Psych 125

  1. WADA Technique
    anesthesizes hemisphere to allow for lateralization of the brain for research. Although temporary it is highly invasive. Used in epilepsy
  2. Transcranial Magnetic Stimulation (TMS/rTMS)
    • -Pulses of magnetic stimulation
    • -Disrupts ongoing cognitive processing
    • -Has been used experimentally to treat depression
    • -Reversible/temporary disruptions
    • -More localized than the WADA technique
    • -cortical excitabilty
  3. Wilder Penfield
    • -Brain Surgeon
    • -applied electric currents to the surface of patient's brains
    • -mapped motor cortex and some somatosensory cortex
    • -Humunculus
  4. CT/CAT Scans
    • -Based on same technolog as x-ray
    • - bone is white, cerebrospinal fluid is dark
    • -diagnose strokes, lesions, tumors, and vascular malformations
    • - Faster than the MRI
    • -Can see better calcium deposits
    • Disadvantages:
    • -uses radiation
    • -poorer resolution than MRI
    • -Most tissue types are better seen with MRI
    • -CT/MRI just look at brain structure
  5. Electroencephalograhy (EEG)
    • -Ongoing electrical activity in large groups of neurons firing in synchrony
    • -Good temporal resolution
    • -Poor spatial resolution
  6. Ictal, Seizure, Epilepsy
    • Ictal - Discharge
    • Seizure - episode
    • Epilepsy - syndrome of multiple seizures
  7. Event-Related Potentials (ERPs "Evoked Potentials)
    • -Time-locked response to specific stimulus
    • - provide excellent temporal resolution of neural processes
    • -Downward signal = depolarization
  8. Positron Emission Tomography (PET)
    • - Metabolism of brain
    • -Radioactive tracer labels blood glucose - scan brain for radioactivity
    • -Active brain areas metabolize more glucose
    • -Measures function
    • -Radioactive
    • - Poor Resolution
    • -One Task at a time
    • - Expensive
    • -SPECT : Cheaper than PET - "poor" PET
  9. Magnetic Resonance Imaging (MRI)
    • -Peel Away at the brain
    • -Grey/White Matter differentiation
    • -Magnetic field aligns hydrogen atoms in brain
    • -radiofrequenct pulse "knocks" atoms out of alignment
    • -atoms "spin back" into place - generates measurable magnetic field
    • -Good Spatial Resolution
    • - Can see diff tissues
    • -Can't have metal, can't see calcium well, takes longer than CT
  10. fMRI
    • -multiple tasks at once
    • -good resolution
    • -poor timing
    • -"brain activity" from blood flow
  11. Vegetative State
    -Patient emerges from coma and appears to be awake but there are no signs of awareness
  12. What is the #1 complaint in Neuropsychological assessment/testing?
    • -Memory problems
    • -NOT #1 problem
  13. Neuropsychological Testing
    -An objective, comprehensice assessment cognitive and behavioral functioning
  14. Reliability
    • -Consistency in measurement
    • -Test retest, split-half, internal consistency
  15. Validity
    • -Measuring what you think you are measuring in this context
    • -Face: surface
    • -construct - concept - are you measuring what you think you are measuring?
    • -content criterion
    • -Goal is to minimize error
  16. Standardization
    Consistent use of a technique
  17. False Positive
    • -Type I error, false alarm
    • -Disease Absent but test was positive
  18. False Negative
    • - Type II error, Miss
    • -Disease present, but test was negative
  19. Sensitivity
    • -Tendency for people to score Positively
    • - 90(positive)/(90+10(negative)) : Calculation column down
  20. Specificity
    • -People w/o condition have (-)
    • -
  21. PPV (positive Predictive Value)
    • 90/(90+20)
    • rows across calculation
  22. NPV (negative predictive Value)
    -calculate rows across
  23. Flexible Battery
    • -Individually Tailored for each patient
    • -"Hypothesis Testing"
    • -biased, might miss things
    • - only choosing tests that are most likely to produce important information
    • -focus on presenting problem - saves time
    • -emphazises WHY a task is failed and not WHETHER a task was failed
    • -Confirmatory bias
    • -subjectivity in interpretation
    • -Not good for research and lacks standardization
  24. Fixed Battery
    • -A pre-determined set of tests used for every patient
    • -Will not omit something since it is not biased
    • -better for research since you get similar responses from patients
    • -consistent, comprehensive
    • -can be very time consuming
    • -Limited in that it is fixed and cannot do additional testing
    • -Omits Qualitative observations
    • -Data limited by original test selection
  25. Domains of Assessment
    • My Soup Lacks Many Hot Peas
    • -Motor
    • -Seonsory and Perceptial
    • -Language
    • -Memory
    • -Higher Cognitive Functioning
    • -Personality and Emotion
  26. Dyspraxia
    • -Dyspraxia = impairment
    • - impaired mental representation
  27. Apraxia
    • -Loss of the ability to carry out or execute learned purposeful movements, despite having the desire and physical ability to perform the movements
    • -Apraxia = Loss
    • Motor representations in parietal lobe, but premotor cortex (including SMA) translates into movements
  28. Sympathetic Nervous System
    -Activation of the arousal state
  29. Parasympathetic System
    -Deactivation of arousal state
  30. Anterior
    -Towards the front or end
  31. Posterior
    -Towards the back or back end
  32. Inferior
    -Below, towards the bottom of body or below
  33. Superior
    Towards the top of the head /body or above
  34. Medial
    towards the middle/midline
  35. Lateral
    away from the midline/middle, toward side
  36. Rostral
    -Toward the nose/face?
