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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intrathecal injection of phenol (ITP) has been used to control intractable pain and spasticity. Direct caustic nerve damage has been postulated as the mechanism of analgesia. Sensation is commonly recovered, suggesting that a spontaneous regeneration process takes place. There is, however, a lack of mechanistic information on ITP therapy. To define morphologically the neurolysis and regeneration phenomena produced by ITP, anesthetized rats were subjected to laminectomy at L5; 5 microl of 22% phenol in saline solution or vehicle (control) was injected. Light and electron microscopy studies of nerve roots were performed at 2, 14, and 60 days after injection. Rats given ITP showed at the early stage a variable amount of roots with signs of infarction characterized by loss of axon-myelin units and thrombosis of intra-root vessels. At 14 days, abundance of macrophages removing debris, open vessels, and nerve sprouts was identified in damaged roots. At this time, non-myelinating glial fibrillary acidic protein-positive Schwann cells were observed in both damaged and apparently undamaged roots. At 60 days, abundance of 2',3'-cyclic nucleotide 3'-phosphodiesterase-positive Schwann cells myelinating newly formed axons was observed in damaged roots. Control rats did not show signs of neural or vascular pathology. Attempting to prevent thrombosis, another group of rats received heparin before ITP; these anti-coagulated rats developed radicular thrombosis, neurolysis, and hemorrhage. In conclusion, neurolysis produced by ITP is associated with acute ischemia (not prevented by heparin) and is followed by vascular, nerve, and myelin regeneration. Our results help understand the lack of efficacy of and some complications by ITP clinical therapy.
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PMID:Nerve root degeneration and regeneration by intrathecal phenol in rats: a morphologic approach. 1711 39

Ultrasound-guided, intraneural chemical nerve block was performed to control intractable limb spasticity and its feasibility was evaluated. Twenty-nine patients showing spastic limb were controlled by 53 intraneural injections of chemical agents, either lidocaine or phenol. The main targets were the sciatic, tibial and musculocutaneous nerves. After identification of the spastic muscle and target nerve, an ultrasound-guided, intraneural injection was administered through a 25-G needle. The average effective duration was 9.1+/-19.6 days in the lidocaine injection group and was 164.5+/-169.4 days in the permanent blocking group with phenol injection. The ultrasound-guided intraneural injection technique was convincing. Intraneural injection of phenol achieved long-lasting improvement of spasticity.
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PMID:Percutaneous chemical nerve block with ultrasound-guided intraneural injection. 1835 55

Cerebrovascular accidents often produce significant pathology, including upper extremity muscle contractures and deformities that may be painful and aesthetically unappealing and that interfere with activities of daily living and hygiene. Orthopaedic intervention may be required to manage these disabilities. Nonsurgical management includes brachial plexus and phenol nerve blocks, which provide temporary relief of painful contractures and allow for a period of spontaneous neurologic recovery of up to 6 months. Definitive surgical procedures should be avoided during this time. After this period, surgical management can be valuable in releasing muscle spasticity, managing painful contractures, and positioning the deformed extremity in a more functional and aesthetically appealing position. Current surgical management is directed at reducing or eliminating muscle spasticity and joint contractures, with the goal of correcting deformities in shoulder adduction, elbow flexion, forearm pronation, wrist and finger flexion, intrinsic muscle spasticity, thumb-in-palm deformity, wrist extension, and finger extension.
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PMID:Orthopaedic management of the upper extremity of stroke patients. 1866 35

Management of spasticity is a major challenge to the rehabilitation team. The initial management has centered on the elimination of externally exacerbating causes, physical therapy, splinting and casting. Medical management has centered on anti-spasticity medication use, but more recently focal treatment methods including phenol blocks and botulinum toxin have been utilized. There has been an increased use of intrathecal baclofen in the management of refractory tone. Dorsal rhizotomy has been advocated for a selective population of children with spasticity. There is no standardized approach to spasticity management and this paper will discuss the importance of evidence-based treatment of spasticity that is adapted for the individual child.
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PMID:[Management of spasticity in children with cerebral palsy]. 1944 46

Most children with paediatric neurotransmitter diseases have global functional deficits secondary to central nervous system damage. Paediatric physiatrists, working in conjunction with a multi-disciplinary team, help to improve physical function by normalizing muscle tone and improving body position. Components of spasticity, rigidity, and dystonia may all need to be considered in a comprehensive treatment programme. Complications of disordered tone include skin breakdown, pain, sleep disturbance, and dysphagia. With an integrated approach to use of medications and equipment as well as implementation of therapy and therapeutic exercise, physiatrists can help maximize functional independence for children with this group of disorders. Pharmacological treatment includes GABA-agonists including baclofen and benzodiazepines, alpha-2 adrenergic agonists, L: -dopa and dopaminergic agents, and dantrolene. Intrathecal baclofen may be used in patients refractory to these medications. In addition, physicians may utilize botulinum toxin, phenol, or surgical interventions such as selective dorsal rhizotomy or tendon lengthening. Pharmacological treatment must be used in conjunction with appropriate adaptive equipment in order to maximize therapeutic benefit. Focus on function in an attempt to increase independence is targeted to improve the child's quality of life. We present a framework and rationale to the management of the functional consequences of the paediatric neurotransmitter diseases.
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PMID:Increasing physical function through physiatric intervention for children with paediatric neurotransmitter disorders. 1944 66

