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Brain and Behavior Exam 2 > Exam2 Review Deck > Flashcards

Exam2 Review Deck Flashcards

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1
Q

What is the path of dorsal column medial lemniscus from sensory resceptors to cortex?

A
  • AB, 1, and 2 fibers enter more medially to spinal cord
  • a few fibers stay around for local processing, most fibers go to f. cuneatus (above T6, lateral) and f. gracilis (below T6, medial) and travel up to synapse in gracilis/cuneatus nuclei in medulla
  • in medulla decussate and ascend contralaterally in medial lemniscus to VPL of thalamus
  • from thalamus go to sensory cortex (S1) cortical layer 4
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2
Q

what is path of spinothalamic tract from sensory receptors to cortex

A
  • Ad, C, 3, 4 fibers enter more laterally to spinal cord
  • travel in lissauers tract 2-5 segments up or down
  • synapse in ipsilateral gray matter
  • decussate via anterior white commissure
  • ascend in contralateral spinothalamic tract to VPL
  • from thalamus to sensory cortex cortical layer 1
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3
Q

what is path of trigeminal somatosensory tracts from sensory receptors to cortex?

A

proprioception and vibration path:

  • AB and group 1/2 enter brainstem in pons
  • synapse in ipsilateral principal trigeminal nucleus
  • cross to join contralateral DC-ML tract
  • synapse in VPM in thalamus
  • fibers project to S1/S2 layer 4

pain and temp path:

  • Ad and C fibers enter brainstem in pons
  • travel into medulla via ipsilateral spinal tract of V
  • synapse in spinal nucleus of CN V
  • cross and join contralateral ascending spinothalamic tract
  • synapse in VPM in thalamus
  • fibers projects to S1/S2 layer 1
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4
Q

What is the somatotopic organization of sensory systems in the brainstem?

A

medulla: no face there, legs = anterior
pons: face = medial, legs = lateral
midbrain:

arms are medial to legs with two exceptions: posterior columns and S1 cortex

  • pain temp systems = no organization
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5
Q

what is the somatotopic organization of sensory systems in the thalamus?

A

thalamus: face/arms medial, legs lateral
- pain temp systems = no organization
* arms are medial to legs with two exceptions: posterior columns and S1 cortex

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6
Q

what is the somatotopic organization of sensory systems in the cortex?

A

cortex: legs medial, face lateral
- pain temp systems = no organization
* arms are medial to legs with two exceptions: posterior columns and S1 cortex

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7
Q

What are the characteristics of AB fibers?

A

sense touch/pressure cutaneously

thick myelinated, fast conducting [but not as fast at group 1, about equal to group 2]

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8
Q

What are characteristics of AD fibers?

A

sense pain/temp cutaneously

thin myelinated slow conducting

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9
Q

What are characteristics of C fibers?

A

sense pain/temp cutaneously

not myelinated slow conducting

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10
Q

What are characteristics of Group 1 [a and b] fibers?

A 
1a = primary to muscle spindle
1b = to golgi tendon organ

sense touch/pressure in muscle

thick myelinated, fasted conduction, biggest fibers

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11
Q

what are characteristics of group 2 fibers?

A

secondary fiber to muscle spindle

sense touch/pressure in muscle

thick myelinated, fast conduction

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12
Q

what are characteristics of group 3 and 4 fibers?

A
  • sense pain and temp in muscle

3: thin myelinated slow conduction
4: not myelinated, slow conduction

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13
Q

What are the 4 areas of S1 and their input info?

A

1, 3b = cutaneous info [Ab]

2, 3a = proprioception [group 1a, 1b, 2]

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14
Q

What is the function of S2?

A

process info during bimanual manipulation
- has representation from both sides of body [via internal capsule fro contralateral body and vai corpus callosum from contralateral S1 or ipsilateral body]

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15
Q

What are the principal input layers of S1 for different sensory modalities?

A

layer 4 = DC-ML

layer 1 = spinothalamic

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16
Q

thalamic VA nucleus: inputs, outputs, function

A

input –> output:
cerebellum/basal ganglia –> frontal cortex

function: motor

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17
Q

thalamic VL nucleus: inputs, outputs, function

A

input –> output:
cerebella/basal ganglia –> M1/PM/SMC

function: motor

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18
Q

thalamic VPL nucleus: inputs, outputs, function

A

input –> output:
medial lemniscus DC-ML –> S1/S2
spinothalamic –> S1/S2

function: somatosensory pain/temp/proprioception from body

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19
Q

thalamic VPM nucleus: inputs, outputs, function

A 
input --> output:
spinal nucleus of V --> S1/S2
principal nucleus of V --> S1/S2
spinothalamic --> S1/S2
solitary nucleus --> gustatory cortex
spinothalamic --> gustatory cortex

function: somatosensory pain/temp/proprioception from face AND taste

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20
Q

thalamic MGN nucleus: inputs, outputs, function

A

input –> output:
superior olive and inferior colliculus of tectum –> auditory cortex [heschl’s]

function: hearing

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21
Q

thalamic LGN nucleus: inputs, outputs, function

A

input –> output:
retina–> visual cortex [calcarine]

function: vision

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22
Q

What do free nerve endings sense?

