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Neuro > Unit III week 2 > Flashcards

Unit III week 2 Flashcards

1
Q

Light

A

electromagnetic radiation that travels in waves

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2
Q

Wave length = ?

Intensity = ?

A

Wavelength = color

Blue = 420 nm
Green = 530 nm
Red = 560 nm

Intensity (amplitude) = brightness

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3
Q

Cornea

A

provides ⅔ refractive (focusing) power for eye, transparent

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4
Q

Lens

A

provides ⅓ focusing power, under neural control and allows for focusing of nearby objects, transparent

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5
Q

Pupil

A

opening through which light enters

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6
Q

Ciliary muscles

A

control size of pupil

Accommodation = contract ciliary muscles, makes lens fatter

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7
Q

Retina

A

at back of inner eye - receptive organ of eye

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8
Q

Optic disc

A

Output neurons = retinal ganglion cells → group together at optic disc → form optic nerve

No photoreceptors at optic disc = blind spot

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9
Q

Photoreceptors

A

(rods/cones): capture light and convert to an electrical signal

Photoreceptors at back of eye - light must pass through all other cells before it reaches the photoreceptors

→ passes electrical signal to bipolar cells and horizontal cells then to ganglion cells

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10
Q

Fovea

A

region of most acuity where other cells are swept aside

-In fovea, 1:1 ratio of photoreceptor → bipolar cell → ganglion cell

As you get more out to periphery, the receptive field is larger - many photoreceptors → one bipolar cell → ganglion cell

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11
Q

Cones

A

mediate color vision, concentrated in fovea, work well only in bright light

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12
Q

Rods

A

color insensitive, work best in dim light

Dominant photoreceptor away from fovea

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13
Q

Horizontal cells

A

Mediates receptive field surround

Photoreceptors release glutamate (excitatory) onto horizontal cells

Horizontal cells release GABA (inhibitory) onto neighboring photoreceptors in field center

Modulate vertical flow of information via LATERAL information flow

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14
Q

Steps of Phototransduction

A

Light comes in, photon absorbed by Vitamin A (attached to membrane protein)

→ RHODOPSIN = opsin (7 transmembrane spanning protein) + retinal (light sensitive molecule)

→ intracellular cascade, activates TRANSDUCIN

→ cGMP phosphodiesterase

→ decrease in cGMP

→ close Ca2+ channels, and cell hyperpolarizes

Cell at -40mV in dark → in light hyperpolarizes to -70 mV (reversal potential of K+)

Increased intensity → increased hyperpolarization

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15
Q

Ganglion cells

A

only cells that make APs - all others communicate by graded changes in membrane potential which alters the rate of exocytosis of NT in a graded fashion

Ganglion cells either have ON center/OFF surround receptive fields or OFF center/ON surround

Get glutaminergic (excitatory) input from Bipolar cells

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16
Q

Bipolar cells

A

either have receptors that are excited by glutatmate (OFF center) or inhibited by glutamate (ON center)

Bipolar cells ALWAYS make excitatory synapses on ganglion cells

Determine receptive field property of ganglion cell!

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17
Q

On center ganglion cells

A

excited by light shining in their centers, inhibited by light in periphery

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18
Q

On center ganglion cells:

Light shone on photoreceptor in center:

→ photoreceptor _________ and releases less _______ onto _______ glutamate receptors of Bipolar cells

→ ______ inhibition of bipolar cells

→ _______ released by bipolar cell

→ ________ of ganglion cell

A

→ photoreceptor hyperpolarizes and releases less glutamate NT onto INHIBITORY glutamate receptors of Bipolar cells → LESS inhibition of bipolar cells → MORE NT released by bipolar cell → excitation of ganglion cell

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19
Q

On center ganglion cells:

Light shone on photoreceptors in surround

1) → photoreceptor _______ and releases __________
2) → reduce excitation of _______ cells
3) → horizontal cells __________ and release ________ onto neighboring photoreceptors in field center
4) → center photoreceptors release ______ glutamate NT onto ______ cells with ________ glutamate receptors
5) → inhibition of ______ cells increase when light shines on periphery
6) → ________ bipolar cell excitatory input to ganglion cell
7) → ________ firing rate of ganglion cell

A

1) → photoreceptor HYPERPOLARIZES and releases LESS GLUTAMATE
2) → reduce excitation of HORIZONTAL cells
3) → horizontal cells HYPERPOLARIZED and release LESS GABA onto neighboring photoreceptors in field center (decrease inhibition)
4) → center photoreceptors release MORE glutamate NT onto BIPOLAR cells with INHIBITORY glutamate receptors
5) → inhibition of BIPOLAR cells increase when light shines on periphery
6) → REDUCE bipolar cell excitatory input to ganglion cell
7) → REDUCE firing rate of ganglion cell

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20
Q

What are the 4 synapses in determining the receptive field properties of ganglion cells

2 excitatory
1 inhibitory
1 ??

A

2 excitatory =

1) photoreceptor→ horizontal cell
2) bipolar cell → ganglion cell

1 ALWAYS inhibitor =
1) horizontal cell → photoreceptor synapses

1 may be: field center photoreceptor → bipolar cell
-excitatory (OFF center bipolar cell, excitatory glutamate receptor on bipolar cell)
OR
-inhibitory (ON center bipolar cell, inhibitory glutamate receptor on bipolar cell)

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21
Q

Rebound Response

A

** after light turned off indicates that light was in the inhibitory part of the receptive field

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22
Q

Off center ganglion cells

A

excited by light in periphery, inhibited by light in center

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23
Q

Color-opponent ganglion cells

A
  • Cones of different color preferences converge in retina to produce ganglion cells with receptive fields partial to particular colors
  • Bipolar cells in fovea connected directly to one kind of cone in field center, and indirectly (via horizontal cells) to cones with a different color preference in field surround

→ Red-green opponents (e.g. RED ON-center and GREEN OFF-surround)

→ Blue-yellow opponents

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24
Q

Pupillary eye reflex

A

shine light in one eye, muscles in iris contract (pupil smaller) → consensual constriction in other eye

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25
Q

Mechanism of pupillary eye reflex (5 steps)

A

1) Light → AP in ganglion cells
2) → Pretectum gets excitatory input from BOTH eyes
3) → synapse in BOTH Edinger-Westphal nuclei (R and L)
4) → excite ciliary ganglion cells (preganglionic parasympathetic motor neurons)
5) → excitation of muscles in BOTH irises

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26
Q

Central visual pathway

optic nerve –> __________ –> ___________

optic tract then synapses in what 4 major regions

A

Optic nerves from two eyes merge at optic chiasm → axons from nasal half of each retina decussate → continue as optic tract

Optic tract stops at:

1) LGN (thalamus)
2) Pretectum
3) Suprachiasmatic nucleus of hypothalamus
4) Superior colliculus

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27
Q

RIGHT optic tract contains axon from where?

A

Right optic tract contains axons from RIGHT side of each retina which see the LEFT side of the visual world → right LGN

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28
Q

Pretectum

A

important for pupillary eye response

gets input from BOTH eyes and projects to BILATERAL Edinger-Westphal nuclei for pupillary eye reflex

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29
Q

Suprachiasmatic nucleus of hypothalamus

A

One stop of optic tract

important for visceral functions of day/night cycle

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30
Q

Superior colliculus

A

One stop of optic tract

coordinates head and eye movements

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31
Q

Lateral Geniculate Nucleus (LGN)

  • represents what visual field?
  • does it have binocular cells?
  • represents termination of what cells?
  • how many layers is its cortex?
  • sends projects out via what and to where?
A

LGN represents CONTRALATERAL visual field

**Gets input from both eyes, but eye origin remains separate in LGN layers → NO BINOCULAR INTERACTION IN LGN

After LGN, axons involved in visual processing fan out in OPTIC RADIATIONS to VISUAL CORTEX

Ganglion cell axons end in LGN

LGN composed of 6 layers

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32
Q

What layers of the LGN represent the contralateral eye

A

Layers 1, 4, 6 → contralateral eye (nasal axons decussated at chiasm)

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33
Q

What layers of LGN represent the ipsilateral eye

A

Layers 2, 3, 5 → ipsilateral eye

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34
Q

Magnocellular ganglion cells

-in what LGN layers?
-responsible for what?
acuity?
receptive field size?
doesn’t do what?

A

Layers 1, 2

spatial vision, motion and depth

Low acuity, large receptive fields, responsive to motion, no color vision (input from rods)

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35
Q

Parvocellular ganglion cells

-in what LGN layers?
-responsible for what?
acuity?
receptive field size?
doesn’t do what?

A

Layers 3-6

object vision, color, form, detail

High acuity, small receptive field, not responsive to motion, color vision (input from cones)

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36
Q

The parvocellular and magnocellular systems do what as they go to the visual cortex?

A

Two systems established in retina, remain segregated at LGN, and travel in separate, but parallel pathways through visual cortex

Parvocellular and magnocellular pathways project to different LGN layers → different layers in V1 → different layers in V2

parvocellular = color, form –> VENTRAL pathway, stripe and interstripe region in V2

Magnocellular = motion, depth –> DORSAL pathway, thick stripe in V2

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37
Q

Visual cortex

A

area 17

above and below calcarine fissure of occipital lobe

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38
Q

Retinotopic map

A

LGN axons radiate to visual cortex (V1) creating a map

Distorted because tiny fovea region has ½ of visual cortex

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39
Q

Hypercolumn

A

each microregion of V1, about 1mm on a side

Layered 1-6

contains simple cells, complex cells, blobs and ocular dominance columns

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40
Q

Input from 10,000 LGN axons, terminate in layer _______ of the visual cortex and create ______ cells that then send axons up and down in same hypercolumn to create ________ cells

Output of each hypercolumn exits layer _____ or _____ to go to higher visual areas

A

layer 4

simple cells send axons up and down in same hypercolumn to create complex cells

Layer 3 or 6

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41
Q

Ocular dominance columns

A

divide each hypercolumn in half for each eye → ganglion cells in a specific region of retina for each eye sends axons to side-by-side slabs of cortex

Cells at border between two eyes = BINOCULAR - receive input from both eyes

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42
Q

Line orientation and the visual cortex

A

lines in visual field lie in different rays of pinwheels

All cells in a vertical column are sensitive to same orientation

Horizontal rows are a pinwheel of different orientations

–> Orientation column pinwheels spin out over cortical surface, interconnected with neighboring hypercolumns

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43
Q

Color information is processed in the visual cortex where?

