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BCSCSAP Review > Neuro-ophthalmology > Flashcards

Neuro-ophthalmology Flashcards

To review high yield N-O topics and concepts.

1
Q

(start 72) When an imaging study fails to demonstrate the expected pathology in relation to the clinical presentation, the clinician’s first step is to..

A

reexamine the study parameters, ideally with a neuroradiologist.

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2
Q

Best quantifies torsional strabismus

A

double Maddox rod - when vertical diplopia is present

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3
Q

Diagnostic of neurosyphilis

A

positive CSF VDRL

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4
Q

Patient presents with intraocular inflammation and positive RPR. Next step?

A

lumbar puncture with CSF examination, followed by antibiotic therapy (series of IV or IM dosing)

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5
Q

Consists of paired subnuclei for the superior rectus, inferior rectus, medial rectus, and inferior oblique muscles as well as paired subnuclei for the pupillary constrictor muscles and single subnucleus for the levator palpebrae

A

CN III nuclear complex

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6
Q

Subnuclei for the superior rectus supply..

A

the contralateral superior rectus muscle

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7
Q

Actions of the superior oblique muscle

A

intorts, depresses, abducts the eye

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8
Q

Presentation of bilateral CN IV palsy

A 
crossed hypertropia (right hyper on left gaze and left hyper on right gaze) extorsion of at least 10 degrees, 
large V-pattern esotropia greater than 25 PD (esotropia greatest on downgaze), and 
chin-down positioning (as hypertropia decreases in upgaze)
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9
Q

Cerebral achromatopsia is a feature of this type of lesion

A

occipital lobe

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10
Q

Pursuit and reflexive saccade movements are initiated in this region

A

parietal lobe, abnormal OKN responses can be seen related to a parietal lobe lesion

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11
Q

Abnormal OKN response. Where is the lesion?

A

Parietal lobe

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12
Q

VF defects commonly present with disc drusen

A

enlarged blind spot and ARCUATE SCOTOMAs

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13
Q

2 ways B-scan can differeniate calcified drusen from papilledema

A

1) highly reflective, calcified drusen maintain high echogenicity with lowering of U/S gain
2) with papilledema, intraorbital portion of ON is widened and will decrease in width with prolonged lateral gaze (30 degree test”); ODD do not produce widening of the intraorbital nerve.

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14
Q

Anatomic location of most ODD

A

anterior to lamina cribosa and posterior to Bruch membrane (lamina choroidalis portion of the intraocular optic nerve)

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15
Q

When does aberrant regeneration occur?

A

after trauma or compression by an aneurysm or tumor but does not occur with microvascular ischemia

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16
Q

What is primary aberrant regeneration?

A

aberrant regeneration without a h/o CN III palsy - evidence of a slowly expanding parasellar lesion - m/c meningioma or carotid aneurysm within the cavernous sinus.

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17
Q

Eyelid retraction in downgaze, eyelid elevation or pupil constriction on attempted adduction, and globe retraction on attempted upgaze

A

aberrant regeneration

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18
Q

Branch of the posterior cerebral artery that supplies the primary visual cortex

A

calcarine branch

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19
Q

Supply most of the blood supply to the skull and its contents. Be specific

A

Common carotid arteries arising from the innominate artery on the right and directly from the aorta on the left

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20
Q

Systemic evaluation for patient with suspected oculopharyngeal muscular dystrophy

A

genetic testing - PABPN1 - encodes for polyadenylate binding protein nuclear 1, only associated gene.

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21
Q

Diagnosis of OPMD (oculopharyngeal muscular dystrophy) relies on this molecular diagnosis

A

expansion of a GCN trinucleotide in the first exon of PABPN1 (commercially available test)

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22
Q

postpartum or recent SSRI + recurrent HA + hemianopic field loss with MRA showing “string of beads” appearance of cerebral arteries.

