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

We sought to identify significant ulnar nerve conduction abnormalities and also to detect ulnar F-wave variable changes in patients with secondary progressive multiple sclerosis (MS). Conventional conduction study was performed unilaterally to ulnar nerves of eight men and 12 women with secondary progressive MS (mean age, 47.5 +/- 6.6 years), having spastic hemiparesis and hand spasticity. A series of 40 electrical stimuli were also delivered to their ulnar nerves unilaterally so as to obtain F waves. The side of examination was ipsilateral to the side of spastic paresis. The following F-wave variables were estimated: F-wave persistence, latency, amplitude, duration, and F chronodispersion. Ten patients with remitting-relapsing MS without any evidence of hand spasticity and 20 age- and gender-matched healthy volunteers served as controls. Motor and sensory conduction study was normal in all participants. The F-wave persistence, latency, and duration parameters and also the F chronodispersion were comparable between groups. The mean and maximum F-wave amplitude values (P = 0.005) and the F mean/M (P = 0.001) and F maximal/M (P = 0.001) ratios were significantly higher than those of controls. Finally, the F-wave amplitude parameters in patients with secondary progressive MS significantly correlated with the degree of spasticity and the duration of disease. Significant amplitude F-wave abnormalities occurred in patients with secondary progressive MS and hand spasticity, emphasizing the contribution of upper motor neurons damage in the genesis of F waves.
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PMID:F-wave characteristics as surrogate markers of spasticity in patients with secondary progressive multiple sclerosis. 2050 76

Although spasticity has been defined as an increase in velocity-dependent stretch reflexes and muscle hypertonia during passive movement, the measurement of flexor muscle paresis may better characterize the negative impact of this syndrome on residual motor function following incomplete spinal cord injury (iSCI). In this longitudinal study Tibialis Anterior (TA) muscle paresis produced by a loss in maximal voluntary contraction during dorsiflexion and ankle flexor muscle coactivation during ramp-and-hold controlled plantarflexion was measured in ten patients during subacute iSCI. Tibialis Anterior activity was measured at approximately two-week intervals between 3-5 months following iSCI in subjects with or without spasticity, characterized by lower-limb muscle hypertonia and/or involuntary spasms. Following iSCI, maximal voluntary contraction ankle flexor activity was lower than that recorded from healthy subjects, and was further attenuated by the presence of spasticity. Furthermore the initially high percentage value of TA coactivation increased at 75% but not at 25% maximal voluntary torque (MVT), reflected by an increase in TA coactivation gain (75%/25% MVT) from 2.5+/-0.4 to 7.5+/-1.9, well above the control level of 2.9+/-0.2. In contrast contraction-dependent TA coactivation gain decreased from 2.4+/-0.3 to 1.4+/-0.1 during spasticity. In conclusion the adaptive increase in TA coactivation gain observed in this pilot study during subacute iSCI was also sensitive to the presence of spasticity. The successful early diagnosis and treatment of spasticity would be expected to further preserve and promote adaptive motor function during subacute iSCI neurorehabilitation.
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PMID:Voluntary ankle flexor activity and adaptive coactivation gain is decreased by spasticity during subacute spinal cord injury. 2058 Jul 13

Spasticity is a sign of upper motor neurone lesion, which can be located in the cerebrum or the spinal cord, and be caused by stroke, multiple sclerosis, spinal cord injury, brain injury, cerebral paresis, or other neurological conditions. Management is dependent on clinical assessment. Positive and negative effects of spasticity should be considered. Ashworth score and the modified Ashworth score are the most used scales for assessment of spasticity. These and other spasticity scales are based on assessment of resistance during passive movement. The main goal of management is functional improvement. A novel 100-point score to assess disability, function related to spasticity (Rekand disability and spasticity score) is proposed. Management of spasticity should be multimodal and should always include physiotherapy or exercise. Oral medications such as baclofen and tizanidine have limited efficacy and considerable side effects, but are easiest to use. Botulinum toxin combined with physiotherapy and/or orthopaedic surgery is effective treatment of localized spasticity. Treatment with intrathecal baclofen via programmable implanted pump is effective in generalized spasticity, particularly in the lower extremities. Neurosurgical and orthopaedic procedures may be considered in intractable cases.
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PMID:Clinical assessment and management of spasticity: a review. 2058 38

