Muscle Hypertonia
Muscle Spasticity
Evaluating the role of botulinum toxin in the management of focal hypertonia in adults. (1/79)
OBJECTIVES: To investigate the effects of EMG guided botulinum toxin (BTX-A) on impairment and focal disability in adults presenting with focal hypertonia. METHODS: A prospective, randomised, double blind, placebo controlled, parallel group trial was carried out with standardised assessment before and at 3 week intervals until 12 weeks after injection, in patients with focal hypertonia affecting upper or lower limbs. Botulinum toxin or placebo was injected with EMG guidance after multidisciplinary assessment. The modified Ashworth scale of spasticity, percentage passive range of joint motion, subjective rating of problem severity, the Rivermead motor assessment scale, a timed 10 metre walk (lower limb patients), nine hole peg test (upper limb patients), and a modified goal attainment scale were used as outcome measures. The patients were 52 adults; 34 male, 18 female; mean age 40.31, range 16-79 years; mean duration of symptoms 35 months (range 3 months to 22 years). Diagnoses included cerebrovascular accidents (23), head injury (12), incomplete spinal cord injury (six), tumour (five), cerebral palsy (three), and anoxic episodes (three). RESULTS: For each variable an overall score for the treatment period was computed by summing the scores from the 3, 6, 9, and 12 week assessments. These overall scores were significantly better in the treated group for the Ashworth scale, percentage passive range of movement, Rivermead lower limb, and subjective rating of problem severity. The significant treatment effect on the Ashworth scale was seen on analysis of variance (ANOVA) at 3 weeks and the subjective rating of problem severity at 3 and 6 weeks. The goal attainment scale score in both groups was similar at 12 weeks. CONCLUSION: Selective use of botulinum toxin to weaken muscles can lead to a reduction in resistance to passive movement about a distal limb joint. This allows for improvements in passive range of movement and focal disability, particularly in patients presenting with focal spasticity of the lower limb. (+info)Functional evidence of a constitutively active population of alpha(1D)-adrenoceptors in rat aorta. (2/79)
After depletion of intracellular calcium stores sensitive to noradrenaline, a spontaneous increase in the resting tone (IRT) when incubated in Ca(2+)-containing solution was observed in isolated rat aorta, but not in tail artery. This IRT does not depend on agonist activation of alpha(1)-adrenoceptors but it is inhibited by prazosin. A close relationship was found between the inhibitory potencies of prazosin (pIC(50) = 9.833), BMY 7378 (pIC(50) = 8.924), and 5-methylurapidil (pIC(50) = 7.883) against IRT and their affinities for cloned alpha(1D)-adrenoceptors. Chloroethylclonidine (100 micromol. l(-1)) did not inhibit the IRT. After depletion of internal calcium stores by noradrenaline in absence of the agonist, loading in Ca(2+)-containing solution also brings about an increase in the inositol phosphate (IP) levels in rat aorta (not seen in tail artery) that is inhibited by prazosin (1 micromol. l(-1)), BMY 7378 (10 micromol. l(-1)), and 5-methylurapidil (10 micromol. l(-1)), thus confirming the results obtained in contractile studies. Chloroethylclonidine (100 micromol. l(-1)) did not inhibit this IP accumulation. The fact that the IRT and the IP accumulation related to it can be selectively inhibited by different alpha(1)-adrenoceptor antagonists suggests the existence of a population of alpha(1D)-adrenoceptors that show constitutive activity in rat aorta, not in tail artery. (+info)Intrathecal baclofen for spastic hypertonia from stroke. (3/79)
BACKGROUND AND PURPOSE: We sought to determine whether continuous intrathecal delivery of baclofen can effectively decrease spastic hypertonia due to stroke. METHODS: Stroke patients with >6 months of intractable spasticity were screened via a randomized, double-blind, placebo-controlled crossover design of either intrathecal normal saline or 50 microgram baclofen. Those who dropped an average of 2 points in either their affected lower extremity side Ashworth or Penn spasm frequency scores were then offered computer-controlled pump implantation for continuous ITB and followed prospectively for up to 12 months. RESULTS: In 21 stroke patients 6 hours after the active drug bolus, the average (+/-SD) lower extremity Ashworth score on the affected extremities decreased from 3.3+/-1.2 to 1.4+/-0.7 (P<0.0001), spasm score from 1.2+/-1.2 to 0.1+/-0.3 (P=0.0224), and reflex score from 2.1+/-1.2 to 0.1+/-0.5 (P<0.0001). The average upper extremity Ashworth score on the affected extremities decreased from 2.8+/-1.1 to 1.8+/-0.8 (P<0.0001), spasm score from 0.7+/-1.0 to 0.2+/-0.4 (P=0.1544), and reflex score from 2.1+/-0.9 to 1.2+/-0.9 (P=0.0004). All active drug scores were statistically different from placebo scores at 6 