REVISION LECTURE Flashcards
Brain
- Frontal lobe
- parietal
- temporal
- Occipital
1. motor cortex prefrontal association cortex 2. sensory cortex parietal association cortex 3. auditory cortex, wernicke's area 4. visual cortex
stroke
types
sudden onset of a focal neurological deficit due to a presumed local disturbance to the blood supply lasting. more than 24 hours
ischaemic - embolus,, thrombus in blood supply to the brain
Haemorrhagic - ICH - bleeding in the brain
SAH - bleeding in the subarachnoid space - between arachnoid membrane and Pia mater.
Stroke signs and symptoms
post stroke deficits
headache, visual disturbance, photophobia, vomiting, cervical stiffness,
LOC
attention, conc, memory issues,
Motor deficitcs, Loss of power, hemiplegia, facial droop.
sensory deficits, neglect, inattention
Spacial problems,
visual disturbance,
visa-spatial issues
cognitive impairment
nutrition continence breathing circulation
motor impairment
hemiparesis weakness paralysis loss of voluntary motor control spasticity increased reflexes
weakness after stroke
UL LL BOTH LIMBS face trunk ADL functional mobility weight transfer
Hemiparesis after stroke
paralysis that effects one side of the body. R/L hemiplegia depending on which side of the body is affected
abnormal tone after stroke
Assess tone?
initial - cerebral shock - low tone - hypotonia
hypertonia- increased tone, spacticity
ash worth scale / modified ashworth scale
use of position charts
hemiasthesia
sensory impairments where is lesion? - sensory cortex / thalamus assess sensation sensory loss - implications for mgmt treatment - sensory reeducation
BAlance
Loss of balance control Loss of automatic postural adjustments Posture - large base of support \+/- ataxia Increased risk of falls
Factors for balance impairment
attention concentration deficits post stroke
Implications for rehabilitation, and learning skills
Relearning movements
Communication
broca’s - motor dusphagia / expressive
Wernicke’s - receptive / sensory dysphagia
aphasia. = motor and sensory dysphagia
reading writing and numeracy affected
Swallow problems - dysphagia
- swallow test formal SLT ASS first 24 hours risk of aspiration pneumonia dehydration / malnutrition video fluoroscopy
mgmt swallow technique modify food consistency positioning - sitting up involve carers
visual deficits
homonymous hemaniopia
visual field defect
visual inattention
visuospatial deficits after stroke somatognosia anosognia unilateral neglect right/ left discrimination
damage non-dominant posterior parietal lobe
Somatognosia
Lack of awareness of body structure and failure to recognise one’s parts and their relationship to one another.
Anosognosia
Severe form of neglect - patient fails to recognise paralysis or deficits
Unilateral neglect
Inability to integrate and use perceptions from one side of the body /environment. Ignores one half of body. Bumps into objects.
Right / left discrimination
Inability to understand concepts of right
and left.
Apraxia
agnosia
body image
body scheme
Apraxia
Inability to perform skilled movements in the absence of loss of motor power, sensation or co-ordination
Agnosia
Lack of recognition of familiar objects.
Body image
Visual & mental memory image of one’s body.
Body scheme
The position of different parts of the body to each other.
Testing for visuospatial deficits
Tests Clock drawing Line Bissection test Cancellation tasks Clinical psychology and OT
Implications in rehabilitation Balance Transfers Falls risk Functional mobility ADL
Common complications post stroke
Seizure Delirium Nutrition Incontinence Pain - Musculoskeletal pain Psychological issues Depression Circulation Deep Vein Thrombus (DVT) Breathing issuesInfection Aspiration pneumonia Urinary tract infection (UTI) Hospital acquired infection Falls Pressure Ulcer Fractures after falls Limb oedema, lack of muscle pump activity / dependent positions
abnormal tone
high - hypertonia
spasticity
rigidity
low - hypotonia
flaccidity
tone define
‘Tone is the resistance offered by muscles to continuous passive stretch’ (Brooks, 1986).
or ‘Clinically [tone] is defined as the resistance that is encountered when a joint of a relaxed person is moved passively’ (Britton, 1998)
Normal tone is a prerequisite for normal movement
Resting level of tension in muscle must be high enough to support against gravity, but low enough to allow movement to occur
Clinically - examiner feels slight resistance when moving a normal limb passively
non - neural
factors contributing to tone
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 factors contributing to tone
Neural Factors
Active tension set-up by stretch reflex
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*
factors contributing to tone
- peripheral and 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
Abnormal tone - spasticity
Definition
‘Velocity-dependent increase in the tonic stretch reflexes with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex’ (Lance, 1980).