A

separated out from spatial information in retina, and handled in central regions of hypercolumns called BLOBS

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44
Q

Parallel processing of visual system

A

requirement that dissimilar dimensions (e.g. color and form) must be analyzed by separate, but parallel, neural systems

For different dimensions of an image(e.g. Shape, color, motion, spatial information) we have analogous systems that use hierarchical processing to construct higher levels of representation in their dimensions

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45
Q

Hierarchical processing of visual system

A

use successive synaptic integrations of highly specific synaptic inputs to construct higher and higher levels of representation of the retinal image until eventually we have cells that respond only to the complete form of an object

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46
Q

Dorsal Pathway from V1 goes through _________ –> _________ –> _________

A

“Thick Stripe” region of V2

Middle Temporal region of V5

Parietal lobe

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47
Q

Dorsal pathway is responsible for what?

A

travels from V1 dorsally to parietal lobe

Spatial vision - Motion, depth perception, WHERE pathway

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48
Q

Lesion to the middle temporal region of V5 results in what?

A

Middle Temporal important for direction and depth

Lesions to MT → impaired motion and depth perception

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49
Q

Ventral pathway from V1 goes through _______ and ________ region of _______ –> ________ –> _________

A

“Stripe” and “Interstripe” region of V2

V4

Temporal lobe

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50
Q

Ventral pathway is responsible for what?

A

travels ventrally from V1 to temporal lobe

Object recognition - color, form, pattern vision, WHAT pathway

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51
Q

Blob cells

A

color only, don’t care about shape, get input from color-opponent neurons

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52
Q

V2 stripe and interstripe region receive inputs from what type of cells in V1?

A

BLOB cells - specific for color

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53
Q

If you have a lesion in V4, what happens?

A

V4 lesions → impairment in color discrimination

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54
Q

Cortical simple cells

A

responsive to lines with certain orientations

Cells with an ON/OFF area that is a narrow line at some preferred orientation that is flanked on each side by OFF/ON areas

Max stimulation by narrow line of light covering all ON areas

Tightly tuned within a few degrees of its best orientation

Cells in the same penetration show same orientation selectivity

Generated by several overlapping LGN and ganglion cells that converge on one cortical cell in area V1 = hierarchical processing

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55
Q

How are cortical simple cells an example of hierarchical processing?

A

several cells with similar but spatially offset receptive fields converge on a higher order cell to create an altogether new type of receptive field (ON/OFF center ganglion cells –> simple cells with lines)

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56
Q

Cortical complex cells

A

receptive fields like simple cells but they abstract for position

Line or edge can be anywhere within receptive field and these cells like to see lines or edges moving across the field

Generated by excitatory synapses onto complex cells by convergence of several simple cells whose positions are slightly offset = hierarchical processing

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57
Q

Binocular Cells

A

receive input from LGN from both eyes

Receptive fields of two eyes are identical in orientation, region of retina, width, and on/off organization

Found at borders of ocular dominance columns

Mediate depth perception - select cells fire when object is certain distance away

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58
Q

Photoreceptor:

Location?
Diffuse light?
Receptive field shape?
Orientation selective?
Binocularly driven?
Position sensitive?
A 
Location - retina
Diffuse light - ok
Receptive field shape - tiny spot
Orientation selective - NO
Binocularly driven - NO
Position sensitive - YES
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59
Q

Ganglion cell

Location?
Diffuse light?
Receptive field shape?
Orientation selective?
Binocularly driven?
Position sensitive?
A 
Location - Retina
Diffuse light - so-so
Receptive field shape - Donut
Orientation selective - NO
Binocularly driven - NO
Position sensitive - YES
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60
Q

Simple cell

Location?
Diffuse light?
Receptive field shape?
Orientation selective?
Binocularly driven?
Position sensitive?
A 
Location - Cortex
Diffuse light - NO
Receptive field shape - Bar
Orientation selective - YES
Binocularly driven - YES
Position sensitive - YES
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61
Q

Complex cell

Location?
Diffuse light?
Receptive field shape?
Orientation selective?
Binocularly driven?
Position sensitive?
A 
Location - Cortex
Diffuse light - NO
Receptive field shape - Edge
Orientation selective - YES
Binocularly driven - YES
Position sensitive - NO
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62
Q

Monocular Deprivation

A

Normally: binocular cells receive inputs from both eyes with receptive field positions and orientation in two eyes being identical

Monocular deprivation during sensitive period of cortex development causes synaptic connections in cortex from deprived eye to degenerate and disappear

DOES NOT recover if deprived eye is reopened for duration of sensitive period - once connections are lost, they are gone for good

BUT retinal ganglion cell and LGN receptive fields remain intact (normal pupillary reflex)

If one eye is deprived at birth, the bands in LGN change - bands from deprived eye are reduced in size, and normal eye bands are expanded

Showed that you either “Use it or lose it”

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63
Q

Binocular Deprivation

A

Use it or lose it hypothesis would predict that cortex would be silent, with few synapses form either eye…WRONG!

Primary visual cortex was mostly normal (but animals were blind in both eyes), lots of binocularly driven cells

Showed that competition between converging synaptic inputs from two eyes, not disuse atrophy, is the mechanism

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64
Q

If left eye was deprived during sensitive period…what happens?

1) if right eye receives normal input
2) if right eye also deprived of vision

A

If right eye received normal visual input, all cortical cells would be driven by right eye

If right eye was also deprived of vision, then cortex will contain many binocularly driven cells, BUT animals were blind in both eyes (if deprived during sensitive period)

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65
Q

Strabismus

A

deviation of one eye

Normal visual stimuli, but each eye saw a different part of visual world

→ Very few binocular cells!

Almost all cells driven exclusively by one eye or the other (half and half)

No sync, no link - synchronous activity from both eyes is necessary to insure proper synaptic connections form during development in visual cortex

Showed: Cells that fire together wire together
-Done via NMDA receptor plasticity mechanism (AMPA upregulation etc.)

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66
Q

Conclusion based on monocular deprivation, binocular deprivation, and strabismus experiments?

A

NOT a use it or lose it mechanism, there is a competitive interaction between contralateral and ipsilateral eye, that requires normal pattern input spatially and temporally so areas of cortex represent same point in space

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67
Q

Sensitive period

A

2-3 year period of time after birth when connections can be altered by visual experience (corresponds with time babies eyes are moving farther apart)

If visual deficits not repaired soon after birth → irreversible damage to vision

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68
Q

Ocular dominance

A

a measure of relative synaptic input to a cell from each eye

-can range from only sensitive to ipsilateral eye, only responsive to contralateral eye, to only responsive to both eyes

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69
Q

Gross Pathology of Alzheimer’s (3)

A
  1. Diffuse atrophy
  2. Area around hippocampus (meso-temporal area) disproportionate
  3. Status spongiosis - present in any severe neurodegeneration
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70
Q

Histology of alzheimer’s

A

must have BOTH neurofibrillary tangles and neuritic plaques

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71
Q

Neurofibrillary tangles ion Alzheimers

  • Composed of?
  • Stained with?
  • Where do they begin?
A

bundles of paired helical filaments in cytoplasm of neurons that displace or encircle the nucleus

a. Filaments primarily composed of hyperphosphorylated forms of tau protein (normally involved in microtubule assembly)
b. Silver stain
c. First tangles begin in transentorhinal cortex

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72
Q

Neuritic amyloid plaques in alzheimer’s

A

beta pleated sheet configuration

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73
Q

Genetics of Alzheimer’s (3)

A
  1. APP on Chr21 → early onset for pts with down syndrome, or increased risk with mutation of APP gene
  2. Presenilin 1 and 2, Chr14 and 1→ altered AB
  3. APO-E4 = highest risk of AD
    - APO-E3 and E2, lower risk of AD
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74
Q

2 variants of frontotemporal lobar degeneration

A

primary progressive aphasia or behavioral variant

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75
Q

Histology of frontotemporal lobar degeneration

A

ubiquitin positive inclusions with TDP-43

1.TDP-43 inclusions usually associated with mutations in progranulin (growth factor secreted in response to injury and/or inflammation)

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76
Q

Pic Disease

A

aggregates of tau in the form of pick bodies

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77
Q

Pick bodies

A

Well demarcated, round, slightly basophilic inclusions in neuronal cytoplasm- aggregates of tau proteins

  • silver stain darkly stains pick bodies
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78
Q

Amyotrophic lateral sclerosis

A

Degeneration of upper and lower motor neurons (anterior horn cells)

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79
Q

Onset of ALS

A

early middle age - rapid course leading to death (due to respiratory failure) in 1-6 years

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80
Q

Clinical manifestations of ALS

A
  1. Lower motor neuron signs: symmetric atrophy and fasciculation
  2. Upper motor neuron signs: hyperreflexia and spasticity
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81
Q

Pathology of ALS (4)

A
  1. Shrinkage of precentral gyrus in severe ALS
  2. Marked depletion of neurons from anterior horn of spinal cord
  3. Ubiquitin-immunoreactive neuronal inclusions
  4. Loss of corticospinal fibers in pyramids of medulla
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82
Q

Pathology of Parkinson’s

A
  1. Depigmentation of substantia nigra and locus ceruleus
    a. Pigment incontinence and pigmentophagy
  2. Lewy bodies: Neurons contain eosinophilic intracytoplasmic round inclusions
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83
Q

Genetics of Parkinson’s (3)

A
  1. PARK1 - alpha-synuclein (AD)
  2. PARK2 - Parkin (AR, juvenile)
  3. PARK3 through 11 - some AD, AR, with differing ages of onset
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84
Q

