Neuropsychology Flashcards

1
Q

Unimodal (Homotypic) Association Cortex

AKA Secondary Association Cortex

A
  • Characteristics:
    • Modality specific: neurons respond almost entirely to a single sensory modality
    • Information processed here comes from the primary sensory (idiotypic) area for that modality
    • Lesions = deficits specific to that sensory modality
  • Components:
    • Upstream: areas 1 synapse away from the primary sensory area
    • Downstream: 2+ synapses away from primary sensory area
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2
Q

Heteromodal Association Cortex

AKA Tertiary Association Cortex

A
  • Constituent neurons are not restricted to a single sensory modality
  • Instead, respond to inputs from multiple unimodal (secondary) areas and other heteromodal areas
  • Lesion = multimodal deficits, involve disruption of inputs from more than one functional area
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3
Q

Major anatomical areas subserving language functions

A
  • Heschl’s gyrus: primary auditory cortex
  • Broca’s area: posterior aspect of the inferior frontal operculum
  • Wernicke’s area: middle, posterior aspects of the superior temporal gyrus banding Heschl’s gyrus
  • Major association fibers and streams
    • Arcuate fasciculus: connects Wernicke’s and Broca’s
    • Ventral/dorsal streams
  • Supramarginal and angular gyri in left parietal
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4
Q

Wernicke-Geschwind model of language processing

A
  • Hearing/speaking:
    • Primary auditory cortex > secondary auditory (Wernicke’s) > (via arcuate fasciculus) > motor/premotor cortex and Broca’s > primary motor cortex > output
    • Broca’s is not just about producing speech, it’s also about planning the motor component
  • Reading/writing:
    • Primary visual cortex > other visual association areas > angular gyrus (tertiary association) > secondary auditory (Wernicke’s) > (via arcuate fasciculus) > secondary motor cortex (Broca’s) > primary motor cortex > output
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5
Q

Role of different temporal lobe regions in language processing

A
  • Middle, inferior temporal areas = naming
    • Posterior inferior = general naming
    • Temporal pole (anterior temporal) = proper noun retrieval
  • Inferotemporal areas = object categorization
  • Superior temporal gyrus and bounded cortex = socio-emotional processing
    • Lateralized between hemispheres
  • Ventral processing stream provides visual input for temporal function
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6
Q

Broca’s Aphasia

A
  • AKA expressive or nonfluent aphasia
  • Slow, effortful, poorly articulated speech
  • Speech is sparse, hesitant, missing function words (agrammatism)
  • Naming and repetition are impaired
  • Paraphasias are rare, comprehension is intact
  • Disturbance in speech planning/production
  • Caused by lesion to the pars operculum and aspects of the pars triangularis of the left inferior frontal gyrus
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7
Q

Wernicke’s Aphasia

A
  • AKA receptive or fluent aphasia
  • Disturbance in comprehension
  • Normal verbal output (fluency is normal)
  • Output is nonsensical, consisting of paraphasic errors, jargon, and neologisms
  • Reading/writing/naming/repetition are impaired
  • Inability to classify phonemes into meaningful morphemes and lexical semantics
  • Caused by lesion to posterior portion of superior temporal gyrus and some cortical tissue banding Heschl’s gyrus
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8
Q

Transcortical Motor Aphasia

A
  • Just like Broca’s but repetition is intact
  • Nonfluent speech with preserved repetition (normal comprehension)
  • Naming is variable
  • Damage is often anterior and/or superior to Broca’s (watershed)
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9
Q

Transcortical Sensory Aphasia

A
  • Just like Wernicke’s but repetition is intact
  • Impaired speech comprehension, intact fluency and repetition
  • Naming is impaired
  • Disorder of semantic processing
  • Lesion: middle and inferior temporal gyri and sometimes inferior occipitotemporal junction
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10
Q