  37. Caudal
    Towards the tail/rear
  38. Dorsal
    Towards the back
  39. Ventral
    Towards the belly
  40. Ipsilateral
    on the same side
  41. Contralateral
    on the opposite side
  42. Bilateral
    on both sides
  43. unilateral
    on one side
  44. The Meninges
    • Protects brain from penetration of foreign objects, and provides support
    • -Dura
    • -Arachnoid
    • -Pia
  45. Sylvyan Fissure (lateral)
    -Located inferior to the Frontal and Parietal lobe, and superior to the temporal lobe
  46. Central (rolandic) sulcus
    • -Located between the frontal and parietal lobe
    • -major dividing point from anterior and posterior brain
    • -also major dividing point between the primary mortor cortex and the primary somatosensory cortex
  47. Frontal Lobe
    • -1/3 of the brain
    • -output based regioon of brain
    • -goal/motor
    • -pre-central gyrus - motor cortex: signal to move, peripheral
  48. Temporal Lobe
    • -Auditory
    • -Language Reception
    • -Limbic System and emotions
  49. Parietal Lobe
    • Sensory/spatial information: where thing are in space
    • Post Central Gyrus
  50. Occipital Lobe
  51. What Lies beneath the Sylvyan Fissure?
    • Insula
    • -Function not well known
  52. What is structure between Wernicke's and Broca's area and what is it called?
    Connective fibers; Arcuate fasiculus
  53. Arcuate Fasiculus
    • Arches between superior temporal lobe ands and inferior frontal lobes
    • connections between language and comprehension and output
    • understand what u hear but harms repetition if you have lesion in arcuate fasiculus
    • Connective fibers between Wernicke's and Broca's areas
  54. Interhemispheric Fissure
    What divides the two hemispheres
  55. Internal Capsule
    • -fibers coming down into a bundle.
    • -area of white matter in the brain that separates the caudate nucleus and the thalamus from the lentiform nucleus
  56. Corpus Callosum
    • - Area in split-brain type that gets severed
    • -93-94% of connection fibers between hemispheres
  57. Central Canal
    • -Cerebrospinal fluid-filled psace that runs longitudinally thorugh the length of the entire spinal cord
    • -Lateral ventricles are the primary source of CSF
  58. Cerebrospinal Fluid
    -Provides some nourishment
  59. What happens if the constant removal of (CSF) fluid is interrupted ?
    • -ventricles are enlarged
    • -Alzheimer's patients
  60. Why would there be no ventricles in the brain?
    -Due to tumors, etc.
  61. Human Diencephalon consists of:??????
    • -Bands of myelinated axons
    • -hypothalamus???
    • -right thalamus
    • -left thalamus
    • -cerebellum
    • -Deeper in the Thalamus
  62. Thalamus
    • -relatively large
    • -2 symmetric large nuclei
    • -relay station
    • -domain-specific information processing
  63. Hypothalamus
    • -Very small
    • -Contains important collection of nuclei
    • -controls autonomic mechanisms (life sustaining mechanisms - thirst, hunger, etc.)
  64. Diencephalic Syndromes
    • -Wernicke-Korsakoff's Syndrome
    • -Vascular Disease
    • -Thalamic Trauma
    • -rare but potentially lethal cause of failure to thrive in infants and yound children
  65. Wernicke-Korsakoff's syndrome
    • -brain disorder due to thiamine deficiency
    • -due to brain damage caused by lack of vitamin B1 (thiamine)
    • -Common in ppl with alcoholism
    • -also in ppl whose bodies do not absorb food properly
  66. Vascular Disease
    -Usually if you have stroke
  67. Limbic System Consists of:
    • -Cingulate Gyrus
    • -Thalamus
    • -Olfactory bulb
    • -Amygdala
    • -Hippocampus
    • -Mamillary body
    • -Hypothalamus
    • -Fornix
  68. Amygdala
    • -survival related processing
    • -also has projections into the hypothalamus
  69. Mamillary body
  70. Limbic System
    -emotion, affect, memory
  71. Basal Ganglia
    • -Situated at the base of the forebrain
    • -associated with a variety of functions, including, voluntary motor control, procedural learning relating to routine behaviors, eye movements, and emotional cognitive functions
    • -Caudate nucleus+putamen+globus Pallidus+substantia nigra+subthalamic nucleus
  72. What structure is involved in Parkinson's Disease?
    Basal Ganglia
  73. Cerebellum
    • -The "little brain"
    • -evolutionarily "old structure"
    • -2 hemispheres
    • -connected by the vermis
    • -coordinated motor behavior
    • -postural adjustments
    • -stores memories for simple motor responses
  74. What Structure is involved in "Ataxia"? and what is it?
    • -Cerebellum
    • -neurological sign and symptom that consists of gross lack of coordination of motor movements
  75. Circle of Willis
    • -serves as a redundancy; if there is a blood blockage in one you can still get blood supply
    • -As many as 15% of us don't have a complete circle
  76. 3 Main arteries?
