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)

The part played in traffic safety by driver illness or disability is uncertain or unknown. So also are the specific identity and degree of the disorders which necessitate the use of driving aids or which completely incapacitate a person from driving. Despite the gravity of the problems, the question of fitness to hold a driving licence is decided throughout the world mainly on the basis of subjective assessment. Controlled experiments exploring the significance of disorders have only been carried out on a restricted scale. In this paper a description is given of a mock car, which is used both for research and individual assessment. It enables the measurement of strength application, steering wheel turn speed, simple reaction times when operating pedals and steering wheel, erroneous reactions, and choice reaction times. Experiments involving 109 able-bodied and healthy persons showed, as expected, that the muscular strength of men was greater than of women, and that men were significantly quicker at carrying out functions which primarily depend upon speed of movement and of strength. Apart from this, however, there were no significant sex-related differences. Almost all variables showed age dependence, this being most pronounced in the case of men. Thirty-two percent of the test candidates committed errors like braking instead of turning the wheel or turning to the wrong side. Neither the incidence nor the seriousness of errors bore any relation to sex or age. Fifty-two persons suffering from paraparesis inferior were compared with the 109 able-bodied subjects. The degree of paresis co-varied with reaction times, but the degree of spasticity only to a minor extent. The results indicate that at a speed of 80 km/h, 'slight paresis' increases reaction distance by around 2-3 m (15%), and 'moderate paresis' by the region of 50 m.
 ...
PMID:Assessing driving capability: a method for individual testing: the significance of paraparesis inferior studied in a controlled experiment. 1567 1

Transcranial magnetic stimulation (TMS) has been successful in the prediction of motor recovery in acute stroke patients with initially severe paresis or paralysis of the upper extremity. Motor evoked potentials (MEP) appear to have a high specificity but a rather low sensitivity with regard to motor recovery. The silent period (SP) has been proposed as an additional factor to the MEP for predicting motor recovery that might optimize the sensitivity of TMS. The authors reviewed the literature and case series focusing on the additional value of the SP to the MEP for predicting poststroke hand motor recovery. Studies that have analyzed the SP for predicting poststroke motor recovery have rather inconsistent results and suffer from heterogeneity in technical methods, methodology, and patient characteristics. In most studies, prolonged SPs have been found immediately after stroke, whereas in the (sub)acute phase thereafter, different patterns of SP duration have been found. These differences are thought to be related to stroke localization, though contraction-induced reduction phenomena and recovery-related intracortical phenomena may also be responsible. Although the SP might be used to identify clinically silent or minor strokes, in acute stroke patients with initial severe paresis or paralysis, the SP seems to have no additional value to MEP for predicting poststroke motor recovery. Nevertheless, the SP (poststroke-reduced SPs and contraction-induced inhibitory phenomena) has been proposed as a prognostic factor for poststroke spasticity. This review emphasizes the significance of the SP in predicting poststroke motor recovery and spasticity. Although the relation among the SP, recovery-related intracortical phenomena, and spasticity remains unclear, a neurophysiologic model underlying the SP is discussed. However, more research is needed on the value of the SP for predicting poststroke spasticity.
 ...
PMID:How salient is the silent period? The role of the silent period in the prognosis of upper extremity motor recovery after severe stroke. 1568 9

Gait analysis and recording of standing position were performed in 38 ambulatory children with myelomeningocele. Thirty-four were independent ambulators and four required a walking aid. All subjects were assigned one of four muscle function groups based on muscle strength. They were also divided into subgroups based on the distinction between flaccid and spastic paresis in the lower limb joints. A comparison was made between the gait pattern of the children with spasticity and that of the children with flaccid paresis in each muscle function group. Spasticity in only the ankle joint muscles influenced the subject's gait and standing position compared to the subgroups with a flaccid paresis. Even larger deviations in gait and standing position were observed when spasticity occurred in muscles at the knee and hip joints. When setting ambulatory goals the presence of additional neurological symptoms such as spasticity and inadequate balance should be taken into consideration.
 ...
PMID:The influence of spasticity in the lower limb muscles on gait pattern in children with sacral to mid-lumbar myelomeningocele: a gait analysis study. 1599 87

Two families of dogs (Australian cattle dogs and Shetland sheepdogs) with an inherited "spongiform leukoencephalomyelopathy" were identified, with widespread vacuolation of white matter of the brain and spinal cord. Affected dogs of both breeds developed tremors at 2-9 weeks of age followed by progressive neurological worsening with ataxia, paresis, paralysis, spasticity, and cranial nerve dysfunction. The modes of inheritance of both families were most likely maternal. The cerebrospinal fluid (CSF) analysis showed elevated ratio of 3-OH butyrate to acetoacetic acid. Mitochondrial DNA sequencing showed a G to A transition at 14,474 nt (G14474A, GenBank accession no. NC002008 ) that results in an amino acid change of valine-98 to methionine (V98M) of mitochondrial encoded cytochrome b. Western blot analysis showed increased levels of core I and core II but decreased level of cytochrome c1 of the complex III and cytochrome c oxidase of the complex IV of the respiratory chain.
 ...
PMID:Canine spongiform leukoencephalomyelopathy is associated with a missense mutation in cytochrome b. 1602 96

