how to differentiate · modified frisen criteria 6 stages grade 0 grade 1 grade 2 grade 3 grade 4...

Are we killing or blinding ourpatients?

Rosa A. Tang, MD, MPH, MBABruce Onofrey OD, RPh, FAAO

Eduardo Villarreal , MDMS Eye CARE –University of Houston

College of Optometry

How to differentiatedemyelinating from toxic optic

neuropathy with a review of drugrelated Neuro-ophthalmic

adverse effects

Rosa A. Tang, MD, MPH, MBABruce Onofrey OD, RPh, FAAO

Eduardo Villarreal , MDMS Eye CARE –University of Houston

College of Optometry

Acute demyelinatingoptic neuritis

• Age: 20-50

• 75% females

• Monocular painfulloss of vision notbeyond 14 days

• Most recover with notreatment

Discuss performanceof brain MRI


• If brain MRI hasWML –risk of MS is60%

• If brain MRI has noWML lesions risk isreduced to 20%



• IV steroids for acuteattack of optic neuritis

• Decision made forimmuno-modulatingtherapy based onMRI findings ,clinical risk for MS.


WHEN GOOD DRUGS GO BAD

NEURO-OPHTHALMICADVERSE EFFECTS [ADR]OF COMMONLY USEDMEDICATIONS

Ocular toxicity

• Systemic medications

– Increase damage with long term use:

a) Use in younger patients for longer term

b) Chronic use issues !

WHO classification

• Certain

• Probable/likely

• Possible

• Unlikely

• Conditional/Unclassified

• Unassessible/Unclassifiable

• Ref: Edwards,IR,Biriell C.: Drug Safety:1995:10:93-102

• The WHO Technical report Series #498,1972.

Learning objectives

• Recognize agents which have potential toproduce Neuro-ocular damage and when canthis be reversed.

• Know when to STOP the drug• Identify early signs and symptoms of ADR.• Standardize your proper management:

– Special testing: when to order ERG, mfERG,etc– Alternative therapies: what if…..– Proper intervals of evaluation: how often to check

– Counseling and do not abandon the blind!!!

What is the target???

• Anterior Sensory : optic nerve

Retina/macula

ON via Glaucoma

• Motor : pupil

EOM

Posterior Visual Pathway

Medications

• Optic nerve

– Accutane

– Tetracyclines

– Phenothiazines

– Ethambutol

– Amiodarone

– PDE inhibitors

Type: disc edema, direct toxicity, increased ICPAION

GLAUCOMAS

• Angle closure glaucoma*

*Other types

Medications

• Retina /macula

– Hydroxychloroquine

– Tamoxifen

– Phenothiazines

– Corticosteroids

– Digoxin

– Interferons

Types: central :CME, macular deposits, pigmentary changes, peripheral changesVascular changes [CRVO,BRVO,CRAO,BRAO] ,electrophysiology changes.

DRUGS AND DILATED PUPIL

Medications

• HMG-CoA reductaseinhibitors

DiplopiaMyositisMG relatedAccommodative-fusionalNystagmus

Fluoroquinolones

TOXIC OPTIC NEUROPATHIES

• Bilateral usually symmetric progressive lossvision. Painless.

• Loss of color vision is constant & more profoundSx than the loss of visual acuity.

• Early cases may present with isolated color visiondeficiencies.

• The hallmark of this disorder is the visual fielddefect consisting of a cecocentral scotomathat begins nasal to the blind spot and

extends to involve fixation on both sides of thevertical meridian.

TOXIC OPTIC NEUROPATHIES

• Nerve fiber layer losses APPEAR first in thepapillomacular bundle sometimes associated with swellingof the nerve fiber layer in the arcuate bundles above andbelow the denuded area between the fovea and optic nervehead (Sadun et al 1994a; 1994b).

• Later in the course of the disease, the temporal optic discappears mildly pale.

