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Clinical Medicine > Phase II Neuro > Flashcards

Phase II Neuro Flashcards

1
Q

what are the 6 components of the neurological examination

A

1) mentation
2) gait and posture
3) CN exam
4) postural reactions
5) spinal reflexes
6) palpation

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2
Q

what 2 tests do we use to assess postural reactions

A

1) proprioceptive tests (ex. knuckling)
2) hopping

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3
Q

what tests do we use to assess spinal reflexes:
- thoracic limb (TL)
- pelvic limb (PL)
- other regions

A

TL: withdrawal, weight-bearing
PL: withdrawal, patellar
Other regions: perianal, cutaneous trunci

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4
Q

what are the functional segments of the spinal cord and which are the enlargements

A
  • C1-C5
  • C6-T2 (TL enlargement)
  • T3-L3
  • L4-S3 (PL and perineum/tail enlargement)
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5
Q

what do the spinal cord enlargements contain

A

LMNs for the limb pairs

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6
Q

what lives in the white vs grey matter of the spinal cord

A

white matter: tracts
grey matter: motor nerve cell bodies

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7
Q

what are the 3(4) sections of the spinal cord white matter

A
  • dorsal funiculus
  • ventral funiculus
  • lateral funiculi (left and right)
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8
Q

in what general area of the white matter are the ASCENDING tracts located

A

dorsolateral

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9
Q

the ascending tracts contain tracts carrying what 3 general categories of information

A
  • conscious proprioception
  • reflex proprioception
  • nociception
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10
Q

what are the 2 conscious proprioceptive ascending tracts and which limbs do they correspond to

A
  • fasciculus cuneatus (TL)
  • fasciculus gracilis (PL)
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11
Q

what are the 2 reflex proprioceptive ascending tracts and what limbs do they correspond to

A
  • rostral spinocerebellar tract (TL)
  • dorsal and ventral spinocerebellar tracts (PL)
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12
Q

what are the 2 nociceptive tracts

A
  • spinothalamic tract
  • fasciculus proprius
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13
Q

what is the proprioceptive pathway

A

sensory receptor -> peripheral sensory neuron -> spinal cord white matter (tract) -> brainstem/cerebellum -> contralateral cortex

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14
Q

what ascending tracts are deepest in the white matter and what does this mean clinically

A

nociceptive (i.e spinothalamic and fasciculus proprius)

means that loss of deep pain is only going to be seen with a severe spinal cord injury (to the dorsolateral spinal cord)

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15
Q

what clinical signs would you expect to see in a patient with a lesion to the dorsolateral spinal cord (i.e. ascending tracts damaged)

A

1) proprioceptive deficits (decreased hopping, knuckling, proprioceptive ataxia)

2) changes in pain perception (hypoesthesia, hyperesthesia, anesthesia)

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16
Q

what are signs of proprioceptive ataxia

A
  • wobble/sway
  • erratic paw placement
  • limbs crossing over
  • abnormal posture
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17
Q

T/F knuckling will always indicate spinal cord dysfunction

A

F (pain, metabolic disease, orthopedic disease, etc.)

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18
Q

Are you more likely to see proprioceptive deficits (ex. knuckling) if there is a peripheral nerve or a tract problem? Why? Are both possible?

A

More likely in the tracts as you would need complete severage or loss of nerve fibers in the entire nerve to see proprioceptive deficits from a peripheral nerve problem. Both are technically possible (ex. severe trauma such as a car accident that severs the brachial plexus)

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19
Q

T/F proprioceptive ataxia is seen in both CNS and PNS lesions

A

F; only CNS

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20
Q

in what general area of the white matter are the DESCENDING tracts located

A

ventrolaterally

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21
Q

what are the 5 descending white matter tracts

A
  • tectospinal
  • rubrospinal
  • vestibulospinal
  • reticulospinal
  • corticospinal
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22
Q

UMN exercises ___________ on LMN

A

descending inhibition (keeps reflexes in check)

