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
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
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
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
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
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
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
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)
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
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”
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
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
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)
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
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)
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
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
- Pts make “body part as tool” errors (like scissor symbol)
- 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
18
Q
Ideational Apraxia
A
- Inability to sequence movements (order)
- Lesion: LEFT frontal damage, primarily seen in dementias
- Frontal lobe planning problem
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
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
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
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)
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
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)
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
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
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
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
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
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
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
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))
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
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
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
- Neglect half of any object regardless of it location in relation to the body space
- Egocentric spatial deficits:
- 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
- Left dlPFC
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
