Neuro-Op Flashcards
• Lesion of CNVI nucleus
will give you an ipsilateral gaze palsy in both eyes and almost always an ipsilateral CN VII palsy.
• Wallenberg syndrome
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.
• To dampen nystagmus with prism:
orient apices TOWARDS the null point (if doing strab surgery you would rotate the eyes away from the null point
• Causes of light-near dissociation:
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).
• Raymond syndrome
CN6 palsy with contralateral hemiparesis (mid poins lesion) and corticospinal tract lesion
• Weber syndrome
CN 3 palsy with contralateral hemiparesis (midbrain lesion)
• Benedikt syndrome
midbrain lesion involving the CN3 nucleus and the red nucleus. Causes an ipsilateral CN 3 palsy and contralateral tremor.
• Claude syndrome
dorsal midbrain lesion which results in ipsilateral CN3 palsy with contralateral ataxia (damage to the superior cerebellar peduncle and 3rd nerve fasciculus)
• Millard-Gubler syndrome
ventral pons lesion which causes ipsilateral facial weakness, ipsilateral abduction deficit and contralateral spastic hemiplegia
• DDx of chronic toxic optic neuropathy
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.
• Dominant optic atrophy
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
• CN 3 nucleus
rostral midbrain causes ipsilateral mydriasis, ipsilateral MR, IR and IO involvement; bilateral levator involvement and contralateral SR involvement.
• For MS
do NOT use infliximab (works on TNF alpha)
• Hydroxyamphetamine testing
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
• Downbeat nystagmus
suggest cervicomedullary junction issue (ie chiari malformation, cerebellar flocculus)
• See-saw nystagmus
suggests parasellar pathology (ie craniopharyngioma)
• Opsoclonus
suggests neuroblastoma, usually from the adrenals
• Periodic alternating nystagmus
suggests issue at cerciomedulary junction, cerebellar nodulus
• Upbeat nystagmus
suggests pathology at cerebellum, medulla, midbrain
• Morning glory disc anomaly
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)
• Parinaud syndrome
sxs of dorsal midbrain syndrome—paralysis of upgaze, defective voluntary convergence, light-near dissociation, convergence retraction “nystagmus”, eyelid retraction (collier’s sign).
• Susac syndrome
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
• Balint syndrome
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
