It provides a brief information about Neuroplasticity to enthusiast willing to know "How we gain daily skills?" and "Changing ability of our brain according to our daily habit."
For more details on study, you can follow the references...
It provides a brief information about Neuroplasticity to enthusiast willing to know "How we gain daily skills?" and "Changing ability of our brain according to our daily habit."
For more details on study, you can follow the references...
“The ability of neurons to change their function, chemical profile or structure is referred to as neuroplasticity.”
Neuroplasticity includes :
- Habituation
- Learning & memory
- Cellular recovery after injury
What is Neuroplasticity? What are neurons? Understand the Framework, Principles and types of Neuroplasticity. Learn about the mechanisms and processes of neuroplasticity. Understand the applications of neuroplasticity.
The ability of the neurons to change their function, chemical profile ( amount and types of neurotransmitters produced) or structure is referred to as neuroplasticity.
The plastic changes in neuron can occur
Physiologically according to activity and skill.
Pathologically due to injury or disease of CNS.
Sensory integration therapy is used to help children to learn to use all their senses together. That is touch,smell,taste,sight and hearing can improve difficulties/problems in children with special need.
Learn more in how the brain functions and how important physical therapy is for recovery.
The basis of neuro rehabilitation.
Brain has an incredible adaptation capacity and here you'll know just how to...explore it
“The ability of neurons to change their function, chemical profile or structure is referred to as neuroplasticity.”
Neuroplasticity includes :
- Habituation
- Learning & memory
- Cellular recovery after injury
What is Neuroplasticity? What are neurons? Understand the Framework, Principles and types of Neuroplasticity. Learn about the mechanisms and processes of neuroplasticity. Understand the applications of neuroplasticity.
The ability of the neurons to change their function, chemical profile ( amount and types of neurotransmitters produced) or structure is referred to as neuroplasticity.
The plastic changes in neuron can occur
Physiologically according to activity and skill.
Pathologically due to injury or disease of CNS.
Sensory integration therapy is used to help children to learn to use all their senses together. That is touch,smell,taste,sight and hearing can improve difficulties/problems in children with special need.
Learn more in how the brain functions and how important physical therapy is for recovery.
The basis of neuro rehabilitation.
Brain has an incredible adaptation capacity and here you'll know just how to...explore it
EFFECT OF MIRROR THERAPY ON UPPER EXTREMITY MOTOR FUNCTION IN STROKE PATIENTSismailabinji
EFFECT OF MIRROR THERAPY ON UPPER EXTREMITY MOTOR FUNCTION IN STROKE PATIENTS
Stroke is one of the main causes of disability around the globe. plegia (complete paralysis) or paresis (partial weakness ) are common following a stroke. According to the Journal of Physical Therapy Science, about 85 percent of stroke survivors will suffer from hemiplegia, and at least 69 percent will experience a loss of motor function in the upper limb.
Although these changes may not be permanent, some people regain partial or full limb function, the road to recovery can be long. But did you know that it is possible to trick the brain into believing what it sees? Mirror therapy is being used more and more in stroke rehabilitation to dupe the brain and restore limb function.
STROKE: is defined as the rapidly developed clinical signs of global or focal disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than of vascular origin. (WHO, 2017)
MOTOR FUNCTION motor function is the ability to learn or to demonstrate the skillful and efficient assumption, maintenance, modification, and control of voluntary postures and movement patterns.
In mirror therapy, a mirror is placed beside the unaffected limb, blocking the view of the affected limb. This creates the illusion that both limbs are functioning properly.
Mirror theory is based on evidence that action observation activates the same motor areas of the brain as action execution. Observed actions lead to the generation of intended actions, engaging motor planning and execution.
Mirror neurons are type of brain cell that respond equally when we perform an action and when we witness someone else perform the same action. They were first discovered in the early 1990s, when a team of Italian researchers found individual neurons in the brains of macaque monkeys that fired both when the monkeys grabbed an object and also when the monkeys watched another primate grab the same object.