    • -Posterior cerebral artery
    • -Middle cerebral artery
    • -Anterior cerebral artery
  77. External processing
    Touch, Pain, Heat
  78. Internal Processing
    • Body position, fever
    • -where you are in space
    • -involves cerebellum
  79. Nocioceptors
    pain receptors
  80. Proprioceptors
    Body position
  81. Limb Kinetic
    • Fine motor coordination (clumsy) - impairment
    • e.g., thread needly, key/lock
  82. Somatosensory System
    • Info sent from body to Thalamus and Contralateral primary somatosensory cortex
    • Each body region is represented in a different cortex region
    • Posterior to the Motor system
  83. Motor System
    • Info is sent TO the body through the Internal capsule (then decusates), Spinal cord, muscles via contralateral projections
    • each body region is represented in different cortical region
    • Motor system is anterior to the somatosensory system
  84. Ideomotor
    • the idea of the movement is impaired
    • still can do the motor behavior spontaneously
    • can't get mental representation to turm into motor act
    • problems generating mental image
    • gestures to command
  85. Conceptual
    Loss knowledge of the behavior (mistaken usage)
  86. Dissociation
    • Sequencing of motor program
    • Fine movements ok, but putting them into sequence is the problem
  87. Stereognosis
    Ability to recognize object by touch
  88. Astereognosis
    • Lose the ability to recognize an object by touch
    • Impairment in sensory
  89. Visual System
    • Information sent from teh retina through the thalamus (LGN) to V1
    • Left/Right visual fields are processed contralaterally
    • Optic Nerve --> Optic Chiasm --> Optic Tract--> Thalamus (LGN) --> Optic Radiation --> Primary Visual Cortex
  90. Lesion in optic chiasm
    Lateral periphery is the blind spot
  91. Lesion in Optic Nerve
    • Right: Right eye visual field is blind
    • Left: Left visual field is blind
  92. Optic Tract
    Blind side is on left lateral side of each eye
  93. Optic Radiation
    2nd quadrant for both eyes is blind
  94. Striate Cortex
    Basically the same as with optic tract lesion...Left half of both eyes is the blind side
  95. Dorsal "Where" Stream
    • Spatial Location
    • Topographical orientation
    • Planning and coordination of movement
    • Deficits: Neglect, Apraxia, and Left-right discrimination problems
  96. Ventral "What" Stream
    • Travels to the temporal lobe
    • Object recognition
    • Matches visual shape to internal representation
    • Deficits: Visual Agnosia
  97. Neglect
    • Deficit in Dorsal Stream
    • Right hemisphere pays attention to both Left/Right
    • Left Hemisphere pays attention to Right only
  98. Anosagnosia
    ppl can learn to compensate for their neglect and become unaware of their disability
  99. Agnosia
    • Failure to recognize previously familiar stimuli
    • Modality-Specific
    • Not due to dementia, aphasia, or unfamiliarity with stimulus
    • May be limited to particular classes of stimuli
  100. Apperceptive Agnosia
    • Inability to recognize or name objects
    • Cannot copy unrecognized objects
    • Strong evidence for sensory-perceptual disturbance
  101. Associative Agnosia
    • Inability to recognize or name objects
    • Generally can copy unrecognized objects
    • Sensory-Perceptual Disturbance cannot explain defect
  102. What agnosia is able to copy unrecognized objects?
    Associative Agnosia
  103. What Agnosia has evidence for sensory-perceptual disturbance?
    Apperceptive Agnosia
  104. What is similar between Apperceptive and Associative Agnosia?
    They both have the inability to recognize or name objects
  105. Prosopagnosia
    • Inability to identify previously familiar ppl by facial features alone
    • Intact ability to identify ppl using nonfacial features (e.g., voice)
    • May extend to nonfacial stimuli
    • May co-exist with object agnosia
    • May take apperceptive and associative forms
  106. What would result in prosopagnosia?
    Posterior Cerebral Artery
  107. Gertsmann Syndrome
    • Dysgraphia/agraphia - deficiency in the ability to write
    • dyscalculia/acalculia - difficulty in learning or comprehending mathematics
    • finger-agnosia - inability to distinguish the fingers on the hand
  108. FFA (fusiform face area)
    • Recognition of strangers, danger, friends
    • But not just faces, also things that we have a lot of experience with (e.g., dog experts)
  109. Topographical Agnosia
    • Person cannon rely on visual cues to guide tthem directionally due to the inability to recognize objects
    • Lesion in right temporal lobe
  110. Heschl's Gyrus
    • Within lateral sulcus (broadman 41 (BA 41)
    • 1st cortical structure to process incoming auditory information
    • runs mediolaterally - towards the center of the brain
    • Transverse Temporal Gyrus
  111. Wernicke's Area
    • Posterior aspect of superior temporal gyrus
    • Secondary auditory cortex
    • (BA 22)
  112. Wernicke's Aphasia
    • Fluency - Yes
    • Comprehension - Poor
    • Naming - Poor
    • Repetition - Poor
    • Receptive aphasia, fluent aphasia
    • Primary deficit is in Language comprehension - both others AND Self
    • speech is fluent but not in proper grammatical form; word meaning is lost
    • patients dont realize they arent making any sense
  113. Broca's Aphasia
    • Expressive aphasia, nonfluent aphasia
    • primary deficit is speech production
    • phonemic paraphasias--little mistakes in language that most ppl dont make - e.g, mixing up syllables
    • Speech is effortful, hesitant, and dysarthric
    • Fluency - No
    • Comprehension - Good
    • Naming - Poor
    • Repetition - Poor
  114. Broca's Area
    • BA 44/45
    • 3rd frontal convolution of the left inferior frontal gyrus
    • Inferior frontal lobe, and superior to the temporal lobe
  115. Supramagrinal Gyrus (BA 40)
    • Integrate visual and spatial information from occipital and parietal lobes with auditory information
    • Portion of the parietal lobe
    • Lesion here may cause Wernicke's aphasia or transcortical sensory aphasia
  116. Angular Gyrus
    • BA 39
    • Integrates other information
    • Plays a role in reading comprehension by matching phonemes to graphemes (sounds to words)
    • Reading and Writing
    • In the parietal lobe, lies near the superior edge of the temporal lobe, and immediately posterior to the supramarginal gyrus
  117. In what Hemisphere is Language lateralized?
    • Left side of the brain
    • ~20% of left handed ppl have bilateral localization
    • ~5% have clear right hemisphere localization
  118. Left Hemisphere
    • Comprehension
    • Production
    • Meaning
  119. Right Hemisphere
    • Emotion in Language
    • Prosody
    • --Aprosodia: Speaking monotone without emotion or tone
    • Greater activation when the complexity of language increases
  120. Aprosodia
    Speaking monotone without emotion or tone
  121. Aphasia
    • Disturbance of language usage or comprehension
    • -- Spoken, written or gestured
    • Not due to motor dysfunction of the mouth/vocal cords
    • Most frequently caused by strokes, and head injury
    • Can develop slowly from brain tumor, infection, or dementia
  122. Dysarthria
    • Having a problem with motor speech resulting from neurological injury
    • characterized by poor articulation of phonemes (sounds of words)
  123. What causes Conduction aphasia?
    Damage to the arcuate fasiculus
  124. Conduction Aphasia
    • Fluency - Yes
    • Comprehension - Good
    • Naming - Good?
