New Final Info Flashcards
Cognition
-ability to turn external timulation to internal motivation
-identify stimui and respond
Association Corticies Inputs
-projections from primary and secondary sensory and motor, thalamus, BS
Association Corticies Outputs
-hippocampus, BG, cerebellum, thalamus
Temporoparietal Association Cortex
-cognitive intelligence
Dorsolateral Prefrontal Areas
-self awareness
-executive function
-goal setting
-plans
Medial Dorsal Prefrontal Areas
-perceives other’s emotion making assumptions
-medial and superior
Ventral Pefrontal Cortex
-connects mood and affects
-medial and inferior
Frontal Lobe Syndromes: Executive Dysfuntion and Loss of Willpower
-Dorsolateral prefrontal cortex < Caudate < GP < Thalamus
-Difficulty planning, initiating, maintaing behavior
Frontal Lobe Syndromes: Disinhibition, irritability, and Impulsiveness
Orbital Cortex < Caudate < Substantia Nigra < Thalamus
-Social judgement, inappropriate behaviors
Frontal Lobe Syndromes: Apathy
Ventral Prefrontal Cortex < Ventra Striatum < Ventral Pallidum < Thalamus
-Apathetic and lack insight
Frontal Lobe Syndromes: Paranoia, Delusions
Medial Dorsal prefrontal Cortex < Ventral Striatum < Ventral Pallidum < Thalamus
-Undrstanding others emotions and beliefs and intentions
Hemispheric Localization & Lateralization
-reduce connection times
-R hand dominance and left
-lateralization occurs at 3-4
Dominant Hemisphere
-usually Left
-motor planning
-math: sequence, analytic calc
-Music: sequential, analytic skill
-Sense of direction: following directions
Nondominant Hemiphere
-usually R
-visual spatial analysis and attention
-Math: estimate quantities
-Music: untrained musicians, complex performance
-Sense of direction: navigating using spatial orientation/awareness
Disconnection Syndromes
-leisons to white matter disrupting connections between cortical areas
Ex: conduction aphasia, corpus callosotomy (split brain procedure for epilepsy)
Consciousness System
-medial and lateral frontoparietal association cortex and arousal circuits of upper brainstem and diencephalon
-AAA: alertness, attention, Awareness
AAA
Alertness: normal functioning of brainstem and diencephalic arousal circuits
Attention: functioning of brainstem and diencephalic arousal circuits and processing frontoparietal association cortex
Awareness: subjective experiences, combine higher order systems, poorly understood
Reticular Formation
-in tegmentum and runs through entire brainstem
Midbrain and Upper Pons: continuous with nuclei diencephalon rostrally, conscious state in forebrain
Pons and Medulla: conntinuous with intermediate zone SC caudally for motor, reflex and autonomic functions
Reticular Acticating System
-in upper brainstem-diencephalic junction where lesion can cause coma with multiple interconnected arousal systems acting in parallel to keepp consciousness
Coma from:
-lesion in rostral RF and related structures
-Massive damage damage tto B cerebral cortex
-Damage to B thalamus
-more caudal or ventrtal don’t cause coma
Maintenance of Alertness
-BS noreinephrine, serotonin, dopamine, ACH, RF w/ glutamate projections
-Posterior hypothalamic neurons
-Basal forebrain
Attention
-brain processes that allocate resources to what matters
-frontoparietal assoxiatiooon cortex
-anterior cingulate gyrus, amygdala, limbic structures
Sustained: viligance, concentration, non distractibility
Switching: change from one task to the other
Selective: able to focus on more than 1
Divided: by performind 2 or more tasks
Dominant Side Language
-Comprehension: wernicke’s, left side
-Motor Planning and production: Broca’s, left
-Angular Gyrus: connected to wernicke’s for comprehending spoken and written language
Non-Dominant Side Language
-Wernicke’s equivalent on R side: comprehends emotional or tone of voice and facial expressions
