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

After atraumatic birth, three neonates presented with muscle hypotonia and weakness. Flaccid paresis of the upper extremities, spasticity of the lower extremities, dissociate sensory loss and autonomic dysfunction developed later. This ruled out the initial, tentative diagnoses of cerebral palsy, spinal muscular atrophy or hereditary neuropathy. Diagnostic imaging revealed marked thinning of the cervical spinal cord in all patients. The possible aetiology of these lesions is considered. In all cases, an antenatal or perinatal infarction is thought to be the most probable cause. Different clinical pictures following intrauterine spinal cord ischemia are discussed. Spinal cord lesion must be considered even after atraumatic birth.
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PMID:Cervical spinal cord atrophy in the atraumatically born neonate: one form of prenatal or perinatal ischaemic insult? 1269 May 68

Botulinum toxin has been used for therapeutic purposes in medicine for more than 20 years. Its effective use now covers more than 50 conditions in a wide variety of areas. Its medicinal use was initially based on its blockade of neuromuscular and neurosecretory transfers. Its use for conditions in the field of specific pain therapy is currently authorized in Germany for spastic torticollis, blepharospasm, hemifacial spasm, spastic equine gait in cases of idiopathic cerebral paresis, and spasticity of the arm following stroke. New publications suggest that it can usefully be employed for numerous other painful conditions. The modes of action known today are not confined to the blockade of cholinergic innervation.Indeed, there is also evidence that therapeutic effects are mediated through a normalization of muscle spindle activity, retrograde intake into the CNS with modulation of the central neuropeptide function, inhibition of sterile neurogenic inflammation, and normalization of endplate dysfunction. In view of the methodological peculiarities of studies in the field of pain therapy, such as injection techniques, injection sites, blind study techniques, dosage etc., the scientific evidence for its use in a wide variety of pain syndromes is still patchy in many areas. For this reason the use of botulinum toxin for these syndromes is only justified after full use has been made of standard therapeutic methods and evaluation in specialized centers. The possibility of considering botulinum toxin in specific pain therapy contexts is a new option for patients and doctors.However, its use calls for detailed knowledge of functional neuroanatomy and extensive practical experience and expertise.
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PMID:[Botulinum toxin in specific pain therapy]. 1269 98

A new therapeutic method for the rehabilitation of central paresis of the upper extremity, especially of fine skilled finger movements, is presented. The therapeutic concept is the activation of reorganization processes in the CNS. These processes are elicited by the induction of proprioceptive input to the CNS which corresponds physiologically to the lost input during active movements. The input is generated by repetitive peripheral magnetic stimulation (RPMS) at the innervation zone of the paretic muscles. The stimulation leads to a motion of the activated muscles. The proprioceptive input is generated by two mechanisms: adequately by activation of mechanoreceptors of the stimulated muscles during the induced contractions and relaxations and inadequately by direct activation of the involved sensorimotor afferents. The method has been applied to 52 patients suffering from spastic paresis of the upper extremity. A simple clinical quantification using the Ashworth scale revealed that spasticity could be remarkably (1-2 points) reduced already by one session of RPMS lasting 15 minutes. In order to get an objective insight into the improvement of active motor performances, a neurophysiological investigation of active finger extensions was performed in eight patients suffering from a central hemiparesis. Following RPMS of the paretic finger extensors, the patients could perform rapid finger extensions with larger displacement and velocity at diminished amounts of EMG activity.
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PMID:Facilitation of skilled finger movements by repetitive peripheral magnetic stimulation (RPMS) - a new approach in central paresis. 1271 22