A

Reversible cerebral vasoconstriction syndrome (RCVS)

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23
Q

Prognosis of RCVS (reversible cerebral vasoconstriction syndrome)

A

resolves within 3 months

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24
Q

T1 MRI with contrast of brain with enhancing lesion of tectum of midbrain would confirm the diagnosis

A

Dorsal midbrain syndrome (Parinaud) syndrome

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25
Q

Signs of dorsal midbrain syndrome

A

1) convergence-retraction nystagmus (co-contraction of EOMs wtih attempted upgaze)
2) Conjugate limitation of vertical gaze (upgaze deficit)
3) skew deviation
4) eyelid retraction in primary position (Collier sign)
5) convergence abnormalities (convergence spasm or convergence palsy)
6) mid-dilated pupils, poorly reactive pupils with light-near dissociation

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26
Q

Most likely cause of diplopia in parinaud/pretectal syndrome

A

Skew deviation

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27
Q

Cause for optic disc edema with exudate in macula start pattern

A

M/c Bartonella henselae, less common syphilis, toxoplasmosis, lyme disease, tuberculosis, viruses. May also be postviral autoimmune process

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28
Q

Most common cause of divergence insufficiency (DI) in an otherwise healthy adult patient?`

A

Connective tissue involution between the superior and lateral rectus muscles causing inferior displacement of the lateral rectus muscles (sagging eye syndrome)

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29
Q

What is divergence insufficiency?`

A

acquired ocular misalignment defined by an esodeviation that is greater at distance than near fixation without lateral incomitance, and without abduction deficits.

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30
Q

Website for BCSC Self-assessment

A

https://bcscap.aao.org/Dashboard

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31
Q

Characteristic optic nerve appearance in dominant optic atrophy

A

Temporal pallor with an area of triangular excavation (wedge-shaped pallor)

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32
Q

Characteristic optic nerve appearance in Leber hereditary optic neuropathy (LHON)

A

Peripapillary telangiectasia

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33
Q

Characteristic optic nerve appearance in glaucoma

A

Superotemporal or inferotemporal notching

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34
Q

Characteristic optic nerve appearance in optic nerve hypoplasia

A

Yellow peripapillary halo with ring of pigmentation

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35
Q

What test would best distinguish a retinopathy from an optic neuropathy?

A

Photostress recovery

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36
Q

Characterized by short severe attacks of pain with cranial autonomic features (ptosis, miosis)

A

Paroxysmal hemicrania

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37
Q

Bouts of unilateral excruciating headaches with autonomic features lasting 15-180 minutes

A

Cluster headaches

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38
Q

Continuous unilateral headache

A

Hemicrania continua

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39
Q

Episodic very brief sharp stabbing stabbing pains/HA with no autonomic features

A

Idiopathic stabbing headache

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40
Q

Specific steps of cocaine test

A

Instill 2 drops of cocaine 4% or 10% in each eye 5 minutes apart

Measure anisocoria 45 minutes to 1 hour

Postcocaine anisocoria >1mm is diagnostic of Horner syndrome on the side of the smaller pupil

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41
Q

Mechanism of cocaine

A

Blocks reuptake of norepinephrine released at sympathetic nerve terminals in the eye causing pupillary dilation, eyelid retraction, conjunctival blanching

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42
Q

Portion of a CN that travels within brainstem

A

Fasicle

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43
Q

What structures lie adjacent to the fascicles of CN III?

A

Substantia nigra + red nucleus -(Benedikt syndrome)

superior cerebellar peduncle - (Nothnagel) (superior cerebellar peduncle + red nucleus = Claude syndrome)

cerebral peduncle - (Weber syndrome)

corticospinal tracts

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44
Q

Nothnagel syndrome

A

CN III + superior cerebellar peduncle

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45
Q

Benedikt syndrome lesion

A

CNIII + red nucleus + substantia nigra

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46
Q

Weber syndrome

A

CNIII + cerebral peduncle

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47
Q

Claude syndrome

A

CNIII + superior cerebellar peduncle + red nucleus

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48
Q

CN IV courses below the

A

Pineal gland

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49
Q

Where does the CN VI nucleus lie?

