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)

Vessels of the microcirculatory bed of the heart in myocardial infarction were studied on the basis of the material of 21 section observations using histological, histochemical methods and the technique of impregnation of films of the epicardium developed by V. V. Kupriyanov. In the ischemic stage in the zone of ischemia and in perifocal areas there were noted signs of increased vascular permeability and impairment of hemodynamics: plethora of the venous department of the microcirculatory system, stasis of the blood in capillaries, spasm and paresis of vessels of the microcirculation. In the necrotic stage in the zone of necrosis there were observed destruction of vessels of the microcirculatory bed; in the peri-infarction zone--drastic plethora of veins, venules and capillaries, higher vascular permeability, leucostasis, leucopedesis, perivascular cellular infiltrates, destruction of vessels of the microcirculatory bed, dilatation of lymphatic vessels; in the intact zone--venous plethora and elevated permeability. In cases of shocks and collapses in vessels of the microcirculatory bed of the heart beyond the zone of necrosis aggregations of erythrocytes were found. In the reparative stage newly formed vessels in the granulation tissue were observed; In the post-infarction scars sinusoid vascular cavities and arteries of the closing type were noted.
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PMID:[Vessels of the microcirculatory bed of the heart in myocardial infarction]. 122 73

A 49-year-old man was hospitalized for slight paresis of the upper left limb. Thrombosis of the right internal carotid artery was documented by arteriography and digital angiography, which showed evidence of an anastomotic blood flow. He went on anticoagulation treatment. Five years later, after an uneventful period, he was referred to our center for the occurrence of a superficial thrombophlebitis: diagnosis of congenital protein C deficiency was possible in the patient as well as in two of his relatives. Two other subjects with congenital protein C deficiency belonging to two different kindreds, whose illness was diagnosed in our center, suffered from myocardial infarction and TIA, respectively, as the only clinical manifestation; a fourth case, previously described, with recurrent superficial thrombophlebitis, suffered from a TIA when on treatment with stanozolol. These cases indicate that arterial thrombosis or TIA is not an uncommon event in congenital protein C deficiency, even in patients without other risk factors for arterial thrombosis.
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PMID:Arterial thrombosis as clinical manifestation of congenital protein C deficiency. 204 65

Aneurysms of the extracranial internal carotid artery are rare but can be responsible for severe complications such as rupture, thrombosis, or embolism. Between 1961 and 1985 we operated on 38 aneurysms of the extracranial internal carotid artery in 35 patients, 22 males and 13 females, whose ages ranged from 6 to 73 years. The underlying causes of aneurysm included atherosclerosis (12 cases), fibromuscular dysplasia (eight cases), a congenital defect (five cases), infection (one case), and trauma (six cases); in six cases aneurysm was secondary to spontaneous dissection. Signs of cerebral ischemia were present in 26 (74%) patients and a cervical mass was found in six. The aneurysm was proximal (i.e., below the angle of the mandible) in 16 patients and distal (i.e., above the angle of the mandible) in 22. After resection of the aneurysm, arterial continuity was restored in 37 patients by resection and grafting (12 cases), resection and anastomosis (11 cases), or arteriorrhaphy (14 cases). One death occurred 13 days after operation due to myocardial infarction. Two patients experienced a reversible neurologic event. Transient paresis of cranial nerves was observed in eight patients. During a follow-up period that ranged from 6 to 30 years, four patients were lost to follow-up and 25 patients remained asymptomatic. Three patients had asymptomatic thrombosis of the carotid artery detected at follow-up investigations. The potential risks of cerebral ischemia and rupture and the satisfactory long-term results achieved with surgery are strong arguments in favor of surgical treatment for aneurysms of the extracranial internal carotid artery.
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PMID:Surgical treatment of extracranial internal carotid artery aneurysm. 781 77

A 65-year-old patient was referred to hospital with suspected myocardial infarction because of left-sided thoracic pain. A paresis of the left recurrent nerve of unknown etiology has been known for three years. Because of shock with anemia, upper gastrointestinal endoscopy was performed. A diverticulum-like lesion in the proximal esophagus was found to be the source of the bleeding. A contrast X-ray examination showed a cavity of approximately 2 x 2 cm originating from the proximal esophagus. Computerized tomography revealed a large mediastinal mass reaching from the thyroid to the diaphragm. An ultrasound-guided fine-needle puncture of this tumor, together with the endoscopical snare biopsies of the esophageal lesion, allowed the diagnosis of an anaplastic thyroid carcinoma with erosion of the esophagus. The patient responded well to palliative radiotherapy. The defect in the proximal esophagus refilled quickly. Nine months after radiotherapy the patient is doing well.
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PMID:[Thoracic pain, shock-inducing gastrointestinal bleeding]. 812 60

