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47 Cards in this Set
- Front
- Back
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What is Amnesia?
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Memory deficit for facts/data
Can be either episodic or semantic Caused by damage to medial temporal areas, medial diencephalic areas, or both |
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What is Anterograde Amnesia?
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Loss of information acquired after onset
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What is Retrograde Amnesia?
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Loss of information acquired before onset
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What are the four features of anterograde amnesia?
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1. Working memory is intact: ability to hold small amounts of information briefly as a task is performed
2. Global loss: regardless of modality or material. 3. Impairment of memory for new events and facts. 4. Learning and expression of skilled performance is intact (procedural memory). |
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What is repetition priming?
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Facilitation of performance based on previous experience with a task.
Ex: word stem completion task |
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What are the four features of retrograde amnesia?
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1. Temporal extent varies with the cause.
2. Temporal gradient: more recent information often more affected than remote information. 3. Over-learned information from early in life tends to be spared. 4. Skilled performance is spared. |
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What is short term memory?
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Usually refers to memories that last less than a few minutes.
STM--> modernized/refined into "working memory" |
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What is long term memory?
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Usually refers to memories that last more than a few minutes.
LTM--> the 3 stage process of storing/using information |
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What are remote memories?
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Memories for long past events.
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What are the stages of memory?
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1. Encoding: provess of placing information into memory storage for later retrieval.
2. Consolidation: "keeping it there" 3. Retrieval: "pulling it out" |
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What is declarative memory?
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The conscious recall of facts or events/experiences
Semantic vs. Episodic |
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What is procedural memory?
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Memory for skills that occur without conscious mediation.
Explicit vs. Implicit |
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What are the two main areas involved in memory?
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Medial temporal lobe area
Medial diencephalic area |
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What is the medial temporal lobe area?
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Hippocampal system
Hippocampal formation: hippocampus, dentate gyrus, and subiculum Parahippocampal gyrus: several cortical areas with connections to the HF, entorhinal cortex (most important), multimodal/association cortex, secondary association cortex. |
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What is the role of entorhinal cortex in memory?
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major input/relay between association cortex and the hippocampal formation
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What is the role of the multimodal/association cortex in memory?
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integrating information from multiple modalities.
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What is the role of the secondary association cortex in memory?
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unimodal, processes information from modality
elaborates |
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What is the role of the medial temporal lobe area?
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Additional major output pathway of HF is the fornix
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What is the role of the fornix?
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carries output information to diencephalon and septal nuclei.
Fornix physically links medial temporal lobe area and medial diencephalic area. |
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What are common causes of amnesia?
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Medial temporal lobe damage: stroke, hypoxia/anoxia, closed head injury, Alzheimer's disease
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What is Herpes Simplex Encephalitis?
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Can cause amnesia
Most common form of viral encephalitis in the U.S. Symptoms: confusion, aphasia, agnosia that gradually resolves to amnesia. Damage to medial/lateral temporal lobe Lesions may be asymmetric (thus, greater verbal or nonverbal deficits) Ex: Clive (semantic memory is spared, episodic memory is impaired), can still play music because of procedural memory skills, knows he loves his wife. |
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What are the structures of the Medial Diencephalic areas?
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Fornix (3 main targets)
1. Mamillary bodies 2. Septal nuclei 3. Anterior thalamic nuclei of thalamus. Dorsal medial nucleus of thalamus also important in memory function. |
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What is Kosakoff's syndrome?
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Cause: Severe thiamine (Vitamin B) deficiency from chronic ETOH abuse and malnutrition
Cell death in the medial diencephalic areas; frontal lobe atrophy. Symptoms: severe memory deficits and personality changes. AA & RA; RA is temporally graded Personality: irritability, apathy, impaired judgement, disinhibition |
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What is procedural memory?
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Different types may involve different brain areas or symptoms.
Skill learning: basal ganglia, cerebellum, motor cortex, posterior parietal cortex (dorsal pathway). Priming: several cortical areas Classical Conditioning: variety of structures, including cerebellum, amygdala, spinal cord non-associative learning: same as classical conditioning |
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What is a "new way" to think of procedural memory?
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Sequence learning: basal ganglia, supplementary motor cortex
Perceptual motor integration learning: posterior parietal cortex, premotor cortex discovered by: Daniel Willingham (University of Virginia) |
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What are the basic divisions of the frontal lobes?
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Premotor
Motor (precentral gyrus) Prefrontal (33% of the entire brains cortex) |
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What are frontal-subcortical circuits?
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A series of parallel frontal-subcortical circuits link frontal regions to subcortical structures.
Circuits are contiguous but remain anatomically segregated. |
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What are the 3 types of frontal-subcortical circuit syndromes?
