ABI and Nudo

Question 1

Intro

Answer 1

• Brain damage (cerebrovascular injury – CVI tumour, TBI, anoxia, degenerative disease, infection, toxins (lead), tumours, seizures
• Stroke
o Infarct – block, loss of function in watershed area
o Haemorrhage – weakness in artery wall, fills with blood, pressure on neurons, med emergency – more often they burst (bleeding brain) confined in meninges of brain = compresses all neurons in area as blood has no where to go, decreased BF = neuronal death
o Ischaemic – clot occluding brain dysfunction
o Intracerebral haemorrhage – bleeding into brain (focal and diffuse brain dysfunction)
o Subarachnoid haemorrhage – bleeding around brain (diffuse brain dysfunction)
• Treatment – early rehab essential
• Major arteries of brain
o Circle of Willis – basic life saving very important – blood can still get to major areas of brain
o MCA (band which lots of infarcts are seen), ACA (very important MCA-ACA sensory and motor cortexes), OCS
o Lenticulostriate arteries subserve the BG – bad strokes (ruled out in many studies)

Question 2

Nudo 1997

Answer 2

• Squirrel monkey MC undergoes functional reorganization with rehab – similar to owl monkeys (sim brain to humans)
• Brain stim map out areas and look at which muscles respond
o Markers – elbow and shoulder area maps (laser burns particular area of brain for fine finger movement) – model of stroke
o Monkeys with no rehab = lesion area much smaller than burned (preserve as much of essential area as possible) – ate with other hand
o Monkeys with rehab = remove ability to use alternative hand by binding it, forces them to use damaged hand
♣ Big food dish to eat out of – when they get better, makes disc smaller so harder for them to eat and so on lesion area same, but maps = neurons of elbow and shoulder response now respond to fingers
♣ Maladaptive plasticity in no rehab, but positive in rehab (change in brain)

Question 3

Taub 2002

Answer 3

• Led to constraint-induced movement therapy (4-weeks post-treatment = change in functional score specific to stroke) – name disliked as people didn’t like limb being bound – drop out of trials
• Now try to promote use of damaged limb and limit others – many different names but based on sound neuro physiology
• Development of learned non-use
o CNS depressed and decrease motor activity
♣ Movement effortful less movement contraction of cortical rep zones
♣ Unsuccessful punishment (pain, failure, incoord) behavior suppression and masked ability
♣ Develop compensatory behavior patterns positive reinforcement less effective behavior strengthened
♣ All lead to learned non-use – normally non-permanent, reversal possible
o Overcoming learned non-use
♣ Any evidence-based therapy and learned non-use (masked recovery of limb use)
♣ Increased motivation affected limb use positive reinforcement further practice and reinforcement
♣ Use-dependent cortical reorganization further practice and reinforcement use-dependent cortical reorg learned non-use reversed; limb used in life situation permanently

Question 4

Sawaki 2008

Answer 4

• 30 stroke subjects in sub-acute phase 3-9 months, randomized into experimental (CIMT immediately after baseline) and control (CIMT post-4 months) – evaluated using TMS at baseline, 2-w post and 4m follow up
• Wolf Motor Function test – both groups improved hand motor function 2-weeks after baseline – experiment group = sig greater improvement in grip force post IV and follow up
• Adjusting for baseline – experimental had increase in TMS motor map compared with control over 4 months (borderline sig)
• Stroke patients (3-9 months) CIMT produced stat sig and clinically relevant improvements in arm motor function that persisted for at least 4 months – enlargement of TMS motor maps, similar to earlier studies of chronic stroke subjects, appears to play an important role in CIMT-dependent plasticity
• CIMT problem developed FES/FET
o Circumvent corticol involvement and attach electrodes to muscle themselves and help person by artificially stim hand opening and closing (used as neuro-prosthetic)
♣ Stroke – neuro-prosthetic – treatments in foot drop (stim TA) – timing right so they contract TA during swing phase so they don’t trip – works well but devices would break down
♣ Some people better when they first started – therapeutic effect?
♣ Rather than removing hand function, can replace it immediately (works best if vol activity combined with stim) – want it to augment existing vol drive)

Question 5

Popovic 2002

Answer 5

• FES therapy – highlighted it works, compared to 3-weeks conventional physio training (both increases some natural recovery – better and more with FES)
• If chronic patients – improve a little but not as much as early rehab patients (essential)
• Golden 3 weeks – seen in monkeys, vast corticol reorganization within weeks (may develop maladaptive plasticity)
• TFES application:
o In addition to usual therapy, stimulation applied only to affected limb, 30 mins daily for 3 weeks, sessions are supervised and assisted by physical therapist, patients are required to self-initiate each trial and to ex specific functional tasks
o Patterned stim is programmed to control flex/ex muscle groups to mimic normal movement synergies
• Positive effects – strengthened atrophied muscle, mod spasticity, improve patient motivation, enhance cortical plasticity

Question 6

Kwakkel 2008

Answer 6

• View effect size – effects of robot-assisted therapy on upper limb post-stroke favours treatment (but small effect size – increasing with newer studies)
• LokoMat = walking robot – made mainly for SCI units but now more in stroke
• Armeao – behind person and acts as exoskeleton, aids with arm movement
• HandCARE – fine finger movements
• Mention VR therapy (stroke rehab) and parabolic screens