Neuro-ophthalmologic Examination of the Neurosurgical Patients

Amgad Hanna, MD and Peter Savino, MD Departments of Neurosurgery and Ophthalmology Thomas Jefferson University December 2005 Agenda

• Abnormal pupils: miosis and mydriasis • Trochlear N palsy • Fundi: NL and abnormal Abnormal pupils Miosis

Not all constricted pupils are caused by carotid dissection V1

Postganglionic (3rd order) Horner’s

Long Cil Nn Central (1st order) Horner’s

Preganglionic (2nd order) Horner’s Causes of Horner’s Syndrome (usually have associated signs and symptoms) Cocaine

NO Mydriasis response NE NE Blocks reuptake NE NE Of NE (90%) NO NE outside vesicles

True Pseudo-Horner’s Horner’s (physiologic anisocoria) (MRI/A H/N – CT Chest) True Horner’s Hydroxyamphetamine test

No response Mydriasis

NE NE Release of NE from No NE NE NE inside vesicles synaptic vesicles NE

Postganglionic Central or Horner’s Preganglionic Horner’s Physiologic Anisocoria Central or Preganglionic R Horner’s Postganglionic R Horner’s Case

• 40 y/o Woman • C/O R swollen eyelid and H/A Upper lid (Muller’s m), lower lid (Lid retractis) Dim Light

Post-Cocaine; True Horner’s Post-Hydroxyamphetamine; Postganglionic Horner’s Carotid Dissection Mydriasis

Not all dilated pupils are caused by P Com aneurysms Parasympathetic and light reflex

Posterior commissure

III

Inf div Short Cil Nn N to inf obl Physiologic anisocoria

• Normal reaction to light • The size difference between both eyes remains the same with dim and bright light • 0.3 – 0.4 mm difference found in 50% of the normal population • Up to 1.5 mm difference could be normal Adie’s Syndrome

• 20-50 y/o • Women 70% • Parasympathetic denervation supersensitivity • Constricts with 1/8% Pilocarpine R Adie’s Pupil R Adie’s Pupil

Near (accomodation)

Light 1/8% Pilocarpine Cholinergic Blockade (Eye Drops) EOMI – No assoc features of III palsy – No consens reaction to light Very Large, No direct response to light – not physiologic 1/8% Pilocarpine – Not Adie’s pupil 1% Pilocarpine – Pharmacologic pupil R Third Nerve Palsy

Diabetic Third Nerve Palsy

Parasympathetic fibers are superficial: supero- medial Ptosis in Horner’s Syndrome (Muller’s muscle)

R Ptosis (Levator Palpebrae Superioris-III) R mydriasis - III R Lateral Rectus - VI R med rectus - III R Sup Rectus – III R Inferior Rectus - III , R SO (no intorsion) - IV

Trochlear Nerve Palsy Anatomy SC III V2 IC V1 IV

C A SCP

CS SO III

IV T SCA PCA

B C D IV EOM Function Testing for RSO palsy

R Hypertropia With L gaze, the R eye is adducted, thus disabling the inferior rectus, leaving the eye to the unopposed elevation action of the inferior oblique With R head tilt, the external With L head tilt, the internal rotation of the R orbit is rotation of the R orbit is balanced by intorsion of the R balanced by extorsion of the R eye by the SO (intorsion & eye by the IO and IR. The IR depression) and the SR action (depression) compensates (intorsion & elevation). for the loss of the SO. R IV palsy Primary Gaze

RSO LIO RIR LSR

R eye hypertropic LSR RSO L Head Tilt Improves R Head Tilt Worse

RSO (intorting) IV nerve palsy Fundi

I can’t see anything in the fundus

• Check the red reflex Cup – nonspecific; 0 – 0.9 Spontaneous venous pulsations

Sharp edges

NL

Nerve fibre layer Pigment epith

Choroidal vessels Acute papilledema NL

Peripapillary nerve fiber layer H/ges

Opacification of peripapillary nerve fiber layer causing blurry disc margins

Disc elevation causing tortuous vessels Early papilledema NL

Disc hyperemia; due to engorgement Opacification of peripapillary nerve fiber layer causing of disc capillaries blurry disc margins; due to axonal swelling and Lost venous pulsations degeneration, and some interstitial edema Chronic Papilledema

(Pseudodrusen) NL

Crystalline deposits covering the vessels, shunt vessels (arrow) Drusen (Pseudopapilledema)

NL

Drusen (pseudopapilledema): hyaline deposits and Chr Papilledema calcification in the disc deep to the arteries – loss of nerve (Pseudodrusen) fiber layer; vessels appear in good focus Postpapilledema atrophy

NL

Disc pale and flat (Dd) Case

• 52 year old woman • Decreased vision R>L for 3 months • Unable to read for 1 month • Height 5’5’’ weight 225 lbs •PMH – Diabetes Mellitus – Hypertension • Medications – Oral contraceptives – Oral hypoglycemics •O/E – VA: OD CF 1 ft, OS 20/70 –R APD B/L papilledema

Paton’s lines

Exudates MRI

T1 T1+C Case

• 33 y/o man presenting with decreased vision in the R eye • VA: OD 20/400, OS 20/25 OD OS Optic atrophy Papilledema Foster-Kennedy syndrome

HTN

NL

AV crossing

Narrow irregular arteries Ischemic

NL

Disc edema & pallor Cotton-wool infarcts H/ges Hollenhorst plaques (Cholesterol emboli) Giant C Arteritis

NL

Pale disc

H/ge Infarct Conclusion

• Neuro-ophthalmology is an important part of the exam of the neurosurgical patient • Exam should focus on the patient’s problem • Be mindful of the differential diagnosis even if the patient is transferred already “labeled”. Some benign conditions can mimic serious neurological or neurosurgical disease Aknowledgements

• Peter Savino, MD Professor of Neurology and Ophthalmology Will’s eye Hospital Thomas Jefferson University

• Molly Gilbert, MD Neuro-ophthalmology fellow Thomas Jefferson University Thank you