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SF2 Unit 4 Memorization Flashcards

1
Q

Projection Neuron

A

Second-order neuron with axon in Ascending Spinothalamic Tract

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2
Q

Interneurons: Inhibit or Excite Projection Neurons

A

inhibit (when active)

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3
Q

Neurotransmitters used by Nociceptors on projection Neurons

A

Gluatamate
Substance P
Calcitonin Gene-Related Peptide (CGRP)

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4
Q

Classes of Endogenous Opioids

A

Enkephalins
Dynorphins
Endorphins

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5
Q

Type of Receptor: Opioid Receptors

A

G-Protein Coupled

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6
Q

C Sensory Fibers

A

from nociceptors

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7
Q

Type of Fibers from Non-Nociceptor Receptors

A

A-Alpha or A-Beta

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8
Q

Principle opioid in dorsal horn

A

enkephalin (mu receptor type)

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9
Q

High concentration of Mu-type Opioid Receptors

A

Periaqueductal Gray

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10
Q

Caused of Pain Wind-Up

A

Repeated firing of C-fiber nociceptors

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11
Q

Hyperalgesia

A

Abnormally increased sensitivity to pain

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12
Q

Released by Microglia during inflammation

A

Interleukins

Brain-Derived Neurotrophic Factor (BDNF)

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13
Q

Discussed Types of Non-Opiate Analgesic Drugs

A

Antidepressants
NMDA Receptor Antagonists (ex: Ketamine)
Anticonvulsants

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14
Q

Rostral portion of developing neural tube; precursor to Telencephalon and Diencephalon

A

Prosencephalon

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15
Q

Diverticulation

A

Process of Rostral Neural Tube differentating and expanding faster than caudal portion

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16
Q

Primary cell type in Neocortex

A

Pyramidal Cells

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17
Q

Apical dendrite of Pyramidal Cells is in the Cortex. Where does it send inferior axons?

A

Corpus Callosum (white matter tract)

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18
Q

Columns (Cortex)

A

Vertical organization / functional unit

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19
Q

Columnopathy

A

Disorder of columnar development in Cortex

ex: Autism Spectrum Disorder

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20
Q

Primary Center(s) for Olfaction in Cortex

A

Piriform and Entorhinal Cortices

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21
Q

Unimodal Association COrtical Area

A

Adjacent to primary cortical area; modality-specific

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22
Q

Heteromodal Association Cortex

A

Receive/process input from multiple modalities; “higher-order” function

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23
Q

Disconnection Syndromes

A

Impairments in fibers that connect cortical regions

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24
Q

Cortical Signs Associated with Dominant Hemisphere Damage

A

Agraphia
Acalcia
Alexia (Pure and other)

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25
Q

Acalcia

A

Inability to perform simple math (Parietal lobe lesion)

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26
Q

Alexia w/agraphia. Lesion?

A

Left angular gyrus (dominant parietal lobe)

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27
Q

Pure Alexia. Lesion?

A

Left occipital lobe and splenium of corpus callosum

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28
Q

Typical sign of Damage to Non-Dominant Cerebral Hemisphere

A

Neglect

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29
Q

Construction Apraxia is an early finding in…

A

Alzheimer’s Disease

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30
Q

Damage to this structure can typically cause Hypersexuality and Hyperaggression

A

Amygdala

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31
Q

Non-Cortical Lesion which can cause Homonymous Hemianopia

A

Damage to Internal Capsule or Lateral Geniculate Nucleus

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32
Q

Destructive Eye Deviation

A

Deviation toward lesion.

Lesioned Frontal Eye Field (Area 8)

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33
Q

Irritative Eye Deviation

A

Deviation away from lesion.

Cause: Seizure

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34
Q

Apraxia

A

Loss of ability to carry out voluntary movement despite intact primary sensory, motor, and language areas

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35
Q

Cause: Subcortical Apraxia

A

May occur due to damage to Subcortical Extrapyramidal Motor System or Thalamus

(Cause of false localization of Apraxia to cortex)

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36
Q

Frontal Release Sign

A

Unmasking of Infantile reflexes by Frontal Lobe

Palmar Grasp, Sucking, Glabellar, Snout, Rooting Reflexes (dont memorize)

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37
Q

Dorsal Stream of Visual Processing

A

“Where” Stream

Motion and spatial information travelling dorsally from primary visual cortex to parietal lobe. Area 17 (V1) to Parieto-Occipital Association Cortex (V5)

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38
Q

Ventral Stream of Visual Processing

A

“What” Stream

Information about size, shape, color, etc. Travels ventrally to Temporal Lobe. Area 17 (V1) to Occipitotemporal Association Cortex

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39
Q

Object Agnosia

A

“Classic Agnosia”. Loss of ability to recognize objects by sight

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40
Q

Cause: Object Agnosia

A

Damage to Ventral “What” Stream

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41
Q

Types of Visual Agnosia Associated with Left Occipital/Temporal Damage

A

Apperceptive - Failure of Perception

Associative - Failure of recognition despite accurate perception

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42
Q

Prosopagnosia

A

Loss of ability to subscribe identity to familiar faces

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43
Q

Cause: Prosopagnosia

A

Bilateral damage to Fusiform Gyrus (Occipitotemporal Gyrus)

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44
Q

Akinetopsia

A

“Motion blindness”

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45
Q

Cause: Akinetopsia

A

Damage to lateral part of occipital lobe

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46
Q

Other name for Deep White Matter of Cerebral Hemispheres

A

Centrum Semiovale

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47
Q

Main Types of Tracts in Deep White Matter of Cerebral Hemispheres

A

Association Fibers
Commissural Pathways
Projection Fibers

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48
Q

Associational Fibers

A

Travel within hemisphere only, connecting areas within the cortex

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49
Q

Arcuate Fibers (U Fibers)

A

Connect adjacent cortical areas (gyri)

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50
Q

Predominant Association Fiber

A

Superior Longitudinal Fasciculus

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51
Q

Superior Longitudinal Fasciculus

A

Associational Fiber; Travels from anterior of front lobe to posterior of occipital lobe

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52
Q

Arcuate Fasciculus

A

Subtract of Superior Longitudinal Fasciculus in Dominant Hemisphere

Connects Broca’s and Wernicke’s Areas

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53
Q

Conduction Aphasia

A

Can speak fluently but incoherent and inappropriate responses.

Result of lesion to Arcuate Fasciculus

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54
Q

Inferior Longitudinal Fasciculus

A

Associational Fiber connecting Temporal and Occipital Poles

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55
Q

Cingulum Fibers

A

Originate from Cingulate Gyrus

Connects emotion centers and Default Mode Network with memory structures (Limbic System/Hippocampus)

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56
Q

Default Mode Network

A

Provides abilities of internal cognition, thought and dialog.

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57
Q

“Theory of Mind”

A

Understanding that we and others have similar motivations. Adjust behavior accordingly.

Structure: Default Mode Network

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58
Q

Uncinate Fasciculus

A

Association Fiber that connects Temporal and Frontal Lobes. Role in empathy and recognition

Uncinated Seizures - emotional affect and olfactory changes

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59
Q

Commissural Pathways

A

Connect the two cerebral hemispheres

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60
Q

Predominant Commissural Pathways

A

Anterior Commissure
Posterior Commissure
COrpus Callosum

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61
Q

Anterior Commissure

A

Commissural pathway connecting temporal lobe, olfactory cortices, and olfactory bulbs.

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62
Q

Posterior Commissure

A

Commissural pathway connecting Pretectal structures (Rostral Midbrain)

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63
Q

Corpus Callosum

A

Commissural pathway which connecting homotypic (“same type”) areas of the cortices/hemispheres

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64
Q

What can a defect in development or resection of the Corpus Callosum lead to?

A

Disconnection Syndromes

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65
Q

Projection FIbers

A

Afferent and efferent pathways that carry information between the brain and spinal cord

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66
Q

Capsule (Cerebral Structure)

A

Fiber bundle traveling through space in cerebrum

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67
Q

Corona Radiata

A

Name for structure formed when fibers fan out to fill hemisphere after traversing capsules

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68
Q

Internal Capsule

A

(Projection) Fiber tract between Thalamus and Lenticular/Lentiform Nucleus

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69
Q

Parts of the Internal Capsule

A

Anterior Limb
Genu
Posterior Limb

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70
Q

Anterior Limb of Internal Capsule (tracts)

A

Most tracts to and from frontal lobe. Includes Frontothalamic and frontopontine tracts

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71
Q

Genu of Internal Capsule (tracts)

A

Corticobulbar Fibers

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72
Q

Posterior Limb of Internal Capsule (tracts)

A

Corticospinal, sensory, and visual/optic radiations. Auditory Radiations.

Retrolenticular portion is here somewhere visual/auditory

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73
Q

Blood Supply: Anterior Limb of Internal Capsule

A

ACA

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74
Q

Blood Supply: Genu of Internal Capsule

A

Lenticulostriate Branches of MCA

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75
Q

Blood Supply: Posterior Limb of Internal Capsule

A

Lenticulostriate Branches of MCA

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76
Q

This-walled arteries susceptible to stroke in brain

A

Lenticulostriate Branches of MCA

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77
Q

Blood Supply: Basal Ganglia

A

Lenticulostriate Branches of MCA

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78
Q

External Capsule

A

Lateral to Internal Capsule (separated by Lentiform Nucleus); Contains Cortico-Cortical Projections

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79
Q

Cortico-Cortical Projections

A

Cholinergic axons connecting basal forebrain to other cortical areas. Found in External Capsule

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80
Q

Extreme Capsule

A

Connects Claustrum with the Insular Cortex

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81
Q

Function: Claustrum

A

Conscious, sustained attention

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82
Q

Function: Insular Cortex

A

Consciousness, emotion, empathy, self-awareness, and also “Theory of Mind”

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83
Q

Principle Component of the Extrapyramidal Motor System

A

Corpus Striatum

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84
Q

Consists of structures surrounding the COrpus Callosum and the Upper Brainstem-Diencephalic Junction

A

Limbic Cortex

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85
Q

Function: Limbic System

A

HOME

Homeostasis, Olfaction, Memory, Emotion

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86
Q

Receives precortical input from all sensory systems except olfaction

A

Thalamus

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87
Q

Internal Medullary Lamina

A

White matter tract dividing Thalamus into 3 (medial, anterior, lateral nuclear groups)

