B And B Test 5

Front 1

Define neuroplasticity and factors that will make it more likely to occur

Back 1

Refers to brains ability to change and reorganize throughout life span

Occurs more readily when we are children

Front 2

How can neuroplasticity occur

Back 2

Neurogenesis, cortical reorganization, neural growth

Front 3

Describe the different types of brain tumors and discuss how they can lead to brain damage

Back 3

Neoplasm: mass of cells growing independently of the body

20% of brain tumors are meningiomas, usually benign, surgically removable. Tumors encapsulated in meninges. Putting pressure on brains.

Malignant tumors are infilitrating

Front 4

Difference between ischemic and hemorhagic strokes

Back 4

Ischemic: blood is cut off to the brain. Thrombosis, a plug forms in the brain. Embolism, a plug forms elsewhere and moves to the brain

Hemorrhage: bleeding in the brain. Blood vessel ruptures

Front 5

How does damage due to ischemia occur?

Back 5

Results from release of glutamate. Glutamate over activates its receptors, especially NMDA receptors, leading to influx of Na+ and Ca2+. Neural death occurs

Front 6

Difference between contusion and concussion

Back 6

Contusion: bruising of the brain

Concussion: bruising of brain and a change in consciousness

Front 7

Coup and Contre Coup concussion

Back 7

Coup: point of impact

Counter Coup: due to impact of brain hitting skull on opposite side of impact

Front 8

Describe what happens in the brain during a seizure

Back 8

When a part of the brain receives an abnormal burst of electrical signals that temporarily interrupt normal electrical brain function

Front 9

How did the removal if the left hemisphere influence the little boy in the video

Back 9

Seizures stopped. Relearn how to talk and walk over years. It was done much slower.

Front 10

Why is it difficult to determine recovery of a function after brain damage.

Back 10

Researchers can't distinguish between true recovery and compensatory changes.

Cognitive reserve: education and intelligence play an important role in recovery.

Adult neurogenesis may play a role too

Front 11

Is the transplanting of different neural cells successful in promoting recovery from brain damage?

Back 11

Can't cure paralysis or parkinsons yet, but there are cases where results do look promising. The research is ongoing.

Front 12

How can exercise help to promote recovery after brain damage?

Back 12

Exercise fights the effects of aging and promotes neurogenesis

Front 13

Schwann Cells

Back 13

Promote neural regeneration

Front 14

Transplanting Fetal Tissue

Back 14

Fetal substantia cells were used to treat MPTP-treated monkeys

Treatment was successful, limited success in humans

Front 15

Transplanting Stem Cells

Back 15

Embryonic cells implanted into damaged rat spinal cord

Rats with spinal damage showed improved mobility

Front 16

Describe H.M.s damage to his brain and the subsequent changes to his memory.

Back 16

Had bilateral removal of temporal lobes and lead to retrograde amnesia and anterograde amnesia. His implicit memory was still intact.

Front 17

Retrograde vs anterograde amnesia

Back 17

Retrograde: memory that did occur

Anterograde: creating new memories

Front 18

What does HM tell us about memory?

Back 18

Medial Temporary lobes involved in memory.

Separate systems exist for implicit and explicit memory

Front 19

Cerebellum

Back 19

Motor movement learning

Front 20

Amygdala

Back 20

Emotional memories

Front 21

Medial-dorsal nucleus dicephalan

Back 21

Korsakoffs Symptoms

Front 22

Hippocampus

Back 22

Spatial locations

Front 23

Perirhinal Cortex

Back 23

Object Recognition

Front 24

Basal Forebrain

Back 24

Alzheimers disease

Front 25

Prefrontal Cortex

Back 25

Temporal order of events and working memory. Tasks involving series of responses.

Front 26

Striatum

Back 26

Habit formation

Front 27

Implicit memory

Back 27

Using past experiences to remember things without thinking about them

Front 28

Explicit memory

Back 28

Conscious, intentional recollection of memory

Front 29

Episodic memory

Back 29

Forming new memories

Front 30

Sematic memory

Back 30

Memory for knowledge and info

Front 31

Korsakoffs Syndrome

Back 31

Occurs after severe alcoholism or thiamine depletion.

Damage in the Medial Diencephalon: Medial Thalamus and Medial Hypothalamus

Early stages: amnesia for episodic memory

Later stages: severe retrograde amnesia develops

Front 32

Alzheimers

Back 32

Early Stages: slight losses of memory, progresses to dementia

Major anterograde and retrograde amnesia for explicit

Deficits in STM and some implicit memory. Implicit sensorimotor is intact

Decreased Acetycholine. Basal forebrain degeneration, basal forebrain strokes can cause amnesia

Damage to medial temporal lobe and prefrontal cortex

Front 33

Process of Long Term Potentiation (LTP)

Back 33

Synaptic changes made my increased use of synapses. Can last for many weeks. Only occurs of presynaptic firing is followed by postsynaptic firing.

3 part process: induction (learning), maintenance (memory), expression (recall)

Front 34

What is LTD?

Back 34

Long Term Depression, opposite of LTP

Front 35

What are smart drugs and how do they work?

Back 35

Nootropics, thought to improve memory. No memory enhancing effects in normal people.

Front 36

Schizophrenia positive symptoms

Back 36

Delusions, hallucinations, inappropriate effect, odd behavior, incoherent speech

Front 37

Schizophrenia negative effects

Back 37

Flat affect, alogia, avolition, anhedonia, catatonia

Front 38

Brain changes in Schizophrenia

Back 38

Temporal lobe abnormalities

Increased dopamine activity

Low blood flow in prefrontal cortex

Glutamate and GABA abnormalities

Front 39

Possible causes of Schizophrenia

Back 39

Genetics, viral infections during gestation, stress, trauma, brain injury

Front 40

Bipolar

Back 40

Extremes highs and lows

Front 41

Unipolar

Back 41

Flat effect. No emotions

Front 42

Mania

Back 42

Great excitement, euphoria, delusions, and overactivity

Front 43

Areas of brain that are dysfunctional in depression

Back 43

Amygdala, medial prefrontal cortex, hippocampus

Front 44

What are some theories of depression?

Back 44

Monoamine theory: depression is associated with decreased activity of serotonin

Neuroplasticity theory: Neuroplastic changes in certain areas associated with expression

Front 45

How might anxiety be treated?

Back 45

Benzodiazepines-valium

Serotonin agonists- don't produce ataxia like benzodiazepines

Antidepressants

Front 46

Five classes of anxiety disorders

Back 46

Generalized anxiety, Phobic Anxiety, Panic Disorders, OCD, PTSD

Front 47

What areas of brain are dysfunctional in anxiety disorders

Back 47

Medial Prefrontal Cortex, hippocampus, amygdala, deficits in GABA and serotonin

Front 48

How might depression be treated?

Back 48

MAOIs, Tricyclic antidepressants, SSRIs, Mood Stabilizers: effective for mania