    • Repetition - Poor
    • Impaired Repetition
    • Lots of hesitations and word-finding pauses
    • May have intact reading abilities
    • Damage to Arcuate Fasiculus
  125. Global Aphasia
    • Fluency - No
    • Comprehension - Poor
    • Naming - Poor
    • Repetition - Poor
    • Overall decrease in language function in multiple domains
    • Most widespread deficits of all the aphasias
    • Generally due to damage in multiple perisylvian regions
  126. What causes Motor Transcortical Aphasia?
    Lesion in the white matter tracts connecting Broca's area to parietal lobe
  127. Sensory Transcortical Aphasia
    • Light Version of Wernicke's Aphasia
    • Wernicke-Like impairments in word comprehension
    • Good repetition
    • Normal recognition of auditory words, but no activation of meaning
    • Reading and writing affected
    • Lesion: Disruption of white matter tracts between parietal and temporal lobes or angular gyrus lesion
  128. Motor Transcortical Aphasia
    • Light version of Broca's Aphasia
    • Broca-like disturbed spontaneous speech; often halting
    • Good Repetition and comprehension
    • Disruption between conceptual word representations and motor speech output
    • Lesion: White matter tracts connecting Broca's area to parietal lobe
  129. Transcortical Motor Aphasia
    • Fluency - No
    • Comprehension - Good
    • Naming - Poor
    • Repetition - Good
  130. what would damage to the Middle cerebral artery cause?
    • supply system affected via stroke
    • global aphasia
  131. Transcortical Sensory
    • Fluency - Yes
    • Comprehension - Poor
    • Naming - Poor
    • Repetition - Good
  132. Difference between Motor Transcortical Aphasia and Broca's Aphasia?
    Good Repetion in Motor transcortical
  133. Anomia Aphasia
    • Severe problem recalling words or names
    • Fluency - Good
    • Comprehension - Good
    • Naming - Poor
    • Repetition - Good
    • Impaired single word production
    • Mostly "everyday" nouns
    • Repetition and comprehension intact
    • impaired storage or access to lexical information
    • damage to inferior parietal lobe or damage within the perisylvian region. Can also be seen in dementia
  134. What does damage to the inferiorparietal lobe or damage within the perisylvian region cause?
  135. Retrograde Amnesia
    Cannot Remember events prior to brain damage
  136. Anterograde Amnesia
    Cannot later remember events that occur after brain damage
  137. What is being used in declarative memory?
    Hippocampus and medial temporal lobe are the most used
  138. What are the structures of the brain that play a role in memory?
    • Basal forebrain
    • prefrontal cortex
    • amygdala
    • mediodorsal nucleus
    • rhinal cortex (on medial surface of temporal lobe)
    • inferotemporal lobe
    • cerebellum
  139. What does damage to the basal forebrain result in?
    prominent anterograde amnesia and confabulation
  140. What is preserved n Korkasoff's patients?
    Implicit priming
  141. What kind of memory was preserved in H.M?
    Procedural and motor skill learning
  142. What structures are implicated in Implicit (non-declarative) memory?
    basal ganglia, cerebellum, and the motor strip
  143. Huntington's Patients
    • Progressive deterioration of caudate nucleus of basal ganglia
    • increased verbal memory, decreased perceptual-motor
    • Huntington's disease (HD) is a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems
  144. Alzheimer's Patients
    • Progressive deterioration of medial temporal structures
    • Increased perceptual-motor, decreased verbal memory
  145. Anoxia
    complete deprivation of adequate oxygen supply
  146. hypoxia
    deprived of adequate oxygen supply
  147. Transient global amnesia
    • syndrome
    • key defining characteristic is temporary but almost total disruption of short-term memory with a range of problems accessing older memories
    • When having an attack, person has almost no capacity to establish new memories
  148. Psychogenic Amnesia
    • Functional or Dissociative Amnesia
    • extreme memory loss caused by extensive psychological stress and that cannot be attributed to a known neurobiological cause
    • Presence of retrograde amnesia, and absence of anterograde amnecia
    • Due to psychological rather than physiological causes and can sometimes be helped by therapy
  149. Infantile Amnesia
    • Inability to recall events from the first 1-3 years of life
    • "Normal" memory loss
  150. What kind of recall is easier for patients with eitehr intact or brain-injury?:
    Recognition as opposed to recall
  151. Retroactive interference
    new information can interfere with old information learned
  152. Remote Memory
    • not a good way of evaluating
    • hard to do valid and good testing for remote memory
    • ask about verifiable personal information or about well-known events or figures in the past
