Chapter 10  Brain Damage and Neuroplasticity <ul><li>Can the Brain Recover from Damage? </li></ul>
Causes of Brain Damage <ul><li>Brain tumors </li></ul><ul><li>Cerebrovascular disorders </li></ul><ul><li>Closed-head inju...
Brain Tumors <ul><li>A tumor (neoplasm) is a mass of cells that grows independently of the rest of the body – a cancer </l...
Brain Tumors <ul><li>Most brain tumors are infiltrating </li></ul><ul><ul><li>Grow diffusely through surrounding tissue </...
Figure 10-1
Figure 10-2 Metastatic brain tumors
Figure 10-3 Professor P’s Acoustic Neuroma
Cerebrovascular Disorders <ul><li>Stroke – a sudden-onset cerebrovascular event that causes brain damage </li></ul><ul><ul...
Cerebrovascular Disorders <ul><li>Cerebral hemorrhage – blood vessel ruptures </li></ul><ul><ul><li>Aneurysm – a weakened ...
Figure 10-4 Angiogram  showing narrowing of the carotid artery--the main blood pathway to the brain
Damage due to Cerebral Ischemia <ul><li>Does not develop immediately  </li></ul><ul><li>Most damage is a consequence of ex...
Damage due to Cerebral Ischemia <ul><li>lnflux of Na +  and Ca ++  triggers: </li></ul><ul><ul><li>the release of still mo...
Figure 10-5
Closed-Head Injuries <ul><li>Brain injuries due to blows that do not penetrate the skull – the brain collides with the sku...
Figure 10-6
Concussions <ul><li>While there is no apparent brain damage with a single concussion, multiple concussions may result in a...
Case 10-2
Brain Infection <ul><li>Invasion of the brain by microorganisms </li></ul><ul><li>Encephalitis – the resulting inflammatio...
 
 
Bacteria versus Viruses <ul><li>http://cubanology.com/Articles/Virus_vs_Bacteria.htm </li></ul>
Brain Infections - Some Causes <ul><li>Bacterial </li></ul><ul><li>Syphilis – may produce a syndrome of insanity and demen...
Neurotoxins <ul><li>May enter general circulation from the GI tract, lungs, or through the skin </li></ul><ul><li>Toxic ps...
Neurotoxins <ul><li>Some antipyschotic drugs produce a motor disorder caused tardive dyskinesia </li></ul><ul><li>Recreati...
Genetic Factors <ul><li>Most neuropsychological diseases of genetic origin are associated with recessive genes. Why? </li>...
Figure 10-7
Neuropsychological Diseases <ul><li>Epilepsy </li></ul><ul><li>Parkinson’s disease </li></ul><ul><li>Huntington’s disease ...
Epilepsy <ul><li>Primary symptom is seizures, but not all who have seizures have epilepsy </li></ul><ul><li>Epileptics hav...
Epilepsy <ul><li>Types of seizures </li></ul><ul><ul><li>Convulsions – motor seizures </li></ul></ul><ul><ul><li>Some are ...
Figure 10-8
Epilepsy <ul><li>Seizures often preceded by an aura, such as a smell, hallucination, or feeling </li></ul><ul><ul><li>Aura...
Figure 10-9 The bursting of an epileptic neuron, recorded by extracellular unit recording.
Partial Seizures <ul><li>Simple </li></ul><ul><ul><li>symptoms are primarily sensory or motor or both (Jacksonian seizures...
Case 10-3
Generalized Seizures <ul><li>Grand mal </li></ul><ul><ul><li>Loss of consciousness and equilibrium </li></ul></ul><ul><ul>...
Figure 10-10
Parkinson’s Disease <ul><li>A movement disorder of middle and old age affecting ~ .5%of the population </li></ul><ul><li>P...
Parkinson’s Disease <ul><li>Associated with degeneration of the substantia nigra whose neurons use dopamine and project to...
Huntington’s Disease <ul><li>Also a progressive motor disorder of middle and old age – but rare, with a strong genetic bas...
Image 10-1
Multiple Sclerosis <ul><li>A progressive disease that attacks CNS myelin, leaving areas of hard scar tissue (sclerosis) </...
Figure 10-11
Multiple Sclerosis <ul><li>Epidemiological studies find that incidence of MS is increased in those who spend childhood in ...