Patient characteristics
Motor abilities
Vision
Trunk control
Non affected limb
Cognitive abilities (Wade DT et al., 2011)
Informing the patient
Possible Negative effect
Environment and required materials
Surrounding
Jewellery and other marks
Mirror
Pathophysiology of TBI is complex and consists of acute and delayed injury. In the acute phase, brain tissue destroyed upon impact includes neurons, glia, and endothelial cells, the latter of which makes up the blood-brain barrier. In the delayed phase, “toxins” released from damaged cells set off cascades in neighboring cells eventually leading to exacerbation of primary injury. As researches further explore pathophysiology and molecular mechanisms underlying this debilitating condition, numerous potential therapeutic strategies, especially those involving stem cells, are emerging to improve recovery and possibly reverse damage. In addition to elucidating the most recent advances in the understanding of TBI pathophysiology, this review explores two primary pathways currently under investigation and are thought to yield the most viable therapeutic approach for treatment of TBI: manipulation of endogenous neural cell response and administration of exogenous stem cell therapy.
این پاورپوینت خلاصه شده فصل شش یکی از کتابهای مربوط به علوم اعصاب است. این پاورپوینت در کارگاه تخصصی توانبخشی دیداری عصبی توسط دکتر علیزاده ارائه شده است.
Maintaining cognitive vitality remains challenging in our rapidly aging society. It has been well documented that as we age, even simple daily tasks become challenging as it increasingly draws cognitive resources from neural pathways outside of the primary Motor Cortex. The purpose of this statement is to explore the potential use of novel motor training as a countermeasure to alleviate cognitive declines in older adults.
This presentation is about geriatric Psychiatry awareness. it contains basic information about what is geriatric psychiatry, which are the main psychiatry disorder found in elderly and how to manage them?. it contains some detailed information about late life depression, delirium and dementia in geriatric population.
Traumatic Brain Injury to temporal lobe and cognitive rehabilitationRavi Soni
This presentation briefs you about temporal lobe basic anatomy, Structures, functions, Mechanisms of Temporal lobe Injury and Cognitive rehabilitation strategies for temporal lobe deficits
Alzheimer's disease: Clinical Assessment and ManagementRavi Soni
This PPT is a seminar on the Alzheimer's disease which was prepared for sensitizing post graduate psychiatry students on the day of World Alzheimer's Day.
Evidence based treatment approaches for prevention of dementiaRavi Soni
This presentation reviews all the available treatment which have been used for prevention of dementia. The evidences were taken from the Cochrane reviews and library.
Relationship of Metabolic syndrome and cognitive impairment has been discussed. Metabolic causes of Dementia and their reversibility has been discussed.
Late onset mania is a kind of Psychiatric illness in which Manic symptoms develops for the first time after the age of 60 years or the continuation of recurrent bipolar illness.
This PPT contains all the important guidelines that are needed to manage a patient of Dementia. It involves diagnosis, psychosocial treatment, non-pharmacological management and pharmacological management. This PPT is prepared from NICE, APA and SIGN guidelines.
This presentation describes various movement disorders and its management strategies with particular focus of management of parkinson's disease. It gives basic overview of the drugs also.
This ppt describes various movement disorders found commonly in elderly persons. It also describes hyper and hypokinetic disorder categorization with cause and pathophysiology of movement disorders.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ocular injury ppt Upendra pal optometrist upums saifai etawah
Brain plasticity after Traumatic brain Injury
1. Brain Plasticity after TBI
DR RAVI SONI
DM GERIATRIC PSYCHIATRY
ASSISTANT PROFESSOR
HOSPITAL FOR MENTAL HEALTH
AHMEDABAD
2. What is Brain Plasticity?
Answer: Brain reacts and adapts in response to
challenge.
Brain Plasticity the capability of the brain to alter its
functional organization as a result of experience.
3. Brain Plasticity
Plasticity in physics : propensity of a material to undergo
permanent deformation under load.
Entire brain structure can change to better cope with the
environment.
Specifically when an area of the brain is damaged and
nonfunctional another area may take over some of the
function
4. Plasticity includes the brain's capacity to be
shaped or molded by experience, the capacity to
learn and remember, and the ability to
reorganize and recover after injury.
