RECOVERY OF FUNCTION

Dr. Ayesha Kousar PT

 Definition
 Recovery of motor performance is defined as the reacquisition of motor patterns thst were present before
the CNS injury.
 In complete recovery , performance of reacquired skills is identical in every way to preinjury
performance.
 Recovery can be further categorizd into two main types:
1-spontaneous recovery: the neuronal changes that results from the repair process occurring within the
cns after the insult, resulting in function being restored in neural tissue intiaaly lost.
2- Function –Induced recovery: the restoration of ability to perform the movement in the same or similar
manner as it was performed before the injury, occurring in response to changes in activity and environment
(e.g., increased use of involve body segments in behaviorally relevant tasks).
 compensation
 Immediately after a brain insult, a cascade of events occurs, producing transient depression of brain
activity.
 diachisis
 Edema
 Intracellular response to injury :
 Denervation supersensitivity
 unmasking of silent synapses
 Neural regeneration ( regenerative synaptogenesis)
 Collateral sprouting ( reactive synaptogenesis)
 Diaschisis

One of the first events following nervous system injury is diaschisis.

 Diaschisis is a transient CNS disorder involving loss of function in a structurally intact brain area because
of loss of input from an anatomically connected injured area of the brain.
 The sudden functional depression of brain regions distant from the primary site of injury can be due to a
reduction n blood flow and/or metabolism.
 It has been proposed that early recovery of function following stroke is due to the resolution of diaschisis.
 The site of the area that has been injured by an acute focal disturbance such as stroke or penetrating brain
injury, and the site of the diaschisis are connected to each other by neurons.
 The loss of the damaged structure disrupts the function of the remaining intact systems and causes a
physiological imbalance. These changes are most pronounced during the first few days following cerebral
infarction or injury.
 Edema
Cerebral edema commonly follows brain injury. Cerebral edema can be local (i.e., adjacent to the primary
injury site) or remote and produces a functional depression in brain tissue that is not part of the primary
injury.
 Intercellular Responses to Injury Intercellular response to injury reflects the formation and regeneration
of synapses (synaptogenesis).

Denervation Supersensitivity Denervation supersensitivity can occur when neurons show a loss of input
from another brain region. In this case, the postsynaptic membrane of a neuron becomes hyperactive to a
released transmitter substance.
 For example, PD causes a loss of dopamine producing neurons in the substantia nigra of the basal ganglia. In
response to this disease-induced denervation, the postsynaptic target neurons in the striatum become
hypersensitive to the dopamine that is released by the remaining substantia nigra neurons. This occurs
through the postsynaptic cells forming more receptors to capture more dopamine. It is interesting that this
denervation supersensitivity occurs only when at least 90% of the nerve fibers in the substantia nigra are
gone. Thus, it occurs only when a critical number of neurons have been destroyed
Unmasking of Silent Synapses
Recruitment of previously silent synapses also occurs during recovery of function. This suggests that structural
synapses are present in many areas of the brain that may not normally be functional because of competition within
neuronal pathways. However, experiential factors or lesions may lead to their being unmasked.

Cortical remapping following peripheral lesions

the neighboring maps expand their receptive fields to cover much of the denervated region. These
representations increased even further in the weeks following denervation (Since the extent of the
reorganization of the cortex was a few millimeters, it was assumed that it occurred because of the
increased responsiveness of existing, previously weak connections.
In humans, reorganization of the somatosensory and motor systems also occurs following amputation.
Researchers have found that stimulation of the face and upper body in patients who have had their upper
limbs amputated can elicit phantom-limb sensation, suggesting that after upper-limb amputation, the
somatosensory representation of the face and upper body expanded to occupy the arm and hand area The
extent of shift in cortical representation was correlated with the amount of phantom sensation (Chen et al.,
2002). This research demonstrates that alterations in cortical mapping occur following peripheral-nerve
lesions or amputation.
 Neurotransmitter release and receptor sensitivity are improved (synaptic
plasticity). Changes in synaptic strength, long-term potentiation (LTP), firm
up neuronal connections and serve as a basis for all memory and learning. It is
important to remember that these neuroplastic changes may be adaptive
(functional) or maladaptive (nonfunctional)
 Recovery of function and enviroment
 Thank-you