Alzheimer’s Disease <ul><li>Most common cause of dementia – likelihood of developing it increases with age </li></ul><ul><...
Figure 10-12 Amyloid Plaques in an Alzheimer Patient’s Brain
Familial Forms of Alzheimer’s Disease <ul><li>Several genes identified as involved in early onset AD </li></ul><ul><li>All...
Figure 10-13
Neuropsychological Diseases - Recap <ul><li>Epilepsy – abnormal electrical activity </li></ul><ul><li>Parkinson’s disease ...
Animal Models of Human Neuropsychological Diseases <ul><li>While animal models only model some aspects of the human condit...
Kindling Model of Epilepsy <ul><li>A series of periodic brain stimulations eventually elicits convulsions – the kindling p...
Transgenic Mouse Model of AD <ul><li>Transgenic – genes of another species have been introduced </li></ul><ul><li>Only hum...
MPTP Model of Parkinson’s Disease <ul><li>The Case of the Frozen Addicts </li></ul><ul><ul><li>Synthetic heroin produced t...
Case 10-4
Figure 10-14
Neuroplastic Responses to Nervous System Damage <ul><li>Degeneration - deterioration </li></ul><ul><li>Regeneration – regr...
Degeneration <ul><li>Cutting axons is a common way to study responses to neuronal damage </li></ul><ul><li>Anterograde  - ...
Figure 10-15
Neural Regeneration <ul><li>Does not proceed successfully in mammals and other higher vertebrates - capacity for accurate ...
Neural Regeneration in the PNS <ul><li>If the original Schwann cell myelin sheath is intact, regenerating axons may grow t...
Figure 10-16 Neural Regeneration
Figure 10-17 Collateral Sprouting
Why do mammalian PNS neurons regenerate and CNS neurons do not? <ul><li>CNS neurons can regenerate if transplanted into th...
Neural Reorganization <ul><li>Reorganization of 1° sensory and motor systems has been observed following damage to: </li><...
Figure 10-18 Reorganization of the Rat Motor Cortex after Transection of Motor Neurons that Control the Vibrissae (whiskers)
Mechanisms of Neural Reorganization <ul><li>Existing connections strenghtened due to a release from inhibition? </li></ul>...
Figure 10-19
Recovery of Function after Brain Damage Poorly Understood <ul><li>Difficult to conduct controlled experiments on populatio...
Figure 10-20 17-20 21-25 26+ 17-21 22-25 26+ 17-19 20-25 26+
Figure 10-21
Treating Nervous System Damage <ul><li>Reducing brain damage by blocking neurodegeneration </li></ul><ul><li>Promoting rec...
Reducing brain damage by blocking neurodegeneration <ul><li>Various neurochemicals can block or limit neurodegeneration </...
Promoting Recovery by Promoting Regeneration <ul><li>While regeneration does not normally occur in the CNS, experimentally...
Promoting Recovery by Neurotransplantation <ul><li>Fetal tissue </li></ul><ul><ul><li>Fetal substantia nigra cells used to...
Case 10-5
Promoting Recovery by Rehabilitative Training <ul><li>Constraint-induced therapy – down functioning limb while training th...
Case 10-6.1
Case 10-6.2
Figure 10-22
Can the brain recover from brain damage? <ul><li>Consider what you now know about the brain’s ability to adapt following b...
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Chapter 10 Brain Damage

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  • Multiple metastatic brain tumors. The arrows indicate some of the more advanced areas of metastatic tumor development.
  • The bursting of an epileptic neuron, recorded by extracellular unit recording.
  • Areas of sclerosis in the white matter of a patient with MS
  • Amyloid Plaques in an Alzheimer Patient’s Brain
  • Reorganization of the rat motor cortex following transection of the motor neurons that control movements of the vibrissae. The motor cortex was mapped by brain stimulation before transection and then again a few weeks after.
