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 70-year-old man who had a sudden onset of right hemiparesis and mutism. The lower extremity was more involved than the upper one. He had a long history of diabetes and chronic renal failure for which hemodialysis was necessary. On August 30, 1990, he had an sudden onset of right hemiparesis and mutism. Neurological examination revealed awake but mute in no acute distress. He could only respond to very simple commands such as opening his mouth or protruding his tongue. He did not appear to understand more difficult questions. In addition, he could not answer verbally. He was totally mute. Cranial nerves appeared intact except for slight right central facial paresis and severe diabetic retinopathy. He had complete paralysis of his right leg and a moderate weakness in his right upper extremity. Deep reflexes were diminished in both upper extremities and absent in the lower limbs. Frotal signs such as grasp and snout reflexes were present. Cranial CT scans revealed an ill-defined low density area in the left parasagittal subcortical area and a part of the anterior cerebral artery territory. The supplementary motor area appeared at least in part to be involved. He was treated with glycerol and other supportive cares, however, his clinical course was complicated by pneumonia, heart failure, septicemia, and he expired two months after his stroke. The patient was discussed in a neurological CPC, and the chief discussant arrived at a conclusion that he had an artery-to-artery embolism at the internal carotid bifurcation resulting in the cerebral infarction mainly in the territory of the anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 70-year-old man with right hemiparesis and mutism]. 836 54

The course of naturally acquired infection with feline immunodeficiency virus was monitored in a cat over an 18-month period after diagnosis. The cat was admitted with diarrhea, poor body condition, a bite wound abscess, gingivitis, chronic fever, and splenomegaly. The cat's condition improved after splenectomy and remained stable for approximately 15 months, then began to deteriorate, as gingivitis, polyuria, polydipsia, pyrexia, multiple cutaneous masses, and hind limb paresis developed. The in vitro response of the cat's lymphocytes to mitogens was suppressed, and absolute lymphocyte counts were low. Spinal lymphosarcoma, disseminated mastocytoma, and presumptive diabetes mellitus were diagnosed after euthanasia. Decreased immune surveillance associated with feline immunodeficiency virus-related immunosuppression possibly played a role in the development of neoplastic disease in this cat.
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PMID:Spinal lymphosarcoma and disseminated mastocytoma associated with feline immunodeficiency virus infection in a cat. 839 90

We analysed retrospectively our clinical experience with 36 cases of mucormycosis. They were seen during the last 15 years. The diagnosis suspected on clinical grounds, was confirmed in 31 cases by finding the hyphae in hematoxylin-eosin stained material obtained from aspirated or tissue biopsy or by isolation of the fungus in culture. Rhinocerebral mucormycosis was diagnosed in 22 patients. Diabetes was the underlying disorder in 20 cases, kidney failure in one and myelodysplastic syndrome in one. Nine had stable and 11 unstable diabetes (ketoacidosis in 10 and hyperosmolar coma in 1). The earliest sign was facial edema, followed by proptosis, chemosis and extraocular muscle paresis. They were treated by extensive surgical debridement, insulin and antifungal drugs with 69% of survival rate. The disseminated mucormycosis was diagnosed at the autopsy in 5 cases, acute leukemia was the underlying disease in 2 of them. Pulmonary mucormycosis was diagnosed in 2 cases, cutaneous form in 2, sinuorbital form in 4 and brain abscess in one patient. Eight of these 9 cases survived after therapy. We emphasize the importance of an early diagnosis. This can only be made in the presence of a typical clinical setting confirmed by finding the hyphae in tissue or culture. Antifungal drugs along with treatment of the underlying disorder and aggressive surgical debridement must follow.
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PMID:Rhinocerebral and systemic mucormycosis. Clinical experience with 36 cases. 898 Dec 94