5. Plasticity: Brain’s ability to change: two
processes
Neurogenesis: new neurons migrate to different
areas
Synaptogenesis: development of connections with
neurons This means that the brain is actually
physically changing in response to information we
receive! “ creation of synapses”
6. Four types of Plasticity
Adaptive plasticity that enhances skill development or recovery
from brain injury
Impaired plasticity associated with cognitive impairment; as in
fragile X syndrome
Excessive plasticity leading to maladaptive brain circuits as in focal
dystonia
Plasticity that becomes the brain's `Achilles' Heel‘ because makes it
vulnerable to injury.
7. How does the brain change?
The brain can change in many ways such as:
A change in the internal structure of the neurons,
particularly at the area of synapses.
An increase in the number of synapses between
neurons.
8. Neuroplasticity occurs in the brain under two
primary conditions:
1. During normal brain development when the immature brain first
begins to process sensory information through adulthood
(developmental plasticity and plasticity of learning and memory).
2. As an adaptive mechanism to compensate for lost function and to
maximize remaining functions in damaged brain.
9. One rule that is more important in Brain
plasticity: Hebb Rule
1. Neurons that fire together wire together!
2. When cells are active together synapses are
strengthened and preserved.
3. The neurons & synapses that are activated
repeatedly are preserved while those who aren’t,
are pruned.
10. Few facts about TBI
The annual
incidence
rate of TBI
579 people
per 100,000.
Number of persons affected per 100,000 (CDC)
11. Brain Injury Cascade
Traumatic Brain Injury
Primary insult-Injury Secondary Insult-Injury
Two
Phases
Etiology: Direct Mechanical Damage Following mechanical damage, etiology being a
cascade of pathophysiological processes.
12. ‘CURE’ for primary Insult is
Prevention
Intervention at Second Phase
process can result into
improvement in outcome post
Injury
Depending on the mechanism
of Injury, the process can
differ
Injury Cascade
13. Phase One:
Injuries typically include direct tissue damage, impaired cerebral blood flow, and
impaired metabolic activity, leading to edema formation and cyto-architecture
changes like membrane permeability.
Contact Forces: contusion, hemorrhage and lacerations throughout
Inertial forces: shearing and/or compression of brain tissue
These forces cause multifocal injuries (usually termed diffuse axonal injury)
affecting axons, blood vessels, junctions between white and gray matter, and
other select focal areas like the corpus callosum and junctions between the
frontal and parietal lobes.
14. Phase Two: Initial Injury
Disruption of Neurons (Neuronal
Depolarization)
Release of Excitatory
Neurotransmitters (Ca++ and Na+)
lead to intracellular breakdowns
Release of Caspases and Calpains
Cell Death
Release of
Caspases initiates
the process of
APOPTOSIS
(Programmed cell
death)
Release of Calpains quickly
leads to necrosis where cells
die as a response to
mechanical or hypoxic damage
and metabolic failure. This
leads to an inflammatory
response with the cells being
removed.
15. Neuroplasticity and Brain function after TBI
Easiest way to conceptualize neuroplasticity after injury to
the brain is to view it simply as re-learning
“the brain will rely on the same fundamental
neurobiological process it used to acquire those behaviors
initially. The basic rules governing how neural circuits adapt
to encode new behaviors do not change after injury” (Kleim
2011)
16. Neuroplasticity and Brain function after TBI
We can view re-establishing function as a re-learning process but
there are two conceptual differences when it occurs after a brain
injury.
First, because neural circuits for a particular function were
previously established during the brain’s neurodevelopmental
process, it may be possible to take advantage of those learned
behaviors if they persist in residual areas of the brain during the
rehabilitation (Kleim, 2011).
This presents as a potentially adaptive circumstance.
17. Neuroplasticity and Brain function after TBI
Second, a more maladaptive consequence which occurs post injury
relates to the concept of learned non-use.
Just as increasing dexterity of motor function leads to increased
motor cortex representation of neural circuitry (and therefore
improved function), non-use can lead to decreased motor cortex
representation, and therefore decreased function (Plowman and
Kleim, 2010).
Research indicates that learned non-use of a paretic limb,
combined with an increased reliance on the unaffected limb can
result in major brain reorganization.