Conduction Aphasia

A
  • Impaired repetition with constant phonemic paraphasias
    • Phonemic paraphasia: substitution, addition, omission of a phoneme (table becomes tadle)
  • Preserved fluency and comprehension
  • Impaired communication (speech sound patterns and motor production)
  • Basically: can talk and understand, but have problems repeating things
  • Naming and writing are variable
  • Lesion: arcuate fasciculus or the supramarginal gyrus (usually inferior parietal lesion)
    • “Transfer deficit between Broca’s and Wernicke’s”
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11
Q

Global Aphasia

A
  • Everything is impaired
    • Naming, repetition, fluency, comprehension
    • Writing is impaired
    • Paraphasic errors are common
    • May be able to respond to basic commands
  • Lesion: very large left lesion, major MCA infarct
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12
Q

Anomia

A
  • Fluency, repetition, and comprehension are good
  • Naming is impaired
    • Word retrieval deficit, so paraphasias are uncommon
  • Tends to be residual of many aphasias as the acute phase transitions to recovery
    • So, little localization value
  • Lesion: generally involve LEFT inferior temporal regions
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13
Q

Alexia with agraphia

A
  • Impaired reading and writing
  • Non-aphasic (naming, comprehension, fluency intact)
  • Lesion: both left supramarginal and angular gyri) (posterior inferior temporal)
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14
Q

Alexia without agraphia

AKA pure alexia, pure word blindness

A
  • Impaired reading with intact writing
  • Non-aphasic (naming, comprehension, fluency intact)
  • Pts engage in compensatory serial letter numbering strategy to put together words
  • Can copy words/sentences but cannot read them
  • Fundamentally is a disconnection syndrome from left to right
  • Prevents direct visual input of info from right hemisphere to the left angular gyrus
  • Lesion: left PCA infarct, destroying mesial aspects of left occipital lobe and splenium of corpus callosum
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15
Q

Primary Acalculia

A
  • Impaired number processing, particularly for calculations
  • Not explained by alexia/agraphia
  • There’s a discrete location for numerical processing and sequencing
  • Lesion: left inferior parietal lobule in intraparietal sulcus (both left supramarginal and angular gyri)
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16
Q

Left Parietal Region for Skilled Motor Movements

A
  • Premotor region contains movement lexicon (praxicon: mapped categories of movement for specific actions)
  • Must be linked to meaning in order to provide for purposeful movement
  • Connections between motor regions and posterior parietal and temporal regions provide meaningful linkage to purposeful movements
  • Damage to these systems = apraxia
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17
Q

Ideomotor Apraxia

A
  • Inability to make gestures or use objects to command
    • Pts make “body part as tool” errors (like scissor symbol)
      • Improved with actual object but still impaired
  • Spatial and temporal errors when pantomiming
    • Posture of hand/fingers is incorrect for object
    • Incorrect movement and/or speed with object
  • Lesion: left inferior parietal lobe
    • Damage to praxicon; movement formulas are damaged
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18
Q

Ideational Apraxia

A
  • Inability to sequence movements (order)
  • Lesion: LEFT frontal damage, primarily seen in dementias
  • Frontal lobe planning problem
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19
Q

Conceptual Apraxia

A
  • Inability to select the correct movement for a given action/object
  • Lesion: possibly left tempoparietal junction, may also be left frontal
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20
Q

Body Schema and Extrastriate Body Area

A
  • Body Schema
  • Proprioception; representation of one’s own body in space (body awareness)
    • Also, nociception, vestibular, auditory, etc.
  • Extrastriate body area (EBA) is Brodmann area 19
    • In anterior region of the occipital lobes bilaterally (bordering posterior temporal and inferior parietal)
    • Responds to stationary and moving human body parts (but NOT the face!)
    • Engaged during planning, execution, imagination of goal directed movements
    • Critical to perception of body
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21
Q

Autopagnosia

A
  • Inability to identify one’s own body parts or those of others
  • Not a language disorder
  • Body schema disorder
  • Left hemisphere disorder
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22
Q

Finger Agnosia

A
  • Inability to name, show, or localize fingers on command
  • Use of fingers is normal though
  • Lesion: LEFT occipitoparietal
    • (both left supramarginal and angular gyri)
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23
Q

