Neurological Physiotherapy - PROM, Tone, Spasticity & Contracture

Muscle Tone

  • Muscle tone = resistance felt when moving a limb passively through range.
  • Related to:
    • Intrinsic stiffness/elasticity
    • Neural component – activation of motor unit.
  • Muscle tone occurs along a spectrum.
    • Hypotonia: lower than normal resistance.
    • Hypertonia: greater than normal resistance.

Upper Motor Neuron Syndrome (UMNS)

  • UMNS = group of motor impairments resulting from damage to the CNS.
  • Positive Features (Muscle Overactivity)
    • Spasticity
    • Dystonia, Spastic dystonia
    • Hyperreflexia
    • Clonus
    • Co-contraction
    • Positive Babinski sign
    • Spasm
    • Associated reactions
  • Negative Features (Reduction in Muscle Activity)
    • Muscle Weakness
    • Loss of dexterity, impaired motor planning and control
    • Fatiguability

Neural Changes Following UMNL & Hypertonia

  • Following an UMNL:
    • Loss of normal descending innervation – both excitatory and inhibitory
    • Possibility of new connections through axonal sprouting
    • Increased sensitivity to pre- and post- synaptic inputs
    • Unmasking of previously inactive synapses
    • Resulting in NET Excitation = Hypertonus

Muscle Changes Following UMNL

  • Muscles have natural viscoelastic properties
    • Sarcomeric actin-myosin cross-bridges
    • Viscosity, elasticity and extensibility of contractile filaments
    • Filamentous connection of sarcomeric non-contractile proteins
    • Osmotic pressure of cells
    • Surrounding (non-muscle) connective tissues
  • With disuse: loss of viscoelastic properties --> increased muscle tone
    • Reduction sarcomere number and fibre size, increase sarcomere length
    • Increase collagen and connective tissue proportion
    • Increases resting discharge of muscle spindles

Hypertonia

  • Hypertonia = increased resistance to PROM associated with UMNL
  • Both neural and local muscle/biomechanical changes
  • Hypertonia ≠ Spasticity but includes spasticity, dystonia and rigidity
  • External triggers usually increase hypertonia

Hypotonia

  • Reduced resistance to passive movement as compared to “normal”
  • Early after UMNL incl stroke - paresis presents as ‘low tone’ “floppy”
  • Patients may have difficulty in generating muscle activity
  • Rx – aim to increase M tone through tactile stimulation, quick stretch, faster muscle activity e.g. strength and power training.

Dystonia

  • Involuntary, sustained or intermittent muscle contractions causing abnormal movements, postures, or both
  • Can be triggered by either postural or task-specific functional activities or spontaneously and occur at rest
  • Spastic Dystonia = persistent posture maintained by spontaneous tonic muscular contraction at rest

Spasticity

  • Damaged UMN means communication between brain and spinal cord is disrupted
  • Net Disinhibition of spinal (stretch) reflex arcs --> Increased excitability muscle stretch reflex / Hyper-reflexia

Definition of Spasticity

  • Spasticity: “A motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper excitability of the stretch reflex, as one component of the upper motor neuron syndrome. ” (Lance 1980)
  • Velocity dependent increase in tonic stretch reflex
  • Also length dependent - muscle group variability
  • May be focal, regional, or generalised
  • Brisk stretch --> abrupt increase tone then decreased resistance = clasp knife

Rigidity

  • Resistance to muscle stretch with passive movement at all rates of passive and active movement - NOT velocity dependent
  • Sustained efferent M hyperactivity
  • Common feature Parkinson’s
  • Often ‘lead-pipe’ in nature – flexors and extensors affected equally
  • Cogwheel rigidity – rigidity felt in presence of underlying (not-visible) tremor

Decorticate and Decerebrate Rigidity

  • Forms of Spastic Dystonia / severe rigidity
  • Decorticate posture – flexion arms +add/IR g/h with extension/IR legs + PF
  • Decerebrate posture – Add/IR g/h, extension elbows with pronation forearm + finger flexion, extension/IR legs with PF, back/neck E
  • Typically responses to noxious stimuli
  • Indicative of significant brain injury

