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PSYC 304 > CH 10: Brain Damage & Neuroplasticity > Flashcards

CH 10: Brain Damage & Neuroplasticity Flashcards

1
Q

Define TUMOUR.

A
  • A mass of cells growing independently of rest of body
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2
Q

Explain difference b/w ENCAPSULATED vs. INFILTRATING brain tumour.

A
  • Encapsulated Tumours = grows w/in their own membrane
  • -> usually are BENIGN Tumours = can be surgically removed w/ little risk of further growth in body
  • Infiltrating Tumours = grows diffusely through surrounding tissues
  • -> usually are MALIGNANT Tumours = difficult to remove/destroy completely
  • -> any cancerous tissue that remains after surgery cont. to grow
  • ie) Gliomas = brain tumours that develop from glial cells
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3
Q

List the 2 types of brain tumours.

A
  1. Meningiomas

2. Metastatic Tumours

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4
Q

Describe MENINGIOMAs.

A
  • Tumours that grow b/w the meninges (=the 3 membranes that cover the CNS)
  • All meningiomas = Encapsulated tumours
  • -> Usually benign tumours
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5
Q

Describe METASTATIC Tumours.

A
  • Don’t originate in brain but grow from infiltrating cells that are carried to brain via bloodstream from some other body part
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6
Q

Define a STROKE.

A
  • Sudden-onset cerebrovascular disorders that cause brain damage
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7
Q

List the 2 types of stroke.

A
  1. Cerebral Hemorrhage

2. Cerebral Ischemia

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8
Q

Describe a CEREBRAL HEMORRHAGE.

A

Cerebral Hemorrhage:
= Bleeding in brain
- Occurs when a cerebral bv ruptures & blood seeps into surrounding neural tissue & damages it
- Commonly caused by burst aneurysm

  • ANEURYSM = ballon-like dilation formed in artery wallet point where elasticity of artery wall is defective
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9
Q

Describe CEREBRAL ISCHEMIA.

A

Cerebral Ischemia:

= disruption of the blood supply to an area of the brain.

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10
Q

Describe the 3 main causes of Cerebral Ischemia.

A
  1. THROMBOSIS
    = a plug called a thrombus is formed & blocks blood flow at with of its formation
  2. EMBOLISM
    = similar to 1., except that the plug, called an emboli, is carried by the blood from a larger vessel, where it was formed, to a smaller one, where it becomes lodged
    - aka a thrombosis that’s taken a trip
  3. ARTERIOSCLEROSIS
    = walls of blood vessels thicken & channels narrow
    –> usually as result of fat deposits
    –> narrowing leads to complete blockage of the bv
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11
Q

List the 2 important properties of ischemia-induced brain damage.

A
  1. Takes a while to develop
  2. It doesn’t occur equally in a all parts of brain
    - -> Particularly susceptible neurons are in certain areas of hippocampus
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12
Q

Describe how GLUTAMATE plays a major role in ischemia-induced brain damage.

A
  • GLUTAMATE = brain’s most prevalent excitatory NT
  • After a bv becomes blocked, many blood-deprived neurons become overactive & release ^^glutamate
  • -> Glutamate over activates glutamate receptors in membranes of postsynaptic neurons
  • -> ^Na & Ca2+ ions enter postsynaptic neurons
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13
Q

Excessive internal Na & Ca [ ]s affects postsynaptic neurons by… (2)

A
  1. Triggering release of excessive amounts of glutamate from the neurons
    - -> Spreads toxic cascade to other neurons
  2. Triggers sequence of internal reactions that ultimately kill the postsynaptic neurons
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14
Q

Define CLOSED-HEAD INJURIES.

A
  • Brain injuries produced by blows that do NOT penetrate skull
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15
Q

Describe a CONTUSION.

A

Contusion:

  • Closed-head injury involving damage to cerebral circulatory system
  • Produced internal hemorrhaging
  • -> results in HEMATOMA = localized collection of clotted blood in organ/tissue = bruise
  • Occurs when brain slams against inside of skull
  • Frequently occurs on side of brain opposite to side struck by blow (bc brain strikes inside of skull on other side of head)
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16
Q

Describe a CONCUSSION.

A

Concussion:

  • Disturbance of consciousness following blow to head & no evidence of a contusion or other structural damage
  • Its effects can last years
  • Effects of repeated concussions can accumulate
  • ie) memory loss in football players
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17
Q

Define a BRAIN INFECTION.

A
  • An invasion of the brain by microorganisms
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18
Q

List the 2 different types of infections of the brain.