-Broca’s equivalent on R side: use of different tones and gestures of communication
Wernicke’s Aphasia
-can form words but do not make longical sense as a language
Broca’s Aphasia
-understands what they want to say but cannot find the words
Logorrhea
-excessive wordiness and repetiveness
Verbal Perservation
-repetittive spoken words
Confabulation
-patient generates a false memory without the intention of deceit
Alexia/Dyslexia
-rerading disorders
Agraphia
-inability to right
Dysarthria
-difficulty speaking because the muscles you use for speech are weak
H.O.M.E
-Homeostasis
-Olfaction
-Memory
-Emotional drives
Limbic Cortex
-corpus callosum
-cingulate
-uncus
-parahippocampal gyrus
-temporal pole
-medial orbitofrontal gyrus
-insula
-hippocamppus
-amygdala
Olfaction
-olfactory n. < olfactory bulb < olfactory tract < primary olfactory cortex < amygdala < olfactory tubercle
Working Memory
-short term storage and handling info
-goal relevant
-need for language, prooblem solving, reasoning, multi tasking
-lateral prefrontal cortex
-temporparietal ass cortex
Declarative Memory
-memories that can be verbalized (explicit memory)
-recongnizes memory for longer term storage
-not stored in medial temporal lobe
-starts in thlamus selecting inut from temporoparietal ass cortex, encoded into med temporal lobe
- Encoding: processing, enhanced by attentiveness, arousal, reviewing
- Consolidation: stabilization of memories
-synapses through long term pootentiatioon (min-hr)
-systemic through med temporal lobe (min-decade) - Retrieval
Declarative Memory: Lobes
Medial Temporal Lobe:
-hippocampus
-fornix: connects hippocampus to mammilary bodies and thalamus
-parahippocampal gyrus
-activated <12yrs
Lateral Prefrontal Cortex:
-voluntary control over medial temp in processing and organizing
-access stored info
-analyzes language
-Retrieval: searches and verifies encooded memories in med temporal
-activated 13+yrs
Episodic Declarative Memory
-personal events
Semantic Declarative Memory
-learned common knowledge unrelated to personal events
Procedural Memory
-implicit or nonconscious
-harder to verbalize
-learned skills or habits
-perceptual skills
Learning Motor sequence: motor and parietal cortices and striatum
Learned Mmt sequence: sup motor areas and putamen/GP
- Cognitive
- Associative
- Automatic
Amnesia
-loss of declarative memory
Retrograde Amnesia
-looses memories prior to injury
-can create new memories
Anterograde Amnesia
-looses memories after injury
-post traumatic amnesia
-cannot create new mems
Separation of Procedural and Declarative
-allow ppl to learn subconsciously w/o remembering learning
-encodes enough info to be able to form mems
Remote Memory
-long term memory
Goal Directed Behavior
-make goal, plan, execute, monitor plan
Lateral PFC: goal directed behavior and working memory
-inhibits bad behavior
-formulates posibilities
Lateral PFC < head of caudate < GPe and PGi < Thalamus
Emotion
-short term subjective experience
-can influence perceptions and actions
-can trigger physiologic responses
Mood
-enduring subjectiv eongoing emotional experience
Emotion Structures
-amygdala
-Medial prefrontal cortex
-thalamus: sadness and depression
-anterior insula: awareness of feelings and internal stimuli
-emotion loop BG
Medial PFC < ventral striatum < thalamus
Amygdala
-produces fear, disgust
-interprets social signals
-important for social behavior and emotional learning
Emotional Regulation
Automatic: subconscious, ignoring, leaving
Voluntary: conscious, choosing to control emotions
Social Behavior
-ventral PFC
-connects with regions ass with mood
-steers behaviors and inhibits undesireable, activates ANS
Ventral PFR < Head caudate < Sub nigra < thalamus
-detects relevant info, self control, understands social disapproval (self awareness)
Affect vs Mood
-mood: feeling
-affect: what i’m showing
Somatic Marker Hypothesis
-gut feelings
