Howard's Anatomy Flashcards
1
Q
olfactory N
A
bulb/N are under frontal lobe= often damaged in acc/deceleration injury. prob in smell affects taste. only sensory modality that bypass thalamus.
2
Q
anosmia
A
early sign of parkinson’s disease- smell tests are used as screen
3
Q
CN3 lesion
A
ptosis (bc ctrl elevator palpebral superiors). eye deviated downward and outwards
4
Q
imaging for CN3 palsy
A
order MRA bc there could be aneurysm of ipsilateral posterior communicating artery
5
Q
superior oblique M
A
pulls N down and interest eye. only CN that decussates. Right CN4 innervates left superior oblique.
6
Q
PSNS eye
A
in edinger westphal nucleus in brainstem.
7
Q
pupil sparing third
A
ex microvascular disease from diabetes.
8
Q
CN3 location
A
emerge from brainstem btw posterior cerebral A and superior cerebellar A. run under posterior communicating A.
9
Q
CN4 location
A
only CN that exits from dorsal aspect of brainstem
10
Q
CN4 damage
A
causes vertical diplopia and pt compensate by tilting head towards shoulder on the unaffected side= side of lesion. can be due to trauma
11
Q
Cavernous sinus contents
A
O TOM CAT: oculomotor nerve, trochlear N, ophalmic branch of CN5, maxillary branch of CN5, internal carotid A, abducent N. O TOM are lateral wall components from superior to inferior. CA ends at lvl of T from O TOM.
12
Q
Cavernous sinus location
A
lateral to sella turcica. border by temporal and sphenoid bones
13
Q
pineal gland
A
secretes melatonin. stimulated by darkness, inhibited by light. usually calcified.
14
Q
melatonin
A
help reg sleep/wake cycle.
15
Q
pinealomas
A
silent until affect midbrain –> visual sx. up gaze. circadian rhythm disruptions. most common type in germinomas.
16
Q
frontal eye fields
A
cortical areas that ctrl eye mvt. deviate eye to pop direction. ban in here produce gaze preference
17
Q
horner’s syndrome
A
ptosis, miosis, anhydrosis/ common in carotid dissection and vertebral artery dissection as part of wallenberg syndrome
18
Q
internuclear opthalmoplegia
A
look right. cannot adduct left eye. abducting nystagmus of right eye. conference preserved. due to lesion in medial longitudinal fasciculus which connect CN3 and CN6. most often seen in MS
19
Q
optic neuritis
A
give 3d IV steroids then oral taper. hasten recovery, delay 2nd demyelinating epic but no long term impact on disease. loss of color vision, particularly red. severe relapses treated with plasmapheresis
20
Q
afferent pupillary defect: due to. evaluate by
A
due to lesion to CN2. evaluate with swinging flashlight test. direct response is impaired. consensual response preserved. so when light on good eye, both constrict. eventual optic pallor.
21
Q
clinical disability in MS correlates most with
A
black holes (permanent axonal damage) and atrophy
22
Q
Uhthoff’s phenomena
A
tendency heat worsen MS sx
23
Q
MS associated with
A
def in Vit D incr risk of dev MS. less common in areas near equator. higher it D- fewer relapses. Epstein-barr virus
24
Q
MS etio
A
1/750. most white females (3:1), 30s. far from equator. move bf age 15- dev risk of new home.
25
MS favorable prog
white, female, younger, sensory sx at onset, full recovery from initial attack, fewer relapses, fewer lesions on baseline mir.
26
MS presentation
optic neuritis, sensory disturbances, weakness, diplopia, ataxia- most common. psych and aphasia not common.most bothered by fatigue
27
L'Hermitte's sign
electrical shock sensation in limbs and body brough on by neck due to path of cervical spinal cord. seen in MS
28
MS dx
mcdonald criteria. dep on 2 attacks with clinical evidence or supportive evidence like MRI or oligoclonal bands in CSF (immunoglobulin patterns in 90% of MS pt)
29
benign MS
no disability, return to normal btw attacks
30
RRMS
never new disability between attacks.
31
secondary progressive MS
no new disability btw attacks followed by steady incr in disability
32
primary progresson MS
steady incr in disability w/o attacks. no tx
33
MS tx
interferon beta or glatiramer acetate (copaxone). decr relapse by 33%. SE: flu like sx, depression. natalizumab (tysabri) - monthly infusion- monoclonal antibody that prevent T cell from crossing BBB. but associated with cases of PML which is sometimes fatal.
34
oral MS meds
fingolimob: block T cell egress from LN. teriflunimode. dimethyl fumarate- BID, long safety profile. novantrone- only approved med for secondary progressive form, limit by cardiotox and potential for leukeia.
35
neuromyelitis optica
devices disease. demyelinating illness characterized by optic neuritis (often bilateral), transverse myelitis with MRI evidence of contiguous SC lesion 3 or more set in length, brain MRI non-diagnostic for MS, NMO-IgG seropositivity. more severe than MS. more in hispanic and AA. W>M. tx for MS would worsen disease. seen with intractable hiccups, N/V bc of lesion in area pastrami
36
NMO IgG
antibody against astrocyte on BBB.
