Spasticity or periodic limb movements?

Lévy, Jonathan; Hartley, Sarah; Mauruc-Soubirac, Elsa; Léotard, Antoine; Lofaso, Frédéric; Quera-Salva, Maria-Antonia; Bensmaïl, Djamel

doi:10.23736/s1973-9087.17.04886-9

Cited by 11 publications

(3 citation statements)

References 34 publications

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“…Trials of dopamine agonists are useful to distinguish dystonia from other forms of spasticity. 26,27 Anticonvulsant drugs are efficacious, especially sodium-channel blockers such as carbamazepine, oxcarbazepine, lacosamide, and lamotrigine, as well as medications with other mechanisms of action, such as levetiracetam, 165 gabapentin, and pregabalin. Phasic spasticity can become cyclical due to ongoing pain acting as a trigger, so providers should work with the patient to remove other noxious stimuli (i.e.…”

Section: Spasticitymentioning

confidence: 99%

Managing the Symptoms of Multiple Sclerosis

Sneha¹,

Lauren²,

Langston³

2023

MRAJ

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Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system that is characterized by recurrent bouts of acute neuroinflammation and chronic neurodegeneration. Treatments for MS are aimed at prevention of disability in the future or restoring function in the present. Prevention treatments disrupt the underlying disease pathology, whereas restorative treatments address not only the disease’s primary effects on the central nervous system, but also secondary effects on other parts of the body and tertiary effects on each patient’s psychosocial functioning. MS symptoms can have primary, secondary, and tertiary components, which can interlock and reinforce each other. Restorative treatment should tease apart these components and address them separately. In this article on symptom management, we focus on treatments that aim to maximize each component of function.

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Section: Spasticitymentioning

confidence: 99%

Managing the Symptoms of Multiple Sclerosis

Sneha¹,

Lauren²,

Langston³

2023

MRAJ

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“…Further, a recent case series evaluated PSG data in both SCI and Multiple Sclerosis from a spasticity clinic population who were typically referred for refractory “spasticity” despite often maximal anti-spasticity therapy. The study explored the possibility that spasticity was, in fact, undiagnosed and/or untreated PLM and showed a substantial reduction in PLM index and arousals from sleep in those with confirmed PLM (≥15 per hour of sleep) treated with a low dosage of pramipexole 97. Taken together, these data suggest that there is likely clinical utility in SCI, especially where movements predominate in supine and during sleep, in assuming the distressing movements are PLM, not excess spasticity and treated with dopaminergic agents as first-line therapy.…”

Section: Management Of Sleep Disorders In Individuals With Scimentioning

confidence: 99%

Impact Of Spinal Cord Injury On Sleep: Current Perspectives

Sankari¹,

Badr²,

Martin³

et al. 2019

NSS

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Sleep disorders are commonly encountered in people living with spinal cord injury (SCI). Primary sleep disorders such as sleep-disordered breathing (SDB), sleep-related movement disorders, circadian rhythm sleep-wake disorders, and insomnia disorder are common conditions after SCI but remain under-recognized, underdiagnosed and therefore remain untreated for a majority of patients. Sleep disturbances in people living with SCI are associated with significant impairments of daytime function and quality of life. Previous reviews have described findings related mainly to SDB but have not examined the relationship between other sleep disorders and SCI. This narrative review examines various sleep abnormalities and related functional and physical impairments in people living with SCI. It discusses new evidence pertaining to management, highlights existing limitations in the literature and recommends future directions for research.

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“…1 The immediate consequences of SCI are motor and sensory deficits with spasticity, such as initiate and coordinate muscle spasticity. 2 Muscle spasticity can lead to uncontrolled body movements, 3 sustained abnormal postures of the affected body part 4 and even muscle damage and rhabdomyolysis sometimes. 5 Muscle spasticity is usually caused by neuromuscular excitability 6 and represents a complicated array of neurological motor disorders.…”

Section: Introductionmentioning

confidence: 99%

Botulinum Toxin Type A Possibly Affects Cav3.2 Calcium Channel Subunit in Rats with Spinal Cord Injury-Induced Muscle Spasticity

Zhu

Zhang

et al. 2020

DDDT

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Introduction: Spinal cord injury (SCI) often causes muscle spasticity, which can be inhibited by using calcium channel blocker. Botulinum toxin type A (BoT-A) shows therapeutic efficacy on spasticity and may exert inhibitory effects on the calcium channel. Methods: A rat model with muscle spasticity was established after SCI via contusion and compression. Different concentrations (0, 1, 3 and 6 U/kg) of BoT-A Botox were injected in the extensor digitorum longus (EDL) muscles of the right hindlimb in the muscle spasticity model. The changes of muscle spasticity and calcium level in EDL muscles were measured after the establishment of SCI-induced spasticity. Ca v 3.2 calcium channel subunit and its mutant (M1560V) were analyzed using Western blot before (input) or after immunoprecipitation with anti-FLAG antibody, and their currents were measured in motoneurons by using whole-cell voltage clamp recordings. Results: SCI induced muscle spasticity, whereas calcium level in EDL muscles and expression of Ca v 3.2 was increased in the SCI model when compared with the sham group (p < 0.05). BoT-A Botox treatment significantly reduced muscle spasticity and calcium level in EDL muscles and Ca v 3.2 expression in a dose-dependent way (p < 0.05). The ratio of biotinylated to total Ca v 3.2 was reduced in the mutant (M1560V) of Ca v 3.2 and lower than that in the wild Ca v 3.2. BoT-A Botox intervention also reduced the current values of calcium channel and the ratio in a dose-dependent way (p < 0.05). Discussion: BoT-A Botox possibly attenuates SCI-induced muscle spasticity by affecting the expression of Ca v 3.2 calcium channel subunit in the rat models. There may be multiple mechanisms for the function of BoT-A Botox. Further work is needed to be done to address these issues.

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Spasticity or periodic limb movements?

Abstract: This study brings new insights on abnormal movements, often misinterpreted as spasticity, and their management. We suggest to include a PSG in the diagnostic approach of uncontrolled spasms prevailing at night or in supine position, to search for PLM, which are easily treatable.

Cited by 11 publications

References 34 publications

Managing the Symptoms of Multiple Sclerosis

Managing the Symptoms of Multiple Sclerosis

<p>Impact Of Spinal Cord Injury On Sleep: Current Perspectives</p>

<p>Botulinum Toxin Type A Possibly Affects Ca<sub>v</sub>3.2 Calcium Channel Subunit in Rats with Spinal Cord Injury-Induced Muscle Spasticity</p>

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