A

pain and temperature

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23
Q

what do meissner corpuscles sense?

A

light touch

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24
Q

what do pacinian corpsucles sense?

A

vibration, pressure

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25
Q

what do merkel discs sense?

A

sustained pressure, position sense

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26
Q

If you have loss of pain and temp on right side starting at T5 coming from contralateral spinothalamic injury, where would the level of injury be?

A
  • fibers descend and take 2-3 spinal segments to reach opposite side so lesion is likely 2-3 segments above this [T2-T3]
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27
Q

Importance/function of cortico-thalamic input?

A
  • modulates output of thalamic relay neurons via feedback and feedforward inhibition
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28
Q

Role of thalamus in controlling states of consciousness [tonic vs burst, transition between]?

A

tonic firing in awake/alert states –> dorsal thalamic relay neurons fire in response to depolarization, allows flow of info to cortex

burst firing in drowsy/deep sleep –> thalamic relay neurons fire in oscillatory manner = blocks flow of info to cortex

to enter tonic state: ACh, histamine, NE depolarize membrane
to enter burst state: 5HT hyperpolarizes membrane

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29
Q

What is effect of thalamic lesion that damages VPL/VPM [thalamic syndrome]?

A
  • contralateral hemianesthesia

- excruciating central pain

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30
Q

What causes a tremor state?

A
  • rhythmic bursts in VA/VLa due to abnormalities in GP-thalamus circuits
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31
Q

What happens if lesion of anterior or MD nuclei in thalamus?

A
  • amnesia –> disrupts amygdala/hippocampus circuitry
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32
Q

What causes absence seizures? what are they?

A
  • due to abnormal sustained TRN GABAergic neuron activity

- characterized by sudden arrest of movement, blank stare, fluttering eyelid, loss of ability to interact

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33
Q

What is path for affective component of pain perception?

A
  • begins in lamina I/V in spinal cord or spinal nucleus of V
  • travels via spinothalamic/trigeminothalamic tracts
  • go to: midbrain periaqueductal gray [PAG], rostral ventral medulla, amygdala, hypothalamus, VM/MD of thalamus –> insula
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34
Q

What is process by which descending modulatory systems inhibit pain transmission?

A

PAG in midbrain and RVM [rostral ventral medulla]

  • -> locus ceruleus [NE], raphe nuclei [5HT]
  • -> release NE/5HT onto local inhibitory interneuron in spine
  • -> they release enkephalin [endogenous opioid] onto synapses in lamina 1, V
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35
Q

What is nociceptive pain?

A
  • physiologic [normal] stimulus-dependent pain

first pain by Ad, second pain by C

spinothalamic nerves get info from Ad/C and Ab, Ab activate inhibitory interneurons = dampen throughput of pain info

referred: group 3/4 terminate on spinothalamic neurons that are also getting Ad/C fibers –> pain perceived to be coming from cutaneous receptive field

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36
Q

What is inflammatory pain?

A
  • pain hypersensitivity due to peripheral inflammation
  • -> have sponatneous and stimulus dependent pain
  • -> protective –> adis in healing

mech: neurochemical mediators secreted by immune cells cause pain fibers to discharge aberrantly –> amplification peripherally and centrally

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37
Q

What is dysfunctional pain?

A
  • same components as inflammatory pain but without evidence of inflammation
  • not protective [does not support healing/repair]
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38
Q

What is neuropathic pain?

A
  • pain felt in absence of stimulus = maladaptive, chronic, debilitating

mech:
- any lesion or disease that causes trauma at nerve terminals/axons can cause irritation of nerves

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39
Q

What is central sensitization?

A
  • synaptic signaling strength of pain paths exaggerated; pain hypersensitivity to normal inputs

mech:

  • increased membrane excitability in peripheral axons via upregulation Na channels
  • increased synaptic efficacy via upregulation glutamate receptors
  • decreased inhibition in local interneuron networks
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40
Q

What is action of enkephalin in top down pain inhibition?

