L6: Abnormal tone Flashcards
what is tone
- resistance offered by muscles to continuous passive stretch
- normal tone= prerequisite for normal mvmt
- resting level of tension in muscle - high enough to support against G but low enough for mvmt
- slight resistant when moving normal limb
non-neural and neural factors
non
-Passive stiffness of a joint & surrounding soft-tissue
Inherent visco-elastic properties of the muscle itself
Compliance of muscles, ligaments & joints (usually limiting factor under normal conditions)
Can vary with age, limb temperature, exercise state
neural Active tension set-up by stretch reflex
Neural
Activation of the contractile apparatus of the muscle
Can vary with age, emotional state
Output of alpha motor neuron, influenced by excitatory and inhibitory synapses from several systems*
peripheral and CNS - factor relating to tone
PNS CNS Muscle spindles (tonic component of stretch reflex)
Golgi tendon organ
Somatosensory receptors (skin, joints, connective tissue, muscles)
Sensory systems (visual, auditory, vestibular)
Limbic system (emotional state)
Motor systems
Interneurons in spinal cord
Higher centres via descending tracts
neural factors - stretch reflex
The stretch reflex is the body’s involuntary response to an external stimulus that stretches the muscles.
Proprioceptors/stretch receptors
muscle spindles - provide information concerning muscle length and the rate of change of length.
Muscle spindle located in the belly of the muscle.
This basic function of the muscle spindle helps to maintain muscle tone and to protect the body from injury. Also contributes to the performance of precise movements.
stretch reflex - cause
The stretch (myotatic) reflex is a direct result of stimulation of the muscle spindle (stretch receptor) – when a muscle is stretched, so is the spindle. Example of the stretch reflex is the knee jerk reflex.
sensory info to CNS
Sensory information is relayed to CNS via sensory neurons during a stretch - concerning the degree of stretch i.e. the change of length (type I a and type II ) and speed of the change (type I a only) on the involved muscle and the exact number of motor units needed to contract in order to overcome stretch
activation of stretch reflex
Activation of the stretch reflex attempts to resist the change in muscle length by causing the stretched muscle to contract
The more sudden the change in muscle length, the stronger the muscle contractions will be.
As fibres contract (shorten), the intrafusal muscle fibres which house the muscle spindle, shorten, so that the muscle spindle is deactivated and their activity ceases.
function of muscle spindle
This basic function of the muscle spindle helps to maintain muscle tone and to protect the body from injury. Also contributes to the performance of precise movements.
suprasinal control via:
Gamma motor neurones set sensitivity of muscle spindle.
Supraspinal control via: Pyramidal tracts Basal ganglia Cerebellum Vestibular system Reticular formation (RAF)
what alters stretch reflex?
Disruption to reflex arc at the level of:
Sensory input
Supraspinal control
Motor output
high tone
hypertonia
spasticity
rigidity
low tone
hypotonia
flaccidity
spasticity
‘Velocity-dependent increase in resistance to passive stretch of a muscle, with exaggerated tendon reflexes’ (Lance, 1990).
‘clasp knife’ phenomenon – abrupt cessation in movement (resistance greater at start of movement), followed by ‘a melting away’ of resistance.
Spasticity - Central
- loss of cortical inhibition
- imbalance in descending pathways
spasticity - peripheral
- altered biomechanical properties of muscle
Spasticity - pathophysiology mechanisms
maybe due to:
abnormal enhancement of the spinal stretch reflexes
Increased muscle spindle sensitivity (via gamma-motoneurone drive).
Increased excitability of central synapses involved in reflex arc.
Loss of inhibition of stretch reflex by descending supraspinal pathways .
causes:
Spasticity
upper motor neuron lesion - anywhere from motor cortex to spinal motor neurons.
common:
- stroke
- spinal cord compression,
- brain damage
- inflammatory lesions of SC
spasticity clincial features
Characteristic involvement of certain muscle groups – predominantly antigravity muscles e.g. UL flexors, LL extensors.
Increased responsiveness of muscles to stretch.
Hyper-reflexia – increased tendon reflexes.
Abnormal resistance to passive movement – the more rapid a limb is moved the greater the increase in tone.
Clasp knife – ‘catch’ followed by ‘melting’ away of resistance.
Clonus – rhythmic oscillations (usually of ankle & foot).