A

Below the 4th ventricle and it’s fasicles pass medial to the superior olivary nucleus

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50
Q

Passes medial to the superior olivary nucleus

A

Fasicles of CN VI

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51
Q

M/c hereditary optic neuropathy

A

Dominant optic atrophy

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52
Q

M/c mutation in DOA

A

OPA1 gene on chromosome 3

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53
Q

Optic neuropathy with cardiac conduction defects

A

Leber hereditary optic neuropathy pre-excitation syndrome

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54
Q

Eye movement dysfunction in congenital ocular motor apraxia

A

Horizontal saccades

Increased latency and intermittent failure of initiation

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55
Q

Nerve that courses along surface of clivus

A

Abducens nerve

Underneath the petroclinoid (gruber) ligament to enter the dorello canal

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56
Q

Structure in brainstem responsible for excitatory burst in horizontal movement

A

Paramedian Pontine Reticular Formation

Located adjacent to the CN VII nucleus

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57
Q

Neural integrator for horizontal movement

A

Nucleus prepositus hypoglossi (NPH)

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58
Q

Excitatory burst cells and neural integrator for vertical/torsional movement

A

Rostral interstitial nucleus of the medial longitudinal fasiculus

(riMFL)

Interstitial nucleus of Cajal (INC)

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59
Q

CN IV palsy with lesion at predescussation fasicular or nuclear level

A

Ipsilateral RAPD without vision or color loss (decussation of nasal pupillary fibers)

Contralateral Horner’s 2/2 proximity of sympathetic fibers

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60
Q

Assessment that may best distinguish between a retinopathy and optic neuropathy.

A

Electrophysiology

Electroretinogram (ERG) and visual evoked potentials (VEP) can be very specific in localizing etiology to retina or optic nerve

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61
Q

Electrophysiology consistent with a retinopathy compared to an optic neuropathy

A

Abnormal ERG and VEP would be seen in a retinopathy whereas a normal ERG and abnormal VEP is highly suggestive of an optic neuropathy.

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62
Q

Within the cavernous sinus, what cranial nerve do the sympathetic fibers run with?

A

CN VI

Sympathetic fibers destined for the dilator muscles leave the carotid in conjunction with CN VI for a few millimeters. Further anteriorly in the cavernous sinus, the sympathetic fibers join the nasociliary branch of CN V1. The sympathetic fibers do not join any of the other cranial nerves within the cavernous sinus.

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63
Q

When does optic neuropathy occur after radiation therapy?

A

on average 18 months and produces subacute optic neuropathy

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64
Q

Where are saccadic eye movements generated?

A

Frontal eye fields located in the frontal lobe, one on each side. Each frontal eye field initiates saccades to the contralateral side.

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65
Q

Where are smooth pursuit eye movements generated?

A

Medial temporal (MT) visual area (V5) in the parietal lobe. Each generates smooth pursuit eye movements to the ipsilateral side.

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66
Q

Name for inability to initiate saccades

A

ocular motor apraxia - results from injury to the frontal lobe or may occur in childhood conditions

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67
Q

Condition visual evoked potential (VEP) testing is most helpful in confirming

A

Demyelinating optic neuropathy. Measures electrical signals over the occipital cortex produced in response to verbal stimulus. Shows increased latency in demyelination

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68
Q

Formed hallucinations + insomnia + excessive daytime somnolence. Where is the lesion?

A

MIDBRAIN - constant hallucinations frequently associated with inverted sleep-wake cycle (peduncular hallucinosis)

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69
Q

Pallinopsia

A

illusion of persistent afterimages that can be a/w visual hallucinations

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70
Q

Region of brain that produces olfactory and gustatory hallucinations, with complex formed hallucinations in the ipsilateral or contralateral field

A

temporal lobe

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71
Q

Lesion to this region of brain commonly cause unformed hallucinations, geometric colors or patterns

A

Occipital lobe

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72
Q

Slowly progressing facial palsies strongly suggest this. Preferred imaging test?

A

MRI brain. Brainstem mass.

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73
Q

Frequent origin of facial myokymia with continuous or undulating contraction of facial muscles

A

intramedullary pons. In children - pontine glioma and adults multiple sclerosis

74
Q

Condition that commonly leads to congenital Horner syndrome

A

Brachial plexus injury (birth trauma)

75
Q

irregular myocytes “ragged-red” fibers and inclusion body abnormalities on EM from a muscle biopsy

A

Mitochondrial myopathy

76
Q

Myotonic discharges seen on electromyography

A

Myotonic dystrophy

77
Q

Infant develops conjugate horizontal nystagmus with null point. OK drum testing shows reversal of normally expected OK nystagmus.

