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At least 37 records · Page 2Linked to original sources
PubMed2002

Changes in hip spasticity and strength following selective dorsal rhizotomy and physical therapy for spastic cerebral palsy.

Hip adductor spasticity and strength in participants with cerebral palsy (CP) were quantified before and after selective dorsal rhizotomy (SDR) and intensive physical therapy. Twenty-four participants with cerebral palsy (CP group) and 35 non-disabled participants (ND controls) were tested with a dynamometer (OP group: mean age 8 years 5 months, 13 males, 11 females; ND group: mean age 8 years 6 months, 19 males, 16 females). According to the Gross Motor Function Classification System (GMFCS), of the 24 participants with CP, eight were at level I, six were at level II, and 10 participants were at level III. For the spasticity measure, the dynamometer quantified the resistive torque of the hip adductors during passive abduction at 4 speeds. The adductor strength test recorded a maximum concentric contraction. CP group spasticity was significantly reduced following SDR and adductor strength was significantly increased after surgery. Both pre- and postoperative values remained significantly less than the ND controls. Spasticity results agreed with previous studies indicating a reduction. Strength results conflicted with previous literature subjectively reporting a decrease following SDR. However, results agreed with previous objective investigations examining knee and ankle strength, suggesting strength did not decrease following SDR.

Adolescent↗
PubMed2001

Classification of gait patterns in spastic hemiplegia and spastic diplegia: a basis for a management algorithm.

Classifications of gait and postural patterns in spastic hemiplegia and spastic diplegiía are presented, based on the work of previous authors. The classifications are used as a biomechanical basis, linking spasticity, musculoskeletal pathology in the lower limbs, and the appropriate intervention strategies. The choice of target muscles for spasticity management, the muscle contractures requiring lengthening and the choice of orthotics are then linked to the underlying gait pattern.

Algorithms↗
PubMed1975

Bovine spastic paralysis: cerebrospinal fluid concentrations of homovanillic acid and 5-hydroxyindoleacetic acid in normal and spastic calves.

Homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were determined in the cerebrospinal fluid (CSF) of 28 normal calves and 29 spastic calves. Concentrations of HVA were significantly (P less than 0.01) lower in spastic calves, whereas differences in 5-HIAA concentrations were not found between normal and spastic calves. These findings indicate that a lower dopaminergic metabolism takes place in the central nervous system (CNS) of spastic calves.

Animals↗
PubMed2005

Quantitative assessment of spasticity in human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis.

People with human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) develop spasticity. The authors examined 34 patients with HAM/TSP in Perú using a device that measures tone in the gastroc-soleus-Achilles tendon unit and provides a quantitative spasticity assessment (QSA). Tone in the 34 patients was more than double that of women with asymptomatic HTLV-I infection. The device may help to track progression in HTLV-I infection.

Adult↗
PubMed2004

Clinical progression and genetic analysis in hereditary spastic paraplegia with thin corpus callosum in spastic gait gene 11 (SPG11).

BACKGROUND: Hereditary spastic paraplegia (HSP) with thin corpus callosum (CC) is a rare neurodegenerative disorder classified as a complicated form of spastic paraplegia. Some patients with HSP with thin CC have previously been described in Japanese families, and the genetic locus was linked to chromosome 15q13-15. OBJECTIVE: Our objective was to further clinically and genetically characterize HSP with thin CC. PATIENTS: We describe the clinical, structural, and functional follow-up and the genetic characterization of 2 sisters aged 26 and 31 years who had severe spastic paraplegia and cognitive impairment. RESULTS: Magnetic resonance imaging revealed a thin CC with progressing frontoparietal cortical atrophy paralleled by cognitive decline. Using transcranial magnetic stimulation, we delineated a lack of transcallosal inhibition. Images obtained with(18)fluorodeoxyglucose positron emission tomography showed reduced cortical and thalamic hypometabolism that decreased further within 4 years. Additionally, combined axonal loss and demyelinating sensorimotor polyneuropathy were present. Because other family members were not affected, autosomal recessive inheritance was considered likely. Genetic analysis of this autosomal recessive HSP was consistent with the linkage to 15q13-15 (markers D15S971, D15S118, D15S994, and D15S659). No mutation was found within the SLC12A6 gene. CONCLUSION: Progressive axonal degeneration occurs in the corticocortical projections, corticospinal tract, and peripheral nerves in HSP with thin CC linking to chromosome 15q13-15 in a German pedigree.

