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103 Cards in this Set
- Front
- Back
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Optic Nerve anatomy:
#fibers, dimensions, length |
1.2 million axons
1.5mm diameter, 3.5mm diamter posterior to lamina cribosa. Intraocular 1mm Intraorbital 25mm Intracanalicular 8-10mm Intracranial 15mm myelination completes after birth from LGB to lamina cribosa |
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Optic nerve blood supply:
intraocular, orbital, intracanalicular, intracranial |
Intraocular: NFL - Central retinal A. Prelaminar - capillaries of Short post. artery
laminar - plexus short post. artery retrolaminar - ciliary and retinal circulation orbital: ophthalmic artery intracanalicular: pial branches of ophthalmic artery intracranial: small Internal carotid artery vessels, ant cerebral a., ant communicating a. |
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saccades
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quick eye movements for refixation. generated by contralateral frontal eye fields of frontal lobes
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smooth pursuit
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eye following movements. generated from ipselateral parieto-occipital lobe
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Tensilon and it's side effects
What is the antedote? |
A inhibitor of acetylcholinesterase. Used in Myasthenia Gravis. Can cause cholinergic crisis: sweating, nausea, vomiting, salivation, fever.
Use atropine as antidote to block Ach receptor sites |
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Caloric vestibular stimulaton
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COWS. refer to fast phase nystagmus. Cold opposite, warm same. bilateral simulation: cold up, warm down. In comatose patient is it all inverse
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Diagnosing Horner's syndrome
Work up for Horner's syndrome |
Use cocaine test (4%, 10%). Cocaine inh reuptake of norepi. In normal people will dilate pupil. In horner's will fail to dilate. It does not indicate level of damage
Use Hydroxyamphetamine 1% (paradrine): releases norepi from nerve terminal. To determine level of damage. If dilation damage is preganglionic at first or second order neuron level. If no dilation damage at level of post ganglionic, third order neuron damage. Work up with: MRI head and Neck, CT chest |
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Explain the sympathetic pathway of the pupil.
Damages at each level |
First order neurons from hypothalamus synapse at level C8-T1 ciliospinal center of budge.
Second order neurons exit T1 course under the subclavian A. then ascend the internal carotid a. to synapse at the superior cervical ganglion. Third order neurons then send post ganglionic fibers to carotid plexus, branch joins V1 pass through ciliary gangion (no synapse) to iris. A branch also goes to the lacrimal gland. Second order damage: mediastinal or apical tumor, pancoast tumor, neuroblastoma Third order damage: ICA dissection, trauma, migrane. |
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Adies tonic pupil. diagnosis
Adies syndrome |
A dilated pupil due to post-ganglionic parasympathetic pupillomotor damage. Occurs in young women, unilateral.
Pupil is dilated, reacts poorly, can become miotic. HAve segmental contraction of pupil. Light near dissociation. Has slow tonic redilation after reaction to near stimuli. Adies sydrome: tonic pupil with decreas DTRs and orthostatic hypotension. pathologically: loss of ganglion cells in ciliary ganglion. Diagnose with dilute pilocarpine .125%, will constrict tonic pupil but not in normal pupils. |
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DDX dilated pupil
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Adies tonic pupil
traumatic mydriasis pharmacologic |
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temporal lobe lesion VF
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Pie in the sky, superior homonymous hemianopia, formed visual hallucination, seizures
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parietal lobe lesion VF
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inf. homonymous hemianopia, hemiparesis, visual perception diffcult, agnosia, apraxia, left - right confusion
OKN asymmetry - difficult to pursuit to side of lesion |
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occipital lobe lesion VF
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macular sparing if post. cerebral a infarction. sparing temporal cresent
Cortical blindness occurs in BL occipital lobe destruction. Pupils are normal, have unformed hallucinations, riddoch phenomenon, antons |
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vascular supply of occipital lobe
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supply by both middle cerebral and post. cerebral A.
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Aberrent regeneration caused by?
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Trauma
tumors aneurysm **Never by vasculopathic ischemic injury |
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Eaton Lambert
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A paraneoplastic syndrome that cause proximal muscle pain, weakness, dysarthria, dysphagia. Assoc with small cell lung carcinoma. there are antibodies made against the presynaptic calcium channels causing impaired release of Ach.