37
optic chiasm tumor cause
bitemporal hemianopsia. lateral side dark
38
pie in the sky
lesion in optic radiations in temporal lobe on contralateral side
39
monocular blindness
lesion of optic N of same side
40
homonymous hemianopsia
lesion of optic tract. dark for the same half of both sides.
41
homonymous hemianopsia with macular sparing
lesion of occipital lobe
42
glossopharyngeal neuralgia
pain in posterior tongue and pharynx
43
carbamazepine
effective 75% pt. tx. trigeminal neuralgia. anti-epileptic. decr efficacy of oral contraceptives
44
trigeminal neuralgia causes
often idiopathic or vascular loop compressing Cn5. may be presenting feature of MS
45
trigeminal neuralgia present
shock like pain over 2nd and 3rd division of CN5. may ultimately need surgical decompression
46
CN5 location
originate in pons. runs through mocker's cave where it synapses with sensory gang in trigeminal ganglion = semilunar or gasserian ganglion where it dev into V1-3. descends into lower brainstem. so medulla pathology can result in numbness of face.
47
M of mastication
have bilateral cortical innervation. so pt with unilateral CNS damage do not have weakness of jaw mvt
48
bell's palsy
most recover well. tx: oral steroids and antiviral (acyclovir) against herpes virus. unilateral mouth droop. can't close ipsilateral eye/ wrinkle forehead. pain behind left ear. and sounds are louder. may have hyperacusis bc CN7 innervate stapedius M. often presenting sx of sarcoidosis
49
ramsay hunt syndrome
herpes zoster infection of CN VII and sometimes CN VIII. can present with painful rash in ear canal and dysfunc of affected nerves
50
bilateral facial N palsies
lyme disease
51
peripheral seventh
lesion in faical nuc in pons or facial nerve itself
52
central seventh
lesion of motor pathway above facial nerve nucleus. CL side
53
conductive hearing disorder
due to damage of ossicles. Weber's test- tuning fork on forehead. sound louder on affected ear. rinne's test- bone conduction louder than air conduction
54
vestibulocochlear nerve damage
if slowly progressive, no dizziness or vertigo bc CNS can accommodate.
55
presbyacusis
progressive bialteral symmetrical age related sensorineural hearing loss. most common form of hearing loss in elderly
56
tensor tympani M's nerve
trigeminal
57
stapedius M's nerve
seventh N
58
muscles that dampen sound when talking or chewing
tensor typani. strapedius. is why hyperacusis can be seen in bell's palsy
59
pure word deafness
damage to primary auditory cortex bilaterally. can hear, speak, write but can' recognize spoken language.
60
CNS lesion v hearing
bc hearing has bilateral rep, CNS lesion rarely cause deafness
61
sensorineural hearing loss
dmage to cholea or CN8. weber test- louder in unaffected ear. Rinne's test- air conduction be louder than bone conduction.
62
otolithic organs
utricle and saccule are perpendicular.
63
utricle
horizontal acceleration
64
saccule
certical acceleraton- elevator
65
meniere's disease
episodes of unilateral hearing loss, tinnitus, fullness of 1 ear, severe episodes of vertigo. may feel like they are thrown to the ground at time s= otolithic crisis of tumarkin. tx: slat restriction and diuretics. caused by rupture of membranous labyrinth- leads to endolymphatic distention and death of hair cells in cochlea
66
benign positional vertigo
vertigo provide by change sin head position- lying down on affected ear. dix-hallpike maneuver used to help dx condition. employee maneuver = series of positional changes to help reposition otolithic material in posterior semicircular cal
67
ototoxic drugs
aspirin-tinnitus. aminoglycoside antibiotics (anything that end in mycin), loop diuretics, chemo agents like cisplatin, carboplatin
68
vestibular neuritis
unilateral vestibular dysfunc associated with n/v, previous UPTI,
69
labyrinthitis:
~ vestibular neuritis but associated with hearing loss and or tinnitus
70
peripheral causes of vertigo
benign paroxysmal positional vertigo, miner's disease, labyrinthitis, ototoxicity, superior canal dehiscence syndrome
71
central causes of vertigo
migraine, MS, mal de debarquement syndrome, cerebellar hemorrhage and infart, vertebrobasilar insuf, vertebral artery dissection, neoplasm
72
nucleus ambiguus
though this, CN9/10 innervate M of pharynx and larynx. path --> dysphagia and dysarthria
73
CN9
taste from posterior 1/3 of tongue, parasympathetics to parotid gland, receives general sensory fiber from tonsils, pharynx, middle ear, post 1/3 tongue
74
CN10
PSNS to multi organ.
