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Muscle Spasms (muscle + spasm)
Selected AbstractsConnecting the dots: trafficking of neurotrophins, lectins and diverse pathogens by binding to the neurotrophin receptor p75NTREUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2003Rafal Butowt Abstract The common receptor for neurotrophins, p75, has important roles in internalization and trafficking of neurotrophins along axons. Recent studies show that an astonishing array of proteins, including lectins, pathogens and neurotoxins, bind the p75 receptor, suggesting that they can hijack and utilize this receptor for trafficking between neuronal populations within the nervous system. Such pathogens include the neurologically important rabies viruses, prion proteins, ,-amyloid and possibly tetanus toxin. These proteins may hijack existing transport machineries designed to traffick neurotrophins, thus allowing the infiltration and distribution of pathogens and toxins among vulnerable neuronal populations with devastating effects, as seen in rabies, prion encephalopathies, Alzheimer's disease and tetanic muscle spasm. The discovery of an entry and transport machinery that is potentially shared between pathogens and neurotrophins sheds light ono trafficking systems in the nervous system and may assist the design of novel therapeutic avenues that prevent or slow the progression of diverse chronic and acute neurological disorders. [source] The use of mandibular nerve block to predict safe anaesthetic induction in patients with acute trismus*ANAESTHESIA, Issue 11 2009A. M. B. Heard Summary Acute trismus can be caused by pain, muscle spasm, swelling or mechanical obstruction. Unfortunately, the cause is not always obvious during pre-operative airway assessment. In this pilot study, we prospectively evaluated mandibular nerve block as a pre-operative tool to identify patients with reversible causes of trismus, namely pain or spasm, in order to allow safe anaesthetic induction. Six patients with unilateral fractured mandibles and trismus received a mandibular nerve block before induction of general anaesthesia. There was an increase in maximal inter-incisor gap after the blocks (median (range) distance: pre-block 16.5 (14,30) and post-block 34 (32,35) mm; p = 0.027), and no further improvement after induction of general anaesthesia (post-induction 37 (30,40) mm; p = 0.276 compared with post-block). There was an improvement in pain scores (p = 0.027), and no side-effects were detected. Pre-operative mandibular nerve blockade appears to reverse trismus caused by pain and muscle spasm, allowing the anaesthetist to decide whether awake intubation is genuinely indicated. [source] Masseter muscle spasm and non-depolarising neuromuscular blocking agentsANAESTHESIA, Issue 9 2004R. Seneviratne No abstract is available for this article. [source] Evidence for Antinociceptive Activity of Botulinum Toxin Type A in Pain ManagementHEADACHE, Issue 2003K. Roger Aoki PhD The neurotoxin, botulinum toxin type A, has been used successfully, in some patients, as an analgesic for myofascial pain syndromes, migraine, and other headache types. The toxin inhibits the release of the neurotransmitter, acetylcholine, at the neuromuscular junction thereby inhibiting striated muscle contractions. In the majority of pain syndromes where botulinum toxin type A is effective, inhibiting muscle spasms is an important component of its activity. Even so, the reduction of pain often occurs before the decrease in muscle contractions suggesting that botulinum toxin type A has a more complex mechanism of action than initially hypothesized. Current data points to an antinociceptive effect of botulinum toxin type A that is separate from its neuromuscular activity. The common biochemical mechanism, however, remains the same between botulinum toxin type A's effect on the motor nerve or the sensory nerve: enzymatic blockade of neurotransmitter release. The antinociceptive effect of the toxin was reported to block substance P release using in vitro culture systems.1 The current investigation evaluated the in vivo mechanism of action for the antinociceptive action of botulinum toxin type A. In these studies, botulinum toxin type A was found to block the release of glutamate. Furthermore, Fos, a product of the immediate early gene, c- fos, expressed with neuronal stimuli was prevented upon peripheral exposure to the toxin. These findings suggest that botulinum toxin type A blocks peripheral sensitization and, indirectly, reduces central sensitization. The recent hypothesis that migraine involves both peripheral and central sensitization may help explain how botulinum toxin type A inhibits migraine pain by acting on these two pathways. Further research is needed to determine whether the antinociceptive mechanism mediated by botulinum toxin type A affects the neuronal signaling pathways that are activated during migraine. [source] Childhood glioblastoma multiforme of the spinal cordJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 4 2006C Oake Summary Astrocytoma accounts for more than 50% of all central nervous system tumours diagnosed, with particular prevalence in the 15- to 34-year-old age bracket, rarely arising in younger children. In 1995, a 7-year-old boy presented in Emergency with a 3-day history of severe radicular back pain and associated muscle spasms, exacerbated by lying on his back. Both bone scan and plain X-rays were unremarkable; however, MRI showed a 3-cm space-occupying lesion at the level of T5-T6. The patient proceeded to biopsy and partial excision of the tumour through laminectomy, histology confirming an anaplastic astrocytoma (glioblastoma multiforme), St