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Neuro Test 2 > Clinical Implications (rebby) > Flashcards

Clinical Implications (rebby) Flashcards

1
Q

4D’s of Brainstem Dysfunction

A

Dysphagia
Dysarthria
Diplopia
Dysmetria

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2
Q

Blockage of PCA or Basilar artery causes ________ Syndrome

A

Anteromedial Midbrain Syndrome (Weber’s)

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3
Q

Patient presents with
* CL hemiparesis
* IL loss of eye movements, paralysis of eyelid, dilated pupil
* CL loss of motor coordination, Lability, Ataxia

What are the primary structures affected? What is the syndrome?

A
  1. Corticospinal Tract
  2. Oculomotor Nerve Nucleus
  3. Red Nucleus

Anteromedial Midbrain Syndrome (Weber’s)

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4
Q

What are 2 symptoms of CN III palsy?

A
  1. Ptosis (droopy eyelid)
  2. Eye deviated down and out
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5
Q

Blockage of AICA leads to ________________ Syndrome

A

Lateral Inferior Pontine Syndrome

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6
Q

Patient presents with
* IL hearing loss
* Dysequilibrium
* IL horner’s syndrome
* IL facial pain
* Decreased tears & salivation
* CL pain and temp sensation lost
* IL weakness of facial expressions

What is the syndrome?

A

Lateral Inferior Pontine syndrome

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7
Q

Name the 7 primary structures affected with Lateral Inferior Pontine Syndrome

A
  1. Cochlear Nucleus
  2. Vestibular Nucleus
  3. Impaired sympathetics
  4. Trigeminal Nerve
  5. Salivatory Nucleus
  6. Spinothalamic Tract
  7. Facial Nerve
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8
Q

Bell’s Palsy is damage to what CN?

A

CN VII

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9
Q

Horner’s Syndrome is what 3 things?

A

Ptosis-eyelid drooping
Miosis-excessive constriction
Anhidrosis- little/no sweat

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10
Q

Thrombosis or stenosis of basilar artery will affect ________ bilaterally and cause ________ syndrome

A

Ventral Pons

Locked-In Syndrome

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11
Q

Patient presents with
* Paralysis below the head
*Paralysis of facial, swallowing, chewing, talking muscles
* inability to abduct eyes

What structures are affected?

A

B corticospinal tracts
B corticobulbar tracts
B abducens nerve nuclei

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12
Q

Which of the following is not affected in Lateral Inferior Pontine Syndrome?

A. Vestibular Nucleus
B. Impaired sympathetics
C. Vagus Nerve nucleus
D. Salivatory Nucleus

A

C. Vagus Nerve nucleus

this is a primary affected structure in Wallenberg Syndrome

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13
Q

Which of the following is not affected in both Lateral Inferior Pontine syndrome and Wallenberg?

A. Solitary Nucleus
B. Salivatory Nucleus
C. Trigeminal Nerve
D. Spinothalamic Tract

A

A. Solitary Nucleus

only in Wallenberg

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14
Q

Blockage of Anterior Spinal Artery leads to ______ Syndrome

A

Medial Medullary Syndrome

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15
Q

Patient presents with
* IL tongue protrusion
*CL loss of vibration, proprioception, light touch
*CL hemiparesis

What structures are affected? What is the syndrome?

A

Hypoglossal Nucleus
DCML
Pyramids

Medial Medullary Syndrome

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16
Q

Blockage of PICA leads to _____ Syndrome

A

Wallenberg/Lateral Medullary Syndrome

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17
Q

Which of the following is not a clinical manifestation of Wallenberg Syndrome?

A. Increased HR
B. Ataxia
C. Horner’s syndrome
D. Can’t abduct eyes

A

D. Can’t abduct eyes

this is a manifestation of Locked In syndrome –> B abducens

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18
Q

In the thalamus, when relay sensory neurons disrupt CONTRALATERAL sensation, what sensation is most commonly affected?

A

Proprioception

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19
Q

What is a common clinical implication of a thalamic lesion?

A

Lateropulsion aka Pusher syndrome aka Contraversive Pushing

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20
Q

In Pusher Syndrome, does the patient push to the strong or weak side?

