Category Archives: P-Z

White Matter


  • Human brain filled w/ nervous tissue, glial cells, and vasculature, weighing avg 1400 grams
  • Estimated 100 billion neurons, each makes contact w/ at least 10,000 others
  • About 50% of adult cerebral volume is occupied by white matter
  • Great majority of white matter in white matter tracts, though some found in gray matter
    • Distinction between gray and white matter therefore relative


  • Word derives from Greek word for marrow (myelos), coined to indicate abundance of white matter in the core or “marrow” of brain
  • Universal fx is to insulate axons and thereby dramatically affect electrical properties
  • Myelin sheath is discontinuous, leaving Node of Ranvier uncovered, to permit more efficient axonal transmission

Glial Cells

  • Of 4 types of glial cells in CNS (oligodendrocytes, astrocytes, ependymal cells, microglia), olig and astrocytes important in structure and fx of white matter
  • Oligodendrocytes are responsible for formation of myelin in CNS (Schwann cells in PNS)
  • Astrocytes found throughout CNS – provide structural support to neurons; in white matter they make contacts at nodes of Ranvier and help to regulate ionic microenvironment

Blood Supply

  • Blood supply for white matter comes from many perforating arteries arise from larger arteries at base of brain
  • Most prominent is Lenticulostriate Arteries

White Matter Tracts

  • Axons in tracts as short as 1 mm (if intracortical) and as long as 1 meter (brain to cord)
  • Tract most common term, but also fasciculus, funiculus, lemniscus, peduncle, bundle
  • Coalesce w/ each other to form rich mass of white matter w/in each hemisphere above internal capsule called corona radiata; still higher is centrum semiovale (subjacent to cortex)
  • May have more white matter in right hemisphere, w/ biggest difference in frontal lobe
  • Three Major Groups of White Matter Pathways
    • Projection
      • Consist of long ascending (corticopetal) and descending (corticofugal) tracts
      • Includes thalamo-cortical radiations; corticospinal and corticobulbar tracts
    • Commisural
      • Connect two hemispheres
      • Corpus callosum biggest (made up of posterior splenium, central body, anterior genu, and ventrally directed rostrum)
      • Other commisures include: anterior (connects olfactory and temporal regions) and hippocampal/fornical (links the fornices)
    • Association
      • Connect cerebral areas within each hemisphere
      • Generally bidirectional
      • Short association fibers (U or arcuate fibers): link adjacent cortical gyri
      • Long ass’n fibers (all terminate in frontal lobe): arcuate fasciculus, superior occipitofrontal fasciculus, inferior occipitofrontal fasciculus, cingulum, uncinate fasciculus


  • Brain electrical organ
  • Speed/efficiency of action potential propagation significantly influenced by degree and integrity of myelination of axons

Action Potential

  • Neurons in brain conduct impulses at velocity of 1 to 120 meters per second
  • Speed influenced by size of axon

Saltatory Conduction

  • Increase of neuronal conduction also conferred by saltatory conduction
  • Myelin sheath interrupted every 1-2 mm by unmyelinated segment called node of Ranvier, which permits the action potential to jump from one node to next

Clinical Neurophysiology

  • Function of white matter indexed w/ EPs or evoked potentials (EEG index of cortical fx)
  • Most familiar: visual, auditory, brainstem auditory (BAEP) and somatosensory
  • Special form of EP is event-related potential (ERP): in general, long-latency waves related to cognitive stimuli
  • Most familiar ERP is P300 (can be affected by both gray and white matter dysfx); thus, P300 and other ERPs are of research interest but don’t have routine clinical application yet


  • Interference w/ normal operations of distributed neural networks by white matter lesions may disturb all aspects of neurobehavioral function. Need to consider if lesion is:
    • Focal or diffuse
    • Static or progressive
    • Associated w/ edema or mass effect
    • Severe enough to cause axonal loss
    • Combined w/ cortical or subcortical gray matter pathology
  • Microscopic level burden of white matter pathology may involve any of 5 components:
    • myelin
    • oligodendrocyte
    • axon
    • vascular system
    • astrocyte

Pathogenesis of White Matter Disconnection

  • Slowed Conduction: if pt given enough time, accurate completion of tasks
  • Absent Conduction: lesion may be severe enough to completely block axonal conduction
  • Focal Neural Network Disruption: e.g., auditory verbal agnosia, conduction aphasia
  • Diaschisis: remote effects of an acute lesion on other regions of the brain; remote area itself intact, so recovery from acute insult eventually leads to partial or complete return of some functioning in temporarily deactivated region
  • Wallerian Degeneration: axonal injury in white matter tract removed from the primary site of pathology; thus, severe white matter lesion may also produce damage in other regions of the tract; may proceed distally thru length of axon or proximally toward cell body; can occur over period of months to years
  • Transsynaptic Degeneration: secondary damage can be seen in neurons linked to those that undergo primary injury; similar to Wallerian degeneration but extends beyond initially damaged neurons; essentially refers to neuronal loss and reactive gliosis in neurons deprived of synaptic input by lesions in adjacent neurons



  • Jun Wada pioneered the technique of injecting sodium amobarbital into the carotid artery to produce a brief period of anesthesia of the ipsilateral hemisphere
  • Injections are now normally made through a catheter inserted into the femoral artery
  • This procedure results in an unequivocal localization of speech, because injection into the speech hemisphere results in an arrest of speech lasting up to several minutes; as speech returns, it is characterized by aphasic errors
  • Injection into the nonspeaking hemisphere may produce no speech arrest or only brief arrest.
  • The amobarbital procedure has the advantage that each hemisphere can be studied separately in the functional absence of the other, anesthetized one (Some institutions do both hemispheres on the same day; others do it on separate days)
  • Memory testing is also performed for each hemisphere. Again, there is no standard procedure, and different institutions perform it differently.
  • In a typical Wada test, a patient is given a “dry run” to become familiar with the tests that will be done during and after the drug injection. This dry run establishes a baseline performance level against which to compare the postinjection performance


  • The Wada procedure starts with the supine patient raising both arms and wiggling the fingers and toes
  • The patient is asked to start counting from 1, and, without warning, the neurosurgeon injects the drug through the catheter for 2 to 3 seconds.
  • Within seconds, the contralateral arm falls to the bed with a flaccid paralysis, and there is no response whatsoever to a firm pinch of the skin of the affected limbs
  • If the injected hemisphere is nondominant for speech, the patient may continue to count and carry out the verbal tasks while the temporary hemiparesis is present, although often the patient appears confused and is silent for as long as 20 to 30 seconds but can typically resume speech with urging
  • When the injected hemisphere is dominant for speech, the patient typically stops talking and remains completely aphasic until recovery from the hemiparesis is well along, usually in 4 to 10 minutes
  • Speech is tested by asking the patient to name a number of common objects presented in quick succession, to count and recite the days of the week forward and backward, and to perform simple object naming and spelling
  • In addition to aphasia and paresis, patients with anesthesia of either hemisphere are totally nonresponsive to visual stimulation in the contralateral visual field. For example, there is no reflexive blinking or orientation toward suddenly looming objects

RESEARCH DATA (Milner, et al.)

  • In a series of studies, Brenda Milner and her colleagues demonstrated that about 98% of righthanders and 70% of left-handers show speech disturbance after sodium amobarbital injection into the left hemisphere and not after injection into the right
  • Curiously, roughly 2% of right-handers have their speech functions lateralized to the right cerebral hemisphere, which is roughly the proportion of righthanded people who show aphasia from right-hemisphere lesions. This finding reminds us that speech is sometimes found in the right hemisphere of righthanded people
  • The results for left-handed patients support the view that the pattern of speech representation is less predictable in left-handed and ambidextrous subjects than in right-handers but that the majority of left-handers do have speech represented in the left hemisphere
  • In these studies, none of the right-handers showed evidence of bilateral speech organization, but 15% of the non-right-handers displayed some significant speech disturbance subsequent to the injection of either side
  • These patients probably did not have a symmetrical duplication of language functions in the two hemispheres; the injection of one hemisphere tended to disrupt naming (for example, names of the days of the week), whereas the injection of the other hemisphere disrupted serial ordering (for example, ordering the days of the week)

Visual System

Eyes and Retina

  • Lens – as light enters the lense, the image is inverted and reversed (so information from the upper visual space is projected to the lower and vice versa; R-L inversion occurs as well)
  • Fovea – central fixation point; region of retina with highest visual acuity; central 1-2 degrees of visual space
  • Macula – surrounds fovea and has relatively high visual acuity; central 5 degrees of visual space
  • Optic Disc – 15 degrees medial to the fovea; where axons leave retina to form optic nerve = blind spot

Two Classes of Photoreceptors

  • Rods – more numerous by 20:1; poor spatial and temporal resolution, do not detect colors; main function is vision in low-level lighting conditions
  • Cones – less numerous (though more highly represented in fovea); high spatial and temporal resolution, detect colors
    • Unlike any other neurons, photoreceptors and bipolar cells do not fire action potentials. Instead, information is conveyed by passive electrical conduction and they communicate through “nontraditional” synapses that release neurotransmitters in a graded fashion

Optic Nerves, Optic Chiasm, Optic Tracts

Probably the most critical information in this chapter is contained in Figure 11.15.

