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BIOPSYCHOLOGY 8e John P.J. Pinel Copyright © Pearson Education 2011 Causes of Brain Damage • Brain tumors • Cerebrovascular disorders • Closed-head injuries • Infections of the brain • Neurotoxins • Genetic factors Copyright © Pearson Education 2011 Brain Tumors! • A tumor (neoplasm) is a mass of cells that grows unrestrained and 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 • Most brain tumors are infiltrating (like tree roots) • About 10% of brain tumors are metastatic – the originate elsewhere, and are carried in bloodstream FIGURE 10.3 An MRI of Professor P.’s acoustic neuroma. The arrow indicates the tumor. Copyright © 2011 Pearson Education, Inc. All rights reserved. Cerebrovascular Disorders • Stroke – A sudden-onset cerebrovascular event that causes brain damage • Infarct – area of dead and dying tissue • Penumbra – dysfunctional area surrounding the infarct tissue – Cerebral hemorrhage (bleeding in the brain) – Cerebral ischemia (disruption of blood supply) • More next slide… 3rd leading cause of death in Canada too Copyright © Pearson Education 2011 Cerebral Hemorrhage! Cerebrovascular Disorders • Cerebral hemorrhage (bleeding in the brain) – Aneurysm – a weakened point in a blood vessel that makes a stroke more likely; may be congenital (present at birth) or due to poison or infection • Cerebral ischemia (disruption of blood supply) – Thrombosis – a plug forms in the brain and blocks blood flow – Embolism – a plug forms elsewhere and is transported in blood to a smaller vessel – Arteriosclerosis – wall of blood vessels thicken, usually due to fat deposits Copyright © Pearson Education 2011 Damage Due to Cerebral Ischemia • Does not develop immediately • Most damage is a consequence of excess neurotransmitter release – especially glutamate (excitatory) • Blood-deprived neurons become overactive and release glutamate • Glutamate overactivates its receptors, especially NMDA receptors leading to an influx of Na+ and Ca2+ • lnflux of Na+ and Ca2+ triggers • the release of still more glutamate • a sequence of internal reactions that ultimately kill the neuron Copyright © Pearson Education 2011 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; hematoma (bruise) forms • Concussions – when there is disturbance of consciousness following a blow to the head but with no detectable evidence of structural damage Copyright © Pearson Education 2011 Infections of the Brain! • Encephalitis – the resulting inflammation of the brain by an invasion of microorganisms • Bacterial infections • Often lead to abscesses, pockets of pus • May inflame meninges, creating meningitis • Treat with penicillin and other antibiotics • Viral infections • Some preferentially attack neural tissues (e.g. rabies) • Others have no special affinity for neural tissue (e.g. herpes) • Some can lie dormant for years n eurotoxins" • May enter general circulation from the GI tract or lungs, or through the skin • Toxic psychosis – chronic psychosis (insanity?) produced by a neurotoxin • The Mad Hatter – hat makers often had toxic psychosis due to mercury exposure during felt preparation • http://www.youtube.com/watch?v=26RTlPgg-tA • Older antipsychotic drugs produce a motor disorder called tardive dyskinesia Copyright © • http://www.youtube.com/watch?v=t_NKRS8lLWA Pearson Education 2011 Genetic Factors • Most neuropsychological diseases of genetic origin are associated with recessive genes--why? • Dominant genes that disturb neuropsychological function tend to be eliminated from the gene pool • Down syndrome: • 0.15% of births, probability increases with advancing maternal age – Far more common in pregnant women under the age of 35 –why? • Extra chromosome 21 created during ovulation • Characteristic facial features, cognitive impairments, other health problems (premature aging, increased risk of Alzheimer’s) Copyright © Pearson Education 2011 Programmed Cell Death • All six causes of brain damage produce damage, in part, by activating apoptosis • Programmed cell death • Neat and organized • Essential to early development Copyright © Pearson Education 2011 Neuropsychological Diseases • Epilepsy • Parkinson’s disease • Huntington’s disease • Multiple sclerosis • Alzheimer’s disease Copyright © Pearson Education 2011 Epilepsy • Primary symptom