A

Weak side

Push with strong side towards the weaker side & accompanied by POSTERIOR push

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21
Q

What type of tumor makes up 10-17% of intracranial neoplasms? (in hypothalamus)

A

Pituitary adenomas

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22
Q

Larger pituitary adenomas can push on surrounding structures (of the hypothalamus) such as _______ _______ and cause _______ _______

A

Optic chiasm

Bitemporal hemianopsia

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23
Q

When there is too much Basal Ganglia inhibition of motor thalamus, PPN, and midbrain locomotor region, this will cause __________

A

Hypokinesia

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24
Q

In Parkinson’s, there is ______ (decreased/increased) dopamine from SNc leading to ________ (under/over) activity of GPi

A

Decreased

Over

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25
Q

fill in the blank with (overactivity/underactivity)

Overactivity of GPi in Parkinson’s leads to _______ in motor thalamus

A

Underactivity (bradykinesia and hypokinesia)

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26
Q

fill in the blank with (moreinhibition/less inhibition)

Overactivity of GPi in Parkinson’s leads to _______ in Pedunculopontine nucleus

A

Less inhibition (rigidity trunk and girdle muscles)

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27
Q

fill in the blank with (overactivity/underactivity)

Overactivity of GPi in Parkinson’s leads to _______ in Midbrain locomotor region

A

Underactivity (freezing and festinating gait)

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28
Q

What are the 2 subtypes of Parkinson’s?

A

Postural Instability Gait Difficulty

Tremor Dominant Subtype

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29
Q

When there is too little Basal Ganglia inhibition, that causes ________

A

Hyperkinetic disorders

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30
Q

In hyperkinetic disorders, there is (more/less) inhibition by the GPi

A

Less inhibition

because

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31
Q

Hyperkinetic disorders affect _____ (which motor pathway)

A

No-Go/Indirect pathway

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32
Q

In hyperkinetic disorders, there’s a _____ of inhibitory neurons in putamen and caudate, so ____ input to GPe

A

Loss

Less (inhibitory)

So GPe inhibits Subthalamic Nucleus (MORE) which excites GPi less so GPi has less inhibition

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33
Q

Dystonia increases with _____ and decreases/completely vanishes with ____

A

Activity and/or emotional stress

Sleep

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34
Q

Injury to Paramedian Pontine Reticular Formation (PPRF) causes loss of

A

Horizontal Gaze center

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35
Q

Injury to Rostral interstitial nucleus in midbrain RF causes loss of

A

Vertical Gaze Center

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36
Q

Injury to Medial Longitudinal Fasciculus causes loss of

A

coordinated activation of B neural circuits

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37
Q

Injury to Vestibular n will cause loss of which 2 reflexes?

A

VOR and Optokinetic Reflex

38
Q

Injury to Frontal eye field will cause loss of CL _______ and ________, and loss of connection with CL ________

A

saccades, smooth pursuit

PPRF

39
Q

Injury to Parieto-occipital-temporal cortex will cause loss of (CL/IL) smooth pursuit

A

IL

whereas frontal eye field does CL smooth pursuit and saccades

40
Q

Injury to Parieto-occipital-temporal cortex may affect the cortex connection to what 3 locations?

A

vestibular nucleus
cerebellum
PPRF

41
Q

Lesion to superior colliculus (optic tectum) causes

A

Increased latency and reduced accuracy, frequency, and velocity of saccades

42
Q

How will injury to basal ganglia affect the visual system?

A

Deficits in initiation of eye movements

43
Q

How will injury to cerebellum affect the visual system?

A

Deficits in correct execution of eye movements

44
Q

Lesion to L optic nerve

A

Loss of vision to L eye

45
Q

Lesion to optic chiasm

A

Bitemporal (heteronomous) hemianopsia

46
Q

Lesion to L optic tract

A

R homonymous hemianopsia

47
Q

Lesion to L Meyer’s Loop

A

R superior homonymous quadrantanopsia

48
Q

Lesion to L V1

A

R homonymous hemianopsia with macular sparing

49
Q

Lesion to primary auditory cortex causes

A

Loss of conscious hearing

50
Q

Lesion to secondary auditory cortex results in …

A

Inability to compare sounds with memories of sounds and categorize them

51
Q

How will a lesion to superior colliculus affect the auditory system?

A

Inability to orient head and eyes toward sound

52
Q

Lesion to Wernicke’s area means…

A

Inability to comprehend speech

53
Q

If SCC signals are not reciprocal, there is impaired ______, ______, and/or ______

A

Postural control
Eye movements
Nausea

54
Q

When the pt has a vestibular disorder, _____ is essential for adaptations in postural/balance systems

A

Vestibulocerebellum

55
Q

Lesion of R posterior parietal cortex causes _______

A

Altered perceptions of personal and extrapersonal space

L hemi neglect

56
Q

Lesion to descending pathway of vestibular system…

A

Balance deficits –> impacts movement abilities/control especially in low-light or uneven surface conditions

57
Q

Vestibular + visual systems linked for ….

