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NS_BTRAN > Unit3_Questions > Flashcards

Unit3_Questions Flashcards

1
Q

Transduction of taste and smell share what common protein?

A

Trp receptors which allow Calcium in

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2
Q

What are the other important proteins for taste?

A

PLCB2, IP3R3

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3
Q

Give an example of how taste and smell can be damaged, and why that happens.

A

Cancer drugs can kill off the epithelium where the taste buds and olfactory neurons are because these cells are continuously dividing.

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4
Q

What is the nucleus for taste fibers?

A

Nucleus of solitary tract

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5
Q

What parts of the tongue are foliate, circumvallate, filiform, fungiform taste buds?

A

Fungiform is anterior 2/3

Circumvallate is posterior 1/3

foliate are lateral, filiform are part of gag reflex (larynx, etc.)

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6
Q

Where are taste and smell integrated?

A

Orbitofrontal cortex (flavor cortex)

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7
Q

Where are smell memories encoded?

A

Entorhinal cortex –> hippocampus

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8
Q

What ion is responsible for smell transduction?

A

Chloride efflux

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9
Q

Where do the solitary tract fibers project to, for taste?

A

Bilaterally to amygdala, hypothalamus, VPM thalamus then to insular cortex

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10
Q

What do most patients present for in terms of food sensory deficit, and what is actually wrong?

A

“I can’t taste” – they actually can’t smell

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11
Q

Where do hearing fibers decussate?

A

Trapezoid body

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12
Q

Where do vestibular fibers decussate?

A

Prior to medial longtiduinal fasciculus

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13
Q

What controls voluntary saccades, and what is the pathway to start them?

A

Frontal eye fields of the frontal lobe are stimulated, and bypass the superior colliculus to project straight to ipsilateral paramedian pontine reticular formation

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14
Q

How fast can saccades move?

A

Up to 700 degrees per second

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15
Q

After that, where do they project to?

A

The PPRF innervates the ipsilateral abducens nucleus, the other fibers join the medial longitudinal fasciculus which decussates to the contralateral oculomotor nucleus

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16
Q

So activation of the left frontal eye field causes what?

A

Look to the right

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17
Q

How do voluntary saccades get transmitted?

A

Parietal eyefields are stimulated by visual cortex, which transmits to the superior colliculus and also removes inhibition of SNPR (NOT PC!) by the caudate to net activate the superior colliculus, which goes to the PPRF (Brainstem gaze center)

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18
Q

What do involuntary saccades bypass?

A

Frontal eye field

ds and Basal ganglia

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19
Q

When are you performing saccades?

A

Always – microsaccades occur even while staring at something.

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20
Q

T/F: An individual with a lesion in the ipsilateral Medial Longitudinal Fasciculus (MLF) would not be able to generate a complete saccade.

A

False

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21
Q

T/F: The velocity at which you perform a saccade can be controlled in voluntary, or visually-guided saccades.

A

False

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22
Q

What happens if the frontal eye field is damaged?

A

Temporary loss of ability to generate saccades.

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23
Q

And if superior colliculus is damaged?

A

Saccades are less accurate and less frequent.

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24
Q

If both FEF and SC are damaged?

A

Permanent loss of saccade generation

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25
Q

One side PPRF innervates what, and causes you to look where?

A

Ipsilateral abducens, contralateral oculomotor; look to the ipsilateral side.

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26
Q

Left lesion to the medial longtiduinal fasciculus causes what, and is associated with what?

A

Internuclear opthalamoplegia

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27
Q

Ipsilateral eye cannot adduct; contralateral eye abducts with nystagmus. You are still able to loo to the left side, but looking to the contralateral side is difficult.
Associated with multiple sclerosis

A

Ipsilateral eye cannot adduct; contralateral eye abducts with nystagmus. You are still able to loo to the left side, but looking to the contralateral side is difficult.
Associated with multiple sclerosis

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28
Q

At what velocity (degrees/sec) do saccades take over in place of horizontal pursuit?

A

50 degrees per second

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29
Q

Nystagmus is named for:

A

Direction of the saccade (the jump)

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30
Q

Absence of the vestibular ocular reflex indicates what?

A

Brainstem damage

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31
Q

Turning your head to the right in the vestibular ocular reflex causes what? Are there decussations?

A

Eyes to pursuit to the left. Decussation occurs via vestibular tract to contralateral abducens nucleus, and decussates from there via the medial longitudinal fasciculus to the (originally) ipsilateral oculomotor nucleus.

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32
Q

Most ocular drugs are made as what type of prodrug?

A

Ester, there are many esterases that allow for conversion to the active form of the drug after the lipid-soluble form allows for penetration into the cornea

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33
Q

What is the drug of choice for open-angle glaucoma? Give information behind it, including what it is, method of action, side effects.

A

Latanoprost, prodrug for PGF2; increases accessory outflow pathway; causes darkening of eyelashes and iris

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34
Q

What drug is the second most-common treatment for open-angle? Name the important one. What’s the mechanism?

A

Beta-blockers; Betaxolol; decreases Gs activity to decrease cAMP to increase PKA which decreases production.

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35
Q

When should you avoid beta blockers for glaucoma treatment? How do they causes issues?

A

Bradycardia, heart failure, COPD, asthma. They can be taken up via nasolacrimal drainage to cause systemic side effects.

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36
Q

What drugs cause decreased production of aqueous humor?

A

Beta-blockers, Alpha-2 agonists, carbonic anhydrase inhibitors

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37
Q

Give one carbonic anhydrase inhibitor’s name

A

Dorzolamide.