is seizures, but not all who have seizures have epilepsy • Epileptics have seizures generated by their own brain dysfunction (not secondary to some other problem such as high temperature or viral infection) • Difficult to diagnose due to the diversity/complexity of seizures Copyright © Pearson Education 2011 Epilepsy • Types of seizures • Convulsions – motor seizures, tonus and clonus, loss of balance and/or consciousness • Some are merely subtle changes of thought, mood, or behaviour • Causes • Brain damage • Genes – over 70 known so far • Faults at inhibitory synapses (e.g. GABA) • Diagnosis • EEG – electroencephalogram • Seizures associated with high amplitude spikes Copyright © Pearson Education 2011 FIGURE 10.8 Cortical electroencephalogram (EEG) record from various locations on the scalp during the beginning of a complex partial seizure. Copyright © Pearson Education 2011 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 – involves the entire brain Copyright © Pearson Education 2011 Parkinson’s Disease • Movement disorder of middle and old age affecting 1-2% of the population • 2.5 times more prevalent in men • Tremor at rest is the most common symptom of the fullblown disorder • Other symptoms: rigidity, difficulty initiating movement, slowness, masklike face • Dementia is not typically seen • No single cause Copyright © Pearson Education 2011 Parkinson’s Disease • Associated with degeneration of the substantia nigra; these neurons release dopamine to the striatum of the basal ganglia • Almost no dopamine in the substantia nigra of long-term Parkinson’s patients • Autopsies often reveal Lewy bodies (protein clumps) in the substantia nigra • Treated temporarily with L-dopa • Linked to about 10 different gene mutations • Deep brain stimulation of subthalamic nucleus reduces symptoms, but effectiveness slowly declines Copyright © Pearson Education 2011 Multiple Sclerosis • A progressive autoimmune disease that attacks CNS myelin, leaving areas of hard scar tissue (sclerosis) • Onset earlier in life • 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) • Seems to have both a genetic and environmental component (interaction effect) … Copyright © Pearson Education 2011 Multiple Sclerosis • Epidemiological studies find that incidence of MS is increased in those who spend childhood in a cool climate • MS is rare among Africans and Asians • Rates are three times higher in women • Smokers higher risk • Higher concordance rate in monozygotes (25%), than dizygotes (5%) Copyright © Pearson Education 2011 Alzheimer’s Disease • Most common cause of dementia – likelihood of developing it increases with advancing old age • Progressive, with early stages characterized by confusion and a selective decline in memory • Definitive diagnosis only at autopsy – must observe neurofibrillary tangles (tangles of protein in neural cytoplasm) and amyloid plaques (clumps of scar tissue comprising a amyloid protein and degenerating neurons) Copyright © Pearson Education 2011 Alzheimer’s Disease • Amyloid plaques are found diffusely in the extracellular neural environment. Neurofibrillary tangles (NFT) on the other hand, form inside neurons. Copyright © Pearson Education 2011 Animal Models of Human Neuropsychological Diseases • Experiments regarding neuropathology are not usually possible with human subjects • Therefore, essential for understanding, predicting and treating disordered/diseased brain states • Animal research is usually a first and critical step prior to human clinical trials • 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 Copyright © Pearson Education 2011 Neuroplastic Responses to Nervous System Damage • The Brain is Plastic (changeable) • Neuroplasticity is the dynamic process of changes occurring in the brain in response to genes and experience (Including damage) • Degeneration – deterioration • Regeneration – regrowth of damaged neurons • Reorganization • Recovery Copyright © Pearson Education 2011 Neural Degeneration • Cutting axons (axotomy) is a common way to study responses to neuronal damage • Anterograde: degeneration of the distal segment – between the cut and synaptic terminals • Retrograde: degeneration of the proximal segment – between the cut and cell body Copyright © Pearson Education 2011 Neural Regeneration • Not great in mammals and other higher