Right-left disorientation

A
  • Inability to identify right/left side of one’s own body or the body of another
  • Lesion: LEFT parieto-occipito-temporal
    • (both left supramarginal and angular gyri)
  • Body schema disorder
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24
Q

Gerstmann’s Syndrome

A
  • Finger agnosia,
  • L/R disorientation
  • Agraphia
  • Acalculia
  • But usually occurs in context of a ton of other deficits from large lesion, so controversial
  • Lesion: left angular gyrus and posterior lobe
    • (both left supramarginal and angular gyri)
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25
Achromatopsia
* Inability to perceive color (pure color blindness) in absence of other visual processing problems * May be dyschromatopsia, varying hues and shades possible * Can affect some object identification (banana vs pickle) * Usually restricted to one visual field (rarely bilateral) * Often co-occurs with other disorders * Lesion: posterior lingual and fusiform gyri (they border the calcarine sulcus) * Ventral occipitotemporal * More common in superior quadrant defects * 70% bilateral lesions, 20% R-sided, 10% L-sided
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Akinetopsia
* Inability to perceive motion, but without deficits in object form perception * Pts perceive object as static and "freezing" and reappearing in different places * Cannot judge distances or quantities well (like, pouring coffee) * Palinopsia = trailing of an image, may be present in mild cases * Lesion: Mt/V5 of the temporo-occipital junction * Medial superior temporal area of the dorsal visual steam * Tends to be bilateral * Can also be caused by systemic issues like seizures
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Apperceptive Visual Agnosia AKA Visual Form Angosia
* Impaired perception of the basic components of object form, particularly with regard to shape * Pts cannot link different aspects of object perception into a coherent whole (shape, form, depth) * Results in inability to identify the target object * Often presents with several other disorders * Lesion: bilateral occipital, occipitotemporal, posterior inferior temporal (including posterior lingual and fusiform gyri) * Disruption of **ventral visual stream** * Also a result of carbon monoxide poisoning
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Associative Visual Agnosia
* Inability to link semantic meaning/concept of an object to its visual form * In the context of otherwise intact perception, sensory function, and preserved ability to ID objects in other sensory modalities * Cannot identify visually presented stimuli, cannot demonstrate use * BUT can sometimes ID it if it's used * BUT can draw what they cannot identify * Disorder is "post perceptual"; occurs in a later stage of processing result in failure of semantic representation leading to a defect in visual identification * Lesions: diffuse but always involve bilateral lateral occipitotemporal cortices, interruption of inferior longitudinal fasciculus * Some fusiform gyrus involvement * Left-sided lesions may be critical * Different from apperceptive agnosia and anomia: * Must be a nonverbal recognition defect * Anomic pts cannot name objects but can still recognize them; agnosics cannot do either
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Prosopagnosia
* Inability to recognize familiar faces, including their own * Can recognize that they're seeing a face and give accurate descriptions of facial features * **Not a perceptual deficit; an identification deficit** * Lesion: bilateral fusiform gyri
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Balint's Syndrome
* Posterior syndrome; **dorsal stream** * Acquired visual disturbance resulting in inability to perceive entirety of visual field with fractioned recognition of parts and associated defects of visually guided reaching and voluntary shifting of gaze * **Ocular apraxia**: impaired voluntary gaze * **Optic ataxia**: impaired hand/eye coordination, cannot grab objects * **Simultanagnosia**: inability to perceive/attend to more than one stimulus * Lesion: bilateral posterior parietal regions involving parietooccipital junction and the intraparietal sulcus
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Ocular Apraxia
* Defect in voluntary direct gaze/volitional eye movement * Pt unable to intentionally look at something * Failure to initiate saccadic eye movement; are chaotic and random * Lesion: may involve higher control of superior colliculi
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Ocular Ataxia