Emotional/Social Intelligence
-ventral premotor
-amygdala
-ant insula
Stress Response
-disruption of 3 systems
-restores after response but can linger due to feelings/thinking
-Somatic: motor neurons increase tension
-ANS: sympathetic activity sends blood flow to muscles and reduces central
-Neuroendoocrine sys: adrenal medulla to release epi
Loss of Goal Directed Behavior
-lack of initiation and follow through
-seen as uncooperative or noncompliant
Apathy
-lack of emotion and insight
-may not care to eat or drink
Emotional Labile
-uncontrolled crying or laughing
-impaired reg of social behaviors
-delusion, mania, depression, anxiety
Personality
Extraversion: ventral PFR
Neurotocism: amygdala, cingulate, medial PFC, hippocampus
Agreeableness: temporoparietal ass, cingulate
Conscientiousness: lateral PFR
Intellect
-develop concepts into reason
Function of ANS
-homeostasis and reproduction (HR, breathing)
-activity of internal organs (metabolism, digestion)
-activity of blood vessels
-Reflexes
Overview of ANS
-Mostly efferent axons not under conscious control of glands, muscles
-afferent carry info from organs to CNS
-controlled by hypothalamus
SNS: T1-L3
PNS: BS, S2-S4
ANS Flow of Info
Visceral/Vascular receptors < Limbic sys, hypothalamus, RF, SC < SNS, PNS, Hormones
ANS Receptors
Mechanoreceptors:
-BP in aorta, carotid sinus, lungs
-Stretch in veins, bladder, intestines
Chemoreceptors:
-02 in carotid and aortic bodies
-H/Co2 in medulla
-GLucose/electrolytes in hypthal
Nociceptors:
-damage to tissue walls and viscera
Thermoreceptors:
-changes in blood temp in hypthal
-external changes to skin
ANS Afferent Pathways
-enter through SC
Visceral Afferents: ascending neurons to BS, Hypthal, thalamus
-CN 7 & 9 Taste
-CN 9 & 10 Viscera: into solitary nucleus of medulla and pons
Visceral Nocicepive: nociceptive tracts relating to referred pain
-cause muscle guarding
BS control of ANS
Medulla: regulation through autonomic efferents in SC and vagus n
-HR, RR, vasoconstrictionn/dilation
Pons: respiration
Diencephalon and limbic role in ANS
-modulation of BS autonomic control
-hypothal
-most visceral input to thalamus is through limbic system
Divisions of ANS
Main:
-SNS: fight or flight
-PNS: rest and digest
Enteric NS: in gut for GI secretions and digestion
Cholinergergic Neurotransmitters
-acetylcholine
-all preganglionic neurons on ANS
-PNS post ganglionic neurons
Adrenergic Neurotransmitters
-Norepineophrine: most SNS postganglionic neurons
-Epinephrine: adrenal medulla
dopamine is precursor to norepinephrine and epinephrine
Preganlionic FIbers
-AB fibers
-neuron from CNS to ganglion
-acetylcholine
Postganglionic FIbers
-C fibers
-neuron from ganglion to effector organ
-acetylcholine (PNS) or norepinephrine (SNS)
Sympathetic NS (pre/post)
Preganglionic Neurons: cell bodies in lateral horn (T1-L3) exit through ventral root
-synapse w/ post neuron in communicating ramus (acetylcholine)
Postganglionic Neurons:
1. Cell bodies in sympathetic trunk to innervate smooth muscle and glands
2. Unpaired cells in ganglia < segmental spinal ganglia < abdominal and reproductive organs
- travel longer distances and closer to organs
Sympathetic NS Efferents
Efferents to Body:
-1 to adrenal medulla
- 2 tracts to periphery and viscera via paravertebral ganglion
- 2 tracts to abdominal and pelvic organs via paravertebral ganglion
T5-L2 pass through trunk w/o synapsing
Efferents to Head:
-originaes in hypothal and synapses in upper thoracic
-preganlionic fibers from upper throacic to cervical (stellate) ganglia via SNS trunk
SNS Function
-promote circulation to organs (increased SNS constricts, decreased dilates)
-fight or flight (dilation to muscles/lungs, contriction to gut, increase BP, BV, glucose)
-body temp regulation (sweating, goosebumps, dilation of skin BV)
Parasympathetic NS
-from BS to sacral cord lateral horns (S2-S4) < to end organs
