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Neural plasticity and recovery of function Lect. Thawatchai Lukseng, M.Sc (Physiology) School of Allied Health Sciences and Public Health Contents: • Introduction – Upper and lower motor neuron lesion – Pathophysiology of ischemic injury • Neuronal plasticity • Recovery of function – Recovery patterns for specific neurological impairments – Prediction of functional recovery 5/24/2017 2 5/24/2017 3 Upper motor neuron and lower motor neuron lesion (UMNL & LMNL) • Corticobulbospinal tract – Corticobulbar tract – Corticospinal tract • Anterior corticospinal tract (10-20%) Uncross • Lateral corticospinal tract (80-90%) Crossed at medulla oblongata 5/24/2017 4 5/24/2017 5 Upper motor neuron 5/24/2017 6 5/24/2017 7 5/24/2017 8 Introduction CNS injury CNS changes Functional recovery Impair cerebral blood flow • Control of CSF • Control of cerebral metabolism 5/24/2017 9 Introduction • Pathophysiology of ischemic injury – Autoregulation of BF – Increased oxygen extraction • Failure of aerobic metabolism (mild) • Disturbed Ca2+ homeostasis (moderate) • Ca2+ overload (severe) 5/24/2017 10 Neural plasticity • Neural (adj.) = involving a nerve or the system of nerves that includes the brain • Plastic (adj.) = soft enough to be changed into a new shape • Neuroplasticity, brain plasticity or brain malleability • The brain's ability to reorganize itself by forming new neural connections • Neurons (nerve cells) in the brain to compensate for injury and disease and to adjust their activities in response to new situations or to changes in their environment 5/24/2017 11 Memory • Memory refers to the storage and retrieval of information. • No absolute boundaries between learning and memory. • Learning and memory may be viewed as a being on a time continuum. 5/24/2017 12 Divisions of Long-term Memory 5/24/2017 13 Locating the Engram • Karl Lashley observed the • Lashley believed that the engram was distributed effects of lesions on rats’ across the cortex. maze learning. • The larger the amount of cortex damaged, the more errors the rats made. 5/24/2017 14 The Delayed Nonmatching to Sample Task • Monkeys with medial temporal lobe damage do poorly on the DNMS task. • The DNMS task requires the ability to form long-term memories. 5/24/2017 15 Long-Term Synaptic Enhancement • Long-Term Potentiation (LTP) ~ Rapid and sustained increase in synaptic efficacy following a brief but potent stimulus • Best studied in the hippocampus • Induction of LTP occurs at the postsynaptic site and requires the conjunction of pre and post-synaptic activity • On the order of hours, days or longer 5/24/2017 16 5/24/2017 17 The Anatomy of the Hippocampus in Humans 5/24/2017 18 Producing Long-Term Potentiation in the Rat 5/24/2017 19 Long-Term Potentiation 5/24/2017 20 LTP and the NMDA Receptor 5/24/2017 21 5/24/2017 22 5/24/2017 23 5/24/2017 24 LTP Shares Characteristics with Long-term Memory • Both LTP and long-term memories last indefinitely. • Both LTP and long-term memories result from very brief input. 5/24/2017 25 The Hippocampus and Human Memory • The right hippocampus is active during spatial memory processing and the left hippocampus is active during verbal memory processing. • Rostral portions of the hippocampus are more active during encoding, and caudal portions are active during retrieval. 5/24/2017 26 Brain injury • Neuron and axon injuries • Degeneration of other neuron – Both above and beneath • CNS dysfunction 5/24/2017 27 Brain recovery • 2 stages • Early (Spontaneous) recovery • 2-3 first days (or 3-4 first weeks) • Reduction of brain edema • Increasing of BF from nearly surroundings • Neural plasticity • • • • 5/24/2017 Depending on use and experience Occur continuously throughout recovery (fast/slow) Short-term functional plasticity (synaptic connection ability) Structural plasticity (neural modifiability) 28 Brain recovery mechanisms • There are many theories that explain this events – von Monakow’s diaschisis theory (1895-1913) • Diaschisis (from edema) – (Diaschisis (from Greek), meaning "shocked throughout") • Resolution of diaschisis – Recovery of synaptic effectiveness • Only emphasize in injured neuron • Depression of axon (from edema) • recovery 5/24/2017 29 Brain recovery mechanisms (cont.) – Denervation supersensitivity • Hypersensitivity of neurotransmitter (NT) of postsynaptic membrane – Recruitment of silent synapses – Neural sprouting • Regenerative synaptogenesis – Old axon (injured) into new axon • Reactive synaptogenesis (collateral sprouting) – Neighboring normal axon Old axon (injured) 5/24/2017 30 Regeneration following in Central Nervous System: Collateral Sprouting 5/24/2017 31 Neuronal Degeneration in Necrosis Anterograde & Retrograde Wallerian degeneration 5/24/2017 32 Regeneration in the Peripheral Nervous System (e.g., spinal cord injuries) 5/24/2017 33 Advantage of neural sprouting mechanisms • Increasing of effectiveness of synapse • Motor relearning • Compensation axonal regrowth • occurs in periphery in mammals • no regrowth in mammalian CNS 5/24/2017 34 CNS PNS 5/24/2017 35 Brain recovery mechanisms (cont.) – Redundancy theory • Various area same function • Believe that violent status depending on normal neurons (not injured) > lesion area – Vicarious function • Latent motor functions of neurons – Functional reorganization • Reorganization to control other movement – Behavioral strategy change • Subsituation • E.g. sensory neuron induce movement • Other movement supplemented the movement dysfunction 5/24/2017 36 Cellular response to learning and memory • How does learning change the structure and function of neuron in the brain? – CNS structural changes occur because of the interaction between both genetic and experiential factors – There appears to be use-dependent competitions among neurons for synaptic connections (transient and long term modification of synapses) – Memory • Required synthesis of new proteins and the growth of new synaptic connections 5/24/2017 37 Recovery of function • Recovery patterns for specific neurological impairments – Recovery of function is fastest during the early weeks and up to 3 months after stroke – Statistically significant recovery occurring for up to 6 months – Some patients continue to recover function between 6 months-1 year but not have statistical significance 5/24/2017 38 Recovery of function (cont.) • Motor recovery – Tend to plateau more quickly than functional recovery – Small motor changes seen after 8-12 weeks – Recovery of arm movement is usually less complete than leg movement – Full arm recovery, if it occurs, is usually complete by 8 weeks – At 3 months, 5% of all stroke have significant shoulder pain and 8% have decreased ROM 5/24/2017 39 Motor homunculus 5/24/2017 40 Prediction of functional recovery • Prognostic indicators – Level of consciousness (GCS) – Hematoma (lesion) size – Age (over 69-poor prognosis), young>old • Sex or side of stroke no relation • Final level of recovery measured 1-3 wks post onset best predictors • Waiting at least 7 days exclude transient deficits patients 5/24/2017 41 Important factors to brain recovery • Age – depending on lesion • • • • Quality of the lesion Experience before ill Training Environment 5/24/2017 42 Summary • Introduction – Upper and lower motor neuron lesion – Pathophysiology of ischemic injury • Neuronal plasticity • Recovery of function – Recovery patterns for specific neurological impairments – Prediction of functional recovery 5/24/2017 43 5/24/2017 44