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
