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Brain and Behavior > Week 1 Lectures > Flashcards

Week 1 Lectures Flashcards

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1
Q

Why is gastrulation the most important stage in development?

A

All of the tissues in the body can be traced back to tissues formed at gastrulation

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2
Q

What are the terminal tissues formed by the ectoderm?

A

Skin and nervous system

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3
Q

Where do signals for differentiation of ectoderm into neural ectoderm come from?

A

Mesoderm - block BMP signaling and allow overlying cells to assume their natural identity

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4
Q

Wnt gradient

A

More wnt at the back end vs. front end –> anterior/posterior character

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5
Q

Neural plate

A

Initial thickening of ectoderm that grows cranial to caudal –> becomes concave after neural folds rotate into formation –>fuses at dorsal midline to form neural canal –> separates from surface ectoderm

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6
Q

Neural crest origination

A

forms from most lateral neuroectoderm –> squeezed out from both neural tube and overlying surface ectoderm

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7
Q

Neural tube closure defect - Spina Bifida

A

defect in vertebral arch formation or neural tube closure resulting in exposure and possible extrusion of spinal cord and meninges

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8
Q

Neural tube closure defect - Meroanencephaly

A

defect in tube closure resulting in the partial absence of the brain (most common nt defect)

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9
Q

Neural tube closure defect - Anencephaly

A

results in total absence of brain

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10
Q

Neural tube closure defect - Exencephaly

A

results in exposure and possible extrusion of the brain

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11
Q

Which supplement during pregnancy reduces closure defects by more than 50%?

A

Folic acid

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12
Q

The rostral end of the neural tube becomes what division of the brain?

A

Forebrain

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13
Q

The caudal end of the neural tube becomes what division of the brain?

A

Hindbrain

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14
Q

In which division of the brain do each of the ventricles form?

A

Forebrain-lateral, Midbrain-third, Hindbrain-fourth

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15
Q

What are the vesicles of the forebrain?

A

Telencephalon and Diencephalon

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16
Q

What is the vesicular name of the midbrain?

A

Mesencephalon

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17
Q

What are the two vesicles of the hindbrain?

A

Metencephalon and Myelencephalon

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18
Q

How many rhombomeres are there?

A

9 - subdivisions of the hindbrain

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19
Q

From what vesicle are the following structures formed? Olfactory lobes, Hippocampus, Cerebrum

A

Telencephalon

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20
Q

From what vesicle are the following structures formed? Retina, Epithalamus, Thalamus, Hypothalamus

A

Diencephalon

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21
Q

From what vesicle are the following structures formed? Cerebellum, Pons

A

Metencephalon

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22
Q

From what vesicle are the following structures formed? Medulla

A

Myelencephalon

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23
Q

The more wnt you have the more ______ the structure.

A

Caudal

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24
Q

What main gene is turned on in areas of low wnt?

A

otx2 transcription factor –> telencephalon to midbrain/hindbrain boundary –> anterior structures

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25
Q

What are the “crucial elements in executing the information from signals to the specificity of cells”?

A

transcription factors

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26
Q

What signal and corresponding gene control anterior/posterior patterning within the forebrain?

A

FGF signals from anterior telencephalon –> upregulate tf Pax6, downregulate tf Emx2 –> ratio of each gradient helps to determine identity of neurons in different regions of telencephalon along anterior/posterior axis

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27
Q

Hox genes

A

Homeotic transcription factors: DNA binding proteins that are expressed in the order in which they are expressed physiologically –> relating to segmental identity along anterior/posterior axis.

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28
Q

Three examples of anterior/posterior positioning.

A
  1. otx2 2. pax6-emx2 3. hox genes/rhombomere identity in hindbrain
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29
Q

A combinatorial code of ___________ defines rhombomere segmental identity even before the cranial nerves that will emerge are apparent.

A

transcription factors

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30
Q

What embryological structure induces the floor plate of the neural tube to relay dorsal/ventral patterning signals?

A

Notochord

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31
Q

What signal is released by the notochord and by the neural tube floor plate to induce ventral patterning?

A

Sonic Hedgehog (Shh)

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32
Q

What signal is released by the neural tube roof plate to induce dorsal patterning?