  153. What does the Weschsler Memory Scale (WM-III) measure?
    visual, verbal and global memory measures
  154. CA Verbal Learning Test (CVLT-II)?
    • Word listening task
    • Quick to administer
    • helps determine where in the enconding and retrieving system it begins to breakdown
  155. Rey-Osterreith Complex figure
    • Visual Memory
    • show complex figure and ask to draw it
    • visuospatial skills
    • immediate and delay recall in visual task
  156. Glutamate
    • corticostriatal, thalamocortical
    • Neurotransmitter that plays a key role in long-term potentiation
    • important for learning and memory
    • sensory neurons use glutamate
  157. GABA
    • basal ganglia
    • inhibitory NT
    • plays a role in regulationg neuronal excitability throughout the nervous system
    • also directly responsible for the regulation of muscle tone
    • amino acid
  158. Dopamine
    • modulates all 3 circuits
    • cortical, subcortical
    • produced in several areas of the brain, including substantia nigra and ventral tegmental area
    • responsible for reward driven learning
  159. Acetylcholine
    • Striatal
    • Neurotransmitter
    • both in the CNS and PNS
    • Neurotransmitter in the Autonomic Nervous system
    • Used in the motor division of the Somatic Nervous system
    • slows HR when functioning as an inhibitory NT, but also behaves as excitatory NT at neuromuscular junctions
  160. Dorsolateral Circuit functions
    • Executive Function: planning, decision making, self-directed goal selection, monitoring, guiding, and directing behavior to achieve goal
    • activation of remote memories
    • environmental independence: internal goals and desires, environment will not tell you what to do
    • Verbal mediation of behavior does not help action/behavior
  161. Dorsolateral Circuit Dysfunction
    • Poor organizational behavior
    • Poor memory search strategies
    • environmental dependency
    • Poor set shifting (Perseveration of task even though it fails)
    • Verbal/Manual dissociations
  162. Orbitofrontal circuit Functions
    • 2 Parallel circuits: Lateral and Medial
    • Personality characteristics: empathy, civility, social appropiriateness
    • environmental independence
    • emotional continence
  163. Orbitofrontal circuit Dysfunction
    • Personality Changes: tactlessness, impulsivity, irritability, antisocial behavior
    • utilization/imitation behavior
    • mood disorders
    • OCD
  164. Orbitofrontal Syndrome
    • Emotional liability (mood Swings)
    • disinhibition
    • criminal behavior
    • unusual/impulsive sexual behavior
    • Often Lack awareness
    • Anosmia
    • Environmental Dependency
    • pseudopsychopathic
  165. Anosmia
    • Lack of functioning olfaction
    • can be either temporary or permanent
    • Hyposmia: decreased ability to smell
    • Hyperosmia: increased ability to smell
  166. Anterior Cingulate Functions
    • Motivated behavior
    • Drive
    • Spontaneity
    • "Personhood"
    • creativity
  167. Anterior Cingulate Dysfunction
    • Akinetic Mutism
    • indifference to pain
    • apathy
    • poverty of speech - no spontaneous speech
    • psychic emptiness
    • excessive conformity
    • --suceptible to being taken advangtage of
    • poor response inhibition
  168. Akinetic Mutism
    • -e.g., will not get up to make food even if hungry
    • cannot translate feelings into drives
  169. Abulia
    • Lack of motivation or desire to perform a task
    • In stroke - results most often from damage to frontal lobes
    • Dementing illness, head trauma, and drug withdrawal can also cause abulia
  170. Supplementary Motor Area
    • Secondary Motor cortex
    • sequencing, timing, proper initiation of voluntary movements
  171. What happens if there is an injury to the Supplementary Motor Area?
    disorder in motor planning, organization and initiation
  172. Cingulate Motor Area
    Emotional or motivational impetus for movement (when reward is involved)
  173. What happens when there is injury in the Cingulate motor area?
    Lack of spontaneous motor activity, reduced speech input
  174. Motor Impersistence
    a form of distractability in which patients only briefly sustain a motor action in response to a command such as "raise your arms" or "Look to the right"
  175. FL Lesion
    • nonlocalized; dementia
    • can produce a return of primitive reflexes
    • Grasp, sucking/"snout', groping, utilization behavior
  176. Symptoms of FL disorder
    • poor motor sequencing
    • Poor initiation of movements
    • dysarthria
    • Apraxia
    • frontal Release signs
  177. Stroke
    • cerebrovascular accident (CVA)
    • focal neurological disorder of abrupt development due to a pathological process in blood cells
    • 3rd leading cause of death in the US
    • 700,000 strokes per year in US
    • women>men, blacks>other ethnicities
    • Reduced/blocked blood flow --> increased HR --> arterial dilation --> increased oxygen extraction ration -->in none of the above help, cell death
  178. Ischemia
    Insufficient blood flow to an area
  179. Infarction
    • sufficient disruption of blood flow to cause significant cell death
    • cell death resulting from ischemia
    • Thrombosis, Embolism - thrombosis most common kind
  180. Hemorrhage
    • rupture of blood vessel
    • most severe form of CVA
  181. Transient Ischemic Attack (TIA)
    • temporary blockage of vessels
    • symptoms similar to stroke: anterior circulation (motor, speech), Posterior circulation (visual, sensory, memory)
    • Lasts several minutes; no more than 24 hrs
    • ~33% will have a stroke
  182. Left Hemisphere Deficits
    • Aphasia
    • Apraxia
    • Agraphia/dysgraphia
    • Right hemiplegia/hemiparesis
    • verbal memory problems
    • right visual field loss
    • local processing deficits
    • depression
  183. Right Hemisphere Deficits
    • Visual-Perceptual Processing
    • Left hemiplegia/hemiparesis
    • nonverbal communication
    • prosopagnosia
    • visual memory
    • left neglect
    • anosagnosia or euphoria
  184. Stroke Risk Factors
    • Age
    • Prior history of stroke
    • Ethnicity (AA have highest rate)
    • Coronary artery disease (CAD)
    • Hypertension (HTN)
    • Hypercholesterolemia (LDL)
    • Diabetes
    • Smoking
    • Obesity
  185. Aneurysm
    • weakened blood vessel wall
    • ballooning
    • risk of rupture
  186. Vascular Dementia (VaD)
    • cognitive delcine secondary to cerebrovascular disease
    • definition challanges
    • multiple types
  187. BinsWanger's Disease
    • Diffuse white matter hyperintensities
    • Focused in teh centrum semiovale and periventricular white matter
  188. What uses 20% of body's oxygen?
    Blood, brain and energy
  189. What is particularly suceptible to osygen deprivation?
  190. CVA Course
    • Reduced/blocked blood flow
    • increased heart rate
    • arterial dilation
    • increased oxygen extraction ration
    • if none of the above help, cell death occurs
  191. What are the Different types of CVA?
    • Ischemia
    • Infarction
    • Hemorrhage
  192. Infarction
    • Cell death resulting from ischemia
    • 2 primary sources:
    • --Thrombosis: most common type, associated with atherosclerosis.
    • --Embolism: associated with arterial fibrillation
  193. What is the most common type of infarction?
  194. Tumors
    • Atypical, uncontrolled growth of cells
    • No functional purpose
    • grows at expense of healthy cells
    • can cause intracranial pressure and swelling
  195. Treatment for Tumors
    • Surgical removal
    • Radiation
    • Chemotherapy - Least effective?