OR
‘Velocity-dependent increase in resistance to passive stretch of a muscle, with exaggerated tendon reflexes’ (Lance, 1990).
Descriptives ‘clasp knife’ phenomenon – abrupt cessation in movement (resistance greater at start of movement), followed by ‘a melting away’ of resistance.
Pathophysiological Mechanisms
Abnormal enhancement of spinal stretch reflexes.
Maybe due to:
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 .
central - loss of cortical inhibition
imbalance in descending pathways
peripheral - altered biomechnaical properties of muscle
change in visco-elastic and connective tissue properties of muscle
Spasticity - causes
UMNL
from motor cortex to spinal motor neurons
common causes: stroke, SC compression, brain damage, inflammatory lions of the spinal cord MS
spasticity - clinical 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
Ax spasticity
ash worth scale modified ash worth scale movement grading severe- no mvmt moderate - poor mvmt mild - good mvmt assoc reactions effort on unaffected side leading to increased tone on spastic side involuntary mvmt - yawning tendon jerks
spasticity -
implications
aims of physio
implications Weakness Decreased movement Abnormal movement Poor posture Soft tissue shortening - contracture Pain Loss of function & adaptive motor behaviour
Normalise tone Maintain normal muscle length Improve ROM Decrease pain Reduce unnecessary complications Improve function Positioning - Abnormal reflex activity Supine - extensor activity Sitting - symmetry and stability Passive movement Movement proximal region of limb Slow passive movements
medical management spasticity
baclofen
GABA derivative, pre and postsynaptic inhibitory effect
diazepam - enhances action of GABA on inhibitory NTS
botulinum toxin - toxin into affected muscle causing presynaptic blockade of Ash release
rigidity
increased resistance to passive movement, constant throughout range of movement
in flexors and extensors
lead pipe rigidity - resistance throughout movement
cogwheel rigidity - additional tremor - superimposed rigidity
causes - extrapyramidal lesions - Parkinson’s disease - caused by functional disturbance of the basal ganglia
rigidity clinical features
Ax
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.Scales tend to disease/condition specific e.g. Parkinson’s disease.
Hoehn and Yahr Scale
Universal Parkinson’s Disease rating Scale (UPDRS)
rigidity
aims of physio
physio mgmt
Assessment Normalise tone Relief of symptoms – stiffness/pain Review – posture, gait, mobility, transfers Record functional performance
Regular re-assessment
Normalise tone
Management of stiffness/pain – heat, Neurotech
Educate re posture
Gait, mobility, transfers – re-education
Optimise functional independence
medical management for rigidity
Medical Mx - Medications include: levodopa, dopamine agonists, anticholinergics and selegiline.
hypotonia
decreased resistance to passive movement
decrease reflexes
hypotonia causes
clinical features
causes Central cerebral shock - post UMNL spinal shock peripheral nerve lesion cerebellar
Clinical features loss of function inability to move against gravity unable to sustain upright posture can't WB ./ TF
UL dysfunction
causative factors
Paralysis / Loss of movement post stroke Muscle weakness Muscle imbalance Abnormal tone Sensory loss Altered alignment / biomechanics Perceptual deficits Immobility Weakness Adaptive soft tissue changes Dependent limb Poor handling Trauma Forced ROM Immobility Prolonged positioning Secondary changes Degeneration
Rotator cuff muscles
functions
Supraspinatus: Shoulder abduction
Post stab: Infraspinatus: External rotation of the shoulder
post stab: Teres Minor: External rotation of the shoulder
Ant stab: Subscapularis: Internal rotation of the shoulder
scapulohumeral dynamics
The Scapulothoracic articulation contributes to both flexion and abduction of the humerus by upwardly rotating the glenoid fossa 60 from its resting position.
