Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a 68-year-old man with anti-phospholipid antibody syndrome who presented slowly progressive pure motor monoparesis(PMM) in left upper extremity as a sign of cerebral infarction. He had history of hypertension and hyperlipidemia. He first noticed clumsiness in left fingers, then weakness of left fingers with drop hand developing gradually in 2 to 6 weeks. He began to feel difficulty in raising left upper arm in 8 weeks and was admitted to our hospital. On admission, he exhibited severe weakness in distal portion and moderate weakness in proximal portion of left upper extremity. Deep tendon reflexes were slightly hyperactive in left side. Muscle strength of right upper extremity and bilateral lower extremities were normal. There was no sensory and autonomic abnormality. Laboratory examination revealed high titer of anti-cardiolipin IgM antibody. Brain MRI demonstrated a small cortical infarction in the right precentral gyrus. Cerebral angiography revealed severe stenosis in right common carotid artery. Other examinations including EMG were unremarkable. PMM in left upper extremity was considered to be caused by the ischemic lesion in the precentral motor cortex. Slowly progressive course might be explained by the hypovolemic factor due to the marked stenosis in right common carotid artery, poor collateral circulation, and abnormal coagulation caused by anti-phospholipid antibody syndrome.
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PMID:[A case of antiphospholipid antibody syndrome with cerebral infarction showing slowly progressive pure motor monoparesis in unilateral upper extremity]. 1121 63

A case is reported of anterior cerebral artery dissecting aneurysm presenting with subarachnoid hemorrhage and cerebral infarction. A 50-year-old man presented with sudden onset of weakness of the left lower limb was admitted to our hospital. CT scan on admission showed a subarachnoid hemorrhage in the interhemispheric fissure and CT on the 6th day demonstrated a cerebral infarction on the right medial frontal lobe. A carotid angiogram 12 hours after the onset showed no aneurysmal lesion, but, the angiogram repeated 11 days after the onset revealed an aneurysmal dilatation with distal narrowing at the right A2-A3 segment. To prevent rebleeding, we performed a wrapping procedure through the interhemispheric route on the 18th day after onset. The postoperative course was uneventful. We reviewed 27 previously reported cases with symptomatic dissecting aneurysm confined to the anterior cerebral artery.
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PMID:[Spontaneous dissection of the anterior cerebral artery presenting subarachnoid hemorrhage and cerebral infarction: a case report]. 1134 13

A 60-year-old, right-handed man suffered from left hemiparesis with upper limb dominance. CT and MRI revealed cerebral infarction of the entire right middle cerebral artery territory. His hemiparesis recovered excellently and residual neurological deficits 6 years later were left hand weakness(grasping power 9 kg vs. 35 kg in the right) and clumsiness. Functional MRI was performed. During right(normal) hand grasping, activation was seen in the left sensorimotor cortex and supplementary motor area. During left(paretic) hand grasping, activation was seen in the left (ipsilateral) sensorimotor cortex, right parietal cortex, and bilateral supplementary motor areas. Near infrared spectroscopic imaging showed similar results. During right hand grasping, left sensorimotor cortex was activated, and during left hand grasping, bilateral sensorimotor cortices were activated with ipsilateral predominance. Transcranial magnetic stimulation of the left motor hand area evoked right hand movement and stimulation of a point near that area evoked ipsilateral left hand muscle movement. Thus, the findings of the three techniques consistently suggest that the recovery of left hemiparesis of this patient was promoted by motor cortical area reorganization including the ipsilateral motor cortex.
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PMID:[Hand motor cortical area reorganization following cerebral infarction evaluated with functional MRI, near infrared spectroscopic imaging, and transcranial magnetic stimulation]. 1159 83

