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.
MS course
-Remitting/relapsing (90% time)-> 2ndary progressive - Primary progressive (10%)
INF-b/Glatiramer Acetate
-INF:Avonex, Rebif, Betaseron -GA: capoxone -MS injection; flu-like SE
Tysabri (Natalizumab)
prevents t-cells from crossing BBB
Fingolimod (Gilyena)
-first oral med -prevents Tcell egress from LN -Bradycardia/macular edema
Aubagio (teriflunimode)
-2nd oral med -category x in pregnancy; Gi upset/reversible alopecia
Dimethyl Fumarate * (Tecfidera)
-3rd oral -Originally for psoriasis in Germany
Novantrone
-Only for 2ndary progressive form of illness -Chemo, possibility of cardiotox/leukemia
EDSS
- Disability in MS; sometimes underestimates morbidity b/c only way to get over 4 is by having ambulation problems
Neuromyelitis Optica
-Devic’s disease -De-myelinating, characterized by optic neuritis -Contiguous spinal cord lesion for 3 levels. -generally more severe than MS, F>>>>M; hispanics/AA’s -oral immunosupressants as tx -Intractable hiccups/n/v; (area postrema)
Trigeminal Neuralgia
-brief, shock like pain over V2, V3 region. Can be triggered by mild stimuli. -Often mistaken for dental disease -Tx: carbamazepine, & other antiepileptcs (phenytoin, neurontin), clonazepam, and baclofen - Artery or vein touching the trigeminal nerve root; ultimatemately sugary might be needed
Trigeminal Nerve
-sensory and muscles of mastication - pons,lower BS-> meckel’s cave-> TG ganglion
CNV-course
-After ganglion, splits into 3; bilateral somatic sensation to face -Afferent for corneal reflex
Bell’s Palsy and treatment
-Problem with CNVII; facial droop, increased sound, -TX: oral steroid/ antiviral ( acyclovir) against herpes virus. Protect Eye.
Ramsey-Hunt Syndrome
Herpes zoster infection of CNVII, CNVIII; painful rash in the ear canal and dysfunction of the affected nerves
CNVII and what diseases give b/l CN VII damage
-Muscles of facial expression; stepedius, submandibular/sublingual glands. taste from ant 2/3 of tongue - b/l nerve palsies commonly from lyme disease/sarcoidosis -
CNVII nucleus
-Nucleus in the pons -nuc/nerve itself lesion-ipsi facial droop - above the nucleus-> contra droop, superior face
CNVIII
-hearing is bilateral ; usually unilateral loss does not mean deafness -Damage to b/l auditory cortex= pure word deafness;its can hear, speak, and write but does not recognize spoken
Weber’s test
-Tuning fork on forehead -Louder with conductive hearing loss
Rinne’s Test
- Near ear and behind on bone -sensorineural loss with conduction better on air
components of 3 semicircular canals
-3 orthagonal canals -utricle- horizonatal -saccule-verticle *otoliths
Central Causes of Vertigo
-Migraine -MS -Mal de Debarquement Syndrome -Cerebellar hemorrhage and infarct - Vertebobasillar insuff - Vertebral artery dissection -Neoplasm
Meniere’s Disease
-Episodes of u/l hearing loss, sense of ear fullness, and episodes of vertigo - Pt’s may feel like they are thrown to the ground -cause:rupture of membranous labyrinth, endolymphic distention and death of hair cells in cochlea tx-salt restriction.diuretics
Benign positional vertigo
episodes of vertigo provoked by changes in head position–usually lying down on affected ear -> Dix0 Hallpike manever-help dix this -Epley maneuver-put metrical back into posterior semicircular canal
Ototoxic drugs
aspirin, aminoglycosides, (“-mycins”), loop diuretics (ie furosemide), cisplatin/carboplatin
Vestibular nueritis
-u/l vestibular dysfunction and may be associated with nausea, vomiting, and previous URI.
Labyrinthitis
-like vestibular neuritis but with hearing tinnitus
CNIX
-w/ CNX, innervates muscles of pharynx, larynx (nuc ambiguous) Lesion-> dysphagia, dysarthria - CNIX: taste post 1/3 tongue (tonsils, pharynx, middle ear, posterior 1.3 tongue)
CNX
-parasympathetic to many organs
Reticular Formation
-Poorly defined area of 100 small neural networks throughoutt bstem. -Multiple connections through cortex-> motor control, sleep and consciousness, pain mod, and habituation
Central Pontine myelinolysis
-demyelinatingw/ rapid correction of longstanding hyponatremia -Most commonly in alcoholica, chronically malnourished, medically ill. -Presents: variably with coma, acute quadraparesis, locked-in syndrome, and signs of bulbar dysfunction. poor prognosis
BSTEM and cranial nerves
Midbrain: CN III & IV Pons: CN V, VI, VII, VIII Medulla: CN IX,X, XI, XII
Brain Stem
-Basal Ganglia -Sensory & Motor between cortex and cerebellum -reticular activation system, nuclei ( Da, 5HT, NE)
Bstem Injury
-“Crossed findings”- ipsi CN., Contralateral S&M -Typically w/ dizziness/vertigo, ataxia, nausea, imbalance, double vision, nystagmus, dysarthria, dysphagia
Cervical Spondylosis
Legs almost cross in front of each other, mild weakness of hip flexors, brisk deep tendon, b/l up going toes
Dorsal Columns/ Medial leminicus
Proprioception/ vibration ipsi; Gracilus fasciculus ( more medial) from legs; Cuneatus fasciculus ( more lateral) from arms - Ipsi to medulla, cross and here they are medial leminicus -VPL/M thalami–> 1mary sensory in cortex
Corticospinal
Descending; motor to same side of body - pyramidal tract, majority crosses here - Anterior horn; ventral nerve root