Dementia with Lewy Bodies

A

1; Second most common dementing disorder in late life

  • Common to have concomitant AD
  • Begins with memory impairment and progresses to movement disorder
  1. Parkinson’s and Lewy Body Dementia appear to represent a clinico-pathologic continuum
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85
Q

Clinical presentation: Dementia with Lewy Bodies (4)

A
  1. Progressive cognitive decline
  2. Fluctuating cognition with pronounced variations in attention and alertness
  3. Recurrent visual hallucinations that are usually well-formed and detailed
  4. Spontaneous features of parkinsonism
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86
Q

Pathology of dementia with Lewy body (3)

A
  1. Cortical atrophy less severe than alzheimer’s
  2. Significant atrophy of limbic system
  3. Lewy bodies present with a-synuclein
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87
Q

Clinical characteristics of Huntington disease

A
  1. Delay of clinical abnormalities until 30-40 years
  2. Course extends 15-20 years
  3. Begins with athetoid movements with progressive deterioration leading to hypertonicity, dementia, and death
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88
Q

Pathology of Huntington disease (2)

A
  1. Progressive degeneration of striatum (Caudate and Putamen) and frontal cortex with neuronal loss and gliosis
  2. Loss of myelinated fibers
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89
Q

Genetics of Huntington disease

A
  1. AD
  2. Increased (more than normal 11-34) of CAG trinucleotide repeats within Huntingtin gene on chr 4p
  3. Preferentially paternal anticipation is due to greater genetic instability in spermatogenesis as compared to oogenesis
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90
Q

Role of frontal lobe (6)

A

i. Voluntary movement
ii. Language fluency (left)
iii. Motor prosody (right)
iv. Comportment
v. Executive function
vi. Motivation

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91
Q

Role of temporal lobe (5)

A

i. Audition
ii. Language comprehension (left)
iii. Sensory prosody (Right)
iv. Memory
v. Emotion

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92
Q

Role of Parietal lobe (6)

A

i. Tactile sensation
ii. Visuospatial function (right)
iii. Attention (right)
iv. Reading (left)
v. Writing (left)
vi. Calculation (left)

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93
Q

Role of occipital lobe (3)

A

i. Vision
ii. Visual perception
iii. Visual recognition

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94
Q

Broca’s aphasia

A

lesion in Broca’s area of left hemisphere (Brodmann areas 45), nonfluent aphasia

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95
Q

Motor aprosody

A

lesion to region equivalent to Broca’s area in right hemisphere

i.Inability to inflect speech with emotion

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96
Q

Traumatic brain injury (3)

A

i. Cortex damaged by direct injury via contusion
ii. Bleeding from damaged blood vessels can also occur → intraparenchymal, subdural, or epidural hemorrhage
iii. Widespread white matter damage called diffuse axonal injury is also typically present

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97
Q

Three frontal lobe syndromes

A
  1. Disinhibition
  2. Apathy
  3. Executive dysfunction
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98
Q

Disinhibition:

  • Where is the lesion?
  • What is it?
A

orbitofrontal cortex lesions

  1. Person can no longer adequately integrate limbic drives into an appropriate behavioral repertoire in the face of social situations where limbic drives are influential and impulse control is critical
  2. Irritability, loss of empathy, impulsivity, hypersexuality, hyperphagia, violence
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99
Q

Apathy:

  • Location of lesion?
  • What is it?
A

medial frontal cortex lesions

1.Loss of motivation

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100
Q

Executive dysfuntion:

  • location of lesion?
  • What is it?
A

dorsolateral prefrontal cortex lesions

  1. Loss of capacity to plan, carry out, and monitor goal-directed action
  2. Problems with altering actions in response to changing environmental stimuli
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101
Q

4 cognitive disorders of temporal lobe

A
  1. Wernicke’s aphasia
  2. Sensory aprosody
  3. Amnesia
  4. Temporal lobe epilepsy
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102
Q

Wernicke’s aphasia

A

auditory comprehension is impaired because of lesion in posterior region of left superior temporal gyrus (Wernicke’s area, Brodmann area 22)

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103
Q

Sensory aprosody

A

diminished ability to comprehend emotional inflection in speech - lesion in right hemisphere analogue of Wernicke’s area

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104
Q

Amnesia related to temporal lobe

A

due to removal of hippocampus bilaterally

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105
Q

Limbic system is in the ______ lobe

A

temporal

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106
Q

Limbic system

A

(fight/flight, feeding, sexuality)

1.Circuit of hippocampus, parahippocampal gyrus, cingulate gyrus, anterior nucleus of thalamus, mammillary bodies, fornix = center of human emotional function

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107
Q

Temporal lobe epilepsy (TLE)

A

a. Related to focal cortical lesions in temporal lobe that produce complex partial seizures
b. Many behavioral phenomena can be associated with these seizures → deepend emotionality, hyperreligiosity, philosophical interests, hypergraphia
c. Interictal state of patients with TLE

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108
Q

Parietal lobe lesion deficits

A

produce deficits in tactile sensation, but also cognition → visuospatial dysfunction, inattention to contralateral space (right parietal with left hemineglect), and reading, writing, and calculation disorders (all with LEFT side lesions)

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109
Q

Hemineglect

A

failure to report, respond to, or orient to sensory stimuli that cannot be explained by primary sensory dysfunction

  1. Inattention to one side of the body or extrapersonal space
  2. Due to RIGHT parietal hemisphere lesions
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110
Q

Why is hemineglect due to right hemisphere lesions?

A

a. Right hemisphere has capacity to attend to both sides of space, whereas left can only attend to contralateral space
b. Thus a right parietal lesion will only permit surveillance of RIGHT hemispace
c. Left hemineglect is more severe and lasting than right hemineglect

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111
Q

Occipital lobe lesions lead to what?

A

visual function → hemianopia, quadrantanopia often

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112
Q

Occipitotemporal cortex:

A

VENTRAL stream, WHAT

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113
Q

Occipitoparietal cortex:

A

DORSAL stream, WHERE

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114
Q

Visual field deficits

A

actually have problems seeing object

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115
Q

Visual agnosia

A

Deficit to occipitotemporal or occipitoparietal cortex causing impairment with recognition - object SEEN normally, but adequately recognized

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116
Q

Lesion causing object agnosia

A

Left occipitotemporal lesion

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117
Q

Lesion causing face agnosia (prosopagnosia)

A

Right occipitotemporal lesion

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118
Q

Lesion causing sumultanagnosia (failure to recognize entirety of visual array)

A

bilateral occipitoparietal lesions

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119
Q

Cerebral disconnection

A

lesion disconnecting one part of brain from another causing behavioral disturbances

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120
Q

2 examples of cerebral disconnection

A

i. Conduction aphasia = linguistic disconnection due to damage to arcuate fasciculus (Wernicke’s area is disconnected from Broca’s area)

ii. Hemispheric disconnection = lesions of corpus callosum
- Surprisingly few effects - get anomia, agraphia, apraxia of left hand

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121
Q

Types of eye movements (4)

A

1) Smooth pursuit
2) Saccades
3) VOR and Optokinetic nystagmus (OKN)
4) Vergence

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122
Q

Smooth pursuit

A

tracking (to keep an object on the fovea)

visually-evoked tracking of movements

Used once object is on or near the fovea

Slower movements to track a moving object

Analyze position, direction of movement, and speed in visual cortex

→ descending command to brainstem conjugate movement pattern generators

Can only maintains foveation at max rate of 50 degrees/sec

Completely dependent on visual input

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123
Q

Saccades

A

rapid, ballistic (to bring an object onto the fovea)

rapid eye movement that brings eyes to a predetermined target or position

Ballistic in character - programmed to foveate a particular target even if target moves after saccade was initiated

Up to 700 degrees/second

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124
Q

Vestibular Ocular Reflex (VOR) and Optokinetic Nystagmus (OKN)

A

combination of pursuit and saccades

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125
Q

Vergence

A

moving the fovea to an object closer (convergence) or farther away (divergence)

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126
Q

Lateral and medial recti –> what movement?

Superior and inferior rectus → what movement?

Superior and inferior oblique → what movement?

A

Lateral and medial recti → horizontal rotation

Superior and inferior rectus → vertical displacement

Superior and inferior oblique → rotation about visual axis, and some vertical movement

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127
Q

contains motor neurons for what extraocular muscles?

Oculomotor (III) nuclei
Trochlear (IV) nuclei
Abducens (VI) nucleus

A

Oculomotor (III) nuclei: medial rectus, inferior and superior rectus, and inferior oblique muscles

Trochlear (IV) nuclei: superior oblique

Abducens (VI) nucleus: lateral rectus muscle

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128
Q

Conjugate Movements

A

eyes move same amount in same direction

EX) VOR: eyeball rotation precisely opposing head rotation

Can be fast (saccades), or slow (tracking movements)
Elicited by visual and vestibular inputs

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129
Q

Optokinetic nystagmus

A

rhythmic pattern of saccades and tracking movements - visually evoked nystagmus due to a moving visual stimulus

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130
Q

Vergence Movements

A

eyes moving in opposite directions

EX) near reflex

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131
Q

Near Reflex

A

both eyes town nasally to focus on near object

Both medial recti contract → pull eyes nasally

Pupils constrict to increase depth of field
-Ciliary muscle contract → lens becomes fatter (for focus on near object)

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132
Q

Pattern generator for horizontal saccades

A

Paramedian Pontine Reticular Formation (PPRF) (near abducens nucleus)

Horizontal saccades driven CONTRALATERALLY - saccade to left driven by activity in right frontal eye field

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133
Q

Important control center for saccades (2)

A

cortex (FEF) and superior colliculus

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134
Q

Frontal eye field

A

anterior to head representation in motor cortex

voluntarily generated saccade

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135
Q

Frontal eye field can activate saccades via two pathways

A

1) Direct to reticular formation

2) Via superior colliculus to reticular formation
- Involves auditory spatial map, retinotopic map, and somatotopic map all superimposed on motor map for the movement resulting from saccade

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136
Q

Change in saccades how?