We report a 72-year-old right-handed man who was diagnosed as having crossed aphasia. He had polycythemia, hypertension and an old cerebral infarction in the right occipital lobe. He was admitted to our hospital because of muscle weakness in the left extremities at the age of 71. In the laboratory data, red blood cells(689 x 10(4)/microliter) and platelets(87.6 x 10(4)/microliter) were increased in number. Brain CT detected a right putaminal hematoma and an old infarct in the occipital lobe on the right. After admission, he developed non-fluent speech, and impairments of auditory comprehension, writing and naming due to the infarction in his right cerebral hemisphere including the middle cerebral artery distribution. The standard language test of aphasia(SLTA) revealed marked impairments in the language function, except for reading kana and kanji words. This writing was severely impaired compared with other language dysfunctions. Auditory comprehension, repetition and reading were impaired at the sentence level rather than at the kana word level. Furthermore, he suffered from left hemiparesis and left unilateral spatial neglect. We diagnosed his impairments of language function as crossed aphasia based on his right-handedness, CT findings and the results of SLTA. His language center was considered to be located in both cerebral hemispheres. Compared with typical findings in reported cases of crossed aphasia, the presence of both non-fluent speech and mutism were consistent with previous observations. However, the marked impairments of auditory comprehension, repetition and naming were different. Polycythemia and hypertension were considered to be the risk factors of cerebral infarction in our patient.
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PMID:[A case of crossed aphasia in a dextral patient with polycythemia]. 1199 62

The aetiology of Hashimoto's encephalopathy is still unknown. A 52-year-old woman with so far unspecific thyroid disorder presented with acute onset of right-sided sensory loss and visual disturbances. The neurological examination revealed a right upper quadrant anopsia and subtle right-sided sensory loss and weakness. The cranial MRI showed a left-sided cerebral infarction. MR angiography demonstrated a stenosis of the proximal segment of the left posterior cerebral artery, which was confirmed by conventional catheter angiography. The patient had no cardiovascular risk factors, no signs of systemic vasculitis, and no thromboembolic disorder. Thyroid function tests showed a subclinical hypothyroidism with plasma TSH level of 12.0 mU/ml, and thyroid antibodies were markedly elevated (hTG-AB 3390 U/ml, TPO-AB > 8000 U/ml). Typical features of Hashimoto's disease were demonstrated by ultrasound and scintigraphic examination of the thyroid gland. To the best of our knowledge, this is the first description of Hashimoto encephalopathy with localised vasculitis of the posterior cerebral arteries and left posterior infarction. It could be shown that the MR angiogram is a feasible tool to demonstrate regression of the vasculitis under glucocorticoid therapy.
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PMID:[Circumscribed vasculitis with posterior infarct in Hashimoto encephalopathy]. 1259 32

Emery-Dreifuss muscular dystrophy (EDMD) is a muscular disorder characterized by 1) early contracture of the elbows. Achilles tendons and post-cervical muscles, 2) slowly progressive muscle wasting and weakness with a humeroperoneal distribution, and 3) life-threatening cardiomyopathy with conduction block. Most of families with EDMD show X-linked recessive inheritance with mutations in the STA gene on chromosome Xq28, which encodes a protein named emerin. A rare autosomal dominant form of EDMD (AD-EDMD) is caused by mutations in lamin A/C gene (LMNA) on chromosome 1q21. Both emerin and lamin A/C are located in the inner surface membrane of the nucleus. A 49-year-old woman was skinny and slow runner from childhood and suspected as having a certain muscular disorder. At 35 years, she was found to have the second degree atrioventricular block. At 45 years, she was admitted to a hospital for right-side hemiplegia after cerebral infarction. Cardiac involvement was also observed including high degree atrioventricular block with chronic atrial fibrillation and frequent paroxysmal ventricular contraction on the electrocardiogram. At 49 years, she was referred to our hospital for further evaluation. She had possible dilated cardiomyopathy with conduction block. She also had muscular atrophy and weakness in all extremities, predominantly in the right-side, and contracture of bilateral Achilles tendon, knee and elbow joints, and postcervical muscles. Biopsied skeletal muscle and electromyogram showed myopathic changes. Since a novel point mutation of Ser303Pro was found in exon 5 of LMNA gene, she was diagnosed as having AD-EDMD and had a permanent pacemaker implantation. Her daughter also had some abnormalities on electrocardiogram. This is the first Japanese case of AD-EDMD. Amiodaron was effective for non-sustained ventricular tachycardia. Early diagnosis and following cardiological examinations and treatments are important and necessary to improve the prognosis of the patients with EDMD.
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PMID:[The first Japanese case of autosomal dominant Emery-Dreifuss muscular dystrophy with a novel mutation in the lamin A/C gene]. 1242 64