There are varying degrees of spontaneous improvement in arm paresis over the first 6 months after stroke. The degree of improvement at 6 months is best predicted by the motor deficit at 1 month despite standard rehabilitative interventions in the ensuing 5 months. Animal studies indicate that the loss of fine motor control, especially individuation of the digits, is due to interruption of monosynaptic corticomotoneuronal connections. Spasticity occurs because of loss of cortical modulatory control on descending brain stem pathways and spinal segmental circuits but is not a major cause of motor dysfunction. Quantitative studies of reaching movements in patients suggest that arm paresis consists of higher-order motor planning and sensorimotor integration deficits that cannot be attributed to weakness or presence of synergies. Cortical stimulation experiments in animals and functional imaging studies in humans indicate that motor learning and recovery after stroke share common brain reorganization mechanisms. Rehabilitation techniques enhance learning-related changes after stroke and contribute to recovery. Future research will benefit from using quantitative methods to characterize the motor impairment after stroke and by applying concepts in motor learning to devise more physiologically based rehabilitation techniques.
 ...
PMID:Arm function after stroke: from physiology to recovery. 1634 95

Botulinum toxin A (BoNT-A) is a potent biological toxin widely used for the management of skeletal muscle spasticity or dynamic joint contracture. Intramuscular injection of BoNT-A causes muscle denervation, paresis, and atrophy. This clinical effect of botulinum toxin A lasts 3 to 6 months, and injected muscle eventually regains muscle mass and recovers muscle function. The goal of the present study was to characterize the molecular and cellular mechanisms leading to neuromuscular junction (NMJ) regeneration and skeletal muscle functional recovery after BoNT-A injection. Fifty-six 1-month-old Sprague-Dawley rats were used. Botulinum toxin A was injected into the left gastrocnemius muscle at a dosage of 6 units/kg body weight. An equivalent volume of saline was injected into the right gastrocnemius muscle to serve as control. The gastrocnemius muscle samples were harvested from both hind limbs at 3 days, 7 days, 15 days, 30 days, 60 days, 90 days, 180 days, and 360 days after administration of toxin. In addition, the gastrocnemius muscles from 1-month-old rats with no injections were harvested to serve as uninjected control group. Muscle samples were processed and mRNA was extracted. Real-time polymerase chain reaction (PCR) and gene microarray technology were used to identify key molecules involved in NMJ stabilization and muscle functional recovery. More than 28,000 rat genes were analyzed and approximately 9000 genes are expressed in the rat gastrocnemius muscle. Seven days following BoNT-A injection, 105 genes were upregulated and 59 genes were downregulated. Key molecules involved in neuromuscular junction (NMJ) stabilization and muscle functional recovery were identified and their time course of gene expression following BoNT-A injection were characterized. This animal study demonstrates that following intramuscular injection of BoNT-A, there is a sequence of cellular events that eventually leads to NMJ stabilization, remodeling, and myogenesis and muscle functional recovery. This recovery process is divided into two stages (aneural and neural) and that the IGF-1 signaling pathway play a central role in the process.
 ...
PMID:How muscles recover from paresis and atrophy after intramuscular injection of botulinum toxin A: Study in juvenile rats. 1660 9

Portosystemic encephalopathy (PSE) is a well-known, common complication of portal hypertension. It is thought to be caused by nitrogenous substances such as ammonia, which are normally cleared from the blood stream by the liver. In cirrhosis and other hepatic disorders with portosystemic shunting (PSS)-- either surgical portosystemic anastomoses (PSA) or spontaneous PSS-- the collateral vessels bypass the liver allowing the accumulation of toxic, ammoniacal substances in the blood and tissues. PSE is characterized by encephalopathy; portosystemic myelopathy (PSM) is characterized by paresis of the extremities, Babinski signs and muscle spasticity in patients with cirrhosis and/or PSS. Usually only the lower extremities are involved. This report presents the first case of this syndrome observed 5 years after a transjugular intrahepatic portosystemic shunt. The 31 year old man with chronic Hepatitis B developed complete spastic paraparesis within 4 weeks after onset of clinical/neurological symptoms, accompanied by an episode of severe hepatic encephalopathy. The transcortical magnetic stimulation showed normal motoric stimulation times to the abductor digiti minimi muscles but no stimulation to the tibialis muscles was seen. Lumbar stimulation to the tibialis muscles, however, was normal. This indicates loss of motor neurons in the spinal cord, a characteristic finding in patients with portosystemic myelopathy. We performed a search of the literature for all reported cases of cirrhosis and/or PSS that developed PSM. However, the intervals between the construction of a shunt and the diagnosis of portosystemic myelopathy were shorter in total portacaval shunts (median 16 months) than in partial, non-portacaval shunts (median 60 months, p < 0.01). This suggests that not only the shunt itself but also the shunted volume contributes to the development of the syndrome Sixty-one patients with PSM have been reported in the literature since 1944. PSE had developed before PSM in almost all cases. PSM occurred from 1 month to 10 years after the creation of portacaval anastomoses (PCA) or splenorenal shunts (SRS) or in cirrhotic patients without shunts. No one type of liver disease or type of shunt appears to predispose to PSM. The mechanisms of PSE and PSM are thought to be similar and of nitrogenous origin, but their pathogenesis remains unknown. Lathyrism, a toxic syndrome with similar symptoms and signs, is caused by the ingestion of a legume, Lathyrus sativa, which contains beta-N-oxalo-L amino-L-alanine (BOAA). This animal model with or without BOAA appears to offer a reliable way of studying PSM experimentally.
 ...
PMID:Portosystemic myelopathy: spastic paraparesis after portosystemic shunting. 1663 7