A
  1. Bacterial infections

2. Viral infections

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19
Q

Describe BACTERIAL INFECTIONS of the brain.

A
  • Bacteria infect brain
  • -> Lead to formation of CEREBRAL ABSCESSES = pus pockets in brain
  • Bacteria = major cause of meningitis = inflammation of meninges
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20
Q

Describe the 2 types of VIRAL INFECTIONS of the brain.

A
  • 2 types of viral infections of NS:
    (a) those w/ particular infinity for neural tissue
    (b) those that attack neural tissue but have no greater affinity for it than other tissues
  • ie) rabies = virus w/ particular affinity for NS
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21
Q

Describe 3 different types of NEUROTOXINS.

A
  1. HEAVY METALS
    - ie) mercury & lead
    - Can accumulate in brain & permanently damage it
    - -> Produce toxic psychosis = mental illness produced by neurotoxin
    - ie) Madhatter = hat makers inhale mercury when making hats
  2. DRUGS USED TO TREAT NEUROLOGICAL DISORDERS
    - Proven to be toxic
  3. Some neurotoxins = ENDOGENOUS = produced by patient’s own body
    - ie) produce antibodies that attack particular components of NS
    - ie) glutamate & ischemic stroke – excessive release of NT can damage brain
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22
Q

Discuss symptoms of DOWN SYNDROME & what causes this disorder.

A

Down Syndrome:

  • Disorder ass w/ presence of extra chromosome 21
  • Results in characteristic disfigurement & intellectual impairment
  • Genetic accident
  • -> Extra chromosome 21 created in egg during ovulation
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23
Q

Describe APOPTOSIS.

A

Apoptosis:
= Programmed cell death
- Critical in early development (eliminates extra neurons)
- Causes brain/neural damage
–> Is activated by tumours, cerebrovascular disorder, closed-head injuries, infections, toxins , & genetic factors
- Slow death (1-2d)
- Gradual, starting w/ shrinkage of cell body
–> parts of neuron die
–> debris packaged in vesicles
–> no inflammation = minimal damage to nearby cells

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24
Q

Describe NECROSIS.

A

Necrosis:
= Passive cell death resulting from INJURY
- Quick death (1-2h)
- Damaged neuron swells & breaks apart, beginning in axons & dendrites &; ending in cell body
–> Fragmentation leads to inflammation
–> Damage other nearby cells

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25
Q

Describe EPILEPSY.

A

Epilepsy:
= Neurological disorder characterized by spontaneously recurring seizures
- Hard to diagnose bc some epileptic seizures don’t affect motor function
–> Rather subtle changes in mood, thought or behaviour

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26
Q

What are some causes of epilepsy (4)?

A
  1. Viruses
  2. Neurotoxins
  3. Tumours
  4. Blows to head
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27
Q

Describe the difference b/w/ FOCAL Seizures & GENERALIZED Seizures.

A
  • FOCAL Seizure = doesn’t involve entire brain

- GENERALIZED Seizure = involves entire brain

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28
Q

Describe Focal Seizures & list the 2 categories of Focal Seizures.

A

Focal Seizure:

  • Epileptic neurons at a focus discharge together in bursts
  • -> Synchronous bursting neurons produce epileptic spiking in EEG
  • -> Spreads to other areas of brain, but not entire brain
  • -> Usually accompanied by total loss of consciousness

Categories:

  1. Simple Partial Seizures
  2. Complex Partial Seizures
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29
Q

Describe Simple Partial Seizures.

A

Simple Partial Seizures:
= Focal seizures whose symptoms are primarily sensory or motor or both
- As epileptic discharges spread through sensory or motor areas of brain, the symptoms spread systematically through body

30
Q

Describe Complex Partial Seizures.

A

Complex Partial Seizures:
= Restricted to temporal lobe
- Patient engages in compulsive, repetitive, simple behaviours (ie. doing & undoing a button)
- Engages in ^complex behaviours that appear almost normal

31
Q

Describe Generalized Seizures & list the 2 categories of Generalized Seizures.

A
  • Discharges begin simultaneously in all parts of brain
  • OR begin as focal discharges that gradually spread through entire brain

Categories:

  1. Tonic-Clonic Seizures
  2. Absence Seizure
32
Q

Describe Tonic-Clonic Seizures - what are its primary behavioural symptoms?

A

Primary behavioural symptoms:

  • Loss of consciousness
  • Loss of equilibrium
  • Tonic-Clonic Convulsion = TONIC (rigid body) then CLONIC (uncontrollable jerking)
33
Q

Describe Absence Seizures - what are its primary behavioural symptoms?