Damage superior colliculus →

Damage to frontal eye field →

Damage superior colliculus and frontal eye field →

A

Damage superior colliculus → saccades less accurate, occur less often, but still happen

Damage to frontal eye field → TEMPORARY loss of ability to generate saccades

Damage superior colliculus and frontal eye field → permanent loss of ability to make saccades

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137
Q

“Blindsight response”

A

occurs with stroke in visual cortex

light flashed in dark room, eyes foveate to light, but the say they didn’t see anything → superior colliculus still drives saccade

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138
Q

6th nerve (abducens) deficit –> ?

A

6th nerve (abducens) → cannot laterally rotate in side ipsilateral to lesion

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139
Q

3rd nerve palsy (oculomotor) → ? (3 symptoms)

A

3rd nerve palsy (oculomotor) → ptosis (drooping eyelid), down and out position of eye (lateral rectus remains intact, but medial rectus not), and mydriasis (pupil dilation)

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140
Q

Children with hydrocephalus → what eye exam findings? (3)

A

setting sun gaze (problems with upgaze) + enlarged pupils + sluggish to react

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141
Q

Parietal Eye Field (PEF)

A

reflexive direction of saccade

→ activate Brainstem Gaze Center (BGC) directly, or indirectly through Superior Colliculus (SC)

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142
Q

Dorsolateral Prefrontal Cortex = DLPC

A

Inhibits reflex saccades, provides advanced planning of saccades

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143
Q

Supplementary Eye Fields = SEF

A

Coordinates saccades with body movement

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144
Q

Substantia Nigra (pars reticulata) = SNPR and saccadic movements

A

Inhibits superior colliculus

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145
Q

Caudate Nucleus = CN

and saccadic movements

A

Inhibits substantia nigra pars reticulata

CN inhibition of SNPR → activation of SC

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146
Q

**Internuclear Ophthalmoplegia

A

Caused by MLF damage resulting in disconnection in the coordination of medial and lateral recti during horizontal gaze movements

Right sided lesion to MLF → when patient looks left, left eye will go lateral, but right eye won’t medially deviate normally

**When looking to the right, eyes move normally!

**NO defect in convergence!

Common in patients with MS

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147
Q

Nystagmus

A

aka vestibular nystagmus

Sawtooth movement of eyes, slow ramp opposite to head rotation, fast saccade to center of eye position

Head turns right, then eyes counter rotate left - if head continues to turn, eyes slowly rotate left until the limit of eye rotation is reached, then snap quickly back (right) to a new fixation point

Direction of nystagmus defined by direction of rapid saccade

148
Q

Refractive Errors (4)

A

nearsightedness, farsightedness, astigmatism, presbyopia

When light doesn’t focus properly on retina, causes blurred vision and difficulty performing daily activities
Vision can be corrected with glasses to help focus light rays more precisely in eye and in turn improve vision

149
Q

Nearsightedness

A

optical power of eye is too large and causes light to focus in front of the retina

150
Q

Farsightedness

A

optical power of eye is too small and causes light to focus behind the retina

151
Q

Astigmatism

A

shape of cornea causes light to focus in front or behind retina

152
Q

Presbyopia

A

results when eye progressively loses ability to focus on near objects

Caused by natural aging as lens becomes less flexible

Around age 40-50 years

Treatment with simple magnifying lenses or bifocals can help improve near vision

153
Q

Basic Eye Exam: (6 components)

A

1) Visual Acuity: one eye at a time at 20 foot distance
2) Visual Fields: look at nose, cover one eye, old up fingers in visual fields
3) Ocular Motility: follow finger left, right, up and down
4) Pupils: round, reactive to light, equal
5) External exam (eyelids, conjunctiva, cornea)
6) Fundoscopic exam (red reflex, disc, retina)

154
Q

Unilateral Red Eye: (8)

A

1) Bacterial/Viral conjunctivitis
2) Iritis
3) Corneal abrasions
4) Corneal ulcers
5) HSV keratitis
6) Herpes Zoster Ophthalmicus
7) Pterygium
8) Subconjunctival hemorrhage

155
Q

Bacterial conjunctivitis

2 common bugs that cause it

A

“Pink Eye”

Inflammation of conjunctiva caused by bacterial infection

Most common = Staph aureus and Strep pneumoniae

156
Q

Bacterial conjunctivitis

Symptoms

A

Red eye with purulent discharge
-minimal loss of vision

More inflammation of conjunctiva than viral (red)

Purulent discharge (white-yellow color)

Eyelid swollen, almost closed

157
Q

Bacterial conjunctivitis

Treatment

A

Antibiotic eye drops for one week

Usually self-limiting, but treatment shortens clinical course and reduces person-to-person spread

158
Q

Viral conjunctivitis

A

More common than bacterial conjunctivitis

Common after URI

Adenovirus most common cause

159
Q

Viral conjunctivitis (3)

Symptoms

A

Moderate inflammation of conjunctiva (pink)

Associated with watery discharge

+/- preauricular lymph node enlargement

160
Q

Viral conjunctivitis

Treatment

A

Hand hygiene so it doesn’t spread to contralateral eye

No specific treatment - self-limiting within a week

Cool compresses and artificial tears

161
Q

Iritis

A

form of uveitis with inflammation of iris

162
Q

Iritis

Symptoms (6)

A 
Can have acute onset
Ocular/periorbital eye pain
Photophobia
Blurred/cloudy vision
Redness (near limbus=junction between cornea and sclera)
Irregular shape of pupil
163
Q

Iritis

Treatment

A
  • Topical steroid drops
  • Dilating eye drops
  • Occasionally topical glaucoma drops

**Second recurrence → systemic workup recommended

164
Q

Corneal abrasions + Symptoms (6)

A

painful scratch involving cornea

Severe eye pain or foreign body sensation with acute onset, tearing, blurred vision, and redness

Exam may show irregular epithelium, slightly cloudy

165
Q

Corneal abrasions

Treatment

A

Mild → artificial tears, topical abx

Large → abx, patching of eye, oral pain meds

NO topical anesthetic eye drops → delay healing process

166
Q

Corneal ulcers

+ causes?

A

(bacterial keratitis): infection of corneal stroma

associated with injury/abrasion, contact lens wear

167
Q

Corneal ulcers

Symptoms (8)

A

acute onset, severe pain, redness, decreased vision, eyelid swelling

White infiltrate seen in cornea

+/- thinning of cornea where infiltrate is present

+/- Hypopyon inside anterior chamber

168
Q

Corneal ulcers

Treatment

A

Small → 4th gen fluoroquinolone

Large → culture + fortified abx (vanco, tobramycin) - REFER

Slow healing, can require weeks of therapy

**Can leave corneal scar with permanent vision loss

If corneal thinning results in perforation, corneal transplant can be performed

169
Q

HSV keratitis:

A

viral infection of corneal epithelium

Primarily HSV-1

One of the most frequent causes of permanent vision loss

170
Q

HSV keratitis:

Symptoms (5)

A

Acute onset with variable symptoms of pain, visual blurring, and watery discharge

Unilateral eye redness (can be bilateral)
Pain
Photophobia
Decreased vision
Tearing
171
Q

HSV keratitis:

Special test

A

Fluorescein on ocular surface shows dendritic epithelial ulcer in branching pattern with terminal bulbs

172
Q

HSV keratitis:

Treatment

A

typically resolves spontaneously

Topical trifluridine
Oral acyclovir

Once healed, may have corneal scar, can cause blurred vision

173
Q

Herpes Zoster Ophthalmicus + Symptoms

A

reactivation of VZV

Symptoms: prodromal period of fatigue, low grade fever, unilateral rash on forehead, upper eyelid, and nose

Includes dermatological involvement of V1 distribution

Unilateral eye pain, redness, decreased vision, photophobia

174
Q

Herpes Zoster Ophthalmicus

special test

A

Fluorescein on corneal surface can reveal multiple swollen lesions with staining around them

175
Q

Herpes Zoster Ophthalmicus

treatment

A

Oral acyclovir or valacyclovir

Neurotrophic cornea may develop

At risk for chronic dry eye and infections requiring chronic artificial tear supplements

176
Q

Pterygium

A

benign fibrovascular tumor
UV induced
Often becomes inflamed

Treatment: artificial tears, sunglasses, vasoconstrictors (short term), conjunctival autograft with tissel glue

177
Q

Subconjunctival hemorrhage

A

ruptured blood vessel under conjunctiva

Can happen in absence of trauma, but can happen with sneezing, coughing, excessive eye rubbing, trauma

Usually asymptomatic

No treatment necessary - resolves in one week

178
Q

Bilateral Red Eye (2)

A

Allergic conjunctivitis

Dry Eyes

179
Q

Allergic conjunctivitis

+ Symptoms (4)

A

occurs when allergens irritate the conjunctiva, seasonal

Symptoms: itching**, eyelid swelling, redness, watery discharge

180
Q

Allergic conjunctivitis + treatment (4)

A

Avoid offending allergens
Topical antihistamine
Topical mast cell stabilizers
Topical steroids

181
Q

Dry Eyes + symptoms (4)

A

common disorder of the tear film

Symptoms:
Foreign body sensation
Blurred vision
Reflex tearing
Condition worsens towards end of day and activities that require attention (Reading, computer work)
182
Q

Causes of dry eye

A

Body not making enough tears

  • Systemic conditions: rheumatoid arthritis, lupus, grave’s disease
  • Medications: antihistamines, pain meds, antidepressants

May also occur if they are producing tears, but it’s just evaporating quickly

183
Q

Special tests: for dry eyes (2)

A

Schirmer’s test

Corneal staining pattern

184
Q

Treatment for dry eyes (5)

A

1) Artificial tears
2) Flaxseed oil, omega-3 vitamins
3) Medicated eye drops to help improve tear production (restasis)
4) Modification of oral medications, treatment of underlying systemic disease
5) Punctal plugs - tear outflow blocked

