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324 Cards in this Set

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What are Paraneoplastic syndromes?
rare neurologic disorders caused by remote effects of cancer in the body leading to autoimmune response.
meningismus?
(meningismus= meningeal irritation) often caused by meningitis OR
SAH, carcinomatous meningitis, or chemical sensitivity.
6 common signs of meningismus?
H.A., Lethargy, Photo & Phonophobia, fever, nuchal rigidity.
Brain Abscess?
Bacterial infection of nervous system that presents as an expanding intracranial lesion, much like a tumor, with a more rapid course.
Common sx of Brain Abscess?
HA, lethargy, fever, nuchal rigidity, nausea, vomiting, seizures, and focal signs determined by location of BA.
Where do epidural abscesses most often occur?
Spinal canal.
What is neurosyphilis? What are the stages?
1. sexually transmitted bacterial infection.
2.
A. Primary syphilis- painless skin lesions occur at site of infection
B. Secondary syphilis: Worse lesions within 6 months involving palms and soles.
C. Tertiary syphilis: Neurological manefestations present.
Consequences of Neurosyphilis?
Meningeal involvement and cranial nerve palsies, especially II, VII, & VIII. Can also have late stages, which are more serious (different card).
Later stages of neurosyphilis:
latency?
3 types and sx?
1. Can occur 4-15 years
2. A. Meningovascular syphilis: chronic meningeal involvement, arteritis (generally midsize vesicles) diffuse white matter infarcts. Can lead to . . .
B:General paresis: accumulation of infarcts with dementia, bx changes, delusions of grandeur, psychosis, UM neuron weakness.
C) Tabes Dorsalis: Different variant can occur with B results in degeneration of spinal dorsal column. Leads to sensory ataxia (highstepping gait) and incontinence.
Lyme Disease:
Cause?
Physical Sx?
Neurological Sx?
1) bacteria carried by deer tick.
2)raised rash
3) Often delayed weeks.
-meningeal signs
-emotional changes
-impair memory and concentration
Most common viral encephalitis?
HSV-1
Sx of HSV
meningial signs, psychotic bx, confusion, and seizures. Focal signs can also be present.
HSV MRI findings in which 2 regions?
Can cause necrosis of bilateral or unilateral temporal and frontal structures.
Transverse myelitis?
inflamation of spinal chord. Transverse suggests it goes across the thickness of the SC.
Progeressive Multifocal Leukoencephalopathy?
-Cause
-MRI
Condition can occur with AIDS or other immunocompromised patients.
-Caused by papovavirus (JC virus) results in gradual demyelenation.
-T2 bright white matter anomalies particularly posterior.
HIV and Toxoplasmosis
-Mechanism
-MRI
-Comes from parasite. Initial exposure from undercooked meat or cat feces is often asymptomatic, but it becomes reactivated with AIDS.
-Creates brain absecess visable on MRI as ring enhancing lesion (dark middle bright ring).
Most common cause of intracranial mass lesion in HIV?
Toxoplasmosis
Why are serological tests for Toxoplasmosi unhelpful?
30% of the general population in US have been exposed.
Cysticerosis?
-Mechanism?
-Sxs?
-Caused by ingestion of the eggs of a pork tape worm.
-Migrates through blood stream leaving small cysts in muscles, eyes, and CNS.
-seizure, ha, nausea, vomit, meningitis, and focal signs.
Name the Prion disorders:
Crutzfeldt-Jakob,
Gerstmann-Straussler- Schneiker disease,
kuru,
fatal familial insomnia
3 Main long tracks of the CNS and their functions?
1-Lateral Corticospinal- Motor
2-Posterior Columns- Sensory (vibration, fine touch, position)
3-Anterolateral Sensory (pain, temp., heavy touch)
Where does the lateral corticospinal tract originate?
Over 50% of fibers come from primary motor cortex the rest come from premotor, supplementary motor, or parietal lobes.
The Corticospinal tract lies in the ___ limb of the internal capsule?
Posterior
What is the order of motor neurons as the Corticospinal tract passes through the internal capsule?
The hemunculous is preserved, i.e beggining with anterior (face, arm, trunk, leg).
Cervicomedullary Junction?
Area where the medulla turns to spine. At the level of the foramen magnum. Also location of pyramidal decussation (where motor tracks become ipsilateral).
What is Crural Monoparesis?
Unilateral leg weakness.
What is Brachial Monoparesis?
Unilateral arm weakness.
In Bell's palsy, paralysis of only the lower 1/2 of the face is associated with ______ motor neuron, whereas full facial paralysis is associated with ____ motor neuron.
Upper; Lower
Where are the cell bodies for sensory neurons located?
Dorsal Root Ganglia
The Posterior Column -Medial lemniscal somatosensory pathway decusates at the level of the ________ _______, whereas the Antolateral pathway decusates at the level of the _____ ________ _________.
1. caudal medulla
2. Cervical Spinal Chord
The Spinothalamic tract is part of what larger group of sensory pathways?
The Anterolateral pathways.
The anterolateral and posterior column sensory tracts go through what nucleas of the Thalamus?
VPL Ventral posterior lateral nucleas
3 Tracts of the anterolateral pathways
-spinothalamic
-spinoreticular
-spinomesencephalic
Gate Control Theory
-Pain modulation occurs as sensory inputs from large fiber non-pain fibers reduce pain transmission through the dorsal horn. This is why shaking your hand may reduce pain from hitting your thumb with a hammer.
Internal Medullary Lamina
Y-shaped white matter structure that segments the thalami into the 3 sepperate regions.
Cranial nerves relay through what thalamic nuclei?
ventral posterior medial
Which Thalamic nucleas is the major relay of information being sent to the frontal association cortex?
Mediodorsal (MD) *can also be called dorsalmedial.
Parestesia?
-abnormal positive sensory phenomena.
Dejerine-Roussy syndrome
Lesions to the thalamus cause severe contralateral pain
Myelopathy?
Term meaning spinal chord dysfunction.
Vibration, fine touch, and proprioception will be ____lateral above the medulla and ____lateral in the spinal chord. In contrast, Crude touch, pain, and temp. will be ___above the C-spine level.
-Contra, ipsi
-Contra
Left PCA stroke can cause alexia without agraphia, if it extends to which structure?
