Neuro-ophthalmic Disease SymposiumDiagnosis and Management Pearls

Mountain West Council of Op-tometrists

Las Vegas, NevadaApril 24, 2010

• Andrew G. Lee, M.D.

• Danica J. Marrelli, O.D.

• Robert P. Wooldridge, O.D.

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Evaluation of diplopia: What is life threatening?Andrew G. Lee, MDChairman of Ophthalmology, The Methodist Hospital, HoustonProfessor of Ophthalmology, Weill Cornell Medical CollegeAdjunct Professor of Ophthalmology, University of IowaClinical Professor of Ophthalmology, UTMB Galveston

• I have no financial interest in the contents of this talk

• I will not be discussing any off label uses of drugs

• Lee’s P’s

• Pain (severe, worst of life) in elderly

• Perception loss

• Pupil involvement

• Progressive proptosis

• Paresthesias or paralysis

• Overview: Lee’s “A”s: The five chances to save a life

• Arteritis (Giant cell)

• Apoplexy (Pituitary)

• Abscess (Mucor)

• Aneurysm (pupil involved third nerve palsy)

• Arterial (carotid or vertebral) dissection

• *At the end I want to give you an additional important take home message

• The 7 “Must Call” triage list (Give to your techs tomorrow)

• Acute painful ophthalmoplegia

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• Acute painful bitemporal hemianopsia

• Acute painful anisocoria (big or small)

• Acute painful visual loss in elderly

• Acute painful (HA) bilateral optic disc edema (papilledema)

• Acute “no light perception” vision

• Acute painful severe HA (“worst pain of my life)

• Beautiful Sunday….but what if it had been Monday 8 AM instead

• Giant cell arteritis: What everyone knows….

• Elderly patient (often female)

• Acute onset headache, jaw claudication, temporal artery pain, neck or ear pain

• Loss of vision (typically due to ischemic optic neuropathy)

• Elevated erythrocyte sedimentation rate (ESR) & C-reactive protein

• But….You should also know that it can be GCA if

• Transient double vision

• Any ophthalmoplegia in elderly

• Ask about GCA symptoms in diplopia in elderly patient

• Patients do not come in with the diagnosis written on their forehead (but sometimes they do)

• The artery on the side of my head hurts

• Delay in GCA diagnosis common

• Br J Rheumatol. 1997 Feb;36(2):251-4. Clinical features in patients with perma-nent visual loss due to biopsy-proven giant cell arteritis. Font et al.

• 146 biopsy + GCA

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• 23 (16%) lost vision

• GCA Sx for average of 1.3 months

• 35% PMR x 10.8 months

• 65% premonitory visual Sx for 8.5 days

• Clear delay in diagnosis in 65% (15)

• Giant cell arteritis can kill people….

• Aortitis

• Systemic vasculitis

• Crow et al. J Gerontol A Biol Sci Med Sci 2009.

• Mortality in GCA: 5-year survival: 67% for controls vs 35% for GCA cases (p < .001)

• Holiday Headache

• 22 y/o woman

• Severe headache

• New diplopia (partial third)

• 20/50? Effort (blurred vision)

• Fundus normal OU

• HVF: “unreliable”

• Thursday 4:45 PM

• Perform a confrontation field

• Beware acute bitemporal field loss

• “Unreliable HVF” = “I have no visual field on this patient!”

• Life threatening diagnosis?

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• Pituitary tumors common

• Incidence of pituitary tumors = 7 per 100K population per year

• As high as 1 in 500 > 65 years

• “The average ophthalmologist should see about one pituitary tumor per year….are you missing your quota?” ----B. Katz MD

• Pituitary apoplexy

• Acute onset

• Usually severe headache

• Bitemporal hemianopsia

• Apoplexy can kill (8%)

• Hypopituitarism (cortisol)

• Emergent scan

• Pituitary apoplexy

• Semple et al. Neurosurgery. 56(1):65-73, 2005.

• 62 patients (Average age 51.1 years)

• Average time presentation: 14 days after ictus

• 81% no previous history of pituitary tumor

• Headache (87%) with diminished visual acuity in 56% (bitemporal hemianopia 34%)

• 73% hypopituitarism; 8% diabetes insipidus

• Acute ophthalmoplegia in a diabetic

• 35 y/o WM with diabetes

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• History of diabetic ketoacidosis

• Complete left ptosis

• Acute onset almost complete left sided ophthalmoplegia

• What should be the evaluation?

