Behavioral Neuro EXAM 2

Phoneme

The smallest unit of sound in a language that distinguishes words (e.g., "p" vs. "b").

Morpheme

The smallest unit of meaning in a language (can be a word or word part, like prefixes and suffixes—e.g., "un-", "-ed").

Syntax

The set of rules that determines the order of words and phrases in a sentence; governs sentence structure

Infant phoneme perception

Can distinguish all phoneme contrasts in any language, but after one year, lose this ability, focusing on their native language's sounds.

Adult phoneme perception

Mostly perceive and distinguish phonemes from their native language; struggle with non-native contrasts.

Phonotactic rules

Language-specific constraints that determine permissible combinations and order of sounds (phonemes) in syllables or words.

Universalist infant

Initially, perceive speech sounds from all languages; this broad ability narrows to native language sounds as they grow.

Formant frequency

Resonant frequencies of the vocal tract that shape speech sounds (especially vowels); distinguish different vowel sounds.

Critical period for language

A time in early life when the brain is highly capable of learning language; after this period, language fluency is much harder to achieve.

Language lateralization and handedness

For most people, language is in the left hemisphere—about 95% of right-handed people, 70% of left-handed people.

Right hemisphere and language

Involved in emotional tone (prosody), sentence organization, meaning from context; damage affects understanding jokes, emotion, and sentence order.

Behavioralist approach to language acquisition

Language is learned through imitation, reinforcement, and interaction with the environment (Skinner).

Innate-grammar approach

Language ability is biologically hardwired (Chomsky); children are born with an internal universal grammar, activated by exposure.

Transitional probability

The likelihood one syllable follows another in speech; used by infants to find word boundaries in continuous speech.

Broca’s aphasia

Non-fluent, effortful speech with grammatical and repetition impairment but relatively preserved comprehension; involves the inferior left frontal gyrus.

Wernicke’s aphasia

Fluent but unintelligible speech ("word salad"), poor comprehension; involves posterior left auditory association cortex and left posterior temporal lobe.

Conduction aphasia

Fluent speech and good comprehension, but trouble repeating sentences verbatim and assembling phonemes; involves left superior temporal gyrus and inferior parietal lobe.

Global aphasia

Nearly complete inability to comprehend or speak, but automatic speech may be preserved; involves widespread damage, often middle cerebral artery stroke.

Transcortical aphasia

Transcortical motor: non-fluent, impaired spontaneous speech, but repetition spared; Transcortical sensory: fluent speech, impaired comprehension and naming, repetition spared; involves areas near but sparing main language areas.

Broca’s area

Responsible for speech production, grammar, and sentence formation; damage leads to impaired speaking and writing.

Wernicke’s area

Responsible for language comprehension (spoken/written); damage causes impaired understanding and nonsensical speech.

Superior temporal gyrus

Involved in phonological processing (sound analysis).

Inferior frontal cortex

Key for speech production.

Inferior parietal lobe

Important for language acquisition and processing.

Insular cortex

Plays a role in language, especially articulation and emotional tone.

Basal ganglia

Supports motor aspects of speech.

Premotor cortex (Exner’s area)

Involved in writing.

Prefrontal cortex

Provides executive control over language.

Anterior cingulate cortex

Initiates and maintains speech.

Cerebellum

In infants, contributes to language production.

Memory, Processing Speed, and Intelligence Across Lifespan

Fluid intelligence and processing speed peak in young adulthood and decline with age; crystallized intelligence and vocabulary grow into older adulthood and remain stable or improve; working/episodic memory declines with age while semantic memory is stable or improves.

Mild Cognitive Impairment (MCI)

A condition involving measurable cognitive decline with preservation of daily function; about 15% develop Alzheimer’s disease within a few years; over time, 50% or more will progress to dementia.

Genetic Factors and Lifespan

Genes control cell aging and repair mechanisms, activate longevity genes rare genetic syndromes can dramatically reduce lifespan; many genes interact with lifestyle and environment to influence longevity.

Lifespan Changes Over 100 Years

In 2025, U.S. life expectancy is around 80 years; worldwide it has doubled since 1900, now about 73 years.

