REVISION LECTURE Flashcards

1
Q

Brain

  1. Frontal lobe
  2. parietal
  3. temporal
  4. Occipital
A
1. motor cortex
prefrontal association cortex
2. sensory cortex parietal association cortex
3. auditory cortex, wernicke's area 
4. visual cortex
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2
Q

stroke

types

A

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.

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3
Q

Stroke signs and symptoms

post stroke deficits

A

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

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4
Q

motor impairment

A
hemiparesis 
weakness 
paralysis 
loss of voluntary motor control 
spasticity 
increased reflexes
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5
Q

weakness after stroke

A
UL LL BOTH LIMBS
face trunk
ADL 
functional mobility 
weight transfer
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6
Q

Hemiparesis after stroke

A

paralysis that effects one side of the body. R/L hemiplegia depending on which side of the body is affected

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7
Q

abnormal tone after stroke

Assess tone?

A

initial - cerebral shock - low tone - hypotonia
hypertonia- increased tone, spacticity
ash worth scale / modified ashworth scale

use of position charts

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8
Q

hemiasthesia

A
sensory impairments 
where is lesion?  - sensory cortex / thalamus 
assess sensation 
sensory loss - implications for mgmt 
treatment - sensory reeducation
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9
Q

BAlance

A
Loss of balance control
Loss of automatic postural adjustments
Posture - large base of support
\+/- ataxia
Increased risk of falls

Factors for balance impairment

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10
Q

attention concentration deficits post stroke

A

Implications for rehabilitation, and learning skills

Relearning movements

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11
Q

Communication

A

broca’s - motor dusphagia / expressive

Wernicke’s - receptive / sensory dysphagia

aphasia. = motor and sensory dysphagia

reading writing and numeracy affected

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12
Q

Swallow problems - dysphagia

A
- 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
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13
Q

visual deficits

A

homonymous hemaniopia
visual field defect
visual inattention

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14
Q
visuospatial deficits after stroke 
somatognosia 
anosognia 
unilateral neglect 
right/ left discrimination
A

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.

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15
Q

Apraxia
agnosia
body image
body scheme

A

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.

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16
Q

Testing for visuospatial deficits

A
Tests 
Clock drawing
Line Bissection test
Cancellation tasks
Clinical psychology and OT
Implications in rehabilitation
Balance
Transfers
Falls risk
Functional mobility
ADL
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17
Q

Common complications post stroke

A
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
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18
Q

abnormal tone

A

high - hypertonia
spasticity
rigidity

low - hypotonia
flaccidity

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19
Q

tone define

A

‘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

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20
Q

non - neural

factors contributing to tone

A

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

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21
Q

neural factors contributing to tone

A

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*

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22
Q

factors contributing to tone

- peripheral and CNS

A

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

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23
Q

neural factors. - stretch reflex

A

the stretch reflex is the body’s involuntary response to an external stimulus that stretches the muscles

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24
Q

Abnormal tone - spasticity

A

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

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25
Spasticity - causes
UMNL from motor cortex to spinal motor neurons common causes: stroke, SC compression, brain damage, inflammatory lions of the spinal cord MS
26
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).
27
factors influencing spasticity
``` positioning stress fatigue pain full bladder infection fear pressure sore constipation increased effort ```
28
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 ```
29
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 ```
30
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
31
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
32
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)
33
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
34
medical management for rigidity
Medical Mx - Medications include: levodopa, dopamine agonists, anticholinergics and selegiline.
35
hypotonia
decreased resistance to passive movement | decrease reflexes
36
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 ```
37
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 ```
38
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
39
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.
40
consequences of UL dysfunction
``` Pain (distraction) Recovery & outcome of rehabilitation Interferes with rehabilitation Interferes with transfers ADL and Independent function Depression Sleep disturbance ```
41
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
42
``` 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.
43
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) ```
44
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 ```
45
supporting UL during TF and mob
sling only used for TF and walking | when in bed or chair remove the sling
46
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
47
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
48
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)
49
implications
Balance control (sitting, standing, walking) Functional mobility Recovery of ADL Safety during movement / transfers
50
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
51
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
52
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
53
ICF
health condition - disorder or disease body functions and structures activities participation environmental and personal factors
54
Outcome measures
instrument used to test or rate a part of your Ax make sure its valid and reliable
55
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 ```
56
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? ```
57
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
58
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
59
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 ```
60
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.
61
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.
62
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
63
lower limb coordination
heel to shin patient in supine lift leg and place heel on knee slide heel down along shin
64
trunk co-ord
tandem walking
65
Dysdiadokokenesis
rapid alternating pronation supination
66
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
67
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. ```
68
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 ```
69
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 ```
70
LMN
neuron who's cell body lies in the CNS and whose axon leaves the CNS through a foramen and terminates on an effector
71
UMN
a neuron which lies entirely in the CNS and causes movement because it terminates on the LMN
72
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.
73
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) ```
74
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 ```
75
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).
76
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 ```
77
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…
78
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 ```
79
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
80
unilateral neglect
Unilateral Neglect common in right sided stroke with left sided hemiparesis WHY – Dominant visuoperceptual centre in right cerebral hemisphere, parietal lobe
81
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
82
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
83
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
84
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 ```