185
Q

Angle Closure Glaucoma

risk factors (3)

A

Risk factors: ethnicity (asian), age (60s-70s), and hyperopia

186
Q

Angle Closure Glaucoma

symptoms (6)

A 
Unilateral, severe eye pain
Nausea
Redness
Blurred vision
Halos around lights
**sight threatening glaucoma
187
Q

Angle Closure Glaucoma

exam findings (5)

A 
Sluggish mid-dilated pupil
Conjunctival injection
Hazy cornea
Shallow anterior chamber
Eye may feel hard on palpation
188
Q

Angle Closure Glaucoma treatment

A

laser peripheral iridotomy

Allow aqueous to gain access to anterior chamber and opens trabecular meshwork

189
Q

Open Angle Glaucoma

+ risk factors

A

Progressive disease of optic nerve

Associated with elevated IOP
-Elevated IOP causes stress on optic nerve → nerve cell damage, enlargement of optic nerve

Risk factors: age, ethnicity, myopia, family history

190
Q

Open Angle Glaucoma

Symptoms

A

Symptoms: Usually do not experience symptoms - slowly causes damage to peripheral vision

191
Q

Cataracts

+ symptoms

A
  • gradual clouding of eye’s natural lens
  • Purpose of lense is to focus light on retina
  • Causes progressive decline in vision as it obstructs light from entering eye

-Symptoms:
Vision like looking through dirty window, color desaturation, or night-time glare and halos

-Develops with age as lens proteins breakdown

-Can occur in younger patients with:
Poorly controlled diabetes
Steroids
Trauma
Radiation
192
Q

Treatment of cataracts

A

Cataracts develop to point that patient’s vision cannot be corrected with glasses, interfering with daily activities → surgical intervention

  • Phacoemulsification: lense removal using ultrasound probe through small incisions
  • Cataract replaced with artificial lens
  • Necessary to allow for functional vision post-op
193
Q

Symptoms of orbital floor fracture

A

pain, ecchymosis, edema, proptosis, enophthalmos, emphysema, nausea/vomiting, bradycardia, diplopia, double vision

194
Q

Basal Cell Cancer of eyelid

A

Commonly involves lower eyelid

Tx = excision with margin control (Mohs surgery) and reconstruction

195
Q

Thyroid Eye Disease

A

Primary inflammatory disease of orbital soft tissue

Get huge swollen eyes due to EOM hypertrophy, hyaluronic acid overproduction, and immune cell proliferation

Autoimmune disease: target is orbital fibroblast

196
Q

Autoimmune mechanism behind thyroid eye disease

A

Autoimmune disease: target is orbital fibroblast

  • Orbital fibroblast expresses TSH-R and ILGF-R
  • Stimulatory autoantibodies (TSI) stimulate orbital fibroblast to produce proinflammatory cytokines and recruit inflammatory cells into orbital soft tissue
  • Leads to production of hyaluronan (glycosaminoglycan, GAG)
  • Lymphocyte infiltration, GAG production, and orbital fibroblast proliferation (adipogenesis) causes EOM hypertrophy

Associated with autoimmune thyroid disease (Graves)
-Dysthyroidism is NOT the cause

197
Q

Treatment of Thyroid Eye Disease

A

1) Typically self-limited disease
2) Immunomodulators during active phase (lasts 18-36 months)
3) Surgery during quiescent phase - make orbit bigger via decompression surgery (take out medial part of orbit so fat, muscles, etc can expand into nose

198
Q

Nasolacrimal duct obstruction

A

blockage in lacrimal duct (below lacrimal sac)

  • Chronic NLDO → epiphora (overflow of tears onto face), chronic dacryocystitis
  • Acute NLDO → Dacryocystitis (infection of lacrimal sac)

Treatment: Dacryocystorhinostomy (DCR)

199
Q

Macula

A

-region in retina = fovea and foveola, central vision

Fovea = central 1.5 mm, sharp central vision
Foveola = central 0.35 mm, small depression in retina
200
Q

Peripheral retina is responsible for what?

A

peripheral and night vision

201
Q

Ora serrata

A

anterior termination of retina (just behind lens and pars plana)

202
Q

Pars plana

A

posterior ciliary body (right behind lens)

203
Q

Retinal pigment epithelium (RPE)

A
  • Provides support for photoreceptor metabolism and provides tight blood-retina barrier
  • Potential space between neurosensory retina and RPE –> fluid/abnormal waste products can collect there
204
Q

Vasculature of retina:

Central retinal artery

Central retinal vein

Capillaries

A

Central retinal artery

  • Branch of ophthalmic artery from internal carotid artery
  • Blood to inner ⅔ of retina
  • Smaller than veins, lighter color

Central Retinal vein - drains blood supply from eye

Capillaries = form inner blood-retina barrier

205
Q

Choroid

A

middle layer between sclera and retina

vascular supply, metabolic and nutritional support

Vascular layer with highest blood flow per tissue weight (provides blood to outer ⅔ of eye)

206
Q

Possible pathologies of choroid (3)

A

1) Uveitis: inflammation of choroid/uveal tissue
2) Choroidal nevus
3) Tumors - mets (melanoma)

207
Q

Sclera

A

outer layer, white, fibrous covering

208
Q

Vitreous

A

main volume of posterior eye (water, hyaluronic acid, collagen)

209
Q

Vascular supply for optic nerve: _______ and _________ branching from ___________ artery

possible disease of optiv nerve (CN II)

A

Vascular supply: ophthalmic artery → posterior ciliary artery branches to optic disc and pial capillaries

Diseases: glaucoma

210
Q

Sub-retinal hemorrhage

A

between retinal pigment epithelium and sensory retinal layer

211
Q

Dot-Blot hemorrhage

common in what disease?

A

common in diabetes, middle layer of retina

-can be present in Non-proliferative diabetic retinopathy (NPDR)

212
Q

Flame hemorrhage

common in what disease?

A

common in HTN

follows nerve fiber layer, inner layer of retina

-can be present in Non-proliferative diabetic retinopathy (NPDR)

213
Q

Preretinal hemorrhage

A

boat shaped

obscures retinal vessels

in front of retinal layer

214
Q

Vitreous hemorrhage

common in what disease?

A

diffuse bleeding into vitreous cavity

obscures retina

common in diabetes

215
Q

Lipid/Exudative disease in the eye

common in what disease?

A

Lipids leak from retinal vessels → common in diabetes

-can be present in Non-proliferative diabetic retinopathy (NPDR)

216
Q

Drusen

hallmark of what disease?

A

yellow circular deposits underneath retina

hallmark of macular degeneration

217
Q

Cotton wool spot

common in what diseases?

A

fluffy white areas, capillary ischemia → common in diabetes and HTN

218
Q

Choroidal nevus

A

benign pigmented neoplasm, asymptomatic, incidental finding

219
Q

Diabetic retinopathy

risk factors (4)

A

1 cause of blindness in working age adults

Risk factors: duration of diabetes, glycemic control, blood pressure, pregnancy

220
Q

Pathophysiology of diabetic retinopathy

A

Microvascular injury to small vessel capillaries → retinal hemorrhage, capillary leakage → ischemia

→ Neovascularization: eye trying to compensate for ischemia, but areas where new vessels are cause problems

Two types: Non-proliferative diabetic retinopathy (NPDR) and Proliferative diabetic retinopathy (PDR)

221
Q

Non-proliferative diabetic retinopathy (NPDR)

A

1 cause of vision loss in DM

Early changes in eye, may be asymptomatic

Includes: Microaneurysms, flame hemorrhage, dot-blot hemorrhage

Diabetic macular edema - retina gets swollen

Hard exudates - lipoprotein leakage from capillaries

222
Q

Proliferative diabetic retinopathy (PDR)

A

More severe, vision threatening

Neovascularization - around optic disc and peripheral retina

Fibrovascular proliferation that pulls on retina

223
Q

Complications of Proliferative diabetic retinopathy (PDR) (3)

A

1) Vitreous hemorrhage - blood vessels leak into vitreous cavity causing complete loss of vision
2) Tractional retinal detachment - fibrovascular tissue pulls neurosensory retina detaches from back wall of eye and Retinal pigment epithelium
3) Neovascularization of iris → neovascular glaucoma because neovascularization of iris blocks egress of fluid from eye

224
Q

Management of diabetic retinopathy (4)

A

1) Glycemic and BP control, screening eye exams
2) Laser photocoagulation
3) Anti VEGF injections
4) Pars Plana Vitrectomy (with vitreous hemorrhage)

225
Q

Hypertensive retinopathy causes what two vascular changes

A

1) Vasoconstriction → arteriolar narrowing

2) Arteriosclerosis → copper and silver wiring, arteriovenous nicking
- When wall of artery gets thick

226
Q

Acute hypertensive retinopathy (3)

A

1) Retinal hemorrhage
2) Macular edema and exudate
3) Optic disc edema (Papilledema if bilateral), especially with acute, severe HTN

227
Q

Central retinal vein occlusion

A

→ extensive retinal hemorrhage and edema

Often related to HTN

Dilated veins, extensive hemorrhage

228
Q

Central retinal artery occlusion

A

→ cherry red spots

“Stroke” to eye

229
Q

Age-related macular degeneration is a disease of the __________

risk factors (4)

A

disease of choroid

Risk factors: age (>75 years), race (caucasians), gender (females), tobacco

230
Q

Dry (nonexudative) Age-related Macular Degeneration (3)

A

1) Drusen - lipoprotein deposits
2) RPE changes - atrophy and hyperpigmentation
3) Geographic atrophy - severe vision loss if in fovea

231
Q

Wet (exudative) Age-related Macular Degeneration

A

more vision loss, less common

  • Blood vessels start to leak and bleed in back of eye
  • Choroidal neovascularization (CNV) = vessels growing out from choroid into retina → subretinal hemorrhage, macular edema, scarring
232
Q

Treatment of Wet (exudative) Age-related Macular Degeneration

A

Anti-VEGF intravitreal injections every 1-2 months

  • First treatment to improve vision in wet AMD
  • Regression of CNV
  • Improved macular edema
233
Q

Optic neuropathies (2)

A

Glaucoma and Papilledema

234
Q

Glaucoma

A

most common optic neuropathy

Damage to nerve fiber layer and optic disc resulting in visual field loss - insidious onset of visual field loss

235
Q

Risk factors of glaucoma (6)

A

age, elevated IOP, race, central corneal thickness, family history, myopia

236
Q

Findings in glaucoma exam (4)

A

Elevated IOP (not in all)

Enlarged Cup/Disc or asymmetry

Optic disc hemorrhage

Visual field defects

237
Q

Treatment of glaucoma

A

*Screening - asymptomatic until end stage

  • Lower IOP
  • Meds → decrease aqueous humor production or increase outflow
  • Laser
  • Surgery - drain fluid from eye to allow fluid to move from inside to outside of eye
238
Q

Papilledema

A

bilateral optic disc swelling due to elevated ICP

→ Blurring of disc margin, sometimes flame hemorrhage on margin

239
Q

Anisocoria

A

unequal size of pupils

can be physiological if it is the same in light and dark

240
Q

Interrupt parasympathetic pupillary fibers –> ?