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38
Q

What is the treatment for open angle glaucoma?

A

Pilocarpine immediately to increase outflow. C.A. inhibitors are good
Mannitol can cause dehydration until surgery.
Definitive treatment is laser iridotomy

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39
Q

What drugs should you avoid in glaucoma?

A

Anticholinergics, sympathomimetics

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40
Q

What is the pathophysiology of closed-angle glaucoma?

A

Iris contacts the trabecular meshwork/canal of Schlemm to block outflow.

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41
Q

Define glaucoma, in terms of numbers.

A

Intraocular pressure greater than 22 mmHg above atmospheric (760 mmHg) [normal is >15]

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42
Q

Describe the metabolic enzymes, in order, to create dopamine

A

Tyrosine –> tyrosine hydroxylase –> L-DOPA –> DDC –> Dopamine –> MAO –> DOPAC –> COMT –> HVA

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43
Q

Describe the metabolic enzymes, in order, to create dopamine

A

Tyrosine  tyrosine hydroxylase  L-DOPA  DDC  Dopamine  MAO  DOPAC  COMT  HVA

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44
Q

Parkinson’s disease is caused by destruction of the ____? How do you treat it?

A

Basal ganglia. Carbidopa and levodopa are first-line therapies.

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45
Q

What is the method of action for carbidopa? Why is it used?

A

Inhibits peripheral dopamine decarboxylase to increase transport to the CNS. Limits systemic effects of dopamine.

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46
Q

What does selegiline do? Why is it preferable to others in its class?

A

Inhibits MAO. It is preferential for MAO-B, which has most effect on serotonin, and least hypertensive issues.

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47
Q

The autosomal dominant form of Parkinson’s is marked by what mutation? Autosomal recessive?

A

Alpha-synuclein Chr4; PARKIN Chr6

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48
Q

Sinemet toxicity is mainly confined to ____ short-term, and ____ long-term.

A

GI toxicity; dyskinesia and psychosis

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49
Q

What advantage does a dopamine receptor agonist have over L-Dopa? Give two examples of drugs in this class.

A

Lower chance of extrapyramidal side effects (dyskinesia)
Pramipexole (Mirapex) is a D2, D3 agonist
Ropinirole is a D2 agonist

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50
Q

What drug facilitates endogenous dopamine release?

A

Amantadine.

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51
Q

What is Entacapone?

A

Comtan, it is a COMT inhibitor (catechol-o-methyltransferase) to prevent the breakdown of L-dopa and dopamine by COMT

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52
Q

What street drug causes parkinsonism symptoms? How can you treat someone on this drug?

A

MPTP. Selegiline will inhibit MAO-B which causes it to become a toxic metabolic MPP+.

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53
Q

What is benztropine’s (Cogentin) method of action? What is the thought process?

A

Anticholinergic to block muscarinic receptors. The idea is decreased dopamine lets ACh thrive due to decreased inhibition and this ACh overactivity causes many Parkinson symptoms.

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54
Q

Which dopamine pathway inhibits movement?

A

D2. Cortex stimulates striatum to stimulate globus palladus externa to stimulate substantia

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55
Q

What is Tourette’s associated with? What are “tics”?

A

OCD. Sensorimotor disorder with motor and verbal manifestations.

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56
Q

How do you treat tics?

A

Only treat them if they interfere with life. The majority resolve spontaneously, only 25% persist.

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57
Q

A patient presents with ataxia and other parkinsonian symptoms that started 2 years ago and is now in a wheelchair. What is the diagnosis?

A

Lewy body dementia

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58
Q

A patient presents with Parkinsonian features and early onset of autonomic instability and postural instability with multiple falls. What is the diagnosis?

A

Progressive supranuclear palsy

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59
Q

Patient doesn’t respond to dopamine-replacement therapy and has autonomic, cerebellar, and Parkinson symptoms. What’s the diagnosis?

A

Multiple systems atrophy

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60
Q

What is the most common adult movement disorder? What is it a disorder of, and what should you avoid?

A

Restless leg syndrome; disorder of restful wakefulness. Avoid sleep study.

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61
Q

Describe a psychogenic movement disorder.

A

Sudden onset, waxing and waning

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62
Q

One of these (in bold) is not typical for sudden onset movement disorder:

A

Poststroke/ischemia, toxin/medications, infection/post-infectious, depression, metabolic, hyperglycemia, autoimmune

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63
Q

Most movement disorders disappear when:

A

You go to sleep

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64
Q

Neurodegenerative disorders are characterized by:

A

Proteins misfolding and aggregating.

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65
Q

Neurofibrillary tangles and neuritic plaques are composed of what, respectively, and are characteristic of what?

A

hyperphosphorylated tau protein and beta-amyloid aggregates; Alzheimer’s

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66
Q

What is tau protein normally part of?

A

Microtubule assembly

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67
Q

Frontotemporal lobe dementia is histopathologically marked by what? What does it stain with?

A

TDP-43 ubiquitin inclusions – Pick bodies. Silver.

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68
Q

Lou Gehrig’s is characterized by degeneration of what structure?

A

Anterior horn of spinal cord and corticospinal tract.

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69
Q

Bunina bodies are histopathologic for what disease?

A

AMLS

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70
Q

Genetics of Huntingtons involves what? What genetic feature is present?

A

AD CAG repeats in Chr4 Huntingtin gene, displays paternal anticipation

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71
Q

What are two drugs to treat essential tremor?