  • Percentage of patients showing improvement following brain injury--within a week of the injury and after 20 years
  • Chapter 10 Brain Damage

    1. 1. Chapter 10 Brain Damage and Neuroplasticity <ul><li>Can the Brain Recover from Damage? </li></ul>
    2. 2. Causes of Brain Damage <ul><li>Brain tumors </li></ul><ul><li>Cerebrovascular disorders </li></ul><ul><li>Closed-head injuries </li></ul><ul><li>Infections of the brain </li></ul><ul><li>Neurotoxins </li></ul><ul><li>Genetic factors </li></ul>
    3. 3. Brain Tumors <ul><li>A tumor (neoplasm) is a mass of cells that grows independently of the rest of the body – a cancer </li></ul><ul><li>~20% of brain tumors are meningiomas – encased in meninges </li></ul><ul><ul><li>Encapsulated, growing within their own membranes </li></ul></ul><ul><ul><li>Usually benign, surgically removable </li></ul></ul>
    4. 4. Brain Tumors <ul><li>Most brain tumors are infiltrating </li></ul><ul><ul><li>Grow diffusely through surrounding tissue </li></ul></ul><ul><ul><li>Malignant, difficult to remove or destroy </li></ul></ul><ul><li>About 10% of brain tumors are metastatic – they originate elsewhere, usually the lungs </li></ul>
    5. 5. Figure 10-1
    6. 6. Figure 10-2 Metastatic brain tumors
    7. 7. Figure 10-3 Professor P’s Acoustic Neuroma
    8. 8. Cerebrovascular Disorders <ul><li>Stroke – a sudden-onset cerebrovascular event that causes brain damage </li></ul><ul><ul><li>Cerebral hemorrhage – bleeding in the brain </li></ul></ul><ul><ul><li>Cerebral ischemia – disruption of blood supply </li></ul></ul><ul><li>3 rd leading cause of death in the US and most common cause of adult disability </li></ul>
    9. 9. Cerebrovascular Disorders <ul><li>Cerebral hemorrhage – blood vessel ruptures </li></ul><ul><ul><li>Aneurysm – a weakened point in a blood vessel that makes a stroke more likely. May be congenital or due to poison or infection. </li></ul></ul><ul><ul><li>Congenital – present at birth </li></ul></ul><ul><li>Cerebral ischemia – disruption of blood supply </li></ul><ul><ul><li>Thrombosis – plug forms </li></ul></ul><ul><ul><li>Embolism – plug forms elsewhere and moves to the brain </li></ul></ul><ul><ul><li>Arteriosclerosis – wall of blood vessels thicken, usually due to fat deposits </li></ul></ul>
    10. 10. Figure 10-4 Angiogram showing narrowing of the carotid artery--the main blood pathway to the brain
    11. 11. Damage due to Cerebral Ischemia <ul><li>Does not develop immediately </li></ul><ul><li>Most damage is a consequence of excess neurotransmitter release – especially glutamate </li></ul><ul><li>Blood-deprived neurons become overactive and release glutamate </li></ul><ul><li>Glutamate overactivates its receptors, especially NMDA receptors leading to an influx of Na + and Ca ++ </li></ul>
    12. 12. Damage due to Cerebral Ischemia <ul><li>lnflux of Na + and Ca ++ triggers: </li></ul><ul><ul><li>the release of still more glutamate </li></ul></ul><ul><ul><li>a sequence of internal reactions that ultimately kill the neuron </li></ul></ul><ul><li>Ischemia-induced brain damage </li></ul><ul><ul><li>takes time </li></ul></ul><ul><ul><li>does not occur equally in all parts of the brain </li></ul></ul><ul><ul><li>mechanisms of damage vary with the brain structure affected </li></ul></ul>
    13. 13. Figure 10-5
    14. 14. Closed-Head Injuries <ul><li>Brain injuries due to blows that do not penetrate the skull – the brain collides with the skull </li></ul><ul><ul><li>Contrecoup injuries – contusions are often on the side of the brain opposite to the blow </li></ul></ul><ul><li>Contusions – closed-head injuries that involve damage to the cerebral circulatory system. A hematoma, a bruise, forms. </li></ul><ul><li>Concussion – when there is a disturbance of consciousness following a blow to the head and no evidence of structural damage. </li></ul>
    15. 15. Figure 10-6