TOXIC OPTIC NEUROPATHY

• MOST COMMON MEDICATION ISETHAMBUTOL > 15 MG/KG/DAY

• MOST COMMON TOXIN ISMETHANOL

OPTIC NERVE TARGET

• Toxic effect associatedto disc edema

DISC EDEMA

IF OPTIC DISC IS EDEMATOUS AND CAUSE ISUNKNOWN I CALL THIS OPTIC DISC EDEMA

[ CPT: 377.00]

WHEN BOTH OPTIC DISCS ARE EDEMATOUSAND I KNOW IT IS DUE TO RAISED ICP, THEN

I USE TERM PAPILLEDEMA [CPT:377.01]

DEFINITIONS

PAPILLEDEMA:2 processes

• CONDITIONS WITHNORMAL IMAGINGAND/OR CSF EXAM(LESS URGENT UNLESSVISION ISCOMPROMISED)

• CONDITIONS WITHABNORMAL IMAGINGAND/OR CSF EXAM(NEED TO MOVE ONTHIS QUICKLY AS MAYTHREATEN LIFE)

AS WE DO NOT KNOW WHICH CONDITION WE ARE DEALING WITH WHENWE FIRST SEE THE PT, I CONSIDER ALL PAPILLEDEMA PTS AS URGENT IN REGARDS TO W/U!!

22

Accutane and disc edema

• Fraunfelder et al 2004– 179 cases of Increased ICP

– Onset in 2.3 months after starting drug

– Derivative of Vitamin A

• Roytman et al 1988– Alteration of lipid concentration of arachnoid

villi

– Impending absorption of CSF16

Tetracyclines

• Bacteriostatic• Ocular side effects:

– Certain: photophobia, blurred vision,discoloration, blue-gray pigmentation, enlargedblind spot

– Probable: Increased ICP, myastheniaaggravated

– Possible: subconjunctival/retinal hemorrhages =anemia, erythema multiforme, Stevens-Johnson

– Conditional: retinal pigmentation (minocycline)

Other drugs linked to disc edema[not all inclusive]

• 1.Lithium

• 2. Danazol

• 3.Steroids

• 4.cimetidine

• 5.All –trans-retinoic acid[ATRA]:leukemias

• 6. Cyclosporine

• 7.Norplant-other BCP?

Idiopathic IntracranialHypertension Treatment Trial

NEI Sponsored Double Blind,Placebo-controlled Clinical Trial

UH College of OptometryRecruitment Center in Texas

Rosa Tang MD,MPH,MBA Neuro-ophthalmologyof Texaswww.neuroeye.com

Idiopathic Intracranial Hypertension TreatmentTrial

18-60 years old

IHH for 6 weeks or less

Reproducible Visual loss on HVF

Bilateral papilledema

Women must use acceptable birth control

INCLUSION CRITERIA


EXCLUSION OF SECONDARY CAUSESOF

Idiopathic Intracranial hypertension orPseudotumor cerebri

EXCLUSION CRITERIA

PAPILLEDEMAModified Frisen Criteria

6 STAGESGRADE 0

GRADE 1

GRADE 2

GRADE 3

GRADE 4

GRADE 5

Modified Frisén Papilledema ScaleGrade 0

no optic disc edema

Modified Frisén Papilledema ScaleGrade I

Hallmark:C-Shaped halo (edema)with a temporal gap of no edema

www.neuroeye.comIdiopathic

Modified Frisén Papilledema ScaleGrade II

Hallmark:The halo of edema becomes

circumferential

Modified Frisén Papilledema ScaleGrade III

Hallmark:Loss of major vessels asthey leave the disc

Modified Frisén Papilledema ScaleGrade IV

Hallmark:Loss of major vesselson the disc

Modified Frisén Papilledema ScaleGrade V

Criteria of Grade IV: + partialor total obscuration of allvessels on the disc

How does the patient with I ICP present?

• Headache (often daily), pulsesynchronous tinnitus, vision loss,transient visual obscurations, orhorizontal diplopia.

• Occasionally on routine eye exam.