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88
Q

Lateral-Posterior Nuclei of Thalamus

A

Ventral Posterolateral (VPL)
Ventral Posteromedial (VPM
Lateral Geniculate
Medial Geniculate

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89
Q

Medial-Posterior Nuclei of Thalamus

A

Lateral Posterior
Lateral Dorsal
Pulvinar

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90
Q

Functional Divisions of Thalamus

A

Anterior/Medial: Limbic
Anterior/Lateral: Motor
Posterior/Medial: Multimodal
Posterior/Lateral: Sensory

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91
Q

Ventral Posterolateral (VPL) Nucleus

A

Thalamic nucleus; sensory from body (medial lemniscus, spinothalamic tracts)

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92
Q

Ventral Posteromedial (VPM) Nucleus

A

Thalamic nucleus; Sensory from head (Trigeminal sensory pathway)

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93
Q

Lateral Geniculate Nucleus

A

(Thalamus) Target for retinal axons. Optic radiations to Primary Visual Cortex

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94
Q

Medial Geniculate Nucleus

A

(Thalamus) Sends auditory radiations to Primary Auditory Cortex

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95
Q

Typical trend with Thalamic syndromes

A

Association with sensation and pain

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96
Q

Paresthesia

A

Aberrant positive sensations (tingling/numbness)

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97
Q

Dejerine-Roussy Syndrome

A

Thalamic Pain Syndrome

Initial presentation complete contralateral lack of sensation. Progression to severe pain. Typically from stroke

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98
Q

Dysesthesia

A

Abnormal, unpleasant sense of touch.

Thalamic sign

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99
Q

Allodynia

A

Subtype of Dysesthesia. Painful sensation induced by normally-innocuous stimuli

Possible thalamic sign

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100
Q

Hemianesthesia

A

Contralateral loss of sensation

Could be from damage to VPL or VPM

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101
Q

Cortical area remodeled by chronic pain

A

Prefrontal Cortex

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102
Q

Catecholamin-o-Methyltransferase

A

Gene/protein involved in pain sensitivity. Regulates enkephalin and catecholamines

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103
Q

Frank Congeital Insensitivity to Pain

A

Complete lack of A-delta and C fibers. Lack affective component of pain

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104
Q

Congenital Indifference to Pain

A

Can distinguish sharp/dull pain. Indifferent to sensations. Lack emotional responses, discomfort, and normal withdrawal from pain.

Normal peripheral fibers

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105
Q

Congenital Insensitivity to Pain w/Anhydrosis

A

Lack pain fibers due to a receptor mutation (cannot bind Nerve Growth Factor). Mutated TRK Receptor makes carrying pain impulse difficult. Difficulty responding to tissue damage/infection

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106
Q

TRK Receptors

A

Nerve Growth Factor (NGF) receptor found on Nerve and Mast Cells.

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107
Q

Importance of Mu Opioid Receptor

A

Most analgesics require Mu activation to work

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108
Q

Naloxone

A

Antagonizes and block Mu opioid receptor

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109
Q

Mechanisms of the Placebo Effect

A

1) Decreased awareness in pain sensitive regions

2) Increased activity in areas involved in top-down pain suppression

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110
Q

Receives projections from Periaqueductal Gray. Abundants 5-HT neurons. Descending projections modulate response to noxious stimulus in Dorsal Horn neurons

A

Dorsal Raphe Nucleus

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111
Q

Nociceptive Pain

A

Pain transmitted to CNS from peripheral receptors

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112
Q

Neuropathic Pain

A

Pain likely derived from nerve injury in CNS/PNS

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113
Q

Phantom Pain

A

Pain memory. Continuing pain after amputation

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114
Q

Most prominent gray matter loss in Chronic Pain

A

Dorsolateral Prefrontal Cortex

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115
Q

Timeline of Behavioral Effects of Chronic Pain

A

Stage 1: Acute Pain
Stage 2: Learned Helplessness
Stage 3: Acceptance of “Sick Role”

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116
Q

FDA-approved SNRIs for peripheral diabetic neuropathy

A

Venlafaxine and Duloxetine

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117
Q

Stroke

A

Acute impairment of blood supply

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118
Q

Ischemic Stroke

A

Loss of blood supply to regions of brain, leading to infarction

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119
Q

Infarction

A

Tissue death (necrosis) from lack of blood supply

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120
Q

Broad categories of Ischemic Stroke

A

Embolic and Thrombotic Stroke

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121
Q

Embolic Stroke

A

Masses (cholesterol/plaques) travel through circulatory system to block small diameter brain vessels

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122
Q

Thrombotic Stroke

A

Build-up of Atherosclerotic plaques within vessel walls. Gradual occlusion (as opposed to sudden)

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123
Q

Treatment: Ischemic Stroke

A

Tissue Plasminogen Activator (tPA). Can break-up clots if administered within 3 hours

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124
Q

Hemorrhagic Stroke

A

Weakening of blood vessel walls leads to rupture then bleed

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125
Q

Intracerebral Hemorrhage

A

Internal bleeding in the brain

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126
Q

Subarachnoid Hemorrhage

A

Rupture of surface blood vessels and build-up of blood/pressure in subarachnoid space. Characterized by sudden onset and ‘Thunderclap Headache’

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127
Q

Neonatal Intraventricular Hemorrhage

A

Bleeding into the ventricles. Elevated risk in premature / low birth weight infants due to autoregulation difficulty

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128
Q

Presentation: Neonatal Intraventricular Hemorrhage

A

Seizure, altered consciousness, and coma

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129
Q

Epidural Hematoma

A

Occasionally follows spontaneous hemorrhage. Rupture of Middle Meningeal Artery. Hematoma does not cross suture lines

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130
Q

Subdural Hematoma

A

Rupture of bridging veins. May cross suture lines

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131
Q

Hematoma seen in Shaken Baby Syndrome

A

Subdural Hematoma

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132
Q

Intraparenchymal Hemorrhage

A

Result of systemic/chronic hypertension. Can be secondary to reperfusion injury after ischemic stroke. Commonly impacts putamen, pons, thalamus, and cerebellum

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133
Q

Defining Feature: Charcot-Bouchard Microaneuryisms

A

Intraparenchymal Hemorrhage

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134
Q

Typical rupture in Intraparenchymal Hemorrhage

A

Lenticulostriate Branches of MCA

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135
Q

Ischemic Core

A

Area immediately impacted by loss of blood flow. Difficulty maintaining ionic homeostasis. Neurons fire in massive bursts (anoxic depolarization)

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136
Q

Anoxic Depolarization

A

Massive bursts of neuronal activity in Ischemic Core

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137
Q

Ischemic Penumbra

A

Periphery of Ischemic core; can be recruited into necrotic area if blood supply not returned

Excitotoxicity from Ca2+ and Glutamate released by Anoxic Deplorization in core.

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138
Q

Peri-Infart Depolarizations

A

Ischemic Penumbral neurons undergo successive rounds of depolarization for hours/days after initial event. Due to local Calcium and Glutamate increase

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139
Q

Cortical Spreading Depression

A

Region outside of Ischemic Core+Penumbra. Shorter depolarizations, Can go without damage

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140
Q

Eosin

A

Pathognomic (condition-specific) stain for stroke-lesioned brain tissue. “Dead reds”

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141
Q

Immediate imagery in stroke

A

Non-Contrast CT scan. Used to rule out Hemorrhagic Stroke prior to tPA administration

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142
Q

Imagery to localized stroke

A

CT scan or Diffusion-Weighted MRI

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143
Q

Cause: Cerebral Hypoperfusion

A

Typically heart failure

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144
Q

Cause of Syncope (fainting)

A

Cerebral Hypoperfusion

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145
Q

Lacunar Infarct

A

Stroke at terminal point of small artery resulting in small infarcted area

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146
Q

Watershed Infarct

A

Occlusion between two major arterial distributions. Combined symptoms from both supplies.

Ex: MCA/PCA

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147
Q

Transient Ischemic Attack

A

Acute episode typically resolved within 30 mins or up to 24 hours. Predictive of major stroke

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148
Q

Amaurosis Fugax

A

“Veil” coming down over one eye. Occlusion of Central Retinal Artery. Indicative of Transient Ischemic Attack

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149
Q

Abulia

A

Loss of willpower / ability to act voluntarily

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150
Q

Akinetic Mutism

A

Slowed/absent body movement and/or speech

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151
Q

Cause: Urinary Incontinence

A

ACA Stroke (genital representation on homunculus)

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152
Q

Area of Hippocampus sensitive to Ischemic Hypoxia

A

CA1 (pyramidal excitatory neurons)

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153
Q

Reason for Macular Sparing in PCA stroke

A

That part of the occipital lobe receives dual MCA/PCA supply

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154
Q

Occlusions associated with Thalamic Stroke

A

1) Penetrating Branches of PCA
2) Posterior Communicating Artery
3) Anterior Choroidal Artery

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155
Q

Weber’s Syndrome

A

Basal Midbrain Sydrome

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156
Q

Claude’s Syndrome

A

Tegmental Midbrain Sydrome

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157
Q

Benedikt’s Syndrome

A

Weber + Claude’s Syndrome

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158
Q

Wallenburg’s Syndrome

A

Lateral Medullary Syndrome

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159
Q

Typical Signs in Cerebellar Stroke

A

Inabiltiy to walk and ataxia. Also: dizziness, headache, nausea, vomiting

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160
Q

Four Brain Waves

A

Alpha, Beta, Delta, Theta

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161
Q

Beta Waves

A

Smallest amplitude. 13-30 Hz Associated with mental activity, alert wakefulness, and REM sleep

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162
Q

Alpha Waves

A

8-13 Hz. Relaxed wakefulness. Most prominent over Parietal and Occipital Lobes.