Among the three main factors of motor impairment that emerge in chronological order following a lesion to central motor pathways, the last two antagonize movement: 1) stretch-sensitive paresis, a reduction of agonist motor unit recruitment upon voluntary command, worsened by antagonist stretch; 2) soft tissue contracture, and 3) muscle overactivity. Types of muscle overactivity include 1) spasticity, an increase in the velocity-dependent response to muscle stretch, measured at rest; 2) spastic dystonia, i.e., chronic tonic muscle activity at rest, sensitive to stretch of the dystonic muscle and 3) spastic co-contraction, an inappropriate degree of antagonistic contraction during voluntary agonist command, sensitive to stretch of the co-contracting muscle. A five-step clinical assessment may closely parallel this phenomenology, in which the first four steps aim at quantifying the antagonistic potential of each muscle group. Step-1 measures passive range of motion, i.e., the angle of arrest upon slow stretch of the muscle group assessed (minimizing spastic dystonia), which provides insight on soft tissue length and extensibility. Step-2 measures the angle of catch or clonus upon fast passive stretch of the muscle group assessed, which provides insight on stretch reflex excitability. Step-3 measures the range of active motion against the muscle group assessed, a net result of agonist recruitment minus the combined resistance from passive soft tissue stiffness and spastic co-contraction in the muscle group assessed. Step-4 measures the maximal frequency of rapid alternating movements along the maximal active range of motion, evaluating Step-3 performance repeatability. Step-5 evaluates active function, using for example a walking test (10 m or 2 min) for lower limb and the Modified Frenchay Scale for upper limb assessment, and perceived function through patient global subjective assessment.
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PMID:Five-step clinical assessment in spastic paresis. 2092 7

A 45-year-old female suffering from severe thoracic pain was admitted to the emergency department of our hospital. Thorough clinical examination revealed paresis of the left lower limb and sensory deficit at the level of the Th4 vertebra. MRI of the thoracic spine demonstrated a lesion at the level of Th1-Th7. Despite initial improvement following i.v. corticosteroid administration, the patient's clinical status deteriorated, with recurrence of myelitis and extension of the lesion to Th12. She developed paraparesis, hyperreflexia and spasticity of both legs, symmetrical sensory deficit below Th4, and sphincter dysfunction. Differential diagnosis included infectious, metabolic, neoplastic/paraneoplastic, and ischemic causes as well as multiple sclerosis. NMO IgG was found positive and led to the diagnosis of longitudinal extensive transverse myelitis (LETM) in the NMO spectrum disorders. Administration of immunosuppressive therapy resulted in gradual improvement of the patient's clinical status and stabilization for five years. In the setting of LETM, patients with antiaquaporin 4 IgGs can present features of coexisting systemic involvement. A thorough differential diagnosis is required to guide appropriate therapy.
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PMID:Neuromyelitis optica spectrum disease with positive autoimmune indices: a case report and review of the literature. 2211 May 10

One of the most important objects of stroke rehabilitation is motor recovery from acute stage to chronic stage. Reorganization theory of motor circuits in the cerebral cortex contributing to recovery following stroke is proposed. In acute stage motor recovery depends on residual corticospinal tract excitability from onset to 3 months (1(st) stage recovery) . In next stage alternative output system is used according to intracortical excitability depending on intracortical disinhibition at the peak of 3 months (2(nd) stage recovery) . At 6 months and beyond training-induced synaptic strengthening becomes better established, and new networks are better reorganized (3(rd)stage recovery) . Stroke rehabilitation programs from acute stage are required depending on this stage theory. With each stage to select and perform the most effective rehabilitation programs are necessary. Two obstruction factors of motor recovery are indicated. One of them is Wallerian degeneration of corticospinal tract. Early Wallerian degeneration of the corticospinal tract that is seen on diffusion weighted MRI was reported. The appearance of Wallerian degeneration at acute stage should be directed to more attention as motor recovery inhibition. Next obstruction factor is development of spasticity from acute stage. Spastic paresis is subjected over time to immobilization of the paretic body part and chronic disuse of the paretic body part, which are avoidable through early rehabilitation intervention. Recently various interventions were proposed for motor recovery. The combination of repetitive transcranial magnetic stimulation and intensive occupational therapy by Abo (2010) are recommended to recovery hand function at chronic stage as 3(rd) stage recovery.
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PMID:[Fundamental theory and practice in stroke rehabilitation from acute stage to chronic stage]. 2227 77

