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)

Development of epilepsy was studied prospectively in a group of 77 consecutive stroke patients. Included were stroke patients less than 75 years old admitted within the first 3 days after the stroke. Excluded were patients with subarachnoid hemorrhage, vertebrobasilar stroke, and patients with other severe diseases. Cerebral angiography, CT, and EEG were performed in all patients. The patients were followed clinically for 2 to 4 years. Seven patients (9%) developed epilepsy. Of 23 patients with lesions involving the cortex, 6 (26%) developed epilepsy. Of 54 patients in whom the cortex was not involved, only 1 (2%) developed epilepsy. Patients with persisting paresis and cortical involvement seem to be at particularly high risk of developing epilepsy, as 50% of such patients (6 of 12) developed the disease.
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PMID:Epilepsy after stroke. 360 Oct 84

A rare case of extracranial internal carotid occlusion with a coexisting ipsilateral internal carotid aneurysm is reported. A 50-year-old male had a sudden onset of severe headache, vomiting and right motor weakness on May 14, 1984. Two days later the patient was transferred to our hospital. On admission he was alert but presented with nuchal rigidity and right moderate hemiparesis. He had an episode of a blunt head injury 12 years previously, but no history of hypertension, diabetes mellitus or cerebral stroke. A computed tomography revealed mild subarachnoid hemorrhage and mild ventricular dilatation. A cerebral angiography did not demonstrate any aneurysms but it revealed occlusion of the right internal carotid artery at the cervical bifurcation. The repeated angiography on May 31 disclosed a saccular aneurysm arising anteromedially at the level of the junction of the right posterior communicating artery and the internal carotid artery. The cervical internal carotid artery remained occluded at the same site. The middle cerebral artery was supplied through the well-developed posterior communicating artery, and the right anterior cerebral artery was supplied through the anterior communicating artery. Clipping of the aneurysm was attempted but it was forcibly trapped because of premature bleeding on June 5. The right V-P shunt was performed for the progressive ventricular dilatation on June 12. The patient was discharged with no paresis on June 20. It has been well known that the uni- or bilateral carotid occlusion, whatever the origins are, are often associated with cerebral aneurysms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Extracranial internal carotid occlusion and coexisting ipsilateral intracranial internal carotid aneurysm]. 361 34

Binswanger, in his 1894 dissertation on the differential diagnosis of general paresis of the insane, described a slowly progressive dementia associated with macroscopic loss of white matter. In recent years interest in Binswanger's disease was rekindled with CT demonstration of extensive white matter low densities in some patients. To define the clinical spectrum, we reviewed 22 consecutive cases in which the CT appearances suggested a diagnosis of Binswanger's disease. Two patients had focal neurological deficits at presentation, but recent anoxic or hypoglycaemic insults could not be excluded as the cause of the CT abnormalities. The 20 remaining patients were demented and showed variable combinations of corticobulbar dysfunction and gait dyspraxia. The duration of symptoms ranged from a few months to several years. Sixty per cent of this group gave a history of discrete stroke events and focal cortical and/or lacunar infarcts were a frequent CT finding. Binswanger's disease is probably due to chronic or acute-on-chronic white matter ischaemia. The association with lacunar and cortical infarctions suggests that a combination of large and small vessel disease produces diffuse ischaemia maximal in white matter watershed zones. Binswanger's disease is clinically differentiated from multi-infarct dementia by its time course.
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PMID:Subcortical arteriosclerotic encephalopathy: Binswanger's disease. 366 81

Of 156 stroke patients prospectively and consecutively evaluated, one-third had a homonymous hemianopia. Of those 52 patients, 46% had a horizontal conjugate gaze paresis at the time of presentation. This gaze paresis was most commonly seen with large hemispheric stroke. The overall prognosis in patients with a gaze paresis was poor. The 30-day case fatality rate was 49% which was significantly higher than for stroke patients presenting with homonymous hemianopia without a gaze paresis.
Stroke
PMID:Horizontal gaze paresis in hemispheric stroke. 376 49

Thirty (2.5%) of 1200 consecutive patients with a first stroke had a spontaneous dissection with occlusion of the cervical internal carotid artery (ICA). A suggestive picture with ipsilateral headache and oculosympathetic paresis was uncommon (17%), so that diagnosis was uncertain before angiography. Seven patients died within one week. During follow-up (mean, 3.2 years) with sequential Doppler ultrasonographic testing, 12 survivors had a good recovery and early reopening of the occluded ICA, and 11 had a poor recovery usually without reopening of the ICA. Recurrence of a dissection occurred in only one patient. Large infarcts causing death or a severe disability were associated with an ICA thrombus and distal emboli; the organization of this intraluminal thrombosis may explain the absence of reopening in these cases while resorption of the intramural hematoma developed. Early heparin sodium therapy may help prevent intraluminal clotting without carrying an important risk of extending the dissection, but its clinical benefit remains unproven. Contrary to current opinions, ICA dissection with occlusion causing cerebral infarction may often carry a severe prognosis.
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PMID:Spontaneous carotid dissection with acute stroke. 381 30