18. Mechanism of Recovery
After injury to the brain, there are two mechanisms whereby functional
improvement may occur.
These are recovery and compensation
Recovery relates to:
1. Restoration of neural tissue initially perturbed after the injury (neural level)
2. Restoration of movement exactly as it was performed prior (behavioral level)
3. Restoration of activity exactly as it was performed prior (activity level)
Recovery therefore relates to lost functions being restored
19. Mechanism of Recovery
Compensation refers to:
1. Recruitment of new neural circuits (neural level)
2. Training of new movement sequences (behavioral level)
3. Training of activity in a new way after injury (activity level)
Compensation relates to the acquisition of new functions or
behaviors to replace those lost after injury
20. Neurological Plasticity Changes during recovery
Two-stage model of recovery with corresponding neurological strategies and recovery vs. compensation distinctions.
21. STAGE ONE: Spontaneous Recovery
Spontaneous recovery: there is resolution of injury and functional
change in close time proximity after injury which plateaus within
three months for focal injury and six months for diffuse injury.
Three processes have been theorized to explain this early recovery
1. Diaschisis reversal
2. Changes in kinematics.
3. Cortical reorganization.
22. Diaschisis Reversal
Diaschisis is a disturbance or loss of function in one part of the brain
due to a localized injury in another part of the brain, and these areas
can be of considerable distance from the lesion area including the
opposite hemisphere (Stein, 2012).
Reversal of Diaschisis: due to resolution of the inflammatory
process, blood flow changes, metabolic changes, edema, and
neuronal excitability
The result of diaschisis reversal is improved function due to intact
brain areas that were previously disrupted now being restored.
23. Changes in Kinematics
The second aspect of early recovery relates to changes in kinematic
(movement) patterns where compensatory patterns are utilized.
The individual begins to complete motor movements in a different
manner, resulting in improved function, sometimes in drastically
different ways than prior to injury.
While these new movements likely contribute to functional
improvement, these compensatory strategies have the potential to
be maladaptive.
24. Cortical Reorganization
The third strategy identified as spontaneous recovery is that the nervous
system undergoes within-area and between-area reorganization or
rewiring.
Cortical reorganization during spontaneous recovery is thought to be
compensatory as different circuits or networks of neurons are utilized post
injury than those utilized pre injury.
While spontaneous recovery occurs in the absence of rehabilitation, there
is certainly the opportunity for overlap of training induced recovery while
spontaneous recovery takes its course.
25. STAGE TWO: Training-induced recovery
Recovery in this stage involves compensation, in that either new
brain areas or neural networks are enlisted to complete previous
functions.
Through the process of training, neuroplasticity is induced.
Adaptive changes after injury are the outcome of new patterns of
activation which include plasticity in areas surrounding the damaged
cortex, reorganization of existing networks or recruitment of new
cortical areas or networks.
26. STAGE TWO: Training-induced recovery
1. Recruitment:
During training-induced recovery, areas which did not make a
significant contribution to that particular function pre-injury now
contribute to function post-injury.
Due to recruitment of neural areas from the undamaged
hemisphere.
Ultimate result is change in motor maps or cognitive functions in the
non-injured hemisphere, allows to take over the motor/cognitive
function of damaged Hemisphere.
27. STAGE TWO: Training-induced recovery
2. Retraining:
Retraining involves the training of residual brain areas, resulting in
reorganization within the cortex and compensation for lost function
(Kleim, 2007).
This often comes in the forms of reorganization within the damaged
hemisphere.
Ultimately, recruitment and retraining involve rewiring or reorganization
of neural networks.
28. Neurobiological Changes after Acquired Brain Injury
After injury to the brain, the processes of neuroplasticity are thought
to be the underpinnings of Recovery.
1. Increases or changes to synapses:
This includes synaptogenesis and synaptic plasticity
Dendrite changes including increased arborization, dendritic growth
and spine growth
Axonal changes including axonal sprouting
29. Neurobiological Changes after Acquired Brain Injury
2. Increased neuron growth:
Neurogenesis in specific brain areas like the hippocampus
subgranular zone of the dentate gyrus and subventricular zone in
some areas, substantia nigra and perinfarcted areas.