* Defect in visually-guided movement * Pt is unable to use vision to accurately coordinate movements to grasp or manipulate objects in visual space * May be restricted to a hemifield or one arm/hand, or can be bilateral and both limbs * Preserved object identification * Lesion: parietal-occipital junction (dorsal stream (where))
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Simultanagnosia
* Inability to attend to/perceive/recognize/ID more than one visually presented stimulusInability to perceive individual parts of a whole * **Left hemisphere sees details**, right hemisphere sees global * Reading is impaired * Akin to neglect (spatial) rather than attentional defect * Pts extinguish previously presented objects with presentation of new objects * Lesion: bilateral parietooccipital junction and inferior intraparietal sulcus
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Posterior regions considered to be heteromodal association cortex
* Superior parietal lobule * Intraparietal sulcus * Inferior parietal lobule * Supramarginal gyrus * Angular gyrus * Middle temporal gyrus * Superior temporal sulcus
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Unilateral Neglect
* Spatial disorder from right posterior damage * Pt fails to report, respond, orient to, explore, or direct attention toward a hemispace contralateral to lesion * Not a result of any sensory, motor, motivation, or other impairment * Can occur in all 3 domains; auditory, visual, and tactile * Can occur in dimensions/frames: * Egocentric spatial deficits: * Vision-centered: reference to visual fields * Head-centered: reference to mid-sagittal plan of head * Body-centered: reference to mid-sagittal plan of body * Allocentric spatial deficits: * Neglect half of any object regardless of it location in relation to the body space * Ex: neglect half of food on plate * Neglect portions of allocentric space while intact to egocentric space * Lesions: right parieto-occipital-temporal area and right frontal involvement * Right inferior parietal, posterior superior temporal involving right angular and supramarginal gyri * Frontal: disconnection between right prefrontal and right posterior heteromodal
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Intentional (motor) neglect
* Failure to respond to a stimulus despite being aware of it * Mostly right frontal (sometimes left frontal)
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Extinction to bilateral simultaneous stimulation
* Seen as denser neglect resolves * Pt can orient to contralesional but when presented with bilateral stim, only respond to ipsalesional
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Other functions affected by neglect
* Left hemisphere functions * Spatial agraphia/alexia * Spatial acalculia * Sleep and dreaming * REM movements stop at midline * Neglect half of space in dreams * Imagery and memory * Neglect left half of objects in mental imagery * Neglect left half of scenes/events from memory * Spatial allochiria
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Spatial Allochiria
* Unilateral neglect * Transposition of details in neglected hemispace into the non-neglected hemispace * Stim from left hemispace is manifested in right hemispace * Occurs in drawing or description of objects * Also occurs in tactile stimulation; sensation to left is felt on opposite body in homologous region * Also occurs in audition; auditory stim is heard in opposite hemispace
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Anosognosia
* Lack of awareness of deficit, denial of illness, * Awareness disorder; disrupts self-awareness * Not a disorder of memory, language, motor, motivation, or attention * Presentation: * Behaviors are inconsistent with patient report (pt that's no clapping will say they're clapping) * Confabulation * Implicit awareness * Lesion: right parietal-occipital-temporal area * Right posterior-inferior parietal and posterior temporal, and right dorsolateral prefrontal (Including insula) * Disconnection between right posterior and right frontal is implicated
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Anosodiaphoria
* Lack of concern for a deficit * Manifestation of neglect and anosognosia * Lesion: right parietal-occipital-temporal area; * Right posterior-inferior parietal and posterior temporal, and right dorsolateral prefrontal (Including insula) * Disconnection between right posterior and right frontal is implicated
42
Asomatagnosia
* Failure to acknowledge ownership of a limb * Manifestation of neglect and anosognosia * Lesion: right parietal-occipital-temporal area; * Right posterior-inferior parietal and posterior temporal, and right dorsolateral prefrontal (Including insula) * Disconnection between right posterior and right frontal is implicated
43
