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)

The strength of 16 muscle groups was measured bilaterally in 38 hemiparetic stroke patients. The relationship between the strengths and gender, weight, age, side of paresis and time since onset were calculated for each muscle group. Although often correlated with the strength of the non-paretic muscle groups; gender, weight and age were very rarely correlated with the strength of the paretic muscle groups. Side of paresis was only correlated with the strength of four non-paretic muscle groups. Time since onset was generally unrelated to strength. Final strength was always correlated with initial strength on the paretic side. These results suggest that cerebrovascular accidents disrupt some of the normal strength relationships on the hemiparetic side, and that the severity of the hemiparesis early in rehabilitation may provide a good indication of the severity to be expected later in rehabilitation.
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PMID:Relationship between static strength and various other measures in hemiparetic stroke patients. 355 12

The time course of tension development produced by fast isometric contraction of the quadriceps femoris muscle for knee extension was examined on eight normal subjects and 14 patients with spastic hemiparesis due to stroke. Tension lag time (TLT), the latency from the onset of EMG activities to the rise of tension, and contraction time (FTmax), the period from the rise of tension to its maximum, were longer in the patients than in the normal subjects. The prolongation of FTmax correlated with the decreased rate of tension development. The results indicated that the temporal characteristics of tension development altered in the spastic paresis, reflecting functional changes in the muscle and motor neurons.
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PMID:The altered time course of tension development during the initiation of fast movement in hemiplegic patients. 357 13

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

For many years, electrophysiological investigations of locomotion were restricted to animals, largely the cat. They concentrated on and emphasized the role of spinal interneuronal networks responsible for the generation of the locomotor pattern. Following the introduction of perturbation impulses and electrical nerve stimulation during stance and gait, information became increasingly available concerning the role of the reflex systems involved in the regulation of gait, their afferent pathways and their control by supraspinal motor centres. During gait monosynaptic stretch reflexes are inhibited. From a knowledge of the behaviour of the cerebral potentials evoked during stance and gait, it can be deduced that during gait the signals of group I afferents are blocked at both segmental and supraspinal levels. Polysynaptic reflex responses are mainly responsible for the compensation of perturbations introduced during gait. They are most probably mediated by group II afferents via a spinal pathway closely connected with the spinal locomotor centres. The functioning of these responses depends on an intact supraspinal control. They are suggested to be incorporated in a more complex e.m.g. pattern mainly determined by central mechanisms. In contrast to the gait condition, segmental stretch reflex activity does contribute to activation of extensor muscles of the leg during fast movements, such as running and hopping. In children at an early stage in the development of gait (around 1 to 2 years of age), as well as in patients with spastic paresis, the polysynaptic reflex responses are reduced or absent, and isolated monosynaptic reflex potentials are present. This suggests a reciprocal modulation of mono- and polysynaptic reflex mechanisms, both being dependant on supraspinal control. When this control is either not yet matured (small children) or impaired (spastic paresis), inhibition of monosynaptic stretch reflexes is absent and associated with a reduced facilitation of polysynaptic spinal reflexes. In spastic muscle hypertonia, the tension developed at the Achilles tendon during gait cannot be explained by gastrocnemius activation alone. In patients with spastic hemiparesis gastrocnemius e.m.g. activity is reduced in the spastic leg as compared to the unaffected one. It can be concluded that the paretic muscle undergoes changes in its mechanical properties, secondary to the supraspinal lesion, which results in the development of spastic muscle hypertonia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of peripheral afferents and spinal reflexes in normal and impaired human locomotion. 362 74

Ninety-three Chinese patients with cutaneous herpes zoster were seen during a 4-year period. Thoracic zoster occurred most commonly, followed by ophthalmic, cervical and lumbosacral zoster. Neurological complications were present in eleven patients (11.8%), the commonest being Ramsay-Hunt syndrome and segmental limb paresis. The clinical picture, pathogenesis, treatment and outcome of segmental limb paresis, myelitis and delayed contralateral hemiparesis following zoster ophthalmicus are discussed. Nine immunocompromised patients received intravenous adenine arabinoside (vidarabine) or acycloguanosine (acyclovir), and no cutaneous or visceral spread occurred in these patients.
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PMID:Herpes zoster and its neurological complications. 367 Dec 48

Muscular deficit, voluntary movement disorders, abnormal movements, and global disturbance of movements are considered. A muscular deficit is part of the Dejerine-Roussy syndrome. It appears as hemiparesis, regressive within days or weeks. A juxta-thalamic capsular involvement can be considered as the origin of this deficit in most cases, especially in hemorrhagic processes even if these are located within the thalamus, on account of mass effect. The occurrence of paresis or paralysis in ischemic processes strictly situated in the thalamus, however, is discussed: the deficit may be limited to parts of limbs; most often, it is not associated with pyramidal symptomatology; recovery is observed in the hand before the inferior limb. To these anatomoclinical facts some data from animal experiments or thalamic stereotaxic surgical procedures in humans must be added. A deafferentiation from the cortex seems to be the main cause of these motor disturbances. Three types of voluntary movement disorders may be encountered: contralateral cerebellar incoordination due to the involvement of the nucleus ventrooralis posterior where the superior cerebellar peduncle ends; homolateral imitative syncinesias, not confined to thalamic lesions, but frequently observed in this location with a particular aspect; contracture. Abnormal movements include choreoathetosic movements, and exceptionally intention and action tremor, and asterixis. They primarily involve the superior limb, but reported cases are not associated with thalamic limited lesions. Global disturbance of movements is observed in the hand or gait. "Thalamic hand" consists of incessant finger movements in the vertical and horizontal planes. They are associated with thalamic dystonia and deep sensibility disorder.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Motor symptomatology of the thalamus]. 378 43