A 27-yr-old woman recreationally inhaled cocaine. Several hours later, she noted chest tightness, back and neck pain, and later bilateral upper-extremity weakness. Physical examination revealed flaccid paresis of the upper extremities. Spasticity at 2 mos after injury, but no detectable weakness, developed in the lower extremities. Cocaine was detected in her urine. Magnetic resonance imaging showed hyperintensity in the anterior cervicothoracic spinal cord. Electrodiagnostic studies of the upper extremities were consistent with anterior horn cell death. Cocaine abuse is associated with cerebrovascular events; spinal cord effects are rarely reported. The patient seems to have an infarct in the anterior spinal artery distribution, with clinical, imaging, and electrodiagnostic findings of upper-extremity lower-motor neuron injury, accompanied by spasticity of the lower extremities. Gray matter has increased susceptibility to ischemia compared with white matter, producing flaccid weakness in the cervical region with isolated arm weakness. Although uncommon, cocaine abuse can cause spinal cord infarction.
 ...
PMID:Spinal cord infarction secondary to cocaine use. 1716 48

Muscle spasticity and paresis are conditions that occur secondary to upper motor neuron lesions. The co-existence of decreased motor unit recruitment and intermittent over-activity generates confusion concerning the effect on muscle fiber characteristics. In order to increase the knowledge about the effect of upper motor lesion on capillarization and muscle fiber composition, the biceps brachii muscle from seven young adults with long duration of spastic paresis and seven age-matched controls were analyzed using morphological and enzyme- and immuno-histochemical techniques. The spastic muscles had a 38% lower capillary density (p=0.002), 30% fewer capillaries around each muscle fiber (p=0.02), and 16% fewer capillaries when related to the fiber size (p=0.04). The frequency of fibers expressing myosin heavy chain (MyHC) IIx increased (30% vs. 4%, p=0.006), while the percentage of fibers expressing MyHC I and MyHC IIa, respectively, decreased (22% vs. 46% and 7% vs. 29%, p<0.01). The high proportion of muscle fibers with low oxidative capacity and low capillary supply indicates that biceps brachii muscle from patients with upper motor lesions fatigue more easily than normal controls. We also observed a significantly higher variability in fiber size for fibers expressing MyHC I (p<0.04), and, in three of the subjects, a small amount of small fibers expressing developmental MyHCs was found. These results suggest that, although intermittent stretch reflex contractions might have an impact on the muscle characteristics in spastic paresis, the muscle phenotypic properties are more adapted to decreased voluntary motor unit recruitment.
 ...
PMID:Decreased capillarization and a shift to fast myosin heavy chain IIx in the biceps brachii muscle from young adults with spastic paresis. 1719 19

Repetitive peripheral magnetic stimulation (RPMS) is a focused and painless stimulation method, in which muscle contractions are elicited by depolarization of the terminal motor branches. Clinical-experimental investigations on different disorders of sensorimotor integration in the last decade have shown that RPMS can be used for the rehabilitation of motor functions after stroke. It is supposed that this therapeutic effect is based on the RPMS-induced proprioceptive inflow to the CNS. To analyze the conditioning effects of RPMS on reorganization of the motor system on cortical level positron emission tomography (PET) is used. Regional cerebral blood flow (rCBF) has been measured using H(2)O(15)-PET in eight patients with arm paresis following focal cerebral ischemic infarction before and after treatment using RPMS on upper arm flexor muscles. Behavioral measures showed a significant improvement of kinematics of finger movements and a reduction of spasticity in the affected arm following RPMS treatment. The recovery was associated with significant increase of neural activation within the superior posterior parietal lobe and the premotor cortex (PM) areas. The increase of activation of the parieto-premotor network following RPMS treatment indicates a significant conditioning effect of RPMS on the cortical level. These results emphasize the positive therapeutic effect of RPMS and describe the physiological bases of its function on the central level.
 ...
PMID:A fronto-parietal network is mediating improvement of motor function related to repetitive peripheral magnetic stimulation: A PET-H2O15 study. 1749 65


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>