Adult↗
PubMed1997

Dosing, administration, and a treatment algorithm for use of botulinum toxin A for adult-onset spasticity. Spasticity Study Group.

Botulinum toxin type A (BTX-A) has been shown to be a safe and effective treatment for focal or segmental muscle overactivity, including spasticity. Local injections of BTX-A are particularly valuable in relieving focal spasticity around a joint or a series of joints. When integrated into an overall spasticity treatment plan with clearly outlined functional goals, BTX-A may offer significant benefits to the appropriately selected adult or pediatric patient. A range of clinical outcome measures are used to evaluate the patient prior to injection. Initial dosing guidelines are offered, though each patient may have a unique drug response profile and set of modifying factors that will be used as a basis for dose adjustments. Clinical benefit usually lasts for approximately 12 weeks, though in some patients the duration of effect may be longer. Assessment of the patient's clinical and functional status is performed at each follow-up appointment, and the contribution of BTX therapy to the goals of the patient and caregiver are evaluated. Other therapeutic options should be considered where appropriate, and the treatment plan revised when necessary. Guidelines for dilution, handling, and office procedure are offered.

Adult↗
PubMed1977

Spasticity: its physiology and management. Part I. Neurophysiology of spasticity: classical concepts.

Spasticity, seen so frequently in clinical situations, presents motor signs resembling those produced experimentally by transecting the brain stem of a cat at the intercollicular level. This paper reviews experimental results which elucidate the roles of different brain regions in the genesis of classical decerebrate rigidity and demonstrate the function of the gamma motor system in the maintenance of the rigidity. Interruption of the gamma-spindle loop of a muscle (i.e. interrupting the monosynaptic reflex arc subserving the stretch reflexes) abolishes rigidity in that muscle. This reflex-mediated gamma support of decrebrate rigidity is also a prominent feature of clinical spasticity, making classical decerebrate rigidity a useful model for studying the neural mechanisms underlying spasticity. Not all rididities, however, are gamma dependent. Those rigidities surviving dorsal root rhizotomy are called alpha rigidity. Alpha rigidity results when a brain lesion disrupts descending systems which normally exert a net inhibitory effect upon alpha motoneurons.

Animals↗
PubMed1977

Spasticity: its physiology and management. Part III. Identifying and assessing the mechanisms underlying spasticity.

Patients with spasticity may have similar motor signs and yet have completely different underlying neural mechanisms. This paper reviews some experimental tests which have been developed to detect and analyze excitatory excesses and inhibitory deficits giving rise to the abnormal motor signs of spasticity. Although at the present time these tests may not lend themselves to routine clinical application, their results are creating a body of knowledge which will become the foundation for diagnosis and treatment of spasticity in the future.

Brain↗
PubMedDate not supplied

Reflex torque response to movement of the spastic elbow: theoretical analyses and implications for quantification of spasticity.