A
  • released by local inhibitory interneurons in spine onto synapses in lamina 1/5
  • presynaptically: decreases NT release from pain/temp Ad and C fibers
  • post-synaptically: causes hyperpolarization of ascending spinothalamic neurons
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41
Q

What is the function of the ciliary body?

A
  • makes aqueous humor

- contains ciliary muscles that change shape of lens

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42
Q

What is the function of the choroid?

A
  • contains connective tissue, blood vessels

provides nutrients

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43
Q

What is a cataract? mech?

A
  • clouding/yellowing of lens –> decrease vision
  • develops slowly with age
    treat: artificial lens replacement
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44
Q

What is glaucoma? mech?

A
  • excess aqueous humor [due to overproduction or under-drain] –> causes increased IOP [pressure] –> optic nerve injury, optic disc atrophy with cupping –> progressive decreased vision [starting with peripheral]
    treat: beta blockers, surgery
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45
Q

what is presbyopia? mech?

A
  • loss of ability to change lens shape [focus near vs far]

- due to normal aging, lens less elastic

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46
Q

what is retinitis pigmentosa? mech?

A
  • progressive retina degeneration
    signs: night/low vision blindness, tunnel vision

slow process –> takes decades

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47
Q

what is macular degeneration? two types?

A
  • degeneration of macula [central retina], fovea –> distortion [straight lines look wavy], central loss of vision [scotoma], blurry vision
    dry: deposition of drusen = yellow stuff under macula, gradual loss of vision
    wet: abnormal blood vessel growth, more rapid loss of vision. treat = VEGF, angiogenesis inhibitors
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48
Q

what is diabetic retinopathy? stages?

A
  • retinal damage due to chronic hyperglycemia
    findings: microaneurysms, hard exudates, intraretinal hemmorrhage, cotton wool spots

early = non-proliferative = asymptomatic

pre-proliferative: damaged capillaries leak blood –> macular edema

proliferative: chronic hypoxia –> new blood vessel formation on retina

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49
Q

What is function of cones?

A

Cones = central vision, color,high spatial resolution, low light sensitivity

  • use parvocellular path, slower
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50
Q

What is function of rods?

A

rods = peripheral vision, light detection, poor spatial detail, more light sensitive, single photon

  • use magnocellular path, faster
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51
Q

What is path of light from periphery through retina to optic nerve?

A
  • light crosses entire retina –> rods/cones –> bipolar –> ganglion –> optic nerve
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52
Q

What are the 3 chambers of the eye? what do they each contain?

A
  • anterior and posterior chambers in front of lens [separated by iris]
  • vitreous body [between back of lens and retina, contains jelly-like substance
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53
Q

What is optic neuritis? presumed pathogenesis?

A
  • inflammatory optic neuropathy
    due to demyelination
  • -> have unilateral loss of visual acuity, pain on eye movement
  • -> high risk of developing MS
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54
Q

What should you think: pt says straight lines appear crooked?

A

dry ARMD [macular degeneration]

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55
Q

What is contained in “nuclear” layers in retina? what about “plexiform” layers?

A 
nuclear = contains cell bodies
plexiform = contains synapse
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56
Q

What layer of retina has ganglion cell axons?

A

nerve fiber layer

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57
Q

What is contained in outer plexiform layer vs inner plexiform layer?

A

outer = synapse between photoreceptors, bipolar cells, horizontal cells

inner = synapse between bipolar, amacrine, ganglion cells

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58
Q

What is the order of cells from out to in in the retina?

A

photoreceptors –>horizontal cells –> bipolar cells –> amacrine cells –> ganglion cells

horizontal = horizontal connections in area where photoreceptors and bipolar cells synapse
amacrine = horizontal connections in area where bipolar and ganglion cells synapse
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59
Q

What is function of interneurons in retina?

A
  • release NT but dont generate AP
    include: horizontal, amacrine, bipolar
  • ganglion: only cells that generate APs
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60
Q

What info does left optic tract carry retrochiasmally?

A

right visual field for both eyes

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61
Q

What info is carried in parietal vs temporal [meyer’s] projections?

A 
parietal = contralateral inferior quadrant in both eyes
meyers = contralateral superior quadrant in both eyes
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62
Q

What happens if left optic nerve lesion?

A
  • left anopia = no vision through left eye
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63
Q

What happens if optic chiasm lesion?

A
  • temporal hemianopia = no vision in temporal half [lateral] of visual field on both sides
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64
Q

what happens if left optic tract lesion?

A
  • right homonymous hemianopia = loss of vision in right half of visual field for both eyes
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65
Q

what happens if right temporal optic radiation lesion?

