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Neurology Clerkship > Cranial Nerves, Brain Stem Reflexes, and Brain Stem Disorders > Flashcards

Cranial Nerves, Brain Stem Reflexes, and Brain Stem Disorders Flashcards

1
Q

What is CN I?

A

Olfactory nerve

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2
Q

Most common causes of impaired smell?

A

Mucosal swelling and inflammation during sinusitis or a URI

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3
Q

Causes of permanent loss of smell?

A

Head trauma (olfactory nerve branches sheared or torn where they pass through the bony cribriform plate)

Tumor near the olfactory lobe at the skull base (eg, meningioma)

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4
Q

What is CN II?

A

Optic nerve

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5
Q

What is CN III?

A

Oculomotor nerve

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6
Q

What is CN IV?

A

Trochlear nerve

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7
Q

What is CN VI?

A

Abducens nerve

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8
Q

Function of the superior oblique?

A

Depresses and abducts the eye

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9
Q

Function of the inferior oblique?

A

Elevates and abducts the eye

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10
Q

Function of the superior rectus?

A

Elevates and adducts the eye

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11
Q

Function of the inferior rectus?

A

Depresses and adducts the eye

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12
Q

Function of the lateral rectus?

A

Abducts the eye

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13
Q

Function of the medial rectus?

A

Adducts the eye

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14
Q

Which muscles may be weak if elevation of the eye appears incomplete?

A

Superior rectus or inferior oblique (or both)

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15
Q

Which muscles may be weak if depression of the eye appears incomplete?

A

Superior oblique or inferior rectus (or both)

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16
Q

Presentation of complete oculomotor nerve lesion?

A

Complete ptosis (levator palpebrae superioris muscle paralysis)

Unopposed LR muscle action -> “down and out”

Pupil of the involved eye is large and unreactive to light directly or consensually (parasympathetic innervation of the pupil is impaired

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17
Q

What is unique about the trochlear nerve?

A

It is the only cranial nerve which exits the brain stem dorsally and decussates to innervate the contralateral superior oblique muscle

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18
Q

Presentation of a trochlear nerve lesion?

A

Impaired downward gaze when involved eye is adducted

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19
Q

Presentation of an abducens nerve lesion?

A

Impaired abduction of the affected eyeball due to ipsilateral LR muscle weakness

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20
Q

Define binocular diplopia.

A

Most common type of diplopia, resolves if the patient coveres either ey

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21
Q

Causes of binocular diplopia?

A

Lesions of CN III, IV, or VI, or their related EOMs; lesions involving the brain stem or cerebellar connections

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22
Q

Define monocular diplopia.

A

Relatively rare, occurs when looking with one eye alone

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23
Q

Causes of monocular diplopia?

A

May occur from a problem in the optical system of an eye, such as a dislocated lens or detached retina, or may be related to a psychiatric disorder

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24
Q

Define nystagmus.

A

Repetitive, oscillatory, jerky eye movements

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25
Q

Lesions that may cause pathological nystagmus?

A

Lesions of the vestibular system, brain stem, or cerebellum

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26
Q

Compare the causes of asymmetrical nystagmus vs. symmetric nystagmus.

A

Asymmetrical (aka more prominent with certain eye movements or positions) - vestibular/brain stem/cerebellar lesions

Symetrical (aka present with virtually all eye movements/positions) - drug toxicity

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27
Q

What is internuclear ophthalmoplegia?

A

Paralysis of EOMs from a lesion between the nuclei involved with lateral gaze (CN 3 and 6) which interrupts the ascending medial longitudinal fasciculus (MLF)

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28
Q

Describe the normal functioning leading to coordinated horizontal gaze (use rightward gaze as an example).

A

Right paramedian pontine reticular formation (PPRF) activates both the right CN 6 in the pons and the left CN 3 in the midbrain so that the R LR and L MR move the eyes to the right

Ascending MLF leaves the R PPRF, decussates early, and rises to join the L oculomotor nucleus

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29
Q

Presentation of a lesion along the main course of the MLF en route from pons to midbrain?

A

Paralysis of adduction of the ipsilateral eye, with nystagmus of the contralateral eye (impaired contralateral lateral gaze)

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30
Q

What are the most common causes of MLF lesions in younger patients and older patients?

A

Younger - MS

Older - ischemic infarction

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31
Q

Describe the pathway leading to the normal pupillary light reflex.

A

Retinal ganglion cells project bilaterally to the pretectal area (rostral to the superior colliculus) -> projects to the EW nucleus of CN III

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32
Q

Effect of an optic nerve lesion on the pupillary light reflex?