• Life threatening diagnosis?

• Cavernous sinus lives close to other structures

• How could a fungal orbital apex lesion be missed on MRI?

• Need contrast to see enhancement

• Fungi are dark on MRI

• No fat suppression can miss lesion

• Super-dangerous because tempting to give steroids to…

• Presumed retrobulbar optic neuritis

• Presumed Tolosa Hunt syndrome

• Aspergillosis of orbital apex

• Complementary roles for CT & MR in fungal orbital apex disease (T2 dark)

• What’s wrong with this picture?

• 60 y/o diabetic man

• New onset ptosis right

• Right adduction, elevation, & depression deficit

• 45 exotropia (XT)

• Diagnosis: “Ischemic third nerve palsy”

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• Plan: “Return 6 weeks”

• Tell your technicians….

• If the patient’s complaint is diplopia or ptosis or….

• If you have to lift a ptotic lid to put in the dilating drops then….

• STOP, come get the doctor before dilating

• Acute pupil involved third n. palsyLife threatening diagnosis?

• Rule of the pupil

• A pupil involved third nerve palsy

• Aneurysm of posterior communicating artery until proven otherwise

• Endovascular treatment

• Highest stakes encounter an eye doctor will see

• Choice of imaging strategy in third nerve palsy

• CT/CTA first to look for SAH/aneurysm in pupil involved third nerve palsy

• MRI/MRA first to look for non-aneurysmal etiologies or do MRI second if CTA nega-tive first

• Catheter angiography if MRI/MRA and CTA not of sufficient quality or insufficient confidence level to rule out aneurysm

• Vertebral dissection & top of the basilar syndrome

• Acute onset homonymous hemianopsia

• Acute onset bilateral progressive ophthalmoplegia

• Paresthesias or paralysis (top of basilar)

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• Initial structural MRI may be normal but DWI might show evolving acute infarct

• May be spontaneous dissection: no trauma

• Dissection can propagate or embolize

• Vertebral artery dissection

• Top of the basilar syndrome

• Bottom line: Its your job

• Lee’s P’s

• Pain (severe, worst of life) in elderly

• Perception loss

• Pupil involvement

• Progressive proptosis

• Paresthesias or paralysis

• Danica J. Marelli, O.D.

• Case 1: 46yo WF

• CC: headache, droopy RUL x 2 days

• POH: unremarkable

• PMH: unremarkable, last physical exam 6 months ago (rou-tine)

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• Meds: Multivitamin

• All: None

• Exam Findings:

• BVA: 20/20 OD, OS

• CVF: FTFC OD, OS

• External Exam & Pupils: See photo

• Questions:

• What is your working diagnosis?

• What diagnostic tests do you need to perform?

• Discussion:

• Sympathetic innervation to the eye: a review

• Horners Syndrome: clinical picture

• Horners Syndrome: pharmacologic testingo Confirmatory testingo Differentiating pre- from post- ganglionic Hornerso Apraclonidine: benefits & pitfalls

• Post-ganglionic Horners: What’s next?

Andrew G. Lee, M.D.Unexplained visual loss in children & adults:

7 easy steps to finding the cause9

• Insure visual loss = actual chief complaint

• Complete eye exam every time (no shortcuts)

• Special effort to detect subtle causes of visual loss

• Formal visual field if unexplained symptoms

• Special tests (e.g., MERG, OCT, fluorescein angiography, neuroimaging if indicated)

• Rule out optic neuropathy or hemianopsia

• Rule out ORGANIC and prove non-organic BEFORE labeling someone as such

• Step 1: Chief complaint = “blurred vision” is not sufficient!

• What do you mean by blurred?

• One eye or both?

• Central or side vision or both?

• Double vision?

• Jumping eyes? (nystagmus)

• Processing of visual information?

• “Blurred vision” may not mean loss of vision (afferent disease)

• Double vision

• Is it double vision?

• Is it monocular or binocular (cover one eye)

• Nystagmus (oscillopsia)

• Is it jumping or moving?

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• Visual processing

• Agnosias (e.g., prosopagnosia, simultagnosia)

• Visual variant of Alzheimer’s disease

• Step 2: Complete eye exam

• By complete I mean….complete (don’t use short cuts in your neuro-op patients!)

