Quiz 2 revision Flashcards
other influences on recovery
Age • Pre-morbid function • Co-morbidities • Isolated or difficult social situation • Patient motivation and attitude
principle 1 of neuroplasticity
Body parts can compete for representation in the brain and
use of body part can enhance its representation
• Representation areas increase or decrease depending
on use
• E.g. the cortical representation of the reading finger in
proficient Braille readers is enlarged at the expense of
the representation of other fingers
• E.g. the representation of tibialis anterior is smaller
after the ankle is immobilised in a cast
In the case of a stroke that damages a body part’s
representation in the primary motor cortex, plasticity
permits some reorganisation that will restore a
representation
• The process must be competitive with all other body parts
principle 2 of neuroplasticity
The premotor cortex can substitute for the motor cortex to
control movement
• While the primary motor cortex has the largest and most
powerful contribution to the function of the corticospinal
tract, the premotor cortex also contributes
principle 3 of neuroplasticity
The intact hemisphere can take over some motor control
• There are ipsilateral corticospinal neural pathways (weak
in humans)
• These pathways innervate many more proximal than
distal muscles
• The transcollosal connections provide another possible
role of the intact hemisphere
• fMRI studies demonstrate that the damaged hemisphere
has increased blood flow when bilateral movements are made
principle 4 of neuroplasticity
Neuroplastic mechanisms can be facilitated
• Physiotherapists can influence cortical reorganisation
after stroke with:
• Rehabilitative techniques
• Sensory stimulation
• Environmental enrichment
MOI for TBI - direct
direct blow to the head
MOI for TBI - indirect
impact from other part of the body
MOI for TBI - blunt
acceleration-deceleration injury commonly resulting in multiple body injuries and widespread brain damage; may causes scalp injuries, skull deformation +/- fractures or depressed fractures +/- perforated dura mater and brain
MOI for TBI - penetrating
open head injury in which the dura mater is breach ed; may be caused by external objects or bone fragments from a skull fracture
Primary brain damage +neuropathic processes
Occurs at the time of injury
• Effects are largely immediate
Neuropathic Processes • Hypoxia • Hypotension • Cerebral metabolic-flow uncoupling • Impairment of cardiovascular autoregulation
secondary brain damage -+ neuropathic processes
Primary injury initiates a cascade of neuropathological processes resulting in more severe and widespread brain damage Neuropathic Processes • Excitotoxicity • Impaired calcium homeostasis • Oxygen free radicals • Inflammatory processes
Intracranial mechanisms for primary brain damage
diffuse
- diffuse axonal injury
focal
- laceration
- contusion
- haemorrhage (subdural, epidural, subarachnoid, intraventricular
intracranial mechanisms for secondary brain damage
-Brain swelling (vasogenic oedema,
cytotoxic oedema)
- Cerebral blood vessel constriction
extracranial mechanisms
hypoxia
hypotension
predictors of outcome following TBI
TBI usually results in immediate loss or impairment of
consciousness
-> period of confusion (PTA)
• Indices of severity of predictors of outcome:
• Depth of coma
• Duration of coma
• Length of post-traumatic amnesia (PTA)
• Depth of coma provides the best clinical picture of a
patient’s current neurological status
• Duration of coma and length of PTA appear to be better
predictors of functional outcome
depth of coma for TBI
The Glascow Coma Scale (GCS) defines the severity of
a TBI within 48 hours of injury
• Most widely used measure of the severity of coma
• Severe = GCS ≤ 8
• moderate = GCS 9-12
• mild = GCS 13-15
Aims of acute neurological physiotherapy management
Provide respiratory care
• Improve respiratory function
• Prevent/ manage respiratory complications
• Optimise musculoskeletal integrity
• Prevent/ minimise/ manage secondary adaptive
changes in soft tissue
• Promote the restoration of motor function
• Discharge planning
Prioritsing physiotherapy assessment 1 and 2
- Cardiorespiratory Assessment
• Life threatening complications must be managed first - Functional Assessment
• Early mobilisation maximises rehabilitation potential
and minimises risk of many complications
• Utilise skills that are unique to physiotherapists
• Recommendations underpin manual handling utilised
by multidisciplinary team
• Patient centred
• Goal directed
• Functional/ task-specific
prioritising physiotherapy assessment #3
assessment of impairments determination of diagnosis determination of prognosis guides physio mgmt D/C planning
minimum requirements of patient to attempt standing
Medically stable/ medical clearance for mobility
• BP, Hb, INR, WB status, ICP, seizures, increasing
neurological deficit
• Cooperative with some level of comprehension
• Pain managed
• DVT screen NAD
• Minimum strength of grade 3 or able to move against
gravity throughout full ROM for hip F/E, knee E, ankle
PF/DF in at least one upper and lower limb
• Attachments managed
• Clinical protocols adhered to
rehab strategies for wernicke’s dysphasia
Picture cards One stage commands Break down questions into key words Use demonstration Use gestures and facial expression Short and simple questions
rehabilitation of broca’s dysphasia
Ask yes/no questions Use visuals scales eg. VAS Give patient time to get words out Use probing questions, e.g. What is it used for? What does it start with?