A

temporal = meyers = pie in the sky

left homonymous superior quadrantopia = loss of vision in left upper quadrant in both eyes

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66
Q

what happens if left parietal optic radiation lesion?

A

right homonymous inferior quadrantopia = loss of vision in right lower quadrant in both eyes

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67
Q

What happens if left visual cortex lesion due to PCA infarct?

A

right homonymous hemianopia with macular sparing = loss of vision in right half of visual field for both eyes but central area spared due to collateral MCA circulation

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68
Q

What is the physiologic blind spot

A
  • region where optic nerve exits retina
  • no photoreceptors
  • on nasal half of visual field
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69
Q

What are the layers of the LGN and their inputs? which are magno vs parvo? which are ipsi vs contra?

A

layers:
1,2 = magnocellular [rods, light]
3, 4, 5, 6 = parvocellular [cones, color]

1, 4, 6 = contralateral
2, 3, 5 = ipsilateral

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70
Q

What is mech for dilation vs constriction of pupil?

A

dilate: dilator pupillae, sympathetic
constrict: sphincter pupillae, PNS via edinger westphal

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71
Q

What is the pupillary light reflex [ex. shine light into right eye]?

A
  • afferents from right CN 2 –> synapse in right pretectal nucleus in midbrain –> activates bilateral edinger-westphal nuclei
  • pupils contract bilaterally via CN3
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72
Q

What is the pupillary near reflex? triad?

A

triad all controlled by CN3 and edinger westphal

  1. accomodation: change lens shape, ciliary muscle
  2. convergence: eye adduction, medial rectus
  3. pupillary constriction, pupillary sphincter
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73
Q

What happens in cranial nerve 3 palsy? cause?

A

cause: aneurysm of posterior communicating artery [Pcom]

signs

  • mydriasis [dilation]
  • ptosis
  • can’t react to light or near
  • down and out gaze
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74
Q

What is tonic pupil?

A
  • dissociation of light-near reflexes due to lesion of ciliary ganglion
    signs:
  • mydriasis [dilation]
  • absent pupillary light reflex [efferent defect]
  • preserved pupillary near reflex
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75
Q

What is argyll-robertson pupil?

A
  • bilateral
  • due to tertiary syphilis, diabetes
  • pupils accomodate [constrict in near reflex] but don’t react [constrict in light reflex]
76
Q

What is horner’s syndrome?

A
  • sympathetic disorder –> associated with lesion of spinal cord above T1
    triad: PAM is horny
  • ptosis [drooping eyelid]
  • anhidrosis [absence of sweating]
  • miosis [constriction]
77
Q

what is afferent papillary defect/marcus gunn pupil?

A
  • due to optic nerve damage or retinal injury
  • affected eye does not constrict as much compared to unaffected eye when you shine light into it
  • test with swinging flashlight
78
Q

What is saccade?

A

rapid eye movement

79
Q

What is optokinetic nystagmus?

A

combination of saccade + smooth pursuits to allow eyes to follow moving object

80
Q

what is vergence?

A

disconjugate eye movements –> allow eyes to focus on near [convergence] or far [divergence]

81
Q

What is abnormality associated wtih PCom aneurysm?

A

CN 3 palsy

82
Q

What is path of CN 3?

A

CN 3 nuclei + edinger westphla in midbrain at level of superior colliculi

  • exit ventral –> pass between PCA/SCA –> cavernous sinus –> superior orbital fissure
83
Q

What is path of CN 4?

A

CN 4 nuclei in midbrain at level of inferior colliculi –> exit dorsally, cross –> cavernous sinus –> superior orbital fissure

84
Q

What is path of CN 6?

A

CN 6 nuclei in pons at facial genu/colliculis –> exits ventrally –> passes under gruber’s ligament –> cavernous sinus –> superior orbital fissure

85
Q

What happens in CN 4 palsy? cause?

A
  • eye up, diplopia, head tilt toward side of lesion

cause: head trauma, congenital deffect

86
Q

what happens in CN 6 palsy? cause?

A
  • ipsilateral eye in [adducted], horizontal diplopia, affected eye can’t abduct
    cause: high ICP
87
Q

What is function of MLF? location?

A

facilitates conjugate horizontal gaze movements between CN 6/CN3

  • located along cerebral aqueduct, 4th ventricle
88
Q

Which lateral rectus and which medial rectus are innervated by the left PPRF?

A

left PPRF –> left lateral rectus, right medial rectus

89
Q

What is the path of innervation upstream to the PPRF?

A

Frontal eye field –> internal capsule –> decussates at midbrain-pontine junction –> PPRF

90
Q

Which direction conjugate gaze does right frontal eye field [FEF] control?