A

Postural control & eye movements

58
Q

Vestibular + auditory systems linked due to….

A

Geography and sharing same CN

59
Q

T/F: Cerebellar dysfunction causes abnormal muscle strength and tone

A

False

60
Q

If cerebellar dysfunction DOES cause abnormal tone, it is hypo/hyper

A

Hypotonia

61
Q

Lesion to any/all areas in cerebellum causes ______

A

Ataxia: jerky, uncoordinated movements of trunk/neck, limbs

62
Q

Lesion to vestibulocerebellum causes

A

Nystagmus: bouncy eye movements
&
Unsteadiness, truncal ataxia, dysequilibrium

63
Q

Lesion to cerebrocerebellum causes

A

Ataxic finger movements
& Dysarthria: slurring of speech

64
Q

Lesion to spinocerebellum causes

A

Dysarthria
Explosive Speech
Limb ataxia
* Dysdiadochokinesia
* Dysmetria (ACTION & INTENTION TREMOR)
Loss of check/rebound
Movement decomposition

65
Q

What is problem with rapid alternating movements?

A

Dysdiadochokinesia

66
Q

What is tendency to under/overshoot when moving to a target?

A

Dysmetria

67
Q

What is shaking of limb during movement called?

A

Action tremor

68
Q

What tends to occur due to delays in agonist burst of activity + in antagonist’s ability to brake?

A

Intention tremor

69
Q

What is it called when there is a quick removal of resistance that causes an exaggerated response?

A

Loss of check/rebound

70
Q

What is it called when you attempt to move one joint at a time?

A

Movement decomposition

71
Q

What is loss of joint position sense?

A

Sensory ataxia

DCML disruption & can improve with visual aid

72
Q

What is an agnosia?

A

Despite having intact vision or hearing, inability to recognize object or sound

73
Q

Agnosia is a disorder of ____ visual stream

A

Ventral

74
Q

Prosopagnosia is …

A

Inability to recognize faces visually

75
Q

Disorder of secondary auditory cortex

A

Auditory agnosia = can’t associate meaning to what you hear

76
Q

Anosagnosia is …

A

Inability to recognize deficits

a reasoning problem

77
Q

Disorder of secondary somatosensory cortex

A

Astereognosia = even with intact light touch sensation, can’t describe object in hand

78
Q

Optic ataxia is a disorder of ____ visual stream

A

Dorsal

79
Q

Optic ataxia is …

A

an inability to use visual info to direct movements

80
Q

Damage to PPC causes

A

Hemineglect

81
Q

Right or Left Hemineglect is more common

A

Left neglect

due to Right hemispheric lesion

82
Q

Damage to primary motor cortex leads to ____, ____, and _____

A

Loss of fractionated movements
Weakness
Dysarthria

83
Q

Lesion to supplementary motor area (acute & long term)…

A

Acutely: hemiparesis, hemiplegia
Long term: anti-phase hand movements

anti-phase is when muscles contract in alternating fashion (aka hands moving to same side so opposite muscles on each arm are contracting)

84
Q

Lesion to premotor cortex causes issues with _____, _____, and _______

A

Speech and automaticity of reaching/grasping
Movement sequences
Posture (axial control) and gait

85
Q

Damage to inferior frontal gyrus can cause…

A

Broca’s Aphasia can be included here (motor of speech)

86
Q

Damage to motor planning areas causes preservation. What is that?

A

Uncontrolled repetition of movement/speech

Remember: Mr. Egg story and how he could not put down his poached egg

87
Q

What is apraxia?

A

Motor planning deficits

88
Q

What is magnetic gait?

A

when the patient has difficulty lifting up their feet and so they have a shuffle or festinating gait

89
Q

What is Ideational apraxia?

A

Inability to use objects appropriately, esp when sequence is necessary

90
Q

What is Ideomotor apraxia?

A

Inability to develop movement sequence, esp to command or to mimic activity

but can do it automatically

91
Q

If someone has true apraxia, how would you describe their gait?

A

Magnetic gait

92
Q

What are the 4 A’s for cerebral cortex disorders?

A

Aphasia: language/communication disorder
Apraxia: motor planning deficits
Agnosia: can’t identify sound/sight
Astereognosis: can’t describe object in hand

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