• A few with abrupt onset of rapiddeterioration of vision.

• Sometimes with neck, back or arm painfrom pressure on nerve root sheaths.

Modified Dandy criteria of IIHRef: Friedman &Jacobson : Neurology :59:1492-1495,2002

• Symptoms and signs of increasedICP

• Otherwise normal neurologicexam

• Normal level of alertness• Neurodiagnostics normal except

elevated ICP• No other cause of increased ICP

present.• The importance of LP

Typical Patient:Clinical Associations

• Obese female ofchildbearing age

• General population:1 : 100,000

• Women 20-44 who are 20%greater ideal body weight:19.3 : 100,000

• Female : Male8 : 1

• Obesity• Recent weight gain• Pregnancy?

Functional Assessment:Visual Field Testing in papilledema

Goldmann visualfield diagram

Study field loss : Classic Inferonasal Step [Grade II}

Automated Humphrey VF

Automated HVF diagram

Medical Treatment IIH

• Weight reduction, low Na+ diet• Repeated lumbar punctures• Diuretics

–Acetazolamide–Furosemide–Topiramate

• High-dose corticosteroids – appear to beeffective but difficult to wean off withoutrebound intracranial hypertension

Surgical Treatment for IIH

• CSF shunting procedures – appears to work but50% eventually fail

• Optic nerve sheath fenestration – seems to bepreferred option

• Gastric weight reduction surgery – maybe formorbid obesity

• Stenting of venous sinus – too early to tell

The Need for a Trial

• IIH treatment data is anecdotal• Optimal management is unknown• Long-term outcomes are unclear• Etiology unknown


Patients randomized for 6 months to:Diet plus DiamoxDiet plus placebo

Rosa Tang MD,MPH,MBA Neuro-ophthalmologyof Texas

www.neuroeye.com

Main entry criteria-NORDIC

• Age 18 - 60 years

• Meets modified Dandy criteria of IIH

• Newly diagnosed (6 weeks or less)

• Presence of papilledema

• HVF shows : PMD -2 dB to -5 dB in the worst eye

IIH AND CVT

• UP TO ~10% of pts presenting as though theyhave IIH end up having underlying CVT

– However this is difficult to image at times and mayrequire the performance of MRV or CTV

CVT-who is at risk ?

• Papilledema patient that is taking :

BCP in women

Drugs: HGHanabolic steroidsEctasy

ERECTILE DYSFUNCTION DRUGS andNON ARTERITIC A.I.O.N. (NAION)

Drugs:- Sildenafil (Viagra)

• Tadalafil (Cialis)

• Vardenafil (Levitra)

PDE: phosphodiesterase type 5 inhibitors

THE BIG THREE

• VIAGRA (Sildenafil – Pfizer)

• CIALIS (Tadalafil – Lilly ICOS)

• LEVITRA (Vardenafil – Bayer/ Glaxco S.K.)

- Est. 170 million Viagra Rx’s has been given

- Est. 23 million men using these drugs

- Est. 1 billion doses (so far)

PDE inhibitors and the eye

• Erectile dysfunction– Dosage dependant

– Can be reversible!!!

– Certain: Transient impairment of blue/green colordiscrimination :changes in color perception (blue)

• FM 100 Hue Test

• Blurred vision - central haze

• changes in light perception, photophobia

– Possible: NA-ION, macular edema

www.neuroeye.com

Nitroglycerine can be deadly

• Nitro + Viagra = ION

B. Onofrey, OD, RPh, FAAO

E.D. DRUGS – WHAT’S THE MESSAGE

• Ask patients if they are using PDE-5 inhibitors (as part ofmedication list)

• NOTE: HBP and/or DM

• Watch for “Discs at Risk”• Consult with patient that there is a ↑ risk of NAION with

PDE-5 inhibitors with HBP, DM, or other vascularcompromise even if there has been no current ocularfindings

• Remember 100 cases out of a billion doses is still a lowincidence of complications

Ethambutol (Myambutol)

