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 studied 22 patients with first stroke and infarct limited to the midbrain on MRI. We selected these patients (8%) from 281 with posterior circulation infarct admitted consecutively into a primary care center. All patients underwent a systematic protocol of investigations including MR imaging and angiography, and echocardiography. Most infarcts fitted well to arterial territories drawn in preestablished templates. Middle midbrain involvement was the most common, mainly in the paramedian territory supplied by the basilar artery. Infarct in the mesencephalic territory of the posterior cerebral artery was less common, while superior cerebellar artery territory infarct was extremely rare, and posterior choroidal artery territory infarct did not occur. The neurologic picture was dominated by eye-movement disorders. Patients with isolated upper or lower midbrain infarct had no localizing clinical findings, but patients with middle midbrain infarct had a localizing picture mainly with nuclear or fascicular third nerve palsies that commonly developed in isolation. Vertical gaze paresis, pure motor hemiparesis, four-limb ataxia from unilateral lesion, and hypesthetic ataxic hemiparesis also occurred. Contrary to a common view, cardioembolism was not a more common etiology than basilar artery stenosis or small-vessel disease.
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PMID:Pure midbrain infarction: clinical syndromes, MRI, and etiologic patterns. 750 Nov 88

It is not easy to predict functional outcome in patients with acute-stage thalamic hemorrhage. We analysed 100 cases of hypertensive thalamic hemorrhage less than 4 cm in diameter, and devised a practical CT classification for predicting the patients' prognoses. On an axial CT scan at the level of the pineal body, four lines were drawn as follows: line (a) between the lateral edge of the anterior horn and the midpoint of the third ventricle; line (b) vertical line to the sagittal line from the midpoint of the third ventricle; line (c) between the lateral edge of the trigone and the midpoint of the third ventricle; line (d) between the lateral edge of the anterior horn and the lateral edge of the trigone. The location of hematoma was divided into three types according to lateral extension as follows: type A (anterior type), center of hematoma located between line (a) and line (b); type P (posterior type), center of hematoma located between line (b) and line (c), and external margin of hematoma localized medial to line (d); type PL (postero-lateral type), center of hematoma located between line (b) and line (c), and showing lateral extension beyond line (d). Then, the correlation between hematoma location and severity of motor paresis at onset and its prognosis was investigated. Severe hemiparesis (MMT: 0-2) was observed in 15.3% of patients with type A, 21.8% with type P, and 59.3% with type PL hematoma in the acute stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Practical CT classification for thalamic hemorrhage: relationship between localization of hematoma and prognosis]. 801 74

A 3-year-old girl with left hemiparesis suffered from bilateral paresis, motor rigidity, gait disturbance, axial hypotonia, dysarthria, apathy, and incontinence. After steroid therapy, mild improvement occurred, but muscle weakness, gait disturbance, and rigidity remained. Leigh encephalopathy was excluded on the basis of muscle biopsy and laboratory findings. Computed tomography and serial magnetic resonance imaging at an early stage revealed right-sided dominant lesions in the putamen and caudate nucleus and later bilateral striatal lesions, appearing as hyperintense signals on T2-weighted images and mixtures of hypo- and hyperintense signals on T1-weighted images. This is the first demonstration of serial magnetic resonance imaging findings in infantile bilateral striatal necrosis.
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PMID:Serial MRI in infantile bilateral striatal necrosis. 802 66