  196. Gliomas
    • infiltrating tumors
    • ~50% of brain tumors
    • arise from glial cells
    • gast-growing
    • typically dont spread
    • Astrocytomas
    • Glioblastoma multiforme
    • Oligodendrogliomas
    • ependymomas
  197. Astrocytomas
    • Glioma Tumor
    • grow more slowly
    • better prognosis
  198. Glioblastoma Multiforme
    • Worse tumor one could get
    • one hemisphere
    • arises in middle age
    • grows very fast
    • poor prognosis
  199. Oligodendrogliomas
    • Rare
    • Usually young adults
    • Glioma tumor
  200. Ependymomas
    • Arise from cells surrounding ventricles
    • Usually in children
    • Glioma Tumor
  201. Noninfiltrating Tumors
    • Encapsulated & differentiated
    • Meningiomas
    • Metastatic Tumors
    • Pituitary tumors
  202. Meningiomas
    • 15% of brain tumors
    • mostly older adults, women
    • arise from arachnoid layer
    • encapsulated outside of brain
    • grows slowly, can be large before any symptoms
    • best prognosis
  203. Metastatic Tumors
    • encapsulated malignant tumors
    • spread from other areas of the body
    • fast-growing
    • usually elderly
    • poor prognosis
  204. Pituitary tumors
    • Usually benign
    • 6-24% of adults
    • often go undiagnosed
    • Nonfunctioning: dont affect pituitary hormones - symptoms arise from pressure on structures
    • Functioning: affect pituitary hormones
    • Good prognosis
  205. Common deficits due to tumors?
    • aphasias
    • visual
    • acoustic
    • endrocrine
  206. What happens if the left visual cortex is damaged/destroyed and the posterior portion of the corpus callosum?
    • Lose ability to read, but can copy words without knowing their meaning
    • Could Write spontaneously, although could not later read what had been written
    • All other aspects of his use and comprehension of language were normal
  207. Alexia
    • Inability to read
    • Word blindness, text blindness or visual aphasia
  208. What happens if you have bilateral destruction of the hippocampal region?
    Permanent memory disorder
  209. What region of the brain is necessary for the memory functions of the speech cortex?
    Left hippocampal region
  210. Isolation of the speech area
    • Hippocampal region preserved
    • Verbal learning
  211. Explicit/Declarative Memory
    When we consciously recollect previous experiences
  212. Implict/Non-declarative Memories
    when past experiences influence current behavior or performance even though we do not consciously recollect them
  213. Performance of amnesics on memory tasks:
    -What is intact?
    -What is impaired?
    • Intact
    • -Delay conditioning, Word completion priming
    • Impaired
    • - Trace conditioning
    • - Associative completion priming
  214. Disorders Affecting Memory
    • Dementias (e.g., Alzheimer's Disease)
    • Toxic Conditions
    • Anoxia or Hypoxia
    • Infarcts
    • Wernicke-Korsakoff's Syndrome
    • Head Injury/TBI
    • Transient Global Amnesia
    • Psychogenic Amnesia
  215. What are the NTs involved in Frontal Lobe Functions?
    • Glutamate (corticostriatal, thalamocortical)
    • GABA (basal ganglia)
    • Dopamine (cortical, subcortical
    • -Modulates all 3 circuits
    • Acetylcholine (striatal)
    • -Open circuit influence
    • Serotonin (cortical, subcortical)
  216. Dorsolateral Circuit Functions
    • Subserves executive function
    • -Behavioral responses to complex problems
    • -activation of remote memories
    • -enviromental independence
    • -shifting/maintaining cognitive sets
    • -generating motor programs
    • -verbal mediation of behavior
  217. Environmental Independence
    internal goals and desires; environment will not tell you what to do
  218. Dorsolateral Circuit Dysfunction
    • poor organization behavior
    • Poor memory search strategies
    • environmental dependency
    • Poor set shifting (perseveration)
    • verbal/manual dissociations
  219. Orbitofrontal Circuit Functions
    • 2 parallel circuits: Lateral/Medial
    • Personality Characteristics
    • -Empathy, Civility, Social Appropriateness
    • Environmental Independence
    • Emotional Continence
  220. Orbitofrontal Circuit Dysfunction
    • Personality Changes: tactlessness, impulsivity, irritability, antisocial behavior
    • Utilization/imitation behavior
    • Mood disorders
    • OCD
  221. Orbitofrontal Syndrome
    • Emotional Lability (mood swings)
    • Disinhibition
    • Criminal Behavior
    • Unusual/impulsive sexual behavior
    • often lack awareness
    • Anosmia
    • Environmental Dependency
    • Pseudopyschopathic
    • (phineas gage)
  222. Anterior Cingulate Functions
    • Motivated Behavior
    • Drive
    • Spontaneity
    • "Personhood"
    • Creativity
  223. Anterior Cingulate Dysfunction
    • Akinetic mutism
    • Indifference to pain
    • apathy
    • poverty of speech
    • psychic emptiness
    • excessive conformity
    • poor respose inhibition
  224. Frontal Release Signs
    • FL Lesions (nonlocalized;dementia) can produce a return of primitive reflexes:
    • -Grasp, sucking/"snout", groping, utilization behavior
  225. How soon can cell death occur without oxygen?
    In as little as 4 minutes
  226. What percentage of ppl that have a Transient Ischemic Attack (TIA) will go on to have a stroke?
  227. Thrombosis
    • Most common type of infarction
    • Associated with atherosclerosis
    • Major Junctures: ICA, VBA
    • stays where it was formed, it is a blood clot that forms when blood cells and fibrin strands clump together. It blocks blood flow