• Pulmonary Tuberculosis Tx

• 822 adverse reports received at Registry– 55 cases reported optic neuropathy– 24 male: 31 female

– Average dose 15mg/kg/day for 235 days todevelop

– 1% w/ dosages at or below 15mg/kg/day

National Registry of Drug-induced Ocular Side Effects2008 (Portland, Oregon)

Ethambutol (Myambutol)Toxicity to ON is dose related

• 50% at a dose of 60-100 mg/kg/day

• 5-6% at a dose of 25 mgrs /kg/day

• 1% at or below 15 mgrs/kg/day

MAY CONTINUE TO LOOSE VISION

DESPITE DISCONTINUATION OF MEDS

ETHAMBUTOL TOXICITY

• AFFECTS MITOCHONDRIAL METABOLICPATHWAYS

• ON starts 2-5 months after start Tx

• AFFECTS THE small caliberPAPILLOMACULAR BUNDLE AXONS.

• Late development of optic atrophy retrobulbar,bilateral ,sometimes asymmetric .

• OCT can detect subtle NF loss before atrophy isobvious.

Ethambutol-who is at high risk

• Patients with renal failure are at particularrisk, owing to reduced excretion of the drug(DeVita et al 1987).

• In a meta-analysis review, Talbert Estlinand Sadun suggest renal function testing inall patients on Ethambutol in order to screenfor even mild renal dysfunction (TalbertEstlin and Sadun 2010).

Ethambutol• Management guidelines

– Baseline exam – VA, pupils, VF :10-2, colorvision, OCT, photos.

– Monthly examination if doses > 15mg/kg/day.

– If visual symptoms occur = DISCONTINUEdrug immediately

Fraunfelder, et al : Clinical Ocular Toxicology 2008Sadun et al: AJO 2009

Ethambutol• Management guidelines: even at “low dose”

– Monthly examination also in “at risk” of toxicity:a) Diabeticsb) C.R. Failure

c) Alcoholicsd) Elderly and childrene) If there is Ethambutol induced peripheral

neuropathy

Fraunfelder, et al : Clinical Ocular Toxicology 2008Sadun et al: AJO 2009

Isoniazid

• Isoniazid, another antimicrobial frequentlyused to treat tuberculosis, is also toxic to theoptic nerves but much less so thanethambutol.

• Optic neuropathies from isoniazid use haveassociated with severe bilateral optic discswelling (Kass et al 1957) and with peripheralneuropathy (Kywosawa and Ishikawa 1981).

• Others have suggested that the visual fielddefects in isoniazid optic neuropathy maytake the appearance of bitemporalhemianopic scotomas (Karmon et al 1979).

AAnti-arrhythmic

Agents• All can produce

reversible orirreversible

decrease in acuity

• Disc edema hasbeen reported


59

Amiodarone (Pacerone)

• Antiarrhythmic

• Certain: blurred vision, photophobia, halos aroundlights - night– corneal golden-brown deposits

– Keratitis Verticillata– IOL brown discoloration

• Possible: Disc edema ?increased ICP ?NAION

Other mechanism?

60Ref: J Natal Med Assoc 2004;96:1477-91. 60

Amiodarone (Pacerone)

• Antiarrhythmic

• Certain: blurred vision, photophobia, halos aroundlights - night– corneal golden-brown deposits

– Keratitis Verticillata– IOL brown discoloration

• Possible: Disc edema ?increased ICP ?NAION

Other mechanism?

60Ref: J Natal Med Assoc 2004;96:1477-91.

Amiodarone Induced OpticNeuropathy

Ref: Macaluso et al: AJO 1999:127:610-2

• Should be a diagnosis of exclusion

• Most pts are vasculopaths so distinctionfrom NAION sometimes difficult

• 57 pts+16 cases reports [WHO registry]

*insidious onset

* bilateral disc edema long duration

[6 months on average]

*milder VF/VA loss

Linezolid

• Linezolid, an oxazolidinone antimicrobial active againstgram-positive infections, has been reported by severalauthors to cause a reversible optic neuropathy (McKinley2005; Rucker et al 2006).