A

Impairs the afferent part of the reflex, so neither pupil constricts with light shined into the affected eye, but both constrict with light in the unaffected eye

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33
Q

Effect of a CN III lesion on the pupillary light reflex?

A

Interrupts the efferent part of the reflex, so the affected pupil never constricts with light in either eye, yet the unaffected pupil constricts with light in either eye

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34
Q

What causes a relative afferent pupillary defect (RAPD)?

A

Partial optic nerve or retinal lesion

35
Q

How is an RAPD tested and how does it appear?

A

Swinging flashlight test - both pupils may initially constrict to light, but after moving the light source back and forth, pupillary dilation occurs because of the relatively reduced afferent input at the affected eye

36
Q

What is the near reflex?

A 
Pupillary constriction
Lens accommodation (thickening)
Convergence of the eyes
37
Q

What is light-near dissociation?

A

Selective disruption of the pupillary light reflex pathway at the pretectal area with connections for the near reflex preserved; presents as pupils only constructing during the near reflex, but not to a light stimulus

38
Q

Classic causes of light-near dissociation?

A

Dorsal midbrain syndrome (aka Parinaud’s) - classically due to a pineal tumor compressing the dorsal midbrain; may also occur from an ischemic infarct
Argyll Robertson pupils in neurosyphilis

39
Q

Cause of Horner’s syndrome?

A

Lesion disrupting the oculosympathetic pathway

40
Q

Presentation of Horner’s syndrome?

A 
Miosis (smaller, constricted pupil which dilates poorly in the dark)
Anihdrosis (decreased sweating in the ipsilateral face)
Mild ptosis (paralysis of the superior tarsal muscle)
41
Q

Describe the oculosympathetic pathway

A

First-order neurons descending down the brain stem

Second-order neurons originate from the interomediolateral cell column in the spinal cord at C8-T2

Third-order neurons arising from the superior cervical sympathetic ganglion ascend up the internal carotid

42
Q

Cause of a lesion of the first-order neurons of the oculosympathetic pathway?

A

Lateral medullary infarction (aka Wallenberg syndrome)

43
Q

Cause of a lesion to second-order neurons of the oculosympathetic pathway?

A

Tumor near the apex of the lung

44
Q

Cause of a lesion to third-order neurons of the oculosympathetic pathway?

A

Neck trauma

45
Q

What is CN V?

A

Trigeminal nerve

46
Q

Sensation over the face and anterior scalp is conveyed to the brain stem by what three branches of CN V?

A

V-1 (ophthalmic) - involves anterior scalp
V-2 (maxillary)
V-3 mandibular - does NOT involve the corner of the jaw or neck

47
Q

Possible causes of sensory deficits not confined to the trigeminal nerve territory?

A

Lesions in the contralateral thalamus or parietal lobe; psychiatric disorders

48
Q

Possible cause of a V-1 territory sensory impairment + ipsilateral CN III, IV, and VI involvement?

A

Lesion at the superior orbital fissure or nearby cavernous sinus

49
Q

Presentation of trigeminal neuralgia?

A

Irritation or inflammation of one of the nerve sensory branches which misfires -> episodic, lightning-like jabs or “electrical shocks” of pain usually in the V2 or V3 territory, often provoked by talking, chewing, or touching the face; no sensory or other CN deficits are found

50
Q

Causes of trigeminal neuralgia?

A

MS lesion at the trigeminal nerve entry region into the pons

Nerve branch compressed by a tortuous or kinked blood vessel (often the superior cerebellar artery)

51
Q

Rx trigeminal neuralgia?

A

Oral anticonvulsants such as carbamazepine, gabapentin, etc.

52
Q

What muscles does the trigeminal nerve innervate?

A

Masseter and temporalis (muscles of mastication)

53
Q

Presentation of a LMN lesion of the trigeminal motor nerve?

A

Rare; produces atrophy and weakness in these ipsilateral muscles with the jaw deviating toward the side of the lesion

54
Q

Presentation of UMN lesions affecting the trigeminal motor nerve?

A

UMN neuron lesion on one side does not produce any jaw deviation or severe weakness; bilateral UMN lesions may cause hyperreflexia of the jaw jerk, since it is a muscle stretch reflex

55
Q

What is CN VII?

A

Facial nerve

56
Q

What does the facial nerve innervate?

A

Originates from facial nucleus in the pons

Innervates ipsilateral facial muscles, from uppermost frontalis to lowermost platysma

57
Q

Presentation of a LMN facial nerve lesion near the stylomastoid foramen?