A

Primary behavioural symptoms:

- Disruption of consciousness ass. w/ cessation of ongoing behaviour, vacant look & fluttering eyelids

34
Q

Describe the treatments for epilepsy (4).

A
  • No cure for epilepsy, but the frequency & severity of seizures can be reduced by anti-epileptic meds
  • -> Though these drugs have adverse side effects & don’t work for everyone

Other treatments include:

  • Stimulation of vagus nerve
  • Transcranial magnetic stimulation
  • Ketogenic diet = high fat, moderate protein, low carbs
35
Q

Describe PARKINSON’s DISEASE (PD).

A
  • Movement disorder of middle & old age

- -> affects 1% of pop >55yo

36
Q

Describe the symptoms of PD.

A
  • Mild initial symptoms = slight stiffness or finger tremor

Symptoms ^severity w/ advancing years ie)

  • Pronounced tremor during inactivity
  • Muscular rigidity
  • Difficulty initiating movement
  • Slowness of movement
  • Mask-like face
  • Pain & depression
37
Q

Describe some treatments for PD (2).

A
  1. L-dopa Injections
    - -> but NOT a permanent solution
    - -> becomes less effective w/ continued use, until its side effects (ie. involuntary movements) outweigh its benefits
  2. Deep Brain Stimulation
    = low-intensity electrical stimulation continuously applied to area of brain via implanted electrode
    - ^controversial
38
Q

Describe the symptoms of HUNTINGTON’s DISEASE.

A

Huntington’s Disease:
= Progressive motor disorder

  • 1st sign - ^fidgetiness
  • Develop rapid, complex, jerky movements of entire limbs (rather than individual muscles)
  • Eventually motor & intellectual deterioration so severe that sufferers are incapable of feeding themselves, control bowels, or recognize own kids
  • NO CURE – death ~15y after presence of 1st symptoms
39
Q

What makes Huntington’s Disease different from PD (3)?

A
  • Unlike PD, it’s:
    > Rare (1:10k)
    > Has simple genetic basis
    > Is always ass. w/ severe dementia
40
Q

Explain the genetic basis of Huntington’s Disease.

A
  • Passed from generation to generation via single mutated dominant gene (huntintin)
  • Dominant = all individuals w/ the gene will have the disorder & pass onto 1/2 offspring
41
Q

Describe MULTIPLE SCLEROSIS (MS) - what happens to the NS?

A

Multiple Sclerosis (MS):
= Progressive disease that attacks the myelin of axons in the CNS
- Attacks in early adulthood
- 1st see microscopic areas of degeneration on myelin sheath
–> Damage to myelin so severe that associated axons become dysfunctional & degenerate
–> Ultimately form many areas of hard scar tissue in CNS (sclerosis = hardening)
= Autoimmune disorder = body’s immune sys attacks part of body as if it were foreign substance

42
Q

Describe the symptoms of advanced MS (6).

A
  • Visual disturbances
  • Muscular weakness
  • Numbness
  • Tremor
  • Ataxia = loss of motor coordination
  • Cognitive deficits & emotional changes in some ppl
43
Q

Describe the symptoms of ALZHEIMER’s DISEASE (AD) - early, intermediate, & advanced stages.

A

Alzheimer’s Disease:

  • Most common cause of dementia in the elderly
  • NO CURE –> Terminal
  • Major genetic component
  • Progressive, early stages = memory loss, attention deficits, personality changes
  • Intermediate stages = concussion, irritability, anxiety, deteriorated speech
  • Advanced stages = ^deterioration
  • -> can’t control simple responses ie) swallowing & bladder control
44
Q

What are the 3 defining characteristics of AD?

A
  1. Neurofibrillary Tangles
    = Tangles of protein in neural cytoplasm
  2. Amyloid Plaques
    = Clumps of scar tissue composed of degenerating neurons
  3. Neuron loss
  • -> All 3 ^prevalent in medial temporal lobe structures
  • ie) entorhinal cortex, amygdala & hippocampus
  • -> all involved in various aspects of memory
  • All 3 also more prevalent in temporal cortex, posterior parietal cortex, & prefrontal cortex
  • -> all mediate complex cognitive function
45
Q

Evaluate the AMYLOID HYPOTHESIS (the evidence for and against it).

A

Amyloid Hypothesis:
= Amyloid plaques are the primary symptom of AD & cause all other symptoms

> SUPPORT:

  • via genetic analysis
  • all 3 diff gene mutations that cause early-onset AD influence the synthesis of beta-amyloid

> AGAINST:

  • via fact that many ppl w/o observable dementia carry ^^amyloid plaques = high-plaque normals
  • However, high-plaque normals have ^^risk of cognitive decline & some develop AD
46
Q

Describe the KINDLING model of epilepsy.