A

Bilateral pregeniculate visual loss - Sensory nystagmus arises when central VA is too poor to develop central fixation

78
Q

Infantile disease that does not produce oscillopsia

A

Infantile nystagmus syndrome (INS) or congenital nystagmus

79
Q

Evaluation for sensory nystagmus (pregeniculate visual loss)

A

optic neuropathy, foveal hypoplasia, retinal dystrophy

80
Q

Two characteristics of infantile nystagmus (INS)

A
  1. Reversal of normal pattern of optokinetic nystagmus (OKN). Patients with INS respond to OKN drum rotation with slow-phase eye movements in the direction opposite to that of rotating OKN drum
  2. Velocity of slow-phase movement increases exponentially with distance from fixation. Increasing velocity waveform is punctuated by foveation periods.
81
Q

Percentage of children with typical INS with no detectable afferent pathway abnormality

A

40%

82
Q

If the pupil affected by Horner syndrome fails to dilate with hydroxyamphetamine, where is the defect

A

Postganglionic neuron - hydroxyamphetamine acts to release NE from the presynaptic terminal. In normal eye or in preganglionic horner syndrome, the postganglionic neuron is intact with normal dilation of pupil.

83
Q

Large vessel vasculitides

A

GCA, Takayasu arteritis

84
Q

Medium-size vessel vasculitis

A

Polyarteritis nodosa and Kawasaki disease

85
Q

Small vessel vasculitis

A

Granulomatosis with polyangiitis

86
Q

Abnormality most frequently associated with ONH drusen

A

Peripheral visual field constriction

87
Q

Ocular findings in neurofibromatosis 1 (NF1)

A

Lisch nodules, prominent corneal nerves, choroidal hamartomas

88
Q

What are lisch nodules

A

hamartomas (tissue normally found at site but in increased amount) flat or dome-shaped iris nodules usually less than 1 mm and tan to dark brown in color. Composed of schwann cells, fibroblast like cells, mast cells

89
Q

What disease are lisch nodules seen and how frequently?

A

NF1 - 10% of children by age 1, 100% by age 10. Presence of 2 or more is criteria for diagnosing NF1

90
Q

Diagnosis of NF1 criteria

A 
6 or more café-au-lait
2 or more neurofibromas
intertriginous freckling
ON glioma
Lisch nodules (2+)
Distinctive osseous lesion
first degree relative with NF1
91
Q

Genetics of NF1

A

NF1 gene on chromosome 17 q11.20, product is neurofibromin, a tumor suppressant. Loss of neurofibromin leads to cell and tumor growth

92
Q

Myopathic facies, frontal balding, ptosis, myopathy affecting distal muscles first. Low intelligence, insult resistance, hearing loss, cardiomyopathy, cardiac conduction abnormalities, testicular/uterine atrophy. Diagnosis and ocular findings?

A

Myotonic dystrophy (dominant, chromosome 19) with pigmentary retinopathy, polychromatic lenticular deposits (“Christmas tree” cataracts), sluggish miotic pupils.

93
Q

Should be performed in every case of typical optic neuritis?

A

MRI brain to assess long-term risk for developing MS over the next 15 years (25% if no lesions, 72% with = 1 lesion)

94
Q

Most important exam finding to help determine risk of corneal ulceration in patient with stroke and facial nerve palsy?

A

Corneal sensation - determine if trigeminal neuropathy present that may eliminate corneal sensitivity - combo of anesthetic cornea and lagophthalmos places these patients at high risk for developing corneal exposure and ulceration.

95
Q

Vesicles along posterior aspect of external auditory canal, over tympanic membrane or over pinna

A

Ramsay Hunt syndrome - Herpes zoster involving the seventh cranial nerve

96
Q

Acquired cases of prosopagnosia result from stroke of which portion of brain

A

bilateral inferior occipitotemporal lobes or right inferior occipital lobe

97
Q

Inability to recognize familiar faces

A

prosopagnosia - disorder of recognition involving visual-visual disconnection

98
Q

Part of brain responsible for processing physical attributes of an object

A

Ventral occipitotemporal pathway

99
Q

Part of brain responsible for visuospatial processing and gulidance of movement towards an object

A

Dorsal occipitoparietal pathway

100
Q

Patient cannot read but can write. What is this called and what part of brain is damaged?

