Spasticity & it’s management

TheraspOT
8 min readSep 4, 2020

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Basics about spasticity & rehabilitation procedures helpful in management of spasticity/hypertonicity.

HYPERTONUS

  • Hypertonus is increased muscle tone. It can occur when a lesion is present in the premotor cortex, the basal ganglia, or descending pathways.
  • Clients with hypertonicity often have difficulty initiating movement, especially rapid movement. Although hypertonic muscles appear to be able to take a lot of resistance,they do not function as normal, strong muscles do. Through the mechanism of reciprocal inhibition, hypertonic muscles inhibit the activity of their antagonists and thus can mask potentially good or normal function of antagonists. some types of hypertonia are:-

a) Cerebral hypertonia- Cerebral hypertonia is caused by traumatic brain injury, stroke, anoxia, neoplasms (brain tumors), metabolic disorders,cerebral palsy, and diseases of the brain. In multiple sclerosis, hypertonia is produced from both spinal and cerebral lesions. It usually occurs in definite patterns of flexion or extension, causing the limb to be pulled in one direction. The re-emergence of primitive reflexes and associated reactions alters postural tone. When an individual is lying supine, muscle tone is less than when the individual is sitting or standing. The tone is at its highest during ambulation. Thus, attention to postural tone is important when positioning a client for splinting or casting.

b) Spinal hypertonia- it results from injuries and diseases of the spinal cord. In slow-onset spinal disease (e.g., spinal stenosis,tumor), there is no period of spinal shock. In traumatic spinal cord injury, spinal shock occurs and is characterized by initial flaccidity. Over time (weeks or months), the flaccidity diminishes and hypertonus develops. The affected extremities first develop flexor and adductor tone. Over time, extensor tone develops and becomes predominant in the lower extremities.

c) Spasticity- Little and Massagli believe that pure spasticity is a subset of hypertonia. It is a motor disorder characterized
by a velocity-dependent increase in tonic stretch
reflexes (muscle tone) with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome(J.W Lance,1980). One of the main systems affected when spasticity is present is the pyramidal system, which consists of the corticospinal and corticobulbar tracts. It is characterized by “clasp-knife phenomenon”.

d) Rigidity- Rigidity is a simultaneous increase in muscle tone of agonist and antagonist muscles. Both groups of muscles contract steadily, leading to increased resistance to passive movement. Rigidity signals involvement of
the extrapyramidal pathways in the circuitry of the basal
ganglia, diencephalon, and brainstem.

Spasticity(epidemiology)

  • spasticity affects approximately 35% of those with stroke, more than 90% with CP, about 50% of TBI patients, 40% of SCI patients, and between 37% and 78% of MS patients.

Pathophysiology

It is not completely understood; however, it is believed to arise from loss of descending inhibitory pathways. Axonal collateral sprouting & denervation super sensitivity may also play a role in development of spasticity.

ASSESSMENT

  • It is helpful to rate spasticity and hypertonia with the client in the same position, preferably at the same time of day, to enhance reliability, because body and head position influence cerebral hypertonus.
  • Clinical assessment of spasticity involves holding the
    client’s limb and moving it rapidly through
    its full range while the client is relaxed.
  • Clinical assessment of rigidity and hypertonia involves
    moving the limb slowly during the range, noting the location of first tone or resistance to movement.
  • Certain scales that are commonly used are:- modified ashworth scale, preston’s hypertonicity scale, Tardieu scale, mild moderate severe hypertonicity scale, etc.

Management

Common rehabilitation methods/techniques/procedures used are:-

  • Muscle strengthening- Bobath stated that
    “heavy resistance training should be avoided in patients
    with upper motor neuron lesions (because)
    in spastic conditions, if disinihibited, the use of effort,
    irradiation, mass patterns and especially tonic
    reflexes to strengthen muscles, will only reinforce
    the few existing abnormally increased reflexes and,
    with it, increase spasticity”. This statement (strength exercises increase spasticity) has been quite controversial. Research studies exist emphasizing on muscle strength exercises in spasticity & haven’t shown as many adverse effects as previously believed. So, if you believe or do not believe that strength training increases spasticity, both of you are right depending upon the approach you are using. A skilled therapist will know when to introduce strength training in the protocol and when to avoid.
  • Pak and Patten reported that there is currently no gold standard to guide the development of strengthening protocols in patients with spasticity. However, based on the clinical studies reviewed, they recommended some
    basic parameters for resistance training. In particular,
    they suggested that: 1) the level of resistance
    should be a one-repetition maximum at 60%-80%,
    reassessed every 2 weeks; 2) the number of repetitions
    per set should not exceed 12 and each set
    (minimum 3 per session) should be composed of 8
    to 10 exercises; 3) the training should be conducted
    3 times per week for a minimum period of 6 to 12
    weeks; 4) functional task-specific activities should
    be incorporated. Moreover, they recommended to
    avoid strength training in: 1) non-neurologically
    stable patients; 2) post-surgical patients; 3) patients
    with severe osteoporosis or acute joint injuries; 4)
    patients with haemophilia or other blood disorders;
    5) patients with severely limited ROM.

