BRAIN DAMAGE AND

NEUROPLASTICITY
Ronald John Recio, M. A., RPsy, EMDRPrac., MBPsS
Pamantasan ng Lungsod ng Maynila
Puso mo.
 FOREWORD……
I hope that the midterms were good for you and that you have sufficiently understood the
basics of anatomy and physiology in relation to psychology. As promised, during the finals
period, we will be focusing more on explaining daily experiences using the interconnection of
psychology and physiology. Expect this period to be an application of what we have learned
previously and integrating them with your own experiences. Fun Fun Fun!
 DEFINITION OF TERMS
• Neoplasms = Abnormal and rapid tissue growth (Tumors)

• Plasticity = Capacity of the nervous system to change their structure and function throughout
life. Plasticity allows cellular regeneration, and form new synaptic connections.

• Recovery = Pag balik sa kwan

• Assisted Daily Living = May kwan pero kwan na.

 CAUSES OF BRAIN DAMAGE: TUMORS
• Tumors or Neoplasms are a mass of cells that grows independently of the rest of the body.

• Around 20% of tumors in the human brain are meningiomas (tumors that grow in between
meninges). All meningiomas are incapsulated tumors (tumors that grow within their own
membrane). Mostly, they are benign. Because of their location, they can influence the brain by
pressure.

• Gliomas = Tumors originating from glial cells. Infiltrating, rapidly growing, and are quite common.

• Most brain tumors are infiltrating. These grow diffusely through surrounding tissue and as a result,
are usually malignant. This means that they are difficult to destroy and any remnants continue to
grow.
 CAUSES OF BRAIN DAMAGE: TUMORS
• Metastatic Tumors: transmission of disease from one organ to another. It is estimated that
about 10% of brain tumors do not originate from the brain.

• Story Telling time

 CAUSES OF BRAIN DAMAGE: STROKES
• Stroke – sudden onset that causes brain damage. In the Philippines, Strokes are the second
leading cause of death. 70% of which is ischemic.

• Depending on the part of the brain affected, common consequences of stroke are amnesia,
aphasia, paralysis and coma.

• Dead tissue produced by stroke is termed as infarct. Surrounding the infarct is a

dysfunctional area called the penumbra.
 HEMORRHAGIC STROKE
• This occurs when a cerebral blood vessel ruptures and blood seeps into the surrounding neural tissue
and damages it. Aneurysms are a common example.

• Aneurysms are balloon like dilations that forms in the wall of an artery at a point where the elasticity
of the arterial wall is defective. This is caused by the weakening of the arterial wall. High Blood
Pressure, atherosclerosis (thickening of the arterial wall caused by plaque build-up), trauma,
heredity, and abnormal blood flow. Mycotic Aneurysms can happen as a result of infection to the
arterial wall.

*** Placques = fat, cholesterol, calcium, and other substances found in blood. All the good stuff ***
 ISCHEMIC STROKE
• Disruption in the blood supply to an area of the brain.

• Thrombosis, (fixed blood clot) Embolism (Traveling Blood Clot) , and Artherosclerosis are
leading causes.

• Damage by ischemic stroke takes up to a day or two to fully develop. Some neurotransmitters
are actually at fault. Much damage comes from the release of excitatory neurotransmitters
(Glutamate is a prime example).
 HOW DO NEUROTRANSMITTERS
NAGPAPALALA NG STROKE?
Once blood vessels become blocked, many blood deprived neurons become overactive and release
excessive quantities of glutamate. Glutamate = over activates glutamate receptors (NMDA Receptors).
Large Na+ and CA2+ ions enter the postsynaptic neurons.

Two ways how excessive NA+ and CA2+ damage = 1. Trigger release of excessive amounts of
glutamate thus becoming toxic and influencing other neurons; and
2. They trigger internal reactions that kill neurons.

Three properties of Ischemic Brain Damage: Takes a while (around 10mins before obvious), does not
occur equally in all parts of the brain (Hippocampus is susceptible, and they vary structure to structure
within the brain.
 CAUSES OF BRAIN DAMAGE:
CLOSED-HEAD INJURIES
• Contusions – damage to the cerebral circulatory system which produces internal hemorrhaging
(Hematoma = parang like pasa)

• Frequently, contusions occur at the opposite side of where the head was hit (Countercoup injury)

• Concussion – Disturbance of consciousness following a blow on the head and there is no evidence of a
contusion or other structural damage.

*** Concussions although are generally scarier when experienced, keribelles lung ***

• Punch-drunk syndrome – general intellectual deterioration (dementia) associated with repeated

concussions
 CAUSES OF BRAIN DAMAGE: INFECTIONS
• Encephalitis – Inflammation of parts of the brain as a result of infection.

• Types Types: Bacterial and Viral

• Bacterial Infections – They often lead to cerebral abscess = pockets of pus in the brain

• Meningitis = Inflammation of the Meninges. Usually has a mortality rate of 25% in adults

• Syphilis = General paresis – insanity and dementia commonly associated

 CAUSES OF BRAIN DAMAGE: INFECTIONS

• Viral Infections – Two types (again) = Those with a particular affinity with neural tissue and those that
attack neural tissue but have no greater affinity for it than for other tissue.