    16. 16. Concussions <ul><li>While there is no apparent brain damage with a single concussion, multiple concussions may result in a dementia referred to as “punch-drunk syndrome” </li></ul><ul><li>When might this occur? </li></ul><ul><li>Can it be prevented? </li></ul>
    17. 17. Case 10-2
    18. 18. Brain Infection <ul><li>Invasion of the brain by microorganisms </li></ul><ul><li>Encephalitis – the resulting inflammation </li></ul><ul><li>Bacterial infections </li></ul><ul><ul><li>Often leads to abscesses, pockets of pus </li></ul></ul><ul><ul><li>May inflame meninges, creating meningitis </li></ul></ul><ul><ul><li>Treat with penicillin and other antibiotics </li></ul></ul><ul><li>Viral infections </li></ul><ul><ul><li>Some viral infections preferentially attack neural tissues </li></ul></ul>
    19. 21. Bacteria versus Viruses <ul><li>http://cubanology.com/Articles/Virus_vs_Bacteria.htm </li></ul>
    20. 22. Brain Infections - Some Causes <ul><li>Bacterial </li></ul><ul><li>Syphilis – may produce a syndrome of insanity and dementia known as general paresis </li></ul><ul><li>Syphilis bacteria are passed to the noninfected and enter a dormant stage for many years. </li></ul><ul><li>Viral </li></ul><ul><li>Rabies – high affinity for the nervous system </li></ul><ul><li>Mumps and herpes – typically attack tissues other than the brain </li></ul><ul><li>Viruses may lie dormant for years </li></ul>
    21. 23. Neurotoxins <ul><li>May enter general circulation from the GI tract, lungs, or through the skin </li></ul><ul><li>Toxic psychosis – chronic insanity produced by a neurotoxin. </li></ul><ul><li>The Mad Hatter – may have had toxic psychosis due to mercury exposure </li></ul>
    22. 24. Neurotoxins <ul><li>Some antipyschotic drugs produce a motor disorder caused tardive dyskinesia </li></ul><ul><li>Recreational drugs, such as alcohol, may cause brain damage </li></ul><ul><ul><li>Neurotoxic effects of alcohol </li></ul></ul><ul><ul><li>Thiamine deficiency </li></ul></ul><ul><li>Some neurotoxins are endogenous – produced by the body </li></ul>
    23. 25. Genetic Factors <ul><li>Most neuropsychological diseases of genetic origin are associated with recessive genes. Why? </li></ul><ul><li>Down syndrome </li></ul><ul><ul><li>0.15% of births, probability increases with advancing maternal age </li></ul></ul><ul><ul><li>Extra chromosome 21 </li></ul></ul><ul><ul><li>Characteristic disfigurement, mental retardation, other health problems </li></ul></ul>
    24. 26. Figure 10-7
    25. 27. Neuropsychological Diseases <ul><li>Epilepsy </li></ul><ul><li>Parkinson’s disease </li></ul><ul><li>Huntington’s disease </li></ul><ul><li>Multiple sclerosis </li></ul><ul><li>Alzheimer’s disease </li></ul>
    26. 28. Epilepsy <ul><li>Primary symptom is seizures, but not all who have seizures have epilepsy </li></ul><ul><li>Epileptics have seizures generated by their own brain dysfunction </li></ul><ul><li>Affects about 1% of the population </li></ul><ul><li>Difficult to diagnose due to the diversity and complexity of epileptic seizures </li></ul>
    27. 29. Epilepsy <ul><li>Types of seizures </li></ul><ul><ul><li>Convulsions – motor seizures </li></ul></ul><ul><ul><li>Some are merely subtle changes of thought, mood, or behavior </li></ul></ul><ul><li>Causes </li></ul><ul><ul><li>Brain damage </li></ul></ul><ul><ul><li>Genes – over 70 known so far </li></ul></ul><ul><li>Diagnosis </li></ul><ul><ul><li>EEG – Electroencephalogram </li></ul></ul><ul><ul><li>Seizures associated with high amplitude spikes </li></ul></ul>
    28. 30. Figure 10-8
    29. 31. Epilepsy <ul><li>Seizures often preceded by an aura, such as a smell, hallucination, or feeling </li></ul><ul><ul><li>Aura’s nature suggests the epileptic focus </li></ul></ul><ul><ul><li>Warns epileptic of an impending seizure </li></ul></ul><ul><li>Partial epilepsy – does not involve the whole brain </li></ul><ul><li>Generalized epilepsy – involve the entire brain </li></ul>
    30. 32. Figure 10-9 The bursting of an epileptic neuron, recorded by extracellular unit recording.