A

Propanolol and primidone

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72
Q

Drugs to treat Tourettes?

A

Tetrabenzine and neuroleptics

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73
Q

Huntingtons?

A

Tetrabenzine, neuroleptics (Haldol)

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74
Q

Describe the pathophysiology of fever.

A

Pyrogens such as cytokines and PGE2 diffuse through the circumventricular organs of the hypothalamus (SFO, OVLT) to the POAH ONLY (no effect on posterior hypothalamus) to raise the temperature set point

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75
Q

What is the primary method for heat maintenance in infants?

A

Non-shivering thermogenesis: sympathetic activity releases norepi  thermogenin/uncoupling protein in brown fat cells  proton gradient creates heat, NOT ATP

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76
Q

What are the direct effects of the hypothalamus on neuroendocrine function?

A

Supraoptic nucleus synthesizes ADH, paraventricular nucleus secretes oxytocin. These diffuse to neurohypophysis of posterior pituitary. They are released upon APs and can modulate behavior.

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77
Q

What are the indirect effects? Give examples (in bold)

A

It releases hormones to the portal circulation to regulate release of hormones from glandular cells of anterior pituitary.
E.G.: CRH  ACTH. GnRH  LH/FSH. PRF  PRL. TRH  TSH. GHRHGH

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78
Q

How does the hypothalamus affect autonomic nervous system?

A

It has direct innervation to preganglionic parasympathetic and sympathetic nerves.

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79
Q

How about hypothalamic effects on somatic nervous system?

A

It innervates upper motor neurons in the brainstem reticular formation.

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80
Q

How does the hypothalamus regulate the sleep-wake cycle?

A

Suprachiasmatic nucleus receives light via retinohypothalamic tract which then forms transcription-translation regulatory loop of key proteins.

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81
Q

What occurs if the cerebral cortex is severed from the hypothalamus? What is the mediator? What is the conclusion of this?

A

How do you destroy this effect?
Sham rage; norepi. The hypothalamic rage response is inhibited by the cerebral cortex. Disconnect the hypothalamus from the brainstem and spinal cord.

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82
Q

What nucleus is the satiety center? The hunger center?

A

Ventromedial; lateral

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83
Q

How does the hypothalamus regulate body temperature to 37 degrees celcius? What is the pathway?

A

Preoptic Anterior Hypothalamus/POAH (Hypothalamic warm receptors and Skin warm receptors activate, skin cold receptors inhibit) activates heat loss mechanisms.
Posterior Hypothalamus/PH (Skin warm receptors inhibit, skin cold receptors activate) activate heat gain mechanisms.

POAH inhibits PH

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84
Q

What are heat loss and heat gain mechanisms?

A

Loss: Vasodilate, sweat, seek cold
Gain: vasoconstrict, shiver, NST, seek warm

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85
Q

Does the body take longer to react to cold or hot temperatures? Why?

A

Cold, there are only central (hypothalamic) warm receptors, no cold receptors, and POAH normally inhibits the PH, so takes longer to start heat gain mechanisms

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86
Q

What are endogenous and exogenous pyrogens?

A

IL-1, IL-6, TNF, interferon are endogenous; bacterial and viral proteins are exogenous. They cross the OVLT to endothelial cells and cause PGE2 production.

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87
Q

Voluntary movement, language fluency, executive function are all functions of the:

A

Frontal lobe (the higher order)

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88
Q

Vision is a function of the:

A

Occipital lobe

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89
Q

Tactile sensation, visuospatial function, attention, reading, writing are functions of the:

A

Parietal lobe (creativity)

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90
Q

Language comprehension, memory, emotion are functions of the:

A

Temporal lobe (think of hearing!)

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91
Q

Brodmann areas 44, 45 are injured in? What lobe?

A

Broca’s aphasia. Frontal.

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92
Q

Most individuals are ___-hemisphere dominant for language

A

Left

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93
Q

Disinhibition results from lesions to what cortex?

A

Orbitofrontal (executive function – the higher order!)

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94
Q

Executive dysfunction results from lesions to what cortex?

A

Dorsolateral prefrontal

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95
Q

Apathy results from lesions to what cortex?

A

Medial frontal

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96
Q

The three previously mentioned conditions (disinhibition, apathy, and executive dysfunction) are more pronounced when:

A

Bilateral lesions are present

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97
Q

Lesions of Brodmann area 22 result in? What lobe?

A

Wernicke’s aphasia. Temporal.

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98
Q

What about Brodmann area 22 on the right?

A

Sensory aprosody.

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99
Q

Hippocampal lesions result in deficits of what?

A

Learning

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100
Q

Hemineglect results from what?

A

Contralateral parietal lobe lesions

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101
Q

Occipitotemporal (ventral) lesions result in ___, while occipitoparietal (dorsal) lesions result in ___

A

Don’t know what; don’t know where

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102
Q

What is the most severe corpos callosal lesion effect?

A

Most are largely asymptomatic, maybe anomia, agraphia, apraxia of left hand

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103
Q

What’s the first step if you suspect aphasia?

A

Complete history and neuro exam. Mental status exam is next.

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104
Q

What is dysarthria?

A

Deficit in motor system leads to inability/disability of speaking.

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105
Q

What is language linked to?

A

Handedness. Most are left-hemisphere dominant.

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106
Q

What is the most common cause of aphasia?

A

Stroke

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107
Q

The arcuate fasciculus is lesioned. What can you expect the patient to demonstrate?

A

Poor repetition, this is conduction aphasia.