A

BMP4

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33
Q

What signal is released by the ectoderm to induce the neural tube roof plate to relay signals for dorsal patterning?

A

BMP4, 7

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34
Q

What extreme defect can loss of shh signaling components result in?

A

Holoproencephaly - defect in birfurction of the forebrain into two lobes resulting in a single holosphere

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35
Q

What pairs of genes are induced by the Shh gradient in dorsal/ventral patterning that also regulate each other in differentiation?

A

Dbx2-Nkx6.1 Pax6-Nkx2.2 Nkx = ventral

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36
Q

Intrinsic lineage

A

As cells arise they inherit their fate from parent cells.

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37
Q

Extrinsic determinants

A

As cells arise, they assume fates based on extrinsic determinants.

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38
Q

What mechanisms do cells derived from other cells employ to take on diverse roles?

A

Intrinsic lineage Extrinsic determinants

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39
Q

Where do the progenitor cells for the PNS come from?

A

Neural crest

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40
Q

What are the two main migration groups for neural crest cells?

A

Along surface ectoderm = non-neuronal melanocytes Ventrally = sensory ganglia, autonomic ganglia, and adrenal neuro-secretory cells

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41
Q

What identity do transplanted neural crest cells take on?

A

They take on the identity of the tissue where they ultimately reside

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42
Q

Neural crest cell fate is controlled by _______.

A

external cues

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43
Q

In the developing CNS, single progenitor cells make one/many different type(s) of neurons.

A

many

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44
Q

Inside-out maturation of the cortex (and type of cell involved)

A

Excitatory luminergic pyramidal-type cells: new neurons migrate past older layers of neurons to assume more superficial positions

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45
Q

Where are inhibitory cells generated?

A

(GABA neurons) - nascent striatum/lateral and medial ganglionic eminences –> migrate to the cortex/cortical sheet

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46
Q

Failure of GABAnergic neuron specification or migration can lead to lack of inhibitory interneurons in the cortex and the associated condition called ____________.

A

Epilepsy

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47
Q

What kinds of proteins are necessary for neuronal migration?

A

Tubulins and tubulin associated proteins

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48
Q

What condition is caused by Lis1?

A

Lissencephaly –> absence of folds and fissures on the surface of the brain

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49
Q

What defect can result in doublecorticin –> thicker cortex and improper migration?

A

Dcx microtubule defect

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50
Q

Which cells have axons that extend from the ventral surface to the pial surface?

A

Radial glia

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51
Q

The _________ is the motile structure at the tip of the neuron.

A

Growth cone

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52
Q

Conserved families of secreted and transmembrane molecules that influence axon trajectories are called _________.

A

Guidance cues

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53
Q

Two main types of signaling molecules/guidance cues

A

Chemotropic - can diffuse at a distance Contact - attached to the cell membrane or ECM Further divided into attractants and repellents

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54
Q

Axon guidance cue: Netrins

A

Chemoattractant secreted at ventral midline of spinal cord and stimulates axons to cross over

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55
Q

Axon guidance cue: Semaphorins

A

Chemorepellent - drive axons away from inappropriate target

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56
Q

Loss of the midline guidance cue receptor ______ perturbs crossing of interneuron axons in the fish brainstem.

A

Robo-3 - guidance receptor that determines whether an axon crosses at the midline

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57
Q

Disruption of robo-3 gene in humans induces what condition?

A

Horizontal gaze palsy - flattened medulla, enlarged 4th ventricle –> can’t look left and right b/c can’t coordinate the two eyes across the midline of the optic chiasm

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58
Q

EphrinAs are expressed at high levels in ______ and are ________ cues.

A

posterior tectum; repellent *only nasal retinal axons can reach posterior locations by expressing low levels of EphA receptor

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59
Q

EphB’s are expressed at high levels in ______ and are _________ cues.

A

ventral tectum; attractant *retinal axons with high levels of ephrinBs are drawn more strongly into the ventral tectum

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60
Q

Changing the size or activity of the muscle target controls the survival of motor neurons: about half of the motor neurons that are formed normally __________.

