Neuro-Op

Question 1

• Lesion of CNVI nucleus

Answer 1

will give you an ipsilateral gaze palsy in both eyes and almost always an ipsilateral CN VII palsy.

Question 2

• Wallenberg syndrome

Answer 2

dorsolateral medullary syndrome) loss of pain and tempo on contralateral side of body and ipsilateral side of face; ipsilateral horners syndrome, ipsilateral ataxia, +/- nystagmus, vertigo, diplopia, hiccups, skew deviation.

Question 3

• To dampen nystagmus with prism:

Answer 3

orient apices TOWARDS the null point (if doing strab surgery you would rotate the eyes away from the null point

Question 4

• Causes of light-near dissociation:

Answer 4

vision loss from severe retina or optic nerve disease, neurosyphilis, adies tonic pupils, parinoud’s (or dorsal midbrain) syndrome (a disruption of light input to the Edinger-Westphal nucleus in the dorsal midbrain, usually compressive, ie mass or hydrocephalus).

Question 5

• Raymond syndrome

Answer 5

CN6 palsy with contralateral hemiparesis (mid poins lesion) and corticospinal tract lesion

Question 6

• Weber syndrome

Answer 6

CN 3 palsy with contralateral hemiparesis (midbrain lesion)

Question 7

• Benedikt syndrome

Answer 7

midbrain lesion involving the CN3 nucleus and the red nucleus. Causes an ipsilateral CN 3 palsy and contralateral tremor.

Question 8

• Claude syndrome

Answer 8

dorsal midbrain lesion which results in ipsilateral CN3 palsy with contralateral ataxia (damage to the superior cerebellar peduncle and 3rd nerve fasciculus)

Question 9

• Millard-Gubler syndrome

Answer 9

ventral pons lesion which causes ipsilateral facial weakness, ipsilateral abduction deficit and contralateral spastic hemiplegia

Question 10

• DDx of chronic toxic optic neuropathy

Answer 10

ethambutol, ethanol, chloramphenicol, hydroxyquinolone, penicillamine, cisplatin, vincristine. Immediate onset: methanol or ethylene glycol toxicity—causes acute diffuse and devastating vision loss with associated disc edema.

Question 11

• Dominant optic atrophy

Answer 11

also called Kjer optic atrophy. Associated with temporal pallor with area of triangular excavation. Characterized by slow loss of vision. Autosomal dominant, blue-yellow (tritan) dyschromatopsia, mild to moderate vision loss (20/40 – 20/200); OPA1 gene

Question 12

• CN 3 nucleus

Answer 12

rostral midbrain causes ipsilateral mydriasis, ipsilateral MR, IR and IO involvement; bilateral levator involvement and contralateral SR involvement.

Question 13

• For MS

Answer 13

do NOT use infliximab (works on TNF alpha)

Question 14

• Hydroxyamphetamine testing

Answer 14

unlike cocaine testing, it hydroxyamphetamine causes a forced release of norepinephrine from both sides so if not a 3rd order horner’s both sides will dilate

Question 15

• Downbeat nystagmus

Answer 15

suggest cervicomedullary junction issue (ie chiari malformation, cerebellar flocculus)

Question 16

• See-saw nystagmus

Answer 16

suggests parasellar pathology (ie craniopharyngioma)

Question 17

• Opsoclonus

Answer 17

suggests neuroblastoma, usually from the adrenals

Question 18

• Periodic alternating nystagmus

Answer 18

suggests issue at cerciomedulary junction, cerebellar nodulus

Question 19

• Upbeat nystagmus

Answer 19

suggests pathology at cerebellum, medulla, midbrain

Question 20

• Morning glory disc anomaly

Answer 20

congenital, usually unilateral, more common in females. Usually poor vision and APD. Associations include serous RDs, occult transsphenoidal basal encephalocoeles, Moya moya disase (get MRI/MRA)

Question 21

• Parinaud syndrome

Answer 21

sxs of dorsal midbrain syndrome—paralysis of upgaze, defective voluntary convergence, light-near dissociation, convergence retraction “nystagmus”, eyelid retraction (collier’s sign).

Question 22

• Susac syndrome

Answer 22

triad of BRAO, bilateral hearing loss and encephalopathy. F>M (3:1). Young adults (20-40), hypothesized to be immune mediated. Treatment starts with methylprednisolone. After 1 month of pred can try IVIG, cyclosporine, MTX, cyclophosphamide

Question 23

• Balint syndrome

Answer 23

bilateral parieto-occipital dysfunction. Classic triad includes optic ataxia, acquired oculoar motor apraxia and simultagnosia (rarely all 3). Optic ataxia is poor hand eye coordination. Ocular apraxia is difficulty initiating saccades. Simultagnosia is failure to understand the whole meaning of the picture, despite understanding its parts (ie, cookie thief picture). For example, you may see difficulty identifying the actual numbers on the ishihara plates, although you may recognize the colors