Somatoparaphrenia
* Denial of ownership of a limb or another part of body * Manifestation of neglect and anosognosia * Lesion: right parietal-occipital-temporal area; * Right posterior-inferior parietal and posterior temporal, and right dorsolateral prefrontal (Including insula) * Disconnection between right posterior and right frontal is implicated
44
Misoplegia
* Emotional attributions (generally hatred) toward a paralyzed limb * Manifestation of neglect and anosognosia * Lesion: right parietal-occipital-temporal area; * Right posterior-inferior parietal and posterior temporal, and right dorsolateral prefrontal (Including insula) * Disconnection between right posterior and right frontal is implicated
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Alexithymia
* Failure to identify one's emotional state * Profound difficulty in describing the way one is feeling * Paucity of dreaming; imagery is devoid of content * Rigid interpersonal interactions * Lesion: right temporal * May also be a disconnection syndrome
46
Aprosodia
* Affective disorder of communication * This is how the right hemisphere is contributing to language in the left * Prosody and emotional inflection in speech * Flat, bland expression * Lesions in right temporal lobe, right inferior frontal (homologue of Broca's), will have an expressive aprosodia * Receptive aprosodia: they can't understand prosody in language
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Major prefrontal cortex functions
* Centralized control: control, integration of internal/external environments via cognitive control of sensory systems, internal states, motor/behavioral output * Executive functions: attention, memory, language, organization, planning, decision making, judgment * Socio-emotional functions: emotion regulation, volitional control, self- and other-awareness, moral reasoning
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3 Major Prefrontal Regions
* Dorsolateral prefrontal cortex (dlPFC) * Connects to posterior parietal cortices, superior temporal sulcus * Orbitofrontal cortex (OFC) * Inputs from sensory modalities and outputs to limbic regions * Ventromedial prefrontal cortex (vmPFC) * Inputs from dlPFC, posterior cingulate, mesial temporal * Outputs to limbic regions and brainstem
49
Dorsolateral Prefrontal Cortex
* Central modulation of attention, working memory * Online monitoring and active manipulation of info * Strategic cognitive control * Lesion asymmetry: * Left dlPFC * Mood fluctuations, generally depressed * Propositional language impairments, poor fluency * Large lesions = Broca's aphasia, left upper extremity hemiparesis with lower right facial droop, possible gaze deviation if FEF is involved * Right dlPFC * Sometimes euphoria * Otherwise, affect is restricted but pt is unconcerned * Non-propositional language impairments; emotional expression is diminished * Large lesions = expressive aprosodia, right upper extremity hemiparesis, gaze deviation if FEF is involved
50
Ventrolateral Prefrontal Cortex
* Regulation of encoding and retrieval of info from posterior association cortices * Mediates selection of goal-relevant info * Acts as an attentional gateway; how are frontal lobes going to use incoming info
51
Dysexecutive Syndrome
* Lesion: lateral aspect of prefrontal cortex * Deterioration of attention and working memory * Poor monitoring and decreased control over active processes * Poor temporal, spatial context for goal-directed behavior * Impaired organization, planning, sequencing, strategizing * Poor cognitive flexibility and control of response choice * Impaired abstract conceptual reasoning for verbal, nonverbal
52
Ventromedial Prefrontal Cortex
* Modulatory control of emotional valence (and possibly a role in emotional output) * Volitional control and motivation * Contextual appraisal of socio-emotional information * Goal selection and decision making for complex and abstract choices * Organization of the temporal aspects of behavior (foresight and planning)
53
Apathetic/Abulic Syndrome
* Lesion: bilateral ventral, mesial aspects of frontal lobes, including anterior cingulate * Diminished capacity to respond to emotionally salient events * Anhedonia * Lack of curiosity * Poor ability to respond to reward/punishment; do not learn from mistakes * Impaired decision making, planning, goal-oriented direction * \*\*If OFC involvement, may also have lack of empathy * Lesion: dorsal-mesial involvement * Apathy: reduction of goal-directed behavior * Abulia: loss of initiative or drive and lack of speech, thought, motor function * Akinetic mutism: extreme apathetic/abulic state with basically no spontaneous activity * Other features of this syndrome: * Generally intact cognitively * Socio-emotional knowledge is normal but they have trouble using it * Large lesions involving orbitofrontal and ventro-mesial cortex results in more socially-disturbed presentation