A

die by apoptosis - a superabundance of neurons are produced and half die off

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61
Q

Which family of proteins promote the survival of neurons from a development pool?

A

Neurotrophins

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62
Q

Neurotrophins interact with what kind of receptor?

A

Trk receptors

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63
Q

Sympathetic proprioceptive cells prefer which neurotrophin?

A

NT-3

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64
Q

Sensory neurons that go to the skin prefer which neurotrophin?

A

NGF

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65
Q

Post-synaptic cells secrete _________ that are required for neuronal survival.

A

trophic factors

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66
Q

What is the fate of secreted neurotrophins?

A
  1. act locally to affect growth cone motilty 2. can be transported retrogradely to the nucleus where they can ‘short circuit” cell suicide (e.g. Nerve Growth Factor)
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67
Q

What happens if a neuron does not receive an appropriate neurotrophic signal?

A

No retrograde transport –> no shortcircuit of suicide –> apoptosis

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68
Q

Which cellular process contributes to babies’ lack of coordination at birth?

A

incomplete myelination (among other activity-dependent processes like visual circuitry)

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69
Q

Anterograde transport: motor, materials

A

Fast: Kinesin; organelles vesicles, membranes Slow: Bulk flow; cytoskeletal and other proteins

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70
Q

Retrograde transport: motor, materials

A

Fast: Dynein; trophic factors, signaling molecules, endosomes, lysosomes

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71
Q

2 mechanisms to disrupt fast axonal transport

A
  1. lack of oxygen/disruption of mitocondrial oxphos 2. anticancer drugs that depolymerize microtubules –> neuropathy
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72
Q

At rest the membrane is more permeable to ____ than ____ and____. this is due to _______.

A

K+; Na+, Cl-; different electrical properties of their respective ion channels

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73
Q

Action potential conduction requires what kind of current flow?

A

Active through the channels and passive current within the shaft of the axon

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74
Q

The distance traveled by depolarizing current in an axon is dependent on what two properties?

A

Length constant and time constant

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75
Q

Where in an axon is the refractory zone?

A

The area of inactivated Na+ channels upstream of a propagating action potential

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76
Q

What are the roles of glial cells?

A
  1. regulation of cell migration and axon guidance 2. formation of BBB 3. trophic and insulating factors 4. modulation of synaptic function 5. injury response
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77
Q

From what germ layer are glial cells derived?

A

mesoderm

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78
Q

Which cells myelinate in the CNS?

A

Oligodendrocytes –> single cell wraps around multiple cell membranes

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79
Q

Which cells myelinate in the PNS?

A

Schwann cells –> single cell wraps around the membrane of a cell

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80
Q

Roles of myelination

A
  1. decreases capacitance of the membrane 2. concentration of channels in one area of membrane –> makes area more excitable
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81
Q

Charcot-Marie-Tooth is a ________ disorder caused by mutations in _____.

A

demyelination; PMP22: peripheral myelin protein 22 –> proximal limb weakness

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82
Q

Which ion drives the release of vesicles into the synaptic cleft?

A

Calcium

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83
Q

The decision to fire an action potential occurs at the site of presynaptic input in the ______ system.

A

PNS

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84
Q

How is action potential propagation different in the CNS than in the PNS?

A
  1. the transmitter may be excitatory or inhibitory 2. The outcome of signaling depends on location, type of receptor, and type of signaling molecule
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85
Q

The decision to fire an action potential in the ____ occurs at the axon hillock.

A

CNS

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86
Q

Myasthenic syndromes involve impaired _______.

A

endocytosis of neurotransmitters

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87
Q

Lambert Eaton myasthenic syndrom affects wht ind of channels?

A

presynaptic Ca2+ channels

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88
Q

Botulinum and tetanus toxins affect proteins involved in what process?

A

vesicle fusion

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89
Q

Synapses in the ______ are plastic throughout development and adulthood.

A

CNS

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90
Q

The primary neurotransmitter in the PNS is ______.

A

Acetylcholine

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91
Q

The probability of neurotransmitter release in the PNS is ______ times greater than that in the CNS.

A

10x

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92
Q

The axon hillock is described as a booster zone because _______.