A

Kindling Phenomenon:
= Progressive development & intensification of convulsion elicited by a series of periodic low-intensity brain stimulation
- Most frequently studied in rats subjected to repeated AMYGDALA stimulation (electrical)

  • Neuroplastic changes underlying kindling are permanent
  • -> A subject kindled & then left unstimulated for months still responds to each low intensity stimulation w/ a generalized convulsion
  • Kindling is produced by distributed (as opposed to massed) stimulation
47
Q

Explain the 2 ways in which the Kindling model of epilepsy models human epilepsy.

A
  1. The convulsions elicited in kindled animals are similar WRT those observed in some types of human epilepsy
  2. Kindling phenomenon itself is comparable to the epileptogenesis (=development of epilepsy) that can follow a head injury
48
Q

Describe the way in which the Kindling model of epilepsy does NOT model human epilepsy.

A
  • Kindled convulsions are elicited

- -> Unlike spontaneous seizures in epilepsy

49
Q

Describe the TRANSGENIC MOUSE models of AD.

A
  • Transgenic = animals w/ inserted genes of another sp
  • In transgenic mouse models of AD, gene mutations that promotes he accumulation of human beta-amyloid are injected into newly fertilized ouse eggs
  • -> Eggs injected into foster mom to develop
  • -> Mutated mice brains contain ^amyloid plaques like those of human Ad
  • -> Display neural loss & memory disturbances
50
Q

Evaluate the 1 problem of transgenic mouse models of AD, & explain its resolution.

A
  • Don’t display neurofibrillary tangles, which are primary symptom of AD
  • -> Resolved by injected human gene mutations that promo accumulation of protein tau
51
Q

Describe the MPTP model of PD, & evaluate the utility of this animal model.

A
  • MPTP = a neurotoxin that produced a disorder in primates that’s similar to PD
  • Non-human primates respond to MPTP the same way humans do
  • -> Display Parkinson motor symptoms, cell loss in the substance nivea, & reduction in brain dopamine
  • Rats are resistant to MPTP
  • Although the MPTP model doesn’t model all aspects of PD, particularly its causation, the model’s proven ^^useful
  • -> Instrumental in development of many treatments & dopaminergic drugs currently in use
52
Q

Define NEURAL DEGENERATION - what is it induced by?

A
  • Neural deterioration & death
  • Component of both brain development & disease
  • Induced by cutting axons
53
Q

List the 2 kinds of Neural Degeneration.

A
  1. Anterograde Degenration

2. Retrograde Degeneration

54
Q

Describe ANTEROGRADE DEGENERATION.

A

Anterograde Degeneration:
= Degeneration of the DISTAL segment of a cut axon (=segment of a cut axon from the cut to the synaptic terminals)
- Occurs quickly following axotomy bc cut separates distal segment of axon from cell body (which is metabolic centre of neuron)
–> Entire distal segment becomes ^ swollen w/in hours
–> Breaks into fragments w/in days

55
Q

Describe RETROGRADE DEGENERATION.

A

Retrograde Degeneration:
= Degeneration of the PROXIMAL segment of a cut axon (=segment of a cut axon from the cut back to the cell body)
- Gradually progresses back from cut to cell body
- Major changes in cell bodies of most axotomized neurones after 2-3d

56
Q

Describe TRANSNEURONAL DEGENEATION.

A

Transneuronal Degeneration:

= Degeneration of a neuron caused by damage to another neuron to which it’s linked by a synapse

57
Q

Describe ANTEROGRADE vs. RETROGRADE Transneuronal Degeneration.

A

ANTEROGRADE = transneuronal degeneration spreads from damaged neurons to the neurons on which they synapse

RETROGRADE =
transneuronal degeneration spreads from damaged neurons to the neurons that synapse on them

58
Q

Define NEURAL REGENERATION.

A

Neural Regneration:

= Regrowth of damaged neurons

59
Q

Compare Neural Regeneration w/in the CNS vs. the PNS.

A
  • Doesn’t process as successfully in mammals & other higher vertebrates as it does in invertebrates & lower vertebrates
  • Is non-existent in CNS of adult mammals, & at best a hit-or-mess in PNS
  • In mammalian PNS: regrowth from proximal stump of damaged nerve begins 2-3d after axonal damage, once new growth cones have formed

see pg 259-261

60
Q

Describe the 1st example of cortical reorganization following damage to the brain, & discuss the mechanisms that might underlie such recognition.