A nuclear oculomotor nerve syndrome is rarely caused by mesencephalic lesions. We describe 5 patients, 4 with unilateral syndrome (3 due to ischemia and 1 to mesencephalic hemorrhage) and 1 with bilateral nuclear ischemia of the third cranial nerve. These patients represent 0.2% of those admitted with cerebral vascular pathology over the last 12 years. Symptoms are consistent with descriptions of the anatomic organization of this nucleus, with peripheral paralysis of the contralateral superior rectus and possible bilateral involvement of the eyelid elevator and the pupillary constrictor muscles. A noteworthy symptom seen in these cases is supranuclear paralysis of the upward gaze on the side of the lesion, with ocular elevation achieved in response to oculocephalic stimuli in 2 cases and with Bell's synkinesis in 4. We analyze the nature of 22 published cases of unilateral nuclear damage and of 14 published cases of bilateral nuclear damage. Unilateral damage may or may not lead to ipsilateral pupillary involvement, uni- or bilateral eyelid ptosis, contralateral ocular hypotropia, and possible horizontal paresis of the contralateral gaze. Associated deficits are hemiparesis or crossed hemiataxia. Unresponsive pupils and bilateral ptosis associated with tetraparesis, bilateral ataxia and altered states of consciousness were seen with bilateral nuclear lesions. Infarction is the main cause (in 32 out of 41) and recovery of full ocular movement is uncommon.
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PMID:[Nuclear oculomotor nerve syndrome due to mesencephalic infarction or hemorrhage. Five cases and a review of literature]. 808 84

Cranial CT scanning was performed in twenty-two patients with severe neurological complications secondary to eclampsia. All patients had repetitive and/or prolonged convulsions. In addition, three patients were in prolonged coma, and three had cortical blindness. One of the patients had central facial paresis, and two had hemiparesis. In seventeen patients, abnormal CT findings were identified. Diffuse cerebral edema was determined in four patients. The most frequent finding was bilateral low-density areas in the parietal and/or occipital lobes (7 cases). In three patients, CT revealed bilateral low-density areas in the basal ganglia. All women but three recovered completely. Two of the three patients who died had intracranial massive hemorrhage. Follow-up CT examinations demonstrated complete resolution of the low-density areas and slight cortical atrophy in three of four patients. Complete recovery of the patients associated with complete resolution of the low-density lesions suggested that these lesions corresponded to edema. We concluded that CT is useful in patients with complicated eclampsia because it may orientate management.
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PMID:The diagnostic value of cranial computed tomography in complicated eclampsia. 811 69

A 37-year-old woman with increasing dyspnoea over several months suddenly developed severe ortho- and tachypnoea as well as cyanosis of the lips and acrocyanosis. Pulmonary angiography revealed massive bilateral pulmonary emboli with a systolic pulmonary artery pressure of 75 mm Hg. Phlebography demonstrated a thrombotic occlusion of the deep veins of the left leg extending to the distal femoral vein. Thrombolysis treatment was started via an indwelling pulmonary artery catheter (500,000 IU urokinase and 10,000 IU heparin as bolus, then 1 mill. IU urokinase and 1,000 IU heparin per hour). After two hours an incomplete left-sided paresis occurred (involving ocular and facial muscles, dysarthria, left arm and left leg) and the thrombolytic infusion was stopped. But cerebral computed tomography (CT) did not demonstrate any intracerebral haemorrhage. The heparin infusion was restarted (partial thromboplastin time between 70 and 90 s). CT examinations during the next few days showed the development of an ischaemic infarction in the distribution of the right medial cerebral artery. Angiography demonstrated occlusion of the right internal carotid artery. The diagnosis of a paradoxical embolus was supported by easy cardiac catheter passage through a patent foramen ovale. Subsequent pulmonary angiography demonstrated a thrombus-free pulmonary arterial circulation with a normal pulmonary arterial pressure. There was gradual and extensive regression of the incomplete hemiparesis.
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PMID:[Paradoxical cerebral embolism during fibrinolysis therapy in deep vein thrombosis and pulmonary embolism]. 820 47