Anne Mayo grade 4. Treatment consisted of a radical course of radiotherapy alone, delivering a total dose of 44.8 Gy at 1.6 Gy per fraction. The treatment comprised of three phases using two oblique wedged fields on a 6 MV linear accelerator. The patient remains disease free 7 years post treatment, with the only effect noted being a slight kyphoscoliosis at the site of the laminectomy and radiation. This report highlights the efficacy of combined surgery and radiation therapy in the management of spinal cord glioblastoma multiforme in preventing tumour recurrence, with acceptable morbidity. Further evaluation of the treatment efficacy would be difficult because of the scarcity of such cases. [source] Evidence for shoulder girdle dystonia in selected patients with cervical disc prolapseMOVEMENT DISORDERS, Issue 4 2002Georg Becker MD Abstract Some patients with cervical disc herniation suffer from persistent nuchal pain and muscle spasms after decompressive surgery despite the lack of clinical and radiological signs for actual spinal root compression. Sonographic examination of the brain in some of these patients showed increased echogenicity of the lentiform nuclei as described in patients with idiopathic dystonia. This has been linked to an altered Menkes protein level and copper metabolism. We suggest a relationship between persistent nuchal pain after adequate cervical disc surgery and dystonic movement disorders. Thirteen patients with persistent nonradicular nuchal pain after at least one cervical disc surgery and without evidence of continuing spinal root compression and 13 age-matched controls were included. All patients had a complete neurological examination, ultrasound, and MRI scan of the brain. In addition, Menkes protein mRNA levels of leucocytes were analyzed in patients and controls. All patients with persistent nuchal pain exhibited a constant tonic unilateral shoulder elevation associated with an ipsilateral hypertrophy of the trapezius muscle. Ultrasound examination showed an increased echogenicity of the lentiform nucleus in one patient unilaterally and in 10 patients bilaterally but in none of the controls. On MRI the T2-values of the lentiform nuclei were found to be higher in patients exhibiting a hyperechogenicity of the lentiform nuclei compared to controls (P = 0.01). In addition, Menkes protein mRNA levels were decreased in patients with cervical disc herniation (P = 0.03). Clinical, neuroimaging, and biochemical findings of this selected patient sample with chronic nuchal pain and muscle spasms after cervical disc surgery resemble alterations in patients with idiopathic cervical dystonia. This suggests a link between both disorders. A peripheral trauma to the nerve roots may precipitate dystonic movements in susceptible patients and chronic dystonic muscle contraction would account for the persistent nuchal pain. © 2002 Movement Disorder Society [source] Differences in circular muscle contraction and peristaltic motor inhibition caused by tachykinin NK1 receptor agonists in the guinea-pig small intestineNEUROGASTROENTEROLOGY & MOTILITY, Issue 2 2000Shahbazian The tachykinin NK1 receptor agonist substance P methyl ester (SPOME) impedes intestinal peristalsis by releasing nitric oxide (NO) from inhibitory motor neurones. Since NK1 receptor agonists differ in their receptor interaction, we set out to compare a range of NK1 receptor agonists including SPOME, septide and GR-73 632 in their effects on propulsive peristalsis and circular muscle activity in the guinea-pig isolated small intestine. SPOME (100,300 n M) inhibited peristalsis by a rise of the pressure threshold at which peristaltic waves were triggered, whereas septide and GR-73 632 (30,300 n M) interrupted peristalsis by causing circular muscle spasms. Separate experiments showed that all three NK1 receptor agonists caused contraction of the circular muscle, which was enhanced by the NO synthase inhibitor NG -nitro- L -arginine methyl ester (300 ,M) and the P2X purinoceptor antagonist suramin (300 ,M). In contrast, tetrodotoxin (300 n M) augmented the contractile effect of septide and GR-73 632 but not that of SPOME. It is concluded that the motor response to NK1 receptor agonists involves release of NO and adenosine triphosphate from inhibitory motor neurones. However, the NK1 receptor agonists differ in the mechanism by which they cause inhibitory transmitter release, which corresponds to differences in their antiperistaltic action. [source] Pain Symptom Profiles in Persons with Spinal Cord InjuryPAIN MEDICINE, Issue 7 2009Yenisel Cruz-Almeida MSPH ABSTRACT Objective., Persistent pain is a common consequence of spinal cord injury. A patient-specific assessment that combines both the identification of pain symptoms and psychosocial factors is needed for a tailored treatment approach. The aim of the study was to define pain symptom profiles and to determine their relationship with psychosocial factors in persons with spinal cord injury. Design., Face-to-face interview and examination. Setting., VA Medical Center and Miami Project to Cure Paralysis, Miami, Florida. Patients., Persons with spinal cord injury (135 men and 21 women) provided detailed descriptions of 330 neuropathic pains. Outcome Measures., The American Spinal Injury Impairment Scale, pain history and measures of pain interference, life satisfaction, locus of control, social support and depression. Results., The exploratory factor analyses and regression analyses revealed three distinct symptom profiles: 1) aching, throbbing pain, aggravated by cold weather and constipation predicted by a combination of chance locus of control and lower levels of life satisfaction; 