Eighty-nine male veterans presenting to a vascular surgery clinic with symptomatic lower extremity atherosclerosis were prospectively screened by duplex scan for asymptomatic carotid artery stenosis (CAS). Their chief complaint was: claudication (90%), rest pain (6%), and ischemic ulcer or gangrene (4%). The mean ankle-brachial index (ABI) was 0.77. Twenty-five CAS > 50% were detected in 18 (20%) patients. Twelve CAS > 75% were detected in 11 (12%) patients. There was no difference between patients with and without CAS > 50% with regards to mean ABI, history of angina, diabetes, hypertension, prior coronary artery bypass, or history of smoking. Carotid bruit was associated with ipsilateral CAS > 50% [p < 0.0001, sensitivity (52%), specificity (88%), positive predictive value (41%), negative predictive value (92%)]. As a result of the screening, eight elective carotid endarterectomies have been performed to date in six (7%) patients with one transient twelfth cranial nerve paresis as the only postoperative complication. We conclude that: (1) male patients presenting with symptomatic lower extremity atherosclerosis have a 20% prevalence of asymptomatic CAS > 50%, (2) there is no correlation between the degree of lower extremity ischemia and CAS > 50%, (3) carotid bruit is significantly associated with CAS > 50%, but has a low sensitivity, and (4) routine CAS screening should be considered for all male patients with symptomatic lower extremity atherosclerosis regardless of whether a bruit is present.
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PMID:Asymptomatic carotid artery stenosis screening in patients with lower extremity atherosclerosis: a prospective study. 923 93

Large subcortical infarctions may be due to cerebral embolism and cause cortical signs more frequently than small subcortical infarctions, which usually result from small-vessel disease and are not associated with cortical findings. We evaluated 51 consecutive patients with a subcortical infarct on CT that was 1.5 cm or larger for a potential carotid or cardiac source of embolism and determined how frequently aphasia, hemineglect, or gaze paresis occurred. A carotid or cardiac embolic source was identified in 63% of the total population with a carotid source occurring in 23% and a cardiac source occurring in 49%. More than one-half of the patients with hypertension or diabetes mellitus had an embolic source, whereas all patients without these risk factors had a possible carotid or cardiac source of embolism. Aphasia or hemineglect occurred in 39% of patients and gaze paresis occurred in 41%. Large subcortical strokes frequently result in a different clinical syndrome and from a different mechanism than small subcortical strokes.
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PMID:Stroke mechanisms and clinical presentation in large subcortical infarctions. 940 42

The encephalomyocarditis virus of the diabetogenic M-strain (EMC-M) is known to cause diabetes in mice. The EMC-M virus has also been shown to cause paresis in some of the infected animals. The clinical features include an acute ascending predominantly motor paralysis, developing within days. This resembles acute idiopathic polyneuritis. The alpha motor neurons would be a possible target for the virus, so two parameters, the total number and the size distribution of motor neurons, were therefore selected for further investigation in 6 mice with neurological involvement and compared with 6 control mice. The optical fractionator method was applied for estimating the total number of motor neurons and the 3D size distribution was estimated using the rotator method in a vertical design. No difference was found in the total number of motor neurons and the size distributions were similar in the 2 groups. This design can be used as a model for the estimation of the total number of motor neurons and their size distribution in other experimental animal models.
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PMID:Total number and size distribution of motor neurons in the spinal cord of normal and EMC-virus infected mice--a stereological study. 941 91

We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.
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PMID:[A 96-year-old man with consciousness disturbance, convulsion, and left hemiplegia of acute onset]. 1006 67