The splenium of the C.C.
Major sign of PCA stroke
Contralateral hemonimous hemianopia
Large MCA strokes often have what gaze phenomena?
Gaze preference toward the side of the lesion.
What % of patients with TIA will have an associated stroke within 3 months time?
15%
What percentage of strokes following TIA occur within 48 hours?
50%
3 conditions that can mimic a TIA
Migraine, seizure, and hypoglycemia.
Transient LOC without other focal features?
-Most common cause?
-Just what it sounds like.
-Cardiogenic syncope
What is hemorrhagic conversion?
When ischemic stroke causes the blood vessels to become fragile leadio
Embolic v.s. Thrombotic infartcts?
Embolic- peice of material (usually clot) develops somewhere and travels to area.
Thrombotic-Clot is formed locally, usually d/t anthroschlerotic plaque.
Lacunar is another term for?
Small vessel infarcts, because they resemble small lakes.
Lipohyalinosis?
hypertension related changes in the blood vessel walls. Common cause of small vessel disease.
Ataxic Hemiparesis
Similar to pure motor hemiparesis, but with associated ataxia on side of weakness. The ataxia is often caused by by damage to proprioceptive or cerebellar circuitry rather than direct injury to the cerebellum.
Hemiballismus
Abnormal involuntary movement on one side. Usually contorting and continuous and of a rotatory nature. (J.C. hypoxia from smoke inhalation)
HA occurs in what % of stroke patients?
25-35%
Seizures occur in what percentage of stroke patients?
3-10%
Common (general) vascular risk factors. These can lead to stroke. (6)
hypertention, hypercholesterolemia, cigarette smoking,
diabetes,
fam hx,
prior hx of stroke or c.v. disease
Stenosis?
Abnormal narrowing of a blood vessel.
What is the initials of the drug that treats acute stroke?
TPA
Bruit?
A "wooshing" sound that is often heard on examination that is sensitive to stenosis (particularly carotid stenosis can be detected below the jaw).
As light passes through the lens it forms an image on the retina that is ____ and ____?
inverted, reversed
Ratio of rods to cones?
-Differences
Rods are 20:1 more common
-Rods have poor spatial resolution and don't detect color, cones are the opposite.
Lesions of the Optic Chiasm cause what visual field defect? Lesions anterior to the chiasm?
Bitemporal, monocular.
What is the anatomy of the extrageniculate visual pathway
-A few fibers in the optic nerve bypass the LGN and project to the Pretectal area and superior colliculus. Diffuse projections from there including to the pulvinar.
Lesions of the optic radiations cause what types of defects?
Homonomous defects of contralateral field.
Temporal lobe lesions can cause what visual field defect?
Contralateral superior homonomous hemianopsia (pie in the sky). This is because the lower optic radiations convey information from the upper visual fields to the lower bank of the calcerine fisher.
Parietal lobe lesions cause what type of visual field defect?
Contralateral inferior hemonomous hemianopsia (pie on the floor)
How is the calcerine fisure organized?
Retinotopically. i.e. the retina is represented in the occipital pole, with more periphreal regions being represented more anteriorally along the calcerian fisure.
Which area of the eye has the greatest cortical representation?
The fovea, despite being a smaller portion b/c of it's higher acuity it has 50% of the PV cortex.
scotoma?
A circumsized area of visual field loss.
Homonymous defect?
A scotoma that involves the same area of visual field in both eyes.
Macular sparing?
Because the fovea has a large representation you can some times get sparing of the most central portion of the visual field, despite the presence of a visual field defect. This also happens because the MCA and PCA provide collateral flow the the portions of the Macula in the occipital pole.
What causes Anterior Ischemic Optic Neuropathy (AION)
Impaired blood supply to the anterior optic nerve.
Infarcts of the LGN typically produce what visual field defect?
Contralateral homonomous hemianopia
The "what stream of visual association cortex" is fed by what artery.
This is the inferior (occipitotemporal) stream and it is fed by the PCA.
The Where stream of visual cortex is fed by what artery?q
This is the superior stream (lateral parieto-occipital). It is fed by watershed regions between the PCA and MCA.
What is optic neuritis?
-Sxs?
Inflamatory demyelinating disorder of the optic nerve. Similar to M.S.
-Eye pain (especially with movement), monocular vision impairment (typically central scotoma, decreased acuity, and color blindness).
What % of individuals with optic neuritis develop MS?
50%
Abnormalities in what areas have been correlated with autism?
Cerebellum, Brain stem, temporal lobes.
Planum Temporale
Area of cortex between Heschel's gyrus and the sylvian fissure. Larger in the left (with difference noted prenatally).
amaurosis fugax?
TIA due to carotid atherosclerotic disease. This causes transient blindness that resolves.
Occular Apraxia?
Difficulty scanning a visual scene.
Dopamine Track associated with extrapyramydal motor disorders?
Nigrostriatal
Pseudobulbar palsy is typical of which dementia?
progressive supranuclear palsy, a subcortical dementia.
Extrapyramidal signs, visual hallucinations and delusions, and memory & attention impairments suggest which dementia?
D with Lewy Bodies
Geshwind's model of agnosia.
Characteristic of his work this was a "disconnection" model, between visual and verbal processes. Specifically, he noted that although agnostics could not name objects they were noted to interact normally with them.
What is the counter arguement to Geshwind's model of agnosia?
most agnostics show both verbal and nonverbal impairments.
Apperceptive agnosia is associated with what brain lesions?
Bilateral involvement of the lateral occipital.
Associative agnosia is associated with what brain lesions?
-bilateral occipitotemporal lesions (e.g. strokes in PCA)
How do you distinguish as agnosic from an agnostic.
-The agnosic can usually describe the object and key functions, but fails to recall the name. Agnosics also do not typically improve, with the use of other senses to detect the stimuli (i.e. holding it in their hand).
Pt's with associative visual agnosia often demonstrate intact drawing of an object. However, their drawings are characterized by?
A peice meal (part-oriented) approach that misses the general gestalt.
What visual impairment is commonly co-morbid with associative agnosia?
Right Homonomous Hemianopia.
Optic aphasia?