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108
Q

The perisylvian region is lesioned. What can you expect of the patient?

A

No speech, no understanding, no repetition, no naming. This is global aphasia.

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109
Q

Brodmann area 22 is lesioned. What can you expect?

A

No auditory comprehension. This is Wernicke’s. Temporal lobe.

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110
Q

Brodmann area 44, 45 is lesioned, what can you expect?

A

Non-fluent speech. This is Broca’s. Frontal lobe.

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111
Q

Which aphasia does the patient not understand they have a deficit?

A

Wernicke’s, B.A. 22

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112
Q

Who will display the best recovery from a lesion? What is the most important thing to offer a patient?

A

Small lesions in younger patients have the best recovery. It’s most important to have the patient adapt to their disability. Most improvement will happen in the first year.

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113
Q

The pure-tone threshold is set at ?

A

0 dB for the normal hearing threshold for each particular pitch

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114
Q

Circles represent the ___ ear

A

Right. ciRcle

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115
Q

Conductive hearing loss manifests on an audiograph as what?

A

Differences in air-bone lines (good bone conduction, poor air)

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116
Q

A choleasteatoma is:

A

Growth in middle ear that can destroy the ossicles. Results in chronic infections as well.

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117
Q

The most common pathology of hearing loss is?

A

Hair cell loss

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118
Q

The most common preventable pathology of hearing loss is?

A

Noise trauma

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119
Q

Presbycusis manifests on an audiogram as:

A

Loss in high frequency hearing

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120
Q

The most common genetic mutation of non-syndromic hearing loss is:

A

Connexin 26

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121
Q

Noise exposure manifests on audiogram as:

A

Bilateral loss of specific frequency, typically 2000-4000 Hz

122
Q

Ototoxic drugs include:

A

Aminoglycosides, loop diuretics, ASA, cancer drugs

123
Q

Meniere’s disease is associated with:

A

Endolympathic hydrops, which causes expansion of endolymph compartment in inner ear

124
Q

Symptoms of Meniere’s include:

A

Vertigo, sensorineural hearing loss (particularly LOW END FREQUENCIES), tinnitus, aural fullness. Usually caused by cytomegalovirus

125
Q

Strial vascularis dysfunction manifests on audiogram as:

A

Flat moderate-severe sensorineural hearing loss

126
Q

The mainstay of sensorineural hearing loss treatment is:

A

Hearing aids

127
Q

T/F: PTSD is not a part of anxiety

A

True

128
Q

What is the relevance of benzos in pathophysiology of anxiety?

A

Decreased binding

129
Q

What part of the brain is hyperactive in anxiety? Hypoactive?

A

Amygdala; orbitofrontal and prefrontal cortex

130
Q

How to treat panic disorders?

A

Start benzos, start SSRIs, titrate off benzos

131
Q

Generalized anxiety disorder is characterized by what 3 symptoms:

A

Worry anxiety tension

132
Q

Tourettes has a high comorbidity with:

A

OCD

133
Q

OCD is marked by hyperactivity of what?

A

Direct pathway, inhibition of thalamus

134
Q

Basal ganglia is more involved in ____, while cerebellum is involved in ___

A

Movement initiation and coordination; moment-to-moment correction of movement

135
Q

What is the size principle?

A

Small motor units (slow fibers) are recruited first because they have high resistance to generate more voltage, then large units (fast fibers) are recruited

136
Q

Difference between fast twitch and slow twitch?

A

Slow has more myoglobin. Fast twitch is either oxidative (more mitochondria, slow fatigue) or glycolytic (less mitochondria, fast fatigue)

137
Q

What is a muscle spindle?

A

Intrafusal fibers innervated by gamma motor neurons in parallel with contractile extrafusal fibers, Afferents detect dynamic (1a, bag) and static (2, chain) stretch and trigger contraction of alpha motor neurons.

138
Q

What is the stretch reflex actually used for?

A

Maintaining muscle tone

139
Q

Are intrafusal fibers contractile?

A

Yes

140
Q

Golgi tendon organs detect what and are innervated by what?

A

Muscle tension, 1B afferents. They are in series of muscle and tendon and get ‘pinched’ when muscle contracts

141
Q

T/F: Stretch reflex inhibits antagonist muscles

A

True, via spinal cord interneuron

142
Q

What receptors detect stepping on a tack?

A

Pacinian (II), free nerve endings (III, IV)

143
Q

Where are central pattern generators, e.g. for locomotion and swimming?

A

Spinal cord, particular thoracolumbar and they interact via commissural fibers to generate rhythm. They generate the alternating flexion-extension for walking etc. and are modulated by descending pathways

144
Q

Gaze orientation is mediated by what structure?

A

Superior colliculus

145
Q

Reticular formation does:

A

Premotor functions such as posture balance anticipatory muscle action, etc. as well as modulatory functions of CV system, ettc.

146
Q

Premotor cortex is involved in:

A

Initiating movement in response to external cue, especially in mirror neuron (same activity in cortex when watching you do something as when I do it)

Either premotore and reticular cortex can initiate complex, multijoint movements!

147
Q

Supplementary cortex is involved in:

A

Rehearsal of movement

Either premotore and reticular cortex can initiate complex, multijoint movements!

148
Q

How does functional recovery from stroke happen?

A

Areas adjacent to damaged cortex can sprout new connections to subserve motor control over the affected body part!

149
Q

Practice leads to what?

A

Expansion of that region of cortex as well as subtle synaptic changes

150
Q

Fasciculations are a sign of a lesion to which motor neuron?