A

→ mydriasis (enlargement), and abnormal reaction to light

Parasympathetic → sphincter constriction (light)

241
Q

Interrupt sympathetic pupillary fibers –> ?

A

→ miosis (constriction), and abnormal reaction to dark

EX) Horner syndrome

Sympathetic → radial dilation (dark)

242
Q

“Light-near dissociation”

A

tonic pupil, dilated pupil that does not respond to light but will constrict during near reflex

243
Q

Left inferior quadrantanopia is a deficit where?

A

lose left lower quadrant in both eyes = homonymous field loss

244
Q

What happens if you damage the optic chiasm?

A

→ lose retinal vision from each eye, get tunnel vision = bitemporal field loss (NOT homonymous)

245
Q

Left optic radiations “Meyer’s Loop” lesion

A

→ lose upper right quadrant in both eyes = Homonymous field loss

246
Q

Homonymous field loss

A

same part of the field with respect to left to right in each eye loss of visual field

247
Q

Left occipital lesion inferior to calcarine sulcus

A

lose upper right quadrant in both eyes = Homonymous field loss

below sulcus → lose vision in upper half of contralateral field

248
Q

Calcarine sulcus lesion, above sulcus

A

above sulcus → lose vision in lower half of contralateral field

249
Q

Posterior vs. anterior region of calcarine sulcus represents what regions of visual field

A

More posterior = more medial part of visual field

250
Q

Optic nerve lesion/optic neuropathy results in what deficits

A

monocular vision loss, color vision impaired

Afferent pupillary defect = hallmark of optic nerve or optic tract disturbance

251
Q

Afferent pupillary defect (APD)

A

problem prior to synapse in LGN

Hallmark of optic nerve or optic tract disturbance

EX) shine light in right eye, both pupils constrict, shine light in left eye, and it dilates = left APD

252
Q

What four questions should you ask to determine source of diplopia

A

1) Is it binocular or monocular?
2) Is it horizontal or vertical?
3) Is it worse left, right, up, or down?
4) Is it worse near or distance?

253
Q

Oscillopsia

A

appearance of movement of visual world, eyes not steady

EX) Nystagmus

254
Q

Types of nystagmus (3)

A

1) Pendular: slow-slow
2) Jerk: fast-slow
3) Mixed: slow-slow + fast-slow

255
Q

Routes of systemic absorption for topical drugs of eye (3)

A

1) Corneal route of absorption
2) Nasolacrimal route of absorption
3) Conjunctival-Scleral route of absorption

256
Q

Corneal route of absorption

A

tears → cornea → aqueous humor → iris → systemic circulation

257
Q

Nasolacrimal route of absorption

A

tears → systemic circulation

258
Q

Conjunctival-Scleral route of absorption

A

tears → conjunctiva → sclera → ciliary body

259
Q

Appearance of drug in aqueous humor is dependent on ______________

A

passive diffusion through cornea

260
Q

Anterior Chamber of Eye

A

pathway for secretion and drainage of aqueous humor

Humor secreted slowly, continuously by cells of epithelium covering ciliary body → drains into canal of Schlemm

261
Q

Primary open angle glaucoma

A

nerve damage, one of most common preventable causes of blindness
Associated with increased IOP

262
Q

Drug targets in glaucoma (especially open angle)

A

PGs = increase aqueous humor outflow

B1 and B2 = increase aqueous humor production

Bicarb increases aqueous humor production

263
Q

Treatment of Primary open angle glaucoma (4 types of drugs)

A

1) PG analog (monotherapy initially)
2) Good response to PA but short of target → add B-BLOCKER or CARBONIC ANHYDRASE INHIBITOR or A2 AGONIST
3) Poor response to PA → discontinue PA, substitute another class (B-blocker or carbonic anhydrase inhibitor)

264
Q

Closed Angle Glaucoma

A

aka ACUTE congestive, narrow angle glaucoma
Less common

Pathophysiology: mechanical blockage of trabecular meshwork by peripheral iris → extreme fluctuations in IOP - requires emergent treatment

265
Q

Goal of treatment with closed angle glaucoma

A

drugs with rapid onset to reduce pressure at time of attack until surgery (iridectomy/laser iridotomy) can be performed

266
Q

Closed angle glaucoma drugs to treat (4) and their mechanism

A

1) Pilocarpine (cholinergic agonist) → induce miosis and contraction of ciliary muscle → free entrance to trabecular space from blockage by iris tissue, increase outflow
2) Apraclonidine and Timolol: given with pilocarpine to synergistically reduce IOP (reduce aqueous humor production)
3) Acetazolamide (Carbonic anhydrase inhibitor) → block formation of humor
4) Mannitol or glycerol → osmotic diuresis → intraocular dehydration

267
Q

________ and _________ can precipitate closed angle glaucoma attacks

A

anticholinergics

decongestants

268
Q

Latanoprost

mechanism and use

A

Prostaglandin analogs

First line medical therapy for treatment of open angle glaucoma

Mechanism: Topical PGF-2a prodrug
Lowers IOP by facilitating aqueous humor outflow through accessory uveoscleral outflow pathway

269
Q

Side effects of prostaglandin analogs (3)

A

brown discoloration of iris, eyelash lengthening and darkening, ocular irritation

270
Q

Brimonidine, Apraclonidine

use and mechanism

A

Alpha-2 adrenergic agonists

Add on second or third line therapy of open angle glaucoma

Mechanism: topical selective a2 agonist

  • Increases uveoscleral outflow of aqueous humor
  • Inhibits formation of aqueous humor
271
Q

A2 agonist side effects for eye administration (3)

A

red eye, ocular irritation, CNS depression

272
Q

Timolol (use for eyes) use and mechanism

A

Beta-adrenergic antagonist

Common treatment of open angle glaucoma

Mechanism: preferential B2 in eye

  • Reduces aqueous humor production via block of B-receptor pathway
  • Decrease ocular blood flow → decrease ultrafiltration required for production
273
Q

Side effects of B-agonists used in glaucoma (3)

A

systemic absorption → bradycardia, heart block, bronchoconstriction

(avoid with asthma, bradycardia, COPD)

274
Q

Dorzolamide

mechanism and use

A

Carbonic anhydrase inhibitors

Add on second or third line therapy of open angle glaucoma

Mechanism:
Inhibit carbonic anhydrase in ciliary body epithelium → reduce formation of bicarb ions → reduce fluid transport and IOP

275
Q

Dorzolamide (carbonic anhydrase inhibitor)

side effects (3)

A

bitter taste, fatigue, kidney stones

276
Q

Pilocarpine

mechanism and use

A

Cholinomimetics

Used to treat open angle glaucoma
Mechanism: Lower IOP by causing contraction of ciliary muscle → facilitates outflow

277
Q

Pilocarpine side effects (3)

A

ciliary spasm → headaches, myopia, dim vision (small pupil)

SLUDGE side effects for muscarinic agonists

278
Q

Direct pathway, D1 vs. Indirect pathway, D2

A

Direct pathway, D1 → coupled to Gs → INCREASES excitatory outflow

Indirect pathway, D2 → coupled to Gi → DECREASES inhibitory outflow

279
Q

Parkinson’s is a primary loss of what dopamine pathway? what are the consequences?

A

Parkinson’s is a primary loss of D1 input, so “foot is off the gas” and “foot is still on the brake”

Decreased striatal DA release and leads to loss of DA “go” signal → decrease motor function

280
Q

Antipsychotic drugs - block D2 receptors → ?

