BOTOX


Why is spasticity important ?

  • Spasticity is a motor disorder charaterized by a velocity dependant increase in the tonic stretch reflex
  • In simpler terms, increased tone or spasticity is the tightness that patients &/or caregivers report with passive movements of the limb
  • Regardless of its cause, spasticity causes significant disability
  • The treatment of spasticity relies on the physician’s assessment of the patient as well as with conversations with the caregiver.

When is spasticity significant ?

  • Spasticity is a clinically relevant medical problem when it interferes with function or care of the patients
  • The lesion alone does not predict the extent or impact of spasticity
  • Other factors such as medications, stress, medical illness, timing of therapy and so on impact the clinical outcome

Choices of treatment of spasticity

  • Several options are available for the treatment of spasticity
  • Splinting, stretching through physical therapy
  • Chemoneurolysis with phenol/alcohol
  • Oral medications such as Dantrolene Sodium, Diazepam, Baclofen, etc
  • Botulinum toxin injections
  • Baclofen pump
  • Rhizotomy

The UMN syndrome

  • The commonest cause of spasticity one sees in neurology is the upper motor neuron syndrome
  • It is the aggregate of positive and negative signs that occur after an upper motor neuron lesion
  • Negative signs are due to loss of a function ordinarily controlled by the lesioned area of brain
  • Positive signs reflect release phenomena, abnormal or exaggerated behaviours and loss of inhibition
  • Positive and negative signs often interact at the same time

Assessment of Spasticity

  • Measures of spasticity include measures of passive movement, measures of voluntary activity, passive and active function,quality of life measures
  • Outcome measures to assess intervention effectiveness could include all of the above plus certain specific assessments
  • However, to date there is no reliable, specific objective measure available,

Assessment tools

  • Measures using nerve conduction and EMG
  • Tendon reflexes
  • Measures of passive activity such as the Ashworth scale, modified Ashworth scale and modified modified Ashworth scale, Tardieu scale,Range of motion,Stiffness and muscle tone,Stretch and stretch reflexes,Pendulum test models,Reflex threshold angle
  • Measures of voluntary activity – performance based measures, gait, balance
  • Functional measures

Modified Ashworth Scale

  • No increase in muscle tone
  • Slight increase in muscle tone manifested at end of ROM
  • Marked increase in muscle tone manifested by a catch in the middle range and resistance throughout the remainder of the ROM, but affected part (s) easily moved
  • Considerable increase in muscle tone, passive movement is difficult
  • Affected part is rigid in flexion or extension


FOR TYPES OF CEREBRAL PALSY - CLICK HERE

Botulinum Toxin Type A

  • This toxin, from the bacteria Clostridia Botulinum, is the most potent known biological toxin and may be responsible for life-threatening paralysis
  • Skeletal muscle is chemically denervated, remaining paralyzed until the nerve supplying the motor end-plate sprouts new axons and forms new synaptic contacts, reestablishing the neuromuscular junction
  • Injection of Botox® directly into the target muscles could have the advantage of reducing muscle spasm without producing sedation.
  • This is in contrast to systemic muscle relaxants
  • Botulinum Toxin Type A prevents the release of acetylcholine by the presynaptic axon at the motor endplates of cholinergic neurons
  • Botulinum Toxin Type A, a 150 KDs protein, binds irreversibly to presynaptic cholinergic nerve terminals, and once internalized, blocks exocytosis of the neurotransmitter acetylcholine .
  • Therefore muscle contraction is inhibited
  • Botox® may produce a prolonged reduction of spasm by producing a partial, reversible denervation of the muscles.
  • Selective weakening of painful muscles in spasm may interrupt the pain-spasm-pain cycle, and facilitate rehabilitationI
  • It has been used therapeutically to produce a partial chemical denervation by injecting minute doses directly into the motor endplate region of the muscle.
  • At the nerve terminal, botulinum toxin type A is thought to induce a temporary chemodenervation through the following steps:
  • The toxin binds to acceptors (yet to be identified) on cholinergic terminals.
  • The molecule is internalized into the nerve ending.
  • Once inside the nerve ending, botulinum toxin interferes with the exocytosis of cholinergic vesicles. This leads to chemodenervation and reduced muscular contractions.
  • Over time, terminal sprouting occurs.
  • Finally, the original functional endplate is re-established and sprouts regress (as reported by Prof. Oliver Dolly's laboratory). At this point symptoms may return in some patients.

Treatment Goals

  • Choice of muscles to inject depends on the goal of treatment as to whether it is meant to be palliative as in the case of improving hygiene, or intended to improve passive or active movements, etc
  • Dosing is decided by past experience, size of the muscle, amount of tone, residual function of the spastic muscles, potential of functional loss that may result from decreased tone and experience of the treating physician


Conclusion

  • Botulinum Toxin Type A is an effective therapy for spasticity secondary to UMN syndrome
  • Treatment with Botox should involve appropriate goal selection
  • Chemodenervation with Botox should be considered as only one component in the management of the condition
  • Dosage selection should be individualized to obtain optimal results
  • Physicians treating patients with Botox should be aware of the different serotypes, formulations and literature in spasticity


BOTOX

Before Botox Toe walking

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Before Botox see foot position

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After Botox both heels - flat