75
intermediolateral cell column
at vertebral level T1-L2. mediate entire SNS innervation of body. nun reside in GM of spinal cord
76
reticular formation
poorly defined area of >100small neural network in brainstem. in motor ctrl, sleep and consciousness, pain modulation, habituation
77
Central pontine myelinolysis (CPM)
demyelinating D that occurs when there is rapid correction of longstanding hyponatremia leading to changes in cell osmolarities and shifts of free water. most common in alcoholics, chronic malnourished, medically ill. present with coma, acute quadraparesis, locked in syndrome, sign of bulbar dysfunc, prog is poor
78
brainstem
contain CN nuclei, components of BG, sensory and motor pathways, connection btw cortex and cerebellum, reticular activating system, nuclei that make NT (dopamine, serotonin, NE)
79
CN location
midbrain: 3,4. pons: v, 6,7,8. medulla: 9, 10,11, 12
80
brainstem injury
crossed findings. CN finding on same side of lesion. motor and sensory on opposite side of lesion. sx- dizziness, vertigo, ataxia, nausea, imbalance, double vision, nystagmus, dysarthria, dysphagia
81
extraaxial mass on brainstem
often at cerebellar pontine angle. meningiomas and schwannomas -CN8.
82
cervical spondylosis
scissors gait: legs seem to cross in front of each other. mild weakness of hip flexors, deep tendon reflexes are brisk with bilateral upping toes.
83
spinothalamic pathway
mediate pain and temperature from opp side of body. primary enter SC through DRG. 2nd order neuron ascend 1-2 lvl as they cross in anterior gray commissure. ascending ptw.y. lesion cause abn 1-2 seg below
84
dorsal column
vibration and proprioception from same side of body. cadet fascicles-most medial- arm. gracile fascicles- fiber from leg. ascending pathway IL where synapse with secondary neuron in medulla --> medial lemniscus (though brainstem ) --> thalamic nuclei --> primary sensory cortex
85
lateral corticospinal tract
pyramidal tract. motor to same side of body. desncending pthwy. cross in pyramids of medulla --> SC
86
ventral posterior lateral nucleus of thalamus
really nun for sensory treats of body and SC. pro to primary sensory cortex of parietal lobe
87
ventral posterior medial nc
relay station for sensory pathway of CN of face and . proj to primary sensory cortex of parietal lobe
88
upper MN signs
incr tone, spacitity, incr reflexes, babinski. benefit from M relaxants like baclofen, botox
89
brown sequard
weakness, loss of proprioception, vibration on same side. loss of P/T on pop
90
central cord lesion
lose P/T in shawl distribution due to spinothalamc tract being affected as it crosses in spinal cord. weakness of M if anterior horn affected. can be due to syrinx/syringomyelia- abnormal fluid collection in spinal cord
91
chiari malformation
congenital disorder defined by downward herniation of cerebellar tonsils into foramen magnum. leading causes of syrinx. manifest as HA and cerebellar x.
92
anterior cord syndrome
weakness bilaterally. loss of P/T bilaterally. reserve proprioception and vibraltion BL. occur bc of occlusion of anterior spinal artery in hypotensive pt. or surgery on abdominal aorta
93
posterior cord syndrome
lose proprioception often have P/T burning sensation in limbs
94
cauda equina
10 N fiber pairs, 5 lumbar, 5 sacral, 1 coccygeal.
95
cauda equina syndrome
often cause by herniated disk at L4-L5 or L5-S1. 1) numbers of genitals, butt, anus due to sacral N root compression= saddle anesthesia 2) lower extremity weakness= often asymmetric
3) decr knee reflexes
4) bowel and bladder retnetion- often later finding
96
conus medullaris
lesion at L1-2 would cause symmetrical weakness with preserved knee reflexes. bowel and bladder incontinence dev early as does impotence.
97
amyotrophic lateral sclerosis
progessive weakness caused by degeneration of MN of brain, CN nuclei, and SC (anterior horn cells). electrophysiologic studies show fascinations, fibrillation, sharp waves. tx: riluzole
98
riluzole
only approved tx for ALS. prevent stimulation of glutamate R. extend survival in pt by several mo
99
B12 def
causes subacute deign of spinal cord. combined- damage of CST and dorsal columns. can present with a normal B12 lvl. elevated homocysteine and methylmalonic acid are more sensitive for dx. megaloblastic anemia, hyperhsegmented neutrophil. can present with psych sx- megaloblastic madness. seen in pt with pernicious anemia (ck anti-parietal cell ab and IF), strict vegetarian diet, post gastric surgery. dev years later bc body has large store of B12. nitrous oxide interfere with B12 metabolism
100
cerebellar dysfunction
ataxia- unsteadiness or incoorination of limbs, posture, gait
hypotonia, intension tremor, gait (legs apart, swaying of body, stagger, reels, lurches),
ocular motor abd: saccadic dysmetria, impaired smooth tracking, fixation abn, nystagmus
scanning speech- ban pauses btw words, ataxia of speech
101
causes of cerebellar dysfunc
toxin (dilatin, alcohol), primary neurodegenerative disease- olivopontocerebellar atrophy, paraneoplastic degen, spinocerebellar ataxia (SCAs), vascular disorder. pathways are double crossed so lesions to cerebellum present with dysfunction on same side of body. midline cerebellum lesion lead of dysfunc of racial muscle that control gain and balance. lesion to lateral lead to limb ataxia
