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Neurological Physiotherapy > Quiz 2 revision > Flashcards

Quiz 2 revision Flashcards

1
Q

other influences on recovery

A 
Age
• Pre-morbid function
• Co-morbidities
• Isolated or difficult social situation
• Patient motivation and attitude
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2
Q

principle 1 of neuroplasticity

A

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

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3
Q

principle 2 of neuroplasticity

A

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

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4
Q

principle 3 of neuroplasticity

A

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

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5
Q

principle 4 of neuroplasticity

A

Neuroplastic mechanisms can be facilitated
• Physiotherapists can influence cortical reorganisation
after stroke with:
• Rehabilitative techniques
• Sensory stimulation
• Environmental enrichment

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6
Q

MOI for TBI - direct

A

direct blow to the head

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7
Q

MOI for TBI - indirect

A

impact from other part of the body

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8
Q

MOI for TBI - blunt

A

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

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9
Q

MOI for TBI - penetrating

A

open head injury in which the dura mater is breach ed; may be caused by external objects or bone fragments from a skull fracture

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10
Q

Primary brain damage +neuropathic processes

A

Occurs at the time of injury
• Effects are largely immediate

Neuropathic Processes
• Hypoxia
• Hypotension
• Cerebral metabolic-flow uncoupling
• Impairment of cardiovascular
autoregulation
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11
Q

secondary brain damage -+ neuropathic processes

A 
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
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12
Q

Intracranial mechanisms for primary brain damage

A

diffuse
- diffuse axonal injury

focal

  • laceration
  • contusion
  • haemorrhage (subdural, epidural, subarachnoid, intraventricular
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13
Q

intracranial mechanisms for secondary brain damage

A

-Brain swelling (vasogenic oedema,
cytotoxic oedema)
- Cerebral blood vessel constriction

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14
Q

extracranial mechanisms

A

hypoxia

hypotension

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15
Q

predictors of outcome following TBI

A

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

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16
Q

depth of coma for TBI

A

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

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17
Q

Aims of acute neurological physiotherapy management

A

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

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18
Q

Prioritsing physiotherapy assessment 1 and 2

A
  1. Cardiorespiratory Assessment
    • Life threatening complications must be managed first
  2. 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
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19
Q

prioritising physiotherapy assessment #3

A 
assessment of impairments 
determination of diagnosis 
determination of prognosis 
guides physio mgmt
D/C planning
20
Q

minimum requirements of patient to attempt standing

A

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

21
Q

rehab strategies for wernicke’s dysphasia

A 
Picture cards
One stage commands
Break down questions into key words
Use demonstration
Use gestures and facial expression
Short and simple questions
22
Q

rehabilitation of broca’s dysphasia

A 
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?
23
Q

autonomic dysreflexia

A 
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
24
Q

Autonomic dysreflexia

A 
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
25
Q

list the 4 clinical courses of MS

A

relapsing remitting
secondary progressive
primary progressive
progressive relapsing

26
Q

aims of physiotherapy- restorative therapy

A

– Optimise performance of everyday activities and
skills/ Maximize functional ability
– Target disuse weakness, spasticity, pain,
incontinence, cardiopulmonary deconditioning;
preserve musculoskeletal integrity

27
Q

compensatory approach

A

– 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

28
Q

clinical presentation MND

A 
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
29
Q

Types of MND

A

– Amyotrophic lateral sclerosis (ALS)
– Progressive muscular atrophy (PMA)
– Progressive bulbar palsy (PBP)
– Primary lateral sclerosis (PLS)

30
Q

define parkinsonism

A

clinical syndrome characterised by a
disorder of movement consisting of tremor, rigidity,
elements of bradykinesia, hypokinesia, akinesia and
postural abnormalities

31
Q

define parkinson’s disease

A

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
32
Q

pathophysiology of Parkinson’s

A 
• 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
33
Q

neurosurgery for PD

A

• 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)

34
Q

gait disturbances in PD

A

• 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

35
Q

define vertigo

A

any sensation of self motion that is not actually occuring. Usually described as world spinning

36
Q

define disequilibrium/imbalance

A

feeling of instability while seated, standing or walking eg. veering while walking

37
Q

define dizziness

A

sensation of disturbed or impaired spatial orientation without false sense of motion eg. light headedness, faintness

38
Q

BPPV

A

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

39
Q

BPPV characteristics

A

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
40
Q

hall pike interpretation - confirmatory diagnosis

A

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

41
Q

BPPV nystagmus

A

latency of 0-40seconds (usually only posterior)
crescendo - decrescendo
reversal upon return to sitting (posterior)
fatigues on re testing (horizontal and posterior)

42
Q

what is a fall

A

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

43
Q

falls may result from

A
  • Loss of balance
  • Tripping
  • Slipping
  • Legs giving away
44
Q

absolute indications to terminate exercise

A

• 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)

45
Q

seating principles for wheelchairs

A
  • 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
46
Q

wheelchair and user measurements

A
  • # 1 USER WEIGHT
  • Seat width
  • Seat depth
  • LL length
  • Seat height
  • Legrest angle
  • Back height
  • Armrest height
  • Seat angle
  • Seat to back angle

Neurological Physiotherapy (13 decks)

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