A

Alexia without agraphia - damage to splenium of the corpus callosum and the left occipital lobe

101
Q

Damage to the midbrain and cerebral peduncle

A

contralateral hemiparesis (Weber syndrome)

102
Q

Damage to red nucleus and substantia nigra

A

contralateral ataxia or tremor (Benedikt syndrome)

103
Q

Damage to dorsal midbrain

A

May involvesuperior cerebellar peduncle and produce contralateral ataxia (Claude syndrome)

104
Q

Dorsal brainstem lesion with CN III nuclear lesion may produce supranuclear eye movement dysfunction. Also known as

A

Nothnagel syndrome

105
Q

Inferior notch would lead to this defect

A

Dense superior arcuate defect

106
Q

Part of optic nerve most sensitive to trauma or sinus surgery

A

Intracanalicular optic nerve

107
Q

What could compress the intracranial optic nerve

A

Sellar masses or internal carotid aneurysms

108
Q

May cause any ocular motility deficit

A

Myasthenia gravis

109
Q

In a patient with an acute optic neuropathy, what symptom suggests the arteritic form?

A

Prior transient monocular visual loss

110
Q

Sudden painful vision loss of right eye followed by similar sx 2 weeks later in her left eye. MRI shows bilateral enhancement of ON. After treatment with methylprednisolone, only minimal visual recovery. Diagnosis?

A

Neuromyelitis optica

111
Q

SE of fingolimod

A

macular edema

112
Q

For patients with MS, what disease-modifying therapy has most often been a/w progressive alteration of mental status resulting from a homonymous hemianopia?

A

Natalizumab in patients with Jacob-Crotzfeld-virus positive - progressive multifocal leukoencephalopathy

113
Q

Confirms diagnosis of horner syndrome

A

cocaine drops (hydroxyamphetamine can localize the lesion producing horners to preganglionic or postganglionic)

114
Q

infant with acquired horner’s syndrome

A

neuroblastoma - originates in either adrenal gland or sympathetic ganglion chain in the retroperitoneum or mediastinum which interrupts papillary sympathetic innervation

115
Q

Most frequent source of childhood orbital metastasis

A

neuroblastoma

116
Q

strabismus, hemorrhage, hyphema, ocular or periocular inflammation, glaucoma, proptosis, hypopyon

A

Rb (m/c leukocoria) but know other presentations

117
Q

Supranuclear ocular motor system responsible for maintaining an image on the fovea during brief head movements

A

vestibular-ocular system

118
Q

Triad of simultanagnosia, optic ataxia, and ocular motor apraxia

A

Balint syndrome (bilateral occipitoparietal lesions)

119
Q

“Where pathway”

A

dorsal occipitoparietal pathway - visuospatial analysis, localization of objects, visually directed movements toward objects

120
Q

“What pathway”

A

ventral occipitotemporal pathway - color, shape, pattern recognition

121
Q

Lesion causes object agnosia

A

lesion to bilateral ventral occipitotemporal pathway (“what pathway”)

122
Q

episodic diplopia lasting 30-60 seconds after sustained activation of cranial ocular motor nerve

A

Ocular neuromytonia - a/w h/o radiation therapy for skull-based neoplasm

123
Q

Neuroimaging finding characteristic of tuberous sclerosis

A

intracranial calcified hamartoma

124
Q

Cerebellar hemangioblastoma

A

von Hippel-Lindau

125
Q

Leptomeningeal vascular malformation

A

Sturge-Weber syndrome (encephalofacial angiomatosis)

126
Q

Next step if more than 1 CN involved

A

Neurological evaluation with neuroimaging, which if normal, LP with cytopathologic examination should be considered.