• Rabies has an affinity for nervous tissue

• Mumps and herpes viruses are examples that can attack the nervous system but usually attack other
parts of the body
CAUSES OF BRAIN DAMAGE: NEUROTOXINS
• Toxic psychosis – chronic psychosis as a result of repeated inhalation of lead and mercury

• Tardive dyskinesia – motor disabilities caused by the effect of certain anti psychotic drugs

• Some neurotoxins are endogenous or are produced by the patients own body. An example is
antibodies that can attack certain parts of the nervous system or glutamate
 COMMON NEUROTOXINS
Lead (paint), Ethanol (Alcohol Poisoning), Nitric Oxide (Viagra), Botox, Tetanus Toxin,
Tetrodotoxin (Puffer Fish)

Aspartame (Diet Soft Drinks; Articifial sweeter), Diacetyl (Alcohol, butter flavouring),
Mercury (Fish), MSG (Pagkain ng Chekwa), Aluminum (Foil used in reheating kwan)
CAUSES OF BRAIN DAMAGE: GENETIC FACTORS
• Most neuropsychological diseases of genetic origin are caused by abnormal recessive genes
that are passed from parent to offspring.

• Down Syndrome (Trisomy 21)

 CAUSES OF BRAIN DAMAGE:
PROGRAMMED CELL DEATH
• Apoptosis – Plays a role in eliminating extra neurons

• Sometimes, damage causes “cell suicide” but this is an evolutionary advantage for our cells
as when opposed to necrosis (dying), apoptosis results in no inflammation. Apoptosis starts
by shrinkage of the cell body and gradually letting the cell die while necrosis happens by the
axon first swelling until it explodes.
 NEUROPSYCHOLOGICAL DISEASE
• Epilepsy

• Parkinson’s Disease

• Huntington’s Disease

• Multiple Sclerosis

• Alzheimer’s Disease
 EPILEPSY
• Epilepsy – Only those who have repeated seizures are diagnosed with this as people could have
seizures and never be repeated (exposure to neurotoxins)

• Convulsions (Motor seizures) – Clonus (tremmors) and Tonus (rigidity) and loss of balance and
consciousness

*** However, some seizures involve subtle changes in behavior, thought, or mood that are not easily
distinguishable from normal day activity“***
 EPILEPSY
• Causes: viruses, neurotoxins, tumors and blows to the head as well as 70 identified genetic
mutations

• Faulty inhibitory synapses (GABAergic synapses) that cause neurons in that area to fire in
synchronous bursts

• Epileptic Auras – psychological changes before convulsions (bad smell, specific thought,
vague feeling of familiarity, hallucinations, or a tightness in the chest). They can tell us
where the location of the epileptic focus is and can warn the patient of an impending seizure.
 EPILEPSY
• Partial Seizures – Does not involve the entire brain. They are not usually accompanied by
total loss of consciousness or equilibrium.

• Simple Partial Seizures (Jacksonian seizures) – primarily sensory or motor or can be both;
symptoms spread systematically throughout the body

• Complex partial seizures - restricted to temporal lobes (temporal lobe epilepsy).

Compulsive, repetitive, simple behaviors referred to as automatisms, however, in more
complex behaviors they appear normal.
 EPILEPSY
• Generalized Seizures – Involve in entire brain. Some are gradual whilst others are almost immediate
simultaneous in the brain.

• Grand mal seizure – loss of consciousness, loss of equilibrium, and violent tonic-clonic convulsion,
tongue biting, urinary incontinence, cyanosis, are common manifestations. *** Hypoxia can
cause brain damage ***

• Petit Mal Seizure – Petit mal absence. Most common in children and they frequently cease in puberty.
Associated with day dreamers.
 PARKINSON’S DISEASE
• Movement disorder that affects 1 to 2% or the elderly population. It is also 2.5 times more prevalent in
males than females

• Tremors become more pronounced during inactivity but not during activity and sleep, muscular
rigidity (stupor), difficulty initiating movement, slowness of movement, and a masklike face. Pain and
depression often develop before motor symptoms become severe

• Widespread degeneration but it is particularly severe to the substantia nigra

 HUNTINGTON’S DISEASE
• Progressive motor disorder of middle and old age but is rare, has a genetic basis and associated with
severe dementia.

• Increased fidgetiness is the first sign. Rapid, complex, jerky movements begin to predominate as the
disease progresses. Eventually, motor and intellectual deterioration becomes more evident in that
sufferers become unable to feed themselves, control their bowels, or recognizing their own children.
There is no cure and life expectancy is 15 years since onset of initial symptoms.

• Cause is the dominant gene called huntingtin. Since it is dominant, all carriers will get the disorder.
 MULTIPLE SCLEROSIS
• Progressive disease that attacks the myelin of axons in the CNS. It typically attacks young adults.
First, microscopic areas of degeneration on myelin sheaths are observed; next, damage to the myelin
becomes so severe that associated axons become dysfunctional and degenerate. Scarring is developed
in the CNS as result.

• Its an autoimmune disorder.

