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Neuroanatomy > Exam VIII > Flashcards

Exam VIII Flashcards

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1
Q

Common etiologies of CVA

A

thrombus (gradual onset), embolism (sudden onset), hemorrhage, TIA

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2
Q

Where to atherosclerotic plaques tend to form?

A

tend to form in vessels with angulations, constrictions, dilations or bifurcations

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3
Q

Factors controlling blood vessel diameter

A

increased [CO2] & [H+], decreased [O2] = vasodilation

vasoconstriction = opposite

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4
Q

Factors controlling blood vessel diameter

A

increased [CO2] & [H+], decreased [O2] = vasodilation

vasoconstriction = opposite

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5
Q

Factors controlling blood vessel diameter

A

increased [CO2] & [H+], decreased [O2] = vasodilation

vasoconstriction = opposite

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6
Q

CVA Signs/Sx

A

Flaccidity, Motor and Sensory Loss (hemiplegia and paresis), Spasticity, deveopment of obligatory synergies, hyperreflexia and return of primitive cutaneous and tonic reflexes, associated reactions, impaired righting/equilibrium/protective extension reactions, homonymous hemianopsia, cognitive/perceptual problems, speech and swallowing difficulties

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7
Q

Flaccidity

A

Thought to be due to abrupt disconnection of UMN’s & LMN’s (diaschisis), can last days, weeks or months

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8
Q

Motor/Sensory loss predominately of LE

A

CL paracentral lobule; CL anterior cerebral artery.

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9
Q

Motor/Sensory loss predominately of UE

A

CL pre and post central gyri; CL middle cerebral artery

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10
Q

Paresis

A

Related to the location and size of the brain injury. Mild weakness often on unaffected side due to fibers of LCST that remain IL

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11
Q

What is spasticity thought to be due to

A

disinhibition of the reticulospinal tract causing excessive muscle contractions of muscles involved in synergistic patterns that are normally inhibited.

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12
Q

UE Spasticity Pattern

A

Scapular retraction, shoulder adduction/IR, elbow flexion, forearm pronation, wrist/fingers flexion

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13
Q

LE Spasticity Pattern

A

hip adduction/extension/IR, knee extension, ankle PF

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14
Q

What is posture of right UE (d/t spasticity) due to

A

contracture, weak actin-myosin bonds, disinhibition of reticulospinal trect

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15
Q

Extension of right LE (d/t spasticity) due to

A

Unopposed input to LE LMN’s by reticulospinal & vestibulospinal tracts (these are not totally dependent on cortical control)

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16
Q

Extension of right LE (d/t spasticity) due to

A

Unopposed input to LE LMN’s by reticulospinal & vestibulospinal tracts (these are not totally dependent on cortical control)

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17
Q

What is an obligatory synergy?

A

Mass patterns of movement elicited by attempts at voluntary movement, reflexes, coughing/sneezing

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18
Q

Synergy Patterns

A

Could be d/t decreased corticospinal input on LMN’s & unopposed vestibulospinal, rubrospinal & reticulospinal input on LMN’s

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19
Q

Reticulospinal tract

A

originates in reticular formation of brainstem, projects bilaterally down through the ventral funiculus to postural muscles & gross limb muscles

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20
Q

What are abnormal reflexes though to be due to?

A

release of normal inhibition by UMN’s.

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21
Q

What do abnormal reflexes interfere with?

A

attempts of volitional movement and with functional mobility. (hyperreflexia, return of cutaneous reflexes, return of tonic reflexes)

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22
Q

Homonymous Hemianopsia

A

loss of half of visual field. Left = loss of left visual field.

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23
Q

Contraversive pushing

A

pt pushes toward the paretic side, often involves lesion in thalamus and/or roght sided cortical lesions causing neglect, can resolve in 6 mo.

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24
Q

Perseveration

A

continuous repetition of words, lesions in the premotor and prefrontal cortex.

