EPPP Part 2 Skills study materials
EPPP Part 2 Skills study resources

EPPP Part 2 Skills: Biological Bases of Behavior

EPPP Part 2 Skills · Work through your exam, one topic at a time.

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Biological Bases of Behavior

Biological Bases of Behavior carries a large share of Part 2 vignettes because the exam asks you to apply neuroscience to a clinical decision rather than to recall a diagram. Expect stems about sudden-onset confusion in an older adult, medication side effects, lateralized cognitive findings, or a behavior traced to a specific neurotransmitter system. Your job is to name the mechanism and predict the next clinical step.

Localization and laterality

  • Left hemisphere: language (Broca area in inferior frontal cortex; Wernicke area in superior temporal cortex), sequential processing, verbal memory.
  • Right hemisphere: visuospatial processing, prosody, sustained attention; right parietal lesions classically produce left hemispatial neglect.
  • Frontal lobes: executive function, inhibition, insight; temporal lobes and hippocampus: declarative memory consolidation; occipital cortex: primary visual processing.
  • Subcortical: basal ganglia (Parkinson's, Huntington's), thalamus (relay station; infarcts can cause amnesia), cerebellum (coordination).

Neurotransmitters and clinical correlates

  • Acetylcholine: nucleus basalis of Meynert degeneration in Alzheimer's disease; anticholinergic drugs (oxybutynin, diphenhydramine) can precipitate delirium.
  • Dopamine: mesolimbic and mesocortical pathways, psychosis; nigrostriatal pathway, movement and extrapyramidal symptoms; tuberoinfundibular pathway, prolactin inhibition.
  • Serotonin: SSRI action and serotonin syndrome (clonus, hyperreflexia, agitation, hyperthermia); norepinephrine: locus coeruleus, arousal.
  • GABA: benzodiazepines and alcohol; withdrawal reduces inhibition and can be lethal. Glutamate: NMDA receptors and excitotoxicity.

Worked example

A 72-year-old woman is brought in with two days of fluctuating confusion, inattention, and vivid visual hallucinations after oxybutynin was added for incontinence. Ask two questions. Is onset acute with attention impaired? Yes, which indicates delirium, not dementia, because dementia is insidious and attention is preserved early. Is there a culprit drug? Yes, anticholinergic burden. Correct action: identify and stop the offending agent, treat underlying causes, provide environmental support and orientation. Anchoring on a new dementia diagnosis would miss a reversible cause.

Traps

  • Equating memory loss with dementia and missing delirium's fluctuating course.
  • Confusing neuroleptic malignant syndrome (rigidity, bradyreflexia, later onset) with serotonin syndrome (clonus, hyperreflexia, earlier onset).
  • Assuming left-hemisphere language dominance for every client; laterality is probabilistic and should be assessed.
  • Attributing depression in older adults to normal aging instead of treating it, when depression can mimic cognitive decline.