-ganglia not interconnected like SNS
Preganlionic Neurons:
-BS Nuclei: CN 3 Edinger Westphal nuc, CN 7 superior salivatory nuc (lacrimal glands), CN 9/10 inferior salivatory nuc and nucleus ambiguus (salivary glands), CN 10 dorsal motor nucleus of vagus (heart, lungs, GI)
Lateral Horn S2-S4:
-pelvic nerves to B/B and external genitalia
PNS Function
-BS: rest and digest (constriction of pupils/lungs, decreased HR, digestion, glycogen synth)
-Sacral: regulates emtying of B/B and erection of penis and clitoris
SNS and PNS Synergy
-some actions are balanced by both systems
-some SNS activities controlling limbs and fac are not countered by PNS
-pupil contriction by PNS not countered by SNS
Breathing Rhythm Generator
-ant medulla blances arousal vs calm
-locus coeruleus responsible for arousal and alertness
-slow breathing inhibits locus c
Freeze, Fight, Flight
Freeze:
-co activation for SNS and PNS to prepare for action and optimize perception of threat
-amygdala recognizes threat < hypothal and ant medulla stimulate SNS < amygdala activates PNS for vagus to decrease HR and medulla to inhibit muscle contractions
Fight/Flight: PNS output decreases and SNS increases
Horner’s Syndrome
lesion of SNS preganglionic n to face ipsi, decreases adrenergic activation of nociceptors
-ptosis: droopy eyelid
-enopthalmos: sunken eye
-miosis: constricted pupil
-imaired sweating
-skin vasodilation (redness)
Peripheral Nerve Injuries
-SNS efferents affect circulation, breathing, sweating in area
SC Injuries
-depends on level and completeness
Complete in lumbar:
-B/B and sexual function
Complete injuries above T5
-homeostasis and temp, BP control
-Autonomic dysreflexia
Autonomic Dysreflexia
-irritantt below level of lesion causes ascending sympathetic unable to reach brain foor inhibition of BP
-contriction of BV and rapid BP increase
-skin below lesion is pale, above is red
-HR slows
-must induce orthostatic hypotension and check irriant
-cannot be stopped once it starts
Brainstem Injuries
-impaires efferent control of BP, HR, R
-dysfunction of CN nuclei
Cerebral injuries
-damage to nuclei in hypothal interferes with homeostasis
Orthostatic Hypotension
-decrease of 20 systolic and 10 diastolic, increased HR
-pooling of blood in limbs
-baroreceptor reflex to contric arteries
-fainting can be gravity reduced
Cause:
SCI, parkinson’s, neuropathy
Syncope
-fainting fom lack of blood flow to brain
Neural reflecive:
-emotional distress or pain or pressure on carotid sinus
-Vasovagal: medulla inhibits SNS and reduces HR
Orthostatic hypotension
Cardiac: arrhythmias or structure
Peripheral Vestibular System
-Vestibular Apparatus
-Semicircular Canals
-Otolithic Organs
Central Vestibular System
Pathways: vestib ganglion < vestib nuclei
-Medial longitudinal fasciculus
-Vestibulospinal tracts (med/lat)
-Vestibulocolic
-Vestibulothalamocortical
-Vestibulocerebellar
-Vestibulorecticular
Vestibulocerebellum
Vestibulocortex
Vestibib Nuc
Vestibular Apparatus
Semicircular Canals: ant, pos, horizontal
-each with an ampulla
Otolithic Organs: utricle, Saccule
Membranous Labyrinth
-separated by perilymph fluid
-filled with endolymph
-hair receptor cells bend with mmt
Semicircular Canals
-Ampulla that contains a crista with a cupula (gelatanous structure containing hair)
-hairs constanly fire AP when at rest and with head mmts to give information about the body in space
-only actively move during rotation of head
Horizontal: head rotation (no)
Ant and Post: pitch and roll (yes)
-R and L Posterior and anterior work in same plane
Ex: Turn to the L, L endolymph shifts toward kinocilium (activating), R endolymph shifts away froom kinocilium
Otolith Organs
Urtricle and Saccule: membranous sac that responds to linear acceleration/decceleration
-have a macula that contains hair cells embedded in a gelatinous mass with microscopic cristals (otoliths) on top