A

the threshold for action potential propagation is low because of the concentration of channels

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93
Q

The larger the membrane time constant of the postsynaptic cell, the longer/shorter the presynaptic potential lasts and the greater the extent of temporal summation.

A

longer

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94
Q

Length constant is dependent on which two factors?

A

conductance of the membrane and shape of the cell

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95
Q

Most excitatory synapses in the CNS form at what location?

A

Spines on the dendrites

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96
Q

Wallerian degeneration in PNS

A

an evolutionary conserved program of axon destruction in response to insult or injury–> Schwann cells wait for macrophages to finish cleaning axonal debris and for the axon to return/regrow

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97
Q

What is the hallmark cellular event in response to a degenerating axon?

A

Change in the distribution of Nissl substance –> RER –> chromatolysis in axotomized motor neurons (lose all the Nissl signal)

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98
Q

Wallerian degeneration in the CNS

A
  1. very slow/poor degeneration and clearance –> microglia instead of macrophages 2. inability to clear the debris is in part what is preventing robust regrowth 3. neighboring neurons are often affected
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99
Q

4 factors that inhibit regeneration in the CNS

A
  1. inhibitory environment for growth - glial scar 2. inhibitory molecules present in CNS myelin - Nogo, MAG, Slit 3. low intrinsic growth potential of adult neurons 4. slow clearance
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100
Q

3 molecules that inhibit axonal regeneration

A

Nogo, MAG, Slit

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101
Q

Inhibition of what gene system has recently been shown to be effective in axonal regeneration?

A

mTOR

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102
Q

of cranial and spinal nerves

A

12 pairs, 31 pairs (8, 12, 5, 5, 1)

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103
Q

The tapered end of the spinal cord ends at ____.

A

L2 vertebra

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104
Q

Meninges extend to what level?

A

S2 vertebra

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105
Q

The space between L2 and S2 is used for what procedure?

A

Lumbar puncture

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106
Q

White matter

A

bundles of axons organized into tracts or fasciculi (wrapped by oligodendrocytes)

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107
Q

Gray matter

A

neuron cell bodies

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108
Q

Dorsal/posterior horns

A

remants of the alar plate –> the dorsal half of the functional neural tube –> sensory neurons

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109
Q

Ventral/anterior horns

A

contain motor neurons

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110
Q

Dorsal root

A

carries all sensory information into an individual spinal cord segment; derived from neural crest –> neurons that give rise to their axonal and dendritic processes outside the CNS –> cell bodies found in ganglia

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111
Q

Ventral root

A

motor; cell bodies of most roots are found in ventral horn (except for some autonomic cell bodies)

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112
Q

The neurons of the ventral horn have a direct/indirect synaptic relationship with corresponding ventral roots.

A

direct

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113
Q

Some/all of the incoming fibers from a dorsal root will synapse on sensory neurons in the dorsal horn.

A

some

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114
Q

T/F Nerve fibers entering the spinal cord via the dorsal roots are of similar size.

A

F

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115
Q

Different size axon fibers correspond to what measure?

A

conduction velocity

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116
Q

What 3 factors distinguish dorsal fibers from one another?

A
  1. fiber diameter 2. degree of myelination 3. sites of termination
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117
Q

If a dorsal root is classified using a roman numeral it is coming from a sensory receptor coming from _______.

A

Skeletal muscle - muscle spindles (Ia) and golgi tendon organ (Ib)

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118
Q

Proprioception

A

term used to describe muscle position sense

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119
Q

Roman numerals for dorsal roots

A

1 = heavily myelinated –> 4 = unmyelinated

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120
Q

If a dorsal root is not categorized by a roman numeral but rather by an alphabetic scheme, it is innervating a receptor in ______.

A

skin –> tactile/touch receptors (A-beta dorsal roots –> slightly less myelinated than 1a/b)

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121
Q

Medial division of the dorsal root

A

course medial to the dorsal horn and largely ignore its superficial layers

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122
Q

1a and 1b fibers synapse in the ______ horn and are involved in _______ contractions of skeletal muscle.

A

ventral; reflex

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123
Q

A delta and cfibers carry _____ and _____ modalities and synapse in the _____ horn.