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23
Q

where can we localize UPN to

A

spinal cord white matter

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24
Q

in what regions of the spinal cord do we tend to see ONLY UMN problems (and no LMN problems)

A

C1-C5 and T3-L3

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25
Q

LMN are confined to the _____ and localized to the (3)

A

PNS; spinal nerves, nerve roots or spinal cord grey matter

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26
Q

Describe the following for UMN:
- paralysis
- reflexes
- muscle tone
- atrophy
- urinary/GI
- clinical signs

A
  • spastic paresis/paralysis
  • normal to increased reflexes
  • normal to increased muscle tone
  • disuse atrophy (slow)
  • incontinence
  • struggling to hold body up, still have voluntary movement but it is abnormal, normal proprioception
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27
Q

Describe the following for LMN:
- paralysis
- reflexes
- muscle tone
- atrophy
- urinary/GI
- clinical signs

A
  • flaccid paresis/paralysis
  • decreased or absent reflexes
  • decreased or absent muscle tone
  • neurogenic atrophy (early and severe)
  • incontinence
  • cannot hold body up, no reflexes, loss of deep pain sensation
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28
Q

Put the following in order of increasing loss of function (and what order is gain of function)

  • nociception
  • proprioception
  • incontinence
  • paresis to paralysis
A

Loss of function:
1) proprioception
2) paresis to paralysis
3) incontinence
4) nociception

Gain of function occurs in the reverse order:
1) nociception
2) incontinence
3) paresis to paralysis
4) proprioception

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29
Q

Shiff-Sherrington posture indicates a lesion where? What are the clinical signs? Why?

A
  • lesion in the L1-L4 grey matter border cells or their axons
  • opisthotonus and increased thoracic limb extensor tone
  • these neurons help co-ordinate the posture of the neck
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30
Q

T/F Shiff-Sherrington posture indicates poor prognosis

A

F: does not indicate prognosis

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31
Q

T/F the spinal cord and brain have no nerve endings

A

T

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32
Q

what 3 structures are involved in EXTREME spinal pain

A

bones, nerve roots, meninges

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33
Q

what do you NOT want to do to assess neck pain if other signs are present

A

vertical/horizontal flexion

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34
Q

what is a nerve root signature

A

single limb lameness (pain) due to nerve damage

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35
Q

what do you see in addition to spinal pain in a patient with concurrent spinal cord disease

A

paresis and ataxia -> proprioceptive deficits

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36
Q

As a lesion moves CRANIALLY in the spinal cord, what happens to proprioceptive ataxia in the thoracic limbs?

A

gets worse

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37
Q

what are the 3 meninges from OUTSIDE to INSIDE

A

dura mater, arachnoid mater, pia mater

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38
Q

the patellar reflex tests the function of what nerve

A

femoral nn

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39
Q

what are the spinal cord segments tested by the femoral nerve and which is the main one

A

L4, L5, L6

L5 is the main one

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40
Q

the flexor reflex tests what nerves

A

radial (thoracic) and sciatic (pelvic)

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41
Q

what spinal cord segments are tested by the flexor reflex and what is the main one

A

Radial:
C7, C8, T1, T2

Pelvic:
L6, L7, S1, S2
L7 is the main one

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42
Q

where does cutaneous trunci synapse

A

C8-T1

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43
Q

the absence of cutaneous trunci reflexes on one side only tells us

A

there is an impaired transmission of sensory signals that synapse between C8-T1 on that side

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44
Q

which is left and which is right:

OS
OD

A

OS: left
OD: right

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45
Q

what are 4 clinical signs of Horner’s syndrome and which is the MINIMAL clinical sign

A
  • miosis (minimal clinical sign)
  • enopthalmos
  • protruding nictitans
  • ptosis
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46
Q

what is the pathway of Horner’s syndrome (normal pathway)

A

hypothalamus -> travels in spinal cord to T1/T2/T3 -> enters sympathetic trunk -> synapses in superficial cervical ganglion -> mediates dilation of the eye

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47
Q

where are the synapses along the pathway for Horner’s syndrome

A

1) at T1/T2/T3
2) at the superficial cervical ganglion

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48
Q

what are the sections of the CNS

A

thalamocortex, brainstem, cerebellum, spinal cord

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49
Q

what are the sections of the PNS

A

peripheral nerves, neuromuscular junctions, skeletal muscles

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50
Q

what are the 2 types of LMNs

A

those leaving the cervicothoracic and lumbosacral enlargements and the cranial nerve motor neurons/ganglia

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51
Q

the perineal reflex tests what nerve? what segments?