A

Involves the nucleus or nerve, causes a relatively severe paralysis of the entire ipsilateral half of the face

58
Q

Cause of ipsilateral facial paralysis + impaired taste over the anterior 2/3 of the tongue?

A

Involvement of the chorda tympani branch of the facial nerve

59
Q

Cause of ipsilateral facial paralysis + hyperacusis?

A

Involvement of the nerve to stapedius

60
Q

Presentation of a facial nerve lesion at the internal auditory meatus aka cerebellopontine angle?

A

Ipsilateral facial paralysis, impaired taste over the anterior 2/3 of the tongue, hyperacusis, and impaired hearing and tinnitus

61
Q

What is an acoustic neruoma?

A

Tumor arising from CN VIII

62
Q

Presentation of a lesion at or near the facial nucleus in the pons?

A

Ipsilateral facial paralysis, impaired taste over the anterior 2/3 of the tongue, hyperacusis, and impaired hearing and tinnitus PLUS ipsilateral weakness of lateral gaze from involvement of the adjacent PPRF and CN VI

63
Q

Distinguish between UMN and LMN lesions causing facial paralysis?

A

If UMN, upper forehead is spared; if LMN, entire half of the face is affected

64
Q

What is CN VIII?

A

Vestibulochochlear nerve

65
Q

What is CN IX?

A

Glossopharyngeal nerve

66
Q

What is CN X?

A

Vagus nerve

67
Q

CN IX and X have similar or shared functions (taste, visceral afferent, visceral efferent -> cannot be tested clinically); they also innervate what muscles, which can cause impaired function of what?

A

Pharyngeal and laryngeal; speech or swallowing

68
Q

Presentation of a glossopharyngeal lesion?

A

Decreased or absent gag reflex ipsilaterally

69
Q

Presentation of a LMN lesion of vagal nerve innervating the palate?

A

Ipsilateral drooping or sagging of the palatal arch with the uvula pointing to the normal side

70
Q

Presentation of a LMN lesion of vagal nerve branches innervating the larynx?

A

Hoarseness from ipsilateral paralysis of vocal cords

71
Q

What CN XI?

A

SPinal accessory nerve

72
Q

LMN lesion of CN XI?

A

Weakened ipsilateral SCM and trapezius

73
Q

CN XII?

A

Hypoglossal nerve

74
Q

What is the most clinically relevant muscle of the tongue innervated by CN XII?

A

Genioglossus muscle -> protrudes each side of the tongue forward

75
Q

Presentation of CN XII LMN lesion?

A

Protruded tongue deviates toward the affected side; eventually would note atrophy and fasciculations/fibrillations

76
Q

In a few patients, the UMNs controlling the CN XII nucleus only arise contralaterally. In that case, what would be seen in an ischemic infarction of the L frontal lobe?

A

Impairs R hypoglossal nucleus, weakening protrusion of the R half of the tongue such that the protruded tongue may deviate toward the side opposite its lesion; in most cases, however, there is dual innervation and an UMN lesion would not cause weakness

77
Q

What are crossed brain stem syndromes?

A

CN involvement on one side and an adjacent fiber tract lesion, creating a clinical sensory or motor deficit on the opposite side

78
Q

Presentation - R pontine lesion involving the R facial nucleus and the R corticospinal tract

A

LMN paralysis of the entire R half of the face and UMN paralysis of the left upper and lower limbs (L hemiparesis)

79
Q

Presentation - L lateral medulla lesion involving the L descending spinal tract of CN V and the L STT (includes afferents from the R side of the cord that have already decussated)

A

Deficits of pain and temperature over the L face and right limbs/bodies

80
Q

Cause of medial midbrain syndrome (Weber syndrome)?

A

Ischemic infarction from an occluded branch of the PCA -> CN III and nearby cerebral peduncle (CST and corticobulbar tract)

81
Q

Presentation of medial midbrain syndrome (Weber syndrome)?

A

Ipsilateral oculomotor nerve lesion and UMN weakness of the contralateral face and limbs

82
Q

Cause of lateral medullary syndrome (Wallenberg syndrome)?

A

Ischemic infarction from an occluded vertebral artery or its PICA branch

83
Q

Presentation of lateral medullary syndrome (Wallenberg)?

A

Pain and temperature impairment in the ipsilateral face and contralateral limbs and body; may also include hoarseness, vertigo, N/V, clumsiness, nystagmus (vestibular nculei), ipsilateral limb dysmetria (inferior cerebellar peduncle), ipsilateral Horner’s syndrome (descending sympathetic tract), ipsilateral palatal and vocal cord paralysis (nucleus ambiguus)

Position sense and strength are always preserved

Neurology Clerkship (25 decks)

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