Biopsychology Chapter 10

Front 1

What is a tumor?

Back 1

mass of cells that grow independently of the body
(neoplasm)

Front 2

Statistics about Tumors

Back 2

20% of meningiomas are encased in meninges

-usually benign, and are surgically removable, but can cause damage through pressure

-most are infiltrating (grow diffusely into surrounding tissue) and malignant – difficult to destroy/remove

-about 10% of brain tumors are metastic (originate elsewhere in the body; usually lungs)

Front 3

Cerebrovascular Disorder
Stroke

Back 3

sudden onset cerebrovascular event that causes brain damage;

2 types:
1) cerebral hemorrhage – bleeding in the brain
2) cerebral ischemia – disruption of blood supply

Front 4

Symptoms of Stroke

Back 4

paralysis, cognitive impairment, aphasia (most common symptom)--> (inability to speak), amnesia (retrograde)

Front 5

Cerebrovascular Disorder
Aneurysm

Back 5

weakened point in blood vessel making stroke more likely; could be congenital, poison, infection, or trauma

peak incidence is at 40-50 years
-sudden severe headache/unconsciousness
-would diagnose with a contrast X-ray

Front 6

infarct

penumbra

Back 6

tissue is dead, where stroke actually happened

where the stroke has spread, but there is still hope for recovery of that tissue

Front 7

Types of Cerebral Ischemia (insufficient blood flow to the brain)

Back 7

Thrombosis: plug forms in brain

Embolism: plug forms elsewhere, moves to brain

Arteriosclerosis: blood vessels thicken from fat deposits

Front 8

Closed-Head Injuries:
Contrecoup Injuries (definition & types)

Back 8

opposite side that you hit gets damaged

-contusion: damaged circulatory system, hematoma forms (bruising)
- concussions: no structural damage, but disturbance of consciousness
- punch drunk syndrome: repeated concussions may result in dementia and intellectual decline

Front 9

Infections of Brain

Back 9

1. Encephalitis: inflammation of the brain due to invasion of microorganisms (viral)

2. bacterial; abscesses, pockets of puss, may inflame meninges, meningitis, syphilis, general paresis, treat with antibiotics.

3. Viral infections; rabies, measles, mumps, influenza, some can lie dormant for years

Front 10

Encephalitis

Back 10

inflammation of the brain due to invasion of microorganisms (viral)

Front 11

Neurotoxins

Back 11

-“poisons” – can enter from lungs or G.I. tract
-some are endogenous (produced by body/autoimmune disorders)

Front 12

Neurotoxin "Diseases"

Back 12

1. Toxic Psychosis: chronic insanity produced by a neurotoxin

2. “The Mad Hatter”: often had elevated levels of mercury exposure from making hats

3. “Crack Pot”- lead lined tea pot, drinking the tea from a broken pot would give lead poisoning

Front 13

Neuropsychological Diseases

Back 13

1. Epilepsy
2. Parkinson's Disease
3. Huntington's Disease
4. Multiple Sclerosis
5. Alzheimer's Disease

Front 14

Epilepsy - types

Back 14

1. Partial : not whole brain → divided into “simple” [sensory or motor] and “complex” [temporal lobes, patient engages in compulsive and repetitive simple behaviours, automatisms]

2. Generalized : whole brain → divided into “Grand Mal” [loss of consciousness + equilibrium, tonic-clonic convulsions, rigidity and tremors, hypoxia (not enough air to brain)] and “Petit Mal” [ not associated with convulsions, disruption of unconsciousness, lose train of thought]

Front 15

Epilepsy - symptoms

Back 15

primary symptom: seizures (although not all who have seizures are epileptic)

-seizures are generated by own brain dysfunction

-some people see aura that signals oncoming seizure

Front 16

Epilepsy - statistics and causes

Back 16

affects up to 1% of the population

- tested with an electroencephalogram (EEG)
-no cure

-causes: brain damage (viruses, neurotoxins, tumors, injuries), genetics (over 70 could be responsible), inhibitory synapses alter GABA