A condition where pts can not name objects visually displayed, but demonstrate recognition through indicating it's use, pointing to it when named, or otherwise demonstrating knowledge of the object. (tactile and auditory naming are preserved).
Balint's Syndrome
-Lesions
-Clinical
Caused by large bilateral parietal lesions (especially severe if frontal lobes affected)
Sxs
1) Simultanagnosia
2)Ocular apraxia (inability to shift gaze voluntarily from a fixation point)
3)Optic ataxia: impairment of visually guided movements as a result of a defect in stereopsis (depth perception).
Receptive Amusia
inability to appreciate characteristics of heard music.
Phonagnosia
inability to recognize familiar person's voices.
Pure word deafness
(also called auditory agnosia for speech, auditory verbal agnosia) is the inability to comprehend spoken language despite the ability to read, write, and speak. Comprehension of nonverbal sounds is also spared.
Lesions associated with pure word deafness.
bilateral cortical-subcortical lesions of anterior superior temporal lobe, with some sparing of Heschel's gyrus.
Auditory sound agnosia
-Lesion location
-Oposite of pure word deafness, can understand words, but inability to recognize sounds (i.e. dog barking).
-Variable lesions, but often same region as pure word deafness, but in the R hemisphere.
Auditory affective agnosia.
-Lesion
-Inability to recognize the affective intonations of speech, despite intact understanding of content.
-Right temporoparietal.
Phonagnosia
-lesion locations
-Deficits in voice recognition.
-Unilateral R hemisphere pts demonstrate difficulties with familiar voices. In contrast, tempotal lobe impairment in either hemisphere can lead to more general voice descrimination.
Astereoagnosia
The equivalent of apperceptive tactile agnosia. A narrower definition would be the inability to recognize shapes in the hand. Often associated with agraphastethia.
Associative tactile agnosia.
Someone can recognize the shape, weight, etc. of object in the hand, but still not name it.
According to Nielson's model, what are the 3 forms of agraphia?
-Aphasic
-Apretic (basically apraxic)
-Isolated
3 main ways to evaluate agraphia?
-Spontaneous writting.
-Writting to dictation.
-Copying.
Exner's area
Area just superior to broca's believed to be associated with agraphia.
Pure Agraphia
-Just what it sounds like, agraphia without any language impairments. Usually includes well produced graphemes, but significant spelling errors.
What is sometimes called parietal agraphia?
Agraphia with alexia, b/c when these occur without aphasia it is often due to parietal lesions.
Which agraphia is often associated with neglect?
Spatial agraphia.
From a neuropsych perspective, what are the 2 cognitive systems available to adults for spelling words.
-Lexical-Relies on sounding words out. Pt's show inability to spell atypical words (i.e. fane for feign).
-Phonological- Pt's will show inability to spell nonsense words, but intact spelling of used words (even complex).
Lexical agraphia has been associated with what cortical region?
Angular gyrus is most common, although other areas occur. Also, the parisylvian region is typically spared.
Brain region most associated with phonological agraphia?
Supermarginal gyrus and the insular cortex proximal to the SMG.
Deep Agraphia
Difficulties spelling nonwords (similar to phonological agraphia), but also . . .
-Greater spelling function words than nouns (i.e. arm > throw).
-Presence of semantic paragraphic errors. This is where you write a word similar in meaning to the target that is not close lexically or phonologically (i.e. propellor for flight).
Semantic Agraphia
-Loss of ability to incorporate meaning in spelling or writting.
-Incorrect homophones may be present (i.e. dough for doe).
-However, both irregular and nonwords are spelled correctly (not lexical or phonemic agraphia).
Ideational Agraphia (Also called Apraxic Agraphia withour Apraxia)
-Not apraxic agraphia because can hold pen, but difficulties with all the motor steps needed to write.
Visual spatial agraphia (constructional agraphia) is characterized by what 3 findings?
-Reiteration of strokes
-Inability to complete a straight horizontal line.
-Insertion of spaces between graphemes.
*Often associated with neglect.
Reiterative agraphia?
-What clinical syndrome is this associated with?
abnormal repetition of phrases, words, letters, etc.
often seen w/ frontal lobe dementia
Apraxias often don't come to clinical attention b/c of their association with what other clinical condition?
-Anosognosia.
Limb Kinetic Apraxia
-Difficulties with fine precise movements (generally 1 limb)
-Hard to distinguish from unilateral Ataxia
-More obvious with distal movements (picking a coin off table).
Ideomotor apraxia?
-Impairment of single components of an action (despite o.k. dexterity). Sepperation between idea of an act and its' performance.
Transative and intransative commands?
-Whether the command assessing appraxia includes use of a tool (transitive- show me how to use a hammer).
Pt's with Ideomotor Apraxia have the greatest difficulties when asked to make what type of movements?
Transative meaning to use a tool (often they show problems with pretending to use transative movements).
-However, is also seen with intransitive movements.
4 broad categories of errors seen in ideomotor apraxia?
-Perseverative (do something from previous task).
-Sequencing error- (i.e. turn the key b4 extending the arm).
-Spatial: The most common error (posture, orientation, movement).
-Timing
3 types of spatial errors seen in ideomotor apraxia?
-Posture
-Spatial Orientation- ex. when pretend to cut bread the knife turns from horizontal plane.
-Spatial movement- Movement at the wrong joints. Ex. rotating the shoulder while pretending to use a scre driver.
Ideomotor Apraxia?
-Difficulties with the execution of individual components of an action. Refers to single action not multi-step.
Liepman's model for ideomotor apraxia?
-The L hemisphere contains "movement formula." Thus lesion to the L. hemisphere cause R hand apraxia. Lesion to the Anterior CC causes apraxia in L hand d/t disconnection.
Goodglass defective symbolization model of apraxia?
-B/C the left hemisphere seems involved in both apraxia and aphasia, this is the idea that the L is involved in symbolization (apraxia being a loss of nonverbal symbolization). Counter- is that not all individuals with apraxia have aphasia.
Geschwind's model of apraxia involves impairment of what tract?
The Arcuate fasciculus.
Representational hypothesis of apraxia (Heilman)?
-The brain stores "Praxicons" (visuo-kinestetic engrams) in the inferior parietal lobe.
What are the 2 causes of ideomotor apraxia, as postulated by the representational hypothesis?