  • Homonymous – visual fields of both eyes are affected
    • Optic nerve is not a true nerve – pathway of retinal ganglion cells (which send axons into optic “nerve”) lies entirely within CNS. Initial portion (anterior to chiasm) = optic nerve; proximal portion (posterior to chiasm) = optic tract
    • Partial crossing of fibers in optic chiasm; therefore, fibers from right hemiretinas (i.e., left visual field) end up in right optic tract (and vice versa)
    • Lesions of optic chiasm – bitemporal (bilateral lateral) visual field defects
    • Lesions of eye, retina, optic nerve – monocular visual field defects
    • Lesions proximal to optic chiasm (i.e. optic tracts, LGN, optic radiation or visual cortex) – homonymous visual field defects
    • Because of location (i.e., ventral surface of brain, beneath frontal lobes and in front of pituitary gland), chiasm is susceptible to compression by pituitary tumors and other lesions

Lateral Geniculate Nucleus and Extragenuclate Pathways

  • Retino-geniculo-striate pathway (See figure 11.6 for visual depiction of pathway)
    • Axons of retinal ganglion cells in optic tract – LGN of thalamus – primary visual cortex
    • Functions in visual discrimination and perception
    • A minority of fibers bypass this pathway to go to the one described below
  • Retino-tecto-pulvinar-extrastriate cortex pathway (i.e., Extrageniculate Visual Pathway)
    • optic tract – brachium of superior colliculus – pretectal area and superior colliculus – relays in the pulvinar and lateral posterior nucleus of the thalamus – numerous brainstem areas and association cortex (lateral parietal cortex, frontal eye fields of prefrontal cortex)
    • Functions in visual attention and orientation (may be involved in “blindsight”

Optic Radiations to Primary Visual Cortex

  • Optic Radiations (see figure 11.8) – axons leaving the LGN fan out over a wide area of white matter
    • Lesion of optic radiation – homonymous defect affecting the contralateral visual field
    • Meyer’s Loop – inferior optic radiation fibers; arc forward into temporal lobe; carry info from the inferior retina/superior visual
      • Temporal lobe lesions – contralateral homonymous superior quadrantopia (“pie in the sky”)
    • Upper optic radiations pass under parietal lobe
      • Parietal lobe lesions – contralateral homonymous inferior quadrantopia (“pie on the floor”)
  • Primary Visual Cortex (see figure 11.8)
    • Lies on banks of calcarine fissure in the occipital lobe
    • Is retinotopically organized (fovea – occipital pole; peripheral regions – anterior along the fissure)
    • Fovea’s cortical representation occupies 50% of the primary visual cortex (despite its small retinal area, b/c it is the region of highest visual acuity)
    • Cuneus (“wedge”) – portion of medial occipital lobe above calcarine fissure
    • Lingula (“little tongue”) – portion of medial occipital lobe below calcarine fissure
    • Upper portion of optic radiation projects to superior bank of calcarine fissure
      • Upper-bank lesions = contralateral inferior quadrant defects
    • Lower portion of optic radiation projects to inferior bank of calcarine fissure
      • Lower-bank lesions = contralateral superior quadrant defects

Visual Processing in the Neocortex

Primary visual cortex (area 17) = striate cortex

  • 2 main streams of higher-order visual processing (after primary and secondary visual cortex):
    • “Where?” – dorsal pathways projecting to parieto-occipital association cortex; analyze motion and spatial relationships between objects and between the body and visual stimuli
    • “What?” – ventral pathways projecting to occipitotemporal association cortex; analyze form; specific regions for colors, faces, letters, etc.

Assessment of Visual Disturbances

  • Visual Acuity:
    • reported using Snellen notation of 20/X
    • visual field defects do not typically affect visual acuity
  • Monocular vs. Binocular visual disturbance – essential for localization, but patient report is often unreliable; “blurred vision” is particularly difficult to interpret (e.g., patient will say they lost the vision in one eye, but they really mean one visual field)
  • Negative phenomena (patients may be unaware)
    • scotoma
    • homonymous visual field defect
  • Positive visual phenomena
    • simple visual phenomena (lights, colors, geometric shapes, etc.) – caused by disturbance anywhere from eye to primary visual cortex
    • fortification scotoma – jagged alternating light and dark zigzagging lines common to migraine
    • pulsating colored lights or moving geometric shapes – suspect occipital seizures
    • formed visual hallucinations (e.g., people or animals) – arise from inferior temporo-occipital visual association cortex; common causes are toxic/metabolic disturbance, alcohol/sedative withdrawal, focal seizures, complex migraine, neurodegenerative conditions (e.g., CJD, LBD), narcolepsy, midbrain ischemia, psychiatric disorders (though auditory more common than visual in latter)
    • release phenomenon – patients with deprivation in part or all of visual field have formed visual hallucinations, especially during early stages of deficit
    • Bonnet syndrome – visual hallucinations occurring in the elderly as a result of impaired vision
  • Terms to Describe Visual Disturbances
    • Scotoma – a circumscribed region of visual loss
    • Homonymous Defect – a visual field defect in the same region for both eyes
    • Refractive Error – indistinct vision improved by corrective lenses
    • Photopsias – bright, unformed flashes, streaks, or balls of light
    • Phosphenes – photopsias produced by retinal shear or optic nerve disease
    • Entopic Phenomena – seeing structures in one’s own eye
    • Illusions – distortion or misinterpretation of visual perception
    • Hallucination – perception of something that is not present

Localization of Visual Field Defects

Visual Field Testing

  • Confrontation testing – the examiner should test their own visual field simultaneously by holding a visual stimulus midway between self and patient
  • Extinction is a sign of visual neglect
  • Formal visual field testing can be done using Goldmann perimetry

Visual Field Defects

Figure 11.15 falls in this section, and is critical for understanding.

  • Retinal lesion – causes monocular scotoma or, if severe enough, monocular visual loss (common cause: retinal infarct)
  • Optic nerve lesion – causes monocular scotoma or monocular visual loss (may be partial or incomplete depending on severity) (common causes: glaucoma, optic neuritis, elevated ICP)
  • Optic chiasm lesion – bitemporal hemianopia (often caused by compression due to lesion; common cause: pituitary adenoma)
  • Retrochiasmal lesion (optic tracts, LGN, optic radiations, visual cortex) – homonymous visual field defects
    • Optic tract lesion (uncommon) – contralateral homonymous hemianopia
    • LGN lesion – contralateral homonymous hemianopia
    • Lower optic radiation lesion (through temporal lobe) – contralateral superior quadrantopia (“pie in the sky”) (common cause: MCA inferior division infarct)
    • Upper optic radiation lesion (through parietal lobe) – contralateral inferior quadrantopia (“pie on the floor”) (common cause: MCA superior division infarct)
    • Entire optic radiation lesion – contralateral homonymous hemianopia
  • Primary visual cortex lesion – common cause: PCA infarcts, tumors, hemorrhage, infection, trauma to occipital poles
    • Upper bank of calcarine fissure – contralateral inferior quadrantopia
    • Lower bank of calcarine fissure – contralateral superior quadrantopia
    • Entire primary visual cortex lesion – contralateral homonymous hemianopia
  • Macular sparing (see figure 11.16) – seen occasionally with partial lesions of visual pathways; occurs because fovea has relatively large representation for its size; term usually used in context of cortical lesions, but other injuries can cause this (e.g., increased ICP)

Blood Supply and Ischemia in Visual Pathways

  • Retina – ophthalmic artery
    • 3 main causes of impaired blood flow:
      • emboli
      • stenosis
      • vasculitis
      • Amaurosis fugax – transient ischemic attack of the retina; browning out or loss of vision in one eye for about 10 minutes (“like a window shade”); should be worked up like any other TIA
  • Optic tracts, optic chiasm, intracranial segment of optic nerves – small branches arising from proximal portions of ACA, MCA, and anterior and posterior communicating arteries
  • LGN – variable blood supply; infarcts may be associated with contralateral hemiparesis or hemisensory loss due to involvement of nearby posterior limb of internal capsule and thalamic somatosensory radiations
  • As optic radiations pass through the parietal and temporal lobes– may be damaged by infarcts to MCA
  • Primary Visual Cortex – PCA; basilar artery supplies both PCAs; bilateral altitudinal scotoma (see figure 11.17) strongly suggests vertebrobasilar insufficiency causing bilateral infarcts or TIAs
  • Inferior occipitotemporal visual association cortex (“what?” stream) – PCA
  • Lateral parieto-occipital visual association cortex (“where?” stream) – MCA-PCA watershed territory

Optic Neuritis

(additional detail on neuro exam and treatment on p. 445)

  • Optic Neuritis – inflammatory demyelinating disorder of the optic nerve that is epidemiologically and pathophysiologically related to MS
    • >50% of patients with an isolated episode of optic neuritis will eventually develop MS
    • typical onset – eye pain, monocular visual problems (monocular central scotoma, decreased visual acuity, impaired color vision)
    • onset acute or gradual (several days to weeks)
    • near complete recovery common in 6-8 weeks
    • may be permanent visual loss

Traumatic Brain Injury

Quick Facts

Open Head Injury – discrete, focal lesions; higher risk for seizures Closed Head Injury – generalized/diffuse cerebral involvement Highest incidence males 16-24 Common Causes MVA, falls (also, industrial, assault, sports)

Risk Factors

  • LD
  • Previous hospitalization for TBI
  • Chronic alcoholism
  • Heart disease and hypertension
  • ADHD
  • Psychiatric illness
  • Seizures
  • Drug abuse
  • Divorce
  • Boxing/soccer
  • Low SES/education
  • Unemployment

Neuropathology of Closed Head Injury

  • Diffuse Axonal Injury (DAI) – breaking/shearing/stretching of myelinated axons
    • Due to acceleration/deceleration and rotational injuries (with subsequent LOC)
    • Occurs over time – compression/stretching, swelling, evolving changes (e.g., changes in glucose transport, blood flow, toxins, etc.)
  • Focal or Subcortical Contusion (FCC) – local abrasions (tearing  hemorrhage; swelling  edematous)
    • Due to coup/contrecoup, depressed skull fx, inertial/rotational force, skull features (e.g., orbital frontal, inferior anterior temporal), hematomas, subcortical bleeds  CVA effects
  • Hypoxic-Ischemic Injury (HII) – infarction in distribution of one artery
    • Due to lack of oxygen, often secondary to physical injuries/chest injuries/airway obstructions
    • Get increased ICP and decreased arterial pressure; results in severe and pervasive memory d/o (because hippocampus requires much oxygen)
    • Edema increases ICP, which increases edema, which increases ICP, and so on…
    • Other secondary insults: from multiple/systemic injuries may get hypoxia/anoxia and fat emboli (fx of femur)
    • Delayed Effects: white matter degeneration (ventricular enlargement), disturbed CSF flow (hydrocephalus)

Primary and Secondary Brain Injury after TBI

  • Primary (immediate on impact)
    • Macroscopic Lesions (contusions at site of impact – coup; contrecoup; laceration)
    • Microscopic Lesions (shearing/stretching of nerve fibers)
  • Secondary mechanisms of brain injury
    • Intracranial hemorrhage
    • Edema in white matter – adjacent to lesion
    • Hyperemia (diffuse swelling)
    • Ischemic brain damage
    • Raised ICP
    • Brain shift/herniation
  • Secondary insult from extracerebral events
    • Effects of multiple systemic injury – e.g., hypoxia, fat emboli
  • Delayed Effects
    • White matter degeneration
    • Disturbed flow of CSF

