WEEK 10 - WHEN THE BRAIN IS DAMAGED

Question 1

Cells of the CNS and PNS

Answer 1

IN CNS

• Oligodendricytes - myelinate the CNS - protecting the axons and neurons
• Astrocytes - star shaped - maintiain the enviornment around the neurons. Also involved in the blood brain barrier, sorting what moves in and out of the brain
• Ependymal cells - produces CSF - within the ventricles of the brain
• Microglia - phagocytose foreign particles

IN PNS

• Schwann cells - creates a myelinated region around neuron axon
• Satellite cells - myelinate and protect the cell body (ganglia) in the PNS

Question 2

Stages of motor recovery after stroke

Answer 2

Stage 1 - flaccid paralysis - no reflexes

Stage 2 - spasticity, hypereflexia, reflex synergic response

Stage 3 - spasticity ++, voluntary movement in synergic patterns only

Stage 4 - spasticity decrease, some movements out of synergy

Stage 5 - spasticity decreases more, only present in quick movements only

Stage 6 - coordination improving, abnormal patterns only with complex movements

Stage 7 - completely normal even through complex movements

Inneurological physiotherapy practice, the assessment toolthat is used to evaluate the stage of motor recovery is theChedoke McMaster Stroke Assessment

Question 3

brain haemorrhages - types

Answer 3

epidural/extradural haematoma - collection of blood within the potential space between the outer layer of the dura mater and the skull

Subdural haematoma - blood collects under the dura mater

Sub- arachnoid haematoma

Question 4

Common aquired conditions - brain, spinal cord and PNS lesions

Answer 4

spinal cord
- spinal cord injury
- meningitis
- tumours

brain lesion
- stroke
- acquired brain injury
- brain infection
- brain tumour

PNS lesion
- MS
- GBS
- Huntingdons chorea
- Poliomyelitis

Question 5

UMN v LMN problems

Answer 5

UMN lesion - e.g stroke, head injury, bleed, brain tumour OR spinal injury OR ALS / MND (only motor)

• increased reflexes
• increased muscle tone/spasticity
  
  • hyper-reflexia
  • hyper-tonia

Spasticity - velocity dependent resistance to movement (stretch). Spasticity results in abnormal movement patterns/synergies

• UL usually into flexion
• LL usually into extension

LMN lesion - e.g poliomyelitis, spinal muscular atrophy, Bells Palsy (only motor),Gulliaine Barre, MS (motor and sensory)

Question 6

Reflexes in UMN lesion?

Answer 6

When there is no damage to your NS, you receive tonic (constant) INHIBITION of reflexes so they are not constantly on every time you lengthen a muscle

When you have UMN damage, you lose inhibitory control from descending pathways.

This means that the reflex arc is NOT inhibited and so there is constant muscle activity

UMN lesion causes abnormal patterns of UL consisting of elbow flexion, wrist flexion and finger flexion is down to

• over-stimulation of the monosynaptic reflex due to removal of descending inhibitory influences (caused by the lesion)

More complex polysynaptic reflexes - reciprocal inhibition

• if inhibitory interneurons are NOT being activated by descending control, then you get increased activation.
• This can lead to co-contraction e.g. around the knee or hip

Question 7

reflexic muscle activation process

Answer 7

1. receptors in intrafusal muscle fibres (muscle spindles and/or golgi tendon organs (in tendons)) detect alteration in muscle length
2. afferent neurons carry this information to the dorsal root of the spinal cord
3. interactions with interneurons in the spinal cord and exits via efferent neurons out of the ventral root
4. efferent neurons carrying stimuli activates the extrafusal muscle fibres, initiating contraction.