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brain damage Flashcards

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1
Q

what are the causes of brain damage

A 
brain tumors 
cerebrovascular disorders 
closed-head injuries 
neurotoxins 
others
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2
Q

brain tumors

A

most brain tumours are infiltrating. they grow diffusely through surrounding tissue. malignant, difficult to remove or destroy.

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3
Q

what percent of brain tumours are metastatic

A

about 10% of brain tumours are metastatic-they originate elsewhere, usually the lungs

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4
Q

what is a neoplasm

A

is a mass of cells that grows independently of the rest of the body- a cancer

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5
Q

meningiomas

A

~20% of brain tumours are meningiomas- encased in meninges. encapsulated, growing within their own membranes. usually benign, surgically removable

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6
Q

stroke

A

a sudden onset cerebrovascular event that causes brain damage. cerebral hemorrhage or ischemia. 3rd leading cause of death and most common cause of adult disability

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7
Q

cerebral hemorrhage

A

bleeding in the brain, blood vessel ruptures. aneurysm or congenital

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8
Q

cerebral ischemia

A

disruption of blood supply. thrombosis, embolism, arteriosclerosis

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9
Q

aneurysm

A

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

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10
Q

thrombosis

A

plug forms

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11
Q

embolism

A

plug forms elsewhere and moves to the brain

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12
Q

arteriosclerosis

A

wall of blood vessels thicken, usually due to fat deposits

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13
Q

cerebral ischemia

A

damage does not develop immediately. most damage is a consequence of excess neurotransmitter release especially glutamate. blood deprived neurons become overactive and release glutamate. glutamate overactive its receptor, especially NMDA receptors leading to an influx of Na+ and Ca++

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14
Q

influx of Na+ and Ca++ triggers

A

the release of still more glutamate. a sequence of internal reactions that ultimately kill the neutron

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15
Q

ischemia induced brain damage

A

takes time. does not occur equally in all parts of the brain. mechanisms of damage vary with the brain structure affected

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16
Q

closed head injuries

A

brain injuries due ti blows that do not penetrate the skull- the brain collides with the skull

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17
Q

types of closed head injuries

A 
coup injuries 
contrecoup injuries 
contusions 
cerebral edema 
concussion
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18
Q

coup injuries

A

injuries in the same side of the brain as the blow

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19
Q

contrecoup injuries

A

contusions are often on the side of the brain opposite to the blow

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20
Q

contusions

A

closed head injures that involve damage to the cerebral circulatory system. a hematoma, a bruise, forms

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21
Q

cerebral edema

A

brain swelling

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22
Q

concussion

A

when there is a disturbance of consciousness following a blow to the head and no evidence of structural damage

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23
Q

neurotoxins

A

may enter general circulation from the GI tract, lungs or through the skin. some antipsychotic drugs produce a motor disorder caused trade dyskinesia. recreational drugs cause brain damage. some neurotoxins are endogenous.

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24
Q

toxic psychosis

A

chronic psychosis produced by a neurotoxin

25
Q

neurological diseases

A 
epilepsy 
multiple sclerosis 
Huntington's disease 
Parkinson's disease 
Alzheimer's disease
26
Q

epilepsy

A

primary symptom is seizures. epileptics have seizures generated by their own brain dysfunction. affects about 1% of the population.

27
Q

why is epilepsy hard to diagnose

A

difficult to diagnose due to the diversity and complexity of epileptic seizures

28
Q

do all who have seizures have epilepsy

A

NO

29
Q

types of seizures

A

convulsions- motor seizures

some are merely a subtle changes of thought, mood, or behaviour

30
Q

causes of epileptic seizures

A

brain damage

genes- over 70 known so far

31
Q

how do we diagnose epilepsy

A

EEG (electroencephalogram

seizures associated with high amplitude spikes

32
Q

Aura

A

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.