Degenerative Events Following Brain Damage

  • Anterograde degeneration (aka orthograde or Wallerian) – degeneration of severed axon
  • Astrocyte activity – invade to remove debris; may seal or scar the area
  • Calcification – large deposits where neural degeneration takes place
  • Chromatolyses – color dissolution (cell Nissel substance breaks down); therefore, no stain uptake and are colorless for microscope
  • Gliosis – replacement of cell bodies by glial cells
  • Necrosis – localized death of individual or groups of cells
  • Phagocytosis – removal of dead cells by mitochondria and astrocytes
  • Retrograde Degeneration – death of remaining axon, cell body, and dendrites after being severed
  • Terminal Degeneration – shrinkage/degeneration of terminals after axon severed
  • Transneuronal Degeneration – death of neurons that innervate or are innervated by damaged or destroyed neuron

Associated Physiological Events

  • Diaschesis
  • Shock (e.g., spinal) – cells everywhere show temporary depression when input removed
  • Edema
  • Blood Flow – decreased CO2, decreased flow, decreased metabolic activity; therefore, decreased overall brain activity
  • Neurotransmitter Releases – levels change
  • Glucose Uptake – decreased metabolic activity (not just due to edema)
  • Changes in electrical activity – can be an index of posttraumatic function
  • Autoneurotoxicity – delayed tissue death due to increased release of glutamate (due to oxygen deprivation; overexcites cells)

Recovery Mechanisms

  • Spontaneous recovery – due to resolution/absorption of hematomas, decreased swelling, normalization of blood flow, return of electrolyte/neurochemical balance
  • Plasticity – neural and/or behavioral resilience (ability to reorganize)
  • Diaschesis (von Monakow) – recovery following temporary disruption of functioning in areas adjacent to the primary damage; inhibited functions slowly reemerge; i.e., reestablishment of unimpaired neurological systems
  • Axonal growth – regeneration of neural elements following injury (axonal sprouting, collateral sprouting from intact neurons – collateral axons grow to replace lost axons or innervate targets); not necessarily beneficial
  • Denervation supersensitivity – postsynaptic receptor sites become more sensitive to neurotransmitter agents in denervated neurons; proliferation of receptors, therefore an increase in response
  • Substitution (not a popular theory) – existing intact brain structures can assume functions previously held by lesioned areas; or, redundancy or duplication of function; unoccupied/unused brain area assumes functions of damaged area
  • Behavioral compensation – new or different behavioral strategy
  • Disinhibition – removal of inhibitory actions of a system (by destruction or pharmacological blocking)
  • Nerve Growth Factor – protein secreted by glial cells; facilitates growth, regeneration, reenervation
  • Regeneration – neurons/axons/terminals regrow and establish previous connections
  • Rerouting – axons/collaterals seek new targets after destruction of old ones
  • Silent Synapses – (hypothetical) present synapse – no evident function until system is disrupted
  • Sparing – certain behaviors or aspects of behavior survive brain damage
  • Transient Collaterals – at some time during development they innervated targets, but were abandoned
  • Vicaration (not a popular theory) – functions of damaged areas can be assumed by adjacent areas
    • Some mechanisms may result in seizures or increased spasticity
    • Growth factors and Ach levels may offer promise

Variables Affecting Recovery

  • Lesion size
  • Age
  • Sex (females less lateralized)
  • Handedness – left less lateralized
  • Intelligence – though really, actual residual deficit may be equal
  • Personality – good: optimistic, extroverted, easy going
  • Better recovery with TBI than with CVA

Measures of Severity

  • Glasgow Coma Scale – use with more severe injuries; eye opening/motor response/verbal response (3-15); alcohol use will lower score
  • Coma duration (or LOC) – good predictor
  • PTA duration – best predictor; important in recording moment-to-moment events; usually about 4X the length of coma
    • Early Stage Recovery – disorientation (time comes last), confusion, agitation, lethargy, severely impaired attention, PTA

Cognitive Deficits

  • Mild TBI – attention, verbal retrieval, emotional distress, fatigue, depression
    • PCS – fatigue, irritability, decreased attention, headache, dizziness, memory deficits, anxiety, insomnia, phonophobia, photophobia, hypochondriacal concern
  • Moderate TBI – headache, memory problems, difficulty with everyday living, frontal and/or temporal lobe damage
  • Severe TBI – cognitive, emotional, and executive dysfunction (especially attention, memory, executive, anomia, pragmatics), social isolation, social dysfunction
  • Bulk of recovery is in first 6-9 months (memory slower than general IQ)
    • Social interaction/personality often biggest change
    • Often bigger PIQ decline than VIQ

Sensory Alterations Following CHI

  • Anosmia
  • Vision (acuity, field, oculomotor, diplopia, photophobia)
  • Dizziness
  • Balance d/o
  • Hearing defects (tinnitus)


  • Stimulation (early period) is useful
  • Forced use is helpful for body parts
  • Practice should be extensive and excessive
  • Training tasks should be relevant to real life
  • Family members, etc. should be included
  • Motivation is important
  • Continue training after plateaus
  • Break tasks down into simple components

Conclusions Regarding Adult TBI

  • Recovery most likely in complex behaviors with many components through behavioral compensation
  • Recovery most pronounced after incomplete lesions (e.g., concussions, penetrating head injury)
  • Recovery unlikely for specific functions controlled by localized brain areas f entire area removed
  • There are “always” residual and permanent deficits; extensive recovery is the exception

Miscellaneous Stuff

  • Akinetic Mutism – ability to respond, but can’t initiate (bilateral lesions of mesial frontal lobes, mesial temporal, cingulate gyrus)
  • Coma – caused by diffuse, severe destruction of white matter along with decreased circulation to brain (therefore, diffuse ischemic cortical dysfunction) – leads to necrosis
  • Coma secondary to hypoxia lasting more than one month carries very bad prognosis (worse than TBI)
  • Coma stimulation programs – outcome research is fairly equivocal; can train a response using backward chaining (but there is no accompanying change in cortical control)
  • GOAT – evaluates PTA
  • Penetrating Head Injury – focal lesion; shock waves and pressure effects may increase the effects seen; see more focal than diffuse effects; much higher rate of seizures than in closed head injury
  • Lashley (was WRONG) – recovery of function expected and easy to explain; principles of mass action and equipotentiality
  • Second Impact Syndrome – repeated concussions over brief periods of timing; typically following an initial brain injury and while still symptomatic
    • Often observed in contact sports
    • Rapid deterioration observed from conscious state to coma and possibly death, minutes to hours following trauma
    • Autopsies reveal loss of autonomic regulation of blood vessel diameter causing cerebral blood volume to rise which leads to increased ICP, diminishes cerebral perfusion and leads to increased risk of fatal brain herniation
  • GOAT – evaluates orientation, first memory recalled after PTA and last memory recalled before accident – Scale of 0-100; Normal = 76-100; Borderline = 65-75; impaired = <66

Classification of Severity of Brain Injury

(re: some variability across papers, but…)

  • LOC – most authors cite LOC of < 20-30 minutes considered “mild TBI”
  • GCS – Mild = 13-15; moderate = 9-12; severe = 3-8

Malingering and Its Differentials

  • Malingering – intentional production or gross exaggeration of symptoms motivated by external incentives
  • Conversion Disorder – change in functioning suggesting a physical disorder. Psychological factors are considered b/c of a temporal relationship b/t a psychosocial stressor and an initiation or exacerbation of the symptoms. However patient is not conscious of intentionally producing the symptoms. Distinguished from malingering due to the intentional production of symptoms and obvious external motivations in malingering
  • Factitious Disorder – voluntary production of symptoms to assume the “patient role” not associated with other clear incentives. E.g., ganser’s syndrome (faking a neurological symptom) and Munchausen syndrome
  • Simulation – feigning symptoms that do not exist
  • Dissimulation – concealment or minimization of existing symptoms

Test Construction


  • Test= systematic method for measuring a sample of behavior
  • Test construction specifying the test’s purpose
    • Generating test items
    • Administering the items to a sample of examinees for the purpose of item analysis
    • Evaluating the test’s reliability and validity
    • Establishing norms

Item analysis

  • Relevance– extent to which test items contribute to achieving the stated goals of testing

To determine relevance:

  • Content appropriateness: Does the item actually assess the domain the test is designed to evaluate
  • Taxonomic level: Does the item reflect the appropriate ability level?
  • Extraneous abilities: Does the item require knowledge, skills, or abilities outside the domain of interest
  • Ethics– to meet the requirements of privacy, the information asked by test items must be relevant to the stated purpose of testing (Anastasi)

Item Difficulty

  • Determined by the Item Difficulty Index (p)
    • values of p range from 0-1
    • calculated by dividing # who answered correctly by total # of sample
    • larger indicate easier items
      • p=1, all people answered correctly
      • p=0, no one answered correctly
    • Typically, items with moderate difficulty level (p=.5) are retained
      • increases score variability
      • ensure that scores will be normally distributed
      • provides maximum differentiation between subjects
      • helps maximize test’s reliability
    • Optimal difficulty level is affected by several factors
      • greater the probability that correct answer can be selected by guessing, the higher the optimal difficulty level
        • for true/ false item, where chance is .50, preferred difficulty level is .75
        • If goal of testing is to choose a number of examinees, the preferred difficulty level will = the proportion of examinees to be chosen
        • if on test, only 15% are to be admitted, the average item difficulty level for entire test should be .15

People in sample must be representative of population of interest, since difficulty index is affected by nature of tryout sample. Study tip- In most situations p=.50 is optimal, except in T/F test, where p=.75 is optimal.