-Damage to the praxicons (believed to be in either the L. supramarginal or angular gyrus) OR the connection between this area & PMC.
What are innervatory patterns (in relation to Apraxia)?
-Heilman's theory- The specific motor plan used for praxis. The supplementary motor cortex is responsible for translating praxicons into innervatory patters.
Conduction Apraxia?
-Pt can pantomime movements to command, but has difficulty imitating transitive movements.
Ideational Appraxia is often associated with what other group of conditions?
Lesion location?
-Dementias
-Believed to be frontal.
How to test for ideational apraxia?
-Have the pt pantomime an activity with multiple steps (i.e. getting a letter ready to mail). Impairment usually seen pantomime> actual object use.
Pantomime agnosia?
Failure to recognize guestures that are being pantomimed (worst Charades player ever:) But they can make guestures.
Conceptual apraxia?
-Pt can make transative movements, but use the wrong one. (ex. hammering motion for screwdriver). Distinguished from agnosia b/c they can I.D. the object.
Pathophysiology for conceptual apraxia?
Posterior L. (Liepman say caudal L. parietal lobe.
Buccofacial Apraxia?
-Pathophysiology?
-Difficulty making movements with face, larynx, pharynx etc. (blow out a match).
-Frontal and central opercula (lid over insula), anterior insula, 1st temporal gyrus (close to opercula).
Constructional Apraxia?
-Not really a traditional apraxia b/c more d/t visual skills.
-Problems with drawing, assembling, or building.
Ocular Apraxia?
-Part of what syndrome?
-Not really an apraxia by classical term.
- Inability to perform purposeful ocular movements
-Balint's
Optic ataxia/apraxia?
Not an appraxia in classical sense.
-Apraxia of visual movements affecting visually guided hand movements.
-Seen as difficulty reaching for object.
Callosal apraxia
-Form of ideomotor appraxia. Unilateral in L hand d/t diconnection of visuokinetic engrams in L. hemisphere from motor areas of R.
The Orbital Frontal region is involved in what aspects of attention?
response initiation; inhibition
Medial Frontal Lobe is involved in what aspects of attention?
intent to respond; consistency of responding; focused attention
Dorsolateral frontal lobes are involved in what aspects of attention?
sequencing; persistence; switching; focus
Limbic systems role in attention?
establishes salience, whereby determining priority of incoming stimuli
Midbrain's role in attention?
arousal and activation
Musalam's model of attention?
2 systems
1.Reticulothalamocortical (bottom up) and
2.Parietal-limbic-prefrontal cortex (top down)
Reticulothalamocortical modulation of attention in Musalam's model?
-Bottom up system-increases arousal by passing sensory information to cortex (global influence on attention without selectivity).
Parietal-limbic-prefrontal modulation of attention Musalam's model ?
(top down)
-Regulates context, motivation, significance, and volition
3 major functions of attention in Posner's model.
1. Orient to sensory stimuly (involuntary)
2. Detecting signals for focal processing (voluntary)
3. Maintaining vigalence and altertness.
2 attentional systems according to Posner and Peterson?
-Posterior-orient, awareness, dorsal visual pathway, cortical connections to parietal lobe.
-Anterior-Signal detection, anterior cingulate, supplementary motor cortex.
Mirsky's model of attention. Hint:derived from factor analysis of npsych data.
1-Focus/Execute-Capacity to concentrate attention and screen out distractors.
2-Sustain (vigilance)
3-Shift (includes selective/divided)
4-Encode (sounds like WM)
5-Stabilize-Reliability of attentional effort.
Cohen, Malloy, & Jenkin's model of attention?
1)Sensory selective attention- Process of selecting what to attend to through (filtering, focussing, disengagement).
2)Attn. capacity and focus-intensity and resources devoted.
3)Sustained (vigilance)
4)Response selection and control (i.e.effortful fascilation of attn.)
Extinction (or called E. to double simultaneous stimulation)
-When sensory systems are tested in 1 side they are normal, but one side becomes impaired when bilateral stimuli.
Extinction is typically mildest in which sensory modality?
Auditory b/c each ear projects to both hemispheres.
3 broad categories of neglect?
-Inattention (sensory neglect)
-Intentional neglect (motor neglect)
-Limbic-Motivational
Akinesia
A type of motor neglect: failure to move the contralateral body part spontaneously (can be eyes, arm, leg, etc.)
Motor Extinction:
A type of motor neglect: The pt does not demonstrate akinesia when asked to move one limb at a time, but doesn't use affected limb when both are needed.
What is "endo-evoked" v.s. "Exo-evoked"
In regards to motor extinction does to the pt move the limb on their own "endo-evoked" or do they move in response to stimuli "exo-evoked"
What is hypokinesia?
Form of motor neglect: The pt does not fail to initiate motor system, but does so after a long time.
Bradykinesia in the context of neglect?
Slow completion of motor tasks in affected limb. This is not restricted to the initation time (hypokenisia).
Motor Impersistence?
In neglect inability to sustain motor act with the affected side.
Allokinesia?
In neglect, pt moves the wrong limb or moves the affected limb in the wrong direction.
Hemispatial neglect?
-Neglect to draw or act on one side of the body. Can also be up/down near/far directions. Tested through line bisection.
Personal neglect?
Failure to recognize or attend to contralateral part of their body. (i.e. deny that their arm is their own, fail to dress affected side).
Anosodiaphoria?
The pt is aware of the deficit, but is not concerned by it. Somewhat similar to anosognosia.
Pathophysiology associated with unilateral neglect?
-Reticular formation, thalamus (nucleas reticularis), cingulate, parietal-occipital-temporal junction.
3 main causes of neglect?
-CVA, tumor, seizures- Diffuse processes are less likely (i.e. TBI, metabolic conditions, or SDH.
Neuroanatomical substrate of achromatopsia?
-inferior surface of the occipital/temporal region.
Cerebral Akinotopsia?
Inability to perceive visual motion.
4 Types of Impairments in topographical knowledge.
-Egocentric Disorientation.
-Heading Disorientation.
-Landmark agnosia.
-Anterograde disorientation.
What is egocentric disorientation?
-Pathophysiology
Topigraphical disorientation secondary to the inability to locate objects in space. Pt's struggle with even familiar terraine.
