ALS Massage: Therapeutic Massage for Amyotrophic Lateral Sclerosis

massage therapy for alsAmyotrophic Lateral Sclerosis aka Lou Gehrig’s Disease is a progressive destruction of motor neurons in the Central and Peripheral Nervous System. The degeneration of motor neurons leads to the progressive and irreversible atrophy of voluntary muscles.

ALS Massage Therapy Treatment:

  • ALS is a motor dysfunction; the patient’s sensation stays intact
  • massage therapy helps increase circulation to reduce muscle stiffness, cramps and spasm. As the disease progresses and patient has decreased activity, increased circulation from massage can help avoid decubitus ulcers
  • massage helps with relaxation, which helps with the overall well being of the patient
  • massage therapy can help manage pain related to degeneration

Massage Therapy techniques to use for ALS Treatments:

  • passive ROM techniques
  • passive stretching techniques
  • vibrations
  • non-aggressive tapotement
  • compression techniques (especially in the limbs)

Massage Indication and Contraindications for ALS:

  • With passive ROM, keep patient’s limbs supported throughout the motion. Move slowly and be aware of the patient’s response and feedback.
  • With passive stretching and passive ROM, move slowly, do not force the movement, and move only to the point of resistance
  • As the disease progresses, patient may not be able to speak so the patient and the therapist may agree on communication signals (eg. answers to yes or no feedback questions through some kind of non verbal communication)

Signs and Symptoms of ALS:

  • Early symptoms of ALS usually include muscle weakness or stiffness.
  • Gradually all muscles under voluntary control are affected, and patients lose their strength and the ability to speak, eat, move, and even breathe
  • muscle twitches in the arm, leg, shoulder, or tongue
  • muscle cramps, tight and stiff muscles, muscle spasms
  • muscle weakness affecting an arm, a leg, neck, diaphragm; fatigue
  • difficulties with speech, swallowing, or motor control of tongue
  • weakness, stiffness, loss of coordination, usually starts distally and progresses toward the core
  • may become painful as muscles atrophy and the skeleton collapses
  • UMN (upper motor neurons) degeneration manifest as progressive spasticity, exaggerated reflex, including gag reflex and positive babinski sign
  • LMN (lower motor neurons) degeneration involved when weakness, atrophy, muscle cramps, and fasciculations( uncontrolled twitching)
  • LIMB ONSET ALS: (70% is spinal variation, with early symptoms in hands or legs)
    • difficulty with fine motor skills in hands (may be first sign); if in the legs, frequent tripping or stumbling is first indication
  • BULBAR ONSET ALS: usually more serious with faster progression
    • Bulbar ALS destroys motor neurons in the corticobulbar area of the brainstem in the early stages of ALS. The corticobulbar area controls muscles of the face, head and neck
    • Changes in voice and speech, harsh, hoarse or strained voice, breathy speech pattern, poor articulation, decrease in range of pitch and loudness of voice, other  Bulbar ALS symptoms include spasms in muscles of the jaw, face, voice box, throat and tongue, inappropriate excessive laughing and crying, brisk jaw jerks, involuntary twitching in the muscles of the tongue, vocal cord spasms causing the sensation that air cannot be moved in or out
    • Bulbar ALS also associated with rapid mood swings or “emotional incontinence”
  • may become painful as muscles atrophy and the skeleton collapses
  • no impact on intellect or memory

3 Types of ALS:

  1. Sporadic (most common) ALS
  2. Familial ALS
  3. Mariana Island type ALS

ALS Etiology:

  • the cause of ALS is unknown
  • when ALS develops, it leads to degeneration of motor neurons in the spinal cord, causing progressive and irreversible atrophy of the patient’s voluntary muscles
  • large motor neurons in lateral aspects of spinal cord (the cells most affected) are replaced with fibrous astrocytes (scar tissue)
  •  accumulation of NT-glutamate in synapses kills postsynaptic neurons – (glutamate: excitatory neurotransmitter), not neutralized or reabsorbed in ALS, eventually damages – even kills motor neuron it’s meant to stimulate

ALS Contributing Factors:

  • genetic susceptibility to damage from free radicals
  • autoimmune disease
  • mitochondrial dysfunction
  • exposure to environmental toxins
  • tangled neural fibers and deposits of abnormal proteins on clumps of cells- leads to degeneration of cytoskeleton of neuron and strangulation of presynaptic axons

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