A

Lower motor neuron

151
Q

The anterior cerebellar lobe is also known as:

A

Spinocerebellum

152
Q

Flocconodular lobe is also known as:

A

Archeocerebellum/Vestibulocerebellum
Posterior cerebellar lobe is a.k.a:
Neocerebellum

153
Q

Corticocerebellum is:

A

Lateral hemispheric lobes

154
Q

Cebellar nuclei, from lateral to medial:

A

Dentate, Emboliform and Globose (these two make up the intersposed), Fastigial

155
Q

Vermis and fastigial nucleus do what? Lesions result in?

A

Axial musculature, posture/balance, head and eye movements; lesions  bilateral deficits

156
Q

Paravermal and intersposed nuclei do what? Lesions result in?

A

Fine-tunes limb movements; ipsilateral deficits (dysmetric, dysdiadochokinesia, tremor)

157
Q

Lateral lobe and dentate nuclei do what?

A

Higher level coordination of movement (planning and initiating movement)

158
Q

Flocconodular lobe does what? What’s it’s nucleus?

A

Balance. Vestibular nucleus…

159
Q

The output of the cerebellum is/are:

A

Deep nuclei

160
Q

To where does the fastigial nucleus send its axons?

A

Vestibular nucleus and pontine reticular formation

161
Q

To where does the intersposed nuclei send its axons?

A

Contralateral red nucleus, and then to the rubrospinal tract

162
Q

To where does the dentate nucleus send its axons?

A

Contralateral ventrolateral thalamus, and then to primary motor and pre-motor cortices

163
Q

Where are somatotopic maps found on the cerebellum?

A

Anterior and posterior lobes only.

164
Q

Motor learning is initiated by error signals from the ___?

A

Inferior olivary nucleus

165
Q

Where do inferior olivary nucleus error signals fire to?

A

Send complex spikes via climbing fibers

166
Q

Net result of a complex spike is?

A

Inhibits simple spikes of parallel fibers, so there is less excitatory parallel fiber innervation of the Purkinje cells when that same movement occurs long-term depression
Cerebellar deficits are always ___:
IPSILATERAL! Only tracts between cerebellum and cortex decussate

167
Q

T/F: Cerebellar lesions result in loss of coordination and strength

A

False, coordination loss only

168
Q

The output cell of the cerebellum is the:

A

Purkinje cell

169
Q

Cells in the Molecular layer are:

A

Inhibitory stellate and basket cells, which inhibit Purkinje cell, as well as parallel fiber of granule cell

170
Q

Cells in Purkinje layer are:

A

Purkinje cells

171
Q

Cells in Granular layer are:

A

Climbing fiber from ION which excites parallel fibers
Inhibitory Golgi cells which inhibit parallel fibers
Excitatory granule cells which becomes parallel fibers
Mossy fibers from pons which excite granule cells

172
Q

In terms of timing of cerebellar neuroelectrical events, what is the order, i.e. how does it make it an inhibitory delay loop?

A

Climbing fibers and mossy fibers directly excite the deep nuclei
Climbing fibers then excite Purkinje cells, which then inhibit the deep nuclei

173
Q

Complex spikes are a result of:

A

Climbing fiber making one AP

174
Q

Simple spikes are a result of:

A

Many parallel fibers making one AP

175
Q

Lesions of the basal ganglia result in deficits on what side of the body?

A

Contralateral side motor axons decussate

176
Q

Striatum receives input from where?

A

Layer V of cerebral cortex

177
Q

Does the caudate or putamen receive information from anywhere else?

A

Sensorimotor cortex has inputs onto the putamen

178
Q

Describe the D1 pathway.

A

Striatum inhibits globus pallidus interna to remove its inhibition of the thalamus, allowing it to output to the motor cortex
Striatum also inhibits substantia nigra (which sends back excitatory neurons to the striatium) to excite the thalamus
Promotes movement

179
Q

Describe the D2 pathway.

A

Striatum activates globus pallidus externa to inhibit subthalamic nucleus to activate globus pallidus interna to inhibit the thalamus
Inhibits movement

180
Q

Substantia nigra has ___ input to the striatium and receives ___ input from striatum.

A

Excitatory, inhibitory

181
Q

Hemiballismus results from lesions to the ___.

A

Subthalamic nucleus

182
Q

Where does the basal ganglia receive sensory input from?

A

It does not get any.

183
Q

Basal ganglia is damaged in ____

A

Metabolic disease

184
Q

What is the nucleus accumbens?

A

Juncture between caudate and putamen, part of limbic system.

185
Q

Huntington’s chorea results from loss of ____.

A

Striatal action on globus pallidus  chorea

186
Q

Period of adaptation to limb length changes depends on what brain structure?

A

Cerebellum

187
Q

What is the adaptive feedforward controller?

A

Cerebellum

188
Q

What cortex predicts motor movements to the premotor cortices?

A

Parietal cortex

189
Q

What structure acts as the comparator?

A

Substantia nigra pars compacta of the basal ganglia

190
Q

Describe what happens when something is heavier than you think it should be.

A

Muscle spindle stretches, ION fires error signal to create LTD in cerebellum, striatum sends dopamine to subthalamic nucleus and thalamus  reconfigure perceptions

191
Q

What is the chemical mediator of learning? What happens to it as you learn?