hours (P<0.05). With up to 12 months of continuous infusion of ITB in 17 implanted patients, the average lower extremity Ashworth score on the affected extremities decreased from 3.7+/-1.0 to 1.8+/-1.1 (P<0.0001), the spasm score dropped from 1.2+/-1.3 to 0.6+/-1.0 (P=0.4282), and the reflex score decreased from 2.4+/-1.3 to 1.0+/-1.3 (P<0.0001). The average upper extremity Ashworth score in the affected extremities decreased from 3.2+/-1.1 to 1.8+/-0.9 (P<0.0001), the spasm score dropped from 0.7+/-1.0 to 0.3+/-0.8 (P=0.8685), and the reflex score decreased from 2.4+/-0.8 to 1.5+/-1.2 (P=0.3337). The average continuous ITB dose required to attain these effects was 268 microgram/d. CONCLUSIONS: Intrathecal infusion of baclofen is capable of maintaining a reduction in the spastic hypertonia resulting from stroke. (+info)Nature and nurture in vitamin B12 deficiency. (4/79)
We report on a child in whom severe nutritional vitamin B12 deficiency was exacerbated by a genetic impairment of the folate cycle, causing reduced CSF concentrations of the methyl group donor 5-methyltetrahydrofolate. Some patients with vitamin B12 deficiency may benefit from high dose folic acid supplementation, even if plasma concentrations are high. (+info)ALG12 mannosyltransferase defect in congenital disorder of glycosylation type lg. (5/79)
In the endoplasmic reticulum (ER) of eukaryotes, N-linked glycans are first assembled on the lipid carrier dolichyl pyrophosphate. The GlcNAc(2)Man(9)Glc(3) oligosaccharide is transferred to selected asparagine residues of nascent polypeptides. Defects along the biosynthetic pathway of N-glycans are associated with severe multisystemic syndromes called congenital disorders of glycosylation. Here, we describe a deficiency in the ALG12 ER alpha1,6-mannosyltransferase resulting in a novel type of glycosylation disorder. The severe disease was identified in a child presenting with psychomotor retardation, hypotonia, growth retardation, dysmorphic features and anorexia. In the patient's fibroblasts, the biosynthetic intermediate GlcNAc(2)Man(7) oligosaccharide was detected both on the lipid carrier dolichyl pyrophosphate and on newly synthesized glycoproteins, thus pointing to a defect in the dolichyl pyrophosphate-GlcNAc(2)Man(7)-dependent ALG12 alpha1,6 mannosyltransferase. Analysis of the ALG12 cDNA in the CDG patient revealed compound heterozygosity for two point mutations that resulted in the amino acid substitutions T67M and R146Q, respectively. The impact of these mutations on ALG12 protein function was investigated in the Saccharomyces cerevisiae alg12 glycosylation mutant by showing that the yeast ALG12 gene bearing the homologous mutations T61M and R161Q and the human mutant ALG12 cDNA alleles failed to normalize the growth defect phenotype of the alg12 yeast model, whereas expression of the normal ALG12 cDNA complemented the yeast mutation. The ALG12 mannosyltransferase defect defines a new type of congenital disorder of glycosylation, designated CDG-Ig. (+info)Managing older patients with urinary retention in the Continence Clinic. (6/79)
OBJECTIVE: To evaluate the effectiveness of the Continence Clinic for managing retention of urine in older patients. DESIGN: Retrospective study. SETTING: Continence Clinic, Fung Yiu King Hospital, Hong Kong. SUBJECTS AND METHODS: Case notes of 58 patients seen at the Fung Yiu King Hospital Continence Clinic from October 1997 to September 2001 were reviewed. The patients had retention of urine with post-void residual volume of more than 200 mL, retention of urine requiring catheterization, or had catheters for unknown reasons. RESULTS: Urodynamic study performed for 22 (38%) patients showed that 12 had detrusor underactivity, six had detrusor hyperactivity with impaired contraction, and four had bladder outlet obstruction. Among the patients who were initially catheterized, the success rate for gradually stopping reliance on urinary catheterization was 84%. The success rate was higher among those who did not undergo urodynamic study than among those who had the study done (95% versus 67%; P=0.03). Reduction in post-void residual volume was observed at the last clinic visits (P<0.0001). Moreover, significant decreases in post-void residual volume were found both for patients who did and did not have urodynamic study. CONCLUSION: Most of the older patients with urinary retention with or without indwelling catheters were treated successfully in the Continence Clinic by appropriate medical therapy. Urodynamic study can be performed for selected patients when managing urinary retention. (+info)Urinary bladder instability induced by selective suppression of the murine small conductance calcium-activated potassium (SK3) channel. (7/79)
