Exam #1 Flashcards

1
Q

Clinical neuropsychology

A

Applied to science that examines the impact of both normal and abnormal brain functioning on a broad range of cognitive, emotional, and behavioral functions

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2
Q

Neuropsychological assessment

A

Use of objective NP tests, systematic observations, interpret findings based on knowledge of NP manifestations of brain-related conditions

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3
Q

Plato (427-347 BC)

A

Brain hypothesis, closest to sky, controlled by soul/spirit, 3 parts: appetite, reason, temper, health related to relationships of body

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4
Q

Aristotle (384-322 BC)

A

Cardiac hypothesis, heart was warm, no evidence

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5
Q

Hippocrates (460-37 BC)

A

Clinical experience and observation, lateralization brought up

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6
Q

Galen (129-199 AD)

A

Pressure on the brain –> motor movement or death, did many dissections

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7
Q

Vesalius (1514-1564)

A

Brain matter, and not ventricles, mediates mental processes

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8
Q

Descartes (1596-1659)

A

“By transmitting info from the soul (in the pineal gland) to nerves and muscles”

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9
Q

Gall (1758-1828) and Spurzheim (1776-1832)

A

Phrenology, first global theory of how the brain works, cortex connects to spinal cord, two hemispheres, Gall thought mental abilities were innate (big eyes=big memory), LOCALIZATION

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10
Q

Lateralization/localization

A

Different regions generate different behaviors (Broca, Wernicke, Gall)

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11
Q

Equipoentiality

A

Many different regions are capable of generating many different behaviors (Flourens, Lashley, Kennard, Basser)

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12
Q

Hierarchy

A

More complex behaviors arise from coordination and integration of more elemental processes (Jackson, Luria)

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13
Q

Modern answers to how brain structures constrain mental events

A

Scientific experiments, double dissociation

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14
Q

Double dissociation

A

Provides strong support for localization and hierarchical organization of function, “symptom A occurs with lesions in one structure but not with those in another, and symptom B occurs with lesions of the other but not the one”

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15
Q

What is inconsistent with double dissociation?

A

Equipotentiality

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16
Q

When did cognitive NP first emerge?

A

WWII-identify cognitive abilities and disabilities for reintegration and rehab, accurate diagnosis of brain disorders (stroke, tumors) in pre-imaging era

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17
Q

Ward Halstead and Ralph Reitan

A

Developed battery of tests with standard administration and scoring, empirically-derived cutoffs, lateralized and localized lesions based on sensory-motor asymmetries, limited assessment of higher cognitive functions

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18
Q

David Wechsler

A

Refined existing IQ tests, using multiple subtests assessing different aspects of verbal and visual-spatial skills, developed attention and verbal and visual memory tests, rigorous psychometric design and large normative samples=improved precision

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19
Q

Edith Kaplan

A

Developed flexible, non-standard assessment approaches, focus on analysis of error types (process approach), tasks tailored to patient

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20
Q

Purposes of NP eval (6)

A
  1. Diagnose medical problem
  2. Diagnose associated cognitive/behavioral problems 3. Educate patient/family
  3. Monitor change
  4. Rehab
  5. Forensic/administrative
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21
Q

NP eval process (4)

A
  1. Gather relevant history
  2. Psychometric assessment
  3. Formulation (identify logically consistent patterns or syndromes)
  4. Recommendations
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22
Q

Quantitative analysis

A

Administered in standard way, scoring of test results, not qualified according to norms, determination of symptoms

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23
Q

Qualitative analysis

A

Not standard, analysis of process and results of tests’ completion, no norms exist, qualification of hierarchical structure of the deficit

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24
Q

Pre-injury data

A

Standardized educational tests, academic record

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25
Q

Post-injury data

A

Demographics, fund of vocab, reading irregular words, combined reading and demographics, best performance method

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26
Q

What factors can affect test scores? (4)

A
  1. Age (preserved/crystallized: verbal and academic skills, acquired knowledge; losses/fluid: novel reasoning, problem solving, memory, motor)
  2. Education
  3. Sex (language less strongly lateralized in females)
  4. Race/ethnicity, cultural bias
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27
Q

3 important principles when integrating test data with other clinical info

A
  1. Avoid the fallacy of affirming the consequent
  2. Be open minded
  3. Apply Occam’s Razor
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28
Q

Diagnosis

A

Identification of the nature of an illness by examining the symptoms

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29
Q

Disease

A

Impairment of bodily functions due to a known, underlying, abnormal condition

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30
Q

Syndrome

A

A group of symptoms which consistently occur together, but unknown pathology

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31
Q

EEG

A

Tracks brain wave patterns

32
Q

SPECT

A

Nuclear radiology study-measures metabolic activity, uses gamma rays and can produce a 3D image, shows HOW the brain works

33
Q

Ways to approach deficit identification (3)

A
  1. Estimating pre-injury function
  2. Deficits on a single test
  3. Patterns of deficits on single test
34
Q

Deficit measurement

A

Standardized approach which allows for comparison of subject to “norm”, allows for ID of statistically probable deficits

35
Q

Pattern analysis

A

Looking at relationships of test scores in a test battery

36
Q

Individual comparison standard

A

Looking at patients’ history, education, school records, prior test scores, etc.