A

pudendal (S1, S2, S3)

52
Q

T/F neuromuscular disease involves lesions of both the UMN and LMN

A

F; it involves the LMN since neuromuscular disease involves the PNS

53
Q

T/F cranial nerves may be impacted by neuromuscular disease

A

T, since they are considered LMNs

54
Q

what is the difference between mononeuropathies and polyneuropathies

A

mononeuropathies: one nerve or a group of adjacent nerves affected

polyneuropathies: simultaneous malfunction of many peripheral nerves

55
Q

how do neuromuscular diseases present (signs on the neurologic exam)

A

Presents like LMN disease
- normal mentation
- CN may be afffected
- paresis/paralysis
- decreased to absent reflexes
- decreased to absent muscle tone
- possible neurogenic atrophy
- possible paresthesia
- expect normal postural reactions unless there is concurrent sensory dysfunction

56
Q

where is the cauda equina located

A

over the lumbosacral junction (with species differences)

57
Q

T/F the cauda equina is part of the spinal cord

A

F, part of the PNS (LMN)

58
Q

what are clinical signs of cauda equina lesions

A
  • NO ataxia
  • may see lumbosacral pain
  • may see abnormal spinal reflexes
59
Q

put the following species in order of shortest to longest spinal cord (i.e which ends before the lumbosacral junction and which extends the furthest past the junction)

  • dog
  • cat
  • horse
  • cow
A

dog, cow, horse, cat

60
Q

what is a telltale sign that a lesion affecting all 4 legs is in the PNS as opposed to the CNS

A

lack of proprioceptive ataxia

61
Q

PNS dysfunctions are characterized by

A

RAT
- reflex deficits
- atrophy (neurogenic)
- tone decreased

62
Q

PNS dysfunctions can be a manifestation of (3)

A

neuropathy, junctionopathy, myopathy

63
Q

T/F ataxia is uncommon with PNS lesions

A

T

64
Q

what 3 “opathies” are clinically indistinguishable

A

polyneuropathies, polymyopathies and junctionopathies

65
Q

describe the expected findings on the neurologic exam for a patient with neuromuscular disease:
- mentation
- cranial nerves
- posture/gait
- postural reactions
- reflexes
- muscle tone
- muscle atrophy
- other comorbidities

A
  • mentation: normal
  • cranial nerves: may be affected
  • posture/gait: paresis/paralysis
  • postural reactions: normal
  • reflexes: reduced to normal
  • muscle tone: decreased to absent
  • muscle atrophy: possible
  • other comorbidities: megaesophagus, aspiration pneumonia, exposure keratitis
66
Q

what are important differential diagnoses for a patient showing signs of neuromuscular disease

A
  • orthopaedic (pain)
  • systemic illness (malaise)
  • lumbosacral disease
67
Q

are presynaptic or postsynaptic neuromuscular diseases associated with SLUDGEM

A

post-synaptic

68
Q

what are examples of myopathies

A

non-inflammatory (acquired, degenerative/inherited, nutritional) and inflammatory (infectious and immune-mediated)

69
Q

what 4 ways can we diagnose myopathies

A
  • CBC/biochem/UA: elevated CK, ALT, AST
  • serum pre and post-exercise lactate
  • electrodiagnostics
  • muscle histopathology
70
Q

how do the clinical signs of hypokalemia differ between cats and dogs and why

A

cats: high shoulders and low head carriage

won’t see low head carriage in dogs as they have a more complete nuchal ligament

71
Q

what is another word for thalamus

A

diencephalon

72
Q

what two regions of the brain control mental status and why is this useful

A

the thalamocortex and the RAS in the brainstem

useful because if we see altered mental status we automatically know the lesion is in the brain