Moderate unilateral weakness of shoulder and hip muscles and limb-kinetic apraxia were observed in 11 patients with frontal lobe lesions on the side opposite to the neurological deficits. On the CT scans, the posterior border of the lesions lay anterior to the precentral gyrus, thus involving the premotor cortex but not the primary motor cortex. In 9 cases, the lesions were caused by a brain infarct, in 2 cases by a tumour. In 1 patient the lesion was purely subcortical. Whereas the paresis affected all hip muscles, in the shoulder mainly those movements associated with abduction and elevation of the arm were disturbed. The EMG showed considerable delays for the preactivation of proximal arm muscles during rapid arm movements, thus interfering with the normal proximal-distal sequencing of muscle action. Limb-kinetic apraxia only became apparent during tasks requiring certain coordinations between both arms or legs. Bimanual interaction was normal. Two patients with proximal hemiparesis and small lesions in the precentral gyrus which have been examined for comparison showed no limb-kinetic apraxia and different distributions of the paretic shoulder girdle muscles. In view of the long-standing controversies as to the functional role of the premotor cortex and the question of specific deficits after lesions of this area, the relevant literature is reviewed.
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PMID:Lesions of premotor cortex in man. 392 94

We studied recovery from hemiparesis in 52 patients who participated in the Hennepin County (Minnesota) Recovery From Aphasia Study. Our intent was to determine the anatomic correlates of recovery from hemiparesis and then to contrast computed tomography (CT)-hemiparesis relationships with CT-aphasia relationships in this same population. Hemiparesis was assessed at one month after onset and again at six months after onset. Computed tomographic scans were obtained five months after onset and analyzed quantitatively for lesion location. The presence or absence of arm paresis was strongly predicted by CT scan findings in the supratentorial corticospinal pathway. However, three of 25 nonparetic patients had lesions in the corticospinal pathway, and one of 22 severely paretic patients lacked an appropriate lesion. This study demonstrated that a small but inherent lack of specificity and sensitivity existed in the predictive power of CT localization of lesions potentially affecting the motor system, suggesting that some caution is necessary in interpreting the lesion-deficit relationships in less well-localized functions, eg, language. Besides considering the lack of precision in localizing with CT, the existence of individual differences both in anatomy and localization of function must be taken into account.
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PMID:The validity of computed tomographic scan findings for the localization of cerebral functions. The relationship between computed tomography and hemiparesis. 395 15

The survival rate was 40% in 10 patients suffering hemorrhage into the pons who were admitted to an acute care facility. This rate is higher than previously reported. In addition to the "classic" pontine hematoma syndrome characterized by coma, quadriparesis, and eventual demise, two more benign syndromes arising from hemorrhage confined to one side of the pons were also recognized. In one of these hemipontine syndromes, hematoma involved both the basis pontis and tegmentum and was associated with hemiparesis, brainstem signs, and preserved consciousness. In the other, hemorrhage was confined to the tegmentum and was associated with gaze paresis, motor sparing, and preserved consciousness. All patients suffering hemipontine hemorrhage survived. An impressive degree of functional recovery occurred in these survivors.
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PMID:The clinical manifestations of pontine hemorrhage. 399 Sep 63

Twenty-five patients with nonhaemorrhagic infarcts of the thalamus were studied clinically and by neuropsychological testing, computerized tomography and somatosensory evoked response (SER) recordings. Our aim was to determine whether the findings in these different tests would form distinct symptom clusters associated with different anatomical territories of the thalamus. Infarction conforming to the tuberothalamic arterial territory caused a facial paresis for emotional movements, severe neuropsychological deficits and a delay of the SER after P14. Infarction conforming to the interpeduncular profundus arterial territory caused a supranuclear vertical gaze paresis, severe neuropsychological deficits and a delay in the P60 component of the SER. Infarction conforming to the anterior choroidal territory caused a hemiparesis, moderate neuropsychological deficits and varied sensory evoked responses. Patients with infarctions conforming to the entire geniculothalamic territory had sensory loss in multiple modalities, minimal neuropsychological deficits and absence of sensory evoked responses after P14. A lacune in this territory caused pure hemisensory loss involving part of the body for the modalities of pain and light touch but not proprioception or vibration. Neuropsychological deficits were uncommon and N32 and N60 were delayed in the SER.
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PMID:Nonhaemorrhagic thalamic infarction. Clinical, neuropsychological and electrophysiological findings in four anatomical groups defined by computerized tomography. 400 33


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