Item Discrimination

  • Extent to which an item differentiates between examinees who obtain high vs low scores
  • Item Discrimination Index (D)
    • identifying the ppl who obtained the upper and lower 27%
    • for each item, subtract the percent of examinees in the lower-scoring group (L) from the percent of examinees in the upper-scoring (U) group who answered it right
  • D= U-L
    • range from –1 to +1.
      • D= +1 if all in upper group and none in lower group answer right
      • D= -1 if none in upper group and all in lower group answer right
    • Acceptable D= .35 or higher
    • Items with moderate difficulty level (.50) have greatest potential for maximum discrimination

Item Response Theory

Classical Test Theory

  • An obtained test score reflects truth and error
  • Concerned with item difficulty and discrimination, reliability, and validity
  • Shortcomings
    • item and test parameters are sample-dependent
      • item difficulty index, reliability coeff, etc likely to differ between samples
    • Difficult to equate scores on different tests
      • score of 50 on one test doesn’t = 50 on another

Item Response Theory (IRT)

  • Advantages over Classical Test Theory
    • item characteristics are sample invariant- same across samples
    • test scorers reported in terms of examinee’s level of a trait rather than in terms of total test score, possible to equate scores from different tests
    • Had indices that help identify item biases
    • Easier to develop computer-adaptive tests, where administration of items of based on examinee’s performance on previous items
  • Item characteristic curve (ICC)-
    • plot the proportion of ppl who answered correctly against the total test score, performance on an external criterion, or mathematically-derived estimate of ability
    • provides info on relationship between an examinee’s level on the trait measured by the test and the probability that he will respond correctly to that item
    • P value: probability of getting item correct based on examinee’s overall level
  • Various ICCs provide information on either 1, 2, or 3 parameters:
    • difficulty
    • difficulty and discrimination
    • difficulty, discrimination, and guessing (probability of answering right by chance)

Study tip Link these with IRT- sample invariant, test equating, computer adaptive tests


  • Classical test theory– obtained score (X) composed of true score (T) and error component (E) where X = T + E
  • True score= examinee’s status with regard to attribute measured by test
  • Error component= measurement of error
  • Measurement of Error= random error due to factors that are irrelevant to what is being measured and have an unpredictable effect on test score
  • Reliability– estimate of proportion of variability in score that is due to true differences among examinees on the attribute being measured
    • when a test is reliable, it provides consistent results
    • consistency = reliability

Reliability Coefficient

  • Reliability Index– (in theory)
    • calculated by dividing true score variance by the obtained variance
    • would indicate proportion of variability in test scores that reflects true variability
    • however, true test scores variance not known so reliability must be estimated
  • Ways to estimate a test’s reliability:
  • consistency of response over time
  • consistency across content samples
  • consistency across scorers
  • Variability that is consistent is true score variability
  • Variability that is inconsistent is random error
  • Reliability coefficient– correlation coefficient for estimating reliability
    • ranges from 0-1
    • r = 0, all variability is due to measurement error
    • r = 1, all variability due to true score variability
    • Reliability coefficient symbolized by rxx .
      • Subscript indicates correlation coefficient calculated by correlating test with itself rather than with another measure
    • Coefficient is interpreted directly as the proportion of variability in obtained test scores and reflects true score variability
      • r= .84 means that 84% of variability in scores due to true score differences while 16% (1.0 – .84) is due to measurement error.
      • If double it, reflects twice as much variability
      • Does NOT indicate what is being measured by a test
      • Only indicates whether it is being measured in a consistent precise way

Study tip Unlike other correlations, the reliability coefficient is NEVER squared to interpret it. It is interpreted directly as a measure of true score variability. r=.89 means that 89% of variability in obtained scores in true score variability.

Methods for Estimating Reliability

  1. Test-Retest Reliability
  • administering the same test to the same group on two occasions
  • correlating the two sets of scores
  • reliability coefficient indicates degree of stability or consistency of scores over time
    • coefficient of stability
  • Source of error
    • Random Factors-Primary sources of error are random factors related to the time that passes
  • Time sampling factors
    • random fluctuations in examinees over time (anxiety, motivation)
    • random variations in testing situation
    • memory and practice when don’t affect all examinees in the same way
  • Appropriate for tests that measure things that are stable over time and not affected by repeated measurement.
    • good for aptitude
    • bad for mood or creativity
  • Higher coefficient than alternate form because only one source of error
  1. Alternate (Equivalent, Parallel) Forms Reliability
  • two equivalent forms of the test are given to same group and scores are correlated
  • consistency of response to different item samples
  • may be over time, if given on two different occasions
  • alternate forms reliability coefficient
    • coefficient of equivalence when administered at same time
    • coefficient of equivalence and stability when administered at two different times
  • Content Sampling-Primary source of error is content sampling
    • error introduced by an interaction between different examinees knowledge and the different content assessed by the two forms
    • items on form A might be a better match for one examinee’s knowledge, while the opposite is true for another examinee
    • two scores will differ, lowering the reliability coefficient
  • Time sampling can also cause error
    • Not good for
      • when attribute not stable over time
      • when scores can be affected by repeated measurement
      • when same strategies used to solve problems on both forms= practice effect
      • when practice differs for different examinees (are random), it is a source for measurement error
    • Good for speeded tests
    • Considered to be the most rigorous and best method for estimating reliability
    • Often not done because of difficulty of creating two equal forms
    • Less affected by heterogenous items than internal consistency
      • higher coefficient than internal consistency (KR-20) when items are heterogeneous
  1. Internal Consistency Reliability
  • Administering the test once to a single sample
  • Yields the coefficient of internal consistency
  • Split half
    • Test is split into equal halves so that each examinee has two scores
    • Scores are correlated
    • Most common to divide by even and odd numbers
    • Problem- produces reliability coefficient based on test scores derived from one-half of the length of the test
      • reliability tends to decrease as length of test decreases
      • split-half tends to underestimate true reliability
      • however when two halves not = in mean or SD, may either under or overestimate
      • corrected using the Spearman-Brown prophecy formula, which estimates what reliability coefficient would have been
      • S-B used to estimate effects of increasing or decreasing length of test on reliability
    • Cronbach’s coefficient alpha
      • Test administered once to single sample
      • Formula used to determine average degree of inter-item consistency
      • Average reliability that would be obtained from all possible splits of the test
      • Tends to be conservative, considered the lower boundary of test’s reliability
      • Kuder-Richardson Formula 20- use when tests scored dichotomously (right or wrong); produces high reliability coeff for speeded tests
      • Sources of error
        • Content sampling: 1) split half: error resulting from differences in the two halves of the test (better fit for some examinees). 2) coefficient alpha: differences between individual test items
        • Heterogeneity of content domain: 1) coefficient alpha only. 2) test is heterogeneous when it measures several different domains. 3) greater heterogeneity, lower inter item correlation –> lower magnitude of coefficient alpha
        • Good for: 1) tests measuring a single characteristic. 2) characteristic changes over time. 3) scores likely to be affected by repeated measures
        • Bad for: 1) speed tests, because produce spuriously high coefficients. 2) alternate forms best for speed tests
  1. Inter-rater ( Inter-scorer, Inter-observer) Reliability
  • When test scores rely on rater’s judgment
  • Done by
    • calculating a correlation coefficient (kappa coefficient or coefficient of concordance)
    • determining the percent agreement between the raters
      • does not take into account the level of agreement that would have occurred by chance
      • px when recording high-frequency behavior because degree of chance agreement is high
    • Sources of error
      • factors related to the raters (motivation, biases)
      • characteristics of the measuring device
        • reliability low when categories are not exhaustive and/or not mutually exclusive and discrete
      • consensual observer drift
        • observers working together influence each other so they score in similar, idiosyncratic ways
        • tends to artificially inflate reliability
      • Improve reliability
        • eliminate drift by having raters work independently or alternate raters
        • tell raters their work will be checked
        • training should emphasize difference between observation and interpretation

Study tip Spearman-Brown = split-half reliability; KR-20 = coefficient alpha; Alternate form most thorough method: Internal consistency not appropriate for speeded tests

Factors that Affect the Reliability Coefficient

  1. Test length– longer the test, larger the reliability coefficient
  • Spearman-Brown can be used to estimate effects of lengthening or shortening a test on its reliability coefficient
  • Tends to overestimate a test’s true reliability
    • Most likely when the added items do not measure the same content domain
    • When new items are more susceptible to measurement error
  • When mean and SD not equal, can over or underestimate
  1. Range of test scores– maximized when range is unrestricted
  • range affected by degree of similarity among sample on attribute measured
    • when heterogeneous, range is maximized
    • will overestimate if sample is more heterogeneous than examinees
  • affected by item difficulty level
    • if all easy or hard, results in restricted range
    • best to choose items in mid-range (p = .50)
  1. Guessing
  • as probability of guessing correct answer increases, reliability coefficient decreases
  • T/F test lower reliability coefficient than multiple choice
  • Multiple choice lower reliability coefficient than free recall

Interpretation of Reliability

  • The Reliability Coefficient
    • Interpreted directly as the proportion of variability in a set of test scores that is attributable to a true score variability
    • R= .84 means that 84% of variability in test score is due to true score differences among examinees, while 16% due to error
    • Coefficient of .80 acceptable; achievement and ability is usually .90
    • No single index of reliability for any test
    • Test’s reliability can vary by situation and sample
  • Standard Error of Measurement
    • Assists in interpreting the individuals score
    • Index of error in measurement
    • Construct a confidence interval around the score
      • estimate range examinee’s true score likely to fall in
      • when raw scores converted to percentile ranks, called percentile band
    • Use standard error of measurement
      • index of amount of error expected in obtained scores due to unreliability of test
    • Standard error affected by the standard deviation and the test’s reliability coefficient
    • Lower standard deviation and higher reliability coefficient, the smaller the standard error of measure (vice versa)
    • Type of standard deviation, so talk about area under the normal curve
      • 68% confidence interval by +/- 1
      • 95% confidence interval by +/- 2
      • 99% confidence interval by +/- 3
    • Problem- measurement error not equally distributed throughout range of scores
      • use of same standard error to construct confidence intervals for all scores can be misleading
      • manuals report different standard errors for different score intervals

Study tip Name “standard error of measurement” can help remember when it’s used- used to construct a confidence interval around a measured (obtained score) Know difference between standard error of measurement and standard error of estimate

  • Estimating True Scores from Obtained Scores
    • Because of measurement effects, obtained test scores tend to be biased estimates of true scores
      • scores above mean tend to overestimate
      • scores below mean tend to underestimate
      • farther from the mean, greater the bias
    • Rather than using confidence interval, can use a formula that estimates true score by taking into account this bias by adjusting the obtained score by using the mean of the distribution and the test’s reliability coefficient.
      • less used
    • Reliability of Difference Scores
      • Compare performance of one person on two test scores (i.e., VIQ and PIQ)
      • Reliability coefficient for the difference score can be no larger than the average reliabilities of the two tests
        • Test A has reliability coefficient of .95 and Test B has .85, difference score will have reliability of .90 or less
      • Reliability coefficient for difference scores depends on degree of correlation between tests
        • more highly correlated, the smaller the reliability coefficient and the larger the standard error of measure


  • Test’s accuracy. Valid when it measures what it is intended to measure.
  • Intended use for tests, each has it’s own method for establishing validity
    • content validity- for a test used to obtain information about a person’s familiarity with a particular content or behavior domain
    • construct validity- test used to determine the extent to which an examinee possesses a trait
    • criterion related validity- test used to estimate or predict a person’s standing or performance on an external criterion
  • Even when a test is found to be valid, it might not be valid for all people

