export_neuroanatomy Flashcards
Occulomotor
CN III 1. edinger-westphal nucleus - GVE - pupillary light reflex 2. oculomotor nucleus - GSE located in the cerebral peduncles supplies many of the eye muscles (except superior obi and lat rectus)
Occulomotor anatomy
_parasympathetic outside, muscle nerves inside -emerges from stem between posterior cerebral and runs under PCOM
Trochlear anatomy and what happens if lesion
superior oblique; only one that decussates and dorsal aspect of brainstem Damage=vertical diplopia; compensate by tilting to unaffected side. can happen from facial trauma
Abducens
-Lateral rectus -Without cannot abduct; have diplopia - Can be damaged by ^ICP - When damaged in BStem lesion can cause facial weakness (bc of facial nucleus that it goes around)
cavernous sinus
* watershed where venous blood drains * lateral wall: CN III, IV, V 1 , V 2 * Internal Carotid * CN VI (Abducens) floating unprotected in the middle, more prone to intracranial pressure damage
NF-I
Chromosome 17 *Glioma & ependymoma Bone abnormalities, Optic Nerve Tumors, lisch nodules, learning disabilities, {large head, short stature, cafe au laid spots}
NF-II
- Ch22q12 -meningioma & glioma * Bilateral 8th nerve masses 1st degree relative with u/l 8th nerve masses or relative with at least 2 of the following: meningioma, glioma, schwannoma, juvenile cataract
VonHippel-Lindau
3p25 AD genetics CNS, retinal *hemangioblastomas, *cc renal carcinoma, pheocytochroma, pancreatic neuroendocrine tumors, pancreatic cysts, endolymphic sac tumors, epididymal papillary cystadenomas.
Li-Fraumeni family cancer syndrome
* Develop tumors while young and in multiple organs * 50% develop cancer by age 30 and 90% by age 70 * have inherited a germ-line p53 mutation (all cells have one mutant p53 allele * just one cell needs to mutate the second p53 allele and cancer develops
Tolosa Hunt Syndrome
Idiopathic granulomatous disease of the cavernous sinus
Pineal Gland
-tumor- Germinomas> pinealoma -Usually silent until affect midbrain causing visual defects (esp upgaze, same as in PSP)
Frontal Eye fields
-Direct saccades to the contralateral side -Stroke- deviation ipsis; seizure, deviation contra
Horner’s Syndrome
-Ptosis, miosis, anhydrosis -Lesion in sympathetic pathway -Common in carotid dissection or vertebral atery dissection ( Wallenburg syndrome)
Miosis
Sympathetic problem; if pupils are too dilated, parasympathetic problem ( CNIII)
Internuclear Ophthalmoplegia
lesion of the MLF; problem adducting one eye and abducting nystagmus in other -Common in MS
MLF
Connects CNIII in midbrain to contralateral CNVI in pons –> conjugate gaze
Optic Neuritis and treatment
-Blurry vision, pain, often subtle color (red) loss - IV steroids ( ie salumedrol) to delay occurrence of 2ndary demyelination; 3 days with oral taper _Severe relapse–> plasmapheresis
Marcus Gunn Pupil
-Afferent pupillary defect (APD) -same size pupils, defected one dilates with light; normal consensual is preserved
MS-imaging
-lesions-classic, enhancing new lesions; classic Dawson’s fingers (periventricular white matter lesions) -Old lesions = “black holes” -Atrophy - Spinal cord lesions cause more disability
MS signs
-Uhthoff’s phenomena: worse with heat - Lhermitte’s- worse with bending neck (cervical spinal cord pathology)
MS
-demyelinating -Low Vit D/EBV -Genetic -F:M (3:1)
MS Presentation
-Optic neuritis, sensory deficits, weakness, diplopia, ataxia; not common for psych problems/aphasia
MS prognosis
good: white race, female gender, younger age, sensory symptoms at onset, full recovery from initial attack, fewer relapses in the years after diagnosis, and fewer lesions on baseline MRI. Note that patients diagnosed at a younger age reach disability milestones at an earlier age, however.
Diagnosis of MS
Diagnosis depends on having two attacks with clinical evidence or supportive evidence including typical MRI or oligoclonal bands in the CSF. Oligoclonal bands are immunoglobulin patterns seen in the CSF of 90% of MS patients. They can be seen in a variety of other inflammatory disorders.