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FN Unit 3 > Neuropsychology > Flashcards

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
Q

Achromatopsia

A
  • 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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26
Q

Akinetopsia

A
  • 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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27
Q

Apperceptive Visual Agnosia

AKA Visual Form Angosia

A
  • 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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28
Q

Associative Visual Agnosia

A
  • 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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29
Q

Prosopagnosia

A
  • 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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30
Q

Balint’s Syndrome

A
  • 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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31
Q

Ocular Apraxia

A
  • 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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32
Q

Ocular Ataxia

A
  • 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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33
Q

Simultanagnosia

A
  • 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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34
Q

Posterior regions considered to be heteromodal association cortex

A
  • Superior parietal lobule
    • Intraparietal sulcus
  • Inferior parietal lobule
    • Supramarginal gyrus
    • Angular gyrus
  • Middle temporal gyrus
    • Superior temporal sulcus
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35
Q

Unilateral Neglect

A
  • 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
36
Q

Intentional (motor) neglect

A
  • Failure to respond to a stimulus despite being aware of it
  • Mostly right frontal (sometimes left frontal)
37
Q

Extinction to bilateral simultaneous stimulation

A
  • Seen as denser neglect resolves
  • Pt can orient to contralesional but when presented with bilateral stim, only respond to ipsalesional
38
Q

Other functions affected by neglect

A
  • 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
39
Q

Spatial Allochiria

A
  • 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
40
Q

Anosognosia

A
  • 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
41
Q

Anosodiaphoria

A
  • 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
Q

Asomatagnosia

A
  • 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
Q

Somatoparaphrenia

A
  • 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
Q

Misoplegia

A
  • 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
45
Q

Alexithymia

A
  • 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
Q

Aprosodia

A
  • 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
47
Q

Major prefrontal cortex functions

A
  • 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
48
Q

3 Major Prefrontal Regions

A
  • 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
Q

Dorsolateral Prefrontal Cortex

A
  • 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
Q

Ventrolateral Prefrontal Cortex

A
  • 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
Q

Dysexecutive Syndrome

A
  • 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
Q

Ventromedial Prefrontal Cortex

A
  • 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
Q

Apathetic/Abulic Syndrome

A
  • 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
54
Q

Orbitofrontal Cortices

A
  • 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
55
Q

Disinhibition Syndrome

A
  • 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
56
Q

Agraphesthesia

A
  • Inability to recognize written letters/numbers traced on skin
  • Postcentral gyrus lesion
57
Q

Astereognosis

A
  • Inability to identify an object by touch only
  • Postcentrral gyrus lesion
58
Q

Tactile Agnosia

A
  • Cannot recognize or name object by touch
  • Lesion to ventrolateral parietal lobe
59
Q

Constructional Apraxia

A
  • Difficulty with simple drawing, assembling blocks
  • Lesion to dorsomedial parietal lobe
60
Q

M1 Infarct Signs

A
  • 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)
61
Q

Superior M2 Infarcts

A
  • 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
62
Q

Inferior M2 Infarct Signs

A
  • 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
63
Q

M3 Infarct Signs

A

Specific to territory in pie-slice shaped wedge of infarction

64
Q

ACA Infarct Signs (A2)

A
  • 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)
65
Q

PCA Cortex Infarct Signs

A
  • 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
66
Q

Central PCA Infarct Signs

A
  • 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
67
Q

Holmes’ Tremor

A
  • Wing-beating
  • Damage to myoclonic triangle (red nucleus triangle with IOC and cerebellum)
68
Q

Dysarthria

A

Speech problem: midline cerebellum (vermis)

69
Q

Tremor when moving vs at rest

A
  • Moving: cerebellum, (hemisphere) lesion
  • At rest: Parkinson’s
70
Q

Dysmetria

A

Past pointing (cerebellum hemisphere lesion)

71
Q

Dyssnergia

A
  • Jerky movements
  • Cerebellum hemisphere lesion
72
Q

Dysdiadochokinesia

A
  • Difficulty making rapidly alterning hand movements
  • Cerebellum hemisphere lesion
73
Q
A
74
Q

Spondylosis

A
  • Arthritic degeneration of vertebra that narrows intervertebral foramina
  • New bone can grow in spinal canal
75
Q

Spinal stenosis

A

Narrowing of spinal cord (SC compressoin)

76
Q

Brown-Sequard Syndrome

A
  • 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
77
Q

Central Cord Syndrome

A
  • 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
78
Q

Syringomyelia

A
  • Intrinsic (internal) spinal cord lesion
  • Bilateral loss of pain and temp over shoulder and lateral arm (like a cape)
79
Q

Anterior Cord (Spinal Artery) Syndrome

A
  • 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
Q

Cauda Equina Syndrome

A
  • 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
81
Q

Conus Medullaris Syndrome

A
  • Compression of conus medullaris
  • Butt sensory loss only
  • Bladder, bowel, and sexual dyfunction
82
Q

Horner’s Syndrome

A
  • 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
83
Q

Dejerne’s Syndrome

A
  • 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
84
Q

Wallenberg’s Syndrome

A
  • 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
85
Q

Benedikt’s Syndrome

A
  • Tremore at rest AND movement
  • PChA in midbrain
86
Q

Weber’s Syndrome

A
  • PChA
  • Cranial Nerve III: ipsilateral D+O eye and contralateral pupil constriction (LMN)
  • Corticobulbar fibers: contralateral UMN face
  • Corticospinal fibers: contralateral UMN body

FN Unit 3 (13 decks)

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