Diagnosis: muscle strength improve with excercise, will not improve with edrophonium. EMG- increase muscle potential with repeated stimulation. |
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Drugs that exacerbate myathenia gravis
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Steroids
antibiotics (aminoglycosides, clinda, erythro) Beta blockers Penicillamine phenytoin curare methoxyflurane lidocaine |
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myathenia gravis
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Weak muscles due to autoimmunity to Ach receptors in motor endplate. Hallmark is fatigability. F > M.
Neonatal form: mother can pass antibodies to child. Congenital form: defect in Ach receptor. Ocular: ptosis, and EOM weakness. Systemic: other muscles invovled, 5% get grave's. Associated with thymic hyperplasia (70%), thymoma. Presentation: ptosis, cogan's lid twitch, ophthalmoplegia, facial muscle weakness, nystagmus, jaw weakness, dysphagia, dysarthria, dyspnea. Diagnosis: tensilon test, EMG, photos, rest test, ice test, Ct chest and look for thymoma. Treatment: Mestinon, steroids, plasmapheresis, immunosuppresion |
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Toxic / nutritrional optic neuropathy
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Painless symetric, progrssive vision loss.
From: ethanol, methanol, digoxin, ethambuthol, chloramphenicol, isoniazid, rifampin, lead, tobacco, alchohol, thiamine/B12 deficiency. Findings: vision <20/200, cecocentral scotoma,disc hyperemia eventually pallor. |
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Leber's hereditary optic neuropathy
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Mitochondrial inheritance (maternal) Occur in males, females are carriers. Onset 15-30yo. Have BL loss of vision over days. Use of tobacco/alcohol can trigger. find: disc hyperemia, peripapillary telangiactasia that dont leak on FA, vessel tortuosity, late ON pallor, cardiac conduction defect.
there is no treatment. provide genetic counseling. |
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Adv and disadv CT scan
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adv: Bone detail, fast use in trauma, can detect FB.
disadv: radiation |
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Adv and disadv MRI.
T1 and T2 |
best for soft tissue, looking at posterior fossa anatomy, no artifact from bone, no radiation.
Contraindicated in metal FB, expensive T1 - blood, fat, mucus, melanin BRIGHT vitreous, CSF, EOM, acute heme DARK T2 - vitreous, CSF BRIGHT blood, fat is DARK. Best for demyelinating lesions. |
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Paramedian pontine reticular formation lesion
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Lesion in pontine. Cause ipsilateral horizontal gaze palsy
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CN 6 nucleus lesion
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cause ipsilateral horizontal gaze palsy
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Test to help diagnose functional visual loss
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Dense defect:fogging refraction, OKN, mirror test, pupil swinging light test, base up prism test
Mild defect: fogging refraction, stereo acuity, red-green glasses |
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One and half syndrome
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Lesion in CN 6 and ipsilaterla MLF. cause ipsilateral gaze palsy and INO.
Only movement is abduction of contralateral eye. convergence is intact. Occur from: MS, basilar a, occlusion, pontine metastasis. |
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Internuclear ophthalomoplegia
WEBINO |
Lesion of MLF, cannot adduct ipsilateral eye with nystagmus on fellow eye.
Can be unilateral or bilateral. Lesion in midbrain (anterior) convergence preserved Lesion in pons (posterior) convergence impaired WEBINO: BL INO |
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vestibular nystagmus
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horizontal, rotary, jerk nystagmus in primary gaze. same in all fields.
due to vestibular disease (infection, menieres, vascular, trauma, toxicity). Peripheral lesion: fast phase to good side, slow to lesion. Can have deafness, tinnitus, vertigo. Central lesion: no localizing |
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Up beat nystagmus
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medullary lesions, midline cerebellar lesions (medulloblastoma)
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Down beat nystagmus
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cervicomedullary junction lesion (arnold chiari)
spinocereberallar intoxication lithium paraneoplastic cerebellar degeneration |
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See-saw nystagmus
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vertical and torsional nystagmus.
suprasellar lesion (CVA, trauma, congenital) Can treat with baclofen |
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Periodic alternating nystagmus
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nystagmus that changes direction.
Vestibulocerebellar system disease treat with baclofen or surgery |
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Convergence-retraction nystagmus
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on upgaze, cause co-contraction of lateral rectus.
Dorsal-midbrain lesion (parinauds, pinealoma, trauma, brain stem, AVM, MS) |
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Dissociated Nystagmus
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asymmetric nystagmus between the eyes. always pathologic
Lesion in posterior fossa |
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Gaze evoked nystagmus
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nystagmus in direction of gaze, fast phase toward lesion.