• Whereas it is probably safe for short courses of therapy, itis often used as a prolonged course of therapy to treatosteomyelitis and other chronic infections.

• Linezolid inhibits translation of bacterial DNA by bindingto bacterial ribosomal RNA subunits (the binding sitesdiffer from those of the macrolides).

• Therefore, its prolonged use may also inhibitmitochondrial protein synthesis.

• In most cases, optic neuropathy has only developed after 3months or more of continuous use.

Other toxics to the Optic Nerve

• Methanol and ethylene glycol deserve special mention, as these agentsare poisons that continue to be implicated in toxic optic neuropathy.

• Methanol is found in poorly distilled alcoholic beverages (“homebrews”). Its ingestion produces a metabolic acidosis as a consequenceof the accumulation of formate, one of its toxic metabolites. Methanolproduces vision loss within hours of exposure and can lead to completeblindness. MRI brain: high T2 signal in basal ganglia and parieto-occipital white matter

• The optic disc is often hyperemic and swollen. Lack of pupillaryreactivity to light usually indicates a poor prognosis (Grant andSchuman 1993).

• Ethylene glycol, the main ingredient in antifreeze, may also produceblindness with a time course similar to that of methanol.

Drug-induced Glaucoma• Topamax• 100 cases reported

• Ref: Fraunfelder et al: Ophth 2004:111:109 • Corticosteroids

Anticonvulsants

• Topiramate (Topamax)• Use to treat: epilepsy, migraine,bipolar

– Acute angle closure glaucoma*

– Weight loss 3.8% per 100 mg

– 100 cases reported of glaucoma in large study

– Certain: glaucoma, mydriasis, VFD, ocular pain

– Probable: blepharospasm, oculogyric crisis

– Possible: scleritis*Fraunfelder FW, Keates EU Ophthalmology 111(1): 109-111, 2004

Drug-induced Glaucoma• Topamax• Acute bilateral secondary

angle closure glaucoma :– Uveal effusion w/secondary

angle closure glaucoma– 2 weeks to develop after

start drug– Tx:

• D/c medication• Hyperosmotic therapy

– Mannitol– Urea

• Cyclopegic• Topical antiglaucoma

Ophthalmology, 111(1): 109-111, 2004

*Myopia up to 8.5 diopters, appears in hoursand disappears in weeks

Steroids (Prednisone)

• Adrenal insufficiency• Inflammatory and allergic disorders• Certain:

– Subcapsular cataracts– Elevated IOP (glaucoma)– Resistance to infection– Papilledema IIH (start/stop)– Myasthenic effect– CSR?

Interferon…. Friend or Foe?

Ref: Tang, R: Editorial. Arch Ophthalmol: 1995:113(8):987

I alfa : tx systemic disorders,CNV ,Hep C and cancers

I beta: MS treatment ,Hep C

Interferons

• Proteins with largemolecular weight

• Against viruses, tumors

• Blocks angiogenesis

• Common side-effect = flu-like symptoms

Ocular :

Reversible vaso-occlusiveretinopathy

– CNP [III reported]

– Eyelash hypertrichosis

Interferons

Types:AlfaBeta

Interferon associated-retinopathy

• IFN-a used for various illnesses [1]10 cases retinal ischemia associated: usually reversible

with discontinuation of tx:– Cotton-wool spot formation 100%

• Axoplasmic flow obstruction - ischemia

– Capillary non-perfusion

– Arteriolar occlusion: severity lessens reversibility– Hemorrhage

1. Guyer D, Tang R et al. Arch Ophthalmol. 1993;111:350-356

Screening in Hepatitis C justified?

• Br J Ophthalmol: 2004 : 12: 88– Tx: Interferon-alfa + ribavirin

– Aim: identify development of Retinopathy

– Methods:• F/u pts for 1 year, n = 25

• FU @ 3-month intervals

– Results:• Retinopathy = 4 cases [2 diabetics and 1 HBP] -reversible in all

– Incidence is low so not justified!!!

