anaplastic carcinoma. It is rarely reported in patients with Down's syndrome. In this report, we describe a Down's syndrome patient with MALT thyroid lymphoma and cerebral infarction. The patient, a 42-year-old man, presented with chest discomfort and bilateral leg weakness of one week's duration. Physical examination of his neck showed a right-sided mass lesion. Neurologic examination revealed decreased muscle power and hyperreflexia in both lower legs. Babinski's sign was present bilaterally. Endocrinologic studies showed subclinical hypothyroidism. A thoracolumbar radiograph showed disc space narrowing. Thyroid sonography revealed a hypoechoic mass lesion in the right lobe of the thyroid gland. Fine needle aspiration cytology of the neck mass demonstrated a large amount of lymphocyte infiltration. An I131 thyroid scan and 24-hour uptake revealed the possibility of thyroid malignancy at the upper poles of both thyroid lobes. Computerized tomography of the brain revealed a lacunar infarct in the posterior aspect of the left putamen. Magnetic resonance imaging of the lumbar spine revealed a healed L4 compression fracture with L4-5 retrolithesis. The patient later underwent a right total thyroidectomy. The pathologic finding showed MALT lymphoma. The patient received steroid suppression therapy, and after nine months of treatment and follow-up, he developed clinical hypothyroidism. Neither local tumor recurrence nor distant metastasis was found.
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PMID:Down's syndrome with mucosa-associated lymphoid tissue, thyroid lymphoma and cerebral infarction. 1074 21

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


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