Mass compressing brain stem (acoustic neuroma, cerebellar tumor), intoxication |
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Brun's nystagmus
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CPA tumor
looking towards lesion - fast phase to lesion, high amplitude, low frequency Looking away lesion - fast phase away from lesion, low amplitude, high frequency |
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Pseudotumor cerebri
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occurs in young, obese, females. elevated intracranial pressure with unknown cause.
present with HA, N/V, visual obscurations, photopsias, CN 6 palsy. Order MRI/MRV head, LP find: papilledema, enlarge blind spot, normal MRI/NRV brain, elevetad LP opening pressure, normal composition. Condition that can cause: endocrine d/o, steroid withdrawl, dural sinus thrombosis, OCP, hypervitaminosis A, tetracycline, isotretinoin. If no VA loss: can observe, wt loss. Mild VA loss, diamox, wt loss. severe Va loss: LP shunt, ON sheath fenestration. |
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Optic neuritis
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Inflammation optic nerve, idiopathic or from systemic disease.
Most common optic neuropathy in young. Common in females. Have acute unilateral VA loss, pain EOM, dischromatopsia, RAPD, VF defect most common diffuse central scotoma > altitudinal > ON can be swollen. DDX: idiopathic, MS, syphillis, sarcoid, lyme, wegeners, sle, devics |
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Anterior ischemic optic neuropathy
Types? |
infarction of he optic nerve head. inadequate perfusion of post ciliary a.
Acute VA loss, dischromatopsia, RAPD, VF loss most common altitudinal or arcuate defects, ON edema. Arteritic: GCA, arteritis affecting post ciliary A. F>M >55, have scalp tenderness, jaw pain, PMR, fever, malaise, wt. loss. Dx elevated ESR, CRP, perform temporal a. biopsy. treat with steroid. Non-arteritic: 50-75yo. Assoc with DM, HTN, collagen vascular disease, ESR normal. no treatment. 25-45% risk of fellow eye. can have crowded disk. |
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Study: Optic neuritis treatment trial (ONTT)
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Evaluated the role of steroids in treatment of optic neuritis.
patients assigned to 3 groups: 1. IV steroids followed by oral pred. 2. Oral pred Only 3. Placebo Results: IV streoid more rapid recovery of vision. decrease incidence of MS in 2 years vs placebo, but no difference after 2 years. Oral pred only have higher recurrence rate. 30% develop MS within 4 years, 38% in 10years. Higher risk of developing MS if previous neuro symptoms and hx of optic neuritis in fellow eye |
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Study: Ischemic optic neuropathy decompression trial (IONDT)
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Results showed that:
1. ON sheath fenestration is not effective 2. surgery has higher risk of loss 3 lines vision. 24% surgical vs. 12% obs 3. at 6 months the observation group have 43% regain 3 lines or more while only 34% surgery patient regained 3 lines or more of VA. |
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Study: Controlled High risk avonex MS prevention study (CHAMPS)
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Ramdomized trial of inferferon B1a. For prevention of MS after demyelinating episode and abnormal MRI.
3 year result, risk of MS lower and fewer MRI lesions in treatment group. |
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CPEO
Kearn-Sayre |
a mitochondrial inherited disease.
Kearn-sayre- ophthalmoplegia, ptosis, retinal degeneration, heart block, path shows ragged red fibers |
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oculopharyngeal dystrophy
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occurs in french canadians, progressive dysphagia, ptosis, CPEO. path shows vacuolar myopathy
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myotonic dystrophy
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myotonia in peripheral muscles, worse in cold, excitement, fatigue. find: christmas tree cataract, pigmentary retinopathy, ptosis, light near dissociation, miotic pupil. Can have cardiac abnormality.
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Parinauds syndrome (dorsal midbrain syndrome)
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90% from pineal tumor. can occur from demyelination, infarction, trauma.
Cause supranuclear palsy on up gaze, mid dilated pupils, convergence retraction nystagmus, light near dissociation, vertical OKN, skew deviation, lid retraction (collier's sign). |
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Trigeminal nerve and branches
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V1 - ophthalmic
V2 - maxillary V3 - mandibular |
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Migraines
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migraines caused by vasospasm of brain vessels.