Factors influencing spasticity
positioning stress fatigue pain full bladder infection fear pressure sore constipation increased effort
assessment spasticity
Ashworth Scale (refer to Neurological Ax)
Modified Ashworth Scale
Movement grading:
Severe - no voluntary movement
Moderate - poor movement
Mild - good movement spasticity on resisted movement
Associated reactions:
Effort on the unaffected side can lead to an tone on spastic side / or effort of one spastic limb can lead to tone in the other spastic limb.
Involuntary movement e.g. yawning = AR
Tendon jerks
spasticity - research/ lab quantification
Wartenburg pendulum test
assess knee extensor response to stretch, & depicts movement of the leg following its drop from a horizontal position while subjects are instructed to relax.
Electrophysiology
EMG
management
Treat underlying causes Symptomatic relief Handling / Positioning Standing frames Avoid noxious stimuli Facilitate normal movementSlow passive movements Splinting Serial casting NMES Medication Surgical - Tendon release
Spasticity - medication
Medication
Baclofen (Lioresal)
GABA derivative, pre & postsynaptic inhibitory effect/better for spinal spasticity.
Diazepam (Valium)
Enhances action of GABA on inhibitory neurotransmitters.
Botulinum toxin/Dysport
Toxin injected directly into affected muscle causes presynaptic blockade of ACh release.
Normally when a message comes from the nerve, acetylcholine is released and the muscle contracts.
When botulinum toxin is added, the release of acetylcholine is reduced and the muscle stays relaxed.
spasticity implications
Weakness Decreased movement Abnormal movement Poor posture Soft tissue shortening - contracture Pain Loss of function & adaptive motor behaviour
spasticity - physio aims
Normalise tone Maintain normal muscle length Improve ROM Decrease pain Reduce unnecessary complications Improve function
spasticity -physio mgmt
Peripheral input to normalise tone Positioning - Abnormal reflex activity Supine - extensor activity Sitting - symmetry and stability Passive movement Movement proximal region of limb Slow passive movements Stretching Weightbearing Ice FES Splinting Serial casting Pain management
patterns of spasticity
decerebrate posture
decorticate posture
decerebrate posture from damage to the brainstem. Arms are adducted and extended with PF of the feet.
decorticate posture from damage to 1/both of corticospinal tracts. Arms are adducted and flexed, wrists and fingers are flexed on the chest.
PF of the feet
Rigidity - presentation and description
Characterised by increased resistance to slow passive movement, which is constant throughout the range of movement.
Present in flexor & extensor muscle groups.
Lead pipe rigidity - resistance felt throughout movement.
Cogwheel rigidity - presence of additional tremor, superimposed on rigidity.
rigidity mechanisms
Enhancement of long latency of stretch reflex (Rothwell, 1994).
Normal stretch reflex composed of short latency (spinal component – normal in rigidity) and long latency (transcortical component – enlarged in rigidity). The longer the long latency, the greater the rigidity.
Damage to basal ganglia, particularly dopamine producing cells in substantia nigra -> distribution of dopaminergic neurons projecting to the corpus striatum which normally modulate direct & indirect pathways within the basal ganglia (allowing for selection of movement pathways).
rigidity causes
Extrapyramidal lesions
(not through the medullary pyramids, extrapyramidal signs and symptoms occur as a result of pathology in the basal ganglia; pyramidal signs occur following an upper motor neurone lesion)
Parkinsonism/Parkinson’s disease – caused by functional disturbance of the basal ganglia.
rigidity features
Increased resistance to relatively slowly imposed passive movements.
Present in both flexor & extensor muscle groups.
Characterised by ‘lead-pipe’ resistance.
Tendon reflexes are normal in contrast to spasticity.
May have superimposed tremor, leading to ‘cogwheel’ rigidity.
factors influencing rigidity
Clinical feature in Parkinson’s Disease, may be accompanied by tremor and bradykinesia.
rigidity assessment
Scales tend to disease/condition specific e.g. Parkinson’s disease.
Hoehn and Yahr Scale
Universal Parkinson’s Disease rating Scale (UPDRS)
UPDRS
The UPDRS scale refers to Unified Parkinson Disease Rating Scale, and it is a rating tool used to gauge the course of Parkinson’s disease in patients. The UPDRS scale consists of the following five segments: 1) Mentation, Behavior, and Mood, 2) ADL, 3) Motor sections, 4) Modified Hoehn and Yahr Scale, and 5) Schwab and England ADL scale. Each answer to the scale is evaluated by a medical professional that specializes in Parkinson’s disease during patient interviews. Some sections of the UPDRS scale require multiple grades assigned to each extremity with a possible maximum of 199 points. A score of 199 on the UPDRS scale represents the worst (total disability) with a score of zero representing (no disability).
rigidity management
Focus on underlying extrapyramidal syndrome.
