NeuroRehabilitation

Factors affecting recovery

psychological: motivation, active participation, awareness into disability eg. Wernicke patients are not aware

Cognitive: cognitive reserve, intelligence, education

Damage: type, extent, location, timing, age, comorbidities

Neurobiological: neural reserve eg. nr. of neurons (premorbid), plasticity, synaptic reorganization eg. Hebbian learning

Negative effects? If motor compensation comes too early ---> some functions that were intact before may become impaired

What is it?

intends to enable patients & their families to live with, manage, bypass, reduce, or come to terms with cognitive deficits

Training, Education, Environmental Adaptation but more specific: Cognitive Training

can apply to any intervention, strategy, technique

Course of recovery after brain damage

  1. Days-weeks: recovery of homeostasis, development of new blood vessels, reduction of diaschisis, spontaneous synaptic changes
  1. Weeks-years: synaptic changes by experience (Hebbian), progress of time, behavioral changes
  1. Hours: saving tissue in the penumbra by trombolysis & trombectomy

Demographics: age, education

Compensation & Substitution

Compensation: reorganization of behavior aimed at minimizing a particular disability, mostly spontaneous, without patient's explicit intention, can be enhanced by effort eg. hemiatopic patients

Substitution: accomplishment of a task by a new method (special form of compensation) e.g.. communication by lip reading in the deaf

Functional recovery

  1. Vicarious function: taking over of the functions of the injured part by distant back up areas with the same functional capacity
  1. Degeneracy: performance of the same function by multiple neuronal systems
  1. Reversal of diaschisis
  1. Redundancy: maintenance of function of a damaged system by parts that were not injured
  1. Spontaneous disappearance of acute effects of traumatic or ischemic lesions e.g. chemical modifications

damaged but surviving neurons can try to re-establish at least some functional connections (through axonal & dendritic sprouting, synaptogenesis)

neuroplasticity is a result of reinforcing or weakening of neuronal synaptic interconnections or of the formation of entirely new synaptic connections

there is no physiology without anatomy

Structural: spines & sprouts

dendritic spines: targets of inputs to a neuron

sprouts: can grow to establish new synaptic contacts

life-long fixed or dynamic, able to change shape & size --> modulators of efficacy of synaptic transmission

Enlargement of dendritic spines, enhanced neuronal activity --> LTP

Spine shrinkage, reduced spine motility, spine pruning --> LTD

Environment enrichment, physical & mental exercise: beneficial effects on spines in hippocampal neurons

Sensory deprivation & stress: adverse effects on learning & spine architecture

spine pathology in dementia & schizophrenia

enlargement of dendritic spines associated with LTP relies on the action of neurotrophins eg. BDNF (controls neuronal connectivity, modulates synaptic strength)

Dentate gyrus (component of hippocampal formation): the only region of human brain with evidence of adult neurogenesis --> flexible, replacing lost neurons, suitable environment for information acquisition, enhanced excitability & facilitated LTP expression in immature neurons

Young vs. Old Brain

Kennard principle not absolute

optimal when the current stage of development & maturation is most favorable to synaptogenesis & glial formation

Aged brain

decline of cognitive functions due to loss of synapses & neuronal connections

volumetric reduction of GM & WM ( cognitive decline correlates more with reduction of WM)

some neurons show normal or overdeveloped dendritic architectures --> maintained capacity for learning & memory

massive numerical decrease of cortical neurons & glia in Alzheimer's dementia & neurodegenerative diseases

difference in spatial & temporal patterns of cortical activations

more diffuse cortical activation in old --> compensatory response to maintain normal/near-normal performance

reduced coordination of brain activity in old --> poor cognitive performance

Attempts to promote Axonogenesis & Neurogenesis

molecular biology techniques

transplantation of neurons & cells, elongation of central axons

"Natural" transplantation: production & migration of progenitor cells towards the injured region

CIMT Contraint-Induced Therapy (learned nonuse)

use of the deafferented limb while the contralateral limb is mechanically restrained --> rearrangements of cortical maps

in aphasic patients eg. restraining gestures & nonvocal communication

the potential for functional recovery may be suppressed through compensation/substitution

Future: couple traditional interventions of rehabilitations (ie. behavioral, cognitive) with advanced neurological treatments eg. brain stimulation, transplantation of stem cells, gene therapies, BMIs

Upper limb recovery after stroke

natural logarithmic pattern of functional recovery can be modified by intensive task-oriented practice (preferably within 6 months poststroke)

Mechanisms that drive recovery after stroke (sometimes limited time-windows)

  1. Salvation of penumbral tissue
  1. Alleviation of diaschisis
  1. Homeostatic & Learning-dependent (Hebbian) Neuroplasticity
  1. Behavioral Compensation strategies

outcome at 3-6 months is highly predictable for upper & lower limb & ADL

skill reacquisition

at the activity level: motor compensation, different end effectors

at the function level: true neurological recovery = restitution of body functions, reappearance of the same end effectors (only possible by replacing lost neurons)

we need to assess the quality of motor performance to distinguish restitution & compensation (clinical outcome measures not suitable) --> Use Kinematic Analysis

we need a translational & multidisciplinary approach & measurements repeated over time