Common - no aura. M=F, throbbing HA Classic - with aura (20%) M=F. Can be triggered followed by hemicranial pain, scintillating scotoma (5-30min), N/V Complicated: assoc hemiplegia, hemiparetic, ophthalmoplegic Childhood: attacks of N/V no HA Acephalic: only aura, no HA retinal: temporary scotoma or monocular blindness, HA can precede or occur later Migraine infarction: focal signs persist > 1 week that correpond to a lesion. |
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Nuclear CN 3 plasy
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rare, contralateral sup rectus paresis and BL ptosis
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nothnagel's
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CN 3 fascicle and sup cerebellar peduncle damage. ipsilateral CN 3 paresis and cerebellar ataxia
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benedikt's
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lesion of fascile with red nucleus: ipsilateral CN 3 paresis with contralateral hemitremor and decrease sensation
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Weber's
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Lesion of fascicle and pyramidal tract. ipsilateral CN 3 palsy with contralateral hemiparesis.
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Claude's
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nothnagel's and benedikts
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Uncal herniation
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uncal herniation compress CN 3
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Post comm. aneurysm
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most common non traumatic aneurysm, painful, involves pupil CN 3 palsy
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photostress recovery test
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cannot be used in VA worst than 20/80. screens macular disease. >90sec to recover after photostress vs ON disease < 60sec.
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Intact bell's phenomenon implies
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supranuclear lesion
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intact doll's head implies
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supranuclear lesion
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failure of doll's head implies
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infranuclear lesion
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Visually evoked cortical potentials
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measures macular function, integrity of primary and secondary visual cortex, optic nerve and tract. Pattern VER used to measure preverbal infants.
Toxic or compressive optic neuropathy: reduction in amplitude demyelination: prolong latency |
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an intact oculovestibular reflex in patient with gaze palsy denotes?
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a supranuclear lesion
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lesion causing ipsilateral horner's and contralateral CN 4 palsy
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midbrain
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Paradoxical pupillary reaction
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CSNB, achromatopsia, leber's congenital amaurosis, optic atrophy, optic nerve hypoplasia
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millard gubler syndrome
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lesion in fasicle of CN 6, 7, and pyramidal tract causing 6th and 7th nerve palsy with contralateral hemiparesis
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raymond's syndrome
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lesion in CN 6 and pyramidal tract causing CN 6 palsy and contralateral hemiparesis
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foville's syndrome
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lesion of CN 6 nucleus and CN 5 and 7 fasciles. cause palsy in 5,6,7, horizontal gaze palsy and ipsilateral horners
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progressive supranuclear palsy
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progressive gaze palsy, early loss of vertical gaze down gaze first, then lose horizontal gaze. no bell's phenomenon present but doll's head intact. Leads to frozen globe, decrease blink, blepharitis, blepharospasm, apraxia eyelid opening, dysarthria, dementia
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millard gubler syndrome
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lesion in fasicle of CN 6, 7, and pyramidal tract causing 6th and 7th nerve palsy with contralateral hemiparesis
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raymond's syndrome
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lesion in CN 6 and pyramidal tract causing CN 6 palsy and contralateral hemiparesis
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foville's syndrome
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lesion of CN 6 nucleus and CN 5 and 7 fasciles. cause palsy in 5,6,7, horizontal gaze palsy and ipsilateral horners
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Optic chiasm anatomy
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55% fibers cross at chiasm, nasal fibers cross, temporal stay. 10mm above pituitary gland
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Knee of von willebrand
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inferonasal retinal fibers cross in the chiasm and course anterior 4mm into contralateral ON before running posterior
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damage to superior colliculus
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sup colliculus invovled in foveation reflexes, injury disrupts eye movement but no VF defect
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magnocellular neurons of LGB
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motion detection
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parvocellular neurons of LGB
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fine spatial resolution and color vision
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primary visual cortex
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contains topographic map of contralateral hemifield. central macular is magnified.
macular region located posterior peripheral VF is located anterior |
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Where is the temporal cresent represented in primary visual cortex?
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temporal cresent only seen by nasal retina of ipsilateral eye.
located most anterior in visual cortex. only site posterior to chiasm that if injured will cause monocular VF. Is also only VF spared after occipital lobe damage |
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What is blood supply of occipital lobe
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middle and posterior cerebral artery
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Horizontal gaze center
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ipsilateral PPRF, ipsilateral CN 6 nucleus, via MLF connects to contralateral CN 3 nucleus
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Vertical gaze center
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in frontal eye fields or superior colliculus --> riMLF --> CN 3, 4
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Gerstmann syndrome
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lesion in dominant parietal lobe cause inferior homonymous hemianopia, acalculia, finger agnosia, left-right confusion.
