Week 4 (part 1 and 2) Flashcards
(22 cards)
Part 1
intro to handling neuro patients
how do muscles change due to misuse
Reduced cross sectional area
Greatest atrophy in antigravity/postural muscles (mainly type I)
Depending on position of disuse:
Lengthened position – increase in number of sarcomeres but shorter
Shortened position – decrease in number of sarcomeres but longer
Reduced pennation angle (due to reduction in sarcomeres) allows greater shortening but less sustained contraction (Postural muscles again)
Changes in length tension relationship
Decreased protein synthesis
Alteration in connective tissue (extracellular matrix) decreased extensibility (titin)
Increased tendon stiffness leads to alteration in force transfer from muscle fibres to muscle attachment
what may Stroke patients experience as a consequence of muscle disuse
Difficulty with wheelchair position or mobility
Feeding problems
Pain
Hygiene (groin, axilla), self care
Communication difficulties
Skin integrity
Impact on functional tasks
Osteoporosis
Influence sleep
Cosmetic deformities
what are the two main treatment strategies for muscle disuse/ ST patients
Stretching
Manual
Splints
Orthotics
Position and Postural Management
Chairs
Beds
24 hours
Stretching:
Physiotherapists undertake stretching during physiotherapy treatment sessions
We can teach carers and family members to stretch as part of a home exercise programme (HEP)
We can use stretching within positioning programs
Physiotherapist can also use Serial casting for a sustained stretch
Splints can be used to maintain range of movement
Orthoses can also be used
Stretching in Neurology is usually a more prolonged stretch than recommended by ACSM due to changes in the muscle structure
what are the foundations for stretching exercises
Stretching exercises
Passive static/dynamic stretching could be carried out periodically but must be performed in conjunction with other rehabilitation treatments.
Prolonged passive stretching should be avoided in favour of more frequent, shorter, and more intense repetitions.
The time for rest between sets should be at least 60 min, and the total time for stretching each day must be no more than 2.5h to avoid the risk of pain.
Static stretching with positioning orthoses
Although positioning orthoses are effective in reducing wrist flexor spasticity in clinical practice, prolonged orthosis use is not encouraged.
what are the aims of positioning
Aims of Positioning:
Encouraging comfort and avoidance of pain
Maintenance of soft tissue length and avoid contractures
Promote hydration and nutrition
Promote orientation for the patient
Avoid aspiration - aspiration pneumonia
Avoid subluxation or pain of the UL (e.g. shoulder pain in stroke)
Maintain appropriate skin integrity
Special Considerations:
Sleep systems
Specialised wheelchairs and beds
Pillows
Towels
Splints/orthotics
Regular turns
Positioning charts
Education
Will be unique to the individual based on their presentation
No one size fits all
Part 2
Neuroplasticity
what is the definition of neuroplasticity
- Enduring changes in structure, function and connections within the nervous system
- The ability of the brain to adapt and reorganise in response to either experience and/or therapy
- This applies to both normal nervous systems and those affected by injury or disease. It gives us the ability to learn and to adapt to changing environments and also the possibility of recovery following injury or disease
- So, although it was believed that the nervous system had no ability to repair, we now know that is not the case
what is the neural response to injury
- There are three possible causes of injury to the nervous system:
- Direct injury to neuron(s)
- Disruption to neural function due to indirect effects of injury – (decreased blood flow, oedema, cerebral metabolism, CSF)
- Synaptic loss from damaged neurons cascades that causes degeneration of neighbouring neurons – leading to further damage
what are the 4 stages of transneuronal definition
1 - Axotomy:
the axon of a neuron is cut
2 - Anterograde Degeneration:
Then the distal portion of the damaged neuron degenerations
3 - Retrograde degeneration:
Then the proximal portion of the damaged neuron may degenerate
4 - Transneuronal Degeneration:
the neurons that synapsed on the damaged neuron may degenerate and so too may neurones on which the damaged neuron synapsed
what is Wallerian Degeneration in the PNS
- Trophic degeneration of the neuron at site of lesion and travels distally from cell body
- Swelling and granulation
- Lasts for 3-4 days
- Myelin degenerates too
- Growth factors promote the growth of axonal buds
- Regeneration begins to occur at 7 days
- Growth occurs at 1-4mm a day
- Process occurs alongside restoration of the Schwann cells
what is Diachisis and Oedema
- Temporary disruption of neural function due to shock of injury or disease
- This can occur locally to the injury or at some distance due to altered metabolism and reduction of blood flow
- Oedema is common around the brain following injury
- Again, can be local or remote
- Can be significant enough to block neural conduction
- Some function is restored when diaschisis and oedema
what are the mechanisms of plasticity
- Denervation Supersensitivity
- Unmasking of silent synapses
- Synaptogenesis
- Collateral sprouting
- Short- and long- term potentiation
- Cortical remapping
what is denervation super sensitivity
- Occurs when there is a loss of input from another area of the brain
- The post synaptic membrane becomes more sensitive to the release of neurotransmitter
- E.g. in Parkinson’s Disease neurons in the basal ganglia are destroyed and therefore produce less dopamine. The post synaptic membranes of the target neurons become more sensitive to the remaining dopamine by forming more dopamine receptors
how does the unmasking of silent synapses
- During recovery previously unused synapses are recruited
- Suggests the existence of structural synapses in the brain that are not normally functional due to competition
what is synaptogensis (regenrative)
- It has been shown in animal studies that there is some ability of injured axons to sprout or regrow
- This occurs within 3 to 7 days of injury
- Not yet established if this process leads to return of function
what is collateral sprouting (reactive synaptogenesis)
eighbouring, uninjured axons sprout to innervate synaptic sites previously activated by the injured neuron
* There has been some research to show the timing of this process is similar to the time for the return of behaviours lost by the original injury
what is short term potentiation
- A change in the performance or output of a synapse in the short term – minutes to hours
- An increase in synaptic strength due to increase in neurotransmitter production and/or altered post synaptic receptors
- “Cells that fire together wire together” – Hebbian theory
- This is the basis of learning
- E.g. remembering a phone number long enough to make a call and then forgetting it
what is long-term potentiation (LTP)
- Change in the performance or output of a synapse in the long term – weeks, months, years
- Not fully understood but related to increase in pre-synaptic neurotransmitter release and structural change of the post-synaptic structure
- This is related to spatial and temporal summation (remember those!) – LTP occurs with high frequency stimulation or pairing of stimulation
- This is how we learn
- E.g. learning a phone number and being able to remember it several years later
what is cortical remapping
- Areas of brain cortex are modifiable by sensory input, experience and learning, as well as response to injury
- For instance:
- The motor and sensory representation of the fingers of the left hand of string players are larger than those of non-string players
- Blind people who read braille activate their primary and secondary visual cortex areas, when reading, whereas those with normal vision do not
- Following amputation of the arm the representation of the arm in the cortex moves into the area no longer in use
- Recovery of hand function following stroke has been associated with extension of the hand area of the cortex into the area normally controlled by the face
- Cortical remapping or reorganisation may not be possible when large areas are damaged.
- In this situation it has been suggested that representation shifts to areas that are functionally related but further from the original site
- Ipsilateral motor pathways (uncrossed) may aid recovery of function
- Cortical remapping is influenced by training
what is the clinical reasoning needed for neuroplasticity
- Use dependent and specific
- Repetition or practice at intensity
- Early intervention is better (first 12 weeks)
- Salience, motivation, feedback and attention
- Environment – sensory, cognitive, social and motor
- Age, genetics, pharmacology, size of lesion and stress
- Adjunct therapies can prime the motor system to enhance neuroplasticity