2) stabbing, penetrating, and constant pain of high intensity predicted by a combination of pain interference, localized pain, powerful others locus of control and depressed mood; and 3) burning, electric, and stinging pain aggravated by touch and muscle spasms predicted by pain interference. Conclusions., Although these results need to be replicated in other spinal cord injury samples, our findings suggest that pain symptom profiles may be a useful way to further characterize pain in a comprehensive assessment strategy. [source] Epidural Infusion of Opiates and Local Anesthetics for Complex Regional Pain SyndromePAIN PRACTICE, Issue 2 2002Sami Moufawad MD CRPS-I consists of multiple signs, including autonomic dysfunction, in the form of edema, vasomotor changes, motor dysfunctions, muscle spasms, tremors and dystonia, as well as burning pain, hypersensitivity and allodynia that could present in any combination. The treatment is progressive physical therapy rehabilitation program. Multiple analgesic modalities have been used to facilitate the rehabilitation program with varying rates of success. The most successful treatment is a multi-disciplinary comprehensive approach, where initial pain control allows for physical and psychological interventions that are believed to be the basis for successful treatment.1 The pain in CRPS-I may be mediated through the sympathetic nervous system, sympathetic maintained pain (SMP) or sympathetic independent pain (SIP)2. [source] Nogo-A antibodies and training reduce muscle spasms in spinal cord-injured ratsANNALS OF NEUROLOGY, Issue 1 2010Roman R. Gonzenbach MD Objective Spinal cord injury (SCI) leads to permanent motor and sensory deficits due to the damage of ascending and descending fiber tracts. In addition, malfunctions such as neuropathic pain or muscle spasms develop in many patients, possibly caused by injury-induced plastic changes of neuronal circuits above and below the lesion. New treatment strategies for spinal cord injury aim at enhancing plasticity and neurite growth, for example, by blocking the key neurite growth inhibitor Nogo-A or its downstream effectors. It is therefore crucial to investigate potential effects of such treatments on malfunctions such as muscle spasms. In addition, locomotor training, now a standard therapeutic tool to improve walking ability in incomplete SCI subjects, can be expected to influence the rearrangement of spinal cord circuits and the development of muscle spasms and other malfunctions. Methods and Results Here we present and validate a new rat model for muscle spasms after incomplete SCI and show that both intrathecal anti,Nogo-A antibody treatment and locomotor training, started early after injury, permanently reduce the development of muscle spasms. Interpretation The results show that an antibody-mediated suppression of the growth inhibitory protein Nogo-A leads to functional recovery and a lower level of malfunctions, suggesting the formation of functionally meaningful connections in the damaged spinal cord. Treadmill training early after SCI also has a beneficial effect. ANN NEUROL 2010;68:48,57 [source] Lumbar Stimulation Belt for Therapy of Low-Back PainARTIFICIAL ORGANS, Issue 1 2009Dejan B. Popovi Abstract We developed the STIMBELT, an electrical stimulation system that comprises a lumbar belt with up to eight pairs of embedded electrodes and an eight-channel electronic stimulator. The STIMBELT is an assistive system for the treatment of low-back pain (LBP). We describe here technical details of the system and summarize the results of its application in individuals with subacute and chronic LBP. The direct goals of the treatment were to relieve pain, reduce muscle spasms, increase strength and range of motion, and educate individuals with LBP in reducing the chances of its reoccurrence. The outcome measures include: a Visual Analogue Scale (VAS), the Oswestry LBP Disability Questionnaire, the Short Form (SF)-12 health survey, and the Manual Muscle Test. The results indicate significant benefits for individuals who use the STIMBELT in addition to the conventional therapy as opposed to only the conventional therapy. [source] Molecular and clinical consequences of novel mutations in the arylsulfatase A geneCLINICAL GENETICS, Issue 1 2009ugowska Metachromatic leukodystrophy (MLD), a severe neurodegenerative metabolic disorder, is caused by deficient activity of arylsulfatase A (ARSA; EC 3.1.6.8), which leads to a progressive demyelinating process in central and peripheral nervous systems. In this study, a DNA sequence analysis was performed on six Polish patients with different types of MLD. Six novel mutations were identified: one nonsense (p.R114X), three missense (p.G122C, p.G293C, p.C493F) and two frameshift mutations (g.445_446dupG and g.2590_2591dupC). Substitutions p.G293C and p.C493F and duplication g.445_446dupG caused a severe reduction of enzyme activity in transient transfection experiments on mammalian cells (less than 1% of wild-type (WT) ARSA activity). Duplication 2590_2591dupC preserved low-residual ARSA activity (10% of WT ARSA). In summary, the novel MLD-causing mutations in the exons 2, 5 and even in 8 of the ARSA gene described here can be classified as severe type 0, leading in homozygosity to the late infantile form MLD. Growth retardation, delayed motor development, gait disturbances, tonic,clonic seizures and non-epileptic muscle spasms were the first onset symptoms in patients with late infantile form of MLD. In individual with juvenile type MLD gait disturbances evidenced the onset of the disease, while in a patient with late juvenile MLD, difficulties at school were displayed. [source] | |||||||||||||||||||||||||