For a long time, primary tumors arising less than 2 cm distal to the carina have presented a contraindication to surgical excision. Tracheal sleeve pneumonectomy technique allows carinal resection and reconstruction but still carries considerable postoperative complications. From 1983 to 1992 we performed 27 right tracheal sleeve pneumonectomies and one left. Fourteen patients had N0 nodes, nine had N1, and five had N2. No anastomotic complications, either fistula or stenosis, were observed. Successful outcome depends on meticulous attention to surgical details and careful anaesthetic management with a new ventilation tube. One patient died on the twenty-second postoperative day from myocardial infarction. Complications included pneumonia (one), vocal cord paresis (two), and pleural empyema without bronchial fistula (one). Conservative treatment allowed complete recovery from all complications. There are seven patients alive at 4 years after operation and one at 5 years. Six patients have been disease-free for between 1 and 32 months. Two patients died free of disease at 13 and 42 months. Two patients died of mediastinal recurrence and 10 of distant metastases within 6 and 54 months.
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PMID:Tracheal sleeve pneumonectomy for bronchogenic carcinoma. 763 86

Results of surgical treatment of kyphoscoliosis complicated with spinal cord injury are presented. There were 16 congenital kyphoscoliosis, 5 idiopathic ones and 4 in course of neurofibromatosis. Increased spasticity was present in 2 patients, spastic paresis in 12 and 11 patients were paraplegic. In 24 cases spinal decompression was performed, in 6 years old boy with spasticity the convex side of the curve was fused. Neurological symptoms ceased in 13 cases, marked improvement was achieved in 6 patients, partial recovery in 1 case, in 5 cases no improvement was accomplished. One patient died 6 weeks after operation due to heart attack. Analysis of results achieved indicates, that surgery in most of kyphoscoliosis complicated with spinal cord injury offers good prognosis.
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PMID:[Results for surgical treatment of kyphoscoliosis complicated with spinal cord injury]. 856 78

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.
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PMID:[A 45-year-old man with peripheral monocytosis and right hemiparesis]. 962 75

A 63 year-old woman who had had mitral valve commissurotomy 12 years earlier was seen because of rheumatic mitral stenosis and left brachial paresis due to cerebral embolism. On clinical evaluation, a diastolic rumble was heard over the mitral area, and the echocardiogram revealed a mass attached to the mitral subvalvular apparatus. The patient was operated on, and both the surgical and histologic findings depicted papillary fibroelastoma. This tumor may occur as an isolated lesion or be associated with mitral valve stenosis or other cardiac abnormalities, and it is an important source of emboli. Early echocardiographic diagnosis, followed by surgical excision, may avoid serious complications such as stroke, myocardial infarction, and sudden death.
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PMID:Papillary fibroelastoma of the mitral valve 12 years after mitral valve commissurotomy. 1054 80

Disruption of the pancreatic anastomosis with resultant sepsis is the cause of nearly 50% of deaths following pancreaticoduodenectomy (PD). Traditionally, the pancreatic remnant is anastomosed to the jejunum. Pancreaticogastrostomy (PG) was introduced as an alternative by Waugh and Clagett in 1946 and by Park, Mackie, and Rhoads in 1967. The purpose of this retrospective review was to assess the safety of PG at a single institution. Between 1986 and 1998 a total of 102 patients underwent PG following PD. The indications for PD were periampullary carcinoma (n = 89), pancreatitis (n = 7), and miscellaneous (n = 6). Altogether, 80 patients underwent the traditional Whipple procedure and 22 the pylorus-preserving Whipple (PPW) procedure. The PG was performed by a single-layer invagination technique to the posterior gastric wall using interrupted silk sutures. Leaks from the pancreatic anastomosis were detected by measuring amylase in fluid obtained from surgically placed drains. Operative mortality was 3.9% (4/102). The cause of death was uncontrolled upper gastrointestinal hemorrhage, sepsis, pulmonary embolus, and cardiac failure secondary to myocardial infarction. The mean operating time was 6.8 hours. Blood transfusion was given in 43 patients (42%), and the mean amount of the transfusion was 2.6 units. Nonfatal complications occurred in 35 patients (34%), and included leaks from the pancreatic anastomosis in 9 (8.8%), leaks from the biliary-enteric anastomosis in 4 (3.9%), and gastric paresis 7 (6.9%). Other complications included abscess, wound infection, colitis, delirium tremens, and hyperbilirubinemia. Discharge occurred 6 to 47 days (median 12 days) postoperatively and was prolonged in patients suffering from a complication. PD is associated with significant morbidity. PG is a safe alternative to pancreaticojejunostomy for managing the pancreatic remnant.
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PMID:Pancreaticogastrostomy following pancreaticoduodenectomy: review of 102 consecutive cases. 1136 81


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