Small conductance, calcium-activated potassium (SK) channels have an important role in determining the excitability and contractility of urinary bladder smooth muscle. Here, the role of the SK isoform SK3 was examined by altering expression levels of the SK3 gene using a mouse model that conditionally overexpresses SK3 channels (SK3T/T). Prominent SK3 immunostaining was found in both the smooth muscle (detrusor) and urothelium layers of the urinary bladder. SK currents were elevated 2.4-fold in isolated myocytes from SK3T/T mice. Selective suppression of SK3 expression by dietary doxycycline (DOX) decreased SK current density in isolated myocytes, increased phasic contractions of isolated urinary bladder smooth muscle strips and exposed high affinity effects of the blocker apamin of the SK isoforms (SK1-3), suggesting an additional participation from SK2 channels. The role of SK3 channels in urinary bladder function was assessed using cystometry in conscious, freely moving mice. The urinary bladders of SK3T/T had significantly greater bladder capacity, and urine output exceeded the infused saline volume. Suppression of SK3 channel expression did not alter filling pressure, threshold pressure or bladder capacity, but micturition pressure was elevated compared to control mice. However, SK3 suppression did eliminate excess urine production and caused a marked increase in non-voiding contractions. The ability to examine bladder function in mice in which SK3 channel expression is selectively altered reveals that these channels have a significant role in the control of non-voiding contractions in vivo. Activation of these channels may be a therapeutic approach for management of non-voiding contractions, a condition which characterizes many types of urinary bladder dysfunctions including urinary incontinence. (+info)The use of casts in the management of joint mobility and hypertonia following brain injury in adults: a systematic review. (8/79)
Many controversies exist regarding the practicality, the theoretical premises, and the supporting evidence for the use of casts in the management of joint hypomobility and hypertonia (ie, increase in joint resistance to passive movement resulting from hyperactivity of the stretch reflex and/or changes in the muscles and connective tissues). The purpose of this review was to determine current best practice for the use of casting in the rehabilitation of adults with brain injury. A systematic review was undertaken to find studies that quantified the effectiveness of casting in adults with brain injury. Thirteen articles that presented experimental or case report evidence on casting were analyzed using Sackett's levels of evidence and were examined for scientific rigor. A grade B recommendation is given for the use of casting to increase passive range of motion or to prevent its loss, and implications for further research are provided. (+info)Muscle hypertonia is a term used to describe an increased tone or tension in the muscles, which can be caused by various medical conditions. This state leads to a reduced ability to stretch the muscle fully, and it may interfere with normal movement. The two main types of muscle hypertonia are spasticity and rigidity.
1. Spasticity: It is a velocity-dependent increase in muscle tone, which means that the resistance to passive movement increases as the speed of the movement increases. This type of hypertonia is often associated with upper motor neuron lesions, such as those caused by stroke, spinal cord injury, or multiple sclerosis.
2. Rigidity: It is a constant and non-velocity dependent increase in muscle tone, meaning that the resistance to passive movement remains consistent regardless of the speed. This type of hypertonia can be seen in conditions like Parkinson's disease.
It is essential to diagnose and manage muscle hypertonia effectively to prevent complications such as contractures, pain, and decreased functional abilities. Treatment options may include physical therapy, medications (like antispasticity agents), orthoses, or surgical interventions in severe cases.
Muscle spasticity is a motor disorder characterized by an involuntary increase in muscle tone, leading to stiffness and difficulty in moving muscles. It is often seen in people with damage to the brain or spinal cord, such as those with cerebral palsy, multiple sclerosis, or spinal cord injuries.
In muscle spasticity, the muscles may contract excessively, causing rigid limbs, awkward movements, and abnormal postures. The severity of muscle spasticity can vary from mild stiffness to severe contractures that limit mobility and function.
Muscle spasticity is caused by an imbalance between excitatory and inhibitory signals in the central nervous system, leading to overactivity of the alpha motor neurons that control muscle contraction. This can result in hyperreflexia (overactive reflexes), clonus (rapid, rhythmic muscle contractions), and flexor or extensor spasms.
Effective management of muscle spasticity may involve a combination of physical therapy, medication, surgery, or other interventions to improve function, reduce pain, and prevent complications such as contractures and pressure sores.