A

right frontal eye field –> left PPRF –> look left [left lateral rectus, right medial rectus]

91
Q

What happens if lesion in left abducens nucleus or PPRF?

A
  • impaired conjugate gaze in both eyes to side of lesion
  • -> try to look left = nothing happens
  • -> try to look right = normal conjugate gaze
92
Q

What happens if lesion in right MLF?

A

INO!
when look righ: fine
when look left: left eye goes and has nystagmus, right eye stays [impaired abduction]

preserved convergence b/c different path

93
Q

INO due to left MLF lesion can be seen when gaze toward which side?

A

when try to gaze right

94
Q

What disease should you think if you see INO in younger vs older pt?

A

INO in younger = usually bilateral = MS

INO in older = usually unilateral = stroke

95
Q

What is the function of the PPRF?

A
  • supranuclear control of eye movements –> PPRF is in the pons, receives signals from frontal eye fields and directs conjugate eye movement via MLF

PPRF initiates conjugate movement

96
Q

What is the vestibulo-ocular reflex?

A
  • eyes move in opposite direction of head rotation to maintain focus on target
97
Q

What is one and a half syndrome[ex on right side]?

A

unilateral lesion of right PPRF and MLF [ie dorsal caudal pons stroke]

  • ipsilateral horizontal gaze palsy
  • ipsilateral INO

look right –> nothing happens [both eyes stay b/c right PPRF lesion]
look right: right eye goes, left eye nothing

98
Q

What is cause of nerve 3 palsy?

A

aneurysm of posterior communicating artery [Pcom]

uncal herniation

99
Q

What happens in frontal eye field lesion?

A
  • gaze preference = ipsilateral gaze deviation to look at the lesion
100
Q

What is path of action VOR if head turns to left?

A
  • endolymph in left horizontal semicircular canal shifts forward and activates nerve VIII
  • projects to ipsilateral vestibular nucleus
  • projects to contralateral CN 6 nucleus and via MLF excite right LR and left MR to turn eyes to the right
  • other projections from vestibular nuc project to ipsilateral CN 6 to inhibit left LR
101
Q

What is caloric testing?

A

way to measure VOR using warm/cold water to generate currents in endolymph of horizontal canals, causes horizontal nystagmus

COWS
cold = opposite –> quick phase of nystagmus toward ear opposite water injected ear
warm = same side –> quick phase of nystagmus toward same side as water injected ear

102
Q

Different roles of inner vs outer hair cells?

A

inner hair cells = 1 row, 95% of auditory fibers, dransduce sound to auditory nerve via pressure waves transmitted through perilymph that cause movement of basilar membrane

outer hair cell = 3 row, support for inner cells, amplify movement of basilar membrane, make otoacoustic emissions [low freq hearing loss = outer hair cells]

103
Q

Parts and function of external ear?

A

outer = pinna + external auditory meatus
pinna - vertical localization of sound
external auditory meatus - magnify sound

104
Q

Parts and function of middle ear?

A

middle = ossicles, tensor tympani, stapedius, eustachian tube
ossicles = malleus, incus, stapes
tensor tympani - attached to malleus, trigeminal = tenses tympanic membrane so you can hear high frequency
stapedius - associated with stapedius, dampens loud noise

105
Q

Parts and function of inner ear?

A

inner = cochlea, canals, vestibule
vestibule - contains utricle + saccule
cochlea - converts sound pressure to nerve pulse
semicircular canals - detect rotational movement

106
Q

Auditory path from ear into CNS?

A

pinna –> external auditory meatus –> tympanic membrane –> oval widnow –> scala vestibuli –> basilar membrane of scala media –> inner hair cell –> auditory nerve

107
Q

If ipsilateral hearing loss what does this mean about location of lesion?

A
  • means it much be in cochlear nucleus or auditory nerve or ear itself
  • from cochlear nuclei, auditory system goes to superior olives and becomes bilateral
108
Q

What is place code?

A
  • cells that respond to highest sound frequences are more posterior
109
Q

What is tonotopy?

A
  • ## sound pitch [frequency] is represented topographically in auditory system
110
Q

What is the process of sound localization?

A
  • inter-aural intensity differences
  • inter-aural timing differences

sound localization in horizontal plane depends on bilateral input to superior olive
in vertical plane = depends on sound reflection at pinna

111
Q

Why important to screen infants for hearing loss?

A
  • critical point in development of hearing and speech wihtin first 6 months
112
Q

What is function of vestibular system?

A
  • head motions and head position in space

- angular rotation [canals] and linear acceleration [otoliths]

113
Q

What is anatomy of the labyrinth?