3. Angiogenesis:
Angiogenesis is the process through which new blood vessels form
from pre-existing vessels.
30. Neurobiological Changes after Acquired Brain Injury
4. Excitability changes:
Excitability refers to the ability of a neuron to generate action
potentials, which is a short-term change in the electrical potential on
the surface of a cell.
It is an all or nothing proposition as it either fires or does not fire
depending on the strength of the potential.
31. Neurobiological Changes after Acquired Brain Injury
The first two items (increase or changes to synapses and increased
neuronal growth) on the list above relate to increases in either the
number of neurons (this occurs in a very limited sense) or the numbers of
synapses or increased strength of existing synapses (this far more
prevalent).
These changes seen post injury are similar to changes seen in the intact
brain in the form of experience dependent learning.
But instead of it being a learning process, it is a relearning process, aided
substantially by rehabilitation.
32. Neurobiological Changes after Acquired Brain Injury
Experience Dependent Learning leads to:
◦ New synapses formation (synaptogenesis)
◦ Strengthening of synapses through changes in dendrites (new dendritic
spine formation), axonal sprouting and long term potentiation (synaptic
plasticity)
Synaptogenesis and synaptic plasticity are the main underpinnings
of cortical reorganization, recruitment and retraining as identified
in Mechanisms of recovery.
33. Findings Related to Neurobiological Changes
Synaptic, Dendritic and Axonal Related Changes:
Loss of synapses with other neurons in affected areas of brain
Dendritic arbors increased in non-affected areas of brain
Axonal sprouting and reorganization occurs
This sprouting has adaptive consequences in that increased axonal growth leads to greater
levels of synapses allowing reinnervation
Restoration of motor/cognitive function through Synaptic Change
This includes synaptogenesis where new synapses form through dendritic growth and axonal
sprouting, and synaptic plasticity which strengthens existing synapses through the process of
long-term potentiation
34. Angiogenesis
Angiogenesis is the process through which new blood vessels form from pre-
existing vessels.
The benefit is return of blood flow to previously damaged areas, which is assists
in establishing metabolic support
An area around the infarct affected by vascular compromise is more than just
dying cells and it is called penumbra – it may be a precursor of neuroplasticity.
Vascular endothelial growth factor (VEGF) is an important factor in post-injury
recovery vascular remodeling which ultimately promotes synaptogenesis and
neurogenesis.
35. Activation and Excitatory Changes
After injury, changes in the excitability of the damaged and intact hemispheres can impact
cortical functioning.
Interhemispheric rivalry model: where there are distinct differences in the excitability of
analogous areas between hemispheres (e.g., motor areas). For example in the damaged
hemisphere there is hyperpolarization (inhibition of neurons) and in the intact hemisphere there
is depolarization (excitation of neurons)
Better recovery is found if activation of the affected-side is more predominant than the
unaffected hemisphere over time. This shift of activation to the unaffected side is “the sign of a
distressed system”
As a long term perspective, if the damaged side was more involved in function, that related to
better outcomes. However, if the patient had to rely on the unaffected side more for
function, that related to poorer outcomes.
36. The maladaptive side of neuroplasticity
Neuroplasticity has also its dark side:
Few examples include
oAddictions to alcohol, elicit substances or prescription drugs,
oPornography addictions,
oSeizure disorders post injury
oPhantom limb pain
oHand dystonia in musicians
oLearning and memory interference and
oChronic pain
37. References
Heidi Reyst, Neuroplasticity After Acquired Brain Injury. Rainbow Rehabilitation Centers.
YouRong Sophie Su, Anand Veeravagu, and Gerald Grant. Chapter 8-Neuroplasticity after
Traumatic Brain Injury. Translational Research in Traumatic Brain Injury.
Kleim JA, Jones TA. Principles of Experience-Dependent Neural Plasticity: Implications for
Rehabilitation After Brain Damage. Journal of Speech, Language, and Hearing Research,
February 2008, Vol. 51, S225-S239. doi:10.1044/1092-4388(2008/018)