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163
Q

Theta Waves

A

4-8 Hz. Most prominent in the young > adult. Awake, drowsy and non-REM sleep states

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164
Q

Delta Waves

A

0.5-3.5 Hz. Non-REM sleep

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165
Q

Current Sink

A

Transient, local excess of (-) charge

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166
Q

Current Source

A

Transient, local excess of (+) charge

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167
Q

Determinant of EEG amplitude

A

Synchronization of firing

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168
Q

Sensory Evoked Potential

A

Average of EEGs recorded during the sensory stimulus

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169
Q

Seizures

A

Caused by abnormal patterns of neuronal activity

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170
Q

Epilepsy

A

Set of diseases characterized by chronic, repeated seizures

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171
Q

Partial Seizure

A

Restricted to one area of the brain

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172
Q

Simple Partial Seizure

A

Retain consciousness but may experience unusual feelings/sensations

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173
Q

Complex Partial Seizure

A

Change of consciousness, including dreamlike experience or loss of consciousness. May be accompanied by Automatisms

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174
Q

Automatisms (Seizures)

A

Repetitious behaviors such as blinking, twitches, mouth movements, walking in a circle

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175
Q

Aura

A

Sensation warning of impending seizure

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176
Q

Secondary Generalizations

A

Spreading of Partial Seizure from well-defined focal area to involve other brain areas

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177
Q

Generalized Seizures

A

Abnormal activation of many areas of the brain. Loss of consciousness. May trigger falls, loss of muscle tone, or massive muscle spasms.

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178
Q

Absence Seizures

A

Appear to be staring into space; may exhibit muscle jerking or twitching

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179
Q

Tonic Seizures

A

Stiffening of muscles esp: back, legs and arms

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180
Q

Clonic Seizures

A

Repetitive jerking movements of muscles on both sides of the body

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181
Q

Atonic Seizures

A

Loss of normal muscle tone; patient may fall down

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182
Q

Tonic-Clonic Seizures.

A

Stiffening of muscles esp: back, legs and arms. Repetitive jerking movements of muscles on both sides of the body (COMBINATION OF TWO)

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183
Q

Postictal Depression

A

Period of depression, with disorientation, drowsiness, or confusion, and altered EEG which may follow a seizure

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184
Q

Medication for Epilepsy

A

Approach 1: Barbiturates and Benzodiazepines. Attempting to enhance GABA neurotransmission

Approach 2: T-Type Ca2+ Channel and/or Use Dependent Voltage-Gated Na+ Channel Blockers. Reduce neuron ability to generate action potential bursts.

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185
Q

Surgery for Epilepsy

A

Temporal Lobe Resection. Most effective with focal epilepsy. Remove part or all of corpus callosum

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186
Q

Rare childhood epilepsys for which CBD is a treatment

A

Lennox-Gastaut Syndrome and Dravet Syndrome

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187
Q

Blood Supply: Inner Retina

A

Central Retinal Artery

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188
Q

Blood Supply: Choricocapillaris

A

Ciliary Arteries (branch of Opthalmic)

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189
Q

Muller Glia

A

Have cell bodies in Inner Nuclear Layer (Retina). Thought to be involved in synaptic formation

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190
Q

Primary Targets of Retinal Projections

A

Lateral Geniculate Nucleus
Superior Colliculus (midbrain)
Prectectum
Hypothalamus

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191
Q

Blood Supply: Lateral Geniculate Nucleus

A

Anterior Choroidal Artery + Small Branches PCA

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192
Q

Geniculocalcarine Tract

A

Primary visual pathway in brain. Connects LGN to Primary Visual Cortex. Tract fibers, known as optic radiations, travel through Retrolenticular Portion of the Posterior Limb of Internal Capsule

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193
Q

Divisions of Geniculocalcarine Tract

A

1) Upper Division (lower half of visual field); ends at Cuneus Gyrus (Upper Area 17)
2) Lower Division (upper half of visual field); ends at Lingual Gyrus (Lower Area 17)

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194
Q

Extrastriate Visual Pathways

A

Projections from Area 17 to Secondary Association Cortical Areas

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195
Q

Prestriate Cortex

A

Secondary Visual Cortex. V2. Both visual streams connect here to refine information from V1.

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196
Q

Superior Colliculus

A

Main player in Extrageniculate Pathway. Highly-sensitive to moving visual stimuli

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197
Q

Regulates control of Saccades (high velocity eye movements)

A

Superior Colliculus

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198
Q

Point of connection of Optic Tract to Superior Colliculus; Superior Colliculus to LGN

A

Brachium of Superior Colliculus

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199
Q

Extrageniculate Pathway

A

Retina -> Superior Colliculus -> Pulvinar -> Extrastriate Cortex

Works parallel to Geniculocalcarine Tract. Assimilates different types of information to construct objects in visual space

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200
Q

Regulates eye’s response to ambient light changes

A

Optic projection to Prectectum, then onward to Edinger-Westphal Nucleus

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201
Q

Edinger-Westphal Nucleus

A

Input from Pretectum. Regulates preganglionic parasympathetic fibers projection to eye.

1) Pupil Constriction
2) Lens Accomodation
3) Eye Convergence

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202
Q

Retinal projection to Hypothalamic

A

Goes to Suprachiasmatic Nucleus (Anterior Ventral Portion of Hypothalamus).

Involved in regulation of Circadian Rhythm and Hormonal Cycles

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203
Q

Progressive Encephalization

A

Evolutionary shift from retinal to primary cortical and then to higher-order visual processing

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204
Q

Binding Mechanism (Visual)

A

Combining multimodal sensation to create perception of external world

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205
Q

Cortical Blindness

A

Loss of conscious perception. Caused by lesion of Area 17 / V1

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206
Q

Blindsight

A

Ability to respond to visual stimuli even with Cortical Blindness. Thought to occur through Extrageniculate Pathway

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207
Q

Anton’s Syndrome

A

a.k.a. Visual Anosognosia

Patient denies losing vision despite Cortical Blindness

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208
Q

Achromatopsia

A

Disorder of color perception. Different from color agnosia/anomia because perception happens but failure to identify

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209
Q

Cause: Achromatopsia

A

Fusiform gyrus lesion (V4)

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210
Q

Metamorphosia

A

Distortion of size and shape. Lesion of Inferior or lateral visual association cortex

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211
Q

Balint’s Syndrome

A

Characterized by Simultagnosia, Optic Ataxia, and Ocular Apraxia.

Lesion: Bilateral lesion of Dorsolateral Parieto-Occipital Cortex (Dorsal Stream)

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212
Q

Simultagnosia

A

Perception of only a portion of visual field at a time; random shifting.

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213
Q

Optic Ataxia

A

Lack of coordination between visual input and hand movements. Inability to reach out and grab objects

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214
Q

Ocular Apraxia

A

Impaired gaze direction; difficulty initiating saccades

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215
Q

P-Type RGCs

A

(90% of RGCs) Small receptive field, sustained responses. Best suited for fine detail and color

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216
Q

M-Type RGCs

A

Large receptive field. Detection of motion

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217
Q

Non-M Non-P RGCs

A

Color-sensitive (???)

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218
Q

Relay Neurons in Lateral Geniculate Nucleus

A

Magnocellular LGN Neurons (correspond to M-Type RGCs)
Parvocellular LGN Neurons (P-Type RGCs)
Intralaminar LGN Neurons (Non-M Non-P RGCs)

Release glutamate at synapses

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219
Q

Stellate Cells (Visual)

A

Receive input from Lateral Geniculate Nucleus in Layer 4 of Primary Visual Cortex)

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220
Q

Blobs

A

Areas of high Cytochrome Oxidase concentration. Neurons in blobs have wavelength-sensitive repsonses to visual stimuli. Important in color discrimination

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221
Q

Channels for Information Processing in Primary Visual Cortex

A

1) M-Channel Neurons
2) Parvocellular, Interblob (P-IB) Channel Neurons
3) Blob Channel Neurons

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222
Q

M-Channel Neurons (Visual Processing)

A

Analyze motion.

Circular center-surround receptive fields; monocular; wavelength insensitive

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223
Q

Directionally Selective Cells

A

Allow for analysis of objects in motion

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224
Q

Simple Cells (Visual)

A

Orientation selective; respond to stimuli in specific angle in “on” zone

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225
Q

P-IB Channel Neurons

A

Analyze object shape/form. Contain Complex Cells

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226
Q

Complex Cells (Visual)

A

Highly orientation selective; No “on” and “off” zones; respond to stimulus anywhere in receptive field; small receptive field

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227
Q

Blob Channel Neurons

A

Analyze color

P-type and Non-M Non-P Type RGCs project; wavelength sensitive; circular receptive field (others are elongated); not orientation or direction selective

228
Q

Hyper Column

A

Small cube of visual cortex containing…

1) complete set of orientationcolumns
2) input form both eyes (complete set of ocular dominance columns)
3) All three information processing channels

229
Q

Parallel Activation Theory

A

Visual info processed in parallel areas of visual system. Perception involves binding of activity in areas processing specific aspects of a single visual object

230
Q

Consequence of missing Critical Period in development of visual cortex

A

early childhood

LGN axon terminals fail to properly innervate Cortical Layer 4

231
Q

Retinal Disparity

A

Mechanism for Near-Field Depth Perception (less than 30 m)

At close range, left and right retina images different; binocular neurons provide basis

232
Q

Mechanisms of Far-Field Depth Perception

A

1) Size (of object)
2) Interposition
3) Linear Perspective
4) Light/Shadow
5) Motion Parallax (nearby objects appear to move faster than distant objects)

233
Q

Fovea

A

Portion of retina with only cones; responsible for high visual acuity

234
Q

Macula

A

Yellow, oval-shaped region surrounding fovea

235
Q

Papilledema

A

Swelling of optic disc in response to increased ICP

236
Q

Non-Papilledema Causes of Optic Disc Swelling

A

1) Long-term hypertension swells retinal vessels

2) Optic Neuritis

237
Q

Optic Neuritis

A

Inflammation of the Optic Nerve. Presents with abnormal pupillary light reflex (Relative Afferent Pupillary Defect too). Common sign in Multiple Sclerosis (typically unilateral and transient)

238
Q

Relative Afferent Pupillary Defect

A

One eye sluggish in comparison to unaffected eye during pupillary light reflex

239
Q

Possible cause of Optic Atrophy

A

Chronic disc swelling

240
Q

Arterio-Venous Nicking

A

(Fundus abnormality) Chronic hypertension stiffens and thickens arteries, leading to vein indentation and displacement.

241
Q

Cotton Wool Spots

A

(Fundus abnormality) Microinfarcts result in Retinal Ganglion axonal damage. Axoplasmic material builds up in nerve fiber layer.

242
Q

Hollenhorst Plaque

A

Cholsterol plaque in the retina (common in geriatric patients with carotid artery disease)

243
Q

Monocular vision loss with “Cherry-red” spot at fovea

A

Central Retinal Artery Occlusion

244
Q

Retinal Detachment

A

Merging of posterior neural retina and cell processes from Retinal Pigment Endothelial layer in embryonic development. These layers get separated.