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25
Left CVA (right hemiparesis) Behavioral differences
difficulties in communication and processing information in a sequential manner, cautious/anxious/disorganized, hesitant to try new tasks, realistic regarding their dysfunctions
26
Right CVA (left hemiparesis) Behavioral differences
difficulty grasping the whole idea of a task, quick and impulsive, overestimate their abilities, safety more of a concern
27
Early warning signs of stroke
- Sudden N/T in face and/or extremities - Sudden confusion and trouble speaking - Sudden difficulty seeing out of one eye - Sudden dizziness and LOB - Sudden severe headache
28
Ischemic umbra
core area of irreversible neuronal damage.
29
Ischemic penumbra
peripheral area of "damaged" neurons (neurons that are vulnerable to extend the stroke) generally takes place in 1st 3-4 hours
30
Lacunar strokes
can affect neuronal cell bodies in the cerebrum, can affect internal capsule (capsular stroke)
31
Pure motor Sxs affects the
posterior limb of internal capsule, basalar pons or pyramids
32
Pure Sensory Sxs
affects the thalamus or thalamocortical fibers
33
Stage 1 of recovery from CVA
Initial flaccidity; no voluntary movement
34
Stage 2 of recovery from CVA
Emergence of spasticity, hyperreflexia and synergies
35
Stage 3 of recovery from CVA
Strong spasticity; voluntary movement possible, but only in synergistic patterns
36
Stage 4 of recovery from CVA
Decline in spasticity and synergies; voluntary control in isolated joint movements emerging
37
Stage 5 of recovery from CVA
Increased voluntary control out-of-synergies; coordination deficits present
38
Stage 6 of recovery from CVA
Control and coordination near normal
39
Stage 6 of recovery from CVA
Control and coordination near normal
40
Multiple Sclerosis
De-myelination of axons in CNS b/t ages 15-50
41
What is MS due to?
immune reaction triggered by a viral infection (possibly Epstein-Berr), Vitamin D deficiency could be a factor. Women 3x more effected
42
Sensory impairments in MS
parasthesias (face, trunk, extremities), decreased position sense, decreased pallesthesia, dysesthesias (burning/aching), Allodynia (light touch causes pain), trigeminal neuralgia, pain, lhermitte's sign
43
Lhermitte's Sign
- “electric-shock” like pain down the spine during flexion of the neck - Possibly caused by “cross-talk” between de-myelinated axons in the white matter of the spinal cord; flexion of neck moves the cord up and causes rubbing of these axons
44
Optic Neuritis
inflammation/demyelination of the optic nerve, often first signs of MS.
45
Optic Neuritis Symptoms
- Pain posterior to eye with movement - Blurred vision - Scotomas (blind spots) - Difficulty seeing in bright light - Difficulty seeing objects of low contrast
46
Motor Impairments of MS
Fatigue, UMN S/S, Paresis, Ataxia, Dysmetria, dysdiadochokinesia (intention tremors), dysphagia, dysarthria, dysphonia
47
Cognitive/Behavioral Impairments of MS
More related to location of lesions vs severity of disease Depression Memory Attention & learning Conceptual reasoning Poor executive functions (planning, organizing, problem solving) Labile Anxiety Bowel/Bladder dysfunction Sexual dysfunction (impotence, decreased libido)
48
Cognitive/Behavioral Impairments of MS
More related to location of lesions vs severity of disease Depression Memory Attention & learning Conceptual reasoning Poor executive functions (planning, organizing, problem solving) Labile Anxiety Bowel/Bladder dysfunction Sexual dysfunction (impotence, decreased libido)
49
Relapsing/remitting
Onset of Sx w/ either full or partial recovery followed by periods of no progression of the disease (when deficit aways resolve b/t episodes = benign)
50
Secondary Progressive
initial relapsing/remitting course followed by progressive course (50% by 10 years, 90% by 25 years)
51
Primary Progressive