consequences of UL dysfunction
Pain (distraction) Recovery & outcome of rehabilitation Interferes with rehabilitation Interferes with transfers ADL and Independent function Depression Sleep disturbance
Hemiplegic shoulder pain
causes
Common post stroke May present early or late Presence of abnormal tone + / - subluxation Sharp pain at end of ROM Experience night pain / diffuse
causes Loss of co-ordinated joint motion Abnormal scapulo-humeral rhythm Inadequate external rotation Lack of downward glide Muscle imbalance, abnormal tone
Forced passive ROM
Incorrect handling / trauma
subluxation mechanism causes presentation diagnosis
Mechanism
Scapula depressed or retracted
Impaired locking mechanism Orientation of scapula & glenoid fossa – up, forward, lateral Slope of fossa - prevents downward subluxation Reinforced by supraspinatus ‘Locking mechanism’ Subluxation Causative factors Paralysis rotator cuff Mal-alignment Abnormal tone Loss of locking mechanism Gravity Weight of limb Presentation \+ / - painful Classification of subluxation*** Inferior subluxation Superior subluxation Anterior subluxation
Mal-alignment shoulder & displaced humeral head
Subjective ‘dragging’
Relieved by passive elevation
diagnosis
palpable dip
pt in sitting
palpate along clavicle out from sc joint
check for gap between lateral cordial border and head of humerus
gap = 1-2 fingers - subluxation.
shoulder hand syndrome
Stage 1 Tender swollen hand Diffuse aching pain Sensitivity Discoloration Warm / moist Loss of movementStage 2 Marked pain and swelling Progressive loss of movement Oedema loss of skin elasticityStage 3 Resolution of pain and oedema Decreased ROM Bone demineralisation Muscle atrophy Soft tissue changes Joint contracture Deformity (flexion)
management of semi shoulder dysfunction
Positioning Handling Normalise tone Education Normalise alignment Posture Facilitate muscle activityPrevent ST shortening Joint mobilisation Restore function Strapping / taping Supports / slings FES/NMES Medication Constraint induced movement Robotics
supporting UL during TF and mob
sling only used for TF and walking
when in bed or chair remove the sling
Pusher syndrome
define
mechanism
The patient leans towards the hemiplegic side in any posture and resists any attempt at passive correction of posture that would move his / her weight towards or across the midline of the body toward the non-affected side’ (Davies, 1985)
Altered perception of body’s orientation in relation to midline / gravity
No correlation with right sided stroke (i.e. L Hemi +/- UN)
Impairment in judging vertical - a change in the perception of midline of their body
clinical findings
Patient leans to hemi side
Resists any attempt to correct posture which moves bodyweight to midline / normal side
Apprehensive re leaning over / WB
Unable to accept weight through unaffected side (if able to WB, may WB on medial border of foot with adduction also)
Demonstrates resistance to passive / active movement toward midline / unaffected side
Over-activity unaffected side UL, LL, trunk
causes
Damage to sensory pathways
Role of posterolateral thalamus
Disturbed neural representation of truncal graviceptive system
Cortical involvement
Insular, opercular as well as temporal regions are possibly involved in the control of upright body position.
Current research indicates that PS in right-hemispheric lesion patients depends on vestibular otolith input, suggesting a link between the system for postural control and the system responsible for processing vestibular otolith information.
Such close interaction would seem useful for processing in multisensory integration centers at the cortical level. (Baier et al 2011 J Neurol)
implications
Balance control (sitting, standing, walking)
Functional mobility
Recovery of ADL
Safety during movement / transfers
PS Ass
mgmt
Assessment Diagnosis made by observation Asymmetrical posture Lack of midline sitting Actively pushes to affected side Verticality & sense of midline Right / Left awareness Visuo-spatial neglect Attention to physical & perceptual deficits to enable appropriate management
Management
Restore sense of verticality
Facilitate midline awareness
Balance training
Regain ability to move actively towards that side with visual cueing & feedback
Regain ability to move actively about in sitting & standing
Physio for PS
Observation based diagnosis.
No reliable measures.
Patient distressed when attempts made to move to normal side.
Preferable to lead patient to move actively to that side.
Balance retraining.
Visual feedback / actively move midline / normal side.
Positioning.
Sitting - small pillow under affected buttock.
Functional movements.
Mirror therapy
hemiplegic gait
Normal gait – what are the characteristics?
