Physiotherapeutic theory of neurorehabilitation
for MS
Introduction MS
Disease mechanisms
Chronic, progressive disease
• Focal auto-inflammation of white matter (demyelination)
o Focal: on particular places in brain (eg. around vesicles)
o Damage can be partial or full
o Central nerves, no impact on peripheral nerves
• Widespread degeneration processes in primarily grey matter in brain
and spinal cord (atrophy)
o Generalized thinning of whole cortex
o Symptom of hippocampus: memory problems, visuospatial
disorder
o Symptom of thalamus: sensory problems
o In spinal cord: more diGicult neuroplasticity, because less
resources to make potentiation
MC Donald diagnostic criteria
Typical areas where inflammation may occur
à You cannot see multigeneral atrophy
A. Periventricular
B. Cortical
C. Optic nerve
D. Infratentorial
E. Spinal cord
,Motor function related CNS
Partial/complete demyelination of corticospinal tract
• Increase in the expenditure of energy
• Makes the neuron to be more fatigable
à Cortical signals have to be stronger to get signals down demyelinated nerve
Cortical thickness (motor cortex)
• Neural reserve: capacity of one’s brain to compensate for possible
deficits of a pathological CNS
• Thickness of cortex necessary to send stronger signals to compensate
• Cortex also degenerates in MS à less capacity to compensate
Central drive: the capacity of the central nervous system to initiate movement
When tipping point reached of compensation in cortex à motor function goes down
,Neural reserve
Cortical thickness
Described as the distance between the innermost and outmost edges of the cortex grey matter
Walking: from automatic to executive controlled
• PwMS presents higher cortical activity for walking than controls
• Frontal areas compensate for lack of motor areas
• Reduced ceiling to perform more complex/demanding tasks
• Amount of cortical activity in the PFC correlates with gait variability
Axonal capacity / connectivity capacity
Axonal neuroplasticity VS (delayed) axonal loss
• Sprouting to compensate for neuronal loss
• Functional rerouting not eGective anymore when too much loss of neurons à symptoms occur
• Longer tract (lower limb): more and earlier chance of problems
, Overview
Progression with relapses
• Acute symptoms: focal auto-inflammation on white matter
• Without or with little bit of remaining damage
o Oligodendrocyte cells partially resolve
for MS
Introduction MS
Disease mechanisms
Chronic, progressive disease
• Focal auto-inflammation of white matter (demyelination)
o Focal: on particular places in brain (eg. around vesicles)
o Damage can be partial or full
o Central nerves, no impact on peripheral nerves
• Widespread degeneration processes in primarily grey matter in brain
and spinal cord (atrophy)
o Generalized thinning of whole cortex
o Symptom of hippocampus: memory problems, visuospatial
disorder
o Symptom of thalamus: sensory problems
o In spinal cord: more diGicult neuroplasticity, because less
resources to make potentiation
MC Donald diagnostic criteria
Typical areas where inflammation may occur
à You cannot see multigeneral atrophy
A. Periventricular
B. Cortical
C. Optic nerve
D. Infratentorial
E. Spinal cord
,Motor function related CNS
Partial/complete demyelination of corticospinal tract
• Increase in the expenditure of energy
• Makes the neuron to be more fatigable
à Cortical signals have to be stronger to get signals down demyelinated nerve
Cortical thickness (motor cortex)
• Neural reserve: capacity of one’s brain to compensate for possible
deficits of a pathological CNS
• Thickness of cortex necessary to send stronger signals to compensate
• Cortex also degenerates in MS à less capacity to compensate
Central drive: the capacity of the central nervous system to initiate movement
When tipping point reached of compensation in cortex à motor function goes down
,Neural reserve
Cortical thickness
Described as the distance between the innermost and outmost edges of the cortex grey matter
Walking: from automatic to executive controlled
• PwMS presents higher cortical activity for walking than controls
• Frontal areas compensate for lack of motor areas
• Reduced ceiling to perform more complex/demanding tasks
• Amount of cortical activity in the PFC correlates with gait variability
Axonal capacity / connectivity capacity
Axonal neuroplasticity VS (delayed) axonal loss
• Sprouting to compensate for neuronal loss
• Functional rerouting not eGective anymore when too much loss of neurons à symptoms occur
• Longer tract (lower limb): more and earlier chance of problems
, Overview
Progression with relapses
• Acute symptoms: focal auto-inflammation on white matter
• Without or with little bit of remaining damage
o Oligodendrocyte cells partially resolve