Blindness in affected area. Associated with head trauma, cataract surgery (complication), and Shaken Baby Syndrome

245
Q

Primary Types of Retinal Detachment

A

1) Rhegmatogenous
2) Tractional
3) Exudative

246
Q

Rhegmatogenous Retinal Detatchment

A

(Most common form) Hole/tear in retina allows fluid to accumulate underneath. Risk increases with age (liquification of Vitreous)

247
Q

Tractional Retinal Detachment

A

Scar tissue on the surface of retina may prompt detachment. Typically in patients with poorly-controlled diabetes

248
Q

Exundative Retinal Detachment

A

Fluid accumulation beneath retina without hole or tear.

249
Q

Scotoma

A

Abnormal blind spot caused by focal lesions in retina

250
Q

Hemianopia

A

Loss of 1/2 of visual field along vertical median

251
Q

Quadrantopia

A

Decreased vision/blindness in 1/4 of visual field

252
Q

Commonality in lesion causing Homonymous Hemianopia/Quadrantanopia

A

Both are Retrochiasmal lesions

253
Q

Visual issue present in Congenital Hydrocephalus (3rd ventricle)

A

Binasal Hemianopia

254
Q

Internal Carotid Artery pushing up against optic fibers can cause what deficit

A

Binasal Hemianopia

255
Q

Binasal Hemianopia

A

Lesioning of uncrossed temporal retinal fibers

256
Q

Bitemporal Hemianopia

A

Lesion of the crossed nasal retinal fibers / optic chiasm

257
Q

Four causes of Bitemporal Hemianopia

A

Pituitary Adenoma
Meningioma
Hypothalamic Glioma
BERRY ANEURYSM in ACA

258
Q

Cause: Contralateral Superior Quadrantanopia

A

Lower Division of Geniculocalcarine Tract Disrupted at Meyer’s Loop

Temporal lobe lesion, LGN innervation of Lingual Gyrus is disrupted

259
Q

Cause: Contralateral Inferior Quadratanopia

A

Upper Division of Geniculocalcarine Tract disrupted.

Parietal lobe lesion in upper territory of MCA. LGN innervation of Cuneus Gyrus disrupted.

260
Q

Motor Subsystems

A

1) Pyramidal Motor System
2) Extrapyramidal Motor System
3) Cerebellar Stuff

261
Q

Functions: Extrapyramidal Motor System

A

1) Motor Programming (planing, initiating, maintaining vol. movements)
2) Habitual Behaviors (procedural learning)
3) Small role in cognition and emotion

262
Q

Key Structures of the Extrapyramidal Motor System (name 5)

A

1) Caudate Nucleus
2) Putamen
3) Globus Pallidus
4) Subthalamic Nucleus
5) Substantia Nigra

263
Q

Make up Lentiform Nucleus

A

Putamen and Globus Pallidus

264
Q

Make up Neostriatum (Dorsal Striatum)

A

Caudate and Putamen

265
Q

Make up Corpus Striatum

A

Caudate, Putamen, and Globus Pallidus

266
Q

Division of Substantia Nigra featuring lots of melanin

A

Pars Compacta

267
Q

Subdivisions of the Substantia Nigra

A

1) Pars Compacta (SNc)

2) Pars Reticularis (SNr)

268
Q

Neostriatal Afferent Pathways

A

1) Cortico-Striatal Pathway [Excitatory/Glutamatergic]
2) Nigro-Striatal Pathway [Modulatory/Dopaminergic]
3) Thalamo-Striatal Pathway [Excitatory/Glutamatergic]

269
Q

Neostriatal Efferent Pathways

A

Both Inhibitory and GABAergic!

1) Globus Pallidus -> Thalamus
2) Neostriatum -> SNr

270
Q

Function: Medium Inhibitory Spiny Neurons

A

Inactive in both pathways (Direct/Indirect) when there is no movement

271
Q

Function: GPi-Thalamic Inhibitory Projections

A

Prevent undesired movement and are tonically-active

272
Q

How do you get movement in the Extrapyramidal Motor System?

A

Thalamic disinhibition

273
Q

Direct (“Go”) Pathway

A

Projects from Striatum directly to GPi or SNr, then onto Thalamus

274
Q

D1 / D2 Receptors Role in Direct and Indirect Pathways

A

Direct - dopamine released onto D1 receptors is excitatory

Indirect - dopamine is inhibitory on D2 receptors

275
Q

Characteristic degeneration in Parkinson’s Disease

A

Dopaminergic neurons projecting from the SNc to Neostriatum [Nigrostriatal Pathway]

276
Q

Motor Symptoms of Parkinson’s (5)

A

1) Resting Tremor
2) Cogwheel rigidity
3) Bradykinesia -> Akinesia (progression)
4) Postural Instability
5) Speech and Swallowing difficulties

277
Q

Myoclonus

A

Involuntary muscle jerkes (agonist muscle)

278
Q

Essential Tremor

A

other names: Familial, benign, or senile

(most common) Tremor of upper extremities, head, tongue, lips, vocal cords

279
Q

Resting Tremor

A

Occurs when limbs relaxed, decreases/disappear during movement. Key feature of Parkinsons’. Typically upper extremities

280
Q

Intention/Ataxic Tremor

A

Produced with purposeful movement toward a target. Worsens when nearing target

Associated with Cerebellar Disease

281
Q

Postural Tremor

A

Occurs when limbs actively held in position; disappears at rest

Associated with MS

282
Q

Genetic Defect in Autosomal Dominant Parkinson’s Disease

A

Alpha-Synuclein Protein/Gene

283
Q

Lewy Bodies

A

Alpha-synuclein aggregates form eosinophillic cytoplasmic inclusions in neuronal body

284
Q

Lewy Neurites

A

Fibrils of insoluble alpha-synuclein polymers deposit in neuronal processes, astrocytes, and oligodendrocytes

285
Q

Pathological abnormality in SNc Neurons in Parkinson’s Disease

A

Abnormal iron accumulation

286
Q

Adjunct therapies to L-Dopa in Parkinson’s

A

Monoamine Oxidase (MAO) Inhibitors [Slow L-Dopa Breakdown]

Catechol-o-methyltransferase (COMT) Inhibitors [Slow dopamine breakdown]

287
Q

On-Off Phenomenon (Parkinson’s)

A

High dose of L-dopa leads to dyskinesia followed by freezing behavior when drug availability decreases

288
Q

Class of Drugs which can induce Parkinson’s-Like Symptoms

A

Anti-psychotics (rigidity and hypokinesia)

289
Q

Wilson’s Disease

A

Copper metabolism disease, causing progressive liver and basal ganglia degeneration. Similar but presents earlier in life than Parkinson’s

290
Q

Distinguishing features of Wilson’s Disease from PD

A

1) Kayser-Flesicher Rings in Cornea (asymptomatic)

2) Choreocathetosis (involuntary twitching/writhing)

291
Q

Huntington’s Disease

A

Autosomal dominant progressive neurodegenerative disease. Heavily impacts Striatum.

Atrophy of caudate makes ventricles appear large; progressed disease show atrophy of cortex

292
Q

Primary Target of Huntington’s Disease

A

Enkephalin-containing Neurons of Indirect (motor) Pathway.

Decrease thalamic inhibition, increase excitation -> Hyperkinetic

293
Q

Symptoms of Huntington’s Disease

A

All four basal ganglia functions

Choreiform movement
Athetosis
Dementia
Tics
Dystonic Posturing
Psychiatric disturbances
294
Q

Ballismus

A

Wild flinging movement of extremities. Basal ganglion lesion (Commonly: Subthalamic nucleus lesion). Hyperkinetic effect (reduced inhibition)

295
Q

Hemiballismus

A

(Most Common). Unilateral (contralateral) flinging movements.

Cause: Unilateral lesion of Subthalamic Nucleus

296
Q

Dystonia

A

Abnormaldistored posturing of limbs, trunk, or face due to sustained contraction of muscles

297
Q

Treatment for Focal Dystonia and types its been successful for

A

BOTOX

Torticollis - Cervical Muscles
Blepharospasm - Orbicularis Oculi
Spasmodic Dysphonia - Vocal Muscles

298
Q

Athetosis

A

Writhing, twisting of limbs, face or trunk

299
Q

Chorea

A

Fluid or jerky movements of varying quality

300
Q

Tics

A

Urge to perform sudden brief action; relief following performance. Can be motor and/or vocal

includes Gilles de la Tourette’s Syndrome

301
Q

Fiber Types: Cerebellar Peduncles

A

Superior - Afferent/Efferent
Middle - Only afferent
Inferior: Afferent/Efferent

302
Q

Afferents in Superior Cerebellar Peduncle

A

Ventral Spinocerebellar Tract
Trigeminal Input
Tectocerebellar Input
Coeruleocerebellar Input

303
Q

Efferents in Superior Cerebellar Peduncle

A

1) Regulate Rubrospinal Tract via Red Nucleus

2) Regulate Corticospinal UMNs via VL

304
Q

Afferents in Middle Cerebellar Peduncle

A

Pontocerebellar fibers to Neocerebellum

305
Q

Subdivision of Inferior Cerebellar Peduncle

A

Juxtarestiform Body (contains the efferents of the Inferior Ped)

306
Q

Afferents in Inferior Cerebellar Peduncle

A

Spinocerebellar System (dorsal, cuneo, and rostral types)
Vestibular System
Afferent from Reticular Formation
Trigeminal System

307
Q

Efferents in Inferior Cerebellar Peduncle (all in Juxtarestiform Body)

A

Fastigial Nucleus and Folcculonodular lobe.

All to UMNs of Vestibular/Reticular Systems

308
Q

Major Cellular Layers in Cerebellum (Deep to Superficial)

A

1) Granule Cell Layer (Tightly packed layer of excitatory interneurons)
2) Purkinje Cell Layer (Purkinje Cell Bodies)
3) Molecular Cell Layer (Location of majority of synapses)

309
Q

Contents of Molecular Cell Layer (Cerebellum)

A

Unmyelinated Granule Cells Axons
Purkinje Dendrites
Interneurons

310
Q

Cerebellar Inputs

A

1) Mossy Fibers (Excitatory)

2) Climbing Fibers (Excitatory)

311
Q

Mossy Fibers

A

Excitatory. Ascend through cerebellar white matter to synapse on Granule Cell denrites

312
Q

Granule Cells

A

Send axons to Molecular Layer, bifurcate to form Parallel Fibers

313
Q

Function: Parallel Fibers

A

Form excitatory synapses with Purkinje Cells

314
Q

Climbing Fibers

A

Excitatory. Project exclusively from contralateral Inferior Olivary Nucleus.