Retrospective clinical analysis with a special focus on pyramidal syndrome expression in the disease course as well as morphological study of brain and spinal structures in all levels of cortical-spinal projection (from brain motor cortex to spinal lumbar segments) have been conducted for 11 section cases of lateral amyotrophic sclerosis (LAS), sporadic type. Two groups of patients were studied: with pronounced pyramidal syndrome (spasticity, hyperreflexia, etc)--7 cases and with some signs of pyramidal deficiency (anisoreflexia, stability of peritoneal reflexes)--4 cases. Pyramidal syndrome in LAS is considered as an emergence of current neurodegenerative process, embracing a significant part of upper motor neurons of both precentral convolution and its axons along the whole length of cerebrospinal axis in the form of cytoplasmic inclusions and axonal spheroids. A presence of pathomorphological changes in other upper segmental structures of motor control reveals their role in pyramidal deficiency. Comparative analysis showed that expression of pyramidal syndrome signs and its correlation to atrophic paresis appearances is specifically determined by the severity of upper and lower motor neurons lesions. With regard to morphological changes in CNS structures, the peculiarities of some pyramidal syndrome appearances in LAS are analyzed.
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PMID:[Pyramidal syndrome in lateral amyotrophic sclerosis: clinico-morphological analysis]. 1278 20

Following stroke, approximately 90% of patients experience persistent neurological motor deficits that lead to disability and handicap. Both pharmacological and physical treatment strategies for motor rehabilitation may be considered. In terms of pharmacological treatment, drugs that may potentially promote motor recovery when added to a regimen of physical therapy include the stimulants amphetamine and methylphenidate, as well as levodopa and fluoxetine. Botulinum toxin A has proven effective and well tolerated in several placebo-controlled trials for the treatment of focal upper and lower limb spasticity, although it has not been shown to improve motor function. The focal injection of botulinum toxin A inhibits the release of acetylcholine into the synaptic cleft, resulting in a reversible paresis of the muscles relevant for the spastic deformity. Other drugs, such as benzodiazepines, antiepileptic drugs and antipsychotics, may have detrimental effects on motor function and should be avoided, if possible. With respect to physical strategies, modern concepts of motor learning favour a task-specific repetitive approach that induces skill-acquisition relevant to the patient's daily life. Constrained-induced movement therapy based on the concept of learned non-use, electromyography-triggered electrical stimulation of the wrist muscles, robot-assisted motor rehabilitation to increase therapy intensity and bilateral practice to facilitate the movement of the paretic extremity are examples in upper limb rehabilitation. Lower limb rehabilitation has been enriched by treadmill training with partial bodyweight support, enabling the practice of up to 1000 steps per session; automated gait rehabilitation to relieve the strenuous effort required of the therapist; and rhythmic auditory stimulation, applying individually adjusted music to improve walking speed and symmetry.
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PMID:Poststroke motor dysfunction and spasticity: novel pharmacological and physical treatment strategies. 1466 87

Local injection of botulinum toxin (BT) is a well-established treatment option for spastic movement disorders in children. BT blocks the release of acetylcholine from the axon terminal into the synaptic cleft of the motor endplate resulting in paresis of the injected musculature. Such localised, temporary chemodenervation of affected muscles can lead to functional gains and may improve the child's daily routine and rehabilitative care. We summarise state-of-the-art treatment of spasticity in children with BT type A, addressing critical issues and introducing recent advances, such as sonography-guided injection of BT and the distal injection of the psoas muscle without the need for general anaesthesia. First-hand experience with BT type B in children is presented.
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PMID:Use of botulinum toxin in pediatric spasticity (cerebral palsy). 1502 70

Head injury can cause extrapyramidal movement disorders such as tremors, parkinsonism, dystonia, chorea, myoclonus, and tics. Pure adventitious movements are rare, but combinations with paresis, spasticity, apraxia, or ataxia occur in approximately 20% of cases of severe head injury, in many cases appearing or evolving in the months following the injury. Tremors may improve in time but many of the other syndromes tend to persist. Reversible causes such as medications or metabolic derangements are occasionally identifiable. Some of these adventitious movements can be improved using neuroactive drugs, botulinum toxin injections, or stereotactic brain surgery.
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PMID:Movement disorders after head injury: diagnosis and management. 1526 58