A parametric model of the human reflex torque response to a large-amplitude, constant angular velocity elbow extension was developed in order to help quantify spasticity in hemiparetic stroke patients, and to better understand its pathophysiology. The model accounted for the routinely observed leveling of torque (i.e., a plateau) at a mean angular increment of 51 degrees +/- 10 degrees s.d. (n = 98) after the initial rise. This torque "plateau" was observed in all eight subjects, and in 98 of 125 trials across 25 experimental sessions. The occurrence of this plateau cannot be explained by decreases in elbow flexor moment arms during elbow extension. Rather, the plateau is attributable to a consistent leveling in muscle activation as confirmed both qualitatively from recordings of rectified, smoothed electromyograph (EMG) activity, and quantitatively using an EMG coefficient model. A parametric model was developed in which the pattern of muscle activation in the stretch reflex response of elbow flexors was described as a cumulative normal distribution with respect to joint angle. Two activation functions, one related to biceps and the other to brachioradialis/brachialis, were incorporated into the model in order to account for observations of a bimodal angular stiffness profile. The resulting model yielded biologically plausible parameters of the stretch reflex response which may prove useful for quantifying spasticity. In addition, the model parameters had clear pathophysiological analogs, which may help us understand the nature of the stretch reflex response in spastic muscles.

Adult↗
PubMed1980

Dynamic motor capacity in spastic paresis and its relation to prime mover dysfunction, spastic reflexes and antagonist co-activation.

Dynamic motor capacity was studied in 24 patients with spastic paraparesis (18 cases) or hemiparesis (6 cases). Torque was recorded with an isokinetic dynamometer in voluntary dynamic knee extensions and flexions at maximum effort and in passive movements at preset speeds of 30, 90 and 180 deg . s-1. EMG was recorded with surface electrodes from the quadriceps and the hamstring muscles. The capacity to accelerate motion up to preset speed was deficient in all patients as compared with healthy subjects. The moment of muscle force in movements at maximum effort was generally more reduced in fast than in slow movements. Spastic restraint in passive movements was low in the great majority of legs examined except in the fastest flexion, where about half showed restraint greater than 10 Nm. In a few cases, spastic reflexes were inhibited in voluntary motion. Most commonly, the restraint was greater in voluntary than in passive movements at equal range and speed. In voluntary motion, antagonist restraint was more common at high than at low speed of motion, and when present at low speed, it usually became greater with increasing speed of motion. It often reached a considerable magnitude, as estimated from EMG and may constitute a crucial component in the motor handicap.

Adult↗
PubMed1989

Early diagnosis of spastic diplegia, spastic hemiplegia, and quadriplegia.

A retrospective study examined early neurodevelopmental behaviors of children with spastic diplegia, spastic hemiplegia, and quadriplegia (spastic, athetoid, or mixed) who had been followed up longitudinally in a high-risk infant follow-up clinic. Compared with peers with normal outcomes, children with all three types of cerebral palsy had significantly lower scores on the Bayley Mental Scale at 4 months of age; children with hemiplegia and quadriplegia also scored significantly lower on the Bayley Motor Scale. On the Movement Assessment of Infants at 4 months of age, the children with hemiplegia and quadriplegia showed significantly higher risk scores than the nonhandicapped group. The Movement Assessment of Infants was more than three times as sensitive as the Bayley Motor Scale in detecting motor abnormalities in 4-month-old infants with diplegia and more than twice as sensitive in detecting early abnormalities of hemiplegia. At 1 year of age, however, the Bayley Motor Scale was extremely sensitive in picking up motor deficits in children with all three types of cerebral palsy.

Cerebral Palsy↗
PubMed2004

The effect of botulinum toxin type-A injection on spasticity, range of motion and gait patterns in children with spastic diplegic cerebral palsy: an Egyptian study.

Spasticity is defined as increased resistance to passive movement, secondary to hyperreflexia after an upper motor neuron lesion. In children with cerebral palsy (CP), it can interfere with mobility and self-care and can contribute to development of fixed myostatic contractures. This study investigated the efficacy of botulinum toxin type-A, a neuromuscular blocking agent that reduces muscle tone, in a variety of neuromuscular disorders, injections in a prospective, 3-month, controlled study involving 40 children with spastic diplegic CP. The patients were divided into two groups: Group 1 (20 patients) entered a botulinum toxin type-A injection+physiotherapy rehabilitation program; Group 2 (20 patients) were given the physiotherapy rehabilitation program only. Patients were assessed at 4, 8 and 12 weeks post-treatment using the Modified Ashworth Scale (MAS), dynamic gait pattern, ankle range-of-motion measurements and quantification of muscle denervation by nerve conduction techniques. The botulinum toxin type-A group demonstrated statistically significantly decreased spasticity, improved gait function and improved range of motion with evidence of partial denervation of the injected muscle compared to the control group. In conclusion, botulinum toxin type-A injections are a well-tolerated, non-surgical technique that can improve overall response to physiotherapy.