Wrap around cell body and proximal dendritic tree of Purkinje Cell. Module Purkinje cell response to input from parallel fibers.

315
Q

Only Cerebellar Output (from the layers)

A

Purkinje Cells

316
Q

Cerebellar Inhibitory Interneurons

A

1) Basket / Stellate Cells

2) Golgi Cells

317
Q

Basket Cells and Stellate Cells

A

Inhibitory interneurons which reside in molecular layer (Cerebellum). Synapse on Purkinje cells. Input from Parallel Fibers.

318
Q

Function: Basket/Stellate Cells (Cerebellum)

A

Promote lateral inhibition of adjacent Purkinje Cells

319
Q

Golgi Cells

A

Reside in Granule Cell Layer (Cerebellum), Dendrites project to Molecular Cell Layer. Receive input from Parallel fibers. Axons relay back in Granule Cell Layer.

320
Q

Function: Golgi Cells

A

Feedback inhibition on Granule Cells

321
Q

Purkinje Cell Ouput: Excitatory/Inhibitory

A

Inhibitory

322
Q

Destination of Purkinje Cell Output

A

Deep Cerebellar Nuclei (exception: Vestibular Nuclei)

323
Q

Deep Cerebellar Nuclei (Lateral to Medial)

A

1) Dentate Nuclei
2) Interposed Nuclei (Emboliform + Globose Nuclei)
3) Fastigial Nuclei

324
Q

Dentate Nuclei

A

Project to:

1) Red Nucleus
2) VL (Thalamus)
3) Inferior Olivary Nucleus

325
Q

Interposed Nuclei

A

Subcomponents: Emboliform + Globose Nuclei

Input: Intermediate part of Cerebellum

Output (via Superior Cerebellar Peduncle):

1) VL (Corticospinal Tract)
2) Red Nucleus (Rubrospinal Tract)

326
Q

Fastigial Nuclei

A 
Input:
1) Vermis
2) Flocculonodular Lobe
Output:
1) VL and Tectum (via Sup. Peduncle)
2) Vestibular System (via Inf. Peduncle)
327
Q

Cerebellar Afferents

A

1) Corticopontine Fibers
2) Spinocerebellar Fibers (many subtracts)
3) Inferior Olivary Complex

328
Q

Corticopontine Fibers

A

Sensory, motor and some visual info from cortex. Brought to ipsilateral Pons via Internal Capsule. Pass through Middle Cerebellar Peduncle into Cerebellum

329
Q

Spinocerebellar Fibers (general)

A

Information about proprioception, touch, pressure and sensation.

Four Subtracts:

1) Dorsal Spinocerebellar Tract
2) Cuneocerebellar Tract
3) Ventral Spinocerebellar Tract
4) Rostral Spinocerebellar Tract

330
Q

Dorsal Spinocerebellar Tract

A

Lower Limb + Trunk. Non-conscious proprioception

Ascends: Ipsilateral through Gracile Fasciulus
Synapses: Clarke’s Nucleus
Enter: Inferior Cerebellar Peduncle

331
Q

Cuneocerebellar Tract

A

Upper Limbs + Trunk. Non-conscious proprioception

Ascends: Cuneate Fasciculus
Synapses: Cuneate Nucleus
Enter: Inferior Cerebellar Peduncle

332
Q

Ventral Spinocerebellar Tract

A

Coordination fo Posture/Lower Limb movement. Double-crosses to stay ipsilateral

Enter; Superior Cerebellar Peduncle

333
Q

Rostral Spinocerebellar Tract

A

Coordination for Posture/Upper limb movement.

Enter: Inferior Cerebellar Peduncle

334
Q

Cerebellar Afferents from Inferior Olivary Nuclear Complex

A

Extrapyramidal nuclei project to Cerebellum via olivary nuclei. Olivecerebellar Fibers arise from Medulla. Decussate before entering Inferior Cerebellar Peduncle.

Conveyed by Climbing Fibers to CONTRALATERAL Cerebellum

335
Q

Cerebellar Afferent (Maybe) Playing Role in Essential Tremor

A

Inferior Olivary Nuclear Complex (Olivocerebellar Fibers)

336
Q

Cerebellar Efferent Functional Areas

A

1) Lateral Cerebellar Hemisphere
2) Intermediate Part / Paramedian Hemisphere
3) Vermal/Median Zone
4) Flocculonodular Lobe

337
Q

Efferent: Lateral Cerebellar Hemisphere

A

Movement planning information to contralateral VL Nucleus (Thalamus)

Efferents project from Dentate Nucleus through Superior Cerebellar Peduncle.

Some efferents also go to Parvocellular Red Nucleus (indirect corticospinal system)

338
Q

Efferent: Intermediate Part / Paramedian Hemisphere (Cerebellum)

A

Coordination of ongoing movements of distal extremities, sent to contralateral VL (Lateral Corticospinal Tract) and Red Nucleus (Rubrospinal Tract)

Efferent project from Interposed Nucleus through Superior Cerebellar Peduncle

339
Q

Efferent: Vermal / Median Zone

A

Proximal trunk movement information. Efferents project from Fastigial Nucleus.

  • To VL and Tectum (via Superior Cerebellar Peduncle)
  • To Vestibular Nuclei (via Juxtarestiform Body)
340
Q

Efferent: Flocculonodular Lobe

A

Vestibulocerebelum influences reflexive equillibrium and balance.

Output to the Median Longitudinal Fascisulus (Ocular Control)

341
Q

Consequence of Damage to Flocculonodular Lobe

A

Nystagmus and Vertigo

342
Q

Most common Cerebellar Infarct

A

PICA Infarct

343
Q

Cerebellar infarct which spares the brainstem

A

Superior Cerebellar Artery (SCA)

344
Q

Cerebellar Symptoms: PICA Infarct

A

Headache, acute vertigo, vomiting, gait/limb ataxia, horizontal nystagmus

345
Q

Cerebellar Symptoms: SCA Infarct

A

Gait/limb ataxia, dysarthria, horizontal nystagmus.

Less common: headache, vomiting, vertigo

346
Q

Truncal Ataxia

A

Wide-based stance and unsteady, irregular “drunk-like” gait

347
Q

Typical Cerebellar Signs (Don’t worry about memorization)

A 
Truncal Ataxia
Hypotonia
Ataxia
Intention Tremor
Dysmetria
Nystagmus
Dysdiadochokinesia
Asynergia/Dyssnergia
Cerebellar Dysarthria
Leaning towards side of lesion
348
Q

Dysdiadochokinesia

A

Inability to perform rapid, alternating movements

349
Q

Asynergia/Dyssnergia

A

Jerky, irregular, arrhythmic movement during planned motor activity

350
Q

Cerebellar Dysarhtria

A

Slowed, slurred, speech, scanning speech (unpredictable stressors/pauses/etc in speech)

351
Q

Cranial Nerve issue seen in Cerebellar Hemorrhage

A

CN VI palsy

352
Q

Motor Issues: Cerebellar Vermis Lesion

A

Effect medial motor system (proximal trunk muscles)

Truncal ATaxia
Ocular Ataxia
Dysarthria
Nystagmus

353
Q

False Localization (reasons) of Ataxia to Cerebellum

A

Lesion of peduncles and pons can also produce ataxia

354
Q

Friedrich’s Ataxia

A

Neruodegenerative disorder targeting dorsal and lateral columns. Autosomal recessive.

Ataxia
Areflexia
Impaired Fine Touch
Vibration issues
Conscious Proprioception effected
Progressive weakness w/ Babinski
355
Q

Symptom Triad: Wernicke’s Encephalopathy

A

1) Cognitive Dysfunction
2) Gait Ataxia
3) Nystagmus

356
Q

Medulloblastoma

A

Malignant, invasive cancer of Posterior Fossa. ~20% of intracranial tumors in young children. Most commonly seen in the Vermis. Tumor may impair CSF flow if grows.

357
Q

Unique Symptom: Medulloblastoma

A

Tinnitus (ringing)

358
Q

Paraneoplasia

A

Autoimmune destruction of Purkinje Neurons. Can be secondary to cancer (don’t quote me on that)

359
Q

Mnemonic: Functions of the Hypothalamus

A

HEAL

Homeostasis (Feeding, Temperature, Sleep/wake cycle)
Endocrine (via Pituitary Gland)
Autonomic (regulation via connections to preganglionic neurons)
Limbic (behavioral, emotion, memory)

360
Q

Location: Pituitary Gland

A

Inferior to Hypothalamus

361
Q

Subdivisions of the Pituitary Gland

A

1) Anterior Lobe (Adenohypophysis)

2) Posterior Lobe (Neurohypophysis)

362
Q

Anterior Lobe of Pituitary Gland (Adenohypophysis)

A

Contains Glandular Cells that secrete hormones into circulation. Regulated by Hypothalamic factors released into Vascular Polar System at Median Eminence.

Formed from ectodermal cells of developing pharynx (Rathke’s Pouch).

363
Q

Posterior Lobe of Pituitary Gland (Neurohypophysis)

A

Contains axon terminal of Hypothalamic neurons which release hormones directly into circulation. Originates from Prosencephalon embryologically.