progresses consistently from initial onset, may have occasional plateaus & minor improvements
52
Progressive Relapsing
Progressive decline with episodes of increased symptoms. Least common
53
Clinically isolated syndrome
Person has an attack suggestive of demyelination but does not fulfill the criteria for MS 30%-70% will later develop MS Should be started on immune-modulating drugs immediately
54
Signs/sxs of MS can be exacerbated by
- Heat = Uhthoff’s Phenomenon (increased body temperature worsens sxs) possibly due to affect on membrane channel proteins) - Stress - Viral or bacterial infections
55
Diagnosis of MS
evidence of plaques in 2 different areas, which occurred at different points in time. two or more attacks of MS S/S during 2 time patterns (2 lasting @ least 24 hours, chronically progressive episodes @ least 6 mo)
56
ALS
Degeneration and loss of motor neurons in the spinal cord, brainstem and cortex - results in UMN & LMN signs/Sx
57
ALS Signs/Sx
Both UMN & LMN LMN: weakness/atrophy, fasciculations (contraction of motor units) respiratory impairments (dyspnea) UMN: spasticity, hyperreflexia, dysarthria, dysphagia, cognitive impairments (frontotemporal dementia), sialorrhea (drooling)
58
Limb onset ALS
limbs affected first
59
Bulbar onset ALS
dysarthria & dysphagia affected first
60
Stages of ALS
I) mild focal asymmetric weakness; hand cramping II) moderate weakness in groups of muscles III) severe weakness, but ambulatory IV) severe weakness; predominately uses w/c V) severe weakness with loss of head control; spasticity noted VI) bedridden with progressive respiratory distress
61
TBI
- Injury to the brain from an external force - The leading cause of death and disability in young adults (1.5-2 million/yr). 50% MVA; 25% falls; 15% assaults/violence; 10% sports (Typical age 15-24)
62
Focal injury TBI
Local injury to brain tissue directly under the impact (coup injury) and/or at a site opposite the injury (coup-contrecoup injury)
63
Diffuse axonal injury (DAI)
Shearing, tearing and retraction of axons (white matter such as the internal capsule) Mechanisms: acceleration/deceleration or rotational forces May result in coma
64
What is normal ICP?
4-15 mmHg.
65
Possible NM impairments from TBI
- Abnormal tone - Primitive postures (decorticate or decerebrate rigidity) - Altered proprioceptive, vestibular and/or visual sensation (poor balance) - Abnormal motor control (hemiparesis, decreased coordination, synergistic patterns) Dysphagia (impaired swallowing) Aphasias (expressive, receptive, global)
66
Possible Cognitive impairments from TBI
``` Altered level of consciousness Memory deficits Perceptual deficits (ideational/ideomotor apraxias, spatial neglect) ```
67
Possible Behavioral impairments from TBI
- Uncontrolled aggression, depression, frustration, anger | - Sexual and emotional disinhibition
68
Subcortical White matter
associational, projection, commissural fibers
69
Associational Fibers
Connect areas in the same hemisphere | Allow hemisphere to function as an integrated whole
70
Superior longitudinal fasciculus
Associational fiber. Connects Wernicke's and Broca's areas
71
Commissural Fibers
interconnect hemispheres. Corpus callosum, anterior and posterior commisures
72
projection fiers
internal capsule - descending fibers = corticospinal, corticopontine, corticobulbar, ascending fibers = thalamocortico fibers
73
Pseudobulbar Palsy
UMN lesion to corticobulbar fibers in the internal capsule. (cortical motor neuron axons projecting to cranial nerve motor neurons) S/S - spastic tongue, hyperreflexic jaw and gag reflexes, slow/slurred speech.
74
True "bulbar" palsy
would be a lesion to the cranial nerves and would exhibit LMN signs/sxs
75
Pure motor symptoms CVA
affects the posterior limb of internal capsule, basalar pons or pyramids
76
Pure sensory symptoms CVA
affects the thalamus or thalamocortical fibers

Neuroanatomy (9 decks)

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