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Neuroanatomy > Exam VIII > Flashcards

Exam VIII Flashcards

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
Q

Left CVA (right hemiparesis) Behavioral differences

A

difficulties in communication and processing information in a sequential manner, cautious/anxious/disorganized, hesitant to try new tasks, realistic regarding their dysfunctions

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26
Q

Right CVA (left hemiparesis) Behavioral differences

A

difficulty grasping the whole idea of a task, quick and impulsive, overestimate their abilities, safety more of a concern

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27
Q

Early warning signs of stroke

A
  • 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
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28
Q

Ischemic umbra

A

core area of irreversible neuronal damage.

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29
Q

Ischemic penumbra

A

peripheral area of “damaged” neurons (neurons that are vulnerable to extend the stroke) generally takes place in 1st 3-4 hours

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30
Q

Lacunar strokes

A

can affect neuronal cell bodies in the cerebrum, can affect internal capsule (capsular stroke)

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31
Q

Pure motor Sxs affects the

A

posterior limb of internal capsule, basalar pons or pyramids

32
Q

Pure Sensory Sxs

A

affects the thalamus or thalamocortical fibers

33
Q

Stage 1 of recovery from CVA

A

Initial flaccidity; no voluntary movement

34
Q

Stage 2 of recovery from CVA

A

Emergence of spasticity, hyperreflexia and synergies

35
Q

Stage 3 of recovery from CVA

A

Strong spasticity; voluntary movement possible, but only in synergistic patterns

36
Q

Stage 4 of recovery from CVA

A

Decline in spasticity and synergies; voluntary control in isolated joint movements emerging

37
Q

Stage 5 of recovery from CVA

A

Increased voluntary control out-of-synergies; coordination deficits present

38
Q

Stage 6 of recovery from CVA

A

Control and coordination near normal

39
Q

Stage 6 of recovery from CVA

A

Control and coordination near normal

40
Q

Multiple Sclerosis

A

De-myelination of axons in CNS b/t ages 15-50

41
Q

What is MS due to?

A

immune reaction triggered by a viral infection (possibly Epstein-Berr), Vitamin D deficiency could be a factor. Women 3x more effected

42
Q

Sensory impairments in MS

A

parasthesias (face, trunk, extremities), decreased position sense, decreased pallesthesia, dysesthesias (burning/aching), Allodynia (light touch causes pain), trigeminal neuralgia, pain, lhermitte’s sign

43
Q

Lhermitte’s Sign

A
  • “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
Q

Optic Neuritis

A

inflammation/demyelination of the optic nerve, often first signs of MS.

45
Q

Optic Neuritis Symptoms

A
  • Pain posterior to eye with movement
  • Blurred vision
  • Scotomas (blind spots)
  • Difficulty seeing in bright light
  • Difficulty seeing objects of low contrast
46
Q

Motor Impairments of MS

A

Fatigue, UMN S/S, Paresis, Ataxia, Dysmetria, dysdiadochokinesia (intention tremors), dysphagia, dysarthria, dysphonia

47
Q

Cognitive/Behavioral Impairments of MS

A

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
Q

Cognitive/Behavioral Impairments of MS

A

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
Q

Relapsing/remitting

A

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
Q

Secondary Progressive

A

initial relapsing/remitting course followed by progressive course (50% by 10 years, 90% by 25 years)

51
Q

Primary Progressive

A

progresses consistently from initial onset, may have occasional plateaus & minor improvements

52
Q

Progressive Relapsing

A

Progressive decline with episodes of increased symptoms. Least common

53
Q

Clinically isolated syndrome

A

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
Q

Signs/sxs of MS can be exacerbated by

A
  • Heat = Uhthoff’s Phenomenon (increased body temperature worsens sxs) possibly due to affect on membrane channel proteins)
  • Stress
  • Viral or bacterial infections
55
Q

Diagnosis of MS

A

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
Q

ALS

A

Degeneration and loss of motor neurons in the spinal cord, brainstem and cortex
- results in UMN & LMN signs/Sx

57
Q

ALS Signs/Sx

A

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
Q

Limb onset ALS

A

limbs affected first

59
Q

Bulbar onset ALS

A

dysarthria & dysphagia affected first

60
Q

Stages of ALS

A

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
Q

TBI

A
  • 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
Q

Focal injury TBI

A

Local injury to brain tissue directly under the impact (coup injury) and/or at a site opposite the injury (coup-contrecoup injury)

63
Q

Diffuse axonal injury (DAI)

A

Shearing, tearing and retraction of axons (white matter such as the internal capsule)
Mechanisms: acceleration/deceleration or rotational forces
May result in coma

64
Q

What is normal ICP?

A

4-15 mmHg.

65
Q

Possible NM impairments from TBI

A
  • 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
Q

Possible Cognitive impairments from TBI

A 
Altered level of consciousness
Memory deficits
Perceptual deficits (ideational/ideomotor apraxias, spatial neglect)
67
Q

Possible Behavioral impairments from TBI

A
  • Uncontrolled aggression, depression, frustration, anger

- Sexual and emotional disinhibition

68
Q

Subcortical White matter

A

associational, projection, commissural fibers

69
Q

Associational Fibers

A

Connect areas in the same hemisphere

Allow hemisphere to function as an integrated whole

70
Q

Superior longitudinal fasciculus

A

Associational fiber. Connects Wernicke’s and Broca’s areas

71
Q

Commissural Fibers

A

interconnect hemispheres. Corpus callosum, anterior and posterior commisures

72
Q

projection fiers

A

internal capsule - descending fibers = corticospinal, corticopontine, corticobulbar, ascending fibers = thalamocortico fibers

73
Q

Pseudobulbar Palsy

A

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
Q

True “bulbar” palsy

A

would be a lesion to the cranial nerves and would exhibit LMN signs/sxs

75
Q

Pure motor symptoms CVA

A

affects the posterior limb of internal capsule, basalar pons or pyramids

76
Q

Pure sensory symptoms CVA

A

affects the thalamus or thalamocortical fibers

Neuroanatomy (9 decks)

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