Study tip When scores are important because they provide info on how much a person knows or on each person’s status with regard to a trait- content and construct When scores used to predict scores on another measure, and those scores are of most interest- criterion related validity

  • Content Validity
    • The extent that a test adequately samples the content or behavior domain it is to measure
    • If items not a good sample, results of test misleading
    • Most associated with achievement tests that measure knowledge and with tests designed to measure a specific behavior
    • Usually “built into” test as it is constructed by identifying domains and creating items
    • Establishment of content validity relies on judgment of subject matters experts
      • If experts agree items are adequate and representative, then test is said to have content validity
    • Qualitative evidence of content validity
      • coefficient of internal consistency will be large
      • test will correlate highly with other tests of same domain
      • pre-post test evaluations of a program designed to increase familiarity with domain will indicate appropriate changes
    • Don’t confuse with face validity
    • Content validity = systematic evaluation of tests by experts
    • Face validity = whether or not a test looks like it measures what it’s supposed to
    • If lacks face validity, ppl may not be motivated
  • Construct Validity
    • When a test has been found to measure the trait that it is intended to measure
    • Abstract characteristic, cannot be observed directly but must be inferred by observing its effects.
    • No single way to measure
    • Accumulation of evidence that test is actually measuring what it was designed to
      • Assessing internal consistency: 1) do scores on individual items correlate highly with overall score 2) are all items measuring same construct
      • Studying group differences: 1) Do scores accurately distinguish between people known to have different levels of the construct
      • Conducting research to test hypotheses about the construct: 1) Do test scores change, following experimental manipulation, in the expected direction
      • Assessing convergent and discriminant validity: 1) does it have high correlations with measures of the same trait (convergent) 2) does it have low correlations with measures of different traits (discriminant)
      • Assessing factorial validity: 1) Does it have the factorial composition expected
    • Most theory laden of the methods of test validation
      • begin with a theory about the nature of the construct
      • guides selection of test items and choosing a method for establishing validity
      • example: if want to develop a creativity test and believe that creativity is unrelated to intelligence, is innate, and that creative ppl generate more solutions, you would want to determine the correlation between scores on creativity tests and IQ tests, see if a course in creativity affects scores, and see if test scores distinguished between ppl who differ in number of solutions they generate
      • Most basic form of validity because techniques involved overlap those used for content and criterion-related validity

“all validation is one, and in a sense all is construct validation” Cronbach

  • Convergent and Discriminant Validity
    • Correlate test scores with scores on other measures
    • Convergent = high corr with measures of same trait
    • Discriminant = low corr with measures of unrelated trait
    • Multitrait-multimethod matrix- used to assess convergent and discriminant
      • table of correlation coefficients
      • provides info about degree of association between 2 or more traits that have been assessed using 2 or more measures
      • see if the correlations between different methods measuring the same trait are larger than the correlations between the same and different methods measuring different traits
    • You need two traits that are unrelated (assertiveness and aggressiveness) and each trait measured by different methods (self and other rating)
    • Calculate correlation coefficient for each pair and put in matrix
    • Four types of correlation coefficients
    • Monotrait-monomethod coefficient = same trait-same method
      • reliability coefficients
      • indicate correlation between a measure and itself
      • not directly relevant to validity, need to be large
    • Monotrait-heteromethod coefficient = same trait-different method
      • correlation between different measures of the same trait
      • provide evidence of convergent validity when large
    • Heterotrait-monomethod coefficient = different traits-same method
      • correlation between different traits measured by same method
      • provide evidence of discriminant validity when small
    • Heterotrait-heteromethod coefficient = different traits- different method
      • correlation between different traits measured by different methods
      • provide evidence of discriminant validity when small

Factor Analysis

  • Identify the minimum number of common factors (dimensions) required to account for the intercorrelations among a set of tests, subtests, or test items.
  • Construct validity when it has high correlations with factors it would be expected to correlate with and low correlations with factors it wouldn’t be expected to correlate with (another way for convergent and discriminant validity)
  • Five steps
    • Administer several test to a sample:
      • administer test in question along with some that measure same construct and some that measure different construct
    • Correlate scores on each test with scores on every other test to obtain a correlation [R] matrix***high correlations suggest measuring same construct
      • low correlations suggest measuring different constructs
      • pattern of correlations determines how many factors will be extracted
    • Convert correlation matrix into factor matrix using one of several factor analytic techniques
      • Data in correlation matrix used to derive a factor matrix
      • Factor matrix contains correlation coefficients (“factor loadings”) which indicate the degree of association between each test and each factor
    • Simplify the interpretation of the factors by “rotating” them
      • pattern of factor loadings in original matrix is difficult to interpret, so factors are rotated to obtain clearer pattern of correlation
      • rotation can produce orthogonal or oblique factors
    • Interpret and name factors in rotated matrix
      • names determined by looking as tests that do and do not correlate with each factor
    • Factor loadings– correlation coefficients indicate the degree of association between each test and each factor
      • square it and determine the amount of variability in test scores explained by the factor
    • Communality– “common variance”
      • amount of variability in test scores that is due to the factors that the test shares in common with the other tests in the analysis
      • total amount of variability in test scores explained by the identified factors
      • communality = .64 means that 64% of the variability in those test scores is explained by a combination of the factors
    • A test’s reliability (true score variability) consists of two components
      • Communality– variability due to factors that the test shares in common with other tests in the factor analysis
      • Specificity– variability due to factors that are specific and unique to the test and are not measured by other tests in the factor analysis
        • portion of true test score variability not explained by the factor analysis
      • Communality is a lower limit estimate of a test’s reliability coefficient
        • a test’s reliability will always be at least as large as it’s communality
      • Naming of factor done by inspecting pattern of factor loadings
      • Rotated matrix: redividing the communality of each test included in the analysis
        • as a result, each factor accounts for a different proportion of a test’s variability than it did before the rotation
        • makes it easier to interpret the factor loadings
        • Two types
          • orthogonal- resulting factors are uncorrelated: 1) attribute measured by one factor is independent from the attribute measured by the other factor 2) choose if think constructs are unrelated 3) types include varimax, quartimax, equimax
          • oblique- factors are correlated: 1) attributes measured are not independent 2) choose if think constructs may be related 3) types include quartimin, oblimin, oblimax
          • When factors are orthogonal, test’s communality can be calculated from it’s factor loadings
          • Communality equals the sum of the squared factor loadings
          • When factors are oblique, the sum of the squared factor loadings exceeds the communality

Study tip

  • squared factor loading provides measure of shared variability
  • when orthogonal, test’s communality can be calculated by squaring and adding the test’s factor loading
  • orthogonal factors are uncorrelated, while oblique factors are correlated


  • Used when test scores are used to draw conclusions about an examinee’s standing or performance on another measure.
  • Predictor– the test used to predict performance
  • Criterion– other measure that is being predicted
  • Correlating scores of a sample on the predictor with their scores on the criterion.

When the criterion related validity coefficient is large, confirms the predictor has criterion related validity

  • Concurrent vs. Predictive Validity
    • Concurrent- criterion data collected prior to or at same time as predictor data
      • preferred when predictor used to estimate current status
      • examples: estimate mental status, predict immediate job performance
    • Predictive- criterion data collected after predictor data
      • preferred when purpose of testing is to predict future performance on the criterion
      • examples: predict future job performance, predict mental illness

Study tip Convergent and divergent associated with construct validity Concurrent and predictive associated with criterion-related validity

  • Interpretation of the Criterion-Related Validity Coefficient
    • Rarely exceed .60
    • .20 or .30 might be acceptable if alternative predictors are unavailable or have lower coefficients or if test administered in conjunction with others
    • Shared variability- squaring the coefficient gives you the variability that is accounted for by the measure
    • Expectancy table- scores on predictor used to predict scores on criterion

Study tip You can square a correlation coefficient to interpret it only when it represents the correlation between two different tests.

  • When squared, it gives a measure of shared variability
  • Terms that suggest shared variability include “accounted for by” and “explained by”
  • If asks how much variability in Y is explained by S, square the correlation coeff
  • Standard Error of Estimate
    • Derive a regression equation used to estimate criterion score from obtained predictor score
    • There will be error unless correlation is 1.0
    • Standard error of estimate used to construct confidence interval around estimated criterion score.
    • Affected by two factors: 1) standard deviation of the criterion scores and 2) predictor’s criterion related validity coefficient
    • Standard error of estimate smaller with smaller standard deviation and larger validity coefficient
    • Larger SD, larger standard error of estimate
    • When validity coefficient = +/- 1, standard error of estimate = 0
    • When validity coefficient = 0, standard error of estimate = standard deviation

Study tip Know difference between standard error of estimate and standard error of measurement. Standard error of estimate is confidence interval around an estimated (predicted) score

Incremental Validity

  • Increase in correct decisions that can be expected if predictor is used as a decision-maker
  • Important- even when a predictor’s validity coefficient is large, use of the predictor might not result in a larger proportion of correct decisions
  • Scatterplot
  • To use, criterion and predictor cutoff scores must be set
  • Criterion cutoff score- provides cutoff for your criterion being predicted, i.e. successful and unsuccessful
  • Predictor cutoff score- provides score that would have been used to hire or not hire
    • divides into positives and negatives
    • postivies= those who scored above the cutoff
    • negatives= those who scored below the cutoff
  • Four quadrants of the scatterplot
  • True positives– predicted to succeed by the predictor and are successful on the criterion
  • False positives– predicted to succeed by the predictor and are not successful on the criterion
  • True negatives– predicted to be unsuccessful by predictor and are unsuccessful on the criterion
  • False negatives– predicted to be unsuccessful by predictory and are successful on the criterion
  • If predictor score lowered number of positives would increase and number of negative would decrease.
  • If predictor score raised number of positives would decrease and number of negatives would increase. (false + decrease)
  • Selection of optimal predictor cutoff based on:
    • number of people in the four quadrants
    • goal of testing
      • goal is to maximize proportion of true positives, high predictor score set because reduces number of false positives
    • Criterion cutoff can also be raised or lowered, but might not be feasible
      • Low scores may not be acceptable
    • Incremental validity calculated by subtracting the base rate from the positive hit rate
      • Incremental validity = Positive Hit Rate – Base Rate
    • Base rate is proportion of people who were selected without use of the predictor and who are currently considered successful on the criterion
    • Positive hit rate is proportion of people who would have been selected on the basis of their predictor scores and who are successful on the criterion
    • Best when:
    • validity coefficient is high
    • base rate is moderate
    • selection ratio is low
    • When incremental validity is also used in determining whether a screening test is an adequate substitute for a lengthier evaluation
      • Positives- people who are identified as having the disorder by the predictor
      • Negatives- people who are not identified as having the disorder by the predictor
    • Criterion cutoff divides people into those who have been dx with the lengthier evaluation as having the disorder or not

