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Copyright © 2007 by Allyn and Bacon
Chapter 8Brain Damage and NeuroplasticityCan the Brain Recover from Damage?
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Copyright © 2007 by Allyn and Bacon
Causes of Brain Damage
Brain tumors Cerebrovascular disorders Closed-head injuries Infections of the brain Neurotoxins Genetic factors
Copyright © 2007 by Allyn and Bacon
Brain Tumors
A tumor (neoplasm) is a mass of cells that grows independently of the rest of the body – a cancer
~20% of brain tumors are meningiomas – encased in meningesEncapsulated, growing within their own
membranesUsually benign, surgically removable
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Meningiomas Common in middle-age to elderly
adults; more women than men Symptoms differ depending on the
site”Frontal LobeLeft SideTemporal LobeParietal Lobe
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Brain Tumors Most brain tumors are infiltrating
Grow diffusely through surrounding tissue
Malignant, difficult to remove or destroy About 10% of brain tumors are
metastatic – they originate elsewhere, usually the lungs
Metastasis: transmission of disease from one organ to another
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Cerebrovascular Disorders-
Stroke – a sudden-onset cerebrovascular event that causes brain damageCerebral hemorrhage – bleeding in the brainCerebral ischemia – disruption of blood
supply Damage depends on the INFARCT 3rd leading cause of death in the US and
most common cause of adult disability
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Strokes
Two Types of Risk Factors:No control:
Age; Gender; Race; Family History; Prior History
Can ControlDiet; obesity; high blood pressure; heart disease; smoking;
high cholesterol; excess alcohol intake; diabetes
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Transient Ischemic Attack (TIA)
Short-term reduction in blood flow to the brain
Symptoms: weakness or tingling in an arm or leg
Usually few minutes Don’t cause brain damage but
warning sign
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Origin and Damage of a Stroke
Right Hemisphere Left Hemisphere: Aphasia Cerebellum Brain Stem
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Cerebrovascular Disorders Cerebral hemorrhage (20%) – blood vessel ruptures
Aneurysm – weakened point in a blood vessel that makes a stroke more likely. Congenital or due to poison or infection.
Congenital – present at birth Cerebral ischemia (80%) – disruption of blood supply
Most common Thrombosis – plug forms Embolism – plug forms elsewhere and moves to the
brain Arteriosclerosis – wall of blood vessels thicken,
usually due to fat deposits
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Damage due to Cerebral Ischemia
Does not develop immediately Most damage is a consequence of excess
neurotransmitter release – especially glutamate Blood-deprived neurons become overactive and
release glutamate Glutamate overactivates its receptors, especially
NMDA receptors leading to an influx of sodium and calcium ions
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Damage due to Cerebral Ischemia
Influx of sodium and calcium triggers: the release of still more glutamatea sequence of internal reactions that
ultimately kill the neuron Ischemia-induced brain damage
takes timedoes not occur equally in all parts of the brainmechanisms of damage vary with the brain
structure affected
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Closed-Head Injuries
Brain injuries due to blows that do not penetrate the skull – the brain collides with the skull Contrecoup injuries – contusions are often on
the side of the brain opposite to the blow Contusions – closed-head injuries that
involve damage to the cerebral circulatory system. A hematoma, a bruise, forms.
Concussion – when there is a disturbance of consciousness following a blow to the head and no evidence of structural damage.
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Concussions
While there is no apparent brain damage with a single concussion, multiple concussions may result in a dementia referred to as “punch-drunk syndrome”
Boxers at risk
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Brain Infection
Invasion of the brain by microorganisms Encephalitis – the resulting inflammation Bacterial infections
Often leads to Cerebral Abscesses, pockets of pus May inflame meninges, creating meningitis Treat with penicillin and other antibiotics
Viral infections Some viral infections preferentially attack neural
tissues
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Brain Infections - Some Causes Bacterial Syphilis – may produce a
syndrome of insanity and dementia known as general paresis
Syphilis bacteria are passed to the noninfected and enter a dormant stage for many years.
Attack the brain approximately 20 years after initial exposure.