364
Q

Regions of the Hypothalamus (Anterior to Posterior)

A

1) Preoptic (small area above optic chiasm)
2) Anterior (from preoptic region to end of chiasm)
3) Tuberal (Tuber Cinerum and above)
4) Posterior (area above/posterior to mamillary bodies; including them)

365
Q

Zones of the Hypothalamus (Medial to Lateral)

A

1) Periventricular
2) Medial
3) Lateral

366
Q

Periventricular Zone of Hypothalamus

A

Thin layer just inside ependymal cell layer of 3rd Ventricle

367
Q

Lateral Zone of Hypothalamus

A

Includes Medial Forebrain Bunle and fibers from Monoaminergic Nuclei in brainstem to cerebrum

368
Q

Medial Forebrain Bundle

A

Axonal pathway connection basal forebrain, hypothalamus, and brainstem tegmentum

369
Q

Functional Groups of Hypothalamic Nuclei (7)

A

1) Feeding and Satiety
2) Sleep and Circadian Rhythms
3) Regulating Factors of Anterior Pituitary Gland
4) Hormone Release from Posterior Pituitary
5) Autonomic Control Centers
6) Memory
7) Thermoregulation

370
Q

(Hypothalamic Nuclei) Feeding and Satiety

A 
Lateral Hypothalamic Area (stimulation inc. feeding)
Ventromedial Nucleus (satiety center; stimulation dec feeding)
371
Q

(Hypothalamic Nuclei) Sleep and Circadian Rhythms

A

Ventrolateral Preoptic Area (VLPO)
Tuberomammilary Nucleus
Suprachiasmatic Nucleus

372
Q

Ventrolateral Preoptic Area (VLPO)

A

(Hypothalamic nucleus) Regulates sleep. Derived from Telencephalon unlike the other nuclei which are diencephalon

Relases GABA and Galanin as inhibitory transmitters

373
Q

Tuberomammilary Nucleus

A

(Hypothalamic nucleus) Histamine from its neurons project to cerebral cortex. Promotes wakefulness

374
Q

Suprachiasmatic Nucleus

A

(Hypothalamic nucleus) Receives light input from retina. Master clock for maintaining circadian rhythms

375
Q

(Hypothalamic Nuclei) Regulating Factors Affecting Anterior Pituitary Gland

A

All projects to Median Eminence where factors are released to control hormone release:

Arcuate Nucleus
Paraventricular Nucleus
Periventricular Area
Medial Preoptic Area

376
Q

(Hypothalamic Nuclei) Regulate hormone release from Posterior Pituitary

A

Supraoptic Nucleus - released Vasopressin

Paraventricular Nucleus - releases Oxytocin

377
Q

Vasopressin

A

aka ADH

Stimulates water retention. Released by Supraoptic Nucleus

378
Q

Oxytocin

A

Stimulates milk ejection, uterine contractions, maternal behavior and bonding. Released by Paraventricular Nucleus

379
Q

(Hypothalamic Nuclei) Autonomic Control Centers

A

Descending fibers from these nuclei travel through Medial Forebrain Bundle to PAG and Reticular Formation.

Relay to Preganglionic PArasympathetic nuclei in brainsted/sacral spinal cord and Preganglionic sympathetics in the Intermediolateral column of Thoracolumbar spinal cord.

Paraventricular Nucleus
Lateral Nucleus
Dorsomedial Nucleus
Posterior Nucleus

380
Q

(Hypothalamic Nuclei) Memory

A

Mamillary bodies receive input from Hippocampal Formation (via Fornix). Project to Anterior Thalamus (Mammillothalamic Tract). Ant Thalamus projects to cingulate gyrus, indirectly going back to hippocampus.

Important circuit for memory formation

381
Q

Hypothalamic Nucleus Degenerated in Wernicke-Korsakoff Syndrome

A

Mamillary Bodies

382
Q

(Hypothalamic Nuclei) Thermoregulation

A

Autonomic Functions: Sweating and Altered Blood Flow
Somatic Functions: Shivering and Panting

Anterior Hypothalamus cools, Posterior Hypothalamus heats up

383
Q

Input Types to Hypothalamus

A

Visceral Sensory (via Medial Forebrain Bundle)
Blood Info
Optic Pathway
Prefrontal/Limbic Areas

384
Q

Output Types from Hypothalamus

A

Regulation of Preganglionic Autonomics
Control Behavior
Endocrine Function

385
Q

Corticotropin Releasing Hormone (CRH)

A

Released from Hypothalamus to Anterior Pituitary.

Targets: Preoptic, Supraoptic, Paraventricular Nuclei

386
Q

Corticotropin (ACTH)

A

aka Adrenocorticotropic Hormone (ACTH)

Released by Anterior Pituitary into general circulation. Stimulates release of corticosteroids from Adrenal Cortex

387
Q

Cortisol Negative Feedback Effect

A

Inhibits Hypothalamus and Anterior Pituitary

388
Q

Pituitary Adenoma

A

Benign, slow-growing tumor of pituitary gland. 85% cause improper secretion.

Large adenoma may compress optic chiasm -> Bitemporal Hemianopia

389
Q

Panhypopituitarism

A

Deficiency of all pituitary hormones. Occurs due to tumor, infarction, autoimmune disorders, or chemotherapy.

Requires hormone replacement therapy

390
Q

Mnemonic: Functions of Limbic System

A

HOME

Homeostasis
Olfaction
Memory
Emotion

391
Q

Cortical Structures of Limibic System

A 
Parahippocampal Gyrus (incl. Entorhinal Cortex)
Cingulate Gyrus
Insular Cortex
Orbitofrontal Cortex
Prefrontal Association Cortex
Hippocampus
392
Q

Subcortical/Diencephalic Nuclei of Limbic System

A

Amygdala
Ventral Striatal Structures
Thalamic Nuclei (Anterior and Mediodorsal Nucleus)
Hypothalamic Nuclei (Anterior, POsterior and Mamillary Nuclei)

393
Q

Midbrain Structures of Limbic System

A

Ventral Tegmental Area (below substantia nigra)

394
Q

Entorhinal Cortex

A

Area 28. Part of Parahippocampal Gyrus. Major relay for I/O between Association Cortex and Hippocampal Formation. Part of Papez Circuit

395
Q

First cortical area to degenerate in Alzheimer’s Disease

A

Entorhinal Cortex

396
Q

Hippocampal Formation

A

Part of Parahippocampal Gyrus. Medial Temporal Lobe. Stores and processes spatial info. Formation of episodic memory.

Consists of: Subiculum, Hippocampus, and Dentate Gyrus

397
Q

Dentate Gyrus

A

Role in memory disorders and possibly depression. Part of Hippocampal Formation. Undergoes neurogenesis throughout life.

398
Q

Intrinsic Hippocampal Circuit

A

Association Cortex -> entorhinal Cortex -> Hippocampus -> 3 major targets

1) Medial and Lateral Nuclei
2) Lateral Septal Nucleus
3) Anterior Thalamic Nucleus

399
Q

Alvear and Perforant Pathways

A

Part of Intrinsic Hippocampal Circuit. Carry fibers from Entorhinal Cortex to Hippocampus

400
Q

Fornix

A

Carries axons out of Hippocampus in Intrinsic Hippocampal Circuit. Curves around ventricular system to Diencephalon and Septal Nuclei

401
Q

Septal Nuclei

A

Function: Endogenous Reward Circuits
Input: Hippocampus, Amygdala, Hypothalamus, and Ventral Tegmental Area

Located in medial wall of anterior horn of Lateral Ventricles.

402
Q

Location: Amygdala

A

Anterior Temporal Lobe

403
Q

Function: Amygdala

A

Interpret and Recall emotional content and olfactory memories, visual inputs, and response. Influences “fight or flight”, mood, and emotion.

404
Q

Stria Terminalis

A

Major output from Amygdala. Connects it to Hypothalamus and Basal Forebrain

405
Q

Amygdala Nuclei

A

1) Corticomedial Nucleus
2) Basolateral Nucleus
3) Central Nucleus

406
Q

Amygdala Inputs

A

Highly-processed sensory info (temporal lobe, olfactory, and limbic areas)

Autonomic Input (Orbitorfrontal cortex, cingulate gyrus, hypothalamus, midbrain tegmentum)

407
Q

Amygdala Outputs

A

Association Cortex and Autonomic Centers (via Stria Terminalis)

408
Q

Symptoms: Amygdala Lesion

A

Docility
Aggression
Outbursts/Rage
Hyperphagia***

409
Q

Limbic-Brainstem Nuclei Connections

A

Reciprocal. Associate limbic function with autonomic and behavior arousal processes

410
Q

Function: Basal Ganglia / Limbic Channel

A

Circuit involved in emotional and motivational drive. Dysfunction leads to neurobehavioral and psychiatric disorders.

411
Q

Medial Diencephalic Structures (Limbic)

A

Important for memory

Thalamus: Anterior Nuclei and Mediodorsal Nucleus
Hypothalamus: Mammillary Bodies

412
Q

Medial Temporal Lobe Structures (Limbic)

A

Important for memory. Consists of Entorhinal Cortex and Hippocampal Formation. Reciprocal connections with Multimodal Association Cortex.

413
Q

Bilateral lesion to either Medial Diencephalic Structures OR Medial Temporal Lobe Structures

A

Loss of declarative or explicit memory

414
Q

Unilateral Lesion to MDS or MTLS (Dominant)

A

Verbal Memory Deficit

415
Q

Unilateral Lesion to MDS or MTLS (Non-Dominant)

A

Visual-Spatial Memory Deficit

416
Q

Kluver-Bucy Syndrome

A

Discovered by removal of Amygdala, Hippocampus, and Anterior Temporal Cortex (bilateral). Similar symptoms from Temporal Resections done for EPILEPSY and Viral Encephalitis

417
Q

Amygdala Hyperactivation Related Disorders

A

Anxiety
Panic Attack
PTSD
Obsessive-Compulsive Disorder (OCD)

418
Q

Infarct in Superior Portion of Basilar Artery

A

Significant memory loss.

PCA, which supplies important limbic regions, branches here. Makes it a bilateral infarct.

419
Q

Possible Result of Contusions in Limbic Areas

A

Contusions more likely than concussion to cause permanent damage. Can lead to seizures

420
Q

Hippocampal Sclerosis

A

Severe Medial Temporal Lobe lesion causes by seizures. Astrocytic scar formation. Memory loss can persist during seizure-free periods

421
Q

Transient Global Amnesia

A

Sudden and temporary onset of Retrograde and Anterograde Amnesia. Coincides with extreme physical exertion or emotional stress

422
Q

Degenerates in Progression to Wenicke-Korsakoff Syndrome

A

MDS Nuclei and Hippocampus. Brings on Amnesia. Confabulation

423
Q

Confabulation

A

Patient provides random answers to questions without attempting to deceive

424
Q

Categorical Types of Memory

A

1) Procedural Memory

2) Declarative Memory

425
Q

Procedural Memory

A

Not directly available to conscious awareness. Skills, habits, experience dependent reflex modications.