*Resistance is more facilitative
to an isometrically contracted muscle than in an isotonic
contraction. As isometric resistance is increased or continued, more motor units are recruited, thereby, increasing the facilitation.*

  • Vibration- There are two types of vibratory methods
    used therapeutically. The first deals with the use of a handheld vibrator to facilitate Ia receptors to enhance agonistic muscle contraction in hypotonic muscles or to facilitate Ia receptors of antagonistic muscle fibers to inhibit hypertonic agonists. High-frequency vibration (100 to 300 Hz or cycles per second) applied to the muscle or tendon elicits a reflex response referred to as the tonic vibratory response.Tension within the muscle will increase slowly and progressively for 30 to 60 seconds and then plateau for the duration of the stimulus.Some researchers found that at cessation
    of the input the contractibility of the muscle was enhanced for approximately 3 minutes.The discrepancy in the research may reflect the way the individual is using the input, both from a direct effect on the motor generator and from supraspinal modulation over the importance of the input, which may affect the overall learning and plasticity of the CNS. To facilitate hypotonic muscle, the muscle belly is first put on stretch, and then vibratory stimuli are applied.
    To inhibit a hypertonic muscle, the antagonistic muscle
    could be vibrated.
  • Vibration is not recommended for infants because the nervous system is not yet fully myelinated and the vibration might cause too much stimulation. Vibration also needs to be used cautiously over skin that has lost its elasticity and is thin (e.g.,that in older persons) because the friction itself from the vibration can cause tearing. Total-body vibration is currently being used to determine if it affects motor performance. Studies have shown that whole body vibration can enhance motor performance in high-level athletes performing sprints and jumps as well as improve trunk stability, muscle tone, and postural control in individuals after stroke while in geriatric rehabilitation. Its application for individuals with neurological dysfunction is inconclusive.
  • Inhibitory pressure- Mechanical pressure (force),
    such as from cones, pads, or the orthokinetic cuff developed by Blashy and Fuchs, provided continuously is inhibitory.That pressure seems most effective on tendinous insertions.
    It is hypothesized that this deep, maintained pressure activates Pacinian corpuscles, which are rapidly adapting receptors. The pressure is applied across the tendon with increasing pressure until the muscle relaxes. Constant pressure applied over the tendons of the wrist flexors may dampen flexor hypertonicity and elongate the tight fascia over the tendinous insertion.
  • Maintained stretch- Once the maintained stretch
    fires the tendon organ, autogenic inhibition of the same
    muscle occurs. A therapist will feel a release of the agonist
    muscle, allowing for elongation of the contractile components. Simultaneously, the tendon organ’s sensory neurons will facilitate motor neurons to the antagonist muscle, thus heightening its sensitivity and potential for activity. There are many ways to apply stretch to the muscles. The therapist can use (1) the hands and their respective muscle power to apply a stretch, (2) a manual weight system of some sort that maintains the stretch through the range, (3) a suspension system (4) the patient’s own body weight against gravity, etc.
  • Joint Receptor Approximation- Approximation of
    the joint mimics weight bearing and facilitates the postural extensor system. Gravity creates approximation and its greatest force is produced down through the body in vertical postures. Approximation should help to stabilize any joint that is in a load-bearing situation by eliciting coactivation of the muscles around the joint in question. Approximation can be used normalize muscle tone i.e increase tone in hypotonic muscles & decrease tone in hypertonic/spastic muscles.
  • Stretch pressure- The muscle belly is the stimulus focus
    of stretch pressure. The therapist slowly applies pressure to the muscle belly. It is used to decrease or release tone in the target muscle, allowing for the (temporary) recovery of voluntary movement. Generally this type of stimulus is applied and maintained for a period of time(e.g., 5 to 10 seconds).
  • Cryotherapy- With prolonged cold the neurotransmission of impulses, both afferent and efferent, is reduced. Simultaneously the metabolic rate within the cooled tissue is reduced. Inhibition of hypertonicity or pain is the goal. However, for effective treatment results, the client (1) should be receptive to the modality,
    (2) should be able to monitor the cold stimulus (sensory
    deficits should not be present), and (3) should have a stable autonomic system to prevent unnecessary adverse effects of hypothermia. cryotherapy has a moderate effect in reducing plantar flexor spasticity after 20 mins of application, indicating short-term benefits in the context of clinical practice.
  • Neutral warmth- Like icing, neutral warmth alters the
    state of the motor generators, either directly or indirectly
    through afferent input. According to Farber, the length of
    application depends on the client. A 3- to 4-minute tepid
    bath may create the same results as a 15-minute total-body-wrapping procedure. As with any input procedure, the effects should be incorporated into the therapeutic session to maximize the results and promote client learning.
  • Rocking- A constant, slow, repetitive rocking pattern, irrespective of plan or direction, generally causes inhibition of total-body responses via the alpha motor neuron but not the spindles, whereas a fast spin or fast linear movement tends to heighten both alertness and the motor responses.
  • Reflex-inhibiting patterns- a term for patterns that counteract the pull of tight or spastic muscles. Since flexor spasticity in the arm is concentrated in shoulder elevators and internal rotators and elbow, wrist, and finger flexors, the tension in these muscle groups can be systematically decreased or “inhibited” by gradually moving the arm into a position that includes shoulder girdle depression and shoulder external rotation, elbow and wrist extension, and an open hand. Rather than passively stretching the spastic muscles into the RIP, B. Bobath (1990) described the use of trunk rotation and shoulder mobilization in the supine position and weight bearing to inhibit flexor spasticity in the hemiplegic arm.
  • Trunk rotation, scapular & pelvic mobilization

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REFERENCES

  • Umphred’s NEUROLOGICAL REHABILITATION, 6th edition.
  • Pedretti’s practice skills in occupational therapy, 4th edition & 7th edition.

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TheraspOT

Bloggers- Sherry Kapoor (BOT, MOT neuro) Rupali Gulati (BOT,MOT peads)