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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gross and microscopic lesions of Bolivian hemorrhagic fever (BHF) are described in 10 rhesus monkeys that survived from 30 to 78 days after subcutaneous inoculation with a dose of 10(3) plaque-forming units (PFU) of Machupo virus, a dose which produces a severe and generally fatal disease. Six of the monkeys had been given low doses of homologous immune globulin when initial signs of infection appeared. Monkeys exhibited clinical signs in two phases. The initial signs of acute infection which began to appear about 1 week following inoculation included: diarrhea, depression, anorexia, dehydration, and skin rash. The survivors of this early phase of the illness usually showed improvement before relapsing into the second (or chronic) phase, which was characterized clinically by central nervous system disturbances including incoordination, tremors, convulsions, paresis, and muscle atrophy. Microscopic lesions were similar in both immune globulin-treated and untreated animals. These included widespread lymphoreticular infiltrates in the walls and adventitia of blood vessels of the brain, spinal cord, pancreas, intestine, liver kidney, adrenal, parathyroid, heart, and skeletal muscle. Diffuse lymphocytic infiltrates not confined to the vascular or perivascular tissues were present to a variable degree in many of these and other organs. Several monkeys exhibited lymphocytic inflammation of the choroid, meninges, peripheral nerves, and ganglia.
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PMID:Pathology of chronic Bolivian hemorrhagic fever in the rhesus monkey. 18 94

An operative case of 12-year-old boy with a saccular aneurysm at the anterior communicating artery was reported. He had episodes of occasional headache during one year before admission. He was attacked by a severe headache associated with nausea and vomiting, and was admitted to Ooita Pref. Hospital under the diagnosis of subarachnoid hemorrhage four days later. On admission physical examinations revealed almost normal findings except for moderate dehydration and a blood pressure of 130/70 mmHg. Routine examinations (blood, serum including total cholesterol, urine, ECG and plain chest X-film) were normal. Neurologically there were lethalgic state, moderate nuchal rigidity and bilateral abducens paresis. Slightly hemorrhagic and xanthochromic CSF was demonstrated by a spinal puncture. An aneurysm was found at the anterior communicating artery on the right carotid arteriogram. The left carotid and the left vertebral arteriograms showed no pathologic findings. Operation via right fronto-temporal approach disclosed a berry aneurysm about 4 mm in diameter arising from the bifurcation of the right anterior cerebral and the anterior communicating artery. There was a plaque presumably an atherosclerotic change at the neck of the aneurysm. Clipping of the aneurysmal neck was done. The aneurysm was not visualized on the postoperative arteriogram, and the patient was discharged in good condition two weeks after the operation. It is true that this patient had a lesion which seemed to be an atherosclerotic plaque at the neck of the aneurysm macroscopically, but he did not have any evidence of generalized atherosclerosis or other metabolic disturbance. This plaque may be of special significance in etiological respect. In general, however, degenerative lesions like atherosclerosis occur predominantly in larger arteries than smaller arteries of the brain. Also the location of this aneurysm was at the anterior communicating artery which is reported to be implicated in anomalous vascularity on occasion. From these facts the authors considered combined congenital and acquired factors in the development of this aneurysm.
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PMID:[Intracranial aneurysm in a child--a case report and some considerations on etiology (author's transl)]. 94 72

Vacuolar degeneration was constantly induced in the CNS of 4-week-old ICR mice by intracerebral or intranasal inoculation of JHM-CC virus, a small plaque mutant of mouse hepatitis virus (JHM). Most animals showed no symptoms or only mild hindlimb paresis. Irrespective of clinical manifestations, the virus was isolated from the CNS up to days 14 to 16. Viral antigen expression in the CNS tissue was most extensive around days 5 to 7 and became undetectable on day 14. Viral antigens were localized almost exclusively to neurons, and the temporal sequence of viral antigen distribution after intranasal inoculation clearly indicated the virus spread through the olfactory and limbic systems into the brainstem and spinal cord, and possible cell-to cell transmission of the virus within the CNS. Vacuolar changes, most conspicuous in the brainstem and spinal cord, were steadily progressive up to 4 weeks after infection, but became indistinct by 4 months. Although the distribution of vacuolar lesions largely agreed with that of viral antigen-positive cells, the severity of vacuolation did not correlate with that of inflammation. Intramyelinic splitting, periaxonal edema, and swollen neurites were major ultrastructural substrates for vacuolar changes. This model could provide a better understanding of new types of neurologic disorders associated with viral infections, including vacuolar myelopathy in AIDS.
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PMID:Vacuolar degeneration in mice infected with a coronavirus JHM-CC strain. 216 Oct 91

The authors report a 46 year-old female who was submitted to a right femoral artery coronary arteriography. During the procedure she presented an upward, downward and convergence gaze paresis; an upbeating nystagmus. A NMRI showed a change in T-2 weighted signal of the left paramedian mesencephalic region. A diagnosis of stroke was made and dextran 40 was prescribed. Vertical gaze paresis progressively disappeared. Convergence paresis and nystagmus improved partially only. The possible pathophysiological basis underlying this clinical picture are: catheter-induced dislodgement of an atheromatous plaque; small thrombi formation and release from the catheter tip; catheter-induced vascular lesion with subsequent thromboembolism or dissection of the intima; cardiac arrhythmia; catheter-induced or contrast medium-induced arterial spasm; a combination of two or more of these.
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PMID:Neurological complications of coronary arteriography. 748 30