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1. Dorsolateral prefrontal syndrome: Executive function deficits and motor programming abnormalities.
2. Orbitofrontal syndrome: personality changes. 3. Anterior Cingulate syndrome: Apathy |
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What are dorsolateral prefrontal syndromes?
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Impairment in executive functions (plan and implement actions towards a goal, flexibility, sequence and prioritizing, proper social interactions).
The abilities are compromised most commonly after damage to the frontal lobe or dorsal lateral prefrontal circuit. |
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What are the categories of executive function deficits?
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1. Deficits in initiation, cessation and control of action.
2. Impairments in abstract and conceptual thinking. 3. Lack of cognitive flexibility and deficits in the response to novelty. 4. Deficits in goal-directed behavior. |
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Explain deficits in initiation, cessation and control of action.
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Psychological Inertia: tendency of body at rest to stay at rest or of a body in motion to stay in motion unless acted on by an outside force.
Initiation difficulty: difficulty starting something (stereotype of a coach potato) Perseveration: difficulty stopping something. |
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Explain impairments in abstract and conceptual thinking.
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Understanding proverbs (can also be effected by education)
Ex: How are two words similar? |
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Explain lack of cognitive flexibility and deficits in response to novelty.
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Cognitive flexibility: ability to look at situations from multiple vantage points and produce a variety of behaviors.
Ideational fluency: old association must be broken and new ones formed. |
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Explain deficits in goal directed behaviors.
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Ability to sequence: What comes before/after, ability to choose which sequence/strategy best allows goal to be reached
ability to shift set and modify strategies: reaching a goal is not always a simple linear progression. ability to self-criticize or self-monitor: "How am I doing?" |
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what is orbitofrontal syndrome?
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"Personality changes" or "changes in emotional control"
Ex: Phineas Gage |
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Where is emotional controlled/regulated in the brain?
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limbic system and anterior cingulate gyrus
regulator: orbitofrontal cortex |
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What is environmental dependency syndrome?
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Behavior triggered by an object in the environment
(described as impulsive) |
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Explain anterior cingulate syndrome.
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Marked apathy
Akinetic mutism (disturbance in motor activity and speech) Lesions to supplementary motor area, can produce "alien hand syndrome" |
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Explain working memory.
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Dorsolateral prefrontal cortex thought to be critically important
Monkey research |
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Explain the epidemiology of TBI
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600,000 new cases/year.
10% require hospital stays 20+ days. Est. that 1-2 million living Americans have sustained moderate-severe trauma Most common in adults <30 years. Caused mainly by MVA's. |
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Explain Penetrating Head Injuries.
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Brain damage via a penetrating mechanism (bullet, knife)
Technically includes injuries that involve skull fractures only, but clinical presentation is more consistent with that of CHI. More often associated with fatalities |
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Explain Closed Head Injury
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Brain damaged because head forcefully comes into contact with another object: does not involve a penetrating wound.
Skull relatively intact. |
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Explain the Neuropathological Effects of a PHI
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Primary Injury: destruction of tissue at site of entry and along path of object, often causes intracranial bleeding and meningeal laceration.
Potential Secondary Effects: destruction of brain tissue during debridement, Ischemia, Edema, Infection, Post traumatic Epilepsy. |
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Explain the Neuropathological Effects of a CHI
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Primary Injury:
-Contusion (bruise): Coup/countercoup, most common damage in the orbitofrontal lesion, frontal pole and anterior temporal region. -Diffuse Axonal Injury: widespread injury often due to shearing as a result of acceleration-deceleration injury. Lesions often involve brain stem, corpus callosum, and white matter. Potential Secondary Effects: Ischemia, Edema, Subdural hematoma, intacerebral bleeding, increased intracranial pressure, hypoxia, post traumatic epilepsy |
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Explain how to measure the severity of a TBI.
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-Loss of Consciousness (LOC): not much consensus.
- Glassgow Coma Scale (GCS): scale from 3-15, bad indicator for mild injury (must score a 13), moderate injury 9-12, severe injury 3-8 -Post traumatic amnesia: disturbance of memory for events that occur immediately following a head injury, interested in length of PTA (episodic vs. semantic memory) <5 min = very mild, ,1 hr = mild, 1-24 hrs = moderate, > 24 hours = severe, 1-4 weeks = very severe. |
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What are the neuropsychological effects of TBI?
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Varies from patient to patient.
Immediately after: disorientation, poor attention, post-traumatic amnesia. Long-term: difficulty with abstract thought and conceptualization, decreased attention, decreased cognitive flexibility, decreased planning abilities, and decreased long term memory |
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What are the behavioral effects of TBI?
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disinhibition
apathy loss of patience agitation or increased temper emotional lability depression |