-Posterior parietal and occipital juncture, bilaterally.
Heading disorientation?
-Pathophys?
-Specific topographical impairment, inability to remember the spatial relations between landmarks in the environment.
-only a few cases (posterior cingulate).
Landmark agnosia?
-Pathophys?
-A type of topographical disorientation where pt fails to recognize land marks (i.e. buildings etc.), but retains spatial knowledge.
-Similar to other visual agnosia occipitotemporal regions (bilateral or R).
Anterograde Disorientation?
-Pathophys
-Topographic d/o w/ spatial and recognition impairments, but is selective to the acquisition of new knowledge.
-Limited cases R. parahippocampal gyrus.
Besides the R. Hippocampus, what other brain region can cause nonverbal memory deficits?
-Mesialdorsal nucleas of the Thalamus
Spatial synthesis-
perceived spatial features of an object that make it “that object”
Inability to recognize facial expressions has been associated with bilateral dammage to what structure?
Amygdala.
What is Balint's syndrome (3 components)?
“Acquired disturbance of ability to perceive the visual field as a while, resulting in unpredictable perception and recognition of only parts (simultanagnosia) which is accompanied by impairment of target pointing under visual guidance (optic ataxia) and inability to shift gaze at will toward new visual stimuli (ocular apraxia)”
Describe L. Hemisphere v.s. R. hemisphere visual constructional apraxia?
-L. hemisphere: drawing is spatially correct, but oversimplified with omission of details
R. Hemisphere: fragmented drawing; may have details but lost whole of picture and spatial relations; may neglect left side.
L. Hemisphere v.s. R. Hemisphere errors on Block design.
L-maintenance of 2x2 configuration, but error with internal details; tend to recognize when incorrect.
R: break configuration, but see internal details; do not appreciate when incorrect; may skew to right space.
4 mitigating factors of childhood cancer and treatment.
-Age: < 5 is bad
-Gender: impairment more prevalent and severe in females.
-Treatment: XRT + intrathecal methotrexate worse than just XRT. XRT dose > 2000 cGy and higher MTX associated with leukoencephalopathy
-Sequence of treatment: lower CNS pathology when IT MTX given before XRT rather than after.
Characteristics of Broca's aphasia.
-Slow halting speech, words misarticulated, often missing function words. Repeating and naming (slightly impaired) comprehension WNL.
Characteristics of Wernicke's Aphasia
-Major disturbance comprehension. There are also morphological, phonemic, and semantic paraphasias. Poor repetition and naming. Speech is fluent
Sxs pure motor speech disorders (anarthria, dysarthria, apraxia of speech).
-Pathophys?
-Only disruption of articulation.
-Outflow of tracks from motor area.
Sxs pure word deafness?
-Pathophys?
-Major:Pt does not recognize spoken words. Spontaneous speech is normal. Repetition often impaired.
-Input tracks from auditory system to Wernicke's.
Sxs transcortical motor aphasia?
-Pathophys?
-Major deficit spontaneous speech (like Broca's), but comprehension and repetition relatively WNL. White matter tracts linking Broca's to parietal lobes.
Sxs transcortical sensory Aphasia?
-Pathophys
Major deficit: single word comprehension, w/ relatively intact repetition.
-White matter connecting parietal to frontal OR portions inferior parietal.
Sxs conduction aphasia?
-Pathophys?
-Main sx, disturbance of repetition. Speech is fluent, but paraphasic. Comprehension is normal.
-Arcuate fasciculous OR cortical connections between broca and wernickes.
Sxs of Anomic Aphasia?
-pathophys?
-Disturbance in single words (especially nouns). Intact comprehension and repetition. Mild speech difficulties can be noted.
-(diverse lesions, but can be inferior parietal, connections parietal and temporal.
Global Aphasia?
-Pathophys
-Just what you think.
-Large portions of parasylvian region.
Sxs of isolation of the language zone (aphasic syndrome)
-Pathophys.
-Disturbance spontaneous speech (slow & halting) & comprehension. Repetition is somewhat better. Echolalia is common.
-Area just outside parasylvian association cortex.
Which classical aphasia is associated with watershed injuries between ACA & MCA?
-MCA & PCA?
-Transcortical motor aphasia.
-Transcortical sensory aphasia.
What are the 2 components of the dual-route model of reading?
-Lexical-Letter strings are matched with learned LS's stored in the "visual word form system"
-Phonological form- Uses sounding out words.
Peripheral & Cental (deep) dyslexias?
-Peripheral dyslexias reflect a deficit of processing the visual aspects of the stimuli.
-Central dyslexia's reflect difficulties in higher order reading functions by which visual forms are associated with meanings. (hint: analogous to perceptual v.s. associative agnosia)
Alexia without agraphia (i.e. pure alexia; letter-by-letter reading).
(peripheral dyslexia)
-Some are unable to read others use letter-by-letter approach.
-Errors of similar letters (i.e. m-n)
-Can have word superiority effect.
Most common peripheral dyslexia?
Alexia without agraphia.
pathophys of alexia without agraphia?
-Typically L occipital area OR regions that provide input to this area (i.e. LGN of thalamus, white matter tracts)
Word superiority effect?
(can recognize it is a word, but not which one).
Can a typical 1st grader have alexia?
-No. Alexia is an acquired deficit in reading. Deficits in the development are called dyslexia or developmental dyslexia.
Neglect Dyslexia
-Pathophys
-Associated with visual neglect. Leave off a portion of the word. Errors occur more commonly when visual info in both fields (double simultaneous suppression).
-Usually R. parietal, but can also occur in L.
Attentional dyslexia?
(Perepheral Dyslexia)
-disturbance in reading multiple words or text, secondary to disturbance in visual attention; single-word reading relatively preserved.
Deep Dyslexia?
(Type of central dyslexia)
-Semantic errors (i.e. castle = knight). Often morphological errors.
-Improved on words with higher immaginability (e.g. table) than low (e.g. passion).
-Functional words (functors) are often ommited (the, which, they, etc.).
-Impairments with nonwords.
Morphological error?
-Errors in prefix or suffix in reading (i.e. reading = readed or read).
Pathophys of Deep Dyslexia?
-Typically large L. parasylvian extending into the frontal regions.