A

pain and temperature; dorsal

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124
Q

Ventral roots are classified as

A

alpha or gamma motor neurons –> all the axons of these cell bodies leave in a ventral root and make skeletal muscle contract via a spinal nerve

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125
Q

Alpha motor neurons

A

neurons whose cell bodies are in the ventral horn and innervate skeletal muscle

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126
Q

Gamma motor neurons

A

cell bodies in the ventral horn and innervate one of the muscle receptors that are found in skeletal muscle (spindle) and alter the sensitivity of muscle spindle

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127
Q

C5-T1 and L2-S2 have large/small ventral horn.

A

large –> more space needed for plexi innervated by these groups (brachial and lumbosacral)

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128
Q

Topographic organization of alpha and gamm motor neurons

A

medial neurons innervate proximal muscles and lateral neurons innervate distal muscles in a limb

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129
Q

The most important tract that plays a role in making skeletal muscles contract voluntarily is ________.

A

the corticospinal tract –> cell bodies in motor cortex –> terminates in spinal cord

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130
Q

Voluntary contraction of skeletal muscle requires an interaction of how many neurons?

A

2 in series

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131
Q

Which neurons are involved in voluntary skeletal muscle?

A

upper motor neuron and lower motor neuron (alpha)

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132
Q

What net effect do upper motor neurons have on muscle stretch reflexes?

A

Inhibitory

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133
Q

Sidedness of skeletal muscle contraction pathway

A

UMN in primary motor cortex (precentral gyrus) –> corticospinal tract –> medulla-spinal cord junction (pyramidal decussation) –> contralateral lateral corticospinal tract –> contralateral LMN in ventral root–> contralateral muscle

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134
Q

decussation

A

oblique crossing of axons

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135
Q

How many neurons are required for general sensory pathways?

A

3: dorsal root ganglion receptor (1st order neuron) –> ipsilateral 2nd order neuron –> cross –> courses in a tract or lemniscus –> 3rd order contralateral thalamus neuron –> contralateral postcentral gyrus

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136
Q

2nd order neuron always crosses midline of body near ______.

A

cell body

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137
Q

Dorsal Column Pathway Medial Lemniscal System

A

three neuron pathway that is conveying proprioceptive and touch modalities to conscious levels of cerebral cortex –> 1st order neurons ignore spinal cord and form ipislateral fasciculi that course to 2nd order ganglia in medulla –> cross midline –> medial lemniscus –> VPL thalamus –> cortex

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138
Q

The upward continuation of the axons that run all the way up the spinal cord to the 2nd neurons are called ___________.

A

Fasciculi

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139
Q

Which fasciculus carries information from the upper/lower halves of the spinal cord to the medulla?

A

cuneatus (t5 and above)/gracilis (t6 and below)

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140
Q

Ventral posterior lateral nucleus

A

area of thalamus that receives communication from 2nd order nuclei in the medulla and transmit that information to specific cortical areas

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141
Q

Anterolateral system responds to what modalities in what kinds of cells?

A

Pain and temperature; A-delta and cfibers

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142
Q

Anterolateral System

A

dorsal root ganglion –> ipisilateral dorsal horn –> cross –> contralteral spinothalamic tract –> contralateral thalamic nucleus –> 3rd axons to cortex

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143
Q

The first axon carrying touch and vibration are long/short.

A

long

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144
Q

The first axon carrying pain and temperature are long/short.

A

short

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145
Q

What modalities are carried in the spinothalamic tract?

A

pain and temperature

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146
Q

The axon of the second neuron in sensory processing must do what?

A

Cross the midline of the CNS

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147
Q

What part of the brain is concerned with proprioception?

A

cerebellum

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148
Q

Spinocerebellar Systems

A

convey unconscious proprioception in ipsilateral tracts: dorsal spinocerebellar (lower limb) and cuneocerebellar (upper limb)

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149
Q

Autonomic pathways in the PNS use how many neurons?

A

3: pre and post ganglionic neurons + hypothalamic axons that synapse on preganglionic neurons

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150
Q

At what spinal cord levels do we find sympathetics?

