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

The purpose of this report is to illustrate the utility of a gait laboratory as a simple, straightforward aid to psychiatric care. The evaluation and management of a patient with spastic paresis and reduced knee flexion in swing (stiff-legged gait), using quantitative gait analysis, are provided. Spastic quadriceps activity during swing was thought to be the cause of reduced knee flexion, based on traditional physiatric history and physical examination. Gait laboratory analysis, including lower extremity kinematic, kinetic and dynamic electromyographic measurements, demonstrated that the quadriceps were not inappropriately active, as had been expected and suggested, instead, that the reduced knee flexion was secondary to dynamic ankle plantar flexor weakness. Modification of an ankle-foot-orthosis and specific exercises to strengthen the ankle plantar flexors were, therefore, prescribed and resulted in kinematic and kinetic improvements at subsequent gait analysis and a subjective feeling by the patient that gait was better. Gait laboratory analysis was useful in determining the optimal rehabilitation plan.
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PMID:An illustration of clinical gait laboratory use to improve rehabilitation management. 799 16

The relative importance of hyperreflexia and paresis in disturbances of voluntary arm movement was studied in a group of patients (n = 25) with spasticity arising from a unilateral ischemic cerebral lesion. Patient performance was evaluated against data obtained from normal subjects (n = 15). Spastic patients achieved lower maximum movement velocities during flexion or extension than did normal subjects. The more marked the paresis of the elbow flexor and extensor muscles of the patients, relative to the strength of the normal subjects, the greater was this reduction in maximum velocity. For a given velocity, however, the time taken to complete a movement and the time to reach the peak velocity were normal. No relationship was found between the degree of impairment of voluntary movement and the level of passive muscle hypertonia in the antagonist. Although overactivity of the antagonist muscle may play some role in disturbance of movements made at low velocities without an opposing load, antagonist activity during movements made against a load (i.e., under more natural conditions) was at or below normal levels, even in those patients with the most marked passive muscle hypertonia. It is concluded that agonist muscle paresis, rather than antagonist muscle hypertonia, plays the dominant role in the disturbance of voluntary elbow movement following stroke.
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PMID:Voluntary movement at the elbow in spastic hemiparesis. 808 Feb 47

Clinical symptoms and patho-anatomic changes in cervical myelopathy due to spondylotic changes are described. The leading symptoms are numbness and clumsiness of upper and lower extremity, mostly combined with gait disturbances. Muscle wasting primarily on the upper extremity leads to the myelopathic hand. Cervical myelopathy can be classified into five main groups: 1. Spastic tetraparesis with numbness and hyperreflexivity of upper and lower extremity. The majority of patients present with the myelopathic hand. 2. Spastic paraparesis with lesion below C6. 3. Spastic tetraparesis, mild or moderate, with deltoid muscle paresis. 4. Amyotrophic myelopathic hand with mild long tract signs. 5. Central cord syndrome due to cervical spondylosis combined with trauma. From the therapeutic aspect, conservative treatment is often unsuccessful. It is important to relieve pressure on the spinal cord, and decompressive procedures, especially posterior laminoplasty techniques, are required. Earlier surgery provides better results.
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PMID:[Symptoms and pathological anatomy of the degenerative cervical spine]. 899 3

Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.
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PMID:Pathophysiology of spastic paresis. I: Paresis and soft tissue changes. 1571 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

The hereditary spastic paraplegias (HSPs) are a heterogeneous group of motorneuron diseases characterized by progressive spasticity and paresis of the lower limbs. Mutations in Spastic Gait 4 (SPG4), encoding spastin, are the most frequent cause of HSP. To understand how mutations in SPG4 affect human neurons, we generated human induced pluripotent stem cells (hiPSCs) from fibroblasts of two patients carrying a c.1684C>T nonsense mutation and from two controls. These SPG4 and control hiPSCs were able to differentiate into neurons and glia at comparable efficiency. All known spastin isoforms were reduced in SPG4 neuronal cells. The complexity of SPG4 neurites was decreased, which was paralleled by an imbalance of axonal transport with less retrograde movement. Prominent neurite swellings with disrupted microtubules were present in SPG4 neurons at an ultrastructural level. While some of these swellings contain acetylated and detyrosinated tubulin, these tubulin modifications were unchanged in total cell lysates of SPG4 neurons. Upregulation of another microtubule-severing protein, p60 katanin, may partially compensate for microtubuli dynamics in SPG4 neurons. Overexpression of the M1 or M87 spastin isoforms restored neurite length, branching, numbers of primary neurites and reduced swellings in SPG4 neuronal cells. We conclude that neurite complexity and maintenance in HSP patient-derived neurons are critically sensitive to spastin gene dosage. Our data show that elevation of single spastin isoform levels is sufficient to restore neurite complexity and reduce neurite swellings in patient cells. Furthermore, our human model offers an ideal platform for pharmacological screenings with the goal to restore physiological spastin levels in SPG4 patients.
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PMID:Gene dosage-dependent rescue of HSP neurite defects in SPG4 patients' neurons. 2438 12