Following injury or disease, the central nervous system (CNS), to varying degrees, loses neurons, synaptic connections and conduction-promoting myelin insulation altering the neural circuitry assembled during development. This "New Anatomy" changes neural processing, bringing spasticity, paresis and paralysis to motor function and altered sensation, numbness and pain to sensory function. Focusing on the effects of CNS damage on the motor subsystems, this review offers a neurophysiological assessment perspective developed within the study of human spinal cord injury and extends it to other CNS disorders. It puts forward the concept that there are essential domains of CNS processing, altered by most neurological disorders, that are temporal, the speed of activation and deactivation, and spatial, the distribution across multiple muscles of motor units selected and activated. Measured through multiple-muscle recordings of selected motor-task performance, these domains can be useful in quantifying the severity of CNS damage and changes achieved through recovery or treatment.
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PMID:Neurophysiological characterization of the 'new anatomy' and motor control that results from neurological injury or disease. 2231 Sep 99

Antispastic medications that are directed to reduce clinical signs of spasticity, such as exaggerated reflexes and muscle tone, do not improve the movement disorder. Medication can even increase weakness which might interfere with functional movements, such as walking. In this chapter we address how spasticity affects mobility and how this should be taken into account in the treatment of spasticity. In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are the consequence of spinal cord injury (SCI). They are generally thought to be responsible for spastic movement disorders. Most antispastic treatments are, therefore, directed at the reduction of reflex activity. In recent years, a discrepancy between spasticity as measured in the clinic and functional spastic movement disorder was noticed, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behavior of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fiber, collagen tissue, and tendon properties (e.g., loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organization. Antispastic drugs should primarily be applied in complete SCI. In mobile patients they can accentuate paresis and therefore should be applied with caution.
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PMID:Spasticity. 2309 14

Poststroke spasticity (PSS)-related disability is emerging as a significant health issue for stroke survivors. There is a need for predictors and early identification of PSS in order to minimize complications and maladaptation from spasticity. Reviewing the literature on stroke and upper motor neuron syndrome, spasticity, contracture, and increased muscle tone measured with the Modified Ashworth Scale and the Tone Assessment Scale provided data on the dynamic time course of PSS. Prevalence estimates of PSS were highly variable, ranging from 4% to 42.6%, with the prevalence of disabling spasticity ranging from 2% to 13%. Data on phases of the PSS continuum revealed evidence of PSS in 4% to 27% of those in the early time course (1-4 weeks poststroke), 19% to 26.7% of those in the postacute phase (1-3 months poststroke), and 17% to 42.6% of those in the chronic phase (>3 months poststroke). Data also identified key risk factors associated with the development of spasticity, including lower Barthel Index scores, severe degree of paresis, stroke-related pain, and sensory deficits. Although such indices could be regarded as predictors of PSS and thus enable early identification and treatment, the different measures of PSS used in those studies limit the strength of the findings. To optimize evaluation in the different phases of care, the best possible assessment of PSS would make use of a combination of indicators for clinical impairment, motor performance, activity level, quality of life, and patient-reported outcome measures. Applying these recommended measures, as well as increasing our knowledge of the physiologic predictors of PSS, will enable us to perform clinical and epidemiologic studies that will facilitate identification and early, multimodal treatment.
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PMID:Toward an epidemiology of poststroke spasticity. 2331 81

Background. Long-term splinting, using static orthoses to prevent contractures, is widely accepted in stroke patients with paresis of the upper limb. A number of stroke patients complain about increased pain and spasticity, which leads to the nonuse of the orthosis and a risk of developing a clenched fist. Objectives. Evaluating long-term use of static hand-wrist orthoses and experienced comfort in chronic stroke patients. Methods. Eleven stroke patients who were advised to use a static orthosis for at least one year ago were included. Semistructured telephone interviews were conducted to explore the long-term use and experienced comfort with the orthosis. Data were analyzed using descriptive statistics. Results. After at least one year, seven patients still wore the orthosis for the prescribed hours per day. Two patients were unable to wear the orthosis 8 hours per day, due to poor comfort. Two patients stopped using the orthosis because of an increase in spasticity or pain. Conclusions. These pilot data suggest that a number of stroke patients cannot tolerate a static orthosis over a long-term period because of discomfort. Without appropriate treatment opportunities, these patients will remain at risk of developing a clenched fist and will experience problems with daily activities and hygiene maintenance.
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PMID:Long-term use of a static hand-wrist orthosis in chronic stroke patients: a pilot study. 2353 61


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