What is the mechanism of skeletal muscle contraction and how are cramps, spasms, or spasticity treated?

Mechanism of Skeletal Muscle Contraction and Treatment of Cramps, Spasms, and Spasticity

Mechanism of Skeletal Muscle Contraction

Skeletal muscle contraction occurs when thin actin and thick myosin filaments slide past each other, driven by cross-bridges that cyclically interact with actin filaments during ATP hydrolysis. 1

Molecular Process

• The myosin cross-bridge exists in two main conformations: a strong-binding state (in the absence of MgATP) where it binds tightly to actin, and a weak-binding state (induced by MgATP binding) where it attaches and detaches rapidly 1
• During ATP hydrolysis, the transition from weak-binding to strong-binding causes the elastic cross-bridge to become deformed and exert positive force, while the transition back to weak-binding upon MgATP binding causes detachment and re-attachment to a new actin site 1
• Excitation-contraction coupling is initiated when an action potential from the somatic nervous system depolarizes the sarcolemma, which is detected by the voltage-gated calcium channel (DHPR), transmitting the signal to ryanodine receptor (RyR1) in the sarcoplasmic reticulum membrane, releasing calcium ions that initiate contraction 2

Mechanical Classification

• Dynamic (isotonic) exercise produces limb movement and includes concentric contraction (muscle fiber shortening) and eccentric contraction (muscle fiber lengthening against gravity) 3
• Static (isometric) exercise results in no limb movement 3

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Treatment of Spasticity

Spasticity is a velocity-dependent increase in muscle tone caused by hyperexcitable stretch reflexes, distinguished from rigidity by its speed-dependence and the clasp-knife phenomenon. 4

Distinguishing Spasticity from Other Conditions

• Spasticity exhibits velocity-dependent resistance (faster stretch produces more resistance), selective muscle involvement (flexors in cerebral lesions, extensors in spinal lesions), and the clasp-knife phenomenon 4
• Rigidity shows constant resistance regardless of speed, uniform involvement of all muscle groups, and originates from extrapyramidal (basal ganglia) lesions 4

Treatment Algorithm for Spasticity

Step 1: Non-Pharmacological Interventions (Initiate Immediately)

Range-of-motion exercises must be performed several times daily to prevent contracture progression in all patients with spasticity. 3, 5

• Implement antispastic positioning and proper body alignment to reduce reflex hyperexcitability 5
• Apply stretching programs and splinting to maintain joint mobility 3, 5
• Use serial casting for established contractures that interfere with function 3, 5
• Consider surgical correction for severe contractures that restrict movement, cause pain, or impede rehabilitation 3, 5

Step 2: Oral Medications for Generalized Spasticity

Baclofen is the preferred first-line oral agent for spasticity, particularly effective for flexor spasms and concomitant pain in spinal cord-related spasticity. 5, 6

• Baclofen is FDA-approved for spasticity from multiple sclerosis, spinal cord injuries, and other spinal cord diseases, specifically for relief of flexor spasms, concomitant pain, clonus, and muscular rigidity 6
• Tizanidine is specifically recommended for chronic stroke patients and is FDA-approved for spasticity management 3, 5, 7
• Dantrolene is an alternative oral agent for generalized spasticity 3, 5
• Gabapentin at 400mg orally three times daily may provide value for spasticity and painful muscle cramping in multiple sclerosis patients, showing statistically significant improvements in Ashworth Scale, Visual Faces Scale, and Kurtzke Disability Scale 8

Critical Pitfall: Do not use benzodiazepines during recovery phases, as they impair neurological recovery and cause excessive sedation 5

Step 3: Focal Spasticity Management

Botulinum toxin injections are the preferred treatment for focal spasticity affecting specific muscle groups, particularly when causing pain, functional impairment, or compromising positioning and skin care. 3, 9, 5

• Botulinum toxin is first-line treatment for focal spasticity, targeting specific motor point zones to achieve optimal spasticity reduction and pain relief 9
• Assess outcome at 4-6 weeks after injection, including reduction in Modified Ashworth Scale score, decreased pain during passive movement, and improved passive range of motion 9
• For hamstring spasticity, botulinum toxin should be considered after documenting specific functional impairments (gait disturbance, difficulty with positioning, pain during passive movement) and verifying failure or intolerance of stretching, range of motion exercises, and splinting 9

Step 4: Advanced Interventions for Refractory Spasticity

Intrathecal baclofen via programmable pump is indicated when oral medications fail at maximum tolerated doses, requiring only 10% of the systemic dose for equivalent effect. 5

• More than 80% of patients show improvement in muscle tone and more than 65% have improvement in spasms with intrathecal baclofen 5
• Critical Warning: Do not abruptly discontinue intrathecal baclofen, as this can be catastrophic and potentially fatal 5
• Selective dorsal rhizotomy or dorsal root entry zone lesion may be considered for intractable spasticity causing pain, poor skin hygiene, or functional impairment 5

Step 5: Technology-Assisted Interventions

• Functional electrical stimulation, neuromuscular electrical stimulation, or transcutaneous electrical nerve stimulation are supported for both upper- and lower-extremity motor outcomes 3
• Neuromuscular electrical stimulation triggered or controlled by electromyography is effective in improving upper-limb motor impairment and ADL function 3

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Treatment of Muscle Cramps and Spasms

Muscle cramps and spasms likely represent related symptoms with a shared pathophysiological component, and cramps may be an under-recognized aspect of spasticity in upper motor neuron disorders. 10

Clinical Recognition

• Muscle cramps are typically regarded as benign muscle overactivity in healthy individuals, whereas spasms are linked to spasticity from central motor lesions, but their clinical resemblance is significant 10
• In upper motor neuron disorders (spinal cord injury, cerebral palsy, traumatic brain injury, stroke), part of the patient's spasms may be attributed to cramps 10

Treatment Approach

• Identify and eliminate external triggers such as constipation, urinary tract infections, or pressure ulcers that can worsen existing spasticity and spasms 11
• Apply the same stepwise treatment algorithm as for spasticity, starting with non-pharmacological interventions (stretching, range of motion exercises) 5, 11
• For painful muscle spasms in multiple sclerosis, baclofen is particularly effective for relief of flexor spasms and concomitant pain 6
• Gabapentin at 400mg three times daily may provide relief for painful muscle cramping in multiple sclerosis patients 8

Common Pitfalls

• Do not neglect non-pharmacological interventions even when medications are effective, as physical modalities remain essential throughout treatment 5
• Recognize that spasms in upper motor neuron disorders may include a cramping component that requires similar management strategies 10