The effects of procaine injected into the substantia innominata (SI) and the amygdala (AM) were compared in AM-kindled rats. Intra-SI injection of procaine (ipsilateral to the kindled AM) caused immediate contralateral hemiparesis lasting for about 30 min, associated with EEG amplitude reduction. When the kindled AM was stimulated at the previously established generalized seizure triggering threshold (GST), 8/15 animals had ipsilateral hemiconvulsive seizure 5 min after the injection. In all the animals, afterdischarge was readily produced with a significant reduction in its duration. When procaine was injected into the kindled AM, there was no paresis or EEG change. AM stimulation at the GST did not evoke afterdischarge 5 min after the injection, although the kindled seizure was reactivated by a more intense stimulus. After 24 hr, all the animals, regardless of the site of procaine injection, responded to GST stimulation with a kindled seizure. The data suggest that: (1) the effect of intra-SI procaine is not due to drug diffusion to the kindled AM, and (2) the kindled AM can gain access to the contralateral hemispheric motor mechanism without participation of the ipsilateral SI.
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PMID:Ipsilateral hemiconvulsive seizure after unilateral injection of procaine into the substantia innominata of amygdaloid-kindled rats. 831 95

Stretch-evoked electromyographic (EMG) activity and torque signals have been studied in elbow joint muscles of both sides of patients with spastic hemiparesis and healthy subjects. In order to reveal differences in the generation of muscle tone between clinical assessment and functional movement, stretches of different velocities and amplitudes were applied during passive and quasi-functional active motor tasks. In spastic patients the strength and duration of the EMG responses following stretching of flexor and extensor muscles during both passive and active tasks were dependent on the stretch velocity and duration, respectively. This effect was seen on both the spastic and unaffected side. Under passive conditions EMG activity after stretching was negligible in the limb muscles of healthy subjects, of small amplitude in unaffected limbs of the patients, but was strong in affected muscles. Under active conditions, the amplitude of the early (M1) component of the EMG signal was larger, while the later components (M2 and M3) were smaller. These differences were due more to a change in reflex gain than to a change in reflex threshold when the stretch velocity signal was the basis for calculation. It is suggested that in spastic paresis, modulation of stretch-induced EMG activity in the spastic limb becomes restricted to a smaller range with a poor ability to switch off under passive conditions. Furthermore, the reflex EMG activity suffers a reduced facilitation under active conditions. In comparison with unaffected limbs the stretch-evoked torque on the affected side was increased under passive conditions (due to the extra EMG activity) and decreased under active conditions (due to a reduced EMG activity). An increased torque to EMG ratio was found in spastic flexor and extensor muscles during active tasks. This is thought to be due to changes in mechanical muscle fibre properties suffered as a consequence of defective muscle activation following cerebral lesions. The consequences for clinical assessment of muscle tone and therapy of spastic movement disorder are discussed.
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PMID:Stretch-induced electromyographic activity and torque in spastic elbow muscles. Differential modulation of reflex activity in passive and active motor tasks. 835 19

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

Four weeks after an attack of pneumonia of unknown aetiology a 40-year-old woman was hospitalized because of a nonpurulent, predominantly basal meningoencephalitis and infratentorial abscesses. She had dysarthria, mild right-sided motor hemiparesis and central paresis affecting the 7th cranial nerve. An area of fluctuating resistance, about 3 cm in diameter, was noticed over the left thigh. Serology indicated inflammatory disease, but there was no immunodeficiency. The CSF showed lymphocytic pleocytosis with mild protein increase but no evidence of infective agent. As tubercular meningitis was suspected she was treated with rifampicin (300 mg i.v. twice daily), isoniazid (300 mg i.v. once daily), streptomycin (800 mg i.m. once daily), cefotaxime (2.0 g i.v. three times daily), fluconazole (200 mg i.v. once daily) and dexamethasone (16-8-8 mg i.v.). She suddenly died two days after admission, probably as the result of central regulatory failure. Generalized nocardiosis involving lung, subcutaneous tissue and brain was revealed at autopsy. Although nocardiosis occurs predominantly in patients under immunosuppression, this infection should be considered in the differential diagnosis of treatment-resistant pneumonia and meningoencephalitis without obvious predisposition.
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PMID:[Generalized nocardiosis with meningoencephalitis in a nonimmunosuppressed female patient]. 837 98


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