A
  1. Cortical Reorganization following damage in LAB ANIMALS:
    - Sensory & motor cortex ideally suited to study neural reorganization bc of their topographic layout
  • Damage-induced reorganization of primary sensory & motor cortices have been studied under 2 conditions:
    (a) following damage to peripheral nerves
    (b) following damage to cortical areas themselves

see pg 262 for 3 influential studies demo cortical reorganization

61
Q

Describe the 2nd example of cortical reorganization following damage to the brain, & discuss the mechanisms that might underlie such recognition.

A
  1. Cortical Reorganization following damage in HUMANS:
    - Use brain imaging techniques to study cortices of blind ppl
    - -> Findings consistent w/ hypo that there’s continuous competition for cortical space by functional circuits
    - W/o visual input to cortex, there’s expansion of auditory & somatosensory cortex, & auditory & somatosensory input is processed in formerly visual areas
    - Functional consequence to this reorganization = blind volunteers have skills superior to those of slighted control on a variety of auditory & somatosensory tasks
62
Q

Describe 2 mechanisms of Neural Reorganization.

A
  1. Strengthening of existing connections, possibly via release from inhibition
    - Indirect support comes from 2 observations:
    (a) reorganization occurs too quickly to be explained by neural growth
    (b) rapid reorganization never involves changes of >2mm of cortical surface
  2. Establishment of new connections by collateral sprouting
    - Indirect support comes from 1 observation:
    (a) the magnitude of long-term reorganization can be too great to be explained by changes in existing connections
63
Q

see Figure 10.8 to see how 2 mechanisms may account for reorganization that occurs after damage to peripheral somatosensory nerve

A

.. do it?

64
Q

Describe the concept of COGNITIVE REVERSE.

A

Cognitive Reverse:
- Thought to play a role in the improvements observed after brain damage that do NOT result from true recovery of brain function

  • ie) brain damage patients who demo improvement bc cognitive reverse allowed them to accomplish tasks in alternative ways
  • Explains why educated ppl are less susceptible to the effects of brain deterioration ass. w/ aging
65
Q

Does adult neurogenesis contribute to recovery from brain damage?

A
  • NO direct evidence that stem cells contribute to recovery!
  • Although stem cells can migrate short distances, there’s no evidence they can migrate from their sites of genesis in hippocampus to distant areas of damage in adult human brain
66
Q

Discuss early work on neuro-transplantation for the treatment of CNS damage.

A
  • Explore possibility of repairing damaged CNS tissue via implanting embryonic tissue near damaged area
  • -> Hope embryonic tissue would mature & replace damaged cells
  • Focused on using as treatment for PD
  • Initial success & reduced symptoms, but patients displayed uncontrollable writing & chewing movements 1yr after surgery
67
Q

Discuss the methods & findings of modern research on neuro-transplantation.

A
  • ^^animal models of all common neurological disorders
  • Suggest stem-cell cultures provide lasting sources of cell transplantation
  • -> Ethical & technical difficulties in transplanting tissue obtained from human embryos
  • -> DIDN’T work out – stem-cell cultures deteriorate as chromosomal abnormalities gradually accumulate during repeated cell division
68
Q

Discuss methods of treating STROKES through rehabilitate treatment.

A
  • Small strokes produce core of brain damage
  • -> Followed by a gradually expanding loss of neural function in the surrounding penumbra
  • Study prod small ISCHEMIC LESIONS in hand area of motor cortex of monkeys
  • -> Initiate program of hand training & practice
  • -> Reduced expansion of cortical damage into surrounding penumbra
69
Q

Discuss methods of treating SPINAL INJURY through rehabilitate treatment.

A
  • Patients incapable of walking were supported by harness over a moving treadmill
  • -> Weight was supported & treadmill provided feedback
  • -> Gradually learn to make walking movements
70
Q

Describe the benefits of cognitive & physical exercise.

A
  • Study benefits of cognitive & physical activity by assessing the neurological benefits of housing animals in ENRICHED environments
  • -> Enriched environ show to ^dendritic branching, the site of synapses, the rate of adult neurogenesis, & the levels of various neurotrophic factors
  • Physical exercise in form of daily wheel running
  • -> Beneficial effects on rodent brain
  • ie) ^adult neurogenesis in hippocampus
  • reduced age-related declines in # neurons in hippocampus
  • improved performance on memory & navigation tests (2 abilities linked to hippocampus)
71
Q

Discuss ways of treating phantom limbs.

A
  • Surgical efforts to control irritation at stump via cutting off stump or various ways of neural pathway b/w stump & cortex
  • -> unsuccessful :(

PSYC 304 (18 decks)

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