• Check relative afferent pupillary defect yourself

• Check color vision & visual field

• Ophthalmoscopy

• High magnification & high clinical suspicion

• Don’t take the shortcut

• M ain Causes For No APD In Unilateral Visual Loss

• M acular disease (e.g. macular hole)

• M edia (cataract, refractive)

• M aking it up (non-organic)

• M issed it (look again!)

• *Bilateral optic neuropathy & retrogeniculate etiologies = normal pupil

• Complete eye exam

• Slit lamp biomicroscopy

• Look after dilation

• Beware oil droplet cataract

• Look for posterior subcapsular cataract

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• Match lens opacity to visual acuity

• Retroillumination

• Look at lens & grade opacities (“NSC/PSC = 20/30” or ≠ “20/30”)

• Step 3: Rule out things you don’t want to end up sending to your neuro-ophthalmologist

• Oil droplet cataract or subtle posterior subcapsular cataract

• Refractive error, keratoconus

• Epiretinal membrane, cystoid macular edema, macular hole, geographic atrophy of retinal pigment epithelium

• Most common etiologies Unexplained anterior segment visual loss in adults

• Mild PSC

• Keratoconus

• Irregular astigmatism

• Use retinoscope & direct (view “in = out”)

• Use the pinhole (also best corrected vision)

• Consider keratometry or topography

• Most common etiologies for unexplained visual loss in a kid

• Uncorrected refractive error

• Unrecognized amblyopia

• Nonorganic overlay

• Poor cooperation

• Incomplete examination

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• Special toys

• Step 4: Formal visual field

• “Unreliable” visual field is the same information as NO visual field per-formed

• Confrontation visual field = minimum

• Media & refractive etiologies rarely produce field defects

• Any respect of vertical meridian significant

• Common errors in evaluation children

• Failure to perform a visual field

• Settling for an “unreliable” automated perimetry as your only visual field

• Failure to complete the exam because of “poor cooperation”

• Assuming that sullen is evidence for non-organic etiology (sullen is nor-mal teen behavior)

• Full Eight Point Exam

• Formal visual field (even if 20/20)

• Homonymous & bitemporal hemianopsia may have 20/20 acuity

• Retrochiasmal disease will have NORMAL structural eye exam (no RAPD, no optic atrophy)

• Normal eye exam does not r/o pathology

• Look At The Macula

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• Subtle macular lesions can be missed without high magnification and high suspicion (e.g. macular hole, cystoid macular edema)

• “WNL” should mean “within normal limits” NOT “WE NEVER LOOKED’

• Most Commonly Missed Posterior Segment Etiologies For Visual Loss

• Epiretinal membrane

• Cystoid macular edema

• Samll macular hole

• Subtle serous retinal detachment

• Retrobulbar optic neuropathy

• Diagnosis and Plan From The Retina Service

• IMPRESSION ‘NOT RETINA’

• PLAN

• “REFER TO NEURO-OPHTHALMOLOGY

• OCT in unexplained visual loss

• Measurement of retinal nerve fiber layer (RNFL)

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• Measurement of retinal thickness

• Detection of subtle macular pathology

• Old relationship with medical retina in organic appearing unexplained visual loss

• Look really hard at macula

• Hallucinate macular pathology

• Do macular photostress test

• Scratch head

• Do a fluorescein angiogram

• Call in medical retina specialist

• Scratch heads together

• OCT in Unexplained visual lossIs it retina or optic nerve?

• Macular edema or macular hole

• Epiretinal membrane

• Cystoid macular edema or subretinal fluid

• Vitreous traction on macula or optic nerve

• OCT can see better than me

• Visual field defect

• OCT: Macula fast scan

• New paradigm

• Macular OCT

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• If OCT sees no pathology then I don’t bother with medical retina consult

• If OCT is normal but seems retinal then still consider fluorescein an-giogram (OCT can not see perfusion)

• OCT has reduced # of fluorescein angiograms that we perform for unex-plained visual loss by 75% or more

• OCT vs. FFA

• Boston VA acquired OCT system in September 2004

• Retrospective review (n =1102)

• Macular edema or age-related macular degeneration (AMD)

• OCT vs. FFA

• Before OCT, 411 FAs (n=314): $297,498

• After OCT: $325,695 (336 FAs at $243,210, 356 OCTs at $82,485)