426
Q

Declarative Memory

A

Conscious awareness. Autobiographical memories and knowledge.

427
Q

Type of memory impaired with Amnesia

A

Declarative Memory

428
Q

Retrograde Amnesia

A

Loss of formed memories. Damage to storage areas

429
Q

Anterograde Amnesia

A

Inability to form new memories. Damage to areas required for consolidation

430
Q

Immediate Memory

A

Sum of all sensory input being procesed at cortical level. Function of relevant High-level sensory / Association Area of Cortex

431
Q

Short-Term Memory

A

Conscious attention allows entrance and required to retain. May involve same cortical areas for immediate memory OR be transferred to Prefrontal Cortex

432
Q

Central Executive Function (memory)

A

Regulates entry of info into Short-Term Memory

433
Q

Long-Term Memory

A

Large, resistant to forgetting. Long-term memory stable but memories in process of consolidation vulnerable

434
Q

Consolidation

A

Thought to occur via strengthening of synapses in Cortical Areas. Makes use of Papez Circuit.

435
Q

Bilateral Damage to Papez Circuit

A

Causes Global Anterograde Amnesia

Least Severe: Just Hippocampus
Mild: Medial Temporal Lobe structure
Severe: Medial Diencephalic Structures

436
Q

Type of Synapses Seeing LTP

A

Glutamate Synapses

437
Q

Location of Glutamate Synapses in Brain

A

Spines of Pyramidal Neurons

438
Q

Targets for Calcium Second Messenger in LTP

A

1) Protein Kinase C
2) Calcium Calmodulin Dependent Protein Kinase II (CaMK II)
3) Nitric Oxide Synthase

439
Q

Mechanisms Enhancing Post-Synaptic Sensitivity in LTP

A

1) Phosphorylation of AMPA/KA Receptors
2) Exocytosis of more AMPA/KA Receptors
3) Increase calcium for vesicle release

440
Q

Retrograde Messaging in LTP

A

Nitric Oxide, release mediated by Calcium in post-synaptic neuron. Enhances Pre-Synaptic Function

441
Q

Reticular System integrates info from all senses except…

442
Q

Neurotransmitters most used in Reticular System

A

Neurons Serotonergic or Noradrenergic

443
Q

Function: Reticular System

A

Most Important: Consciousness and Arousal

444
Q

Principle Columns of Reticular System

A

1) Lateral Column
2) Medial Column
3) Median Column

445
Q

Lateral Column of Reticular System

A

Contains Parvicellular Neurons that receive afferent fibers from neighboring brainstem regions

446
Q

Medial Column of Reticular System

A

Magnocellular and Gigantocellular neurons that give rise to efferents

447
Q

Median Column of Reticular System

A

5HT Neurons of the Raphe Nuclei. Involved in modulatory activity throughout Brain + Spinal Cord

448
Q

Reticular Levels working together on Alertness/Consciousness

A

Diencephalon, Mesencephalon (Rostral Reticular Formation), and Rostral Pons

449
Q

Reticular Levels Working together on Motor, Reflex, Autonomic Function. Also function with CN Nuclei

A

Caudal Pons (Caudal reticular formation) and Medulla

450
Q

Reticular Nuclei: Telencephalon

A

Nucleus Basalis of Meynert

451
Q

Reticular Nuclei: Diencephalon

A

Reticular Nucleus of the Thalamus

452
Q

Reticular Nuclei: Midbrain

A

Periaqueductal Gray
Dorsal Raphe Nucleus
Ventral Tegmental Area
Substantia Nigra, Pars Compacta (SNc)

453
Q

Reticular Nuclei: Pons

A

Nucleus Locus Coerulus

Pedunculo-Pontin Nucleus / Laterodorsal Tegmental Nucleus

454
Q

Reticular Nuclei: Medulla

A

Nucleus Raphe Magnus
Rostral Ventral Medullar
Nuclei of Medullary Reticular Formation

455
Q

Nucleus Basalis of Meynert

A

(Reticular System) Selective Attention, alertness and memory processes. Heavily impacted by Alzheimer’s.

Input: Ventral Tegmental Area (DA), Raphe Nuclei (5HT), Nucleus Locus Coeruleus (NE)

Output: Project widely to Cortex (bypass Thalamus) and Amygdala (ACh)

456
Q

Reticular Nucleus of the Thalamus

A

(Reticular System) Gates activity of Thalamocortical Relays and ARAS. Only Thalamic nucleus with no projections outside of Thalamus.

457
Q

Dorsal Raphe Nucleus

A

(Reticular System) Assists in regulation of consciousness, attention and mood. Widespread forebrain projections with no thalamic relay.

Primary site of 5HT Neurons in Reticular Formation

458
Q

Ventral Tegmental Area

A

(Reticular System) Memory, attention, motivation.

Part of Mesolimibic DA Reward Pathway (prject to Nucleus Accumbens)

Part of Mesocortical DA Reward Pathway (Project to Cortex)

459
Q

Physiology of Reward Seeking

A

Dopamine released before the reward is actually received

460
Q

Nucleus Locus Coerulus (Blue Nucleus)

A

(Reticular System) Ascending/Descending projections to limbic structures, dorsal horn, and cortex.

NE Neurons Modulate: ARAS, arousal, selective attention, stress responses, pain modulation, and mood

461
Q

Pedunculo-Pontine Nucleus / Laterodorsal Tegmental Nucleus

A

(Reticular System) Largest sites of ACh production in brain. Involved in wakefulness, REM Sleep, and ARAS. Widespread cortical projections via Thalamus

462
Q

Reticular Nuclei which must be inhibited for sleep to occur

A

Pedunculo-Pontine Nucleus and Laterodorsal Tegmental Nucleus

463
Q

Nucleus Raphe Magnus

A

(Reticular System) 5HT neurons involved in pain modulation. Receives projection from PAG and projects down to Dorsal Horn

464
Q

Rostral Ventral Medulla

A

(Reticular System) Glutamatergic neurons with descending projections to Spinal Cord. Modulate ascending transmission of pain (similar to PAG)

465
Q

Cardiovascular and respiratory regulation centers

A

Medullary Reticular Formation

466
Q

Ascending Reticular Activating System (ARAS)

A

Responsible for consciousness, wakefulness, arousal, and attention. Filters out noise information.

PRIMES cortex to receive sensory input.
SHUNTS information that is life-threatening/frightening to Amygdala

467
Q

Location for many ARAS Nuclei

A

Ponto-Mesencephalic-Diencephalic Regions of Reticular Formation

468
Q

Main ARAS Pathways

A

1) Aminergic Nuclei – activated during woke state

2) Cholinergic Nuclei – wake state and REM sleep

469
Q

Aminergic Nuclei of ARAS

A

Project Directly to Cortex

1) Nucleus Locus Coerulues (NE)
2) Raphe Nuclei (5HT)
3) Tuberomammillary Nucleus (Histamine)

470
Q

Cholinergic Nuclei of ARAS

A

Project to Cortex via Thalamus

1) Pedunculo-Pontine Nucleus (ACh)
2) Laterodorsal Tegmental Nuclei (ACh)

471
Q

Minimally Conscious State

A

Periods of responsiveness/wakefulness with minimal and variable awareness

Visual tracking, sleep/wake cycle, highly-variable EEG

472
Q

Locked-In Syndrome

A

Lesion preventing corticospinal and corticobulbar motor output. Sensory function and consciousness are spared

473
Q

Catatonia

A

Abnormality of movement from behavioral / mental problems

474
Q

Pathology/Lesion: Akinetic Mutism / Abulia / Catatonia

A

Impaired Frontal Lobe and Dopaminergic function. Apathy and deficits in response initation

475
Q

Vegetative State

A

Periods of wakefulness but no awareness. Persistent vegatative state is more than a month with no evidence of change

No visual tracking
Sleep/wake cycle present but variable
No volutional behavior but may arouse to pain

476
Q

Coma

A

Prolonged loss of consciousness with severe impairment of Cortical and Diencephalic-Upper Brainstem Activating System Function.

Unresponsive to sensory input but primitive reflex may be present

477
Q

Brain Death

A

Irreversible unconsciousness with complete loss of brain function and ability to breath

478
Q

Causes of Coma (3)

A

1) Bilateral Lesion in upper brainstem affecting ARAS
2) Bilateral Compromise/Destruction Brain Hemisphere
3) Large bilateral Thalamus lesion

479
Q

Major Dopamine Pathways in Brain

A

1) Nigrostriatal Pathway (Extrapyramidal System)
2) Meso-Limbic Projections
3) Meso-Cortical Projections
4) Tubero-Infundibular Projection

480
Q

Meso-Limbic Projections

A

Major dopaminergic reward pathway.

Ventral Tegmental Area -> Nucleus Accumbens

481
Q

Meso-Cortical Projections

A

Dopaminergic pathway for working memory and attentional aspects of motor initiation.

Ventral Tegmental Area -> Cortex (mainly Prefrontal)

482
Q

Tubero-Infundibular Projection

A

Dopaminergic Pathway inhibiting synthesis and release of Prolactin.

Arcuate Nucleus -> Anterior Pituitary

483
Q

“Typical” Anti-Psychotic

A

Alleviate positive symptoms of Schizophrenia. Exacerbate negative symptoms.

Possible irreversible side effect: Tardive Dyskinesia (involuntary, repetitive movements)

484
Q

“Atypical” Anti-Psychotic

A

Cause fewewr Extrapyramidal side-effects than “Typical” type.

Complications: Weight gain, Type 2 Diabetes, Prolactinema (hormone secreting tumor)

485
Q

Important Brain Serotonin Pathways

A

1) Dorsal Raphe Nucleus - modulates mood

2) Nucleus Raphe Magnus - modulates CNS Pain transmission

486
Q

Purposes of Sleep (probable)

A 
Energy conservation/replenishment
Consolidation
Tissue Restoration
Clear Brain Metabolites
Renormalization of Synaptic Strength/Number
487
Q

Controlled by Circadian Rhythms

A 
Sleep-Wake Cycle
Hormone Secretion
Blood Pressure
Body Temperature
Urine Production
488
Q

Nucleus regulating activity of Pineal Gland

A

Suprachiasmatic Nucleus

489
Q

Function: Pineal Gland

A

Secrete melatonin

490
Q

Sleep Load

A

“Drive” to sleep

491
Q

Brain Waves during Awake State

A

Beta Waves (high frequency, low amplitude)

492
Q

Sleep Stage 1

A

Drowsy period.