Synaptic Density Lifespan Changes

Synaptic density rises in infancy, peaks in childhood, is pruned in adolescence, stabilizes in adulthood, and declines during aging; age-related brain changes involve synaptic loss rather than neuron loss.

Dementia Types

Alzheimer’s disease (most common—progresses from memory loss)

vascular dementia (due to reduced blood flow/strokes)

frontotemporal dementia (personality/language changes)

Lewy body dementia (hallucinations/movement issues)

Parkinson’s disease dementia.

Pathological Changes in Alzheimer’s Disease

Extracellular amyloid beta plaques

intracellular neurofibrillary tangles (hyperphosphorylated tau)

neuron/cortical loss (especially in hippocampus and cortex)

cholinergic neuron loss, cerebral amyloid angiopathy, gliosis/inflammation, genetic risk (APP, presenilins, ApoE4).

Amyloid Beta Plaques

Aggregates of amyloid beta peptides (mainly Aβ40 and Aβ42).

Neurofibrillary Tangles

Aggregates of hyperphosphorylated tau protein, a microtubule-associated protein.

Secretases and Alzheimer’s Disease

Alpha-secretase is protective, cleaving APP to block toxic Aβ formation;

beta-secretase (BACE1) and gamma-secretase create Aβ, promoting plaque formation.

Alzheimer’s Disease Prevalence and Incidence

In 2025, more than 7.2 million Americans (11% of 65+) and about 55–57 million people globally have Alzheimer’s; both prevalence and incidence are rapidly rising due to aging populations.

Apolipoprotein E (ApoE) and Alzheimer’s

ApoE2 is protective

The ApoE4 allele promotes amyloid beta aggregation and decreases clearance, raising risk; ApoE4 also affects tau, cholesterol, immunity, and synaptic plasticity.

Environmental Risk Factors for Alzheimer’s

Low education

traumatic brain injury

smoking, inactivity

poor cardiovascular health, diabetes

obesity

social isolation.

Visualizing Amyloid Plaques in Living Brain

PET scanning with specific radiotracers that bind to amyloid plaques.

Lewy Body Dementia Features

Associated with visual hallucinations and REM sleep behavior disorder.

Seizure

Temporary disruption of brain function caused by excessive electrical activity in neurons.

Epilepsy

Chronic condition characterized by recurrent, unprovoked seizures.

Generalized Seizure

Seizure involving both hemispheres of the brain simultaneously.

Focal Seizure

Seizure that starts in a specific group of neurons; may spread to become generalized.

Aura

Warning sign that occurs before a seizure; seen in focal seizures.

Ictal

The period during an active seizure.

Post-Ictal

Recovery phase after a seizure has ended.

Tonic Seizure

Seizure type marked by sudden muscle stiffness and loss of consciousness.

Clonic Seizure

Seizure type marked by rhythmic jerking movements.

Absence Seizure

Brief, generalized seizure of sudden onset and termination. Usually presents as blank stare; EEG shows 3-Hz spike-and-wave discharges.

EEG Spike-and-Wave

A pattern seen in absence seizures: 3-Hz generalized spikes and slow waves across the entire brain.

Excitotoxicity

Neuronal damage and dysfunction caused by excessive excitatory neurotransmission, especially glutamate; contributes to seizures.

Paroxysmal Depolarizing Shift

Abrupt, large depolarization in a group of neurons, triggered by glutamate, GABA, adenosine, and endocannabinoids.

Convulsant

Substance or drug that increases excitation or blocks inhibition, thereby promoting seizure activity.

Anticonvulsant

Drug that blocks excitation or increases inhibition to suppress seizure activity.

GABA Receptors

Inhibitory neurotransmitter receptors; insufficient activation promotes seizures.

Glutamate (AMPA & NMDA Receptors)

Excitatory neurotransmitter and its receptors; excessive activation leads to seizure activity

(AMPA: quick excitation, NMDA: prolonged excitation).

EEG Alpha Waves

Frequency 8–13 Hz; normal relaxed wakefulness.

EEG Beta Waves

Frequency 13–30 Hz; active thinking and concentration.