A

Antipsychotic drugs - block D2 receptors → can cause “Pseudoparkinson’s” because you can’t inhibit your inhibitory pathway (can’t take foot off brake) → drug induced movement disorder

281
Q

Testing of CN II (4)

A

Ocular Nerve

1) Visual acuity: use best corrected vision
2) Visual fields
3) Direct ophthalmoscopy
4) Pupillary exam (size, shape, equality, reactivity, convergence)

282
Q

Direct ophthalmoscopy

A

Check red reflex, then focus on red reflex to focus on optic fundus (disc + cup in middle of disc + Macula + arteries and veins)

283
Q

Oculomotor nuclei/nerve

A

seen in upper midbrain (next to Edinger-Westphal Nucleus)

  • III runs between PCA and superior cerebellar artery
  • Does all EOM except for LR (6) and SO (4)
  • CN III palsy → down and out, mydriasis (unopposed sympathetic)
284
Q

Horner’s syndrome (3)

A

sympathetic dysfunction, worse in dark

Ptosis (droopy eyelid), miosis (small pupil), and anhidrosis

285
Q

Trochlear nuclei

A

lower midbrain

Eyes of creepy bald man - MLF = circles under guy’s eyes

Nerve exits DORSALLY (only motor nerve that exits dorsally)

Innervates contralateral SO muscle

People tend to tilt head to compensate for IV palsy

286
Q

VI Abducens Nucleus and Nerve

A

Nucleus seen on pontine section

exits at ventral midline at junction between pons and medulla → innervates LR

Vulnerable to hydrocephalus 6th nerve palsy → eye deviates medially and is unable to abduct beyond midline

Send axons to ascend in contralateral MLF to III nerve nuclei (medial rectus adductor)

287
Q

Trigeminal Nuclei (4)

A

1) Motor nucleus
2) Principal Sensory Nucleus
3) Spinal Trigeminal Nucleus
4) Mesencephalic nucleus

288
Q

Motor nucleus of trigeminal

A

motor for muscles of mastication (medial to sensory nucleus)

Mouth/tongue may deviate to affected side

289
Q

Trigeminal nerve enters/exits at what level of brainstem

A

enters at level of middle cerebellar peduncle

290
Q

Principal Sensory Nucleus

A

fine touch and vibration sense of face (more lateral to motor) → contralateral VPM

V1 - includes tip of nose and forehead
V2 - Maxilla and upper lip
V3 - Lower lip and chin

291
Q

Spinal Trigeminal Nucleus

A

(located in medulla) → contralateral VPM

Continuous with substantia gelatinosa in spinal cord

Spinal trigeminal tract travels down spinal cord

292
Q

Mesencephalic nucleus

A

proprioception from muscles of mastications → synapses in motor nucleus
→ Jaw Jerk Reflex

293
Q

VII: facial nerve

A

Motor structure, exits ventral to vestibulocochlear nerve

Travels up/around abducens nucleus before exiting brainstem

Controls muscles of facial expression

Taste of anterior ⅔ of tongue via chorda tympani nerve, terminates in nucleus solitarius

294
Q

Divisions of facial nerve

A

Rostral → upper half of face
-Innervated by contralateral AND ipsilateral face motor cortex

Caudal → lower half of face
-Only gets innervation from contralateral face motor cortex

295
Q

EX) stroke in L motor cortex of face region causes what facial features on upper vs. lower face

A

stroke in L motor cortex

→ R rostral face will be OK because still get motor innervation from ipsilateral side

–> R caudal (lower) face will droop

= CENTRAL FACIAL PALSY

296
Q

EX) Bell’s palsy, peripheral nerve damage (cut facial nerve), or damage to facial nucleus itself causes what facial features on upper vs. lower face?

A

→ ipsilateral UPPER AND LOWER half of face will be droopy

= PERIPHERAL FACIAL PALSY

297
Q

IX: Glossopharyngeal responsible for what? (3)

A

1) Pain, temp of post ⅓ of tongue → trigeminal nucleus
2) Taste post ⅓ of tongue → Nucleus solitarius
3) Gag reflex: afferent limb of gag reflex via IX

298
Q

Dorsal motor nucleus of vagus responsible for what?

A

→ parasympathetic outflow to thoracic and abdominal visceral

299
Q

XII: hypoglossal

exits where?
UMN vs. LMN damage causes what?

A

Exit between olive and pyramid

Damage to hypoglossal nerve/nucleus → tongue will deviate toward damaged side (LMN)

Damage to motor cortex will point away from side of lesion (UMN)

300
Q

KNOW LOWER PONS AND UPPER-MID MEDULLA SECTIONS!!!!

A

look at the lab slides!

DO IT

301
Q

Ageusia vs. Anosmia

A

Ageusia = loss of taste

Anosmia = loss of smell

302
Q

Smell receptor cells are _________________ and project via CN ____ (#) to ___________ (primary sensory nucleus in CNS)

A

ciliated bipolar neurons

CNI

Olfactory bulb

303
Q

Taste receptor cells are _________________ and project via CN ____ (3 #’s) to ___________ (primary sensory nucleus in CNS)

A

Modified epithelial cells (that synapse onto nerve fiber from cranial ganglion cell)

CN VII (facial, ant 2/3), CN IX (glossopharyngeal, post 1/3), and CN X (vagus, epiglottis and oropharynx)

Nucleus of solitary tract

304
Q

Chemesthesis receptor cells are _________________ and project via CN ____ (#) to ___________ (primary sensory nucleus in CNS)

A

Free nerve ending of cranial ganglion cell

CN V (mostly)

Spinal trigeminal nucleus (pain pathway for face)

305
Q

Taste

A

provides information to brain on chemical composition of food

306
Q

Two types of channels for taste transduction

What do they sense?

A

1) Ion channels (sour/pH, salty): ions can permeate ion channels directly to depolarize cell

2) Second messenger systems (bitter, umami, sweet)
- Umami detects glutamate

307
Q

Tastebuds

4 kinds of tastebudes

A

consist of 50-100 taste cells

1) Fungiform papillae
2) Circumvallate papillae
3) Foliate papillae
4) Filiform papillae

308
Q

Taste cells

A

Taste cells have limited lifespan (10-30 days) undergo continuous replacement by specialized basal stem cells

Taste cells individually sensitive to just ONE class of taste stimuli

CNS extracts info from POPULATION of afferent fibers activated by a particular chemical stimulus to determine sensory characteristics

-Individual afferent neurons innervates several receptor cells

309
Q

Mechanism of taste particle activation of taste

A

Depolarization of taste cells (Ca2+ and Na+) → release NT from basal part of cell

ATP acting on P2X receptors on nerve fibers - crucial for taste info transmission

310
Q

Fungiform papillae

A

located on anterior ⅔ of tongue

Innervated by chorda tympani branch of facial nerve

311
Q

Circumvallate papillae

A

located on posterior part of tongue

Innervated by glossopharyngeal nerve

312
Q

Foliate papillae

A

located on sides of the tongue

313
Q

Filiform papillae

A

non-taste papillae, tactile organs

314
Q

Posterior taste buds

A

oropharynx and epiglottis

more involved in consummatory reflexes (swallowing, choking) than with conscious appreciation of taste quality

innervated by vagus nerve

315
Q

Central taste pathway:

Primary afferents from tongue run through:

_______ (anterior ⅔ of tongue)
__________ (posterior ⅓ of tongue)
_______ (epiglottis and oropharynx) nerves

→ synapse on second order neurons of ______________

A

Primary afferents from tongue run through

FACIAL (VII) (anterior ⅔ of tongue)
GLOSSOPHARYNGEAL (IX) (posterior ⅓ of tongue)
VAGUS (X) (epiglottis and oropharynx) nerves

→ synapse on second order neurons of IPSILATERAL NUCLEUS OF SOLITARY TRACT (NST)

316
Q

Nucleus of solitary tract

A

receives ipsilateral input from VII, IX, and X for taste

Organized orotopically - map of oral cavity in nucleus so anterior parts of mouth represented anteriorly in nucleus

projects to BILATERAL VPM THALAMUS

317
Q

Central taste pathway:

Nucleus of Solitary Tract –> ___________, ____________ and ___________, and ____________

A

Bilateral VPM of thalamus

Bilateral Hypothalamus and Amygdala

Reflex nuclei of brainstem

318
Q

VPM of thalamus gets taste info from ______ and projects taste info to ________ for what?

A

Nucleus of solitary tract

Insula (taste cortex)

conscious appreciation of taste

319
Q

Hypothalamus and amygdala get taste info from ________ and is responsible for what aspects of taste?

A

Nucleus of solitary tract

subconscious reactions to taste and control of appetite, etc.

320
Q

Reflex nuclei of brainstem get taste info from ___________ and are responsible for what 3 actions?

A

Nucleus of solitary tract

1) Nucleus ambiguus (gagging)
2) Nucleus ambiguus and hypoglossal nucleus (swallowing)
3) Superior and inferior salivatory nucleus (salivation)

321
Q

orbitofrontal cortex

A

“Flavor” cortex

Gets projections from primary gustatory area (anterior insula) and from olfactory areas of insula

Responsible for integration of taste and smell → perception of FLAVOR

322
Q

Olfaction

A

inform brain (via olfactory bulb) of quantity and odorous quality of volatile chemicals that enter the nose

323
Q

Olfactory neuroepithelium

A

covered with thin layer of mucous in which odorants dissolve and interact with olfactory receptor proteins on cilia

324
Q

Olfactory neurons

A

Bipolar neurons: send single, thin, unmyelinated axon towards olfactory bulb as part of olfactory nerve (CN I)

Exposed to external environment, subject to bacterial attack, viruses, and environmental toxins

Continually undergo neurogenesis and replacement → vulnerable to mitotic inhibitors used in cancer treatment

325
Q

Olfactory receptors

A

seven transmembrane spanning regions, G-protein coupled receptors, dendrites bind odor molecules

  • Each olfactory receptor neuron predominantly expresses one olfactory protein receptor
  • Each odorant can stimulate a number of receptors
326
Q

Olfactory transduction

1) Odorant binds receptor protein → associated with _______ → activate _____ → local ______ generation → open _________ channel, allowing _____ and ______ ions in (does NOT cause depolarization on its own)
2) Local increase in [____] → open adjacent ________ channels → _____ flows ____ of cell → further depolarization → cell driven to threshold, AP is fired

A

1) Odorant binds receptor protein → associated with G protein → activate AC → local cAMP generation → open cAMP gated ion channel, allowing Na+ and Ca2+ in (does NOT cause depolarization on its own)
2) Local increase in [Ca2+] → open adjacent Ca2+ gated chloride channels → Cl- flows OUT of cell → further depolarization → cell driven to threshold, AP is fired

327
Q

Olfactory glomeruli

A

Axons of olfactory neurons penetrate ethmoid bone (cribriform plate) → converge on glomeruli at outer layer of olfactory bulb

Glomeruli contain input from 1000 axons (1000 olfactory neurons)

-Olfactory receptor neurons expressing the same olfactory receptor protein project axons to SAME glomerulus

328
Q

How are different odors represented in the olfactory bulb?