• 3 adverse events occurred with FAs (0.73), at a cost of $688 per 100 pa-tients

• Purchase price recovered after 4 months

• Bottom line

• OCT shows macula at micron level

• OCT sees better than me even with a contact lens or high magnification with high suspicion

• OCT has replaced fluorescein as my first ancillary test of choice for structural macular pathology

• Fluorescein still useful for perfusion (OCT can not see macular ischemia or show leakage)

• Step 5: Special techniques: OCT

• OCT helpful in unexplained visual loss16

• “Poor man’s neuro-ophthalmology consult”

• “? Mild temporal pallor” if normal visual field, normal OCT, normal acuity then likely physiologic pallor

• “Poor man’s” medical retina consult

• “Poor man’s” glaucoma consult

• Is this nerve pale? Mild pallor? Temporal pallor? Optic atrophy?

• OCT can see better than me

• Am I pale?

• Consider Ancillary Testing

• Fluorescein angiography/OCT

• If I see something funny in the macula

• Electrophysiology if it “smells like retina”

• Big blind spot with normal peripapillary retina

• Ring scotomas

• Photopsias

• Diffuse retinal arteriolar narrowing

• Unexplained visual loss

• 60 y/o WF with painless progressive loss of vision bilaterally for 3 weeks

• “Swirling and flashing lights”, night blind

• Exam 20/40 OD and 20/50 OS

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• Mild vitritis OU

• Retinal vascular attenuation

• Optic atrophy OU

• Cancer associated retinopathy

• Small cell carcinoma of the lung (90%)

• Breast CA, GYN CA, non small cell lung CA, lymphoma

• Retinal antibodies (e.g., 23 kD recoverin)

• Multifocal Electroretinogram(MERG )

• Focal electrical response of photorecepters and bipolar cells

• Does not detect ganglion cell or axonal response (at present)

• Step 6: Rule out optic neuropathy

• Look for subtle signs of optic neuropathy

• Decreased color vision

• Relative afferent pupillary defect

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• OCT abnormal

• Mild disc pallor or disc edema

• Abnormal visual field

• If you miss a non-optic nerve cause for visual loss (PSC, ERM, refrac-tive) it is no big deal

• If you miss an optic neuropathy it could be a big deal (compressive optic neuropathy)

• Step 7: Prove non-organic before labeling patient non-organic

• Non-organic = preferred term

• Outdated terms or terms which imply psychologic motivation (hysterical, malingerer)

• Do you really know they are faking?

• Do you know their motivation?

• They might be organic with overlay!

• Cases

• 75 y/o WF from the “Psych” ward x 2 wks

• Acute onset visual loss OU

• HM acuity OU

• Pupils reactive and no RAPD

• Ophthalmology found a normal eye exam

• Fundus WNL OU

• Visual field “unreliable”

• Sometimes she says she can see: “You are wearing a white coat, doc-tor.”

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• She denied she was blind: “I can see, of course I can see”

• Visual Loss OU

• MRI: Bilateral occipital infarcts

• Pupil & fundus normal in cortical loss

• Bilateral and symmetric visual loss

• “Unreliable” visual field is not same thing as a NORMAL visual field

• Anton syndrome: Cortically blind patients may confabulate or deny they are blind!

• WE ONLY SEE WHAT WE LOOK FOR. WE LOOK FOR ONLY WHAT WE KNOW

• GOETHE

• A warning….

• You find a cataract (good)

• You take out cataract (great)

• Perfect case & you tell patient so (awesome)…They think you are a great doctor

• Vision does not improve post op (bad)

• Now you notice optic atrophy (worse)…& RAPD, & VF defect….(Hmmm was that there before?)

• Now you have to explain to patient why they need an MRI & neuro-op consult (very bad)…We find a tumor..they think you are really bad doc-tor

• Versus exact same scenario but….