    31. 33. Partial Seizures <ul><li>Simple </li></ul><ul><ul><li>symptoms are primarily sensory or motor or both (Jacksonian seizures) </li></ul></ul><ul><ul><li>symptoms spread as epileptic discharge spreads </li></ul></ul><ul><li>Complex – often restricted to the temporal lobes (temporal lobe epilepsy) </li></ul><ul><ul><li>patient engages in compulsive and repetitive simple behaviors – automatisms </li></ul></ul><ul><ul><li>more complex behaviors seem normal </li></ul></ul>
    32. 34. Case 10-3
    33. 35. Generalized Seizures <ul><li>Grand mal </li></ul><ul><ul><li>Loss of consciousness and equilibrium </li></ul></ul><ul><ul><li>Tonic-clonic convulsions </li></ul></ul><ul><ul><ul><li>-rigidity (tonus) and tremors (clonus) </li></ul></ul></ul><ul><ul><li>Resulting hypoxia may cause brain damage </li></ul></ul><ul><li>Petit mal </li></ul><ul><ul><li>not associated with convulsions </li></ul></ul><ul><ul><li>A disruption of consciousness associated with a cessation of ongoing behavior </li></ul></ul>
    34. 36. Figure 10-10
    35. 37. Parkinson’s Disease <ul><li>A movement disorder of middle and old age affecting ~ .5%of the population </li></ul><ul><li>Pain and depression commonly seen before the full disorder develops </li></ul><ul><li>Tremor at rest is the most common symptom of the full-blown disorder </li></ul><ul><li>Dementia is not typically seen </li></ul><ul><li>No single cause </li></ul>
    36. 38. Parkinson’s Disease <ul><li>Associated with degeneration of the substantia nigra whose neurons use dopamine and project to the striatum of the basal ganglia </li></ul><ul><li>Almost no dopamine in the substantia nigra of Parkinson’s patients </li></ul><ul><li>Treated temporarily with L-dopa </li></ul><ul><li>Linked to ~10 different gene mutations </li></ul>
    37. 39. Huntington’s Disease <ul><li>Also a progressive motor disorder of middle and old age – but rare, with a strong genetic basis, and associated with dementia. </li></ul><ul><li>Begins with fidgetiness and progresses to jerky movements of entire limbs and severe dementia </li></ul><ul><li>Death usually occurs within 15 years </li></ul><ul><li>Caused by a single dominant gene </li></ul><ul><li>1 st symptoms usually not seen until age 40 </li></ul>
    38. 40. Image 10-1
    39. 41. Multiple Sclerosis <ul><li>A progressive disease that attacks CNS myelin, leaving areas of hard scar tissue (sclerosis) </li></ul><ul><li>Nature and severity of deficits vary with the nature, size, and position of sclerotic lesions </li></ul><ul><li>Periods of remission are common </li></ul><ul><li>Symptoms include visual disturbances, muscle weakness, numbness, tremor, and loss of motor coordination ( ataxia ) </li></ul>
    40. 42. Figure 10-11
    41. 43. Multiple Sclerosis <ul><li>Epidemiological studies find that incidence of MS is increased in those who spend childhood in a cool climate </li></ul><ul><li>MS is rare amongst Africans and Asians </li></ul><ul><li>Strong genetic predisposition and many genes involved </li></ul><ul><li>An autoimmune disorder – immune system attacks myelin </li></ul><ul><li>Drugs may retard progression or block some symptoms </li></ul>
    42. 44. Alzheimer’s Disease <ul><li>Most common cause of dementia – likelihood of developing it increases with age </li></ul><ul><li>Progressive, with early stages characterized by confusion and a selective decline in memory </li></ul><ul><li>Definitive diagnosis only at autopsy – must observe neurofibrillary tangles and amyloid plaques </li></ul>
    43. 45. Figure 10-12 Amyloid Plaques in an Alzheimer Patient’s Brain
    44. 46. Familial Forms of Alzheimer’s Disease <ul><li>Several genes identified as involved in early onset AD </li></ul><ul><li>All affected genes are involved in synthesis of amyloid or tau, a protein found in the tangles </li></ul><ul><li>Not clear what comes 1 st – amyloid plaques or neurofibrillary tangles </li></ul><ul><li>Declined acetylcholine levels is among one of the earliest changes seen </li></ul>
    45. 47. Figure 10-13