A

T1-L2

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151
Q

Lesions in the neck at about T1 result in what condition? What about lesions in the brainstem affecting the same kinds of nerves?

A

Peripheral Horner’s syndrome vs Central Horner’s Syndrome

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152
Q

Which spinal cord segments control sphincteric function and micturition?

A

S2-S4

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153
Q

Preganglionic sympathetic signaling molecule is ________.

A

Acetylcholine

154
Q

Postganglionic sympathetic signaling molecule is _______.

A

Norepinephrine

155
Q

Dorsal spinocerebellar tract

A

dorsal root ganglion –> ipsilateral clarke’s nucleus in dorsal horn –> via the inferior cerebellar peduncle to cerebellar cortex

156
Q

Cuneocerebellar tract

A

dorsal root ganglion –> ipsilateral 2nd order neuron in Brain stem –> via cerebellar peduncle to cerebellar cortex

157
Q

Main sections of the spinal cord

A
  1. Dorsal = sensory (afferent) 2. Ventral horn = motor (efferent) 3. Intermediate = sensory motor circuits 4. Dorsal column = axons of large diameter mechano/proprioceptors
158
Q

Spinal reflexes

A

involve incoming sensory information which will enter from spinal nerves to the dorsal horn (large diameter axons) and branches toward the brainstem and to the local spinal cord segment (synapse on motor neurons or on interneurons)

159
Q

Muscle spindle organ is sensitive to what?

A

small changes in muscle length

160
Q

Where are muscle spindle organs distributed?

A

in the main belly of the muscle; 10fold smaller than the associated skeletal muscle fiber; in parallel with the muscle fibers

161
Q

Where are golgi tendon organs distributed?

A

clustered at the two musculotendonous junctions

162
Q

What are golgi tendon organs sensitive to?

A

tension changes (muscle contraction)

163
Q

Intrafusal muscle fibers

A

contained within the capsule containing spindle and are innervated by gamma motor neurons as opposed to alpha motor neurons which innervate everything outside the capsule

164
Q

Two types of intrafusual fibers

A
  1. Dynamic fibers = initially stretch with skeletal muscle but secondarily relax –> respond to changes in length 2. Static fibers (majority) = stretch along with extrafusual fibers and hold the same length –> respond to maintenance of length
165
Q

Dynamic intrafusal fibers contribute information about ________.

A

Rapid changes in length –> phasic length change

166
Q

Static fibers provide information about ______.

A

the need to maintain muscle contraction to hold a position

167
Q

Two types of innervation of muscle spindle

A

dynamic = 1 unique gamma neuron static = 1 unique gamma neuron + 1 generic group 2 sensory neuron *1 generic 1A sensory neuron wraps all the fibers in a muscle spindle

168
Q

Striations in intrafusual muscles are limited to which region of the fibers?

A

the tips of the fibers –> regions that are contractile

169
Q

Why is the central region of the muscle spindle devoid of striations?

A

contraction results in increase in tension in the central region that generates the signal for the spindle

170
Q

Where are gamma motor neuron endings found in spindles?

A

At the edges of the contractile tips of the spindle where the contractile apparatus is

171
Q

Where are sensory neuron endings found in spindles?

A

in the noncontractile central region

172
Q

The transducing event in both muscular sensory organs is mediated by _________.

A

stretch responsive ion channels

173
Q

T/F The 10-12 fibers within each golgi tendon organ are innervated by the same alpha motor neuron.

A

F –> enables the golgi tendon to monitor the tension in the muscle in a graded fashion

174
Q

What kind of sensory neuron innervates the fibers of the golgi tendon organ?

A

sensory 1b axon –> enters capsule –> compression of tendon organ upon muscle contraction compresses tips of sensory neuron and this activates stretch-sensitive ion channels

175
Q

Why is passive muscle stretch a bad way to generate action potentials at the golgi tendon organ?

A

the majority of the tension change is absorbed by the viscoelastic properties of the muscle belly, leaving little tension to affect the golgi organ

176
Q

What factor contributes to the ability of skeletal muscle spindles to continue to be responsive to increases in length from a shortened position?

A

gamma motor neuron system

177
Q

In slow movements, gamma neurons to what kind of muscle fibers are activated?