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• Pre-Op: “I think that you have a cataract but if it doesn’t improve your vi-sion there are other things we have to consider including a specialist consult but it is reasonable to start here.” (10 seconds extra time)

• Post-op: “Your vision didn’t improve as much as I would like after surgery remember when we talked about possibly needing to look harder. I am referring you to Dr. X and ordering an MRI”

• A tumor is found…Patient: “Thanks a lot doc, you saved me, you are a great doctor

• Most Common Errors In Unexplained Visual Loss

• Failure to check for RAPD

• Failure to perform a formal visual field

• Failure to perform a confrontation field in an unreliable formal field pa-tient

• Failure to get best corrected vision (contact lens, over-refraction, retinoscopy)

• Jumping to conclusions = non-organic

• Seven steps in unexplained visual loss

• Insure visual loss = actual chief complaint

• Complete eye exam every time (no shortcuts)

• Special effort to detect subtle causes of visual loss

• Formal visual field if unexplained symptoms

• Special tests (e.g., MERG, OCT, fluorescein angiography, neuroimaging if indicated)

• Rule out optic neuropathy or hemianopsia

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• Rule out ORGANIC and prove non-organic BEFORE labeling someone as such

Hysteria and MalingeringRobert P. Wooldridge, O.D.

• Hysteria

• Mental disorder that impairs physical functions with no physiological ba-sis; sensory motor symptoms include seizures, paralysis, temporary blindness; increase in stress or avoidance of unpleasant responsibilities may precipitate

• Subconscious response

• Patient believes he/she has a real problem

• But may have something to gain

• Malingering

• Conscious attempt to deceive for personal gain

• Functional Overlay

• Patient has a true organic disease/problem

• But also has a functional component

• The Usual Suspects

• Hysteria:

• Young: 9-13yo most common

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• Adults possible

• Female>>>>>>Male

• Malingering

• Late teens to adults

• Common Complaints

• Loss of Vision

• Monocular or binocular

• Central or peripheral

• Usually sudden in onset

• Can be dated/connected to an event

• Sometimes vague, uncertain

• Hints of Hysteria

• Reads every line at same slooooow speed, letter by letter

• Ambulates well despite C/O severe LOV

• Severely constricted CVF

• NO APD despite severe unilateral LOV

• Diagnostic Steps

• Careful history

• Refraction

• Full examination

• Stereo

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• CT

• PUPILS!

• Visual Field-Never make a diagnosis without it!

• DFE

• Loss of vision

• 1. Refractive error

• 2. Media opacity

• 3. Macula

• 4. Optic nerve

• 5. Amblyopia-there has to be a cause!

• 6. Hysteria/malingering

• Amblyopia v. Hysteria

• History of poor VA?

• Prior eye exams? (get records)

• Have you ever been 20/20?

• Must have a reason to have amblyopia

• Strabismus

• Refractive

• Obscuration

• NLP Loss of Vision Tricks

• Optokinetic drum

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• Measuring tape, ruler

• Mirror: eye tracking

• 20/50 to 20/400

• Refraction with slow, patient VA

• Telescopic lens suggestion

• Polaroid slide with OU open

• Telescopic lens

• Cyclopleged

• Close OU

• Spin every dial while saying:

• I am putting in a very strong telescopic lens

• *If there is anything wrong, this lens will make you see well*

• Isolated lines; Start at 20/10

• Move up chart slowly

• Lots of positive encouragement be patient for each letter

• Confrontation VF

• Perform at normal two feet

• Again across room

• If cylindrical (tubular), not physiologic

• Mimic finger motions in areas of “blindness”

• Goldmann VF/ Tangent Screen

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• Spiraling isopters

• Inversion of isopters

• Management

• Discuss with parent alone

• Some attempt to determine reason for childs response

• Assure child of healthy eyes

• Give child a way to get better

• Drops

• Glasses

• Voodoo magic

• Parent to reinforce positive feedback

• Billing Coding

• 300.11 Conversion disorder

• Hysterical blindness, deafness, paralysis

• Def.: Mental disorder that impairs physical functions with no physiologi-cal basis; sensory motor symptoms include seizures, paralysis, tempo-rary blindness; increase in stress or avoidance of unpleasant responsi-bilities may precipitate

• Marrelli:

• Case 2: 21 yo WM

• CC: Horizontal diplopia x 3 days

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• HPI: no pain, no headache, no pupil problems

• POH: unremarkable

• PMH: unremarkable

• FH: unknown

• Meds: None

• Exam Findings: See EOMS

• Questions:

• What is the problem with motility?

• Where is the lesion?

• What is the most likely etiology given the patient’s age & health status

• Discussion:

• What is the Clinically Isolated Syndrome?

• What should we do about patients with CIS?

• What is the current thought on treatment of CIS?