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Orbitofrontal Cortices
* Empathy and self-context; role of the self in relation to others * Impulse control and regulation of salient drives/motivations * Social comportment and online monitoring * How a person carries themselves, dressing properly, behaving in a civilized manner
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Disinhibition Syndrome
* Prominent personality changes * Lack of impulse control; pt may be wildly inappropriate * Insensitive, lacking empathy or remorse * Terrible interpersonal skills * Impaired insight * Pathological features: * Hoarding * Inappropriate sexual behaviors * Stimulus-bound and utilization behaviors may become prominent * Patients reflexively use whatever is in sight * Lesion: orbitofrontal cortex
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Agraphesthesia
* Inability to recognize written letters/numbers traced on skin * Postcentral gyrus lesion
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Astereognosis
* Inability to identify an object by touch only * Postcentrral gyrus lesion
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Tactile Agnosia
* Cannot recognize or name object by touch * Lesion to ventrolateral parietal lobe
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Constructional Apraxia
* Difficulty with simple drawing, assembling blocks * Lesion to dorsomedial parietal lobe
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M1 Infarct Signs
* Hemiparesis of lower half of contralateral face * Hemiparesis of contralatera upper and lower extremities * Sensory loss from contralateral face and arm, minor leg * Ataxia of contralateral extremities (minor leg) * Lack of muscle control/coordination * Gaze preference to side of lesion * Contralateral visual field defects * LEFT: Speech impairments (global aphasia) * RIGHT: perceptual impairments (hemispatial neglect)
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Superior M2 Infarcts
* Hemiparesis of the lower half of contralateral face * Hemiparesis of contralateral upper extremities (no leg!) * Sensory loss from contralateral face and arm (no leg!) * Ataxia of contralateral upper extremity * Lack of motor control/coordination * Gaze preference to side of lesion * LEFT: Broca's aphasia * \*No visual loss
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Inferior M2 Infarct Signs
* Contralateral tactile agnosia * Contralateral visual field defects * LEFT: * Wernicke's aphasia * Gerstmann's syndrome * Agraphia, acalculia, R/L disorientation, finger agnosia * RIGHT: perceptual impairments * Hemispatial neglect, constructional apraxia
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M3 Infarct Signs
Specific to territory in pie-slice shaped wedge of infarction
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ACA Infarct Signs (A2)
* Hemiparesis of the contralateral leg, pelvic floor * Incontinence * Sensory loss from contralateral leg, perineum * Ataxia of contralateral leg (motor control/coordination) * Apraxia (difficulty motor planning) * Slowness and lack of spontaneity * Akinetic mutism * No effort to communication (superior PFC)
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PCA Cortex Infarct Signs
* Contralateral visual field defects * Cortical blindness if bilateral * Visual form agnosia * Memory and naming deficits, disorientation * LEFT: alexia with agraphia * Alexia: inability to read * Agraphia: inabiity to write * RIGHT: Prosopagnosia
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Central PCA Infarct Signs
* Thalamic syndromes * Involuntary movements * Chorea * Intentional tremor * Hemiballismus * lesion in subthalamic nucleus * Hyperkinetic disorder like the choreas, but affecting more proximal limb movements * Very intense movements * Contralateral hemiparesis * 3rd nerve palsy: down + out
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Holmes' Tremor
* Wing-beating * Damage to myoclonic triangle (red nucleus triangle with IOC and cerebellum)
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Dysarthria
Speech problem: midline cerebellum (vermis)
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Tremor when moving vs at rest
* Moving: cerebellum, (hemisphere) lesion * At rest: Parkinson's
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Dysmetria
Past pointing (cerebellum hemisphere lesion)
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Dyssnergia
* Jerky movements * Cerebellum hemisphere lesion
