copyright © 2007 by allyn and bacon chapter 8 brain damage and neuroplasticity can the brain...

Copyright © 2007 by Allyn and Bacon

Chapter 8Brain Damage and NeuroplasticityCan the Brain Recover from Damage?

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Causes of Brain Damage

Brain tumors Cerebrovascular disorders Closed-head injuries Infections of the brain Neurotoxins Genetic factors


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


Meningiomas Common in middle-age to elderly

adults; more women than men Symptoms differ depending on the

site”Frontal LobeLeft SideTemporal LobeParietal Lobe


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


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


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


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


Origin and Damage of a Stroke

Right Hemisphere Left Hemisphere: Aphasia Cerebellum Brain Stem


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


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


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


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.


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


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


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


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


Neurotoxins

Some antipsychotic drugs produce a motor disorder caused tardive dyskinesiaSymptoms

Recreational drugs, such as alcohol, may cause brain damage


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


Programmed Cell Death

Apoptosis – cell suicide – involved in all forms of brain damage discussed thus far

Apoptosis is adaptive Ex. Rett’s Syndrome


Neuropsychological Diseases

Epilepsy Parkinson’s disease Huntington’s disease Multiple sclerosis Alzheimer’s disease


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


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


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


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


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


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


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


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


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)


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


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


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


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


Neuroplastic Responses to Nervous System Damage

Degeneration - deterioration Regeneration – regrowth of damaged

neurons Reorganization Recovery


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


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


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


Neural regeneration


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


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


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


Treating Nervous System Damage

Reducing brain damage by blocking neurodegeneration

Promoting recovery by promoting regeneration

Promoting recovery by transplantation

Promoting recovery by rehabilitative training


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


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


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


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


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?

copyright © 2007 by allyn and bacon chapter 8 brain damage and neuroplasticity can the brain...

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