TAMOXIFEN

• Reduces incidence of breast cancer by up to75%

• Originally used in elderly, post-menopausalwomen to prevent recurrence of cancer

• Now in young women for

prophylaxis

• Produces vision loss?


Tamoxifen Maculopathy

• Occurs in 6% of patients within 6 monthsof low dose therapy (20mg/D)

• Reversible early, not reversible later• White crystalline macular deposits


Tamoxifen-Patient Management

• Pre-TX baseline evaluation with emphasison macular function and appearance[OCT-photo]

• Evaluate every 6 months thereafter or prndecrease in central acuity

• Also monitor for cataract!!!


75

Hydroxychloroquine (Plaquenil)

• Tx of rheumatoid arthritis and lupus

• Dermatologic conditions

• Inflammatory disorders

43 76

Plaquenil

• 20 cases reported with low doses(<6.5mg/kg/d)

• Toxicity after 5 years treatment

• Maculopathy– Bilateral

– “Bulls-eye”• ABCR mutation - predisposed to develop

toxicity* Shroyer et al

77

• Guidelines: high Risk [AAO 2005]:• Age: >60 years.

– Duration: > 5 years of therapy– Dosages : >6.5 mgr/Kg– Renal/liver dysfunction– Habitus: Obese, thin or elderly– Concomitant retinal disease.Beware of :– Early changes - relative paracentral scotomas– Beware as changes are IRREVERSIBLE

PLAQUENIL

78

PLAQUENIL

• Baseline examination: after start of drug– Within first year of therapy

– Amsler grid, VA, color testing ,VF ?mfERG

• Follow up:– high risk : at least yearly if asx.

– low risk patients : every 2 years.

– Annual or bi-annual if patients have been

> 5 years on the drug.

46

• Toxic MaculopathiesCloroquineThioridazinePLAQUENILOther : maculopathies, cancer related

retinopathies

81

Phenothiazines

• Antipsychotics

• Side-effects– Certain: night blindness, color distortion (red-

green)• Corneal pigmentary deposits

• Punctate keratitis

• Lens - stellate anterior cortical changes

– Probable: retinal changes, Horner’s sx, MG

– Possible: optic atrophy, papilledema30

MACULAR EDEMA

• 1. Epinephrine

• 2. prostaglandins

• 3. Steroids: CSR more likely link .

• 4.Fingolimod [Gilenya]

• 5.Other

Vigabatrin (SABRIL)Ref: Sergott et al : Neuro-ophthalmology 2010:34:20-35

• Irreversible inhibitor of GABA-T

• Refractory complex partial seizures

• Monotherapy in infantile spasms

VigabatrinRef: Durnian et al : Eye:2008:22:559-563

• Irreversible inhibitor of GABA-T

• Structural analysis NFL shows

• Injury to both:a. the photoreceptors in the

outer retina .

b. The retinal GC and their

axons in inner retina.

c. Secondary optic atrophy


• Induces retinopathy characterized by:

1.Irreversible ,bilateral constricted

VF both eyes in >30% of pts ranging

from mild to severe [Lundbeck]

2.Slow onset: nasal step first

3.Abnl ERG

4.Seen between 3 mo to 12 mo of tx

5.Once a pVFD is detected

it does not regress after D/C drug


After month 1 [baseline] of Tx do testsevery 3 months if ASX :

• Visual field testing (when able):– Perimetry : Goldmann or automated

– Confrontation: misses early VF defects

• Testing when not able to do VF– ERG

– OCT

Evidence-based review of recommendations for VisualFunction Testing in patients treated with Vigabatrin

