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Neuro Block 4 - KJ > Limbic System II > Flashcards

Limbic System II Flashcards

1
Q

What causes Urbach-Wiethe disease?

A

Bilateral Amygdala lesions

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2
Q

What symptoms are associated with Urbach-Wiethe disease?

A

[Bilateral amygdala lesions]

  • Impaired recognition of emotion (in facial expression)
  • –Inability to judege “like” emotions (ex: fear vs. anger, surprise vs. happy)
  • Memory loss especially of information with emotional content
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3
Q

What are the symptoms of PTSD?

A
  1. Re-experiencing phenomena (flashbacks)
  2. Avoidance (of situations similar to original trauma)
  3. Hyperarousal (hypervigilance - high anxiety)
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4
Q

What is the etiology of PTSD?

A
  • Inc. amygdala activity (in fMRI)!

- Dec. medial prefrontal cortex activity

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5
Q

What does the medial prefrontal cortex do to the amygdala in PTSD?

A

It plays a role in inhibiting the amygdala in PTSD.

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6
Q

What does imaging show in Parkinson’s?

A

Dec. in neurons in the substantial nigra

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7
Q

What are the core features of schizophrenia?

A

Fragmentation of mood, thought and movement.

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8
Q

What are positive and negative symptoms of Schizophrenia?

A

Positive - delusions, hallucinations

Negative - social withdrawal

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9
Q

What is the incidence of schizophrenia?

A

1% of US population

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10
Q

What is happening on a neurochemical basis in schizophrenia? What is the “dopamine hypothesis”?

A

Dopamine hypothesis - schizophrenia caused by Inc. DA receptor activity.

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11
Q

What does haloperidol do?

A

It is an anti-psychotic used for schizophrenic patients. It blocks dopamine receptors

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12
Q

What are the side effects of anti-psychotic haloperidol?

A

It causes motor dysfunction (parkinsonian-like) and is not effective in some people.

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13
Q

What is clozapine?

A

It is an atypical anti-psychotic used to treat schizophrenia.

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14
Q

What is clozapine’s mechanism?

A
  1. It blocks DA recpetor: rapid off rate
  2. Blocks 5HT receptors
  3. Blocks glutamate reuptake (increases glutamate in synapse)
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15
Q

What is the “glutamate hypothesis”?

A

-Schizophrenia somehow causes a block in NMDA glutamate receptor

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16
Q

What is Phencyclidine (PCP)?

A

“Angel dust” - blocks NMDA glutamate receptor

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17
Q

What is a testament for schizophrenia based on the glutamate hypothesis?

A

Increase glutamate receptor activity!

18
Q

What are the symptoms and incidence (treated in US) for depression?

A
  • Lethargy, Anhedonia (loss of pleasure), loss of sleep

- 15% of individuals, 20% of women

19
Q

What is the “monoamine” hypothesis of depression?

A

Depression is caused by a decrease in NE and/or 5HT receptor activity.

20
Q

What are the three main mechanisms for anti-dpressants?

A
  1. Monoamine Oxidase (MAO) inhibition
  2. Tricyclics (Imipramine)
  3. SSRIs (Fluoxetine)
21
Q

What do anti-depressants try to do?

A

Increase NE or 5-HT!

22
Q

What do SSRIs (Fluoxetine/Prozac) do?

A

-Serotonin Specific Reuptake Inhibitors

Block repute of 5HT through the transporter on the pre-synaptic cell

23
Q

What do tricyclics (Imipramine) do?

A

Block re-uptake of NE & 5HT (block transporter)

24
Q

What is monoamine oxidase (MAO) inhibitors?

A

Inhibit metabolism/degradation of NE or 5HT.

25
Q

What causes Korsakoff’s Syndrome?

A
  • Chronic Alcoholism –> leads to:

- Vitamin B1 deficiency (Thiamine)

26
Q

What is damaged in Korsakoff’s syndrome?

A

Mammillary body or mamillothalamic tract.

27
Q

What symptoms does Korsakoff’s syndrome cause?

A
  • Disorder of immediate memory (no new memories)
  • Disorientation (in space & time)
  • Confabulation (respond to “Where are you?” by making up a place)
28
Q

What deficits does Kluver-Bucy Syndrome involve?

A
  • Described in monkeys

- Bilateral surgical removal of amygdala, hippocampus and temporal cortex (much of temporal lobe)

29
Q

What clinical conditions can cause bilateral medial temporal lobe damage?

A

Encephalitis, Stroke, etc.

30
Q

What are the symptoms of Kluver-Bucy Syndrome?

A
  1. Oral tendencies (all objects in mouth)
  2. Changes in emotions (neutral affect, little emotion - changes in amygdala)
  3. Hypersexuality (Inc. in # & variety of sexual activities), No reservations, always trying to make the conversation sexual [Due to changes in pathway to hypothalamus]
  4. Visual agnosia - Psychic blindness, inability to discriminate visual stimuli [damage to visual pathways in temporal lobe]
31
Q

What is alzheimer’s dementia?

A

Chronic pressive deterioration of brain with district developmental stages.

32
Q

What are the symptoms of Alzheimer’s dementia?

A
  1. Loss of memory
  2. Mood disorder: Anxiety, depression
  3. Loss of motor function
  4. Complete loss of cognitive function
33
Q

What is the incidence of alzheimer’s?

A

> 85 years, 50% will have AD

34
Q

What is the etiology/what does alzheimer’s brain look like?

A
  1. Loss of cholinergic output to hippocampus [nucleus basalis] <– cholinergic nerves
  2. Loss of neurons in multiple brain areas
  3. Presence of neurofibrillary tangles (NFTs: phosphorylated tau proteins) and beta-amyloid plaques (extracellular)
  4. Huge ventricles, more space between gyri (bc gray matter is being lost)
35
Q

Why do we treat early onset AD patients with Donepezil (Aricept)?

A

It blocks acetylcholinesterase (ACh esterase) which causes an Inc. in ACh!

36
Q

What is chronic traumatic encephalopathy?

A

CTE - Progressive neurodegenerative disease caused by repeated head trauma [ex: football, soccer]

37
Q

What are the symptoms of chronic traumatic encephalopathy?

A
  • -Cognition: memory impairment, anterograde amnesia, executive dysfunction, goal-directed behaviors [prefrontal cortex]
  • -Mood: depression, apathy
  • -Behavior: Impulse control, Aggresiveness
38
Q

What is the incidence of chronic traumatic encephalopathy?

A

Symptoms between ages 30-50, risk factors = head trauma

39
Q

What are the causes of chronic traumatic encephalopathy?

A

Linked to participation in contact sports in which subjects are exposed to mild traumatic brain injury (TBI) or concussions

40
Q

What is the etiology of chronic traumatic brain injury?

A

Generalized brain atrophy: Prefrontal cortex, temporal lobes (amygdala, hippocampus), and parietal lobes. NFTs are present (neurofibrillary tangles)

Neuro Block 4 - KJ (12 decks)

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