    46. 48. Neuropsychological Diseases - Recap <ul><li>Epilepsy – abnormal electrical activity </li></ul><ul><li>Parkinson’s disease </li></ul><ul><ul><li>progressive motor disorder without dementia </li></ul></ul><ul><li>Huntington’s disease </li></ul><ul><ul><li>progressive motor disorder with dementia </li></ul></ul><ul><li>Multiple sclerosis </li></ul><ul><ul><li>autoimmune disorder that affects motor function and strikes early </li></ul></ul><ul><li>Alzheimer’s disease - dementia </li></ul>
    47. 49. Animal Models of Human Neuropsychological Diseases <ul><li>While animal models only model some aspects of the human condition, they can provide insight </li></ul><ul><li>Kindling model of epilepsy </li></ul><ul><ul><li>Experimentally induced seizure activity </li></ul></ul><ul><li>Transgenic mouse model of Alzheimer’s </li></ul><ul><ul><li>Mice producing human amyloid </li></ul></ul><ul><li>MPTP model of Parkinson’s </li></ul><ul><ul><li>Drug-induced damage comparable to that seen in PD </li></ul></ul>
    48. 50. Kindling Model of Epilepsy <ul><li>A series of periodic brain stimulations eventually elicits convulsions – the kindling phenomenon </li></ul><ul><ul><li>Neural changes are permanent </li></ul></ul><ul><ul><li>Produced by stimulation distributed over time </li></ul></ul><ul><li>Convulsions are similar to those seen in some forms of human epilepsy – but they only occur spontaneously if kindled for a very long time </li></ul><ul><li>Kindling phenomenon is comparable to the development of epilepsy (epileptogenesis) seen following a head injury </li></ul>
    49. 51. Transgenic Mouse Model of AD <ul><li>Transgenic – genes of another species have been introduced </li></ul><ul><li>Only humans and a few related primates develop amyloid plaques </li></ul><ul><li>Genes accelerating human amyloid synthesis introduced into mice </li></ul><ul><ul><li>Plaque distribution comparable to that in AD </li></ul></ul><ul><ul><li>No neurofibrillary tangles </li></ul></ul>
    50. 52. MPTP Model of Parkinson’s Disease <ul><li>The Case of the Frozen Addicts </li></ul><ul><ul><li>Synthetic heroin produced the symptoms of Parkinson’s </li></ul></ul><ul><ul><li>Contained MPTP </li></ul></ul><ul><li>MPTP causes cell loss in the substantia nigra, like that seen in PD </li></ul><ul><li>Animal studies led to the finding that deprenyl can retard the progression of PD </li></ul>
    51. 53. Case 10-4
    52. 54. Figure 10-14
    53. 55. Neuroplastic Responses to Nervous System Damage <ul><li>Degeneration - deterioration </li></ul><ul><li>Regeneration – regrowth of damaged neurons </li></ul><ul><li>Reorganization </li></ul><ul><li>Recovery </li></ul>
    54. 56. Degeneration <ul><li>Cutting axons is a common way to study responses to neuronal damage </li></ul><ul><li>Anterograde - degeneration of the distal segment – between the cut and synaptic terminal </li></ul><ul><ul><li>cut off from cell’s metabolic center </li></ul></ul><ul><ul><li>swells and breaks off within a few days </li></ul></ul><ul><li>Retrograde – degeneration of the proximal segment – between the cut and cell body </li></ul><ul><ul><li>progresses slowly </li></ul></ul><ul><ul><li>if regenerating axon makes a new synaptic contact, the neuron may survive </li></ul></ul>
    55. 57. Figure 10-15
    56. 58. Neural Regeneration <ul><li>Does not proceed successfully in mammals and other higher vertebrates - capacity for accurate axonal growth is lost in maturity </li></ul><ul><li>Regeneration is virtually nonexistent in the CNS of adult mammals and unlikely, but possible, in the PNS </li></ul>
    57. 59. Neural Regeneration in the PNS <ul><li>If the original Schwann cell myelin sheath is intact, regenerating axons may grow through them to their original targets </li></ul><ul><li>If the nerve is severed and the ends are separated, they may grow into incorrect sheaths </li></ul><ul><li>If ends are widely separated, no meaningful regeneration will occur </li></ul>
    58. 60. Figure 10-16 Neural Regeneration
    59. 61. Figure 10-17 Collateral Sprouting
    60. 62. Why do mammalian PNS neurons regenerate and CNS neurons do not? <ul><li>CNS neurons can regenerate if transplanted into the PNS, while PNS neurons won’t regenerate in the CNS </li></ul><ul><li>Schwann cells promote regeneration </li></ul><ul><ul><li>Neurotrophic factors stimulate growth </li></ul></ul><ul><ul><li>CAMs provide a pathway </li></ul></ul><ul><li>Oligodendroglia actively block regeneration </li></ul>