Sergott, R., Wheless, J., Smith, M., et alNeuro-ophthalmology, 34(1),20-35,2010

PatientstreatedFor complexPartialseizures

Birth Control pills: BRVO,CRVO, hypercoagulability

Reduction of ocular perfusionpressure

• Systemic antihypertensive drugs

90

Other medications

• Tamsulosin (Flomax)– a-adrenergic antagonist - BPH, HTN

– Certain: Floppy iris syndrome *, amblyopia

• Biphosphonates (Actonel)– inhibits bone resorption - hypercalcemia, Paget’s disease

– Certain: anterior uveitis, episcleritis, irritation

– Possible: retrobulbar neuritis, diplopia, CNP

– Scleritis w/ Avedia = 6-48 hrs post injection*

Medications

• HMG-CoA reductaseinhibitors

DiplopiaMyositisMG relatedAccommodative-fusionalNystagmus

Fluoroquinolones

92

HMG-CoA reductase inhibitors

• Lipitor– Hypolipidemic drugs - statins

– MYOPATHY

– DIPLOPIA

– 256 case reports - diplopia, ptosis orophthalmoplegia• average age 64.5

• Dosage varied

• Diplopia - 8.3 months post-treatment76

93

Fluoroquinolones

• Ciprofloxacin

• Tequin

• Levaquin

• Avelox

73 94

Fluoroquinolones

• Intefere with DNA replication

• Inhibiting bacterial DNA gyrase

• Tendinitis and tendon rupture

• DIPLOPIA

74

95

Fluoroquinolones

• 171 case reports of diplopia

• 76 men: 91 women

• Ages range 6-95 years, median 51.6

• 17 presented with concomitant tendinitis

• Median time = 9.6 days

75

MYASTHENIA

• Neuromuscular JunctionDisease

• IS NOT INHERITED• IS AN AUTOIMMUNE

DISEASE that targets the Achreceptors

DRUGS AND MYASTHENIAType ofdrug

Drug

Anesthetics** General anesthetics: benzodiazepines, ketamine, propanediol ether,proparacaine, methoxyflurane and others

Local anesthetics: lidocaine, procaine, and others

Neuromuscular blocking drugs: vecuronium, atracurium, succinylcholine,and others

Antibiotics Aminoglycosides: gentamycin, tobramycin, kanamycin, neomycin,streptomycin, netilmicin

Fluoroquinolones: ciprofloxacin, norfloxacin, pefloxacin, prulifloxacin(Rossi et al 2009)

Ketolides: telithromycin (Perrot et al 2006)

Macrolides: erythromycin, azithromycin, clarithromycin

Polypeptide antibiotics: vancomycin, colistin, polymyxin B

Penicillins

Tetracycline

Sulfonamides

Others: clindamycin, nitrofurantoin, ritonavir

DISORDER OF ACCOMMODATION AND

OF VERGENCE

• VERY COMMON

• MANY DRUGS: antidepressants

Avodar [dutasteride]Detrol[Tolterodine]

These drugs used for “bladder control” inour MS pts for example can be a factoron these problems with accommodationand vergences

NYSTAGMUS DRUG INDUCED

• GAZE EVOKED: Jerk nystagmus due toproblem with gaze holding

• Occurs with attempted lateral or upwardgaze.

• Seen more commonly with :• ANTICONVULSANTS : phenytoin, [Dilantin]

carbamazepine [Tegretol]• sedatives [ phenobarbiturates]• antidepressants and lithium.• Alcohol

NYSTAGMUS DRUG INDUCED

• BILATERAL PERIPHERALVESTIBULOPATHY

• May be accompanied by dizziness andtinnitus.

• May have hearing loss associated.

• Occurs with ototoxicity of aminoglycosides

Bottom Line

Do a baseline evaluation and recheck patient asoften as needed.

You have been given cluesif exam is monthly,3 months or 6 months.

Know your patient medical status.Keep an eye on the literature

and stay friendly with your lawyerDr Rosa Tang, MD,MPH,MBA

email: [email protected]: www.neuroeye.com

phone:713-942-2187

mailto:[email protected]

how to differentiate · modified frisen criteria 6 stages grade 0 grade 1 grade 2 grade 3 grade 4...

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