Continuous intrathecal baclofen infusion (CIBI) for spasticity of spinal and cerebral origin has been practised for over two decades. More recently, it has been used for severe spasticity of cerebral origin in children. Intrathecal baclofen (ITB) appears most beneficial in severe spastic tetraparetics or tetraplegics, but the evaluation of the outcome of ITB and the benefit of the treatment are largely subjective. The evidence base for this treatment has been questioned, in particular for ambulant children, mainly because of the lack of objective outcome measures. Fifty-two spastic tetraparetic children have been treated by this method in Nottingham, from 1998 to 2003. This represents a large homogeneous series of CIBI in children with severe spasticity of cerebral origin. We carried out a prospective audit of our experience, morbidity and observations during that period. We identified that the lack of a suitable scoring system for the evaluation of effectiveness and benefit is a drawback. As a result of these observations a multicentre randomized controlled trial on ITB in tetraplegia-paresis and ambulant children is advocated.
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PMID:Treatment of childhood spasticity of cerebral origin with intrathecal baclofen: a series of 52 cases. 1532 24

The gait-lab at Klinik Berlin developed and evaluated novel physical and pharmacological strategies promoting the repetitive practise of hemiparetic gait in line with the slogan: who wants to relearn walking, has to walk. Areas of research are treadmill training with partial body weight support, enabling wheelchair-bound subjects to repetitively practice gait, the electromechanical gait trainer GT I reducing the effort on the therapists as compared to the manually assisted locomotor therapy, and the future HapticWalker which will allow the additional practise of stair climbing up and down and of perturbations. Further means to promote gait practice after stroke was the application of botulinum toxin A for the treatment of lower limb spasticity and the early use of walking aids. New areas of research are also the study of D-Amphetamine, which failed to promote motor recovery in acute stroke patients as compared to placebo, and the development of a computerized arm trainer, Bi-Manu-T rack, for the bilateral treatment of patients with a severe upper limb paresis.
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PMID:Recovery of gait and other motor functions after stroke: novel physical and pharmacological treatment strategies. 1550 76

The pathophysiological mechanisms underlying the development of spasticity are not clear, but the excitability of the disynaptic reciprocal inhibitory pathway is affected in many patients with spasticity of different origin. Patients with genetically identified autosomal dominant pure spastic paraparesis (ADPSP) develop spasticity and paresis in the legs, but usually have no symptoms in the arms. Comparison of the spinal and supraspinal control of the legs and arms in these patients may therefore provide valuable information about the pathophysiology of spasticity. In the present study, we tested the hypothesis that one of the pathophysiological mechanisms of spasticity in these patients is abnormal corticospinal transmission and that this may lead to decreased reciprocal inhibition. Ten patients and 15 healthy age-matched control subjects were investigated. The patients were all spastic in the legs (with hyperactive tendon reflexes, increased muscle tone and Babinski sign), but had no neurological symptoms in the arms (except for one patient). Disynaptic reciprocal Ia inhibition of flexor carpi radialis (FCR) and soleus (SOL) motoneurons was measured (as the depression of the background FCR and SOL EMG activity and as the short latency inhibition of the FCR and SOL H-reflex evoked by radial and peroneal nerve stimulation). In addition, the latency of motor evoked potentials (MEPs) in the FCR muscle and the tibialis anterior (TA) muscle was measured. In the patients, the mean reciprocal inhibition was normal in the arms, while it was significantly decreased in the leg compared with the healthy subjects. In the patients, the average latency of MEPs in the FCR muscle was normal, while the latency to the MEP in TA muscle was significantly longer than that found in healthy subjects. Four patients, however, differed from the other patients by having significant reciprocal inhibition in the leg and a significantly shorter latency of TA MEPs than found in the other patients. The six patients without reciprocal inhibition in the leg instead had significant short latency facilitation of the SOL H-reflex and a longer TA MEP latency than seen in the healthy subjects and in the four patients with retained reciprocal inhibition. These findings support the hypothesis that disynaptic reciprocal inhibition and short latency facilitation are involved in the development of spasticity and, furthermore, they suggest a positive correlation between impairment of corticospinal transmission and decrease of reciprocal inhibition/appearance of reciprocal facilitation.
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PMID:Reciprocal inhibition and corticospinal transmission in the arm and leg in patients with autosomal dominant pure spastic paraparesis (ADPSP). 1550 21


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