37
Q

True difference

A

Reflecting brain damage, measurable difference

38
Q

Error variance

A

The portion of the variance in a set of scores that is due to outliers and measurement errors

39
Q

Patient factors for deficits (3)

A
  1. Effort
  2. Alertness
  3. Random variability (number of items, standardization of test admin, environmental distractions)
40
Q

What statistically defines a deficit?

A

Below 2/3 of standard deviation

41
Q

Hindbrain (2)

A
  1. Myelencephalon

2. Metencephalon

42
Q

Myelencephalon

A

Medulla: cardiovascular system, breathing, skeletal muscle tone

43
Q

Metencephalon (2)

A
  1. Pons: balance, vision, auditory processing

2. Cerebellum: involved in balance and motor control

44
Q

Forebrain

A

Diencephalon

45
Q

Diencephalon (2)

A
  1. Thalamus: contains nuclei that receive sensory info and transmit it to cortex
  2. Hypothalamus: contains nuclei involved in control of the ANS and pituitary gland
46
Q

Limbic system

A

Memory and emotion, amygdala (fear and aggression), hippocampus (consolidation of new memories)

47
Q

Basal Ganglia (3)

A
  1. Globus pallidus
  2. Caudate nucleus
  3. Putamen
    Involved in control of movement
48
Q

3 principles of sensorimotor function

A
  1. Hierarchal organization
  2. Motor output is guided by sensory input
  3. Learning (experience) can change the nature and locus of sensorimotor control
49
Q

Reflex arc

A

Neurons carry a message from stimulated receptors to the correct effectors

50
Q

Sensory neuron

A

Carries the message from the receptor to the CNS (sensory input is afferent)

51
Q

Motor neuron

A

Carries the message from the CNS to the effector (motor output is efferent)

52
Q

Association neurons (interneurons)

A

Connects sensory neuron to motor neurons in the CNS (integration)

53
Q

Knee-jerk reflex

A

Simple stimulus response, sensory neuron directly connects to motor neuron in spinal cord, “closed loop” response (no influencers)

54
Q

Mechanical receptors

A

Transduce energy from touch, vibration, and stretch and bending of skin, muscle, internal organs, and blood vessels

55
Q

Chemoreceptors

A

Respond to various chemicals on the surface of the skin and mucous membranes

56
Q

Thermoreceptors

A

Detect heat and cold

57
Q

Nocioceptors

A

Serve as monitors to alert the brain to damage or threat to damage which can be mechanical or chemical

58
Q

Hapsis

A

Identify objects with touch, it is the perception of fine touch and pressure

59
Q

Proprioception

A

Perception of the location and movement of limbs/body

60
Q

Where does somatosensory info enter the spinal cord?

A

Through the dorsal root ganglion and synapse ipsilaterally in the dorsal column nuclei of the spinal cord

61
Q

What 2 somatosensory receptors are transmitted separately?

A

Hapsis and nociception

62
Q

2 main somatosensory pathways

A
  1. Dorsal spinothalamic tract for proprioception and hapsis that crosses in the medulla
  2. Ventral spinothalamic tract for nociceptive info which crosses over in the spinal cord
63
Q

Thalamic pain (higher level disorder)

A

Initial hemianesthesia, later hypersensitivity, increased by light touch, change in temp or other sensory/affective stimuli, location of lesion-posterolateral thalamus

64
Q

Astereognosia/graphesthesia (higher level disorder)

A

Failure to recognize objects in presence of intact hapsis and feature identification, location of lesion-contralateral parietal association cortex

65
Q

Pathognonomic sign

A

Presence means that a particular disease is present beyond any doubt

66
Q

PPAC

A

Receives input and integrates that input to facilitate the execution of functions that require diverse information, part of association cortex, determines original position of the body and objects around the body in space

67
Q

DLPFAC

A

Higher cognitive functions such as switching attention, working memory, maintaining abstract rules, and inhibiting inappropriate responses, part of association cortex, evaluates external stimuli and initiates voluntary reactions

68
Q

Hierarchal organization of SSS

A

Association cortex–>Secondary motor cortex–>primary motor cortex–>brain stem motor nuclei–>muscle

69
Q

Where does the PPAC have outputs to in motor cortex?

A

DLPFAC, secondary motor cortex, frontal eye fields

70
Q

Where does the DLPFAC have outputs to

A

Secondary motor cortex, primary motor cortex, frontal eye field

71
Q

Secondary motor cortex

A

Functioning in organization and sequential timing of movement as well as “internal intention to move”, creates “instructions”

72
Q

Primary motor cortex

A

Controls the movements of the muscles and plans out the coordinated activity of the muscles, executes movements

73
Q

Hemiparesis/hemiplegia (simple motor disorder)

A

Difficulty/inability to move limb, location of lesion-anywhere along cortico-spinal tract (ipsilateral to deficit if spinal cord lesion, contralateral to deficit if supra-medullary lesion)

74
Q

Apraxia (higher cortical motor disorder)

A

Inability to perform skilled movements in presence of preserved single muscle group and muscle strength, location of lesion-left hemisphere, corpus collosum

75
Q

Ataxia (disorder of coordinated movements)

A

Inability to coordinate goal-directed movements in presence of preserved muscle strength and appropriate motor programs, location of lesion-cerebellum or dorsal columns (proprioception)