Front 17

Kindling Model of Epilepsy

Back 17

-convulsion response becomes progressively stronger with repeated administration; neural changes are permanent

-if kindled, can leave untouched for months, but next stimulation will produce convulsions, they have to be distributed over time, once every day not every 5 minutes

-comparable to head injury epilepsy

Front 18

Parkinson's Disease - symptoms

Back 18

tremor at rest (most common)
-difficult time initiating movement
-muscular rigidity

Front 19

Parkinson's Disease- statistics and causes

Back 19

-dementia is not typical
lower incidence in coffee drinkers and smokers


-no single cause – neurotoxins, brain injuries, genetics, pesticides

-associated with degeneration of the substantia nigra; release dopamine to striatum of the basal ganglia – L. Dopa would help

Front 20

MPTP Model of Parkinson's Disease

Back 20

case of frozen addicts – synthetic heroin produce the same symptoms

-contained MPTP; causes cell loss in substantia nigra
- “deprenyl” – can slow progression of Parkinson’s Disease

Front 21

Huntington's Disease- symptoms

Back 21

fidgety movements: jerky, random, uncontrollable movements, more fluid
-CHOREA→ severe motor and intellectual, starts in striatum (basal ganglia)

Front 22

Huntington's Disease- statistics and causes

Back 22

degenerative motor/cognitive disorder
-death within 15 years
-symptoms at about 45 years
-transmission by single dominant gene, 50% chance to pass it on
-gene code for protein is Huntingtin neurotoxin

Front 23

Multiple Sclerosis- symptoms

Back 23

-visual disturbances, weakness, numbness, tremor, more common in females than in males

Front 24

Multiple Sclerosis- statistics and causes

Back 24

autoimmune disease → attacks CNS myelin, leaving areas of scar tissue
-periods of remission is common
- higher rate in cooler climates…may have something to do with vitamin D
-some genetic component
-smokers are higher risk
-no cure, but drugs to slow progression

Front 25

Alzheimer's Disease- symptoms

Back 25

selective decline in memory, confusion, mood swings, language breakdown, long term memory los, loss of bodily functions

Front 26

Alzheimer's Disease- statistics and causes

Back 26

-1/10 over 65, 35% over 85
amyloid plaques [clumps of scar tissue] and neurofibrillary tangles [threadlike protein in neural cytoplasm]- slowly destroy the hippocampus

*hippocampus and amygdala both have important roles in memory; complex cognitive functions…prefrontal cortex, temporal cortex and parietal cortex

Front 27

Transgenic Model for Alzheimer's Disease

Back 27

only humans and a few related primates can replicate the tangles, which shows maybe amyloid plaques are responsible for symptoms

Front 28

Neuroplasticity - Neural Degeneration

Back 28

cutting axons to study response (axotomy)

1. Retrograde – slower, proximal segment
2. Anterograde – degeneration of the distal segment between cut and synaptic clefts, faster

Front 29

What reduces Neural Degeneration?

Back 29

1. Apoptosis inhibitor protein
2. Estrogens
3. Nerve growth Factor

Front 30

Neuroplasticity- Neural Regeneration (What increases?)

Back 30

1. Schwann cells – capable of regeneration in peripheral nervous system

2. Oligodendrocytes – can’t regenerate in central nervous system, actively inhibit growth
-2 ways: either create new connections or strengthen existing connections

Front 31

Neuroplasticity- Neurotransplantation

Back 31

-transplanting fetal tissue
-limited success (~15%)
- MPTP treated monkeys
-stem cells – embryonic stem cells implanted into damaged rat + spinal cord…improved mobility

Front 32

Rehabilitation

Back 32

-constraint-induced therapy : tie down the functioning limb while training the impaired limb creates a competition among neuron to foster recovery

-facilitated walking – treat spinal cord injury

- physical exercise and environmental play a role

Front 33

phantom limb

Back 33

chronic pain often accompanies.
-Kamachandrion’s hypothesis: reorganization of somatosensory cortex following amputation