Study tip

  • Predictor determines whether a person is positive or negative
  • Criterion determines whether person is false or positive
  • The scatterplot on the test may not have the same quadrant labels

Relationship between Reliability and Validity

  • Reliability places a ceiling on validity
    • when a test has low reliability, it cannot have a high degree of validity
  • High reliability does not guarantee validity
    • test can be free of measurement error but still not test what its supposed to
  • Reliability is necessary but not sufficient for validity
  • Predictor’s criterion related validity cannot exceed the square root of its reliability coefficient
    • If reliability coefficient of predictor is .81, validity coefficient must be <.90
  • Validity is limited by reliability of predictor and criterion
    • To obtain a high validity coefficient, reliability of both must be high

Correction of Attenuation Formula

  • Estimate what a predictor’s validity coefficient would be if the predictor and the criterion were perfectly reliable (r=1.0)
  • Need
  • the predictor’s current reliability coefficient
  • the criterion’s current reliability coefficient
  • criterion-related validity coefficient
  • Tends to overestimate the actual validity coefficient

Criterion Contamination

  • Accuracy of a criterion measure can be contaminated by way in which scores on the criterion measure are determined.
  • Tends to inflate the relationship between the predictor and a criterion, resulting in artificially high criterion-related validity coefficient
  • If eliminate it, coefficient decreases
  • Make sure that individual rating ppl on criterion measure is not familiar with performance on predictor.


  • When a predictor is developed, items that are retained for final version are those that correlate highly with criterion.
  • However, can be due to unique characteristics of try out sample
  • Predictor “made” for that sample, and if use same sample to validate the test, the criterion related validity coefficient with be high
  • Must cross validate a predictor on another sample.
  • Cross validation coefficient tends to shrink and be smaller than the original coefficient. Smaller the initial evaluation sample, the greater the shrinkage of the validity coefficient


  • Norm Referenced Interpretation- comparing to scores obtained by people in a normative sample
    • Raw score is converted to another score that indicates standing in norm group
    • Emphasis is on identifying individual differences
    • Adequacy relies on how much person’s characteristics match those in sample
    • Weaknesses
      • Finding norms that match person
      • Norms quickly become obsolete

Percentile Ranks-

  • raw score expressed in terms of percentage of sample who obtained lower scores.
  • Advantage: Easy to interpret
  • Distribution always flat (rectangular) in shape regardless of shape of raw score distribution because evenly distributed throughout range of scores (same # of ppl between 20 and 30 as between 40 and 50)
    • Nonlinear transformation: distribution of raw scores differs in shape from the distribution of raw scores
  • Disadvantage: ordinal scale of measurement
    • Indicate relative position in distribution, do not provide info on absolute differences between subjects
    • Maximizes differences between those in middle of distribution while minimizing differences between those at extremes
    • Can’t perform many mathematical calculations on percentiles

Study tip

  • Linear = distributions look alike
  • Nonlinear = distributions look different

Standard Scores

  • indicates position in normative sample in terms of standard deviations from the mean
  • Advantage: permits comparison of scores across tests
  • Z score: subtracting mean of distribution from raw score to obtain a deviation score, then dividing by distribution’s standard deviation
    • Z = (X – M)/SD
    • Following properties
  • mean = 0
  • SD = 1
  • All raw scores below mean are negative, all above mean are positive
  • Unless it is normalized, distribution has same shape as raw scores

Linear transformation Normalized by special procedure if think normal distribution in pop and that non-normality is error

  • T score: Mean of 50, standard deviation of 10 (essentially, multiply z times 10, and add 50)
    • 26% of scores fall within one standard deviation from the mean
    • 44% of scores fall within two standard deviations from the mean
    • 72% of scores fall within three standard deviations from the mean

Study tip Can calculate percentile rank from a z-score using the area under the normal curve. Percentile rank of 84 = z score of 1 50% fall below the mean and 34% (half of 68%) fall between the mean and 1SD, so50+34= 84

Age and grade equivalent scores

  • score that permits comparison of performance to that of average examinees at different ages or grades
  • easily misinterpreted
    • highly sensitive to minor changes in raw scores
    • do not represent equal intervals of measurement
    • do not uniformly correspond to norm referenced scores


  • Interpreting scores in terms of a prespecified standard.
  • Percentage score on type: indicates percentage of questions answered correctly.
    • A cutoff score in then set so that those above pass, and those below fail
  • Mastery (criterion referenced) testing: specifying terminal level of performance required for all learners and periodically administering test to assess degree of mastery
    • to see if performance improves from program or not
    • if deficiencies seen, given remedial instruction and process repeated until passes
    • goal not to identify differences between examinees, but to make sure all examinees reach same level of performance
  • Regression equation/ expectancy tables: interpreting scores in terms of likely status on an external criterion

Study tip Link percentile ranks, standard scores, and age/grade equivalents with norm referenced interpretation Link percentage scores, regression equation, and expectancy table with criterion referenced interpretation


  • Ensure that use of measures does not result in adverse impact for members of minority groups
  • Used to:
  • alleviate test bias
  • achieve business or societal goals (“make up” for past discrimination, allow for greater diversity in workplace)
  • increase fairness in selection system by ensuring that score on single instrument not overemphasized
  • Only first justification has been widely accepted, and only under certain circumstances (when predictive bias demonstrated)
  • Involve taking group differences into account when assigning or interpreting scores
    • Bonus points- adding a constant number of points to all ppl of a certain group
    • Separate cutoff scores- different cutoff scores for different groups
    • Within-group norming- raw score converted to standard score within group
    • Top-down selection from separate lists- ranking candidates separately within
      • Groups and then selecting top-down from within each group in accordance with a prespecified rule about number of openings. Often used by
      • Affirmative action to overselect from excluded groups
    • Banding: considering ppl within a range as having identical scores. May be
      • Combined with another method to ensure minority representation
    • Section 106 of the Civil Rights Act prohibits score adjustment or use of different cut off scores in employment based on race, color, religion, sex or national origin
      • Sackett and Wilk: may take group membership into if doing so can be shown to increase accuracy of measurement or accuracy of prediction without increasing the adverse impact of the test
        • banding found legal in one case
        • banding with minority preference may be useful for balancing competing goals of diversity and productivity and legal under the Act

Correction for Guessing

  • Ensure examinee does not benefit from guessing
  • When tests corrected, best to omit rather than guess
  • Corrections involve calculating a corrected score by taking into account:
    • the number of correct responses
    • the number of incorrect responses
    • the number of alternatives for each item
      • Corrected score = R – (W/n-1) where
    • R = number of right answers
    • W = number of wrong answers
    • N = number of choices per answer
    • When the correction involves subtracting points from scores, the resulting distribution will have a lower mean and a larger SD than the original distribution
    • Experts generally discourage correction for guessing
      • unless considerable number of items omitted by some of the examinees, relative position of examinees will be same regardless of correction
      • correction ahs little or no effect on test’s validity

Only time justified is for speeded tests


Substance Abuse

Note: methodological problems are common in studies of neuropsychological outcome of substance use due to high rate of co-morbidities and polysubstance use.


Acute Effects

  • One of the most widely investigated and abused illicit drugs in the US.
  • High doses can create rapid motor activity, rambling speech, impaired judgment, paranoid and psychotic behavior, irritability, and anxiety.
  • EEGs show marked reduced Alpha power in frontal and temporal regions.

Prenatal Cocaine Exposure

  • Newborn infants who are exposed to cocaine in utero are more likely to have reduced gestational age, length, and head circumference. Low birth weight has also been implicated in some studies.
  • Often behavioral or temperamental problems emerge, typically by age 3.
  • Cocaine exposed infants can show increased tone and motor activity, jerky movements, startles, tremors, back arching and signs of CNS and visual stress. Also reported are difficulties with auditory skills, excitability, and lethargy.
  • Heavily cocaine-exposed infants show more jitteriness and attentional problems compared to lightly and non-exposed infants.
  • Longitudinal studies of prenatally exposed toddlers and preschoolers typically show low average to average cognitive abilities but tend to be highly distractible and can have significant difficulties with speech and language development, peer interactions, and fine motor coordination.

A few longitudinal studies

  • Cocaine use within 72 hours (acute) is associated with specific neuropsychological impairments, including deficits in memory, visual-spatial processing, and concentration.
  • After two weeks of abstinence, deficits are noted in the areas of psychomotor speed, memory, and concentration.
  • These deficits are consistent with deficits seen in dopamine depletion disorders such as Parkinson’s and progressive supranuclear palsy.
  • Problems with planning and impulsivity have also been reported.
  • CT studies show evidence of cerebral atrophy in chronic users.


  • Stimulant toxicity may include repetitive teeth grinding, skin picking, perseverative speech or behavior, preoccupation with one’s own behavior and mental activity, suspiciousness, paranoia with auditory and visual hallucinations, hyperactivity, confusion, convulsions, and even life-threatening conditions such as cardiovascular collapse and high fever progressing to death.
  • Withdrawal from stimulants can produce extreme depression, fatigue, extreme somnolence, and apathy. Persistent mood and anxiety problems may last for several months.
  • Neuropsychological studies indicate symptoms associated with CNS damage, including disruptions in memory, concentration, and abstract reasoning.
  • Exposure of infants to methamphetamines prenatally produces similar symptoms as are found in cocaine exposed babies. These include lethargy, tremor, and increased intraventricular hemorrhage.


  • Associated with low birthweight, miscarriage, prematurity, microcephaly, and intrauterine growth retardation.


  • Associated with spontaneous abortions, premature rupture of membranes, preterm delivery, perinatal death, low birth weight, and deficits in learning and behavior.


  • A CNS depressant.
  • Impairment in visual-motor skills, integration of sensory stimulation, and information processing become apparent at blood levels of 100 mg (about the point when one feels intoxicated).
  • Higher blood levels eventually can result in sedation, CNS depression, stupor, and even coma. *Tolerance and physical and psychological dependence develop over time with diagnosable alcoholism; this diagnosis can usually be made after 3 to 15 years of prolonged use.
  • Rarely do children or adolescents experience seizures, hallucinations, or the DT’s which are frequently experienced by adult users.