Muscle strength for knee extension, both isokinetic and isometric, and walking capacity, maximum velocity and walking rate, were examined in 11 post-stroke hemiparetic patients. The degree of spasticity of the affected lower extremity was not related to the isokinetic and isometric torques, or to the walking capacity. Although both the isokinetic and isometric torques decreased on the affected side compared to the non-affected side, the rate of decrease was remarkable in isokinetic torque at fast velocities. The walking capacity was well correlated with isokinetic torque of the affected side at fast velocities but not isometric torques. These results suggest that reduction of muscle strength at rapid movements is an essential feature of spastic paresis and is primary cause of motor disabilities such as impaired locomotor function.
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PMID:Relationship of muscle strength for knee extension to walking capacity in patients with spastic hemiparesis. 400 20

EMG denervation activity was studied in patients without peripheral neuron disorder but with upper motor neuron lesions. The time course of such central denervation activity, the local distribution and the quantitative relationship between denervation activity and the degree of paresis and spasticity were also studied. A total of 101 patients, who had developed hemiplegia or hemiparesis as a result of a cerebral vascular accident, underwent needle electromyographic examination at regular intervals in proximal and distal muscle groups. The maximum observation time was 1 year. Denervation activity in cases of central paresis first occurred 2-3 weeks after stroke. This could be observed most frequently in the distal arm and hand muscles. In the course of weeks and months the frequency of the denervation activity decreased in parallel with the development of spasticity and the increasing voluntary innervation. The occurrence and the dynamic properties of the denervation activity in cases of central paresis support the assumption of a trans-synaptic degeneration of alpha-motoneurons and of a compensating segmental "sprouting" of afferents.
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PMID:Denervation activity in the EMG of patients with upper motor neuron lesions: time course, local distribution and pathogenetic aspects. 619 9

In 31 patients with completed stroke (n = 30) or PRIND (n = 1) a brain SPECT with 123I-labeled amphetamines was performed. In 14 (= 45%) of the respective patients--suffering from long-lasting hemiplegia--crossed cerebellar diaschisis was present. The interval between onset of the disease and time of examination varied between 1 week and 7 years. On the other hand, patients without crossed cerebellar diaschisis did not, with one exception, suffer from hemiplegia. It is likely that this phenomenon is caused by the reduction of spino-cerebellar stimuli due to the paresis of the respective extremities.
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PMID:[Cause of crossed cerebellar diaschisis in cerebrovascular disease]. 633 45

We studied 44 patients (group I: 9 with insignificant disease and group II: 35 with significant coronary artery disease) by nuclear angiography during the controlled increase in heart rate by atrial pacing to evaluate the effect of 20 mg of sublingual nifedipine on left ventricular function. Left ventricular volumes were calculated using count-derived changes: end-diastolic (EDE), end-systolic (ESE), stroke volume (SVE) and cardiac output equivalents (COE) and ejection fraction (EF) and ejection rate (ER) were calculated during basal sinus rhythm (C) and at the maximal atrial pacing (AP) rate with and without nifedipine. In normal subjects, AP decreased ventricular volumes. The administration of nifedipine decreased blood pressure but had no further effect on left ventricular volume. In the ischemic ventricle, AP produced reversible ventricular wall paresis with a smaller decrease in EDE, an increase in ESE and a significant fall in EF. Nifedipine induced a striking improvement in EF and ER. This was probably a consequence of afterload reduction and increased coronary blood flow.
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PMID:The effect of nifedipine on normal and ischemic left ventricular function during atrial pacing stress. 647 65

The authors present an adaptive biotraining technique employing automatic portable devices designed for post-stroke patients with secondary motor disturbances. The principal feasibility of a directed central reorganization and formation of new motoric skills in post-stroke patients with the paresis of upper extremities is demonstrated. The principles of correcting motor disturbances, developed for this cohort of patients, have enabled the authors to theoretically substantiate and introduce into clinical practice this effective method of functional therapy based on the active mobilization of brain reserves.
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PMID:[Use of portable biotechnological feedback devices in a system of active rehabilitative therapy in patients with post-stroke movement disorders]. 662 34


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