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oculomotor apraxia
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saccadic palsy. have head thrusting to look at target. fast phase absent on OKN, normal pursuit.
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olivopontocerebellar atrophy
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can be herditary or sporatic, early adulthood. eye movements slow down in all directions leads to complete ophthalmoplegia. have cerellar and pontine atrophy
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ocular bobbing
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due to hemorrhage
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ocular myoclonus
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pendular nystagmus assoc with uveal beating
due to hypertrophy of inferior olives |
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opsoclonus
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rapid chaotic eye movement in all directions, persist in sleep unlike spasmus nutans. A paraneoplastic syndrome from metastatic neuroblastoma
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CN 3 anatomy
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nucleus in midbrain --> exits ventral midbrain pass between post cerebral and superior cerebellar --> lateral to ICA --> cavernous sinus wall --> into superior orbital fissure divides to inferior and superior div.
1 subnucleus serves both levator palpebrae contralateral subnucleus serves SR. Superior division: LP and SR Inferior division: MR, IR, IO, iris sphincter, ciliary muscles |
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CN 4 anatomy
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nucleus in caudal mesencephalon --> exit dorsal at level of inferior colliculus --> decussates pass between post cerebral and superior cerebellar a. --> travel in wall of cevernous sinus --> enters orbit via superior orbital fissure outsite annulus zinn --> to sup oblique
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CN 4 nuclear syndrome
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CN 4 palsy with contralateral horner's or INO
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CN 6 anatomy
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nucleus in dorsal pons (medial CN 7) --> exits inferior pons ventral --> climbs over clivus --> under gruber's ligament through dorello's canal --> enter cavenous sinus --> into orbit via superior orbital fissure --> to lateral rectus
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gradenego's syndrome
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inflammation or abcess of petrous apex (mastoiditis) following ostitis media --> CN 6 palsy with ipsilateral decrease hearing, facial pain and paralysis
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CN 6 subarachnoid space syndrome
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increaseICP can push the brainstem down stretching the CN 6 at where it is tethered between pons and dorellos canal. (30% in pseudotumor)
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Pseudo-gradenego's syndrome
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cause by: nasopharyngeal CA, CPA tumors, petrous bone fracture, basilar aneurysm, clivus chordoma.
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trigeminal neuralgia
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compression of CN 5 root, cause severe facial pain usual at maxillary and mandibular division, get imaging, treat with cabamazepine or surgery
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CN 7 anatomy
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exits at CPA --> enters internal auditory canal with the nervus intermedius, cochlear, and vestibular nerves --> facial n. canal --> exits temporal bone via stylomastoid foramen --> branches in parotid gland. supply facial muscles, lacrimal and salivary, post 2/3 tongue, external ear sensation, dampens stapedius
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CN 7 supranuclear palsy
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damage of precentral gyrus of cerebral cortex cause contralateral paralysis of voluntary facial muscles of upper and lower. reflex and emotional movements preserved
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CN 7 brain stem lesion
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ipsilatral upper and lower facial weakness, can be from tumor or vascular cause
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CN 7 peripheral lesion
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most common facial nerve palsy. Bell's palsy a idiopathic facial n palsy of upper and lower face. if assoc with facial twitching or spasm suspect tumor. 70% recover in 6 weeks
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benign essential blepharospasm
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bilataral involuntary and forceful contraction of obicularis. absent during sleep. treat with botox
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hemifacial spasm
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unilateral contractions of facial muscles. due to vascular compression of CN 7 at brian stem, present at sleep, get imaging
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DDX of multiple CN palsies. CN 3,4,5, 6
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lesion at:
cavernous sinus superior orbital fissure brain stem Mimics: MG, CPEO, TAO, orbital pseudotumor |
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pathway of pupil light reflex
parasympathetic innvervation |
ON --> chiasm --> optic tract --> pretectal n. --> cross to both EW n. -> travel in CN 3 synapse in ciliary ganglion --> post ganglionic fibers via short ciliary n to cilary body and iris sphincter
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What does not cause RAPD
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cataract, amblyopia, acute papilledema, refractive error, function VA loss, any leison posterior to LGB.
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