-displacement of otoliths sttimulate neurons
Uricle: Horizontal mmt
Saccule: vertical mmt
Cervical-Ocular Reflex
-postural adjustments of head in response to SCC
-substitution for VOR when absent
Vestibulo-Spinal Reflex
-postural tone and adjustments of the body for balance while maintaining equilibrium
Medial Longitudinal Fasciculus
-Bilateral connections to extraocular eye muscles and superior colliculus
Cerebello-Thalamocortical Pathways
-ascending pathway
-lateral and superior vestib colliculi < thalamus < posterior parietal cortex
Vestibular System Function
-provides CNS info of head and body
-stable visiono while head is moving
-internal refernce to determine appropriateness of sensory info
Vestibulo Occular Reflex
-head and eyes move in diff direction to maintain view
-opp lateral rectus activate to move eyes in same direction
Activation of hair cells
-movement that bends hair toward kinocilium causes depolarization and activation
-movement that bends hair away from kinocilium causes hyperpolarization and deactiviation
Otolith Ocular Reflex
-input from otoliths
-output to eye muscles
-controls horizoontal and vertical eye mmts
-via linear VOR
Benign Parooxysmal Positional Vertigo
-BPPV
-most common
-crystals from utricle or saccule (MC) fall into SCC (PSCC MC)
-cause change in endolymh viscosity and fire nerve signals
-brief vertigo and nystagmus
Canalithiasis (MC):
-otoconia fall off and free float in PSCC
-latent onset of vertico and nystagmus after provoking
-disappears in 1 min
Cupulolithiasis:
-otoconia fall off and adhere to cupula of PSCC making cupula denser around endolymph
-immediate vertigo is persistent until head moved
-nystagmus
Nystagmus
-non voluntary rhythmic oscillation of eyes
-named by fast phase
-can be suppressed by fixation
-viewed with frenzel or infared goggles
CNS:
-smooth pursuit and saccades (cerebellum and brainstem)
-often follows gaze
-typically vertical, constant
Peripheral Vestib:
-Slow phase: VOR
-fast phase: corrective saccade
-usually horizontal
BPPV:
-named by torsion (canal) and rotary component toward lesion
-Upbeat and rotary for PSCC
Physiologic: induced by normal stimuli; spinning
Pathologic: abnormal, 4 types
Neuritis/Labyrinthitis
Neuritis: no hearing loss
Labryrinthitis: hearing loss and tinitis
-infection/inflammation causing hypofunction
-fireing rate affected
-long lasting 3-7d
-nystagmus fixed on good side in all 3 degrees of gaze
Acoustic Neuroma
-tumor on cochlear n
Endolymphatic Hydrops/Meniere’s
-chroonic condition of inner ear
Fistula/Dehiscence
-trauma, fluid exchange, tears
Vesibular Hypofunction
-damage to inner ear or vestib n
-affects VOR and VSR
-unilateral: dizzy
-bilateral: moving images
Spontaneous Nystagmus
-cns or pns vestib problem
Positional Nystagmus
-paroxysmal or static
-Torsional: BPPV or brainstem
-Down/upbeat: cerebellar dysfunction
Gaze evoked Nystagmus
-eyes drift toward center, contantly corrective
Congenital Nystagmus
-birth
Neuroplasticity
-neural capacitty to alter brain function, neurotransmitters and structure
-memory and learning
-healing from damage
Mechanisms: habituation, new experiences, recovery after injury
Learning
-change in behavior from knowledge and practice
-process of acquisition
Memory
-process that knowledge is encoded, stored and recalled
-product of learning
Motor Learning
-learning new strategies from moving
-permanent changes in behavior
-increases activity of thalamocortical pathways
-parallel pathways aid in efficiency and redundancy
Performance
-temporary change in motor behavior
Habituation
-simple form of neuroplasticity
-supression of repetitive non-noxious stimuli
-after rest, response can be ilicited to same stimulus
Short term: changes in neurotransmitter and concentration of Ca
Long term: repeated stimulation causeing structural changes