33
Q

partial epilepsy

A

does not involve the whole brain

34
Q

generalized epilepsy

A

involve the entire brain

35
Q

simple partial seizures

A

symptoms are primarily sensory or motor or both (Jacksonian seizures). symptoms spread as epileptic discharge spreads

36
Q

complex partial seizures

A

often restricted to the temporal lobes (temporal lobe epilepsy). patient engages in compulsive and petite simple behaviours- automatisms. more complex behaviours seem normal

37
Q

grand Mal generalized seizures

A

“big trouble” loss of consciousness and equilibrium. tonic-clonic convulsions. rigidity (tonus) and tremors (clonus). resulting hypoxia may cause brain damage

38
Q

Petit mal generalized seizures

A

“small trouble”. not associated with convulsions. a disruption of consciousness associated with a cessation of the ongoing behaviour

39
Q

Multiple Sclerosis

A

a progressive disease that attacks CNS myelin, leaving areas of hard scar tissue (sclerosis). nature and severity of defects vary with the nature, size and position of sclerotic lesions. periods of remission are common.

40
Q

symptoms of multiple sclerosis

A

visual disturbances, muscle weakness, numbness, tremor, and loss of motor coordination (ataxia)

41
Q

risks for multiple sclerosis

A

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. genetic predisposition and many genes involved

42
Q

what type of disorder is multiple sclerosis

A

an autoimmune disorder- immune system attacks myelin

43
Q

what can be done about MS

A

drugs may retard progression or block some symptoms

44
Q

Neuroplastic responses to nervous system damage

A

degeneration - deterioration
regeneration- regrowth of damaged neurons
reorganization
recovery

45
Q

degeneration

A

cutting axons is a common way to study responses to neuronal damage. anterograde and retrograde

46
Q

anterograde degeneration

A

degeneration of the distal segment- between the cut and synaptic terminal. cut off from cell’s metabolic centre. swells and breaks off within a few days

47
Q

retrograde degeneration

A

degeneration of the proximal segment- between the cut and the cell body. progresses slowly. if regenerating axon makes a new synaptic contact, the neuron may survive

48
Q

Neural regeneration

A

does not proceed successfully in mammals and other higher vertebrates- capacity for accurate axonal growth is lost in maturity. regeneration is virtually non-existent in the CNS and adult mammals and unlikely, but possible, in the PNS

49
Q

Neural regeneration in the PNS

A

if the original Schwann cell myelin sheath is intact, regenerating axons 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

50
Q

why do mammalian PNS neurons regenerate?

A

CNS neurons can regenerate if transplanted into the PNS, while PNS won’t regenerate in the CNS. Schwann cells promote regeneration. neurotrophic factors stimulate growth. CAMs (cell adhesion molecules) provide a pathway. oligodendroglia actively block regeneration

51
Q

Neural reorganization

A

reorganization of primary sensory and motor systems has been observed following damage to: peripheral nerves, primary cortical areas. remapping can occur within minutes

52
Q

How/why does damage lead to reorganization?

A

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 alone

53
Q

recovery of function after brain damage

A

difficult to conduct controlled experiments on populations of brain damaged patients. can’t distingue 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 lay a role in recovery

54
Q

treating nervous system damage

A

reducing brain damage by blocking neurodegneration.
promoting recovery by promoting regeneration
promoting recovery by transplantation. promoting recovery by rehabilitative training

55
Q

reducing brain damage by blocking neurodegeneration

A

various neurochemicals can block or limit neurodegeneration. apoptosis inhibitor protein- induced in rats via virus. nerve growth factor- blocks degeneration of damaged neurons. estrogens- limit or delay neuron death

56
Q

promoting recovery by promoting regeneration

A

while regeneration does not normally occur in the CNS, experimentally it can be induced. elicited inhibition of oligodendroglia and regeneration can occur. provide Schwann cells to direct growth

57
Q

promoting recovery by neurotransplantation

A

fetal tissue- fetal substantia nigra cells used to treat monkeys. treatment was successful. limited success with humans.
stem cells- rats with spinal damage “cured”, but much more research is needed

58
Q

promoting recovery by rehabilitation training

A

constraint-induced therapy. down functions limb while training the impaired one- create a competitive situation to foster recovery.
facilitated walking as an approach to treating spinal surgery

59
Q

cognitive rehabilitation

A

memory, attention, executive functions

bio psych (6 decks)

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