Outcomes Following Alcohol Cessation

  • Following cessation, older subjects show improvement after prolonged alcohol use but remain in the impaired range on a variety of neurocognitive tests.
  • This is not the same for younger individuals under the age of 35 to 40 who usually return to normal performance levels within about one month after cessation.
    • This is at least the finding in younger alcoholics who have drank six years or less.
  • After initial sobriety, alcohol dependence in younger adults (ages 18 through 35) have found few deficits in language skills, attention, motor skills, intelligence, memory, and executive functions.

Neuroimaging Findings

  • Neuroimaging studies have demonstrated that chronic alcoholism in older adults produces widespread brain damage, but such evidence has not been apparent with children and younger adults.
  • The frontal lobes are uniquely sensitive to alcohol abuse although postmortem studies have implicated temporal and parietal lobes as well.
  • Clinical signs associated with damage to frontal cortex associated with alcohol abuse include emotional apathy, disinhibition, poor attention, and abnormal perseverative responding.
  • Drug abuse combined with heavy alcohol use, which is often typical, show significantly smaller cerebellar vermes. White matter changes can also occur.

Glue Sniffing

  • Neuropsychological deficits include abnormalities in attention, memory, visual-spatial functions, complex cognition, naming, and problems with reading or writing. Deficits in manual dexterity, visual scanning, and verbal memory have also been reported.
  • Neuropsychological deficits appear to be dose related.
  • In one study, diffuse atrophy of cerebral hemispheres, cerebellum and, in severe cases, the brainstem were evident in 88.8% of subjects studied.
    • Of note, this study was confounded because of polysubstance (e.g., amphetamines, marijuana, and alcohol) use.


  • Research is limited but take home message is that there is a dose-response relationship, with greater marijuana use resulting in greater deficits.
    • Memory appears to be the most significant cognitive area affected, and memory efficiency has been noted as the primary difficulty, at least during active marijuana use.
  • In long-term users (>30 years):
    • Neurocognitive problems were noted in sustained attention (a continuous performance test).
    • Short-term memory effects have also been reported, although these have been described as subtle or subclinical.
  • In younger adults, MRI studies have shown evidence of cerebral changes, including large left lateral ventricles, temporal lobe dilation, and damage to the caudate nucleus and basal ganglia.
    • The subjects in the above imaging study were users for a period of 3 to 11 years, but polysubstance use was again a confounding factor.

Somatosensory Pathways

Basic Facts

  • Somatosensory: bodily sensations of touch, pain, temperature, vibration, and proprioception (limb or joint position sense)
  • Two main pathways: See Table 7.1, Figure 7.1, 7.2
    • Posterior column – medial lemniscal pathway: conveys proprioception, vibration,

fine/discriminative touch

    • Anterolateral pathways: include spinothalamic tract and other associated tracts that convey pain, temperature, crude touch
    • Some aspects of touch carried by both pathways; not eliminated in isolated lesions to either pathway
  • Four types of sensory neuron fibers have specialized peripheral receptors that subserve

different sensory modalities, classified by axon diameter (see Table 7.2)

  • Dorsal root ganglion: neuron cell bodies; bifurcated stem axon – one conveys sensory info from periphery, other carries info into spinal cord through dorsal nerve roots
  • Dermatone: peripheral region innervated by sensory fibers from a single nerve root level; dermatomes for different spinal levels form a map over the surface of the body (see Figure 8.4)

Posterior column – medial lemniscal pathway:

See Figure 7.1, 7.4

ML Pathway > decussate in medulla > thalamus > posterior limb of internal capsule > primary somatasensory cortex

  • Large diameter myelinated axons carry proprioception, vibration, fine/discriminative touch; enter spinal cord via medial portion dorsal root entry zone
  • Many of the axons enter the ipsilateral posterior columns to ascend all the way to the posterior column nuclei in the medulla
  • In addition, some axon collaterals enter the cord central gray matter to synapse onto interneurons and motor neurons
  • Somatotopic organization: See Figure 7.3, add on laterally as it ascends; gracile fasciculus: medial, info from legs/lower trunk; cuneate fasciculus: lateral, info from upper trunk above to about T6 and arms/neck; first order sensory neurons that have axons in these synapse onto second-order neurons in nucleus gracile and nucleus cuneatus
  • Axons of the second-order neurons decussate as internal arcuate fibers and then form medial lemniscus on the other side of the medulla
  • Medial lemniscus axons terminate in the ventral posterior lateral nucleus (VPL) of the thalamus
  • Neurons of the VPL project through the posterior limb of the internal capsule in the thalamic somatosensory radiations to reach the primary somatosensory cortex
  • Touch for the face conveyed via analogous path – trigeminal lemniscus (see ch. 12)

Spinothalamic tract and other anterolateral pathways:

  • small diameter unmyelinated axons carrying pain, temperature info also enter cord via dorsal root entry zone but make first synapse immediately in cord gray matter mainly in dorsal horn marginal zone (lamina I) and deeper in dorsal horn (lamina V)
  • Some axon collaterals ascend/descend a few segments in Lissauer’s tract before entering central gray
  • Second-order central gray sensory neurons cross over in spinal cord anterior (ventral) commissure to ascend anterolateral white matter
  • Takes 2-3 spinal segments for decussating fibers to reach opposite side – lateral cord lesions affect

contralateral pain/temp a few segments below

  • Somatotopic organization: feet most laterally represented
  • Thalamus next major relay which projects via thalamic somatosensory radiations to primary somatosensory cortex
  • Pain/temp for face carried by analogous path – trigeminothalamic tract (see ch. 12)
  • Some crude touch also when posterior columns damaged
  • consists of 3 tracts: spinothalamic, spinoreticular, spinomesencephalic
  • Spinothalamic: discriminative pain/touch, e.g., location/intensity; main relay ventral posterior lateral nucleus (VPL); projections to other thalamic nuclei – intralaminar and medial nuclei such as mediodorsal; lamina I & V
  • Spinoreticular: emotional and arousal aspects of pain; terminates medullary-pontine reticular formation which projects to intralaminar thalamic nuclei (centromedian) – project diffusely to entire cortex and thought to be involved in behavioral arousal; lamina 6 – 8
  • Spinomesencephalic: pain modulation; projects to midbrain periaqueductal gray matter and superior colliculi; lamina I & V


See Figure 7.1, 7.2, 6.1

Primary somatosensory cortex:

  • postcentral gyrus; areas 3, 1, and 2
  • thalamaic VPL and VPM nuclei convey somatosensory info to the cortex
  • Somatotopic organization: face most laterally and leg, most medially
  • Conveys info to secondary somatosensory association cortex in the parietal operculum (superior margin of Sylvian fissure); somatotopic organization
  • Further processing occurs in association cortex of posterior parietal lobule including areas 5 and 7
  • Extensive connections with motor cortex
  • Lesions produce cortical sensory loss (see KCC 7.3)


See Table 7.3, Figure 7.6

Basic Facts:

  • “Inner chamber/bedroom” in Greek
  • Important processing station; nearly all pathways that project to cortex do so via relays in the thalamus- major sensory relay station
  • Nuclei receive dense reciprocal feedback connections from cortical areas. In fact, cortical thalamic projections outnumber thalamocortical projections
  • See ch. 14-17
  • Divided into: medial, lateral, and anterior nuclear groups by internal medullary lamina (y-shaped, white matter) – it’s nuclei called intralaminar; midline thalamic nuclei (thin, adjacent 3rd ventricle); thalamic reticular nucleus (lateral aspect)
  • 3 main categories of nuclei: relay, intralaminar, and reticular

See Figure 7.7, 7.8

Relay Nuclei:

  • Makes up most of thalamus
  • Lateral: all sensory but olfaction have specific relays; VPL, VPM; lateral geniculate nucleus (LGN) – visual (ch. 11); medial geniculate nucleus (MGN) – auditory (ch. 12); ventral lateral nucleus (VL) – cerebellum/basal ganglia motor
  • Anterior: limbic pathways (ch. 18)
  • Nonspecific nuclei: widespread projections; e.g., pulvinar: posterior, large, pillow-shaped, behavioral orientation; mediodorsal nucleus (MD): major relay to frontal association, cognitive functions

Intralaminar Nuclei:

  • Within internal medullary lamina
  • Input from numerous pathways, reciprocal cortical connections; sometimes classified with other “nonspecific” relay nuclei
  • 2 functional regions: caudal intralaminar nuclei – include centromedian nucleus, and mainly basal ganglia (ch. 16); rostral intralaminar nuclei – basal ganglia and inputs from ascending reticular activating system (ARAS) to cortex, maintaining alert/conscious state (ch. 14)

Reticular Nucleus:

  • Lateral; only nucleus that does not project to cortex
  • Regulates thalamic activity
  • Receives input from other thalamic nuclei and cortex and then projects back to thalamus
  • Almost pure population of inhibitory GABAergic neurons
  • Other inputs from brainstem reticular activating system and basal forebrain may modulate alertness/attention (ch. 14, 19)



  • Abnormal positive sensory phenomena
  • Character and location can have localizing value; e.g., posterior column lesions (medial lemniscal pathways) = tingling, numbness, tight bandlike feeling around trunk/limbs (See 7.1, page 276)
  • Dejerine-Roussy syndrome: parietal/primary sensory cortex lesions; severe contralateral pain
  • Lhermitte’s sign: cervical lesions; electricity-like feeling running down back to extremities with neck flexion
  • Radicular pain: nerve root lesions; radiates down limb in dermatomal distribution; numbness/tingling; provoked by movements stretching nerve root
  • Peripheral nerve lesions can cause – are of nerve distribution (See KCC 8.3)*Other terms: dysesthesia (unpleasant); hyperpathia/allodynia (painful)

Summary of Types of parathesias depending upon location

  • Lesions of anterolateral pathways – sharp, burning or searing pain
  • Lesions of parietal lobe or primary sensory cortex – numb or tingling, but pain can also be present
  • Thalamus – severe contralateral pain ‘’’ dejerine-roussy syndrome’’’

Spinal cord lesions:

See Table 7.4

  • major disability; involve motor, sensory, autonomic paths
  • Signs/sx’s obvious when sensory level and motor dysfunction correspond to level of lesions (See KCC 7.4)
  • Reflex abnormalities: e.g., abnormal sphincter help confirm diagnosis
  • In subtle cases, minor sensory/motor changes, back/neck pain, or fever may be only clues
  • In acute severe lesions, often initial phase of spinal shock: flaccid paralysis below lesions, loss of tendon reflexes, decreased sympathetic outflow – decreased blood pressure, absent sphincter reflexes, and tone
  • Myelitis: infectious or inflammatory (See KCC 5.9, 6.6)

Sensory loss: patterns and localization

(See pages 278-285):

  • Primary somatosensory cortex: contralateral; discriminative touch/joint position most severely affected but all modalities may be involved; all primary senses can be relatively spared but cortical sensory loss (extinction, or decreased stereognosis, and graphesthesia, (ch. 3) present (See KCC 19.6)
  • VPL/VPM/thalamic somatosensory radiations: contralateral; may be more noticeable in face/hand/foot than trunk/proximal extremities; sometimes with no motor deficit
  • Lateral pons or lateral medulla: contralateral pain/temp loss for body but ipsilateral for face (See KCC14.3)
  • Medial Medulla: contralateral vibration/joint position loss (ch. 14)
  • Spinal cord: See KCC 7.
  • Nerve roots or peripheral nerves: distal symmetrical polyneuropathies cause bilateral sensory loss in a “glove and stocking” distribution in all modalities; specific lesions cause sensory loss in specific territories (See KCC 8.3, 9.1)

Spinal cord syndromes:

See pages 280-283, Figure 7.10

  • Transverse cord lesion: all sensory/motor paths partially/completely interrupted; often a sensory level corresponding to lesion level; common causes – trauma, tumor, MS
  • Hemicord Lesions: Brown-Sequard syndrome: See page 280; lesions lateral corticospinal = ipsilateral upper motor neuron weakness; posterior columns = ipsilateral loss vibration/joint position sense; anterolateral = contralateral loss pain/temp
  • Common causes – MS, tumors, penetrating injuries
  • Central cord syndrome: small lesions in spinothalamic fibers cause bilateral regions of suspended sensory loss to pain/temp; cervical lesions cause classic cape distribution; sacral sparing (loss below lesions except in this region)
  • Posterior cord syndrome: posterior column lesions cause loss of vibration and position sense below lesion level
  • Anterior cord syndrome: loss of pain/temp below lesion level; anterior horn lesions = lower motor neuron weakness at lesion level


Olfactory Disturbances (4 Types):

Quantitative Abnormalities

  • Loss or reduction of sense of smell (anosmia or hyposmia)
    • Can be from the nasal, neuroepithelial, or central level
    • if bilateral, patient usually complains of ageusia (loss of taste)
  • Increased olfactory acuity (hyperosmia)
    • very rare, if exists

Qualitative Abnormalities

  • distortions or illusions of smell (dysosmia or parosmia)
  • May be associated with depressive illness

Olfactory Hallucinations/Delusions

  • Always of central origin
  • Most often due to temporal lobe seizures (uncinate fits)

Higher-order loss of discrimination (Olfactory Agnosia)

  • Perceptual aspects intact, but deficits in recognition


Stages of Sleep

Sleep staging is done via an overnight sleep study or polysomnogram (PSG) that includes, at a minimum, EEG, an electro-oculogram (looking at eye movement), and an electromyelogram (looking at skeletal muscle movement, usually on chin). Most PSGs have additional leads to examine limb movement and respiration. As of 2007, the American Academy of Sleep Medicine recognized 3 non-REM sleep stages, plus REM:


On EEG, predominantly low amplitude, relatively fast alpha activity (8-13 waves/sec) during relaxation or mixed alpha and beta activity (>13 waves/sec) accompanied by fast eye activity during vigilant/alert wakefulness.

N1 (Non-REM stage 1)

Very light sleep. EEG slows down, but remains low amplitude. Theta waves appear (medium amplitude, 4-7 waves/sec). Stage 1 is usually brief, and is a transition between wakefulness and Stage 2.

N2 (Non-REM stage 2)

EEG continues to show predominantly theta activity, with the introduction of sharp waveforms called K-complexes and brief bursts of beta activity called sleep spindles.

N3 (Non-REM stage 3)

“Slow Wave Sleep”, incoporates what had previously been called Stages 3 and 4 NREM. Deep sleep. EEG reflects high amplitude, low frequency delta waves (< 4 waves/sec). Most parasomnias (sleepwalking, night terrors) arise from N3 sleep.

REM (Rapid eye movement)

Sometimes called “paradoxical sleep” because the EEG looks like wakefulness (quick, mixed frequency, low amplitude) but the person is asleep. Can be distinguished from wakefulness by evidence of rapid eye movements and very low skeletal muscle tone. Most dreaming (and nightmares) occur during REM.

Other info about sleep stages:

  • Muscle tone & activity is greatest in wakefulness, declines in stages N1 – N3, and lowest during REM
  • At birth, roughly half of sleep is REM
  • With age, slow-wave and REM sleep diminishes, leaving mostly light sleep. Most rapid decline in REM occurs during early childhood. Most rapid decline in N3 (slow-wave sleep) occurs during adolescence. However, general trend towards decline evident throughout development.
  • In a healthy young adult, slow-wave sleep occurs mostly during the first ½ of the night, REM mostly during the second ½. Most of sleep is spent in stage 2 (about 50%), REM (about 25%), or Stage 4 (about 10-15%).

Important points for neuropsychologists

  • Adequate sleep quantity and quality are essential for daytime functioning, with the most marked effects of poor sleep seen in sustained attention/vigilance, coordination, and emotion regulation. There can also be effects on memory retrieval and aspects of executive functioning (EF). Finally, emerging evidence suggests that sleep is essential to long-term memory consolidation as well.
  • Sleep generation and regulation is dependent on a broad system that includes the brainstem through the diencephalon and limbic system. Any neurological condition or injury that affects a portion of this system can impact sleep. Dementing conditions are often accompanied by sleep disturbances, as is Parkinson’s Disease.
  • Many psychotropic meds can affect sleep. If sleep is a complaint, consider whether meds are contributing.
  • Sleep is particularly important in the epilepsies, as sleep deprivation can promote seizures, and seizures can occur during sleep (in some cases, sleep is the time they occur most).
  • The sleep-wake cycle is influenced by two processes:
    • Time spent awake relative to time recently spent asleep. During wakefulness there is a build-up of sleep pressure, roughly reflected in basal forebrain adenosine levels, that quickly dissipates during sleep, especially N3 (slow wave) sleep. In healthy sleepers, sleep pressure is greatest just prior to sleep onset and, of the two processes, tends to be the major contributor to sleep onset.
    • The circadian rhythm, which is an endogenous rhythm which roughly approximates 24 hrs in healthy sleepers, and which is entrained to a 24-hr cycle mostly by bright light exposure. A major marker, core body temp, is usually lowest at 2-4 am, highest in late afternoon. Consequently, this rhythm helps sustain wakefulness even as sleep pressure builds, and sustains sleep even as sleep pressure dissipates.
  • There are over 80 different sleep disorders. Two of the most important to know as a neuropsychologist are:
    • Narcolepsy: Misalignment of the various aspects of sleep. For example, aspects of REM can intrude into wakefulness during cataplexy (sudden loss of muscle tone during wakefulness, often when excited) or occur right around sleep onset or offset (hypnagogic and hypnopompic hallucinations, sleep paralysis in which person is awake but unable to move). There is also excessive daytime sleepiness, which is treated with stimulants.
    • Obstructive Sleep Apnea: Repetitive obstruction and/or collapse of the airway during sleep, especially seen during REM sleep, conventionally defined as occurring > 10 times/hour in adults or >5 times/hour in children. Results in frequent brief arousals and intermittent hypoxia, daytime sleepiness, poor daytime vigilance, motor uncoordination, depression, and ADHD symptoms in young kids. May cause memory and EF deficits, too.

Sensitivity and Specificity

We sometimes use tests to try to detect diseases, setting a cutoff value on the test to indicate whether or not the individual has the disease. Of course, our tests are not perfect, so test results may not match reality/truth. As shown in the table below, a person can either truly have (+) or not have (-) the disease, and the test can either say the person has (+) or do not have (-) the disease. We use the terms positive predictive power, negative predictive power, sensitivity, and specificity to describe how well the test decision matches reality in a population of individuals.

Has Disease No disease
Test=true True positive False positive
Test = healthy False Negative True Negative

Positive Predictive Power (PPP) = True Positive divided by [True Positive + False Positive]

  • The reference value (i.e., the demoninator) for PPP is TOTAL WHO TEST POSITIVE FOR DISEASE.

Negative Predictive Power (NPP) = True Negative divided by [True Negative plus False Negative]

  • The reference value for NPP is TOTAL WHO TEST NEGATIVE FOR DISEASE.

Sensitivity – ability to pick out individuals with disease; the True Positive rate of a test

Sensitivity = True Positive / [True positive + False Negative]

  • The reference value for sensitivity is TOTAL WHO REALLY HAVE DISEASE.

Specificity – ability to pick out individuals without disease; the True Negative rate of a test

Specificity = True Negative / [True Negative + False Positive]

  • The reference value for specificity is TOTAL WHO REALLY DO NOT HAVE DISEASE.

Base Rate Summary

The base rates of the disease in the general population affect predictive power (Bayesian analysis).

Positive predictive power (PPP) – probability that an individual who receives an abnormal test score actually has the disorder of interest

  • PPP is determined by the test’s sensitivity and specificity in the context of base rate info
  • Even w/ 90% sensitivity and specificity, if base rate is relatively low (condition is rare), the majority of individuals who exhibit that sign or test score will not have the condition.
    • In unreferred population of 1,000 children and 4% base rate for ADHD, 40 children are expected to have ADHD.
    • Using a test w/ 90% sensitivity and specificity, only 27% of children who receive an abnormal score on the test can be expected to actually have disorder. That’s more than a random guess (which would yield only 4% success in identifying kids with the disorder), but it’s still not great.
ADHD present No Adhd
Abnormal score 36 96 PPP= 36/(26+96) = 27%
Normal score 4 864 NPP= 864/{864+4) = 99%

Sensitivity: 36/(36+4) = 90% Specificity: 864/(864+96) = 90%

  • As illustrated in the chart below, the best Positive Predictive Power comes with high prevalence and high specificity.
50% 43% 10% 1% 0.1% 0.04%
90% 91 88 53 9 1 0.4
95% 95 94 69 17 2 0.8
99% 99 99 92 50 9 4
99.9% 99.9 99.9 99 91 50 29