A

Dopamine, increases initially with the reward only, then starts to only show up when you do the thing that you think should get you the reward, and not on reception of the award itself

192
Q

The most important refractive structure for the eye is the

A

Cornea (2/3), lens is only 1/3

193
Q

Light in the photoreceptors results in hyperpolarization because rhodopsin causes:

A

cGMP destruction

194
Q

What are the two excitatory connections in the retina?

A

Bipolar cell synapses on ganglion cells, Surrounding photoreceptors to horizontal cell synapses

195
Q

What is the one inhibitory connect?

A

Horizontal cells to photoreceptors

196
Q

The visual system is primarily interested in what?

A

Light-dark contrast

197
Q

What is the thalamic nucleus for the eye?

A

LGN

198
Q

The parvocellular system is in what LGN layers? It deals with what?

A

3-6, color, form, detail, acuity

199
Q

The magnocellular system is in what LGN layers?

A

1,2, motion, depth, motion

200
Q

Ipsilateral eye goes to what LGN layers?

A

Layers 2,3,5 (can remain concentrated)

201
Q

Contralateral eye goes to what LGN layers?

A

Layers 1, 4, 6 (gets separated)

202
Q

Color is handled by what structure of the visual cortex?

A

Blob hypercolumns

203
Q

Binocular cells arise in what area of the visual cortex?

A

In between ocular dominance columns

204
Q

RF shape of photoreceptors is ___

A

Tiny spot

205
Q

RF shape of ganglion cell is ___

A

Donut

206
Q

RF shape of simple cell is ___

A

Bar

207
Q

RF shape of complex cell is ___

A

Edge

208
Q

What’s the big difference between simple and complex cells?

A

Complex cells are not position sensitive, only motion sensitive

209
Q

Which cells are binocularly driven?

A

Simple and complex cells.

210
Q

T/F: Color opponent cells arise because cones connect to one field center and indirectly to cones with a different color preference…

A

True, just needed this here for review

211
Q

The parietal lobe receives which vision pathway? What is it responsible for? What stripes does it get?
Dorsal; spatial (the “where”); thick stripe

A

Temporal lobe?

Ventral; object (the “what”); strip and interstripe

212
Q

What sides do category 1 and 7 cells drive?

A

1 = contralateral; 7 = ipsilateral

213
Q

What occurs if one eye is deprived of vision in the sensitive period?

A

Synaptic connections degenerate and disappear

214
Q

What occurs if there is strabismus as a baby?

A

Each eye sees different part of the world, thus there are many monocular cells and very fiew binocular cells

215
Q

What occurs if both eyes are deprived of vision in the sensitive period?

A

Behaviorly blind, but normal receptive fields… Higher order cells are disrupted, the primary visual cortex is normal…

216
Q

What is the cerebral anatomic significance of monocular/binocular deprivation?

A

Ocular dominance columns are competing – if optic nerve doesn’t fire AP during development, corresponding ocular dominance hypercolumn doesn’t form

217
Q

What is the molecular basis in formation of ocular dominance hypercolumns?

A

NMDA receptor presynaptically, trophic factor release postsynaptically which diffuses to presynaptic terminal

218
Q

The afferent limb of pupillary light reflex ends where?

A

Pretectal nucleus, bilaterally

219
Q

Efferent limb of pupillary reflex begins where?

A

Edinger-Westphal nucleus…

220
Q

How do you get macular sparing?

A

Lesion to the optic radiations – posterior 1/3 has MCA and PCA collateral circulation

221
Q

Where is the lesion in a homonymous superior quadrantanopia?

A

Meyer’s loop, inferior (temporal pathway)

222
Q

What happens if one eye is deprived, then opened and then the other eye is deprived? What does this resemble?

A

Reopened eye recovers, the newly deprived eye loses synaptic connections. Repeated monocular deprivation resembles nystagmus in developmental terms

223
Q

Where is the lesion in a homonymous inferior quadrantanopia?

A

Baum’s loop, Optic radiation, superior (parietal pathway)

224
Q

Bitemporal hemianopia?

A

Optic chiasm, be on the lookout for pituitary adenoma symptoms (feeling cold, weight issues)

225
Q

What is the pathophysiology of a down-beat nystagmus?

A

Chiara malformation (lesion at cervicomedullary junction)

226
Q

What is the triad of a Horner syndrome?

A

Ipsilateral miosis, ptosis, and anhidrosis. Due to sympathetic trunk lesion.

227
Q

What is the difference between astigmatism and far/nearsightedness?

A

Astigmatism is due to the shape of the cornea. Near/farsightedness is due to the refractive power of the eye (cornea and lens).

228
Q

What things can you see with a funduscopic exam?

A

Corenea, lens, iris, vitreous humor, optic disc (medial from fovea), retina, vessels

229
Q

What about a homonymous hemianopia?

A

Optic tract

230
Q

Why does presbyopia occur? What do we lose focus on?

A

Lens becomes less flexible as we age; lose focus on near objects.

231
Q

A patient presents with pink conjunctiva and watery discharge, what is the most common causative agent? What should you do?

A

Adenovirus (non-enveloped dsDNA)
No specific treatment, advise on hand washing, maybe cold compresses and artificial tears. If serious inflammation, steroids

232
Q

A patient presents with red conjunctiva and thick discharge, what are the 2 most common causative agents? What should you do?

A

Staph aureus and Strep pneumo, both G+ cocci

4th generation fluoroquinolone attacks DNA gyrase. Avoid gentamicin

233
Q

What are the 3 parts of the uvea?

A

Iris, ciliary body/pars plana, choroid

234
Q

A patient presents with an irregularly shaped pupil and redness near the limbus (junction of cornea and sclera), what do you do?