Peripheral facial paresis is a serious clinical and social problem. The effect of physical therapy in 44 patients aged 13-80 was studied. Idiopathic peripheral facial paresis was the cause of mimic muscles dysfunction in 75% of our patients. Medical treatment was conducted according to the established program, consisting in applying combined physical, thermal, electrotherapeutic procedures, exercises and massage. All the patients were examined before physical therapy and after I and II series of procedures, based on Pietruski's evolution table of paresis scored in point and percent scale. Patients between age 13-44 demonstrated 47-50% mimic facial muscles efficiency before the treatment, after I series of procedure it amounted to 80-90% and after the II series to 90-100%, so all the symptoms of paresis disappeared. Similar values were scored by patients aged 45-64 years. Minimal percentage of improvement of mimic facial muscles (57%) was noticed in patients aged 65-80 years The increase of the score was evaluated in the studied group after two stages of treatment. It seems to be best in the younger patients. In the examined group the best improvement evaluated as regression of the symptoms was found in patients with idiopathic peripheral facial paresis. The process of improvement was very slow and not full among patients who additionally suffered from co-existing diseases. Patients with diabetes improved by 57%, with arterial hypertension by 53%, the patients with obesity only by 43% after two cycles of treatment.
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PMID:[Physical therapy in peripheral facial paresis]. 1187 10

A 47-year-old man lost his consciousness and brought to our hospital by ambulance. On admission, he had aphasia and upper right limb paresis. Diffusion weighted MR image of the brain on admission showed multiple high intensity areas in the left middle cerebral artery (MCA) territory. Brain angiography performed on the 2nd hospital day revealed the left MCA severe stenosis. We started intravenous antithrombotic therapy on the 1st day. The left carotid angiography on 12th day demonstrated that the left MCA stenosis was improved. He had medical history of hypertension, diabetes mellitus and gout. But he had only slight atherosclerosis, and had no arrhythmia and patent foramen ovale. Blood chemistry test showed marked hypoproteinemia and hyperlipidemia, and urine examination showed proteinuria. He was diagnosed as nephrotic syndrome for the first time. Nephrotic syndrome brought hypercoagulability, so we suspected that nephrotic syndrome concerned with brain infarction.
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PMID:[A case of brain infarction with nephrotic syndrome]. 1282 May 63

Previous studies demonstrated that porcine encephalomyocarditis virus (EMCV) caused acute and persistent infection in the myocardium, central nervous system, and spleen of non-human primates (cynomolgus macaques); and it productively infected primary human cardiomyocytes, suggesting that the virus may pose a risk in pig-to-human transplantation. Recently, transplantation of myocardial and pancreatic tissues from acutely infected pigs transmitted the virus to recipient mice, resulting in acute fatal EMCV disease. Here, we examined whether porcine islet cells (PICs), which are under clinical trial for treatment of type I diabetes in humans, are susceptible to porcine EMCV, and whether EMCV-infected PICs could function in vivo to reverse diabetes. PICs were infected with EMCV in vitro for 5 h, and resulting insulin production compared with that produced by uninfected PICs. Subsequently, infected PICs were transplanted intra-abdominally or under the kidney capsule of C57BL/6 mice, and both virus transmission and PIC function analyzed. PICs were highly susceptible to porcine EMCV, resulting in a 1500-fold increase in production of infectious virus within 5 h of inoculation and cytolysis that destroyed up to 50% of cells within 96 h. However, as long as they were viable, infected PICs produced insulin at levels comparable with uninfected PICs. Intra-abdominal transplantation of 2000 PICs, infected with one plaque forming unit (pfu) per cell of porcine EMCV, into C57BL/6 mice transmitted the virus resulting in acute fatal EMCV disease characterized by hind limb paresis and paralysis and acute respiratory distress in 40% of recipient mice. More importantly, transplantation of 2500 EMCV-infected PICs under the kidney capsule of diabetic C57BL/6 mice (glucose level > or =350 mg/dl) reversed diabetes in 83% of recipient mice (glucose level < or =170 mg/dl); however these mice succumbed to acute EMCV disease transmitted by the xenograft 5 days after transplantation. EMCV infection does not appear to affect insulin production by PICs, but infected xenografts can transmit the virus to recipient animals, resulting in severe disease.
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PMID:Transplanting encephalomyocarditis virus-infected porcine islet cells reverses diabetes in recipient mice but also transmits the virus. 1496 78


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