    61. 63. Neural Reorganization <ul><li>Reorganization of 1° sensory and motor systems has been observed following damage to: </li></ul><ul><ul><li>peripheral nerves </li></ul></ul><ul><ul><li>primary cortical areas </li></ul></ul><ul><li>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 </li></ul><ul><li>Contralateral somatosensory cortex of monkeys whose arm sensory neurons cut 10 years before--cortical face area expanded into original arm area. </li></ul><ul><li>Transection of motor neurons to rat vibrissae muscles </li></ul><ul><li>Studies show scale of reorganization possible is far greater than anyone assumed possible </li></ul>
    62. 64. Figure 10-18 Reorganization of the Rat Motor Cortex after Transection of Motor Neurons that Control the Vibrissae (whiskers)
    63. 65. Mechanisms of Neural Reorganization <ul><li>Existing connections strenghtened due to a release from inhibition? </li></ul><ul><ul><li>Consistent with speed and localized nature of reorganization </li></ul></ul><ul><li>New connections established? </li></ul><ul><ul><li>Magnitude can be too great to be explained by changes in existing connections </li></ul></ul>
    64. 66. Figure 10-19
    65. 67. Recovery of Function after Brain Damage Poorly Understood <ul><li>Difficult to conduct controlled experiments on populations of brain-damaged patients </li></ul><ul><li>Can’t distinguish between true recovery and compensatory changes </li></ul><ul><li>Cognitive reserve – education and intelligence – thought to play an important role in recovery of function – may permit cognitive tasks to be accomplished new ways </li></ul><ul><li>Adult neurogenesis may play a role in recovery </li></ul>
    66. 68. Figure 10-20 17-20 21-25 26+ 17-21 22-25 26+ 17-19 20-25 26+
    67. 69. Figure 10-21
    68. 70. Treating Nervous System Damage <ul><li>Reducing brain damage by blocking neurodegeneration </li></ul><ul><li>Promoting recovery by promoting regeneration </li></ul><ul><li>Promoting recovery by transplantation </li></ul><ul><li>Promoting recovery by rehabilitative training </li></ul>
    69. 71. Reducing brain damage by blocking neurodegeneration <ul><li>Various neurochemicals can block or limit neurodegeneration </li></ul><ul><li>Apoptosis inhibitor protein – introduced in rats via a virus </li></ul><ul><li>Nerve growth factor – blocks degeneration of damaged neurons </li></ul><ul><li>Estrogens – limit or delay neuron death </li></ul><ul><li>Neuroprotective molecules tend to also promote regeneration </li></ul>
    70. 72. Promoting Recovery by Promoting Regeneration <ul><li>While regeneration does not normally occur in the CNS, experimentally it can be induced </li></ul><ul><li>Eliminate inhibition of oligodendroglia and regeneration can occur </li></ul><ul><li>Provide Schwann cells to direct growth </li></ul><ul><li>Transplanting of olfactory sheathing cells </li></ul>
    71. 73. Promoting Recovery by Neurotransplantation <ul><li>Fetal tissue </li></ul><ul><ul><li>Fetal substantia nigra cells used to treat MPTP-treated monkeys (PD model) </li></ul></ul><ul><ul><li>Treatment was successful </li></ul></ul><ul><ul><li>Limited success with humans </li></ul></ul><ul><li>Stem cells </li></ul><ul><ul><li>Rats with spinal damage “cured”, but much more research is needed </li></ul></ul>
    72. 74. Case 10-5
    73. 75. Promoting Recovery by Rehabilitative Training <ul><li>Constraint-induced therapy – down functioning limb while training the impaired one – create a competitive situation to foster recovery </li></ul><ul><li>Facilitated walking as an approach to treating spinal injury </li></ul>
    74. 76. Case 10-6.1
    75. 77. Case 10-6.2
    76. 78. Figure 10-22
    77. 79. Can the brain recover from brain damage? <ul><li>Consider what you now know about the brain’s ability to adapt following brain damage, can it “recover”? </li></ul><ul><li>If so, what conditions promote recovery? </li></ul>
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