-Occasionally posterior lesions.
-Some argue involvement of the R. hemisphere.
Phonological dyslexia
-pathophys?
(Type of central dyslexia)
-Just what it sounds like.
-Pt's read real words fine, but can't do nonwords.
-Associated with a variety of lesions (most often supramarginal or angular gyri).
-some times R.
Surface Dyslexia?
(Type of Central Dyslexia)
-Inability to read irregular words (i.e. yacht), but intact regular and nonwords.
Surface Dyslexia is associated with what group of conditions?
-Often found in dementias. Alternatively, believed to be related to focal lesions.
Commisurotomy
-Disconnection of all 3 cerebral commisures
-Corpus callosum
-anterior commisure
-hippocampal commisures (go across fornix)
*Some cases masa intermedia
The posterior 1/5 of the corpus is fed by which major artery?
-PCA
-synopsis of 4 major points of findings in patients with split-brain (callosotomy).
1.Social Ordinariness- Look WNL.
2.Lack of interhemispheric transfer. (e.g. inability to i.d. object with R. hand, despite palpating in L).
3.Hemispheric Specialization: E.g. naming items better in R. than L. hand.
4. Compensatory phenomena-Got better with time.
Intermanual conflict. (e.g. diagonistic dyspraxia)
Sx following callosotomy (usually acute), where hands work in cross purposes (e.g. one hand button up shirt while other unbutton). Also seen in CC tumors or stroke.
Alien Hand Syndrome
-Pathophys (particularly when persistent).
Similar to intermanual conflict. Seen in callosotomy pts.
-CC particularly involving Mesial frontal cortex.
L hemianomia
-In split-brain pt inability to name objects shown to only the L. visual field.
L. Hemialexia
-In split brain pts inability to read words shown in the L. Visual field.
How to test audition in split brain pt's.
-Because hearing has ipsilateral, as well as contralateral tracts, this is tested by dichotomous listening (i.e. different but accoustically similar info in each ear). This works b/c the ipsilateral projection is suppressed by stronger contralateral.
What 2 auditory phenomena are noted in split brain pt's?
-L hemisphere suppresion of ipsilateral verbal input. In normals verbal info. is better heard in R. ear. This split is > dramatic in split brain pts.
R. Hemisphere suppresion of nonverbal ipsilateral input.-The R. hemisphere typically involved in interpreting prosody. Better interpretation of language prosody for info. presented in L. ear.
L. tactile anomia?
In callisotomy pt's the inability to name objects held in the L. hand.
Primary (pure) acalculia v.s. secondary acalculia?
-1 model of acalculia.
-Primary A. refers to A. that cannot be attributed to defects in other domains.
-Secondary A. refers to A. that can be (at least in part) attributed to attention, memory, ect.
Alcalculia with alexia and agraphia of numbers?
-Pathophys?
-Impaired reading or writing of #'s causes acalculia (may or maynot be associated with aphasia).
-Generally L. hemisphere (typically parietal).
Acalculia of the spatial type.
-Pathophys?
-Acalculia d/t probs lining up columns in math etc. May also be a problem reversing #'s (i.e. 6 for 9).
-R. hemisphere
Anarithmetria
-Pathophys
-Similar to primary acalculia in Berger or Grewel's model. This is A. that is not associated with other cog. deficits (from Hecaen's model).
-Generally L. hemisphere, but also (less common) in R.
Selective impairment of syntactic processing in Arabic Numeral Processing.
A specific acalculia. The Pt comprehends #'s read to them. When writing #'s prints fine, but hard time (e.g "two-hundered and twenty = 20020.
Selective impairments of operation symbol comprehension (e.g. asymbolic acalculia)?
-Can not interpret signs (i.e. forgets + means add).
Selective impairment in calculation ability?
form of acalculia. The pt can recall math concepts, but fails to do even simple calculation. (e.g. understands algebra but not 2+2).
Dissociation of arithmetic Operations?
-Pathophys?
-Inability to do certain opperations. (e.g. the pt can add and subtract, but cannot multiply or divide.
-limited cases L.
Selective impairment in digit naming?
-Pt can't name digits, despite intact comprehension and math equation skills.
When pt's with R. hemisphere lesions are compared to those with L. hemisphere, which ones show the highest rates of acalculia?
L. hemisphere (particularly L. parietal).
Autopagnosia?
-Inability to name body parts on self, examiner, or pictures.
Most acalculias are associated with predominantly L. or bilateral lesions. What is a common acalculia that is generally associated with R. (particularly post-rolandic).
-Acalculia of the spatial type.
AD constitutes what % of all the dementias?
50-80%
What is the prevalance of dementia in 65-70 year olds?
-How does it increase after that?
-1%
-For each 5 years the %age doubles until 85 when all bets are off!
70-75 = 2%
75-80 = 4%
80-85 = 8 %
>85 = 20-50%
2 most prominent risk factors of dementia?
-Gettin' old and family risk.
What are the major genetic factors for AD?
-How does familial and non-familial AD differ?
-APOE - (onset typically age 50-75)
-Alz. precursor gene chromosome 14
-Presenilin 1 gene(chrzm. 14)
-Presenilin 2 gene (chrzm 1)
B- they only differ in age of onset.
How is education related to AD?
-Very low ed. attainment raises risk (i.e. <8th grade raises risk 2-3X).
-Cognitive performance at 20 can be predictive of AD.
Head trauma & AD
-Earlier TBI can be a risk factor (need more study). Some suggest APOE-4 may link the 2.
Heart conditions that pose risk for later AD?
-What other (non-neuro) medical condition is associated?
-Artherosclerosis, hx of stroke, hypertension, or carotid artery disease.
-Diabetes.
2 medical treatments that may be protective factors against AD?
-Estrogen replacement tx.
-Non-steroidal anti-inflamatory drugs.
-Smoking is mixed, some studies say lower risk others say raise risk.
How do older non-demented individuals perform on list learning tasks?
-Reduced learning, particularly as the length of the list increases. However, recall is as good as younger pt's (in contrast to clear impairment in AD).
How is delirium distinguished from dementia?
-The main thing is course (delerium is acute rapid onset). Additionally, impairments in arousal and attention generally suggest delirium.