A

No systemic workup necessary if first time, but if second time then yes look for systemic disorder

235
Q

A patient presents with foreign body sensation after being poked in the eye, how do you visualize for an abrasion? How do you treat?

A

Fluorescein stain with blue light. Antibiotic ointment, do not give anesthetic eye drops – delays healing process

236
Q

A patient presents with white fluid in the anterior chamber of the eye. What is this and what’s the diagnosis? What causes it?

A

Hypopyon; corneal ulcer. Infectious or trauma, especially if contact lens wearer. Treat with 4th generation fluoroquinolone if small, culture if large

237
Q

A patient presents with a shard of glass in the cornea. What should you do?

A

Ask what they were doing, check under eyelids as it might have migrated. Remove it.

238
Q

Schirmer’s test is a test for what condition?

A

Dry eyes… Insert paper strips into eyes to measure tears.

239
Q

How do you treat dry eyes with oral supplements?

A

Flax oil, omega-3’s

240
Q

You see abnormal dendritic keratin deposits in a patient’s left eye, which also has redness. What is the diagnosis? How do you treat?

A

HSV-1. One of the most frequent causes of permanent vision loss. Most cases resolve spontaneously but can treat with Acyclovir oral or topical trifluridine.

241
Q

A patient presents with red lesions over the upper face including the tip of the nose. What is the diagnosis? Treatment?

A

VZV reactivation (shingles), oral Acyclovir.

242
Q

What are the risk factors for pterygium?

A

UV light.

243
Q

A patient presents are getting fucking decked at a bar with a very red eye. What’s the treatment?

A

Subconjunctival heme will usually resolve spontaneously, but you should get a full history and do an eye exam for other pathology.

244
Q

Which is the more common glaucoma subtype?

A

Chronic open angle.

245
Q

Advanced age, diabetes, steroids, trauma, and radiation are risks factors for:

A

Cataracts

246
Q

What type of orbital fracture is more likely in children?

A

Roof fractures / Buckle

247
Q

What type of orbital fracture is more likely in adults?

A

Floor / Blowout

248
Q

What thyroid etiology is associated with orbital disease? What is the target?

A

Graves disease, but this is due to auto-inflammation, NOT thyroid disease! Orbital fibroblast is the target as it expresses TSH-R and ILGF-R and so it produces GAGs, fibroblast proliferation  extraocular muscle hypertrophy

249
Q

How do you treat the orbital complications of Graves disease?

A

Immunomodulators when in active phase which lasts 1-3 years – follow with clinical activity score then orbital decompression surgery once quiescent

250
Q

What’s the function of Muller’s muscle?

A

The superior tarsal elevates the upper eyelid

251
Q

What is the most common eyelid skin cancer?

A

Basal cell 90%

252
Q

What is the opening of the lacrimal drainage system?

A

Punctum –> canaliculi

253
Q

A patient presents with epiphora (tear overflow) and chronic dacryocystitis (inflammation of lacrimal sac). What’s the treatment?

A

Surgery – dacryocystorhinostomy

254
Q

Where are cones concentrated in the retina?

A

Fovea

255
Q

What are in the foveolar?

A

Photoreceptors ONLY

256
Q

What is a good surgical approach point for the eye?

A

Pars plana

257
Q

Presence of yellow subretinal deposits suggests what etiology?

A

This is drusen, it suggests macular degeneration

258
Q

Presence of cotton wool spots suggests what? What’s the likely etiology?

A

Capillary ischemia; malignant hypertension

259
Q

What is the most common cause of blindness in working adults?

A

Diabetic retinopathy, particularly when it causes macular edema

260
Q

A patient presents with proliferative diabetic retinopathy. What is the treatment?

A

Anti-VEGF injections to inhibit the neovascularization of the iris
On funduscopic exam you see copper and silver wiring. What’s your diagnosis?
Arteriosclerosis – hypertensive retinopathy

261
Q

What’s the most common cause of blindness in people older than working age?

A

Age-related macular degeneration especially in smoking white women

262
Q

What is the pathophysiology of dry AMD?

A

Drusen (yellow lipoprotein deposits), and atrophy of the epithelium can treat with antioxidants

263
Q

What is the pathophysiology of wet AMD? How do you treat?

A

Choroidal neovascularization. Anti-VEGF antibodies. Fibrotic disciform scar suggests it’s end-stage.

264
Q

Where are ‘floaters’ located?

A

Vitreous humor, especially in the posterior region

265
Q

0.3 is the normal ratio for what structures?

A

Cup-to-disk some eyes can be up to 0.7

266
Q

What is the most common optic neuropathy? What is primary vs. secondary due to?

A

Glaucoma; primary is due to eye anatomy, secondary is due to neovascularization.

267
Q

T/F: Glaucoma manifests as increased IOP

A

False, 15% can have normal IOP, BUT TREATING IOP IS ALWAYS BENEFICIAL!

268
Q

Patient presents with bilateral optic disc swelling and blurring of the disc margins, What’s the diagnosis?

A

Papilledema

269
Q

Parasympathetic division mediates pupillary ___, while sympathetic mediates ___

A

Constriction, dilation

270
Q

Where must a lesion be to produce macular sparing?

A

Occipital lobe – think posterior cerebral artery. If it’s a superior vision field defect, it’s the inferior occipital lobe, vice versa. If it’s a hemianopia, it’s the entire occipital lobe.