Lead to Dementia and insanity
Viral Rabies – high affinity for
the nervous system Symptoms Time between expo and Sx
Mumps and herpes – typically attack tissues other than the brain
Viruses may lie dormant for years
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Neurotoxins
May enter general circulation from the GI tract, lungs, or through the skin
Toxic psychosis – chronic insanity produced by a neurotoxin.
The Mad Hatter – may have had toxic psychosis due to mercury exposure
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Neurotoxins
Some antipsychotic drugs produce a motor disorder caused tardive dyskinesiaSymptoms
Recreational drugs, such as alcohol, may cause brain damage
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Genetic Factors
Most neuropsychological diseases of genetic origin are associated with recessive genes. Why?
Down syndrome 0.15% of births, probability increases with
advancing maternal age Extra chromosome 21 Characteristic disfigurement, mental
retardation, other health problems
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Programmed Cell Death
Apoptosis – cell suicide – involved in all forms of brain damage discussed thus far
Apoptosis is adaptive Ex. Rett’s Syndrome
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Neuropsychological Diseases
Epilepsy Parkinson’s disease Huntington’s disease Multiple sclerosis Alzheimer’s disease
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Epilepsy
Primary symptom is seizures, but not all who have seizures have epilepsy
Epileptics have seizures generated by their own brain dysfunction
Affects about 1% of the population Difficult to diagnose due to the diversity
and complexity of epileptic seizures
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Epilepsy
Types of seizures Convulsions – motor seizures Some are merely subtle changes of thought, mood, or
behavior Causes
Brain damage Genes – over 70 known so far
Diagnosis EEG – Electroencephalogram Seizures associated with high amplitude spikes
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Epilepsy
Seizures often preceded by an aura, such as a smell, hallucination, or feelingAura’s nature suggests the epileptic focusWarns epileptic of an impending seizureMay give a clue as to the location of the tumor
Partial epilepsy – does not involve the whole brain
Generalized epilepsy – involve the entire brain
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Partial Seizures
Simple symptoms are primarily sensory or motor or both
(Jacksonian seizures) symptoms spread as epileptic discharge spreads
Complex – often restricted to the temporal lobes (temporal lobe epilepsy) patient engages in compulsive and repetitive simple
behaviors – automatisms more complex behaviors seem normal ½ of seizures fall in this category
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Generalized Seizures Grand mal
Loss of consciousness and equilibriumTonic-clonic convulsions
-rigidity (tonus) and tremors (clonus)Resulting hypoxia (shortage of oxygen) may
cause brain damage Petit mal
not associated with convulsionsA disruption of consciousness associated with
a cessation of ongoing behaviorCommon in children and stops at puberty
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Parkinson’s Disease A movement disorder of middle and old
age affecting ~ .5%of the population 2.5 times more in males Pain and depression commonly seen
before the full disorder develops Tremor at rest is the most common
symptom of the full-blown disorder Dementia is not typically seen No single cause No familial history
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Parkinson’s Disease
Associated with degeneration of the substantia nigra whose neurons use dopamine
Almost no dopamine in the substantia nigra of Parkinson’s patients
Treated temporarily with L-dopa Linked to ~10 different gene mutations
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Huntington’s Disease
Also a progressive motor disorder of middle and old age – but rare, with a strong genetic basis, and associated with dementia.