73
Q

what is the order of mental status from most to least response to stimuli

A

alert - depressed - stuporous - comatose

74
Q

what are clinical signs consistent with depressed mentation

A

drowsiness, inattention, decreased response to environmental stimuli

75
Q

depressed mentation indicates a lesion in:

A

brainstem (ARAS) or thalamocortex

76
Q

what are clinical signs consistent with stuporous mentation

A

unconscious, decreased response to external stimuli, still arousable with a painful stimulus

77
Q

stuporous mentation indicates a lesion in:

A

brainstem (ARAS) - there is a partial disconnection

78
Q

what are clinical signs consistent with comatose mentation

A

unconscious, no response to any external stimuli

79
Q

comatose mentation indicates a lesion in

A

brainstem (total disconnect of ARAS)

80
Q

a disoriented mentation indicates a lesion in:

A

thalamocortex or vestibular system

81
Q

what cranial nerves nuclei live in the:

thalamus

A

CN II

82
Q

what cranial nerves nuclei live in the:

midbrain

A

CN III, CN IV

83
Q

what cranial nerves nuclei live in the:

pons

A

CN Vm

84
Q

what cranial nerves nuclei live in the:

medulla

A

CN Vs, CN VI -> CN XII

85
Q

how can we simplify the division of the CN nuclei in the brain

A

CN II in the thalamocortex, CN III -> XII in the brainstem

86
Q

what is the pathway of the menace response

A

CN II (ipsilateral) -> thalamocortex (contralateral) -> cerebellum (ipsilateral) -> CN VII (ipsilateral)

87
Q

what is the pathway of the PLR

A

CN II in -> thalamus -> midbrain (brainstem) -> CN III out

88
Q

what CN are involved in physiological nystagmus

A

CN III, IV, VI, VIII

89
Q

what is the role of the MLF

A

connects CN III, IV, VI, VIII in the midbrain

90
Q

describe the pathway of physiological nystagmus

A

inner ear receptors sense movement -> info travels down CN VIII to the brainstem (vestibular nuclei) -> info travels through the MLF to CN III, IV, VI -> info carried to the left and right eyes

91
Q

what is the pathway of the palpebral reflex

A

CN V -> brainstem -> CN VII out

92
Q

what is the pathway of nasal septum stimulation

A

CN V -> brainstem -> cerebral cortex

93
Q

masticatory and temporal muscles are innervated by

A

CN V (motor)

94
Q

facial symmetry of ears, nose and lips is controlled by

A

CN VII (facial)

95
Q

laryngeal function is controlled by

A

CN IX, CN X

96
Q

tongue function is controlled by

A

hypoglossal (CN XII)

97
Q

what section of the neurological exam does lesions in the thalamocortex not involve

A

spinal reflexes (only in the spinal cord, does not go to the brain)

98
Q

what mentation might we see in a patient with a thalamocortical lesion

A
  • depressed
  • delirium/disorientation
  • behavioural changes
99
Q

why might we see proprioceptive deficits with an almost normal gait in a dog with a thalamocortical lesion

A

because most of movement is controlled by the brainstem (thalamocortex just responsible for voluntary movement)

100
Q

what types of signs might we see in a patient with a thalamocortical lesion

A
  • changes in mentation (depressed, delirium, disorientation)
  • wandering, pacing, head pressing
  • head and body turn (ipsilateral)
  • mild hemiparesis (contralateral)
  • circling (ipsilateral)
101
Q

what CN tests would we expect to be altered in a patient with a thalamocortical lesion

A
  • menace response (contralateral)
  • nasal septum sensation deficit (contralateral)
102
Q

what clinical sign is a dead giveaway that a lesion is in the thalamocortex and how do we interpret it