A
  • semicircular canals = bony canals in orthoganol planes [horizontal, anterior, posterior], filled with perilymph, have swelling at one end = ampulla from which sensory epithelium hangs
  • otoliths = filled with endolymph, surrounded by perilymph
  • utricle = horizontal, saccule = verticle
114
Q

What symptoms associated with central vestibular damage vs peripheral?

A

central: severe imbalance/ataxia, persistent, nystagmus not inhibited by fixation of eyes, changes direction with gaze
peripheral: ataxia, gait veers toward lesion, N/V, hearing loss, fullness in ear, acute, often position dependent, delayed nystagmus away from side of lesion

115
Q

What is the path from inner ear to vestibular cortex?

A
  • canal/otolith primary afferents get info from hair cells –> form CN VIII cochlear portion
  • terminate in vestibular nuclei in medulla/caudal pons
  • cross at midline –> VP of thalamus –> vestibular cortex
116
Q

What is the function of vestibulo-thalamo-cortical path?

A

conscious perception of balance

117
Q

What is the function of lateral and medial vestibulo-spinal tracts?

A 
lateral = balance and postural control in spinal cord
medial = maintains stability of head and neck as body moves
118
Q

what is the function of vestibulo-autonomic projects?

A

control BP, HR, respiration, etc in response to posture

–> this can go wrong in elderly = orthostatic hypotension

119
Q

How do you distinguish conductive vs sensorineural hearing loss?

A

conductive = air bone gap, air
- air conduction decreased, bone conduction normal

sensory neural

  • AC = BC = both depressed
  • usually bilateral
120
Q

what are common causes of conductive hearing loss?

A

due to outer or middle ear

  • ear wax
  • fluid
  • eustachian tube swelling
  • tympanic membrane perforation
  • otosclerosis [genetic fixation of stapes]
121
Q

what are common causes of sensorineural hearing loss?

A

due to middle or inner ear

  • aging [high freq lost]
  • genetic [middle freq lost]
  • noise [high freq lost]
  • acoustic neuroma [ low speech discrimination]
  • meniere’s disease [bilateral]
122
Q

What is utility of tuning fork tests [weber, rinne]?

A

weber = lateralizes toward conductive hearing loss, away from sensorineural hearing loss

rinner = normally AC > BC; in conductive B > AC

123
Q

What is utility of tympanometry?

A

test movement of ear drum by presenting tone

124
Q

what is utility of audiogram?

A

way to diagnose hearing loss

    • establish pure tone threshold for air and bone
    • test speech reception threshold for each ear
    • provide speech discrimination score
125
Q

How do you distinguish vertigo from imbalance/disequilibrium/lightheadedness?

A 
vertigo = false sense of motion
imbalance = sensory disturbance
disequilibrium = feels off balance, drunk
lightheaded = feels faint
126
Q

What is anatomy of cochlea?

A
  • bony cavity, coils on itself
  • 3 compartments:
    scala vestibuli = in
    scala media = membrane middle endolymph
    scala tympani = out
127
Q

What is acute unilateral vestibular loss?

A

due to virus in inner ear, acoustin neuroma, injury to inner ear

  • gait ataxia toward lesion
    • romberg
  • sudden onset vertigo, N/V, nystagmus
128
Q

What is meniere’s?

A

due to distension of membranes of inner ear [too much endolymph]

  • episodic, spontaneous vertigo
  • lasts hours
  • accompanied by N/V
  • unilateral hearing loss, fullness, tinnitis
129
Q

What is BPPV?

A
  • otolith/otoconia dislodged and float in endoluymph, go to posterior canal
  • abrupt positional vertigo
  • 5-10 sec latency of nystagmus
  • dix hallpike
130
Q

What is bilateral vestibular loss?

A
  • age related, head trauma, aminoglycosides

- absent caloric response in both ear, ataxia, oscillopsia [perception of oscillating vision]

131
Q

what happens in lead poisoning?

A

children: acute encephalopathy, IQ impairment
adult: ab pain, writ drop
burtons lines = discoloration of upper gums

132
Q

What happens in mercury poisoning?

A

= mad hatter –> irritability, shyness, red cheeks, tremor

- encephalopathy, peripheral neuropathy, seizures

133
Q

What happens in arsenic poisoning?

A
  • encephalopathy, N/V, renal failure, garlic breath
134
Q

what happens in thallium poisoning = rat poison?

A

vomiting, diarrhea, paresthesias late hair loss

135
Q

What happens in manganese poisoning?

A

bradykinesia [looks like parkinsons], hyperreflexia, confusion

136
Q

What is marasmus?