Meningiomas of the cerebellopontine angle (CPA) represent a clinically and surgically interesting entity. The opportunity of complete surgical excision and the incidence of impairment of nerval structures largely depend on the tumour biology that either leads to displacement of surrounding structures by an expansive type of growth or to an enveloping of nerval and vascular structures by an en plaque type of growth. As the origin and the direction of growth are very variable, the exact tumour extension in relation to the nerval structures and the tumour origin can be identified sometimes only at the time of surgery. Out of a series of 230 meningiomas of the posterior skull base operated between 1978 and 1993, data of 134 meningiomas involving the cerebellopontine angle are presented. There were 20% male and 80% female patients, age at the time of surgery ranging from 18 to 76 years, on the average 51 years. The clinical presentation was characterized by a predominant disturbance of the cranial nerves V (19%), VII (11%), VIII (67%) and the caudal cranial nerves (6%) and signs of ataxia (28%). 80% of the meningiomas were larger than 30 mm in diameter, 53% led to evident brainstem compression or dislocation and 85% extended anteriorly to the internal auditory canal. Using the lateral suboccipital approach in the majority of cases and a combined presigmoidal or combined suboccipital and subtemporal approaches in either sequence in 5%, complete tumour removal (Simpson I and II) was accomplished in 95% and subtotal tumour removal in 5%. Histologically the meningiotheliomatous type was most common (49%) followed by the mixed type (19%), fibroblastic (16%), psammomatous (7%), hemangioblastic (7%) and anaplastic (2%) types. Major post-operative complications were CSF leakage (8%) requiring surgical revision in 2% and hemorrhage (3%) requiring revision in 2%. While the majority of neurological disturbances showed signs of recovery, facial nerve paresis or paralysis was encountered in 17%, and facial nerve reconstruction was necessary in 7%. Hearing was preserved in 82% with improvement of hearing in 6%. The variability of tumour extension, the implications and limitations for complete surgical excision are discussed along with the experiences from the literature.
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PMID:Meningiomas of the cerebellopontine angle. 873 4

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

A paresis isolate of equid herpesvirus 1 (EHV1, Ab4/8) and a plaque-purified virus derived from it (EHV1, Ab4/13), induced long-term suppression of both mitogenic and antigen-specific lymphocyte proliferations in adult outbred ponies. Peripheral blood mononuclear cells (PBMC) taken from a pony after EHV1 infection suppressed the in vitro function of normal cells but serum did not. This showed that the observed immune suppression was associated with circulating PBMC and/or their products rather than circulating soluble factors such as antigen or immune complexes. The results suggested that productive infection of lymphocytes by EHV1 was unlikely to result in the observed in vitro effects. Moreover, prostaglandin release from monocytes was not likely to have caused the observed suppression, because lymphocyte responsiveness was not restored in the presence of indomethacin.
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PMID:Equid herpesvirus-induced immunosuppression is associated with lymphoid cells and not soluble circulating factors. 1063 Jul 90

A postmortem case of an atypical form of dural graft associated Creutzfeldt-Jakob disease (CJD) is described. A 42 year old man developed progressive spastic paresis 163 months after a cadaveric dura mater graft. He presented with no myoclonus and very late occurrence of periodic synchronous discharges on EEG. The prion protein (PrP) gene was homozygous for methionine at the polymorphic codon 129. Neuropathological examination disclosed plaque-like PrP deposits with atypical distribution of synaptic PrP accumulations in the brain. This patient represents an atypical form of dural graft associated CJD characterised by unusual clinicopathological features.
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PMID:Atypical form of dural graft associated Creutzfeldt-Jakob disease: report of a postmortem case with review of the literature. 1130 72

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

We present five cases of patients diagnosed of a facial nerve tumoral lesion localised at the Geniculate Ganglion and all of which underwent surgical resection. The initial symptoms were in four cases of peripheral facial nerve paralysis and in the fifth case facial paresis. Two trans-mastoid extralabyrinthine approaches were performed and one through a combined path (middle fossa and trans-mastoid) with reconstruction of the facial nerve through a termino-terminal graft. In the fourth case, an approach through fossa media was done, and did not include nerve reconstruction but palliative treatment with a palpebral gold plaque. In the fifth case, a modified trans-labyrinthine approach with facial-hypoglossus termino-terminal anastomosis. Histological diagnosis was 3 neurinomas and 2 hemangiomas. Of the termino-terminal grafts two managed a functional Grade III of the House-Brackmann classification. The third one sustained a Grade VI and therefore a suspension with temporal muscle was carried out. The patient with facial-hypoglossus anastomosis is in a functional Grade IV. Geniculate ganglion tumors are in their majority benign and their treatment is the total resection of the tumor. Nerve reconstruction can be primary or deferred with the aid of a nerve graft or anastomosis, being necessary palliative techniques when resection is not possible.
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PMID:[Geniculate ganglion tumors. Therapeutic and reconstructive management]. 1546 16


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