A

static fibers

178
Q

In fast and uncertain movements, gamma neurons to what kinds of muscle fibers are activated?

A

dynamic fibers (as well as static gamma neurons in more controlled fast movements)

179
Q

Golgi tendon organs have a linear/exponential response to muscle force.

A

linear

180
Q

Cell bodies of all sensory neurons are located where?

A

dorsal root ganglion

181
Q

All sensory neurons have excitatory/inhibitory effects on their target neurons.

A

excitatory

182
Q

Reciprocal innervation

A

when sensory information comes into the spinal cord it will have two opposing actions for the muscles of a particular joint –> excitation of the alpha motor neurons + a parallel inhibition of alpha motor neurons to muscles with opposing force (e.g. extensors vs. flexors)

183
Q

T/F spinal cord reflexes are under a lot of CNS regulation.

A

T

184
Q

Why is the myotactic (stretch) reflex the fastest somatic reflex in the body?

A
  1. involves a single synapse in the spinal cord 2. the 2 neuronal components are fast conducting, large diameter
185
Q

Myotactic stretch reflex pathway

A

patellar tendon tap –> stretch of the tendon –> 1A sensory neuron activation via muscle spindle –> synapse on alpha motor neuron –> excite alpha motor neuron in the same (homonymous) muscle –> activation; in parallel, 1A sensory neuron synapses on 1A inhibitory interneuron –> inhibit the activity of alpha motor neuron on opposite muscles

186
Q

The golgi tendon organ reflex pathway

A

when there is an increase in alpha motor neuron activity to a contracting muscle –> 1B sensory neurons increase firing –> spinal cord –> excites two interneurons –> reduces homonymous muscle tension and increases tension on the opposing muscle

187
Q

Why does the golgi tendon reflex involve muscles on either side of the joint?

A

To ensure feedback and prevent the movement from exceeding the goal

188
Q

Withdrawal reflex

A

Ipsilateral flexion + contralateral extension (graded in intensity and follows reciprocal innervation rule)

189
Q

Withdrawal reflex pathway

A

stimulus –> pain receptors (group 3 and 4) –> spinal cord –> excites ipsilateral flexion + inhibits ipsilateral extension of one leg + excites contralateral extension and inhibition of contraleteral flexion in opposite leg (to support the leg withdrawing from the stimulus)

190
Q

T/F all sensory neurons end in the ipsilateral (to the side of their origination) side of the spinal cord.

A

T

191
Q

Descending control of spinal reflexes comes from where?

A

Motor cortex (mostly) + somatosensory cortex –> corticospinal tract (axoaxonic presynaptic synapses near termination of sensory neurons)

192
Q

Why does descending control signals of spinal reflexes synapse at the dorsal root termination of sensory neurons?

A

so that the sensory signal that has branched off before entry into the spinal cord is unperturbed by regulatory signals and can tell the brain exactly what happened at the muscle

193
Q

T/F regulation in the spinal cord can reverse the activity of a neuron based on state (resting vs locomotion).

A

T –> different interneurons with different functions can be engaged in different states

194
Q

PNS

A

any neuron that is at least in part, outside the CNS as well as associated glial cells and their effector cells (skeletal muscles) *diseases cause numbness and/or weakness

195
Q

Diseases of the sensory neurons are called _______.

A

Sensory neuronopathy

196
Q

Diseases of the motor neurons are called _______.

A

Motor neuronopathy

197
Q

Diseases of the nerve roots are called _______.

A

radiulopathy

198
Q

Diseases of the nerves are called _______.

A

neuropathy

199
Q

Diseases of the neuromuscular junction are called _______.

A

myopathy

200
Q

If both sensory and motor symptoms occur, what kinds of conditions might a patient have?

A

neuropathy or radiculopathy

201
Q

Causes of sensory neuropathies

A
  1. toxins (e.g. cisplatin) 2. anti-Hu/ANNA1 antibodies (paraneoplastic syndrome) 3. Sjogren’s
202
Q

Type grouping

A

Upon denervation of a muscle group, compensative fibers sprout from neighboring motor units in an attempt to renervate the damaged region. Because of this, large groups of neurons innervated by a single motor unit are found clustered instead of widely distributed as normal.