A

balanced starvation
- see in < 1 yo
mental changes, growth retardation

137
Q

what is kwashiorkor?

A

not enough protein

  • see in 1-3 yo
  • muscle wasting, big belly
138
Q

What happens in vit A toxicity?

A
  • ICP [pseudotumor cerebri], alopecia, teratogen
139
Q

What are the neuro effects of thiamine deficiency?

A
  • painful peripheral neuropathy
140
Q

what are neuro effects of pyridoxine [B6] deficiency?

A
  • peripheral neuropathy, microcytic anemia, convulsions

– seizures in infants < 180 mo

141
Q

what are neuro effects of folic acid [B9] deficiency?

A
  • neural tube defects
142
Q

what are neuro effects of cobalamine [B12] deficiency?

A
  • subacute combined degeneration [posterolateral column disease]
  • -> parastehsias [pins/needles], loss of vibration/position sense
  • spastic + ataxic weakness progressive
    • babinski
  • optic atrophy
143
Q

What is wernicke’s encephalopathy?

A
  • due to thiamine deficiency, alcoholism
  • untreated leads to korskoffs
  • lesion of thalamic nuclei
  • ataxia, opthalmoplegia, gaze palsies, confusion
144
Q

what is korsakoff’s psychosis?

A
  • due to thiamine deficiency, alcoholism

- severe memory deficit, confabulation, dementia

145
Q

What makes olfactory system unique compared to other sensory systems?

A
  • cell bodies of primary afferents directly in olfactory epithelium
  • continuous turnover
  • no thalamic relay
  • ipsilateral
146
Q

Path of olfactory from periphery to cortex?

A
  • cilia of olfactory receptor cells
  • ipsilateral to folfactory bulb
  • olfactory tract
  • olfactory cortex
147
Q

Path of gustatory from periphery to cortex?

A
  • taste cells synapse to primary afferents from branches of CN VII [anterior 2/3], IX [posterior 1/3], X [back of tongue]
  • project to nucleus of solitary tract
  • to thalamus [VPM] via central tegmental tract
  • to primary gustatory cortex via internal capsule

== exclusively ipsilateral

148
Q

Causes of olfactory dysfunction?

A
  • URI, sinus infection

- head trauma

149
Q

Causes of gustatory dysfunction?

A
  • ipsilateral loss of taste from anterior 2/3 tongue = lesion of CN VII root
  • viral infection
  • head trauma
150
Q

Difference alpha and gamma motoneurons [organization, fibers they innervate, function]

A 
alpha = innervate extrafusal, force generating
gamma = intrafusal, control and adjust sensitivity of muscle spindle
151
Q

What is a motor unit?

A
  • one motor neuron and all the fibers it innervates
152
Q

What is function/innervation of muscle spindle?

A
  • record muscle length and rate of length change
153
Q

What is function/innervation of golgi tendon organs?

A

record tension generated at myotendinous junction during contraction

154
Q

What are the components of deep tendon reflex?

A
  • group 1a/2 sensory afferent sense muscle stretch
  • synapse on alpha motor neurons of same muscle that gave rise to afferents as well as synergistic
  • also info goes to inhibitory group 1a interneurons that inhibit motor neuron of antagonistic muscles
  • aMN causes stretched muscle to shorten/contract
155
Q

What is pyramidal vs extrapyramidal motor system?

A

extrapyramidal = cerebllum, basal ganglia

156
Q

what is the path of corticospinal tract from M1 to muscle?

A
  • descends
  • crosses at medulla in great pyramidal decussation
  • descends contralaterally

role = fine motor control of distal muscles

157
Q

What is role of descending motor paths in static posture?

A
  • lateral VST and medial [pontine] RST –> tonic excitation of anti-gravity extensors
  • purkinje cells [cerebellum] –> inhibi lateral VST
  • cerberal cortex –> stimulate lateral [medullary] RST –> inhibits extensor MNs
158
Q

Whats spasticity vs rigidity?

A 
spasticity = UMN damage --> hyperactive myotatic reflex, hypertonia of anti-gravity
rigidiy = damage to basal ganglia, hypoactive myotatic reflexes, hypertonia in extensors and flexors, cog wheel
159
Q

Functional impairment of each of different motor cortical areas?

A

M1 = motor execution. lesion = loss of fine motor control

PM [premotor] = sensory guided movement, severe impairment in performing sensory guided motor tasks

SMA/M2 = internally generated movement, impaired self-initiated tasks, impairment in tasks taht require bimanual coordination

160
Q

Presentation of UMN vs LMN lesion?