Robert P. Wooldridge,O.D.Transient Monocular Loss of Vision

• Carol W

• 68 yo WF

• H/O blow out Fx OS 1992

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• Repaired; asymptomatic

• S/P Phaco/IOL OU 2007

• MH: HTN, dyslipidemia, S/P PFO closure, pacemaker, acid reflux, osteopenia

• Allergies: sulfa,cipro, hydrocodone, Percocet, Lortab, Tramadol, Flagyl, Morphine

• 12/13/07

• Routine postop visit

• Notes two episodes of dinner plate-sized blurry area with jagged edges OS

• Pain OS a few times a week

• VA 20/20 OU

• Ant seg, DFE normal

• Dx: Migraine with aura

• 2/08/08

• Routine po visit

• C/o irritation/mild pain OS

• VA 20/20 OU

• Pupils/motility NL

• SLE, DFE normal

• VF as seen

• 2/28/08 RPW exam

• C/o pain OS-dull ache since phaco 4 mos. ago

• Never had pain prior to surgery

• Nothing makes pain better or worse

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• No pain on movement

• 4 episodes of transient LOV x 20 mins.- believes OS only

• central scotoma increases in size with jagged edges

• No subsequent HA, nausea, or other symptoms

• No H/O migraines in past

• Exam

• VA 20/15 OU

• SLE: Ant. Seg normal

• IOP 13 OU

• DFE: Normal OU

• VF: Repeat necessary?

• What is Your Impression?

• 1. Ophthalmic migraine

• 2. Pain related to old orbital Fx

• 3. Retrobulbar optic neuritis

• 4. Temporal arteritis

• What is Your Plan?

• 1. Refer to PCP or neurologist for migraine Rx

• 2. CT scan orbits

• 3. CBC/ESR/CRP

• 4. MRI brain

• Impression/Plan

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• 1. Pain OS- no apparent cause

• 2. Transient LOV OS

• Plan:

• 1. PF qid, Xibrom bid OS

• 2. CBC, ESR, CRP, CMP

• 3. Doppler U/s carotids

• 4. Cardiovascular exam by cardiologist

• With echo with bubble

• 5. Already on ASA

• 6. Cover each eye during episode to confirm laterality

• Follow-up

• 1. CBC, ESR, CRP, CMP normal

• 2. Echocardiogram reveals ASD-atrial septal defect

• 3. Doppler U/S carotids: + plauque

• 4. Reports plaque “behind eye”

• Cardiologist rx’es Plavix, ACE inhibitor, statin, Coreg

• No additional episodes

• Transient Monocular Blindness

• Acute, transient LOV in one eye

• Ascending or descending curtain or total LOV

• Lasts seconds to minutes

• Complete recovery

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• Possible Causes

• Transient retinal ischemia

• Embolus, arteritis

• Impaired retinal perfusion

• Carotid artery stenosis

• Onset over 5 minutes

• Lasts minutes to hours

• Slow to recover

• Temporary vasospasm

• Constriction of retinal vessels

• Diagnosis of exclusion!

• Plan

• 1. Rx: one ASA qd

• 2. CBC, ESR, CRP, stat

• CMP, lipid profile, fasting glucose

• PT (prothrombin time), PTT (partial thromboplastin time),

• Protein C, Protein S

• 3. Doppler US of carotids

• 4. Echocardiogram

• R/O source of emboli

• R/O PFO (patent foramen ovale)

• 5.+/- MRI/MRA

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• Steps in Determination

• Onset

• Sudden

• Laterality

• Monocular v. Binocular

• Unilateral v Bilateral

• Difficult to determine

• Did patient cover one eye to check?

• Hemianoptic VF loss

• Characteristics Indicating True Transient LOV

• Inability to read

• Vision loss restricted to hemisphere

• Presence of slowly expanding scotoma or scintillation

• Accompanying neurologic symptoms suggesting hemispheric brain dysfunction

• Etiology

• Ischemic

• Usually embolus from carotid artery

• Aortic arch or heart secondary possible sources

• Ocular vasospasm

• Systemic hypotension

• Arteritis pailledema (rare)

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• Hyperviscous/hypercoagulable state (rare)

•• Binocular Transient LOV Causes

• Migraine (most common)

• Ischemia

• Seizure

• Migraine

• Scintillations (80%)

• Fortifications (20%0

• March(20%)

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