Hemiplegic gait
Characteristics that are common after stroke
Assessment approach
Management/Rx
Walking essential independent living / function & ADL
ICF
health condition - disorder or disease
body functions and structures
activities
participation
environmental and personal factors
Outcome measures
instrument used to test or rate a part of your Ax
make sure its
valid and reliable
Falls after stroke
25% contributory factors cognitive impairment, inattention anosognia balance co-ordination muscle weakness sensory loss visual disturbance BERG Falls are difficult to predict Assess at individual level: balance, history of falls, perception, what activities they need to do after discharge, risk of consequences Falls are difficult to prevent Focus on patient’s participation goals and undertaking activities safely, consider education to cope with falls, education to rise from the floor and bone health
neurological exam
How to conduct a sensory system exam Light touch Sharp blunt Vibration Sensory inattention Special sensory tests Graphaesthesia / stereognosis How to assess JPS? How to assess coordination? How to assess tone?How to assess balance? Gait exam How to examine trunk ? How to assess for subluxation? How to describe a functional mobility task? How to facilitate a STS?
objective Ax - sensory system
cutaneous sensations
pain
temp light touch pressure
2 point discrimination
prop sensation
vibration joint position sense
movement
integrative sensation
bilateral simultaneous sensory application
posterior column medial lemiscal pathway conveys:
Conveys:
Proprioception (awareness of position of muscles, tendons, joints & body movements).
Fine discriminative touch (ability to feel exactly which part of body is being touched).
Stereognosis (ability to recognise by feel the size,shape and texture of an object).
Vibration sense.
Weight discrimination (ability to determine the weight of an object).
DISTAL TO PROXIMAL
anterolateral pathways
Including spinothalamic tract (anterior & lateral) and other associated tracts that convey: Pain Temperature sense (hot / cold) Crude touch (poorly localised) touch Pressure Tickle Itch
joint position sense
Joint Position Sense
Upper limb
Patients eyes open demonstrate.
Hold distal phalanx DIP joint index finger .
Illustrate bent & straight.
Patient closes eyes & is asked to report if joint is bent or straight.
Test distal joints first.
Lower limb
As above DIP joint, test hallux.
tiger order sensation
Higher Order Sensation*
Graphesthesia - ability to recognize writing on the skin purely by the sensation of touch.
Stereognosis/tactile gnosis - ability to perceive & recognise the form of an object using cues from texture, size, spatial properties, and temperature (mediated by the posterior column-medial lemniscus pathway). Stereognosis tests determine whether or not the parietal lobe of the brain is intact.
Sensory inattention /sensory neglect - patient recognises stimuli when presented independently but recognises only one side when stimulus is presented simultaneously. Indicates Parietal lobe lesion.
The above cannot be tested unless primary sensation intact bilaterally.
co-ordination
Finger-tip to nose test
Hold finger at arms length in front of patient. Ask patient to touch the finger with index finger then touch their nose. Change speed/position of target.
Repeated movements
lower limb coordination
heel to shin
patient in supine
lift leg and place heel on knee
slide heel down along shin
trunk co-ord
tandem walking
Dysdiadokokenesis
rapid alternating pronation supination
objective Ax
tone
Muscle Tone Assessment Procedure
Assessment Steps (position supine lying)
1. OBSERVE Appearance of limb
2. Palpation / Feel muscle
How does it react to stretch PROM – UL, LL, Trunk
3. PROM; Proximal to distal direction for test
Grading Ashworth Scale or Modified Ashworth – next slide
ash worth scale
No increase in muscle tone. Slight increase in muscle tone - manifested by a catch & release or by minimal resistance at the end of the range of movement when the affected part(s) is moved in flexion/extension. Slight increase in muscle tone, manifested by a catch followed by minimal resistance through the remainder (less than half) of the range of movement. More marked increase in tone through most of the range of movement but affected part(s) easily moved. Considerable increase in muscle tone, passive movement difficult. Affected part(s) rigid in flexion or extension.
functional mobility
balance sitting, standing, static dynamic, functional bed mobility rolling lying to sitting transfers level of Ass pattern of mvmt? BOS Stability posture balance tests
objective Ax - Gait
Appropriately undressed Starting position Initiation of gait Level of assistance Use of aid/device Alignment StabilityBase of support Swing phase Stance phase Arm swing Trunk rotation Foot placement/clearance Timing/co-ordination
LMN
neuron who’s cell body lies in the CNS and whose axon leaves the CNS through a foramen and terminates on an effector
UMN
a neuron which lies entirely in the CNS and causes movement because it terminates on the LMN
abnormal mvmt
What types of Abnormal Movement are there?