Sensitization
-strengthening response to stimuli preceded by noxious stimuli
-more complex than habituation
-alters K+ allowing longer AP and more neurotransmitter
Long term: increased strength of existing, new proteins, new synapses, modified current synapses
Assoociative Learning
-person can predict association
-conditioning
-2 neurons activated causes protein altering
Long term: new protein synthesis with formation fo new synapses
Classic Conditioning
-1 stimulus to another
-weak stumulus and response paired with stronger stimulus
-pavlov
Operant Conditioning
-behavior to consequences
-trial and error: behavior shaped by internal throughts and motivation
-consequences: reinforcement to strengthen behavior and punishment to weaken
Implicit Procedural Learning
-skills and habits
-must be performed by learner
-basal ganglia loops
Explicit Learning
-coonscioous processes with end product of acquiring knowledge
-prefrontal cortex, limbic
Long Term Potentiation
-similar to pottentiation
-requires stimuli at the same location
-weak is facilitatied if stimulated in ass with stronger (associativity, specificity and cooperativity (pre and post working together))
-increased neurotransmitter
Shorter term: functional changes only
Long term: protein synthesis
Hippocampus and temporal lobe for spatial memory that can be verbalized
Long Term Depression
-similar to habituation
-acticate weak synapses
Specificity
-only highly actice will exibit LTP
-selective memory
Cooperativity
-requires >1 neuron working togetther
-pre and post together
Associativity
-contributing fibers and post synaptic cells working together
Implicit and explicit memory
-can shift between each
-used in most learning activities
Early Cognitive Phase
-high attention
-activation inc then dec in dorsolateral PFC, sensorimotor coorticies, parietal and cerebellum
-sesnory feedback
-performance witth rapid improvement
Associative Phase
-motor/sensory apthways active but less
-inc in cerebellar activity and basal ganglia
-executive function needed
-new skills, compare results
-refine skill
-slower improvements
Autonomous Stage
-primary cortex remains activice but decreased
-more automatic basal ganglia
-increased accuracy
-stable performance
Brain Injury
-cell death causes <excitotoxicity <release glutamate < destroy post synaptic neurons < increased Ca and K < more glycolysis needed < breaking down cell < cellular inflammation from arachidonic acid < free radicals < cellular edema
Axonal Injury
injury < axons retract away < wallerian degeneration < distal segment dies < glial cells clean up < cell body degenerates through chromatolysis < post synaptic cell may die
Axon Injury Regrowth
Sprouting: new branch of intact axon
Collateral sprouting: neighbo r neuron reinnervates
Regenerative sprouting: damaged neuron sends new sorts to new target
Schwann cells regrow axon 1mm/day, exercise day 5 helps
-PNS
Diffuse Axonal Injury
-DAI
-TBI from high velocity injuries cause widespread tearing
-CNS
Neurite Outgrowth inhibitor
-NOGO
-glial scars revent aconal regeneration in CNS
Cell Body Death
-always causes neuron death
Synaptic Changes after Injury
Recovery of synaptic effectivenss
-resolution of edema
Denervation hypersensitivity
-increased post synaptic receptors
Synaptic Hypereffectiveness
-presynaptic terminals are damaged and post receive it all
Unmasking of silent synapses
Principles of Plasticity
- Use it or lose it
- Use and improve it
- Specificity
- Repetition matters
- Intensity matters
- Time Matters: work at diff times
- Salience Matters: meaningful tasks
- Age
- Transference: can enhance aquisition of similar behaviors
- Interference: one experience can interfere with another behavior
Voluntary Movement 3 Phases
Target identification: post parietal cortex
Planning of action: premotor areas of frontal cortex
Execution of action: primary motor