We describe success with local thrombolytic therapy given to a patient 24 hours after onset of left middle cerebral artery (MCA) occlusion. A 53-year-old man was admitted 18 hours after onset of disorientation, motor aphasia, and right upper and lower limb weakness. Computed tomography (CT) showed an area of slightly decreased density in the deep left frontal white matter. A stable Xenon CT cerebral blood flow study revealed mildly decreased perfusion in the left MCA territory, which showed negative cerebrovascular reactivity. FLAIR method magnetic resonance images demonstrated an area of slight hyperintensity in the left frontal white matter. Angiography showed atherothrombotic left MCA occlusion. 24 hours after clinical onset of occlusion, we successfully performed local thrombolytic therapy with urokinase. The patient's neurological status improved immediately. While indications for local thrombolysis in cerebral infarction presenting more than 6 hours after onset have not been established, we experienced success in the present patient who presented 18 hours after onset.
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PMID:[Successful local thrombolytic therapy for atherosclerotic middle cerebral artery occlusion 24 hours after onset: case report]. 1261 56

Computed tomography (CT) is the initial radiological investigation of patients with an acute neurological event. A 64-year-old woman presenting with generalised weakness and headache for two days was diagnosed on CT to have subarachnoid haemorrhage. Digital subtraction angiography confirmed the cause to be a ruptured posterior communicating artery aneurysm. The patient was treated by neuroradiological intervention using occlusive coils. The CT features of subarachnoid haemorrhage are discussed. Accurate CT interpretation is essential to direct appropriate investigations and management in patients with stroke, particularly as acute cerebral infarction may occasionally mimic subarachnoid haemorrhage. The role of magnetic resonance (MR) imaging in evaluation of cerebral infarct is also discussed.
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PMID:Clinics in diagnostic imaging (91). Subarachnoid haemorrhage. 1500 3

We report on a 32-year-old woman who developed reversible cortical blindness and right-sided weakness after cesarean section at 36 weeks of gestation, due to preeclampsia. An initial brain MRI demonstrated high signal intensity lesions in the bilateral occipito-parietal and left frontal lobes on T2-weighted and diffusion-weighted imaging. All of the lesions showed low signal intensity on apparent diffusion coefficient (ADC) map, which were compatible with cytotoxic edema, and MR angiography (MRA) showed diffuse vasospasm of the intracranial vessels. A follow-up brain MRI showed that most of the lesions disappeared and the vasospasm also resolved. This case suggests that the cytotoxic edema in preeclampsia may evolve differently from the pattern in cerebral infarction and explains the relatively benign course of the neurological signs in preeclampsia.
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PMID:A case of reversible postpartum cytotoxic edema in preeclampsia. 1517 18

We report stroke in a 62-year-old woman who had been on hormone replacement therapy (HRT), estrogen plus progestin, for more than 8 years. She experienced two episodes of transient ischemic attack (TIA), manifesting as right-sided weakness, that persisted for 10-20 min. Magnetic resonance angiography (MRA) obtained before complete stroke, demonstrated severe stenosis of the left middle cerebral artery, without evidence of cerebral infarction. Twenty days after the TIA she suffered a complete stroke corresponding with the site of stenosis. Her protein S activity was low 29%. In the context of the recent findings of the US Women's Health Initiative, we concur that the safety of long-term HRT should be considered carefully, especially in women with a history of TIA and confirmed cerebral artery stenosis.
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PMID:Cerebral thrombosis in a postmenopausal woman on HRT. 1563 31


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