A

seizures: lesion is contralateral to side of seizures

103
Q

T/F neck pain is possible in a patient with a thalamocortical lesion

A

T

104
Q

how do we differentiate a thalamocortical from a vestibular lesion

A

both will have circling (ipsilateral) but only vestibular will have a head TILT (ipsilateral) as well as other vestibular signs (ex. nystagmus)

105
Q

what are focal seizures

A

abnormal activity in one region of a cerebral hemisphere

106
Q

what is a generalized seizure

A

abnormal activity in both cerebral hemispheres

107
Q

what is usually impaired with generalized seizures

A

consciousness

108
Q

what part of the neurologic exam would we not see any changes in a brainstem lesion

A

spinal reflexes (same reason as the thalamocortex)

109
Q

what mentation might we expect to see in a patient with a brainstem lesion

A

depression, stupor, coma

110
Q

does decerebrate or decerebellate rigidity have a better prognosis

A

decerebellate

111
Q

decerebrate rigidity indicates a lesion in ______________ whereas decerebellate rigidity indicates a lesion in _______________

A

rostral midbrain (brainstem); cerebellar peduncles or rostral cerebellum

112
Q

with a brainstem lesion, we might expect to see deficits in what cranial nerves

A

CN III - XII

113
Q

how would postural reactions be altered in the case of a brainstem lesion

A

ipsilateral deficits and abnormal gait (since much of movement is controlled by the brainstem with only voluntary movement coming from the thalamocortex)

114
Q

how do clinical signs differ depending on if there is a bilateral or unilateral CN Vm deficit

A

bilateral: dropped jaw
unilateral: atrophy of masticatory mm on that side

115
Q

what are 2 signs of lesions to CN III, IV, or VI

A

1) strabismus
2) abnormal PLR (dilated eye) -> CN III deficit

116
Q

what is unique about the pathway of CN VII

A

passes close to the middle/inner ear -> can be impacted by disease in the middle/inner ear

ex. with an inner ear infection you might be changes in the palpebral reflex as well as facial paralysis/asymmetry

117
Q

how can we differentiate if CN VII lesions are in the CNS or PNS

A

CNS: will see changes in mentation, changes in other CNs, proprioceptive deficits, tetraparesis (UMN)

118
Q

what causes facial spasm? how can we differentiate from fibrosis

A

hyperactivity in CN VII; if fibrosis, absent palpebral reflex (whereas if hyperactivity of CN VII would still see a palpebral reflex)

119
Q

what components make up the vestibular system:
- PNS
- CNS

A

PNS:
- inner ear receptors
- CN VIII

CNS:
- vestibular nuclei (brainstem)
- cerebellum

120
Q

what are the 5 outputs of the vestibular system

A

1) extraocular mm. via the MLF and vestibulomesencephalic tract
2) skeletal mm. via the MLF and vestibulospinal tract
3) vestibulocerebellum via the vestibulocerebellar tract
4) vomiting center via reticular formation
5) somatosensory cortex via internal capsule and medial geniculate bodies

121
Q

what are the 3 types of pathological nystagmus

A

vertical, horizontal, rotatory

note: can also change directions with different head positions

122
Q

the fast phase of nystagmus is usually (towards/away) from the side of the lesion

A

away

123
Q

T/F CN VII originates from the brainstem and travels with CN VIII at the level of the inner ear

A

T

124
Q

why might you see Horner’s syndrome in a patient with peripheral vestibular disease

A

the pathway of Horner’s syndrome travels and synapses in the superficial cervical ganglion, which is in the inner ear

this makes it susceptible to deficits if there is peripheral vestibular disease originating in the inner ear

125
Q

what type of nystagmus is observed with a CNS lesion and what with a PNS lesion

A

CNS: horizontal, vertical, rotatory or changing

PNS: horizontal or rotatory

126
Q

what makes diagnosing bilateral vestibular lesions difficult

A

no head tilt or nystagmus, only signs are wide based stance with bilateral ataxia and wide head excursions (side-side)

127
Q

why do we see head tilt opposide to the lesion with paradoxical vestibular lesions

A

the cerebellum is doing too much -> moves head tilt away from lesion

Clinical Medicine (8 decks)

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