Cerebral palsy is a disorder that primarily affects the neurologic system but secondarily affects the musculoskeletal system through the effects of spasticity, dystonia, and other movement disorders. The treatment of cerebral palsy requires a multidisciplinary approach with treatment aimed at modulating the movement disorder through oral medication, injectable drugs (phenol, botulinum toxin), and physical and occupational therapy. Treatment of the neurologic effects of the central movement disorders include selective dorsal rhizotomy, intrathecal baclofen pump placement, and potentially deep brain stimulation. Although any effect on tone is temporary, orthopedic surgery has an important role in the treatment of the musculoskeletal deformities and contractures present in the child with cerebral palsy. Orthopedic surgery improves function by lengthening the musculotendinous structures, transferring tendons, performing osteotomies to reduce dislocated joints, and normalizing rotation and fusion of selected joints to improve stability. Neurosurgical techniques are not as widely used, but may reduce spasticity in select individuals. The combined approach of managing tone and normalizing the biomechanics of the spine and upper and lower extremities through orthopedic surgery and neurosurgery and subsequent rehabilitation is the cornerstone of treatment of the child and adult with cerebral palsy.
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PMID:Surgical management of spasticity in persons with cerebral palsy. 1976 17

This article will discuss many of the key concepts regarding chemodenervation and neurolysis in the management of spasticity. Topics that will be discussed include techniques for localization, strengths and limitations of various agents (botulinum toxin, phenol, and alcohol), the value of combination therapies, and the role of nerve blocks (diagnostic and therapeutic). With advancing technology have come newer methods to improve accuracy of localization for the performance of chemodenervation and neurolysis such as electromyographic guidance, electrical stimulation, and ultrasound guidance. During the last 2 decades, the addition of botulinum toxin chemodenervation as an adjunct to traditional neurolysis, medication, and therapy modalities has expanded the field of treatment of intramuscular hyperactivity in upper motor neuron syndrome. The technique of diagnostic blocks as predictors of response and the therapeutic value of nerve blocks will be discussed.
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PMID:Chemodenervation and nerve blocks in the diagnosis and management of spasticity and muscle overactivity. 1976 19

This series of articles for rehabilitation in practice aims to cover a knowledge element of the rehabilitation medicine curriculum. Nevertheless they are intended to be of interest to a multidisciplinary audience. The competency addressed in this article is 'The trainee consistently demonstrates a knowledge of the pathophysiology of various specific impairments including spasticity'. Spasticity is an extremely common feature of chronic neurological conditions and, if badly managed, it can result in pain, contractures and pressure sores, all of which can impact on function. It is therefore essential that a multidisciplinary management strategy is in place to help the individual manage their particular situation through education with timely access to interventions including instigation of a physical management programme and medication such as baclofen, tizanidine, dantrolene, benzodiazepines and gabapentin. Further treatment options for focal spasticity are botulinum toxin and phenol nerve blocks or intrathecal baclofen or phenol for predominant lower limb spasticity. Ongoing assessment with the use of appropriate outcome measures can both guide choice of treatment and monitor efficacy.
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PMID:Rehabilitation in practice: Spasticity management. 2036 Jan 50

Patients with hemiplegia frequently suffer from pain and have a limited range of motion (ROM) of the shoulder. The common pattern of shoulder movement in a patient with spastic hemiplegia is primarily adduction and internal rotation. Spasticity of the subscapularis muscle limits the abduction, external rotation and flexion of the shoulder. Injection of botulinum toxin or application of phenol can reduce the spasticity of the subscapularis muscle and various techniques to inject this muscle have been reported. We injected five patients with hemiplegia with botulinum toxin using our previously reported inferior approach, which is easy, safe and effective. We observed a reduction in pain and spasticity and improvement in the ROM of the shoulder for all patients.
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PMID:Botulinum toxin injection of the subscapularis muscle. 2059 73

Phenol is a neurolytic agent used for management of spasticity in patients with either motoneuron lesions or stroke. In addition, compounds that enhance muscle contractility (i.e., polyphenols, etc.) may affect muscle function through the phenol group. However, the effects of phenol on muscle function are unknown, and it was, therefore, the purpose of the present investigation to examine the effects of phenol on tension development and Ca(2+) release in intact skeletal muscle fibers. Dissected intact muscle fibers from Xenopus laevis were electrically stimulated, and cytosolic Ca(2+) concentration ([Ca(2+)](c)) and tension development were recorded. During single twitches and unfused tetani, phenol significantly increased [Ca(2+)](c) and tension without affecting myofilament Ca(2+) sensitivity. To investigate the phenol effects on Ca(2+) channel/ryanodine receptors, single fibers were treated with different concentrations of caffeine in the presence and absence of phenol. Low concentrations of phenol significantly increased the caffeine sensitivity (P < 0.01) and reduced the caffeine concentrations necessary to produce nonstimulated contraction (contracture). However, at high phenol concentrations, caffeine did not increase tension or Ca(2+) release. These results suggest that phenol affects the ability of caffeine to release Ca(2+) through an effect on the ryanodine receptors, or on the sarcoplasmic reticulum Ca(2+) pump. During tetanic contractions inducing fatigue, phenol application decreased the time to fatigue. In summary, phenol increases intracellular [Ca(2+)] during twitch contractions in muscle fibers without altering myofilament Ca(2+) sensitivity and may be used as a new agent to study skeletal muscle Ca(2+) handling.
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PMID:Phenol increases intracellular [Ca2+] during twitch contractions in intact Xenopus skeletal myofibers. 2072 58


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