A

Odor-related map of glomeruli present in olfactory bulb

Olfactory receptor neurons expressing the same olfactory receptor protein project axons to SAME glomerulus

Odor epithelium has receptor cells with common receptor scattered throughout epithelium, but odorants can activate more than one receptor type
–> Identification of odor entails recognition of the PATTERN of activity across all glomeruli of olfactory bulb

329
Q

Central olfactory pathway:

Olfactory bulb –> _________ tract –> what 4 regions?

A

Lateral olfactory tract

1) Piriform cortex (primary olfactory cortex in lateral olfactory gyrus + uncus)

2-3) Olfactory tubercle and Amygdala

4) Entorhinal cortex

330
Q

Piriform cortex gets ________ info from _______ and projects it to _____________

A

olfactory

olfactory bulb

Orbitofrontal cortex directly or via MD nucleus of thalamus

331
Q

Olfactory tubercle and amygdala get ______ info from _________ and projects it to ________ for what purpose?

A

olfactory

olfactory bulb

Hypothalamus

Visceral reactions, homeostasis

332
Q

Entorhinal cortex gets _______ info from _______ and projects it to _______ for what purpose?

A

olfactory

olfactory bulb

Hippocampus

Memories

333
Q

PROP receptors for taste

A

detect propylthiouracil, people differ in sensitivity to PROP

Differences in sensitivity → diet preferences and tolerance for bitter tasting medicines

Higher bitter sensitivity → eat less veggies, more nutritionally related diseases

334
Q

PROP receptors and respiratory bacterial disease

A

“Bitter” receptors located in nasal cavity, trachea, and bronchi can detect bacterial signaling molecules → detect presence of lots of bacteria, and epithelial cells mount local defense and alert innate immune system

Same receptor used to detect PROP (propylthiouracil)

→ People unable to detect PROP have higher incidence of respiratory bacterial disease

335
Q

Hypothalamus and limbic system

A

hypothalamus connection with limbic system allows for initiation of motivated behaviors and integration of emotional expression with sensory and environmental cues

336
Q

Fornix connects _______ with ________

A

connects hippocampus with mammillary bodies

337
Q

Stria terminalis:

connects _______ with ____________

A

connects amygdala with hypothalamus

338
Q

Medial forebrain bundle: connects _________ with _________ and ________

A

connects hypothalamus with prefrontal cortex and septum

339
Q

Mammillothalamic tract sends info from ___________ to ___________

A

info from mammillary bodies of hypothalamus to anterior nucleus of thalamus (efferent neural pathway)

340
Q

Limbic system

A

responsible for modulating emotional expression such that it is appropriate to the situation

341
Q

Sham rage

A

dissociation of rage response from appropriate environmental context

Observed when hypothalamus disconnected from higher brain areas, but hypothalamic connections to brainstem/spinal cord remain in tact.

Ventromedial nucleus opposes Dorsomedial nucleus and balance between the two results in coordinated response

342
Q

Hypothalamus

A

coordinates endocrine, autonomic, and somatic motor responses in order to achieve homeostasis in a broad range of physiological parameters including body temperature, blood pressure, fluid and electrolyte balance, and body weight

Role in reproduction and emotional expression

Located at floor of third ventricle, and is ventral-most part of diencephalon

Interconnected with autonomic nuclei of brainstem and spinal cord

Regulates pituitary gland

343
Q

Hypothalamus compares what input to biological set point –> generate output signal via visceral and somatic motor, neuroendocrine, and behavioral responses

A

INPUT:

Contextual information (cerebral cortex, amygdala, hippocampal formation)

Sensory inputs (visceral and somatic sensory pathways, chemosensory and humoral signals)

344
Q

Location of preganglionic:

sympathetic neurons

parasympathetic neurons

A

Preganglionic sympathetic neurons: located in intermediolateral column T1-L3

Preganglionic parasympathetic neurons: located in brainstem nuclei (III, VII, IX, X) and S2-S4

345
Q

Hypothalamic neurons innervate upper motor neurons in _______________ → UMN then project to LMN that innervate skeletal muscle

what actions does this region mediate?

A

brainstem reticular formation

Organizes/initiates complex activities that require both somatic and autonomic responses (vomiting, laughing, crying, facial expressions) and motor activities required for maintenance of homeostasis (chewing, swallowing)

346
Q

Neuroendocrine function of hypothalamus

A

both direct and indirect via posterior and anterior pituitary

347
Q

Anterior pituitary

A

indirect

Hypothalamus synthesizes and releases hormones into hypothalamo-pituitary portal circulation that regulates release of hormones from glandular cells of ant. Pituitary

NO dilution of hypothalamic hormones in general circulation

348
Q

Posterior pituitary

A

DIRECT

Hormones of posterior pituitary (vasopressin/ADH, oxytocin) made by neurons in supraoptic (SON) and paraventricular nuclei (PVN) of hypothalamus and transported down axons of neurons to post. Pit.

Hormones stored in axon terminals until AP signals their release DIRECTLY into general circulation

349
Q

The hypothalamus receives afferent visceral sensory information from baroreceptors, gastric/cervical stretch via what tract?

A

Nucleus of solitary tract

350
Q

Circumventricular organs (4)

A

Regions of hypothalamus lack BBB, have fenestrated capillaries - crucial for humoral afferent input to hypothalamus

1) Organum vasculosum of lamina terminalis (OVLT)
2) Subfornical organ
3) Median eminence
4) Posterior pituitary

351
Q

The __________ nucleus of the hypothalamus controls circadian rhythms and gets input via the _____________ tract

A

Suprachiasmatic

retinohypothalamic tract

352
Q

Suprachiastmatic nucleus

A

hypothalamic region that gets light information from specialized retinal ganglion cells

“Central Clock”

Important for entraining our endogenous circadian rhythms to environmental light/dark cycle

Can generate rhythms without exogenous info, but light input “entrains” clock to daily environmental light-dark cycles

Peripheral clocks (e.g. liver) entrained by central clock

353
Q

Hypothalamus role in water balance:

Sensory input to hypothalamus telling you are thirsty from where (2)

A

1) Hypothalamic osmoreceptors - OVLT and SFO (circumverential regions) monitor osmolality
2) Baroreceptors monitor cardiovascular volume

354
Q

Hypothalamus role in water balance:

What does the hypothalamus do when it is notified you are thirsty? (2)

A

1) Release ADH from SON and PVN into POSTERIOR pituitary

2) Make you drink water!

355
Q

Hypothalamus and body weight/food intake regulation:

Ventromedial nucleus/Paraventricular nucleus vs. Lateral hypothalamus

A

Ventromedial nucleus = satiety center

Lateral hypothalamus = hunger or feeding center

356
Q

Ventromedial nucleus of hypothalamus and appetite:

lesion –> ?
Stimulation –> ?

A

Ventromedial nucleus = satiety center

Lesion → increase food intake, marked obesity

Stimulation → inhibit urge to eat

357
Q

Lateral hypothalamus and appetite:

A

Lateral hypothalamus = hunger or feeding center

Lesion → anorexia, starvation, decreased responsivity to food

Stimulation → induce food intake

358
Q

What are some ways our body increases heat production (4)

A

1) Basal metabolic rate
2) Exercise
3) Shivering
4) Non-shivering thermogenesis

359
Q

Non shivering thermogenesis (NST)

A

infants have lots of brown fat

Can increase heat production by increasing catabolic activity of this tissue

———-(below this line is less important, but good to read)———-
Due to release of NE onto brown fat cells by sympathetic nerve fibers → signal activation of thermogenin (uncoupling protein 1) in brown fat

Thermogenin = H+ ion channel in inner mitochondrial membrane, expressed exclusively by brown fat cells

Allows dissipation of proton motive force as heat without producing ATP = uncoupling oxidative phosphorylation

360
Q

How does our body increase heat loss?

A

1) Heat flow to skin (sympathetic control of blood flow to skin)
2) Sweating (sympathetic control)

361
Q

Thermoreceptors in preoptic anterior hypothalamus (POAH)

Excitatory input from where?
Inhibitory input from where?

what happens if you lesion this area?

A

specialized receptor neurons within POAH that generate APs at frequency proportional to local temperature

Increase firing with increased temp at POAH region→ induce heat loss mechanisms (panting, sweating, vasodilation, cooling behavior)

Get inhibitory synaptic input from cutaneous cold receptors and excitatory input from cutaneous warm receptors → both weak inputs

Lesion → hyperthermia

362
Q

Temperature regulation in posterior hypothalamus

Excitatory input from where?
Inhibitory input from where?

what happens if you lesion this area?

A

Excitatory input from: cutaneous COLD receptors

Inhibitory input from: cutaneous warm receptors

DO NOT directly monitor local brain temp (like POAH does)

Excitation of these neurons induces heat gain mechanisms (shivering, vasoconstriction, seeking warmth)

Lesion → hypothermia

363
Q

Interaction of POAH and posterior hypothalamus

A

Cells in POAH are tonically active at normal body temp, and their activity inhibits cells of posterior hypothalamus

Temp drops below certain threshold → POAH drops firing rate → release posterior hypothalamus from inhibition

364
Q

Fever:

induced by _______ to increase __________ of the thermoregulatory system –> causes what physiological responses?

A

Induced by pyrogens (fever producing agents) → increase “set-point” of thermoregulatory system

→ activate physiological responses normally evoked by cold (vasoconstriction, shivering, etc. until core body temp rises to a new level

365
Q

What happens when pyrogens are injected directly in POAH region?

What about when pyrogens are injected into posterior hypothalamus?

A

Fever develops when pyrogens injected into POAH region, but NOT when injected into posterior hypothalamus, pons or cerebral cortex

366
Q

_________ are released by the immune system –> ____________ (circumverential organ) to induce local production of _________ in the hypothalamus.

This then acts directly on __________ (region of hypothalamus) to increase temperature set point → vasoconstriction, shivering, blanket

A

Cytokines (IL-1)

OVLT

PGE2 made in hypothalamus

PGE2 acts directly on POAH cells of hypothalamus

Neuro (8 decks)

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