Limbic System II Flashcards by Kayla Schenheit

What causes Urbach-Wiethe disease?

Bilateral Amygdala lesions

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What symptoms are associated with Urbach-Wiethe disease?

[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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What are the symptoms of PTSD?

Re-experiencing phenomena (flashbacks)
Avoidance (of situations similar to original trauma)
Hyperarousal (hypervigilance - high anxiety)

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What is the etiology of PTSD?

Inc. amygdala activity (in fMRI)!

- Dec. medial prefrontal cortex activity

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

It plays a role in inhibiting the amygdala in PTSD.

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What does imaging show in Parkinson’s?

Dec. in neurons in the substantial nigra

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What are the core features of schizophrenia?

Fragmentation of mood, thought and movement.

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What are positive and negative symptoms of Schizophrenia?

Positive - delusions, hallucinations

Negative - social withdrawal

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What is the incidence of schizophrenia?

1% of US population

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

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

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What does haloperidol do?

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

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What are the side effects of anti-psychotic haloperidol?

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

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What is clozapine?

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

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What is clozapine’s mechanism?

It blocks DA recpetor: rapid off rate
Blocks 5HT receptors
Blocks glutamate reuptake (increases glutamate in synapse)

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What is the “glutamate hypothesis”?

-Schizophrenia somehow causes a block in NMDA glutamate receptor

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What is Phencyclidine (PCP)?

“Angel dust” - blocks NMDA glutamate receptor

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

Increase glutamate receptor activity!

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

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

- 15% of individuals, 20% of women

What is the “monoamine” hypothesis of depression?

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

What are the three main mechanisms for anti-dpressants?

Monoamine Oxidase (MAO) inhibition
Tricyclics (Imipramine)
SSRIs (Fluoxetine)

What do anti-depressants try to do?

Increase NE or 5-HT!

What do SSRIs (Fluoxetine/Prozac) do?

-Serotonin Specific Reuptake Inhibitors

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

What do tricyclics (Imipramine) do?

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

What is monoamine oxidase (MAO) inhibitors?

Inhibit metabolism/degradation of NE or 5HT.

What causes Korsakoff's Syndrome?

- Chronic Alcoholism --> leads to: | - Vitamin B1 deficiency (Thiamine)

What is damaged in Korsakoff's syndrome?

Mammillary body or mamillothalamic tract.

What symptoms does Korsakoff's syndrome cause?

- Disorder of immediate memory (no new memories) - Disorientation (in space & time) - Confabulation (respond to "Where are you?" by making up a place)

What deficits does Kluver-Bucy Syndrome involve?

- Described in monkeys | - Bilateral surgical removal of amygdala, hippocampus and temporal cortex (much of temporal lobe)

What clinical conditions can cause bilateral medial temporal lobe damage?

Encephalitis, Stroke, etc.

What are the symptoms of Kluver-Bucy Syndrome?

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]

What is alzheimer's dementia?

Chronic pressive deterioration of brain with district developmental stages.

What are the symptoms of Alzheimer's dementia?

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

What is the incidence of alzheimer's?

>85 years, 50% will have AD

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

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)

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

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

What is chronic traumatic encephalopathy?

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

What are the symptoms of chronic traumatic encephalopathy?

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

What is the incidence of chronic traumatic encephalopathy?

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

What are the causes of chronic traumatic encephalopathy?

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

What is the etiology of chronic traumatic brain injury?

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