Involuntary Muscle Spasms

  • Occur in any neurological condition with UMNL – MS, SCI, TBI
  • Involuntary movements in muscle groups – spontaneous or triggered

Flexor Spasm/Withdrawal

  • Activation excites flexor and inhibits extensor motor neurons
  • May be exaggerated and desynchronised --> Flexor spasms

Extensor Spasm

  • Flexor response may involve contralateral extension
  • Cutaneous stimulation of groin, buttock and posterior leg, plus proprioceptive input at hip

Hyperreflexia

  • Loss of inhibitory activity from descending motor pathways --> disinhibition of spinal reflex circuits --> exaggerated deep tendon reflexes

Clonus

  • Hyper-reflexive sign
  • Regular, Repetitive and Rhythmic contraction
  • Rapid/sudden and maintained stretch of muscle leads to clonus
  • Clonus sustained for 5+ beats is clinically abnormal

Babinski Sign

  • Normal adult response is plantar-flexion
  • Positive = extension large toe and fanning other toes

Associated Reactions

  • Involuntary activity in one limb that is associated with voluntary movement effort made in other limbs

Co-Contraction

  • Contraction of agonist elicits stretch reflex contraction in antagonist

Possible Consequences of Hypertonia

  • Impairment:
    • Pain
    • Muscle imbalances and abnormal movement patterns --> injury or contracture
    • Skin integrity
    • Fatigue
  • Activity:
    • Posture and seating
    • Task completion
    • Gait
    • Personal hygiene, pADL
  • Participation:
    • Involvement work, sport, home/family roles

Contracture

  • Physical shortening of muscle or other soft tissues around joint, loss PROM
  • Hypertonic muscles that remain in a shortened position can lead to contracture
  • Occurs along a spectrum from muscle tightness to fixed deformity
  • May lead to unwanted biomechanical changes, musculoskeletal deformity, joint capsule and ligament changes, reduced function, pain and pressure areas
  • Need to differentiate in Ax: Contracture v Spasticity v Rigidity
  • Aim to PREVENT!!!!

Spasticity, Contracture and Hypertonia Relationship

  • Spasticity and contracture are both impairments that results in hypertonicity, however the hypertonia of spasticity is neurally mediated
  • The increased tone of contracture is non-neural but biomechanical in origin

Assessment of PROM, Tone and Spasticity

  • PROM Ax in Neuro PT
    • Marked muscle weakness – joint integrity --> handling
    • Sensory changes

The Modified Ashworth Scale (MAS)

  • Often stated as measuring spasticity but given no change in speed is measuring tone
  • Grades tone according to the amount of resistance to passive movement

Tardieu

  • Measures Quality and Angle of muscle reaction
  • Typically complete V1 – slow, and V3 – fast

Management Principles Hypertonia

  • Hypertonus – influenced by sensory input, intrinsic effort and global postural demands
  • Hypertonus can be temporarily reduced by providing additional sensory input
  • Hypertonus can be reduced by actively or passively improving postural stability
  • Increasing usable strength and motor control and reducing task effort

Management of Spasticity Non-pharmacological

  • Removal of noxious stimuli that increase hypertonicity
  • Physical modalities
    • Stretching ?
    • Splints/braces ?
    • Serial Casting
    • EMS / FES
    • Surgery

Management Principles Spasticity

  • Spasticity: Botulinum (BoNT)Toxin Injection “Botox”
    • BoNT = neurotoxin: blocks presynaptic transmission of ACH at neuromuscular junction
    • Need to address ROM, strength and task specific practice to maximise benefit

Management Contracture

  • Focus on prevention
  • Limited effect prolonged stretching or other Rx once occurred/contracted
  • No effect botulinum toxin if contracture
  • Strengthen antagonistic M groups through ROM +/- E-stim
    Eccentric training agonist