What 2 domains are better assessed in the Orientation-Memory-Concentration test than in the MMSE.
-Memory and EF (look at the name).
Anterograde amnestic syndrome?
-A clinical term for the neuropsych pattern of dementia characterized predominantly by anterograde amnesia. Of course, the most common cause is AD.
Besides the obvious, what areas are associated with Frontotemporal dementia?
-Subcortical include thalamus, neostriatum, or anterior white matter.
2 types of language syndromes seen in FTD?
-Semantic Dementia: anomia and comprehension.
-PPA: Includes prominent expressive impairments.
What is the most likely syndrome associated with the visual spatial type of dementia?
-AD
Clinical features that suggest something other than AD?
-Sudden onset
-Focal neurological findings.
-Seizures and gait disturbance (at the onset).
Cholinergic projection neurons in the Nucleas basalis, diagnal band, and the septum often demonstrate what pathology? in what dementia condition?
-neurofibrillary tangles
-AD
Early and late onset AD differ in what way related to language function?
-Early is more likely to demonstrate language impairments early in the disease.
How does fine motor speed vary between dementias?
-Some slowing can be seen in early AD, but it is less prominant. In contrast, slowing is often seen in subcortical dementias (i.e parkinsons). HIV and vacular also have suibcortical involvement.
What is more common "pure" vascular pathology causing dementia or vascular dementia associated with AD?
-Vascular with AD (2x)
How does "pure" vascular dementia differ from AD in regards to the NP profile?
Vascular dementia has a variable np profile, as might be expected given the differing causes. But generally speaking pts show more of a frontal or subcortical profile.
What are the main signs of dementia with lewy bodies?
-Gait and balance disturbance
-visual halucinations and delusions
-Fluctuating cognitive status
-sensitivity to DA blocking drugs
-Of course, dementia.
DLB v.s. AD on neuropsych?
Hard to distinguish, but DLB has slightly better memory and slightly worse EF.
What is the prototypical pathology associated with FTD.
Pick's disease, although other causes occur.
Primary progressive aphasia age of onset?
-Relatively younger.
Primary progressive Aphasia is often associated with impairment in what academic skill?
Writing, whereas reading is often preserved until late in the course.
Supranuclear Palsy Sxs?
-Motor deficitsm & extrapyramidal signs
-Vertical eye movement disorder (diagnostic).
-Gaze paresis (loss of downward gaze).
-Brady kinesia
Pathophys of Supranuclear palsy?
-Due to degeneration of multiple structures including the superior colliculus, red nucleus, dentate nucleus, subthalamic nucleus and globus pallidus
Corticobasal Degeneration sxs?
-Dementia related to supranuclear palsy
-sxs ideomotor apraxia, limb dystonia, myoclonus, sensory deficits.
-NP has more EF involvement
Etiology of huntington's?
-Autosomal dominant. Gene mutation leads to excessive trinucleotide repeats on chromosome 4.
Age range of onset in huntingtons.
20-40
Neurophys of Huntington's
caudate and the putamen, with mild impact on cortex. (sibcortical)
NPsych of huntington's
Slowing and EF worse than memory.
What is the annual incidence of HIV dementia after the diagnosis of HIV?
7% per year following HIV dx.
Npsych profile HIV dementia?
-Psychomotor slowing is prominent.
-2 is memory (in early stages worse recall than recognition).
-3 visual constructional skills, without other parietal signs like anomia, dycalculia.
Hallerverorden-Spatz disease
Rare inherited and progressive illness with late childhood or early adolescent onset, characterized by dementia with spasticity and rigidity, dystonia or chorea. Caused by an accumulation of iron in the brain. There is no current cure.
Syndenham’s Chorea
Affects children between the ages of 5 and 15

Associated with rheumatic fever and Pandas
Also frequently associated with tics, tourette’s, ADHD and dystonia
ways to measure internal reliability?
-split-half (spearman brown)
-coefficient alpha
-Kuder Richardson
What is the Kuder Richardson coefficient used for?
-Internal reliability for yes/know questions.
4 Broad forms of reliability?
-Internal consistency
-Test retest
-alternate forms
-Interater
Formula for creating confidence intervals from the SEM?
-68% C.I. = + or - 1 SEM
-95% C.I. = +/- 2 SEM
-98% C.I. = +/- 3 SEM
Formula for SEM
SD times (Square Root 1-reliability)
Messik's model of test validity
1.Content-
2.substanitive-theoretical rational for the test and responses.
3-structural-fidelity of scoring structure to the structure of construct.
4-generalizability
5-External- Convergent/divergent
6-Consequential- Consequences of test use related to bias, fairness.
Convergent and divergent validity fit into what type of validity in a 3 part model.
Construct.
Formula for sensitivity?
True pos. / True pos. + False neg.
(/ means divided by)
i.e. How many of the total people with depression (by gold standard) did the test detect?
Formula for specificity?
True neg. / True neg. + False pos.

-i.e. How many of the total ss without the condition (by gold standard), did the test reject.
positive likelihood ratio?
Combines sensitivity and specificity, it indicates the odds that a positive test comes from a true positive. i.e. a PLR = 3 means that a pt with a +predictor is 3x's as likely to have the condition. PLR=1 means random classification.

PLR= sensitivity/ 1-specificity
Positive predictive power?
-The probability that a pt with a + test has the true condition (by gold standard).

-PPP= True pos./ True pos. + false pos. (i.e. The proportion of SS that positive that have the condition).
Negative Predictive Power
-This is the probability that a pt with a neg. test result does not have the condition.

NPP= True neg. / true neg. + false neg. (i.e. what proportion of those who test neg. don't have the condition.
The relationship between base rate and PPP & NPP
As the base rate increases, PPP will increase, whereas NPP will decrease. The converse is true as the baserate declines.
A ROC curve is used for what?
It graphically displays the trade off of sensitivity and specificity that occurs as a criteria score is raised or lowered.
Bayesian probability table?
-A method of looking at sensitivity and specificity across different test scores (as opposed to ROC curves).
Test scores are in the columns, with test scores across the top and baserates on the side. Each cell has sensitivity& specificity.
Item discrimination index?
-looks at how well any item distinguishes, by examining those who did well on the test (Good) v.s. those who didn't (poor).
