Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present survey, we investigated the side effects of anticonvulsants in 248 epileptics who had been taking medicine for a long time. About half of the patients had been given anticonvulsant treatment for more than 11 years. The main results were as follows: Subjective symptoms: many kinds of gastrointestinal symptoms, general fatigability and sleepiness. slight pain in bones, joints or muscles and headache were found. Neurological symptoms: finger tremor at rest, diminished or decreased ankle reflex, and cerebellar symptoms such as ataxic gait, dysarthria, nystagmus and diplopia were found. Other clinical symptoms: gingival hyperplasia, hirsutism, dermatitis and edema were observed. Biochemical examinations: indicated that the total bilirubin was decreased in 4.4%, serum AL-P was elevated in 26.2%, the total serum cholesterol increased above 200 mg/dl in 17.7% and decreased below 150 mg/dl in 8.9%, and serum P and K were reduced in 31.5% and 2.4%, respectively. Hypocalcemia was found in only four cases (1.6%). Hematological examinations: serious disturbances were not found in hematopoietic functions, although prothrombin time was delayed in 18 of 40 patients examined.
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PMID:Study of the side effects of long-term anticonvulsant treatment. 721 11

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80

BACKGROUND Antiphospholipid antibody syndrome (APS) is a systemic autoimmune disease associated with arterial and venous thromboembolism and pregnancy complications. There have been several reports of APS with systemic lupus erythematosus (SLE) complicated with aortic dissection. However, none of them has been primary APS, which is APS without SLE. CASE REPORT A 42-year-old woman with primary APS and APS nephropathy on warfarin and aspirin therapy presented with coma due to cerebellar hemorrhage. The effect of warfarin was immediately reversed with prothrombin complex concentrate. We performed emergent evacuation of the hematoma, and her level of consciousness improved to normal on postoperative day (POD) 1. She had acute hypertension on arrival, which was resistant to multiple antihypertensives and was stabilized on POD 3. She also had exacerbation of chronic kidney disease after using contrast and prothrombin concentrate complex, and was on temporary renal replacement therapy from POD 3. Aortic dissection was found accidentally on echocardiography on POD 7, and she was subsequently treated medically. She was transferred to the rehabilitation hospital with mild dysarthria and truncal ataxia on POD 59. CONCLUSIONS We report the first case in the English literature of primary APS complicated with cerebellar hemorrhage and aortic dissection. Acute hypertension following hemorrhage and exacerbation of APS nephropathy likely triggered the dissection of the aortic wall, the integrity of which might have been compromised by longstanding antiphospholipid antibody and vasa vasorum thrombosis.
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PMID:Primary Antiphospholipid Antibody Syndrome Complicated with Cerebellar Hemorrhage and Aortic Dissection: A Case Report. 3182 51