autonomic dysreflexia
Lesions at or above T6 • Causes an imbalanced reflex sympathetic discharge, leading to potentially dangerous hypertension • Life threatening condition • Medical emergency • Can cause seizures, retinal hemorrhage, pulmonary oedema, renal insufficiency, myocardial infarction, cerebral hemorrhage, and death
Autonomic dysreflexia
Signs – Increased blood pressure – Redness in the face – Severe headache – Heavy sweating • Common causes – Blocked urine catheter – Fracture – Burn injury – Hangnail • Symptoms resolve when cause is removed
list the 4 clinical courses of MS
relapsing remitting
secondary progressive
primary progressive
progressive relapsing
aims of physiotherapy- restorative therapy
– Optimise performance of everyday activities and
skills/ Maximize functional ability
– Target disuse weakness, spasticity, pain,
incontinence, cardiopulmonary deconditioning;
preserve musculoskeletal integrity
compensatory approach
– Prevent unnecessary disability and handicap
– Improve individuals quality of life
– Ensure that interventions are relevant to person’s
needs and desires; collaborate to set meaningful
goals
– Manage fatigue
– Teach use of mobility aids, transfers; modify
clinical presentation MND
The clinical presentation tends to be incidious and depends on the part of the CNS affected – Lower motor neurone degeneration - main features are weakness, wasting and fasciculation of the muscles – Upper motor neurone degeneration leads to weakness and muscle wasting but the
Types of MND
– Amyotrophic lateral sclerosis (ALS)
– Progressive muscular atrophy (PMA)
– Progressive bulbar palsy (PBP)
– Primary lateral sclerosis (PLS)
define parkinsonism
clinical syndrome characterised by a
disorder of movement consisting of tremor, rigidity,
elements of bradykinesia, hypokinesia, akinesia and
postural abnormalities
define parkinson’s disease
clinical syndrome of
Parkinsonism associated with a distinctive pathology
- Typically a slowly progressive degenerative disease
- Primarily related to a lack of dopamine
- Most common disease affecting the basal ganglia
pathophysiology of Parkinson’s
• Reduction in dopamine – Disturbance of the central dopaminergic pathway from the substantia nigra to the striatum • Depigmentation and neuronal loss in the in the substantia nigra • Presence of lewy bodies with consequent changes to neural conduction in the nigrostriatal pathway – Basal ganglia, brainstem, spinal cord and cortex
neurosurgery for PD
• Thalamotomy
– Lesioning procedure, not widely used now
• Deep Brain Stimulator
– High frequency electro-stimulation through permanent
implanted electrodes in the brain
– Battery implanted in chest wall below clavicle and
connects to DBS by subcutaneous wire
– Mimics lesioning procedure without destroying brain
tissue; can be performed bilaterally; stimulation can be
adjusted postoperatively; reversible
• Deep Brain Stimulator (cont.)
– Subthalamic nucleus (bradykinesia and rigidity)
– Thalamus (tremor)
– Globus Pallidus (dyskinesia)
gait disturbances in PD
• Slowness of movement
• Difficulty in initiation
• Typical PD gait: short, shuffling steps, uneven step
lengths, flexed posture, reduced arm swing, decreased
angular displacement of the lower limb joints
• Freezing and festination
• Reduced stride length is the biggest contributor to
reduced speed and inefficient turning
• Disturbances amplified walking backwards
• Significantly increased falls risk
define vertigo
any sensation of self motion that is not actually occuring. Usually described as world spinning
define disequilibrium/imbalance
feeling of instability while seated, standing or walking eg. veering while walking
define dizziness
sensation of disturbed or impaired spatial orientation without false sense of motion eg. light headedness, faintness
BPPV
Otoconia (calcium carbonate) fall from the utricle into one of the semicircular canals
movement of the head ( in relation to effected canal) - abnormal stimulation of the cupula sends false signals to brain that the head is moving. vertigo and nystagmus may result
Majority of BPPV is canalithiasis : otoconia free floating
less common cupulolithiasis : otoconia adhere to the cupula resulting in a maintained excitation of the semicircular canal
BPPV characteristics
vertigo
- may be associated with nausea, vomiting, imbalance, difficulty concentrating
- provided by head movements or changes in body position
- usually looking up and down, lying down or getting up from bed, rolling over onto the effected side
short lasting (canalithiasis) (5-30 secs) occurs repeadedly with these movements (not typically a one off episode
hall pike interpretation - confirmatory diagnosis
patients symptoms concurrently with nystagmus
posterior - Right - right rotational and upbeating
posterior - left - left rotational and upbeating
anterior - right - right rotational and down beating
anterior - left - left rotational and down beating
BPPV nystagmus
latency of 0-40seconds (usually only posterior)
crescendo - decrescendo
reversal upon return to sitting (posterior)
fatigues on re testing (horizontal and posterior)
what is a fall
Fall: an event which results in a person coming to rest
inadvertently on the ground or other lower level
• Do not include an intentional change in position
• Do include when a person inadvertently comes to rest on
furniture, against a wall or other object or person
falls may result from
- Loss of balance
- Tripping
- Slipping
- Legs giving away
absolute indications to terminate exercise
• Suspicion of a myocardial infarction or acute myocardial infarction
• Onset of moderate-to-severe angina
• Drop in systolic blood pressure (SBP) below standing resting pressure or
drop in SBP with increasing workload accompanied by signs or symptoms
• Signs of poor perfusion, including pallor, cyanosis, or cold and clammy skin
• Severe or unusual shortness of breath
• CNS symptoms
– e.g., ataxia, vertigo, visual or gait problems, confusion
• Serious arrhythmias
– e.g.: second / third degree AV block, atrial fibrillation with fast ventricular
response, increasing premature ventricular contractions or sustained
ventricular tachycardia
• Technical inability to monitor the ECG
• Patient’s request (to stop)
seating principles for wheelchairs
- Maximise surface area contact
- Maintain or improve postural alignment
- Provide a stable base of support
- Decrease abnormal tone influences
- Promote increased sitting tolerance
- Enhance cosmesis
wheelchair and user measurements
- # 1 USER WEIGHT
- Seat width
- Seat depth
- LL length
- Seat height
- Legrest angle
- Back height
- Armrest height
- Seat angle
- Seat to back angle