-IDI= %P - %F / n of 1 group.
where %p = the percentage of the Goods also passed the item and %F is what % of the Poors passed the item.
-Range -1 to 1. >.35 is acceptable.
Item Charectoristic curve
-basically plots the proportion of people who got an item right against total performance. P value: os tje probability of getting any 1 item right based on total test score.
How do reliability estimates differ from other correlations?
-Rxx is never scored to interpret it.
What is the top down selection from sepperate lists approach to alleviating test bias?
-In a test that is culturally unfair, this approach involves dividing groups into different groups and taking the best from each group. (i.e. the top 5 white candidates, top 5 black candidates, etc.)
What is "banding" as it relates to test bias?
-Consider ppl within a certain range as having identical scores. Can be used to level the playing field.
Hypokinetic movement disorders v.s. hyperkinetic?
-Parkinsons is a HypoKD (rigidity, slowing, etc.) Huntingtons is a HyperKD (jerking uncontrollable movements).
Ventral striatum?
-What is the largest part of the VS?
Region where the caudate fuses with the putamen. They also connect through "cellular bridges" that have a striped appearance, thus "striatum."

-The Nucleas accumbens.
Lentiform nucleas consists of?
-Putamen & GP, b/c of it's lense shape.
Most inputs to the BG come through what structures?
-The striatum
Most outputs from the BG exit through which structure?
-The internal segment of the GP and the substantia nigra (pars reticula portion).
What part of the BG is most important for input of motor control pathways?
Putamen
Most cortical inputs to the striatum use what NT?
Glutamate, b/c most are excitatory.
The pars compacta projects from what to where?
-What is the effect?
-It is a nucleas within the substantia nigra, which projects to the putamen through the dopaminergic/nigrostriatal pathway.
-That pathway is excitatory to some cells and inhibitory to others.
What part of the thalamus has inputs to the BG?
-Nuclei within the intramedulary lamina (dividing strip) project to putamen.
Serotonin inputs to the BG come from where?
-Raphe nucleas.
Main outputs from the BG come from what areas?
-The GP (internal segment, which is medial) and the substantia nigra (pars reticula portion).
What structures of the BG are associated with what aspects of motor control?
-The pars recticula of the substantia nigra contols head and face.
-The GP is associated with the rest of the body.
Outputs from the BG use what NT?
-GABA
The main outputs of the BG include?
Thalamus: (by way of Thalamic fasciculous).
-Ventrolateral:
-Ventral anterior
-Intralaminar nuclei (centromedian & parafascicular)
-medio dorsal nucleas
****Nonthalamus***
-Internal GP and substantia nigra project to reticullar formation.
-Pars reticular of SN projects to superior colliculus.
2 intrinsic BG pathways and their eventual impact on what they output to?
-The Direct Pathway, ultimately has an excitatory (net) effect on the Thalamus.
-The indirect pathway has an inhibitory (net) effect on the Thalamus.
What effect does DA have in the BG pathways?
-Variable. The Direct pathway DA is excitatory. The Indirect pathway DA is inhibitory.
Thus the combined effect on the Thalamus is excitatory.
What are the BG pathways involved in parkinsons?
DA pathways out of the SN pars compacta.
-Also ACh- travels through spiny neurons, which synapse on the indirect pathway.
Pathophys of hemiballismus?
-subthalamic nucleas
Relationship between late stage huntingtons and the internal BG pathways?
-In late stages both the direct and indirect pathways degenerate, resulting in sxs more like parkinsons.
What are the 4 channels of output from the BG to the frontal lobes?
-Alternative nomenclature?
1.Motor Channel
2. Occular Motor Channel
3. Prefrontal Channel
4. Limbic Channel
*Note other nomenclature distinguishes between a Dorsal striatal pathway (1-3) and a ventral pathway (4).
The nucleas basilis of Meynert is the major area of innervation for which NT?
Ach
2 main systems of the brain involved in memory functions?
-Medial temporal lobe areas (i.e. hippocampus, parahippocampal gyrus)
-Medial diencephalic areas
(i.e. Medio-Dorsal nucleas and anterior nucleas of thalamus, mamilary bodies, and other diencaphalic structures near the 3rd vent.)
Besides the medial temporal regions and the medial diencephalic regions, what other regions are involved in memory>
-White matter: This is how both of those systems communicate with cortex.
-Basal forebrain
Major portions of Lymbic system?
Limbic had SOBBB
1. Limbic Cortex- parrahypocampal gyrus, cingulate, etc.
2. Hyppocampal formation
3.Amygdala
4.Diencepahlon (whole thing)
5.Septal nuclei
6.Olfactory Cortex
7.Basal forebrain
8.Basal ganglia
9.Brain stem
What are the components of what get's called the limbic cortex?
1.Parahippocampal gyrus
2.Cingulate
3.Orbital Frontal (medial part).
4. Pole (temporal pole)
5.Insula (anterior portion).
Entorinal cortex?
-Major input and output relay of hippocampus and association cortex.
What is the Hebb Rule?
-When Axon A excites axon B repeatedly and persistently efficiency increases through some metabolic or growth process.
"nerves that fire together, wire together."
*Relates to long term potentiation.
What other drug can Fluoroquinolones be synergistic with?
B-lactam antibiotics
List the connections in the Papez circuit.
-Subiculum of HC to the
-Fornix
-mamalary nuclei
-through the mamalothalamic tract to the Anterior Thalamic N.
-Internal capsul to the . . .
-Cingulate through the cingulum to the . .
-parahippocampal gyrus
-Entorhinal cortex to the . .
-Hippocampus
Medial lobe memory systems communicate with the association cortex through?
-bidirectional connections via the entorhinal cortex.
List the main components of the medial diencephalic memory areas?
-Thalamus (medial dorsal N., Anterior N.m internal medullary lamina, mammillary bodies, (as well as other 3rd ventricle structures).
Learning of skills (procedural learning?) is associated with what regions?
-BG, cerebellum, motor cortex.
What BG structure have been associated with habbit learning?
-The caudate (also tied to OCD pathology).
What region is associated with classical conditioning?
Cerebellum.
What structure is associated with classically conditioned fear responses?
-Amygdala.
Ribot's law.
-Vulnerability to memory loss is inversely related to age of memory.