Loss of co-ordination - cerebellar lesion
Bradykinesia - Parkinson’s disease (slowed movement)
Involuntary movement - tremor / chorea (brief, involuntary, non-rhythmic movements)
Intention tremor - cerebellar
Non-intention tremor - Parkinson’s
Loss of range - contracture
Loss of voluntary movement UMNL, CVA.
cause of abnormal muscle power
Possible Causes of Abnormal Muscle Power (Weakness), can you discuss them? Muscle pathology Neuromuscular junction defect Central - UMNL Anterior horn cell damage/pathology Nerve root injury Nerve plexus Peripheral – Peripheral nerve lesion (PNL)
Asess muscle tone
How to Assess Muscle Tone - Assessment Steps Appropriately undress, prepare model, expose limbs Patient comfort/safety Preparation of environment and patient Supine lying Observation; Appearance of limb Palpation; Feel muscle Passive ROM, How does it react to stretch – UL, LL, Trunk, Proximal to distal direction for test Compare both sides Grading – Use Ashworth Scale
posterior column - medial lemiscal pathway
Proprioception (awareness of position of muscles, tendons, joints & body movements).
Fine discriminative touch (ability to feel exactly which part of body is being touched).
Stereognosis (ability to recognise by feel the size,shape and texture of an object).
Vibration sense.
Weight discrimination (ability to determine the weight of an object).
anterolateral pathways
Including spinothalamic tract (anterior & lateral) and other associated tracts that convey: Pain Temperature sense (hot / cold) Crude touch (poorly localised) touch Pressure Tickle Itch
sensory system
Primary Sensation Light touch Temperature Pinprick / pain Vibration sense Joint position sense 2 point discrimination
Dermatomes – remember CNS vs PNSSensory Testing Instructions Clear instructions / demonstration What you need? Light touch - cotton wool Vibration - tuning fork Pinprick - neurotips Temperature - test-tubes hot / cold Find level of normality Test both sides Review rules for sensory testing Distal to proximal testing See handout
joint position sense
Upper limb
Patients eyes open demonstrate. Clear communication
Hold distal phalanx DIP joint index finger .
Illustrate bent & straight.
Patient closes eyes & is asked to report if joint is bent or straight.
Test distal joints first.
Lower limb
As above DIP joint, test hallux.
Don’t hold the nail, REMEMBER…
co ordination
Upper Limb Finger-tip to nose test Hold finger at arms length in front of patient. Ask patient to touch the finger with index finger then touch their nose. Change speed/position of target. Repeated movements Lower Limb Heel to shin test - Patient in supine. Lift leg and place heel on knee. Slide heel down along shin. Trunk Tandem walking Other test - dysdiadokokenesis
broca’s area
wernicke’s area
speech problems
Broca’s Area
Inferior frontal gyrus of dominant hemisphere (usually the left)
Associated with motor or expressive dysphasia
Wernicke’s Area
Temporal lobe
Sensory or receptive dysphasia
dysphasia
expressive / motor - broca’s
receptive / sensory - wernickes
Speech problems common in left sided stroke with right sided hemiparesis
WHY – Dominant speech centre in Left cerebral hemisphere
Note - there can be exceptions to this simple clinical rule
unilateral neglect
Unilateral Neglect common in right sided stroke with left sided hemiparesis
WHY – Dominant visuoperceptual centre in right cerebral hemisphere, parietal lobe
sit to stand
Sit to stand
Risk assessment 1 or 2 physios, brakes on, position of plinth
Moving to edge of bed
patients feet on floor, physio supports pelvis, depress unilaterally and walk opposite pelvis forward and vice versa.
Foot position, and support hemiplegic lower limb as appropriate
Preparation environment, use of lifting belt
Care of hemiplegic UL web arm sling, proximal arm support, note thumb grip from MH notes
Rocking, trunk forward ‘nose over toes’
Flexion and extension
Steady in initial standing, caution re hypotension/unsteadiness
stand to sit
Stand to sit
Risk assessment 1 or 2 physios, brakes on WC, position of chair
Moving to edge of chair
Turn around until can feel chair at back of legs
Foot position, and support hemiplegic lower limb as appropriate
Physio assists patient to place unaffected hand on arm rest
Care of hemiplegic UL web arm sling, proximal arm support, note grip from MH notes
Bending knees, controlled descent into chair
Reposition in sitting, hips back, support to UL
check for hemi shoulder subluxation
Patient in sitting
Palpate from the SC joint along the clavicle to the AC joint
Check for a gap between the lateral acromial border and the head of the humerus
A gap of 1-2 fingers indicates subluxation is present
shoulder support stroke care
reduce pain Counteract traction imposed on joint by weight of limb + gravity Prevent stretch to capsule +ST Stabilisation / align Provide proprioceptive feedback Promote awareness