EEG Delta Waves

Frequency 0.5–4 Hz; deep sleep or coma.

EEG Theta Waves

Frequency 4–7 Hz; drowsiness and early sleep stages.

Mesial Temporal Sclerosis

Atrophy and cell loss in the medial hippocampus; common cause of focal epilepsy.

Seizure Focus

Abnormal brain region responsible for initiating seizures; identified by EEG.

Status Epilepticus

Continuous seizure activity lasting longer than 5 minutes without return to baseline.

Kindling

Process where repeated, sub-threshold brain stimulation increases susceptibility to seizures over time.

Genetic Causes of Epilepsy

Mutations in genes encoding ion channels, enzymes, or neurotransmitter processes can predispose to epilepsy.

Other Causes of Seizures

Infection, trauma, genetic predisposition, structural brain abnormalities.

Thalamocortical Pathways

Axonal connections allowing spread of focal seizures via normal brain circuitry.

Focal to Bilateral Seizure

Focal seizure that spreads to involve both hemispheres, becoming generalized.

Wakefulness

EEG shows beta waves (13–30 Hz), characterized by low amplitude and high frequency.

Stage N1

(Non-REM 1, Light Sleep)

Stage N2

(non-REM 2)

Stage N3

(non-REM 3, Deep Sleep/Slow Wave Sleep)

REM Sleep (Rapid Eye Movement)

EEG features sawtooth waves resembling beta waves; characterized by vivid dreaming, muscle atonia, fast irregular EEG, and rapid eye movements.

Insomnia

Difficulty falling, staying asleep, or early awakening; common, multifactorial, treated with CBT

Fatal Familial Insomnia

Rare inherited prion disease causing progressive insomnia, autonomic and cognitive decline; no cure.

REM Sleep Behavior Disorder

Acting out dreams during REM, often in older men; linked to neurodegeneration; treated with melatonin or clonazepam.

Narcolepsy

Excessive daytime sleepiness, cataplexy, sleep paralysis due to orexin loss; treated with stimulants.

Sleep Apnea

Breathing stops during sleep, snoring, fatigue; common in obesity; treated with CPAP and lifestyle changes.

Restless Legs Syndrome

Urge to move legs, worse at night/rest, associated with dopamine and iron; improved by drugs and iron supplements.

GABA and Galanin

Neurotransmitters that promote sleep.

Orexin/Hypocretin

Neurotransmitter that keeps you awake; its loss leads to narcolepsy.

Acetylcholine

Triggers REM and dreaming.

Monoamines (Serotonin, Norepinephrine, Histamine)

Promote wakefulness.

Circadian and Homeostatic Drives

Systems that regulate sleep and dreaming; circadian is driven by the SCN, homeostatic by sleep debt/adenosine.

REM ON Cells

Cholinergic neurons in the pons, active during REM sleep.

REM OFF Cells

Serotonergic (raphe) & noradrenergic (locus coeruleus), inactive during REM sleep.

Sleep Spindles

Short EEG bursts (12–16 Hz) generated in the thalamic reticular nucleus, marking N2 sleep.

Sleep Stage Cycle

N1 → N2 → N3 (deep) → REM; each cycle lasts 90–110 minutes, early cycles have more N3, later cycles have more REM.

Physiological Changes in Sleep Stages

Stage 1: muscles relax; Stage 2: body temp drops, spindles; Stage 3: lowest heart/breathing, restoration; REM: active brain, muscle paralysis, irregular heart/breathing.

Suprachiasmatic Nucleus (SCN)

Hypothalamic master clock synchronizing body rhythms, controls sleep timing and melatonin.

Sleep Drive

The urge to sleep, determined by homeostatic buildup (adenosine/time awake), circadian timing (SCN), and external/behavioral factors.

Slow Waves Generation (NonREM)

Synchronized oscillations between up

Sleep Changes with Age

More fragmented, lighter sleep with less N3/deep sleep, earlier bed/wake times, and increased sleep disorders.

VLPO (Ventrolateral Preoptic Nucleus)

Brain region in the hypothalamus that inhibits arousal pathways to promote sleep onset.