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

Eighteen patients whose mean age was 61 years were referred to us with acute aortic occlusion from 1977 to 1985. Ten patients had cardiac emboli (group I) and eight had aortoiliac occlusive disease (group II). Fourteen of these patients had paresis or paralysis. Diagnosis was prompt but the time lapse from onset of symptoms to revascularization averaged 18 hours (group I, 10.3 hours; group II, 26.1 hours). All 10 patients in group I had embolectomy alone; of the eight patients in group II, two had transfemoral thrombectomy and six had bypass procedures. The perioperative mortality rate was 40% in group I and 62.5% in group II. Complications developed in 12 patients (nine died); renal failure occurred in 11, compartment syndrome in nine, adult respiratory disease syndrome in three, acute myocardial infarction in three, disseminated intravascular coagulation in two, and paraplegia in one. No amputations were required in the nine survivors and limb function was restored in eight of these patients. Acute aortic occlusion sets in motion a chain of events that threatens life and limb. Prompt diagnosis and revascularization by the simplest operation are required to decrease morbidity and mortality.
 ...
PMID:Acute aortic occlusion--a multifaceted catastrophe. 374 30

This is the first report of brachial plexus inflammation associated with clinical herpes zoster paresis. A 78-year-old female with a 3-week history of herpes zoster of the C4, C5, and C6 dermatomes developed left upper arm monoplegia. She died from an acute myocardial infarction. Post-mortem provided a rare opportunity to study the neuropathology of herpes zoster motor involvement. Histology of the brachial plexus showed extensive lymphocytic infiltration, myelin breakdown, and preservation of axons without vasculitis. The cervical spinal cord showed perivascular lymphocytic cuffing and no anterior horn necrosis. We suggest, the brachial plexus inflammation was a distal extension of a dorsal ganglionitis. Brachial plexus neuritis may be a direct cause of reversible upper limb paresis in herpes zoster. We demonstrate the motor neuropathy is an inflammatory demyelinative process consistent with the recovery observed in a number of patients. We postulate post-herpetic neuralgia may be related to an ongoing inflammatory process.
 ...
PMID:Herpes zoster brachial plexus neuritis. 910 Nov 5

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.
 ...
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.
 ...
PMID:[A 45-year-old man with peripheral monocytosis and right hemiparesis]. 962 75

We review our two-team operative technique and results of anterior retroperitoneal lumbosacral spine exposure for diskectomy, partial corpectomy, and spinal instrumentation. Seventy-two patients with lumbar spondylosis and associated symptomatic radiculopathy had this exposure between January 1, 2000 and January 1, 2002. A single disc space was isolated in 54 patients. Multilevel exposure was achieved in 18 patients. Main outcome measures included intra- and postoperative complications, blood transfusion requirements, duration of ileus, incidence of erectile/sexual dysfunction, and length of hospital stay. A single small bowel enterotomy and iliac vein laceration, both repaired primarily, were the only intraoperative complications. Perioperative blood transfusions were required in 13 patients (18%). Mean length of postoperative ileus was 3.5 days and average length of hospital stay was 5 days. Postoperative complications occurred in 7 patients (9.7%). These included erectile dysfunction (2), transient unilateral lower extremity paresis (1), acute acalculous cholecystitis (1), femoral vein thrombosis (1), pneumonia (1), and acute myocardial infarction (1). There were no genitourinary or other major vascular injuries. A two-team approach for lumbosacral spine instrumentation via anterior retroperitoneal exposure capitalizes on unique specialty-specific surgical skills. This paradigm facilitates safe lumbosacral spine surgery and major perioperative complications are rare.
 ...
PMID:Anterior retroperitoneal lumbosacral spine exposure: operative technique and results. 1261 53

Morbidity and mortality rates from heart diseases are highly represented in geriatric-aged patients, but these patients also have supporting diseases. Acute coronary syndrome includes unstable angina and acute myocardial infarction with and without ST elevation. The aim of this study was to make a retrospective morbidity analysis of patients admitted to the emergency department. The study is made for a period of three years (from 1998 to 2000). It includes 588 patients divided by age (395 were 65-75 years old; 193 were older than 75 years) and sex (there were 326 men and 262 women). Comorbidity and mortality were investigated. Patients with one, two, three, and more than three supporting diseases were 6.29%, 23.13%, 68.53%, and 2.04%, respectively, of the total number. The most frequent geriatric patients had heart failure, followed by endocrinological diseases (type 2 diabetes, obesity, struma), neurological diseases (insultus, paresis), and chronic kidney diseases (pielonephritis, nephrolithiasis). The combination of hypertension, heart failure, and type 2 diabetes had the highest comorbidity frequency. The mortality rate for 1998 was 8.81%, for 1999 7.74%, and for 2000 13.41%. The mortality rate at the first 12 hours at the beginning of the acute coronary syndrome was 66.6%. Geriatric patients suffer from many diseases, and at the beginning of the onset of acute coronary syndrome they have multiorganal failure. Elderly patients are a high-risk contingent in intensive coronary care units.
 ...
PMID:Acute coronary syndrome, comorbidity, and mortality in geriatric patients. 1524 1