Theta Waves (slightly lowered frequency, high amplitude)

493
Q

Sleep Stage 2

A

Lower frequency, higher amp waves than Stage 1. Presence of Sleep Spindles and K-Complex

494
Q

Sleep Spindles

A

Periodic bursts of activity (1-2 seconds) seen in Sleep Stage 2. Promotes consolidation of motor memory in young adults

495
Q

K-Complex

A

EEG pattern during Stage 2 sleep every two minutes

496
Q

Sleep Stage 3

A

Deepest level of Sleep. Slow Wave Sleep (SWS).

Delta Waves (low frequency, high amplitude)

497
Q

EEG and Physiology: REM Sleep

A

EEG similar to wake state. Increase in BP, HR, and metabolism

498
Q

Characteristic of REM SLeep

A 
Dreaming
Visual Hallucinations
Increased Emotion
Lack of self-reflection
lack of volitional control
paralysis of large muscles
penile erection
499
Q

REM Rebonund

A

REM deprivation makes you go straight to REM sleep at next opportunity

500
Q

Activation of Thalamus (sleep)

A

Causes (test animal) to fall asleep when activated

501
Q

Blocks sensory input during sleep

502
Q

Secreted by Hypothalamus to Promote Waking

A

Orexin and Hypocretin

503
Q

Central Apnea

A

Efferent signal to diaphragm insufficient for inspiration. Most common in early NREM sleep.

Ondine’s Curse - severe form, breathing stops in sleep

504
Q

Narcolepsy

A

Excessive daytime sleepiness. Inhibition of generation of REM sleep dysfunctional. Patients lose Orexin/Hypocretin-synthesizing neurons.

Lose muscle control during episodes (cataplexy)

505
Q

REM Sleep Behavior Disorder (RBD)

A

Kick, punch, and act out aggressive dream scenarios. Mainly men over 50. Associated with inc. incidence of Parkinson’s Disease

Brainstem disorder preventing muscle paralysis

506
Q

Sleep/Aging

A

Sleep lighter and shorter. Need same amount

Less SWS and fewer Sleep Spindles, Pineal gland produces less melatonin. Fewer VLPO neurons.

507
Q

Yerkes-Dodson Law

A

We function best at moderate level of arousal (stress)

508
Q

Active Pathways During Stress

A

1) HPA Axis

2) Adrenal-Medullary System

509
Q

Physiological Effect of Cortisol

A

Increase energy mobilization.

Regulates immune system

510
Q

Adrenal Medullary System

A

Hypothalamus -> Sympathetics -> Adrenal Medulla -> Release of Norepinephrine

511
Q

Effects of Norepinephrine

A

Increased HR, Respiration, BP

512
Q

General Adaption Syndrome (Stress)

A

Stage 1 - react to stress
Stage 2 - adaption to stress; sustained cortisol release
Stage 3 - Depletion

513
Q

Dementia

A

Progressive memory impairment with at least one of these…

1) Aphasia
2) Agnosia
3) Apraxia
4) Executive Function Disturbance

514
Q

Alzheimer’s-Type Dementia

A

Progressive, irreversible, and uncurable. Plaques, tangle in brain. Early/Late Onset Breakpoint 65 yo. Typically die from infection or aspiration; caused by pneumonia, brain hemorrhage, or compromised BBB

515
Q

Alzheimer’s Global Atrophy

A

Most pronounced in…

Hippocampus, Temporal Lobe, and Frontal Lobe.

Narrowing of gyri, widening of sulci, and enlarged lateral/3rd ventricles

516
Q

Most pronounced type of neurodegeneration in Alzheimer’s Disease

A

Cholinergic Neurons

517
Q

First area to show pronounced loss in Alzheimer’s

A

Entorhinal Cortex (Area 28)

518
Q

Cholinergic-Neuron heavy nucleus degenerating in Alzheimer’s and heavily-impacted in all dementias

A

Nucleus Basails of Meynert

Impaired:
Selective Attention
Cortical Activation
Memory Processes

519
Q

Hallmark Symptoms of Alzheimer’s Disease

A

5 A’s

Anomia
Aphasia
Apraxia
Agnosia
Amnesia
520
Q

Anomia

A

Deficit in expressive language. Fluent, correct speech. Work hard to avoid forgotten word.

521
Q

Idomotor Limb Apraxia

A

Most common form of Apraxia in Alzheimer’s Disease

522
Q

Alzheimer’s Amnesia

A

Specific loss of…

Episodic Memory
Semantic Memory (what words mean)
Procedural Memory

523
Q

“Sun Downing” or “Late-Day Confusion”

A

Severe late afternoon/evening mood disturbances observed in AD

524
Q

Later stage Alzheimer’s introduces some more severe symptoms…

A

Inability to respond to environment, control movement, communicate.
Paranoia
Cachexia/Dehydration (forget how to chew/swallow)

Death is typically due to pneumonia or cerebral hemorrhage

525
Q

Pathophysiology List for Alzheimer’s

A 
Tau Hyperphosphorylation
Amyloid Beta accumulation
Granulovacuolar Degeneration
Cholinergic Degeneration
Glutamatergic Dysfunction
Decrease in Dendritic Shafts, Spines, and Synapse #
Gliosis
526
Q

Tau Hyperphosphorylation

A

Happens within neocortex. Generates Neurofibrillary Tangles (NFTs)

527
Q

Neurofibrillary Tangle Impact (structures) by Stage of AD

A

Early: Medial Temporal Lobe
Mid: Association Cortex
Late: Primary Cortical Areas

528
Q

Senile Plaques

A

Plaques formed by Amyloid beta accumulation in Alzheimer’s

529
Q

Granulovacuolar Degeneration (GVD)

A

Fluid-filled space and granular debris that accumulates in neurons in AD

530
Q

Glutamatergic Dysfunction in AD

A

Amyloid B is toxic to these neurons. Glutamate availability and NMDA receptors are affected

531
Q

Gliosis in AD

A

Sporadic astrogliosis and localized microgliosis around the Senile Plaques.

532
Q

Precursor to Amyloid B

A

Amyloid Precursor Protein (APP). Cleaved by Secretases

B and Y Secretases start to cleave in Alzheimer’s, producing Amyloid B. Perhaps BBB / perfusion issue??

533
Q

Post-Operative Cognitive Dysfunction

A

Presents similar to Alzheimer’s but suddent onset and transient

534
Q

Early Stage Treatment of AD

A

Acetylcholinesterase Inhibitors (first line). Mostly just slow decline

535
Q

Acetylcholinesterases used in Early Stage AD Treatment

A

Donepezil (Aricept)
Galantamine (Razadyne)
Rivastigmine (Exelon)

536
Q

Moderate-Severe AD Treatment

A

Continue first-line. Add Memantine (Namenda) – noncompetitive NMDA Antagonist.

Reduces neurotoxicity in Glutamergic dysregulation to minimize neuron death. Minor improvements and slows accumulation of Tau Tangles.

537
Q

Dependence

A

Need for continued drug use to avoid withdrawal

538
Q

Addiction

A

Uncontrollable cravings, inability to control use, compulsive use, and use despite harm to self/others

539
Q

Drug Use: Pathway driving Wanting/Drive to Reward

A

Ventral Tegmental Area (Wanting/Drive) -> Nucleus Accumbens (Reward)

540
Q

Lasting change in chronic drug use in brain

A

Synapses strengthened and decreased sensitivity to Dopamine

541
Q

Hijacked Brain Centers in Drug Use

A

Prefrontal / Orbitorfrontal Cortex
Basal Ganglia (Striatum)
Anterior Cingulate Cortex
Amygdala

542
Q

Role of Drug Activation of Amygdala

A

Adds emotional context to memories

543
Q

Epidemiology

A

Study of distribution/determinants of health-related states/events in specified populations, and the application of this study to control health problems

544
Q

Major Components Studied in Epidemilogy

A

1) Frequency of Disease
2) Distribution
3) Determinants

545
Q

Classical Epidemiology

A

Studies at risk population to prevent disease in total population

546
Q

Incidence

A

New occurrences of disease, injury, or death during time period

547
Q

Prevalence

A

Number of patients who have disease – old and newly-diagnosed – at a given time

548
Q

Point Prevalence

A

Prevalence at a certain point in time

549
Q

Period Prevalnce

A

How many people had disease at any time during the period

550
Q

Screening

A

Search for unrecognized diseases or health condition by means of rapidly applied tests, procedures, or examinations in apparently healthy individuals.

551
Q

Lead Time

A

Treatment time advantage gained by screening (period between earliest possible diagnosis and diagnosis point by traditional means)

552
Q

Types of Screening

A

1) Mass Screening
2) High-Risk Screening
3) Multi-Phasic Screening

553
Q

Validity

A

Ability of test to distinguish who has disease, and who does not

554
Q

Sensitivity

A

Ability of test to identify correctly WHO HAVE the disease

555
Q

Specificity

A

Ability of test to identify correctly who DO NOT HAVE the disease

556
Q

Mass screening test: better sensitive or specific

A

Sensitive (no need to follow negatives)

557
Q

Tests in Treatment Decisions: better sensitive or specifc

A

Specific. Don’t want to treat false positive

558
Q

Qualitative Studies

A

Ethnographic observations, open-ended semi-structured interviews, focus groups, and key informant interviews. Review results and identify paterns

559
Q

Cross-Sectional Study

A

Survey of population at single point in time. Quick.

560
Q

Disadvantages to Cross-Sectional Studies

A

1) HArd to draw cause-effect about risk factors

2) Neyman Bias

561
Q

Neyman Bias

A

Chronic and milder cases of disease more likely to survive than more aggressive types. Issue with Cross-Sectional Studies

562
Q

Cross-Sectional Ecological Studies

A

Relate frequency of characteristic and some outcome occuring in same geographic area

563
Q

Types of Bias in Case-Control Studies (4)

A

1) Confounding Bias
2) Memory Bias (cases tend to remember exposure to risk factor better)
3) Selection Bias
4) Interviewer Bias

564
Q

Selection Biases in Case-Control Studies

A

1) Sampling Bias
2) Incident-Prevalent Bias
3) Berkesonian Bias

565
Q

Berkesonian Bias

A

Increases rates of hospitalization due to exposure AND outcome

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