  228. Embolism
    • Associated with atrial fibrillation
    • breaks off and travels through the blood system
    • Arrythmia in heart
  229. What happens when thrombosis causes right hemisphere lesions?
    Greater functional impairment
  230. What happens when thrombosis causes left hemisphere lesions?
  231. Embolism Effects
    • 14% of strokes
    • Happen fast without transient ischemic attacks (tia's)
    • Tend to further "downstream"
    • -smaller lesions
    • tend to occur in younger individuals
    • often abrupt onset without headache or TIA's
  232. Hemorrhagic Stroke
    • Rupture of blood vessel within the brain
    • Hematoma: pooling of blood in the brain
  233. Hematoma
    • Pooling of blood in the brain
    • Either Intracranial
    • -within the cerebrum
    • Or Subarachnoid/subdural
    • -Bleeding into the meningial spaces
  234. Arteriovenous Malformation (AVM)
    • Abnormal communication between arteries and veins
    • "steals" blood from other areas
    • High leak potential
  235. Mechanism of Damage for Traumatic Brain Injury
    • Traumatic forces shear the axon
    • Retrograde degeneration
    • anterograde degeneration
  236. Penetrating head injuries
    • Object lodged in brain
    • Deficits from direct damage
    • Possible infection and bleeding
  237. Closed Head Injuries
    • Injury to head that doesn't enetrate skull
    • -Acceleration vs. deceleration
    • -Coup vs. contrecoup
    • --Impact injury at site of impact
    • --contrecoup injury opposite of impact
  238. Coup
    impact injury at site of impact
  239. Contrecoup
    injury opposite of impact
  240. Edema
    • intracranial pressure
    • swelling of brain leading to intracranial pressure
    • no ventricles and no sulci
  241. Herniation
    • ICP
    • Hematoma
  242. Complications of TBI
    • Edema
    • Herniation: ICP;herniation
    • Hemorrhage
    • Skull Fractures
    • Seizures
  243. Brain Herniation
    brain becomes displaced and deformed
  244. Brain Hemorrhages
    • subdural hematoma
    • epidural hematoma
  245. Posttraumatic Epilepsy
    • arises from scar tissue
    • more common in penetrating injuries
    • onset may be delayed
    • children more suceptible (to seizures and epilepsy in general)
    • temporal epilepsy
    • possible genetic influence
  246. Skull fractures
    • linear
    • depressed
  247. Concussions
    • "Mild head injury"
    • Symptoms: Minimal loss of consciousness (<20 mins), confusion, headache, nausea/vomiting, blurred vision/pupils dilated, temporary retrograde/anterograde amnesia
  248. Acute Treatment of Head Injury
    • Assess "ABC": airway, breathing, circulation
    • Neurological exam
    • diagnostic imaging
    • reduce intracranial pressure
  249. Neuropsychology of Head Injury
    • Attention deficits: dorsal frontal
    • Mood Changes: patients more labile
    • Personality changes: Frontal lobe syndrome
    • Posttraumatic Amnesia
    • Post Concussion syndrome
    • Malingering
    • Cogniform disorder: adopting a "sick role
  250. Approaches to Rehab: Function (restitution)
    • focus on underlying impairment
    • belief that "memory can be repaired
    • Least effective approach cognitively
  251. approaches to rehab: Performance (Substitution)
    • Focus on compensation
    • learning a new way to do things
  252. Specific Strategies: APT
    • Attention Process Training (APT)
    • Sohlberg/Mateer
    • Sustained attention
    • selective attention
    • alternating attention
    • divided attention
  253. Attention process Training (APT)
    • developed in Canada
    • designed to rehabilitate retention
    • where memory breaks down
  254. Sustained Attention
    • 5-10 Minutes
    • continuous performance task
  255. Selective Attention
    • Ability to ignore competing demands for our attention
    • ignore irrelevant infomation
  256. Alternating attention
    shift back and forth from one thing to another
  257. Divided Attention
  258. External aids
    • Specific strategies for memory
    • best for mild impairments
    • e.g. diaries
    • pagers/voice organizers are more helpful for severe problems
  259. Vanishing Cues
    • Teaches large amount of complex knowledge
    • possibly taps into implicit memory systems
    • Specific strategy for memory
  260. Errorless learning
    • Specific strategy for memory
    • explicit memory is needed to learn from mistakes
    • preventing mistakes capitalizes on intact implict memory
  261. Recall and Recognition in Adulthood
    • Number of words recognized is stable with age
    • Number of words recalled declines with age
  262. Intelligence and Aging
    • Verbal scores are stable with age
    • Nonverbal scores decline with age
  263. Reducing Cognitive Decline
    • Live in favorable environment: above average education, Complex and intact families
    • Be involved in complex, stimulating activities : reading, travel, cultural activities, etc
    • Be married to spouse of high cognitive status
  264. Aging: Conclusion
    • Only certain types of memory decline with age
    • IQ does not show a drastic decline
    • The ability to learn does not change
    • Plenty to counter the effects of age: stop smoking, exercise, eat a healthy diet, engage in learning activities, stay in touch with friends, family, communities
  265. Dementia
    • Not normal aging
    • Dementia is NOT a disease, but a syndrome caused by many different diseases
  266. Some Causes of Dementia: Cortical
    • Alzheimer's Disease
    • Frontortemporal Demetia
    • Primary Progressive Aphasia
    • Pick's Disease
  267. Some subcortical Causes of dementia
    • Parkinson's disease
    • Huntingtons's Disease
    • Progressive supranuclear palsy
    • Creutzfeldt-jakob disease
  268. Some Mixed Causes of Dementia
    • Vascular dementia (CVD/MID)
    • Dementia with Lewy Bodies
  269. Alzheimer's Disease (AD)
    • Syndrome (vs. Specific disease entity)
    • Irreversible and progressive deterioration of intellect and personality : Usually begins with mild memory impairments, Overtime, all cognitive domains are affected. Ultimately leads to patient being bedridden and helpless, and eventually, death.