• Common symptoms of advanced MS are visual disturbances, muscular weakness, numbness, tremors,
and ataxia (motor coordination), cognitive deficits and emotional changes occur in some patients.
STORY TIME!
 ALZHEIMER’S DISEASE
• Most common cause of dementia. Sometimes onset is at 40 but likelihood is greater with
advancement of age. The disease is progressive. Symptoms include confusion, irritability, anxiety,
and deterioration of speech. In advanced stages, deterioration to the point of simply swallowing and
controlling the bladder are difficult.

• Neurofibrillary tanglea and beta-amyloid placques have been seen consistent with post mortem
analysis of neural tissue. The prevalant parts of damage are seen in the entorhinal cortex, amygdala,
and the hippocampus.

• Alzheimer’s Disease has a great genetic component (50%).

 NEURAL DEGENERATION
• Neural Degeneration – Brain development and Disease

• Influenced by Glial Cells by either the activity of degenerating neurons or by the cause of degeneration.

• Two kinds: Anterograde (degeneration of the segment from lesion to synaptic terminals) and Retrograde
(segment from lesion back to the cell body)

• Anterograde degeneration = quickly after a lesion (DUH). Retrograde degeneration progresses

gradually (2 to 3 days before it become obvious)
 NEURAL REGENERATION
• - Regrowth of a damaged Neuron is not successful in vertebrates and higher mammals. We lose this
ability once we mature. In the CNS, virtually nonexistent whilst hit-or-miss for the PNS.

• In the PNS, regrowth from the proximal nerve stump usually begins in 2 to 3 days after axonal damage
(growth cones appear).

• What happens next depends on the nature of the injury: 1. If myelin is intact, growth happens within it at
a speed of a few millimeters a day; 2. If peripheral nerve is severed and the cut end is a few mm,
Regenerating axon tips often grow into incorrect sheaths and thus are guided into incorrect destinations;
Lastly, 3. If the stumps are too far, regeneration becomes meaningless as they just form a tangle of kwan.
 NEURAL REGENERATION
• CNS neurons are not capable to regenerate. Actually, PWIDI PIRO DIPINDI. Some can regenerate
as a result of transplantation. Sa PNS namern, we’re not exactly sure but something about the
environment promotes regeneration

• Schwann Cells clear cellular debris and scar tissue resulting from neural degeneration and promote
regeneration in the PNS by producing neurotrophic factors (biomolecules, mostly peptides and small
proteins that support growth, survival, and differentiates development and maturity of neurons) and
cell-adhesion molecules (CAMs).

*** Neurotriphic Factors = growth cones and new axons; CAMs = Pathway ***
 NEURAL REGENERATION
• Oligodendroglia – Do not clear debris or stimulate cellular regeneration in the CNS. Actually, kwan
to ih, kuntrabida kasi kwan ba; they actively block regeneration.

• Astrocytes form glial scars after injury that forms as a barrier to axonal regrowth and actively
releases chemicals that inhibit axonal regrowth. Ganun talaga ih.

• Collateral sprouting – When an axon degenerates, axon branches grow out from adjacent healthy
axons and synapse at the sites vacated by the degenerating axon. Pwede sa nodes of Ranvier or sa
axon terminals.
GLIAL SCAR EXAMPLE
 NEURAL REORGANIZATION
• Reorganization happens through life experiences. As a response to injury, neurons can also
reorganize themselves

• Ex. Blind people are more skilled at auditory and somatosensory ability than that of sighted
individuals. Cool no?

• Two mechanisms: 1. Strengthening of existing connections through inhibition, and 2. establishment

of new circuits as a result from collateral sprouting.
 SUPPORT FOR BOTH MECHANISMS
1. Reorganization often occurs too quickly to be explained by neural growth, and rapid
reorganization never involves change of more than 2 millimeters of cortical surface.

2. Magnitude of long-term reorganization can be too great to be explained by existing

connections.

*** Di lang itong dalawa ang kwan. Puede din kasi na yung mismong may dameyds mag iba
din ng kwan. Iksplin ko na lang ***
 RECOVERY OF FUNCTION AFTER
CNS DAMAGE
• Poorly understood because improvements are modest and virtually nonexistent.

• Other compensatory changes also interfere with understanding the CNS

• Cognitive Reserve (intelligence) = improvements observed after brain damage BUT it doesn’t
result from true recovery.

*** Para madali ma-gits, kwan, intelligence makes you do things in alternative ways. So ma
compensate mo brain damage in a different way despite na di maayos yung kwan. ***
 BOOM BULAGA!!!
STEM CELLS = No compelling evidence that they promote
cellular regeneration past a few months.
 NEUROPLASTICITY AND THE
TREATMENT OF CNS DAMAGE
• Neurotransplantation = ya esta en la moda!

• Treating stroke: Neurons seem to be in a competitive situation: they compete with other neurons for
synaptic sites and neurotrophins.

• Treating Spinal Injury: Sige lang ng sige sa pag balik ng function. Iksplain ko guyth.

• Cognitive and physically active people = less likely to contract neurological disorders; and if they do,
their symptoms tend to be less severe and their recovery better.