Topic 10 brain damage and neuroplasticity
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Topic 10 Brain Damage and Neuroplasticity. Can the Brain Recover from Damage?. Causes of Brain Damage. Brain tumors Cerebrovascular disorders Closed-head injuries Infections of the brain Neurotoxins Genetic factors. Brain Tumors.

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Topic 10 Brain Damage and Neuroplasticity

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Topic 10 Brain Damage and Neuroplasticity

Can the Brain Recover from Damage?


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 meninges

    • Encapsulated, growing within their own membranes

    • Usually benign, surgically removable


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


Cerebrovascular Disorders

  • Stroke – a sudden-onset cerebrovascular event that causes brain damage

    • Cerebral hemorrhage – bleeding in the brain

    • Cerebral ischemia – disruption of blood supply

  • 3rd leading cause of death in the US and most common cause of adult disability


Cerebrovascular Disorders

  • Cerebral hemorrhage – blood vessel ruptures

    • Aneurysm – a weakened point in a blood vessel that makes a stroke more likely. May be congenital or due to poison or infection.

    • Congenital – present at birth

  • Cerebral ischemia – disruption of blood supply

    • 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 Na+ and Ca++


Damage due to Cerebral Ischemia

  • lnflux of Na+ and Ca++ triggers:

    • the release of still more glutamate

    • a sequence of internal reactions that ultimately kill the neuron

  • Ischemia-induced brain damage

    • takes time

    • does not occur equally in all parts of the brain

    • mechanisms 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”

  • When might this occur?

  • Can it be prevented?


Brain Infection

  • Invasion of the brain by microorganisms

  • Encephalitis – the resulting inflammation

  • Bacterial infections

    • Often leads to 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.

  • Viral

  • Rabies – high affinity for the nervous system

  • 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 antipyschotic drugs produce a motor disorder caused tardive dyskinesia

  • Recreational drugs, such as alcohol, may cause brain damage

    • Neurotoxic effects of alcohol

    • Thiamine deficiency

  • Some neurotoxins are endogenous – produced by the body


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


Autistic Disorder

  • A chronic disorder whose symptoms include failure to develop normal social relations with other people, impaired development of communicative ability, lack of imaginative ability, and repetitive, stereotypical movements.


Possible causes

  • Biological

    • Autism was once believed to beacquired through interactions with hostile, withdrawn parents.

    • Research and mental health professionals are convinced autism is caused by biological factors.

    • Between 2 and 3 percent of siblings of people with autism are themselves autistic.

    • There is a 70 percent concordance rate for monozygotic twins.


Possible causes

  • Phenylketonuria (PKU)

    • A hereditary disorder caused by the absence of an enzyme that converts the amino acid phenylalanine to tyrosine; causes brain damage unless a special diet is implemented soon after birth.

  • Brain pathology

    • Heritable aspect of autism suggests the disorder is a result of structural or biochemical abnormalities in the brain.

    • Researchers have found evidence for structural abnormalities in the brains of autistics, but so far we cannot point to any single abnormality as the cause of the disorder.


Attention-Deficit/Hyperactivity Disorder

  • A disorder characterized by uninhibited responses, lack of sustained attention, and hyperactivity; first shows itself in childhood.

  • ADHD is the most common behavior disorder that shows itself in childhood.

  • ADHD is seen in 4 to 5% of grade school children.


Possible causes

  • Genetics

    • There is strong evidence from family and twin studies for hereditary factors in a person’s likelihood of developing ADHD.

  • Learning

    • Some evidence suggests impulsive and hyperactive behaviors are a result of a steep delay of reinforcement gradient.


Possible causes

  • Biological

    • There is evidence to suggest that abnormalities in dopaminergic transmission play a role in ADHD.

  • Brain structures

    • Studies of brain structure of people with ADHD do not reveal any localized abnormalities, though the total volume of their brains is approximately 4% smaller than normal.


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 feeling

    • Aura’s nature suggests the epileptic focus

    • Warns epileptic of an impending seizure

  • 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


Generalized Seizures

  • Grand mal

    • Loss of consciousness and equilibrium

    • Tonic-clonic convulsions

      • -rigidity (tonus) and tremors (clonus)

    • Resulting hypoxia may cause brain damage

  • Petit mal

    • not associated with convulsions

    • A disruption of consciousness associated with a cessation of ongoing behavior


Parkinson’s Disease

  • A movement disorder of middle and old age affecting ~ .5%of the population

  • 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


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 sever dementia

  • Death usually occurs within 15 years

  • 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

  • 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


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


Animal Models of Human Neuropsychological Diseases

  • While animal models only model some aspects of the human condition, they can provide insight

  • Kindling model of epilepsy

    • Experimentally induced seizure activity

  • Transgenic mouse model of Alzheimer’s

    • Mice producing human amyloid

  • MPTP model of Parkinson’s

    • Drug-induced damage comparable to that seen in PD


Kindling Model of Epilepsy

  • A series of periodic brain stimulations eventually elicits convulsions – the kindling phenomenon

    • Neural changes are permanent

    • Produced by stimulation distributed over time

  • Convulsions are similar to those seen in some forms of human epilepsy – but they only occur spontaneously if kindled for a very long time

  • Kindling phenomenon is comparable to the development of epilepsy (epileptogenesis) seen following a head injury


MPTP Model of Parkinson’s Disease

  • The Case of the Frozen Addicts

    • Synthetic heroin produced the symptoms of Parkinson’s

    • Contained MPTP

  • MPTP causes cell loss in the substantia nigra, like that seen in PD

  • Animal studies led to the finding that deprenyl can retard the progression of PD


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 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


How/why does damage lead to reorganization?

  • Strengthened existing connections due to a release from inhibition?

    • Consistent with speed and localized nature of reorganization

  • Establishment of new connections?

    • Magnitude can be too great to be explained by changes in existing connections


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 successful

    • Limited success with humans

  • Stem cells

    • Rats 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?


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