    • Course: 8yrs(average), 2-3 years to 15-20 years
  270. Risk Factors of AD
    • Age
    • Female gender
    • lower education and occupational levels
    • traumatic brain injury (TBI)
    • Genetics: 1st degree relatives, twin studies. Linked to mutated and other genes
  271. Biology of AD
    • neuronal degeneration
    • general brain atrophy
    • decay of acetylcholine system
    • decreased cerebral metabolism
    • beta-amyloid plaques
    • neurofibrillary tangles
  272. What are the key enzymes involved in Beta-Amyloid plaque formation?
    • Alpha-secretase
    • Beta/gamma secretase
  273. What are the different protein fragments involved in Beta-Amyloid plaque formation?
    • P3 - alpha/gamma: harmless
    • 40 - Amino acid string: beta and gamma: harmless
    • 42 - Amino acid string: beta and gamma: TOXIC
  274. Microtubules
    • Structural support
    • Pathways for: Nutrients, Waste products, NTs
    • Made of Tubulin

    In AD: excess tau protein builds up; Tau binds with Tubulin and tacles the microtubules
  275. Neuropsych Profile: Memory - AD
    • Loss of semantic associative networks : "bird" vs. "robin"
    • Relatively spared memory systems: STM; some non-declarative memory (motor skill learning, perceptual priming)
  276. Neuropsych Profile - Language and Speech - AD
    • Early stages: Anomic aphasia (i.e., word finding and naming difficulties)
    • Mid-to-late stages: comprehension problems and problems repeating info
    • Late stages: declines in fluent conversational output
  277. Neuropsych Profile - Visual-Spatial Functioning - AD
    • Everyday disorientation
    • complex clinical tasks affected first
    • even simpler clinical tasks begin to be affected as the disease progresses
  278. Neuropsych Profile - Attention/Orientation - AD
    • Simpler attentional tasks are intact until later stages of the disease
    • More complex tasks show decline even in early stages
    • Disorientation is a major source of behavioral problems: wandering and confusion
  279. Neuropsych Profile - Executive Functioning - AD
    • Disorganization and leaving tasks unfinished
    • Perseveration and loss of mental flexibility (dorsolateral prefrontal cortex)
    • Repetition of behavior (forgetful?)
    • Loss of metacognitive awareness/self-monitoring
    • Impaired ability to organize, plan, and use appropriate problem-solving strategies
  280. Neuropsych Profile - Motor & Sensory Functions - AD
    • relatively preserved - but declinees with advanced disease
    • olfaction is the only sense impaired - from even the mild stages of the disease since it is right next to the hippocampus
  281. Personality/Mood - AD
    • apathy
    • depression
    • irritability
    • paranoia
    • the differential diagnosis between depression and dementia is often difficult
  282. Cholinesterase inhibitors
    • helps memory
    • pharmacologic treatment for cognitive
    • stops breakdown of acetylcholine
    • most helpful in early stages of disease
  283. Memantine
    • Prevents premature cell death
    • Pharmacologic treatment for cognitive
    • there isnt much benefit
  284. Mild Cognitive Impairment (MCI)
    • "transitional zone" between normal cognition and Alzheirmer's disease
    • Not severe to meet criteria for other dementias
  285. Parkinson's Disease
    • PD occurs as a result of degeneration of the pigmented dopamine containing neurons of the pars compacta of the substantia nigra
    • Idiopathic: genetics, environmental toxins, sporadic
    • 1.5 - 2Xs more likely to occur in males
  286. What happens with the Dopamine depletion in PD?
    • less dopamine=less movement
    • when dopamine production is stopped, the neuron can no longer transmit signals to the next neuron
  287. Motor Symptoms: Parkinson's
    • Resting tremor (pill rolling)
    • Rigidity (cogwheeling)
    • Stooped posture
    • imparied righting reflex/poor balance
  288. Negative Motor Symptoms of PD
    • Bradykinesia
    • Hypokinesia
    • Gait disturbance: slow, festinating, freezing
    • Masked facies
    • slowed speech
    • Decreased voice amplitude
    • Ocular disturbances: decreased blink rate/light accomodation, slowed saccades
  289. Bradykinesia
    Slow movement. Bradykinesia is often associated with an impaired ability to adjust the body's position. Bradykinesia can be a symptom of nervous system disorders, particularly Parkinson's disease, or a side effect of medications.
  290. Hypokinesia
    Decreased bodily movement
  291. Bradyphrenia
    • Slowed thinking
    • implicated usually in Parkinson's
  292. Parkinson's Disease Treatments
    • Medications: L-dopa = dopamine precursor; Anticholinergics
    • Surgery: Pallidotomy, thalotomy, deep brain stimulation
  293. Huntington's Disease
    • Most common inherited neurodegenerative disorder
    • Age of diagnosis: average 40yo, range: ~20-40 yo
    • autosomal dominant neurodegenerative disease
  294. Progressive Supranuclear Palsy (PSP)
    • prototypical subcortical dementia
    • median age of onset: 65 yrs
    • Median survival: 6yrs
    • Commonly misdiagnosed as PD where PD treatment is ineffective for this dementia
    • Cell loss and neurofibrillary changes in multiple regions of the basal ganglia, brain stem, and cerebellum
  295. PSP cognitive symptoms
    • prefrontal/executive (disproportionately impaired)
    • -perseveration
    • -grasping reflex
    • -utilization behavior
    • -poor orientation
    • -slowed or impaired reasoning
    • -apathy
    • -inertia
    • Language:
    • -slowed speech, dysarthria
    • -process/comprehension relatively spared
  296. PSP treatment
    • no effective treatments exist
    • dopaminergic agents help some patients, but most are not
  297. Creutzfeldt-Jakob Disease
    • Subacute Spongiform Encephalopathy
    • Prion disease
    • --disease-causing cellular proteins
    • --Forms plaque
    • --Forms sponge-like “holes” in brain
    • 1 per 1 millionīŽ Most contract it in their 50’s-60’s
    • Extremely rapid progression
  298. CJD Motor Symptoms
    • Myoclonus: involuntary twitching/jerking
    • extreme startle reflex
    • cerebellar dysfunction: ataxia
    • extrapyramidal dysfunction: akinesia or akasthesia
Card Set
Psych 125
Neuropsychology and Assessment