A 
UMN = spastic, hyperreflexia, + babinksi
LMN = flaccid, hyporeflexia, atrophy, hypotonia, distribution in particular area, fasciculations
161
Q

ALS: presentation, course, management, differential

A

combined anterior horn + pyramidal tract

  • spasticity, clumsiness, hyperactive reflex, + babinksi
  • weakness, wasting, fasciculations
  • need to show disease above foramen magnum otherwise could be cervical spondylosis
162
Q

How do you differentiate disorder of motor cortex vs brainstem vs anterior horn vs peripheral motor neuropathy vs neuromuscular junction vs muscle

A

motor cortex: UMN = spastic
internal capsule = contralateral motor + sensory
brainstem = crossed signs
spinal cord anterior horn = LMN –> ipsilateral weakness/atrophy/fasciculations
peripheral neuropathy = distal weakness
NMJ = fluctuating weakness, fatigable muscles, limb weakness
muscle = proximal weakness,

163
Q

What is effect of corticobulbar vs LMN lesion for facial nerve?

A

s

164
Q

What is effect of corticobulbar vs LMN for hypoglossal nerve?

A

s

165
Q

What is presentation of brown-sequard?

A

below lesion:

  • ipsilateral loss of proprioception,UMN deficits [spastic]
  • contralateral loss of pain/temp

at level

  • ipsilateral LMN deficits
  • ipsilateral loss of all sensation
166
Q

What is presentation of syringomyelia?

A
  • bilateral loss of pain/temp sensation in the area

- seen with chiari 1

167
Q

what is presentation of conus medullaris lesion?

A

suddne onset, bilateral L1, L2

  • symmetric weakness and saddle anesthesia
  • LMN bladder/bowel develops early
168
Q

what is presentation of cauda equina lesion?

A
  • gradual onset, asymmetric, L4, L5, S1 nerve roots
  • asymmetric flaccid paralysis/hypotonia, saddle amnesia, radicular/sharp pane

LMN bladder/bowlel develops late

169
Q

What is presentation of complete spinal cord transection?

A
  • bilateral loss of sensation below lesion + para/quadriplegia
170
Q

What is presentation of posterolateral column disease?

A
  • demyelination of dorsal columns, corticospinal tracts

- paresthesia in hands and feet, + romberg, impaired proprioception

171
Q

What is presentation of anterior spinal cord syndrome?

A
  • happens in upper thoracic chord

- bilateral loss of motor control, loss of pain/temp sensation, preserved mechanosensation

172
Q

What is presentation of disc prolapse?

A

s

173
Q

What is presenation of spondylolisthesis?

A

s

174
Q

What is presentation of tabes dorsalis?

A
  • due to tertiary symphilis
  • degerneation of dorsal columns –> progressive impaired sensation/proprioception and sensory ataxia
    no deep tendon reflex, + Romberg
175
Q

What is presentation of spinal tumor?

A
  • pain, numbeness, UMN spasticity/bowel + bladder
176
Q

What is presentation of epidural abscess?

A
  • back pain, radiculopathy
177
Q

What is spinal shock?

A

immediate areflexia [LMN sign] and motor paralysis below level of shock, reflex gradually returns, reveals true UMN lesion

178
Q

Why do lesions in brainstem cause more symptoms than in cerebrum?

A

lots of fiber tracts running in small apce

179
Q

What are “crossed signs”

A

face effects on opposite side from body effects

180
Q

What is wallenberg syndrome?

A
  • lateral medulla, affects CN V, CN 9, 10, 11 in nucleus ambiguus
    • loss of pain in ipsi face, contra body
  • hoarse voice, dysphagia, decreased gag
  • nystagmus, N/V, vertigo, gait ataxia,
  • horners
181
Q

What are defining features of a brainstem syndrome?

A

crossed signs –> ipsilateral symptoms of face from cranial nerves, contralateral symptoms on body

182
Q

Medial lesion vs lateral lesion which affects motor vs sensory?

A

ventromedial lesion = affects motor, corticospinal

dorsolateral = affects sensory, spinothalamic

183
Q

What is rubrospinal tract?

A
  • contributes to movement of upper limb

- from red nucleus, immediately cross and descend lateral funiculus

184
Q

What is tectospinal tract?

A

coordination of head movements

  • originate superior colliculus
  • crosses near origin and descends to cervical levels only
185
Q

What is function of corticoreticulospinal tract?

A

maintenance of posture during complex movement

186
Q

What is inverse myotatic reflex?

A
  • Group 1b afferents sense tenson on GTO
  • inhibit homonymous aMNs and synergists to terminate contraction
  • excite antagonits

Brain and Behavior Exam 2 (21 decks)

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