127
Q

CN palsy most commonly a/w IIH

A

CN VI (unilateral or bilateral)

128
Q

Facial nerve palsy combined with hearing loss and vestibular dysfunction

A

Cerebellopontine (CPA) angle mass

129
Q

M/c CN involved in sarcoidosis

A

CN VII (parotid gland)

130
Q

Recurrent unilateral or bilateral facial paralysis + chronic facial swelling and lingua plicata (furrowing of tongue)

A

Melkersson-Rosenthal syndrome

131
Q

“salt and pepper” retinopathy + ptosis and ophthalmoplegia

A

Kearns-Sayre syndrome (variant of chronic progressive external ophthalmoplegia, AD) Cardiac conduction defects may be fatal if untreated

132
Q

Patient with intraocular inflammation and testing reveals positive RPR test. Next step

A

Lumbar puncture with CSF exam f/b antibiotic therapy

133
Q

What does the CN III nuclear complex contain

A

paired subnuclei for 4 extraocular muscles the superior rectus, interior rectus, medial rectus, inferior oblique, paired subnuclei for the pupillary constrictor (Edinger-Westphal) and single subnucleus for the levator palpebrae muscles (central caudal nucleus)

134
Q

Clinical sign expected in bilateral fourth CN palsies

A

V-pattern esotropia (esotropia greatest on downgaze), chin-down positioning (as hypertropia decreases in upgaze)

135
Q

How could one differentiate a parietal lobe lesion from an occipital lobe lesion?

A

Parietal lobe initiates pursuit and reflexive saccade movements - abnormal OKN responses. Occipital lobe lesion will have intact OKN response - results in cerebral achromatopsia

136
Q

How would examiner elicit impaired OKN response

A

moving targets toward the lesion, inducing attempts to use the damaged pursuit pathway

137
Q

Homonymous hemianopia with reduced OKN response with target moving toward the affected side

A

Parietal lobe lesion

138
Q

Complication following 3rd CN palsy suggestive of nonischemic cause?

A

Aberrant regeneration - most commonly produces eyelid retraction in downgaze, eyelid elevation or pupil constriction on attempted adduction, and globe retraction on attempted upgaze.

139
Q

Branch of the posterior cerebral artery that supplies the primary visual cortex

A

Calcarine branch

140
Q

Systemic evaluation should be performed on a patient with suspected oculopharyngeal muscular dystrophy

A

Genetic testing for PABPN1 which encodes for polyadenylate binding protein nuclear 1

141
Q

Severe recurrent headaches with or without focal neurologic deficits and/or seizures with segmental constriction of cerebral arteries that resolves within 3 months occurring after postpartum period or exposure to vasoactive substances (SSRIs)

A

Reversible cerebral vasoconstriction syndrome (RCVS)

142
Q

Middle-aged woman postpartum with light sensitivity, blurred vision, hemianopic visual field loss and “string-of-beads” on MRA

A

Reversible cerebral vasoconstriction syndrome (RCVS)

143
Q

Dorsal midbrain syndrome features. What is the cause of diplopia?

A 
Convergence-retraction nystagmus
Upgaze deficit
Skew deviation (diplopia)
Eyelid retraction
Convergence abnormalities
Poorly reactive pupils with light-near dissociation
144
Q

Most common cause of divergence insufficiency in healthy adult

A

Connective tissue involution between the superior and lateral rectus muscles.

145
Q

What is divergence insufficiency (DI)

A

An acquired ocular misalignment defined by an esodeviation that is greater at distance than near fixation without lateral incomitance and without abduction deficits.

146
Q

Good exam technique for monocular vision loss.

A

Vertical prism dissociation test. A 4 prism diopter lens is placed base-down in front of the eye with better vision. If they can read the upper and lower images of a vertical prism dissociated 20/20 line, it can prove normal visual acuity.

147
Q

Exam findings with aberrant regeneration of CN III?

A

Eyelid retraction with adduction or pupillary miosis with supraduction, adduction or infraduction

148
Q

Workup for NSOI

A

Crohn disease, SLE, RA, DM, MG, ankylosing spondylitis (Cytoplasmic staining pattern (c-ANCA), ANA, ACE, lysozyme, IgG4

149
Q

NSOI occurs in these patterns

A

5 patterns: M/c are extraocular muscles (myositis), lacrimal gland (dacryoadenitis), anterior orbit (scleritis), orbital apex, or diffuse inflammation throughout orbit.

150
Q

Optic nerve finding most characteristic of dominant optic atrophy?

A

Wedge-shaped optic nerve pallor.