Contracted flexor tendon leading to flexural deformity is a common congenital defect in cattle. Arthrogryposis is a congenital syndrome of persistent joint contracture that occurs frequently in Europe as a consequence of Schmallenberg virus infection of the dam. Spastic paresis has a hereditary component, and affected cattle should not be used for breeding purposes. The most common tendon avulsion involves the deep digital flexor tendon. Tendon disruptions may be successfully managed by tenorrhaphy and external coaptation or by external coaptation alone. Medical management alone is unlikely to be effective for purulent tenosynovitis.
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PMID:Diseases of the tendons and tendon sheaths. 2453 64

Clinical symptoms and patho-anatomic changes in cervical myelopathy due to spondylotic changes are described. The leading symptoms are numbness and clumsiness of upper and lower extremity, mostly combined with gait disturbances. Muscle wasting primarily on the upper extremity leads to the myelopathic hand. Cervical myelopathy can be classified into five main groups: 1. Spastic tetraparesis with numbness and hyperreflexivity of upper and lower extremity. The majority of patients present with the myelopathic hand. 2. Spastic paraparesis with lesion below C6. 3. Spastic tetraparesis, mild or moderate, with deltoid muscle paresis. 4. Amyotrophic myelopathic hand with mild long tract signs. 5. Central cord syndrome due to cervical spondylosis combined with trauma. From the therapeutic aspect, conservative treatment is often unsuccessful. It is important to relieve pressure on the myelon, and decompressive procedures, especially posterior laminoplasty techniques, are required. Earlier surgery provides better results.
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PMID:[Clinical symptoms and patho-anatomic changes in cervical myelopathy]. 2824 74

In this review, we will work around two simple definitions of two different entities, which most often co-exist in patients with lesions to central motor pathways: Spasticity is "Enhanced excitability of velocity-dependent responses to phasic stretch at rest", which will not be the subject of this review, while Spastic dystonia is tonic, chronic, involuntary muscle contraction in the absence of any stretch or any voluntary command (Gracies, 2005). Spastic dystonia is a much less well understood entity that will be the subject this review. Denny-Brown (1966) observed involuntary sustained muscle activity in monkeys with lesions restricted to the motor cortices . He further observed that such involuntary muscle activity persisted following abolition of sensory input to the spinal cord and concluded that a central mechanism rather than exaggerated stretch reflex activity had to be involved. He coined the term spastic dystonia to describe this involuntary tonic activity in the context of otherwise exaggerated stretch reflexes. Sustained involuntary muscle activity in the absence of any stretch or any voluntary command contributes to burdensome and disabling body deformities in patients with spastic paresis. Yet, little has been done since Denny-Brown's studies to determine the pathophysiology of this non- stretch or effort related sustained involuntary muscle activity following motor lesions and there is a clear need for research studies in order to improve current therapy. The purpose of the present review is to discuss some of the possible mechanisms that may be involved in the hope that this may guide future research. We discuss the existence of persistent inward currents in spinal motoneurones and present the evidence that the channels involved may be upregulated following central motor lesions. We also discuss a possible contribution from alterations in synaptic inputs from surviving or abnormally branched sensory and descending fibres leading to over-activity and lack of motor coordination. We finally discuss evidence of alterations in motor cortical representational maps and basal ganglia lesions.
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PMID:On Denny-Brown's 'spastic dystonia' - What is it and what causes it? 2916 22

Spastic paresis is a common feature of an upper motor neuron impairment caused by stroke, brain injury, multiple sclerosis and other central nervous system (CNS) disorders. Existing national and international guidelines for the treatment of adult spastic paresis tend to focus on the treatment of muscle overactivity rather than the comprehensive approach to care, which may require life-long management. Person-centered care is increasingly adopted by healthcare systems in a shift of focus from "disease-oriented" towards "person-centered" medicine. The challenge is to apply this principle to the complex management of spastic paresis and to include an educative process that engages care providers and patients and encourages them to participate actively in the long-term management of their own disease. To address this issue, a group of 13 international clinicians and researchers used a pragmatic top-down methodology to evaluate the evidence and to formulate and grade the strength of recommendations for applying the principles of person-centered care to the management of spastic paresis. There is a distinct lack of clinical trial evidence regarding the application of person-centered medicine to the rehabilitation setting. However, the current evidence base supports the need to ensure that treatment interventions for spastic paresis should be centered on as far as reasonable on the patient's own priorities for treatment. Goal setting, negotiation and formal recording of agreed SMART goals should be an integral part of all spasticity management programs, and goal attainment scaling should be recorded alongside other standardized measures in the evaluation of outcome. When planning interventions for spastic paresis, the team should consider the patient and their family's capacity for self-rehabilitation, as well as ways to enhance this approach. Finally, the proposed intervention and treatment goals should consider the impact of any neuropsychological, cognitive and behavioral deficits on rehabilitation. These recommendations support a person-centric focus in the management of spastic paresis.
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PMID:A comprehensive person-centered approach to adult spastic paresis: a consensus-based framework. 2926 92


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