Ankle Joint↗
PubMed1998

Spasticity, mental retardation, macrocephaly and distinct craniofacial appearance: confirmation of a new subtype of complicated spastic paraplegia?

Spasticity, mental retardation, macrocephaly and distinct craniofacial appearance: confirmation of a new subtype of complicated spastic paraplegia?: In this report, we describe a 30-year-old female with mental retardation, spastic paresis, epilepsy, macrocephaly and distinct craniofacial appearance. Probably, she suffers from the same condition as the two sibs described by Fryns et al., in 1994 (2).

Adult↗
PubMed2001

Botulinum toxin type A management of spasticity in the context of orthopaedic surgery for children with spastic cerebral palsy.

Cerebral palsy is the most common cause of physical disability affecting children in developed countries. Although cerebral palsy is, by definition, a 'static encephalopathy' the associated musculoskeletal pathology is progressive and current definitions are therefore somewhat inadequate. Understanding the stages of the musculoskeletal pathology is fundamental to understanding current management strategies, including spasticity management, strengthening programmes and deformity correction by orthopaedic surgery. In this review, a number of new management strategies are described, in which spasticity management by intramuscular injections of botulinum toxin type A and deformity correction, by orthopaedic surgery, are combined.

Animals↗
PubMed1977

Spasticity: its physiology and management. Part II. Neurophysiology of spasticity: current concepts.

A review is presented of current information about the structural and functional details of the muscle spindle, denervation supersensitivity, neurotrophism, regenerative capabilities of the peripheral and central nervous systems, CNS plasticity as revealed by recovery of function following brain lesions, and the secondary functional consequences of long-term spasticity. If this recent basic information is to have any practical impact, it must ultimately be incorporated into our concepts of spasticity and applied to our clinical evaluation and treatment procedures.

Brain↗
PubMed1977

Spasticity: its physiology and management. Part IV. Current and projected treatment procedures for spasticity.

Today's prescriptions for treating spasticity may include pharmacological, surgical, or physical procedures. All derive their rationale from the classical concepts of decerebrate rigidity and of brain organization as discussed in Part I. This paper describes the advantages and disadvantages of these current treatment procedures and proposes that recent discoveries about the "recovery" capabilities of the central nervous system may influence the means for managing spasticity in the future.

Forecasting↗
PubMed1987

The treatment of spasticity in multiple sclerosis: a double-blind clinical trial of a new anti-spastic drug tizanidine compared with baclofen.

The anti-spastic effect of a new drug, tizanidine, was compared with that of baclofen in a double-blind clinical trial; 40 seriously handicapped patients with multiple sclerosis (MS) were randomly allocated treatment with one or the other drug for a 6-week period. The antispastic effect was evaluated by clinical criteria. The optimal daily dose of both drugs varied considerably from patient to patient, and was on the average 23 mg for Tizanidin and 59 mg for baclofen. To the extent an antispastic effect was observed, the 2 drugs appeared to be equally effective when given at a 1:2 ratio (mg tizanidine: mg baclofen). Side effects of both drugs were sleepiness, muscular weakness and dry mouth. Tizanidine had a mild depressive effect on blood pressure. Sudden withdrawal of both drugs was accompanied by a transient relative increase of spasticity in approximately half the patients. There were no other changes suggesting physical or psychological dependence. The present study underscores that neither baclofen nor tizanidine are ideal antispastic drugs, and emphasize the need for further research.

Adult↗