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Neural plasticity and recovery of function

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Neural plasticity and recovery of function Lect. Thawatchai Lukseng, M.Sc (Physiology) School of Allied Health Sciences and Public Health – PowerPoint PPT presentation

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Title: Neural plasticity and recovery of function


1
Neural plasticity and recovery of
function
Lect. Thawatchai Lukseng, M.Sc (Physiology) School
of Allied Health Sciences and Public Health
2
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

3
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4
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

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6
Upper motor neuron
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9
Introduction
CNS injury
CNS changes
Functional recovery
  • Impair cerebral blood flow
  • Control of CSF
  • Control of cerebral metabolism

10
Introduction
  • Pathophysiology of ischemic injury
  • Autoregulation of BF
  • Increased oxygen extraction
  • Failure of aerobic metabolism (mild)
  • Disturbed Ca2 homeostasis (moderate)
  • Ca2 overload (severe)

11
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

12
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.

13
Divisions of Long-term Memory
14
Locating the Engram
  • Lashley believed that the engram was distributed
    across the cortex.
  • Karl Lashley observed the effects of lesions on
    rats maze learning.
  • The larger the amount of cortex damaged, the more
    errors the rats made.

15
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.

16
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

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18
The Anatomy of the Hippocampus in Humans
19
Producing Long-Term Potentiation in the Rat
20
Long-Term Potentiation
21
LTP and the NMDA Receptor
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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.

26
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.

27
Brain injury
  • Neuron and axon injuries
  • Degeneration of other neuron
  • Both above and beneath
  • CNS dysfunction

28
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
  • Depending on use and experience
  • Occur continuously throughout recovery
    (fast/slow)
  • Short-term functional plasticity (synaptic
    connection ability)
  • Structural plasticity (neural modifiability)

29
Brain recovery mechanisms
  • There are many theories that explain this events
  • von Monakows 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

30
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)

31
Regeneration following in Central Nervous System
Collateral Sprouting
32
Neuronal Degeneration in Necrosis Anterograde
Retrograde
Wallerian degeneration
33
Regeneration in the Peripheral Nervous System
(e.g., spinal cord injuries)
34
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

35
CNS
PNS
36
Brain recovery mechanisms (cont.)
  • Redundancy theory
  • Various area ? same function
  • Believe that violent status depending on normal
    neurons (not injured) gt 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

37
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

38
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

39
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

40
Motor homunculus
41
Prediction of functional recovery
  • Prognostic indicators
  • Level of consciousness (GCS)
  • Hematoma (lesion) size
  • Age (over 69-poor prognosis), younggtold
  • 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

42
Important factors to brain recovery
  • Age
  • depending on lesion
  • Quality of the lesion
  • Experience before ill
  • Training
  • Environment

43
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

44
The End
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