Medications include: levodopa, dopamine agonists, anticholinergics and selegiline.
Dopamine deficiency results in change in setting of background tone resulting in rigidity, review Basal Ganglia.
physio aims for rigidity
-Assessment Normalise tone Relief of symptoms – stiffness/pain Review – posture, gait, mobility, transfers Record functional performance
physio management for rigidity
Regular re-assessment Normalise tone Management of stiffness/pain – heat, Neurotech Educate re posture Gait, mobility, transfers – re-education Optimise functional independence
Spasticity summary
Spasticity UL flexors, LL extensors Velocity dependent increase in tone, clasp-knife Increased Increased spinal stretch reflex gain Upper motor neurone (pyramidal) sign
rigidity summary
Flexors & extensors equally Constant throughout movement, lead-pipe Normal Increased long-latency component of stretch reflex Extrapyramidal sign
Low tone - hypotonia - presentation
- low state of tone
- decreased resistance to passive mvmt
- decrease in reflexes
hypotonia pathophysiological mechanisms
Unclear
Hypotonia secondary to an acute insult may occur as a result of neural shock - results in reduced neuronal conduction & communication breakdown with the nervous system.
Prolonged hypotonia – reduced levels of arousal & central drive -> insufficient alpha motor neurone excitation. Also associated problems with cortical communication with cerebellum & basal ganglia.
Presence of hypotonia beyond 3 months is an indicator of poor prognosis.
hypotonia - causes
Central cerebral shock – post UMNL
Spinal shock
Peripheral nerve lesion
Cerebellar
Hypotonia clinical feature
Loss of function
Inability to move against gravity
Inability to sustain upright posture
Inability to weight bear / transfer
Hypotonia implications for physio
Loss of function Inability to move against gravity Inability to sustain upright posture Inability to weight bear / transfer Muscle is prone to atrophy Change in length leads to change in strength
Aims for physio for hypotonia
Maintain ‘idea’ of movement, PROM. Protect limb / joint Adequate support Positioning Promote tone - facilitatory techniques Facilitate muscle activity Strengthen
physio mgmt for hypotonia
Stability and approximation
Handling and positioning – ‘optimum’ level of support, as too much may be counterproductive. Use of weight bearing & sustained postures. Facilitate movement, increase speed of movement.
Base of support – smaller BOS, higher COG.
Increase sensory input – handling (increased proprioception), brushing/stroking, tapping, ice brushing.
Splints
PNF
Education / awareness / prevent trauma
FES / NMES
guidelines for assessment of spasticity
A - Any patient with motor weakness should be assessed for the presence of spasticity as a cause of pain, as a factor limiting activities or care, & as a risk factor for the development of contractures.
B - In any patient with spasticity, local and general factors that may cause increased tone (e.g. pain) should be identified and alleviated.
C - In any patient where spasticity is causing concern, simple procedures to reduce spasticity should be used, including exercise, stretching and positioning.
D - For more active treatments, specific goals should be set & monitored using appropriate clinical measures (e.g. numerical rating scales, Ashworth scale).
guidelines for management of spasticity
A - Any patient who has increased tone sufficient to reduce passive or active movement around a joint should have their range of passive joint movement assessed as a prelude to starting preventative actions.
B - For any patient whose range of movement at a joint is reduced or at risk of becoming reduced;
A programme of passive stretching of all affected joints on a daily basis should be taught to the patient and/or carers.
Management may include prolonged positioning of muscles in a lengthened position to maintain range of motion, (AUS, 2005).
Inflatable arm splints should not be used routinely, (RCPUK, 2008).
If stretching alone does not control contractures, serial casting around a joint should be considered as a treatment for reducing contractures , (RCPUK, 2008; AUS, 2005)
serial casting
used to help decrease muscle tightness and allow for better function and movement of a joint
UL flexors - clinical patterns for spasticity
- IR shoulder flexed wrist pronated forearm clenched fist flexed elbow thumb in palm deformity
LL extensors - clinical patterns for spasticity
equinovarus stratal toe stiff knee flexed knee adducted thighs