151
Q

ON exam with yellow peripapillary halo with ring of pigmentation

A

Optic nerve hypoplasia

152
Q

ON exam with peripapillary telangiectasia

A

Leber hereditary optic neuropathy (LHON)

153
Q

Test to best distinguish a retinopathy from an optic neuropathy

A

Photostress recovery

154
Q

Several episodes per day of severe left-sided orbital and temporal pain that lasts 5-10 minutes, occasionally a/w left ptosis and miosis..

A

Paroxysmal hemicrania - form of trigeminal autonomic cephalgia a/w short bouts of pain highly responsive to indomethacin

155
Q

Difference between cluster headache and paroxysmal hemicrania

A

both may have autonomic features but cluster headache have longer duration (15-180 minutes)

156
Q

Hemicrania continua

A

continuous unilateral headaches

157
Q

Why does an internal carotid dissection produce pain and horner syndrome?

A

involvement of sympathetic fibers in the wall of the carotid artery

158
Q

Earliest pathologic change to occur in KCN?

A

Bowman layer - focal discontinuities

159
Q

Ocular motility abnormality classically included in dorsal midbrain syndrome?

A

Convergence-retraction nystagmus

160
Q

Retraction of the eyelids in primary position

A

Collier sign

161
Q

What structures lie adjacent to the fascicles of CN III?

A

Substantia nigra

CN III passes adjacent to the superior cerebellar penduncle, cerebral peduncle, red nucleus, substantia nigra, corticospinal tracts.

162
Q

Brainstem structure that generates horizontal saccades

A

Paramedian pontine reticular formation

163
Q

What supranuclear structure if damaged can be a/w diplopia and strabismus

A

thalamus

164
Q

Continuous unilateral undulating contraction of the orbicularis oculi and most of the facial muscles

A

Facial myokymia - Pontine glioma or demyelination (MS) signifies intramedullary disease of the pons involving CN VII nucleus or fasicle

165
Q

Trigeminal neuralgia can result from what artery coming in contact with the trigeminal root in the subarachnoid space?

A

Superior cerebellar artery

166
Q

Left CN III nucleus lesion

A

bilateral ptosis, left adduction and depression deficit, right elevation deficit.

167
Q

Horners with anhidrosis limited to the ipsilateral forehead

A

lesion at or distal to the superior cervical ganglion (third order Horner syndrome)

168
Q

Interruption of central (first order) or preganglionic (second order) neuron causes

A

anhidrosis of the ipsilateral head, face, neck. May produce Harlequin syndrome, one-half of face is pale and other half normal or reddish (white is lesion denervated sympathetics supersensitivity to circulating adrenaline)

169
Q

Term for illusion of object that moves in elliptical path rather than straight line

A

Pulflrich phenomenon

170
Q

Ability to see moving, but not static objects in a blind hemifield (statokinetic dissociation)

A

Riddoch phenomenon

171
Q

Preservation of a visual image after removal of original stimulus

A

Palinopsia - may be illusory (triggered by contrast and/or motion) or hallucinatory (a/w homonymous VF loss and caused by cortical lesions)

172
Q

Inability to perform visually guided movements

A

Optic ataxia

173
Q

Difference between myelinated retinal nerve fiber layer at ON margin versus optic disc drusen

A

retinal vessel obscuration

174
Q

Nystagmus worse in down and lateral gaze to either side. What structure is most likely to have a lesion

A

Flocculus of the cerebellum

175
Q

Cause of downbeat nystagmus

A

vestibulocerebellum (nodulus, uvula, floccus, parafloccus of the cerebellum)

176
Q

Cause of upbeat nystagmus

A

medulla

177
Q

Cause of parinaud syndrome

A

dorsal midbrain

178
Q

Cause of seesaw nystagmus (where is the lesion)

A

parasellar region/diencephalon

179
Q

Transient monocular vision loss a/w eye pain that improves when patient lies down

A

Ocular ischemic syndrome

180
Q

Findings on DFE in ocular ischemic syndrome

A

midperipheral dot-blot hemorrhages and dilated veins due to low central arterial pressure. +/- episcleral injection and aqueous flare due to ischemic uveitis

BCSCSAP Review (13 decks)

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