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Neurology > Howard's Anatomy > Flashcards

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.

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2
Q

anosmia

A

early sign of parkinson’s disease- smell tests are used as screen

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3
Q

CN3 lesion

A

ptosis (bc ctrl elevator palpebral superiors). eye deviated downward and outwards

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4
Q

imaging for CN3 palsy

A

order MRA bc there could be aneurysm of ipsilateral posterior communicating artery

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5
Q

superior oblique M

A

pulls N down and interest eye. only CN that decussates. Right CN4 innervates left superior oblique.

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6
Q

PSNS eye

A

in edinger westphal nucleus in brainstem.

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7
Q

pupil sparing third

A

ex microvascular disease from diabetes.

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8
Q

CN3 location

A

emerge from brainstem btw posterior cerebral A and superior cerebellar A. run under posterior communicating A.

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9
Q

CN4 location

A

only CN that exits from dorsal aspect of brainstem

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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

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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.

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12
Q

Cavernous sinus location

A

lateral to sella turcica. border by temporal and sphenoid bones

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13
Q

pineal gland

A

secretes melatonin. stimulated by darkness, inhibited by light. usually calcified.

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14
Q

melatonin

A

help reg sleep/wake cycle.

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15
Q

pinealomas

A

silent until affect midbrain –> visual sx. up gaze. circadian rhythm disruptions. most common type in germinomas.

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16
Q

frontal eye fields

A

cortical areas that ctrl eye mvt. deviate eye to pop direction. ban in here produce gaze preference

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17
Q

horner’s syndrome

A

ptosis, miosis, anhydrosis/ common in carotid dissection and vertebral artery dissection as part of wallenberg syndrome

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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

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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

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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.

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21
Q

clinical disability in MS correlates most with

A

black holes (permanent axonal damage) and atrophy

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22
Q

Uhthoff’s phenomena

A

tendency heat worsen MS sx

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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

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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.

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25
Q

MS favorable prog

A

white, female, younger, sensory sx at onset, full recovery from initial attack, fewer relapses, fewer lesions on baseline mir.

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26
Q

MS presentation

A

optic neuritis, sensory disturbances, weakness, diplopia, ataxia- most common. psych and aphasia not common.most bothered by fatigue

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27
Q

L’Hermitte’s sign

A

electrical shock sensation in limbs and body brough on by neck due to path of cervical spinal cord. seen in MS

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28
Q

MS dx

A

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)

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29
Q

benign MS

A

no disability, return to normal btw attacks

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30
Q

RRMS

A

never new disability between attacks.

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31
Q

secondary progressive MS

A

no new disability btw attacks followed by steady incr in disability

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32
Q

primary progresson MS

A

steady incr in disability w/o attacks. no tx

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33
Q

MS tx

A

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.

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34
Q

oral MS meds

A

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.

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35
Q

neuromyelitis optica

A

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

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36
Q

NMO IgG

A

antibody against astrocyte on BBB.

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37
Q

optic chiasm tumor cause

A

bitemporal hemianopsia. lateral side dark

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38
Q

pie in the sky

A

lesion in optic radiations in temporal lobe on contralateral side

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39
Q

monocular blindness

A

lesion of optic N of same side

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40
Q

homonymous hemianopsia

A

lesion of optic tract. dark for the same half of both sides.

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41
Q

homonymous hemianopsia with macular sparing

A

lesion of occipital lobe

42
Q

glossopharyngeal neuralgia

A

pain in posterior tongue and pharynx

43
Q

carbamazepine

A

effective 75% pt. tx. trigeminal neuralgia. anti-epileptic. decr efficacy of oral contraceptives

44
Q

trigeminal neuralgia causes

A

often idiopathic or vascular loop compressing Cn5. may be presenting feature of MS

45
Q

trigeminal neuralgia present

A

shock like pain over 2nd and 3rd division of CN5. may ultimately need surgical decompression

46
Q

CN5 location

A

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
Q

M of mastication

A

have bilateral cortical innervation. so pt with unilateral CNS damage do not have weakness of jaw mvt

48
Q

bell’s palsy

A

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
Q

ramsay hunt syndrome

A

herpes zoster infection of CN VII and sometimes CN VIII. can present with painful rash in ear canal and dysfunc of affected nerves

50
Q

bilateral facial N palsies

A

lyme disease

51
Q

peripheral seventh

A

lesion in faical nuc in pons or facial nerve itself

52
Q

central seventh

A

lesion of motor pathway above facial nerve nucleus. CL side

53
Q

conductive hearing disorder

A

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
Q

vestibulocochlear nerve damage

A

if slowly progressive, no dizziness or vertigo bc CNS can accommodate.

