Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 86-year-old woman who developed dementia, gait disturbance, speech disturbance, and right hemiparesis. The patient was well until March of 1979 when upon wakening up on one morning she noted slurring of her speech and weakness in her left upper and lower extremities. These symptoms cleared up during the next several months, however, she noted weakness in her left leg again in May 1985. In 1988, her posture became stooped and she walked in small steps. In 1990, she developed memory disturbance and difficulty in naming. In March 1993, she developed weakness in her right hand; she was treated with aspirin and amantadine HCl, however, she deteriorated during the next two week period, and was admitted to our hospital on March 27, 1993. On admission, she appeared alert, however, she could not answer verbally to questions; she could only utter unintelligible sounds. Apparently she was markedly demented. Her blood pressure was 170/98 mmHg, and general physical examination was unremarkable. Cranial nerves were grossly normal except for marked non-fluency in her word expression. She could not stand or walk, and apparently her right upper and lower extremities were paralyzed with some contracture. Deep reflexes were normally active without asymmetry. Chaddock sign was positive bilaterally. Sensory examination was difficult. Pertinent laboratory examination included WBC 13,000/microliters, BUN 152mg/dl, creatinine 3.75mg/dl, CRP 20.1mg/dl; a chest X-ray film revealed pneumonic shadow in the upper and the middle right lung fields. Cranial CT scan revealed multiple lacunar infarctions in both basal ganglia and cerebral white matters; periventricular lucency was also noted. She was treated with antibiotics and intravenous fluid. Acid-fast bacilli were recovered from sputum, and she was transferred to another hospital for the treatment of pulmonary tuberculosis. After its treatment she returned to our hospital on July 8, 1993, when her condition was complicated with aspiration pneumonia. On admission, she was semicomatose, and no intelligible words were heard. Right facial paresis of the central type was noted. She was unable to stand or walk, and her right upper and lower extremities were paretic. Deep reflexes were increased with extensor toe sign on the right. She was treated with chemotherapy and intravenous fluid, however, her clinical course was complicated with respiratory as well as urinary tract infections. She developed cardiac as well as renal failure and expired on September 25, 1993.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 86-year-old woman with dementia, gait and speech disturbance, and right hemiparesis]. 754 29

A total of 2840 patients with pulmonary tuberculosis and bronchial asthma were studied. Antigens are shown to induce a systemic vascular response with elevated systolic pressure in the pulmonary artery, peripheral venous spasms. There is activation of the sympathoadrenal system and desensitization of beta-adrenoreceptors with lower levels of cyclic adenosine monophosphate (CAMP). There is a direct correlation between the CAMP levels and the cardiac output, between those and the pulmonary systolic pressure (PSP). This determines hyperkinetic hemodynamics in tuberculosis with the volume- and pressure-loaded heart. Paresis of pulmonary circulation, as well as hypokinetic hemodynamics occur as a result of an allergic immunological reaction in severe fibrocavernous processes in the area of tuberculosis. There is a direct correlation between the circulating immune complexes and CAMP. In bronchial asthma microcirculation is impaired due to antigenic exposures and elevated intrathoracic pressure. Pulmonary capillary reduction in restrictive processes results in higher levels of CAMP and right-to-left shunt, leading to hypoxemia. In obstructive pulmonary diseases, hypoxemia is caused by hypoventilation and impaired ventilation-perfusion ratios.
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PMID:[Development of chronic cor pulmonale in restrictive and obstructive pulmonary dysfunctions]. 798 11

Tuberculosis is still the most frequent granulomatous laryngeal disease. Absence of pathognomonic symptoms and change in clinical pattern frequently leads to misdiagnosis and delayed treatment. Hoarseness is the commonest symptom of laryngeal tuberculosis and constitutional symptoms are usually rare. However dysphonia can be caused by many other more common conditions. Hoarseness can be a symptom of organic (nodules and polyps of vocal folds, tumors, vocal fold paresis) or functional (functional dysphonia, laryngeal conversion disorder, paradoxical vocal folds motion) conditions. Rarely systemic diseases as amyloidosis, sarcoidosis, Wegener's granulomatosis or tuberculosis can cause vocal dysfunction too. That is why laryngeal tuberculosis is often forgotten in case of persistent hoarseness. In this article, we present a case of a young previously healthy woman, complaining of persistent hoarseness with no other leading symptoms. Though endoscopic image suggested a malignancy, histology showed granulomatous lesion. Detailed examination revealed laryngeal and pulmonary tuberculosis resistant to rifampicin.
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PMID:Dysphonia - the single symptom of rifampicin resistant laryngeal tuberculosis. 2835 69

38-year-old married woman presented with multiple spontaneous painful ulcers that had involved both forearms for the previous month, along with a single episode of generalized tonic-clonic seizures, with no residual palsy or paresis. She complained of photosensitivity and diffuse hair loss for the past 6 months. She also had had arthralgia for the previous 3 years, which had initially involved the small joints of the fingers (especially the proximal interphalangeal joints) and gradually progressed to involve the larger joints. There was no history of recurrent oral ulcers, psychosis, thromboembolic events, or any other skin lesions. Two years previously, she had taken antitubercular treatment for pulmonary tuberculosis.
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PMID:Systemic Lupus Erythematosus Presenting as Livedoid Vasculopathy over the Forearms. 2991 33