Begins with fidgetiness and progresses to jerky movements of entire limbs and severe dementia
Death usually occurs within 15 years; no cure Caused by a single dominant gene 1st symptoms usually not seen until age 40
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Multiple Sclerosis
A progressive disease that attacks CNS myelin, leaving areas of hard scar tissue (sclerosis)
Nature and severity of deficits vary with the nature, size, and position of sclerotic lesions
Periods of remission are common Symptoms include visual disturbances, muscle
weakness, numbness, tremor, and loss of motor coordination (ataxia)
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Multiple Sclerosis Epidemiological studies find that incidence of
MS is increased in those who spend childhood in a cool climate
MS is rare amongst Africans and Asians Twice more common in females Strong genetic predisposition and many genes
involved An autoimmune disorder – immune system
attacks myelin Drugs may retard progression or block some
symptoms
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Alzheimer’s Disease
Most common cause of dementia – likelihood of developing it increases with age
Progressive, with early stages characterized by confusion and a selective decline in memory
Definitive diagnosis only at autopsy – must observe neurofibrillary tangles and amyloid plaques
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Familial Forms of Alzheimer’s Disease Several genes identified as involved in early
onset AD All affected genes are involved in synthesis of
amyloid or tau, a protein found in the tangles Not clear what comes 1st – amyloid plaques or
neurofibrillary tangles Declined acetylcholine levels is among one of
the earliest changes seen
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Neuropsychological Diseases - Recap Epilepsy – abnormal electrical activity Parkinson’s disease
progressive motor disorder without dementia Huntington’s disease
progressive motor disorder with dementia Multiple sclerosis
autoimmune disorder that affects motor function and strikes early
Alzheimer’s disease - dementia
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Neuroplastic Responses to Nervous System Damage
Degeneration - deterioration Regeneration – regrowth of damaged
neurons Reorganization Recovery
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Degeneration
Cutting axons is a common way to study responses to neuronal damage
Anterograde - degeneration of the distal segment – between the cut and synaptic terminal cut off from cell’s metabolic center swells and breaks off within a few days
Retrograde – degeneration of the proximal segment – between the cut and cell body progresses slowly if regenerating axon makes a new synaptic contact, the neuron
may survive
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Neural Regeneration
Does not proceed successfully in mammals and other higher vertebrates - capacity for accurate axonal growth is lost in maturity
Regeneration is virtually nonexistent in the CNS of adult mammals and unlikely, but possible, in the PNS
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Neural Regeneration in the PNS
If the original Schwann cell myelin sheath is intact, regenerating axons may grow through them to their original targets
If the nerve is severed and the ends are separated, they may grow into incorrect sheaths
If ends are widely separated, no meaningful regeneration will occur
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Neural regeneration
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Why do mammalian PNS neurons regenerate? CNS neurons can regenerate if
transplanted into the PNS, while PNS neurons won’t regenerate in the CNS
Schwann cells promote regenerationNeurotrophic factors stimulate growthCAMs provide a pathway
Oligodendroglia actively block regeneration
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Neural Reorganization
Reorganization of 1° sensory and motor systems has been observed following damage to: peripheral nerves primary cortical areas
Lesion one retina and remove the other – V1 neurons that originally responded to lesioned area now responded to an adjacent area – remapping occurred within minutes
Studies show scale of reorganization possible is far greater than anyone assumed possible
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Recovery of Function after Brain Damage Difficult to conduct controlled experiments on
populations of brain-damaged patients Can’t distinguish between true recovery and
compensatory changes Cognitive reserve – education and intelligence –
thought to play an important role in recovery of function – may permit cognitive tasks to be accomplished new ways
Adult neurogenesis may play a role in recovery
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Treating Nervous System Damage
Reducing brain damage by blocking neurodegeneration
Promoting recovery by promoting regeneration
Promoting recovery by transplantation
Promoting recovery by rehabilitative training
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Reducing brain damage by blocking neurodegeneration Various neurochemicals can block or limit
neurodegeneration Apoptosis inhibitor protein – introduced in rats
via a virus Nerve growth factor – blocks degeneration of
damaged neurons Estrogens – limit or delay neuron death Neuroprotective molecules tend to also promote
regeneration
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Promoting Recovery by Promoting Regeneration While regeneration does not normally
occur in the CNS, experimentally it can be induced
Eliminate inhibition of oligodendroglia and regeneration can occur
Provide Schwann cells to direct growth
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Promoting Recovery by Neurotransplantation Fetal tissue
Fetal substantia nigra cells used to treat MPTP-treated monkeys (PD model)
Treatment was successfulLimited success with humans
Stem cellsRats with spinal damage “cured”, but much
more research is needed
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Promoting Recovery by Rehabilitative Training
Constraint-induced therapy – down functioning limb while training the impaired one – create a competitive situation to foster recovery
Facilitated walking as an approach to treating spinal injury
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Can the brain recover from brain damage? Consider what you now know about the
brain’s ability to adapt following brain damage, can it “recover”?
If so, what conditions promote recovery?