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Dysdiadochokinesia
* Difficulty making rapidly alterning hand movements * Cerebellum hemisphere lesion
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Spondylosis
* Arthritic degeneration of vertebra that narrows intervertebral foramina * New bone can grow in spinal canal
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Spinal stenosis
Narrowing of spinal cord (SC compressoin)
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Brown-Sequard Syndrome
* Result of a hemisection of SC * Symptoms * **Dorsal column**: ipsilateral loss of 2-point discrimination, vibration, conscious proprioception, kinesthesia * **Lateral corticospinal tract:** ipsilateral UMN signs * **Spinothalamic tract:** contralateral loss of pain and temp
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Central Cord Syndrome
* Lesion develiping within the spinal cord (usually cervical) * Bilateral loss of pain and temp over a limited area at levels involved (ventral white commissure but NOT STT) * Sacral sparing (again, NOT STT) * UMN signs like exaggerated reflexes if it reaches lateral corticospinal tract * Disproportionally greater motor impairment in upper vs lower extremities * LMN signs like atrophy if it reaches the ventral horn * Possibly autonomic if levels T1-T2 * DCML is probably just fine
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Syringomyelia
* Intrinsic (internal) spinal cord lesion * Bilateral loss of pain and temp over shoulder and lateral arm (like a cape)
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Anterior Cord (Spinal Artery) Syndrome
* Complete bilateral motor paralysis below level of lesion * Complete bilateral loss of pain and temp sensation below the level of lesion * Sparing of 2-point discrimination, vibration sense, kinesthesia (bc that’s all DC system) * If this lesion occurs in the cervical cord: * Loss of CN XI function (paresis/paralysis of SCM and trapezius) * Respiratory difficulties due to paralysis of diaphragm (phrenic nucleus)
80
Cauda Equina Syndrome
* Results from a pathological process (disc herniation, tumor, etc.) leading to spinal stenosis * Affects the dorsal and ventral roots forming the cauda equina * Symptoms: * Weakness of leg and foot (LMN signs) * "Saddle anaesthesia" - loss of pain, temp, 2-point touch over S1-S5 dermatomes * Loss of knee and ankle reflexes - damage to ventral roots * Urinary retention (flaccid bladder) - due to roots S3 and 4 being affected * Loss of tone in external anal sphincter due to damage to S3-S5
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Conus Medullaris Syndrome
* Compression of conus medullaris * Butt sensory loss only * Bladder, bowel, and sexual dyfunction
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Horner's Syndrome
* Damage to Central Tegmental Tract above T1 * Hemi loss of sympathetic function on the ipsilateral side, resulting in: * Ptosis: droopy eyelid, impairment of Muller's muscle, a smooth muscle adjoining the levator palpebrae superioris muscle (helps to keep eyelid raised) * Miosis: constricted pupil; impairment of the dilator pupillae muscle * Anhydrosis: inability to sweat * Rubrosis: hyperameia - flushed skin * Enophthalmos: sunken eye; impairment of Landstrom's muscle, microscopic smooth muscle fibers located within the fascia bulbi of the eye which help retain the eye in its normal forward position
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Dejerne's Syndrome
* AKA medial medullary syndrome * Anterior spinal atery occlusion in **medulla** * Symptoms: * **Pyramids:** Contralateral UMN signs to muscles (LCST) * **Hypoglossal:** ipsilateral tongue movement (points to lesional side) * **Medial Lem:** contralateral fine tough + proprioception
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Wallenberg's Syndrome
* AKA Lateral medullary syndrome * PICA infarction in medulla * Symptoms: * **_R facial pain/temp, L body pain/temp_** * Nucleus ambiguus: ipsilateral dysphagia, displaced uvula, flaccid vocal ford * Spinal nucleus and tract of V: ipsilateral pain, temp from face * Spinothalamic tract: contralateral pain, temp sensation * Hypothalamospinal tract: Horner's syndrome * Inferior cerebellar peduncle: ipsilateral ataxia (lack of input from spinocerebellar tracts) * Vestibular nuclei: vertigo, nausea * Reticular formation: hiccups
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Benedikt's Syndrome
* Tremore at rest AND movement * PChA in midbrain
86
Weber's Syndrome
* PChA * Cranial Nerve III: ipsilateral D+O eye and contralateral pupil constriction (LMN) * Corticobulbar fibers: contralateral UMN face * Corticospinal fibers: contralateral UMN body