vertebrates (inverts are more successful at it) • Capacity for accurate axonal growth during early development is lost at maturity • Regeneration is virtually nonexistent in the CNS of adult mammals and hit-and-miss in the PNS • Mammalian PNS regeneration begins 2-3 days after axonal damage - 3 outcomes possible… Copyright © Pearson Education 2011 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 (this is why limbs with nerve damage have variable prognoses for recovery of function) • If ends are widely separated, no meaningful regeneration will occur Copyright © Pearson Education 2011 Neural Regeneration • Why no regeneration in the mammalian CNS? • Brain and vertebrae offer good protection • Schwann cells have abilities oligodendroglia do not: • Schwann cells clear neural debris resulting from neural degeneration and promote/guide regeneration • Produce both neurotrophic factors and celladhesion molecules • Oligodendroglia live longer after nerve damage and inhibit axonal regeneration Copyright © Pearson Education 2011 Neural Reorganization • The adult mammalian brain can however, reorganize itself in response to experience – Reorganization of primary sensory and motor systems has been observed in laboratory animals following – Damage to peripheral nerves – Damage to primary cortical areas Copyright © Pearson Education 2011 Cortical Reorganization Following Damage in Humans Brain-imaging studies indicate there is continuous competition for cortical space by functional circuits • e.g. Auditory and somatosensory input may be processed in formerly visual areas in blinded individuals Copyright © Pearson Education 2011 Mechanisms of Neural Reorganization • What accounts neural reorganization? Thefor human brain • 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 Copyright © Pearson Education 2011 Mechanisms of Neural Reorganization The human brain Copyright © Pearson Education 2011 Recovery of Function after Brain Damage • Difficult to conduct controlled experiments on populations of braindamaged patients because: • Can’t distinguish between true recovery and compensatory changes • Eg decline in swelling or new strategies • Cognitive reserve – education and intelligence – thought to play an important role in recovery of function – may permit cognitive tasks to be accomplished in new ways Copyright © Pearson Education 2011 Neuroplasticity and the Treatment of Nervous System Damage • Reducing brain damage by blocking neurodegeneration • Promoting recovery by promoting regeneration • Promoting recovery by transplantation • Promoting recovery by rehabilitative training Copyright © Pearson Education 2011 Reducing Brain Damage by Blocking Neurodegeneration • Various neurochemicals can block or limit neurodegeneration Apoptosis inhibitor protein Nerve growth factor Estrogens • Neuroprotective molecules tend to also promote regeneration Copyright © Pearson Education 2011 Promoting CNS Recovery by Promoting Regeneration • While regeneration does not normally occur in CNS, experimentally it can be induced, directing growth of axons by: • Transplanted Schwann cells • Transplanted olfactory ensheathing cells • Caution: two studies here and recovery is only partial Copyright © Pearson Education 2011 Promoting Recovery by Neurotransplantation • Transplanting fetal tissue • Fetal substantia nigra cells used to treat MPTP-treated monkeys (PD model) • Treatment was successful • Limited success with humans • Transplanting stem cells • e.g. Embryonic stems cells implanted into damaged rat spinal cord improved mobility • Again, not perfect recovery Copyright © Pearson Education 2011 Promoting Recovery by Rehabilitative Training • Monkeys recovered hand function from induced strokes following rehab training • Constraint-induced therapy in stroke patients – tie down functioning limb while training the impaired one – performance of affected arm improved + increased motor cortex for area controlling that arm • Facilitated walking as an approach to treating spinal injury • Cognitive and physical exercise • Active individuals are less likely to contract neurological disorders (correlational finding) • If they do, symptoms are less severe and recovery is better • Enriched environments and regular physical activity work for animals with neurological trauma Copyright © Pearson Education 2011