55
Q

presbyacusis

A

progressive bialteral symmetrical age related sensorineural hearing loss. most common form of hearing loss in elderly

56
Q

tensor tympani M’s nerve

A

trigeminal

57
Q

stapedius M’s nerve

A

seventh N

58
Q

muscles that dampen sound when talking or chewing

A

tensor typani. strapedius. is why hyperacusis can be seen in bell’s palsy

59
Q

pure word deafness

A

damage to primary auditory cortex bilaterally. can hear, speak, write but can’ recognize spoken language.

60
Q

CNS lesion v hearing

A

bc hearing has bilateral rep, CNS lesion rarely cause deafness

61
Q

sensorineural hearing loss

A

dmage to cholea or CN8. weber test- louder in unaffected ear. Rinne’s test- air conduction be louder than bone conduction.

62
Q

otolithic organs

A

utricle and saccule are perpendicular.

63
Q

utricle

A

horizontal acceleration

64
Q

saccule

A

certical acceleraton- elevator

65
Q

meniere’s disease

A

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
Q

benign positional vertigo

A

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
Q

ototoxic drugs

A

aspirin-tinnitus. aminoglycoside antibiotics (anything that end in mycin), loop diuretics, chemo agents like cisplatin, carboplatin

68
Q

vestibular neuritis

A

unilateral vestibular dysfunc associated with n/v, previous UPTI,

69
Q

labyrinthitis:

A

~ vestibular neuritis but associated with hearing loss and or tinnitus

70
Q

peripheral causes of vertigo

A

benign paroxysmal positional vertigo, miner’s disease, labyrinthitis, ototoxicity, superior canal dehiscence syndrome

71
Q

central causes of vertigo

A

migraine, MS, mal de debarquement syndrome, cerebellar hemorrhage and infart, vertebrobasilar insuf, vertebral artery dissection, neoplasm

72
Q

nucleus ambiguus

A

though this, CN9/10 innervate M of pharynx and larynx. path –> dysphagia and dysarthria

73
Q

CN9

A

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
Q

CN10

A

PSNS to multi organ.

75
Q

intermediolateral cell column

A

at vertebral level T1-L2. mediate entire SNS innervation of body. nun reside in GM of spinal cord

76
Q

reticular formation

A

poorly defined area of >100small neural network in brainstem. in motor ctrl, sleep and consciousness, pain modulation, habituation

77
Q

Central pontine myelinolysis (CPM)

A

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
Q

brainstem

A

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
Q

CN location

A

midbrain: 3,4. pons: v, 6,7,8. medulla: 9, 10,11, 12

80
Q

brainstem injury

A

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
Q

extraaxial mass on brainstem

A

often at cerebellar pontine angle. meningiomas and schwannomas -CN8.

82
Q

cervical spondylosis

A

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
Q

spinothalamic pathway

A

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
Q

dorsal column

A

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
Q

lateral corticospinal tract

A

pyramidal tract. motor to same side of body. desncending pthwy. cross in pyramids of medulla –> SC

86
Q

ventral posterior lateral nucleus of thalamus

A

really nun for sensory treats of body and SC. pro to primary sensory cortex of parietal lobe

87
Q

ventral posterior medial nc

A

relay station for sensory pathway of CN of face and . proj to primary sensory cortex of parietal lobe

88
Q

upper MN signs

A

incr tone, spacitity, incr reflexes, babinski. benefit from M relaxants like baclofen, botox

89
Q

brown sequard

A

weakness, loss of proprioception, vibration on same side. loss of P/T on pop

90
Q

central cord lesion

A

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
Q

chiari malformation

A

congenital disorder defined by downward herniation of cerebellar tonsils into foramen magnum. leading causes of syrinx. manifest as HA and cerebellar x.

92
Q

anterior cord syndrome

A

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
Q

posterior cord syndrome

A

lose proprioception often have P/T burning sensation in limbs

94
Q

cauda equina

A

10 N fiber pairs, 5 lumbar, 5 sacral, 1 coccygeal.

95
Q

cauda equina syndrome

A

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
Q

conus medullaris

A

lesion at L1-2 would cause symmetrical weakness with preserved knee reflexes. bowel and bladder incontinence dev early as does impotence.

97
Q

amyotrophic lateral sclerosis

A

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
Q

riluzole

A

only approved tx for ALS. prevent stimulation of glutamate R. extend survival in pt by several mo

99
Q

B12 def

A

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
Q

cerebellar dysfunction

A

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
Q

causes of cerebellar dysfunc

A

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

Neurology (18 decks)

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