271
Q

Describe the retinotopic map (the visual field as represented on the calcarine sulcus)

A 
It’s as if you’re reading successive pages going from inner to outer.
Thus 1 (THE FOVEA) is top left, 2 is bottom left, 3 top right, 4 bottom right.  Then the next circle does the same thing. Of course the nasal half is represented on the contralateral lobe, temporal half is ipsilateral lobe.
272
Q

What is the end of the afferent leg of the pupillary reflex?

A

It’s CN II, and it ends at the LGN of thalamus

273
Q

What are the actions of the trochlear nerve?

A

Depress and intort the eye.

274
Q

What’s the pharmacologic treatment for any nystagmus?

A

Klonopin this is the most common one from Pelak’s chart.

275
Q

Give the equation for dB level of a sound.

dB = 20 * log(P1/P2) where P2 = 20 * 10^-6 N/m2

A

What’s the threshold for human hearing?

1000 Hz

276
Q

Where is the impedance mismatch of the ear?

Between middle and inner ear.

A

How does the ear overcome the impedance mismatch?
P=F/A
The tympanic membrane has 20x the surface area of the stapes, which increases pressure
Malleus is long as fuck – creates a lever to increase force by 1.3x, which increases pressure

277
Q

Where is the basilar membrane? What does it house?

A

Between the scala media and tympani; houses organ of Corti which has the hair cells

278
Q

Where’s the endolymph? How is it made?

A

Scala media; stria vascularis pumps in K+ constantly.

279
Q

What structures enable hair cells to save energy?

A

Tip-links

280
Q

Where do low frequencies vibrate at in the ear?

A

Nearest the apex/helicotroma, where it’s thick, furthest from the entrance
High frequencies vibrate near the base where it’s thin, closest to the entrance so these are lost first

281
Q

What neurotransmitter do IHCs release?

A

Glutamate via mechanotransduction opening voltage gated calcium channels

282
Q

Why are OHCs not the main player?

A

They receive 1 auditory nerve fiber per 10 hair cells… While 1 IHC receives 10-30 ANFs

283
Q

What is the protein responsible for OHC moving?

A

Prestin

284
Q

Where do optoacoustic emissions emanate from?

A

Active OHCs make them which causes them to act as a loudspeaker

285
Q

How is pitch generated?

A

ANFs are phase locked and only respond to certain frequencies

286
Q

Where does the auditory system decussate?

A

Trapezoid body first; also to the other inferior colliculus afterwards

287
Q

Where must a lesion be to produce unilateral deafness?

A

Caudal to and including the CN II nucleus.

288
Q

Interaural level delays are a result of what? What are they useful for? Where are the handled centrally?

A

Because the head is an obstacle. Useful for localizing high frequency sounds. Lateral superior olive.

289
Q

Interaural time delays are a result of what? What are they useful for? Where are the handled centrally?

A

Because the ears are spaced apart. Useful for localizing low frequency sounds. Medial superior olive. ITDs rely on phase locking – if the auditory nerve is damaged, you cannot use ITDs.

290
Q

Monoaural spectral delays arise because of what? What are they useful for?

A

Pinna. Useful for localizing high-frequency sounds along the vertical axis.

291
Q

Unilateral lesions of the inferior colliculus or above result in what?

A

Deficits in sound source localization contralateral to the lesion – there is no unilateral deafness

292
Q

At Brodmann area 41, high frequency sounds are localized where? Low frequency sounds?

A

Low=anterior; High=posterior

293
Q

What vestibular structure responds to horizontal movement? Vertical?

A

Utricle; saccule

294
Q

T/F: Movement of the head results in deflection of the cupula, such that the hair cells are depolarized by endolymph entry to release neurotransmitter, which will cause the otherwise quiescent nerve fibers to fire action potentials which will relay to the vestibular nucleus.

A

False, the nerve fibers fire APs even at rest, this causes them to fire APs more frequently.

295
Q

T/F: The contralateral side of the ampulla (side you’re moving away from) hyperpolarizes

A

True, the ipsilateral side (side you’re moving towards) depolarizes

296
Q

T/F: Constant acceleration followed by constant deceleration will produce increased firing rates above the mean, and then decreased firing rates below the mean at the respective nerve fiber of one ampulla.

A

True

297
Q

T/F: As long as you’re moving, the ampulla of the respective structure will depolarize.

A

False, it’s about acceleration; at a constant velocity they will catch up, i.e. the cupula will return to normal position, endolymph will leave, you’ve adapted.

298
Q

By how many degrees are the horizontal semicircular canals separated from the horizontal when the head is upright?

A

30 degrees

299
Q

Testing the vestibulocular reflex involves pouring cold water and hot water into the ear. What are the normal responses to this?

A

Immediate vertigo, nausea, twisting of head and body. Hot water induces nystagmus to the side of the water by increasing activity of the vestibular nerve, cold water induces nystagmus to the contralateral side by reducing activity of the vestibular nerve

300
Q

What do aminoglycosides damage in the ear?

A

Preferentially OHCs, particularly the transduction channels

301
Q

T/F: IHCs only respond to a certain range of sound, i.e. they are phase locked to certain frequencies. Their resting potential is -50 mV and upon the proper signal they will fire APs which will travel via cochlear nuclei to the contralateral auditory cortex (temporal lobe, Brodmann area 41).

A

False, IHCs only release neurotransmitter, they do not fire APs.

302
Q

Where is the lesion in a downbeat nystagmus?

A

Cervicomedullary junction – this is not congenital type of nystagmus (…but it’s related to Chiari malformation per a previous lecture…)

NS_BTRAN (21 decks)

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