203
Q

EMG findings in neuropathy

A
  1. Action potential amplitude doubles b/c of increased fibers/motor unit from renervation 2. Increased action potential duration 3. Decrease in the number of motor units in the muscle
204
Q

EMG findings in chronic denervation

A

Denervated muscles have regular automatic firing at a low amplitude.

205
Q

Amyotrophic Lateral Sclerosis (ALS)

A

relatively common disease; relentlessly progressive lost of motor neurons (no sensory involvement) –> begins in bulbar muscles, arms, or legs –> UMN findings –> idiopathic

206
Q

Spinal Muscular Atrophy (SMA)

A

relentless progressive loss of motor neurons in babies –> 4 stages –> caused by loss of SMN1 gene

207
Q

What gene results in an unstable transcript resulting in spinal muscular atrophy?

A

SMN2 gene

208
Q

The intensity of spinal muscular atrophy is dependent on _______.

A

The proportion of unstable SMN2 transcript that is produced.

209
Q

Herniation of the nucleus pulposus results in what condition?

A

radiculopathy AKA pinched nerve

210
Q

What are the most common spinal levels involved in radiculopathy?

A

cervical (C7) and lumbosacral (L5)

211
Q

Symptoms of neuropathies

A
  1. weakness and muscle atrophy 2. diminished/absent reflexes pain 3. sensory loss of large and small fiber modalities
212
Q

Which kinds of axons are most affected by neuropathy?

A

long axons in distal places

213
Q

T/F axons are the majority of cell volume.

A

T

214
Q

T/F transport in axons could require years.

A

T

215
Q

T/F energy failures anywhere in an axon could lead to failure of the whole axon.

A

T

216
Q

Mutations in which dynein transport genes can cause spinal muscular atrophy and hereditary motor neuropathy 7B?

A

DYNC1H1 (dynein heavy chain 1) DCTN1 (dynactin)

217
Q

Mutations in which kinesin transport genes can cause hereditary sensory neuropathy

A

KIF1A KIF5A

218
Q

Mutations in what gene can cause syndromic inherited neuropathy?

A

TUBB3

219
Q

Charcot-Marie-Tooth neuropathy is caused by duplication of what gene?

A

PMP22 –>overexpression and destabilization of myelin

220
Q

Deletion of one copy of PMP22 results in what condition?

A

Palsy –> HNPP

221
Q

The precipitating event at the NMJ is what?

A

AP causes calcium release which triggers vesicle release and fusion with the membrane

222
Q

Which sodium gated channel propagates action potentials in skeletal muscle?

A

Nav1.4

223
Q

What molecule is cleaved by botulinum toxin at the NMJ?

A

Snap25

224
Q

What molecule do nerve gases bind to at the NMJ

A

AChE

225
Q

What toxin blocks Nav1.4?

A

tetrodotoxin

226
Q

Autoantibodies against alpha-P/Q calcium channels (in the NMJ) are found in what condition?

A

Lambert-Eaton Myasthenic Syndrome –> presynaptic –> decreased release of vesicles –> FLUCTUATING symmetric proximal weakness at rest (may improve during exercise due to increased calcium concentration with repetitive depolarization) *30% young women with specific HLA *70% secondary to paraneoplastic squamous lung cancer (diagnostic for the cancer)

227
Q

In what condition are autoantibodies against ACh receptors in the NMJ found?

A

myasthenia gravis –> autoantibodies to receptor or MuSK –> lower response to the ACh

228
Q

Safety Factor

A

The difference between the endplate potential and -50 mV is known as the safety factor –> most muscles in the body get enough ACh during a synaptic release to contract –> deficiencies can be presynaptic (not enough ACh) or postsynaptic (not enough receptors) –> “when the safety factor falls below 0, you go weak’

229
Q

Increase in the amplitude of the compound action potential of the muscle is indicative of what kind of defect?

A

presynaptic –> residual buildup of calcium facilitates greater release of ACh all the way up to normal levels (100% release)

230
Q

Decrease in the amplitude of the compound action potential of the muscle is indicative of what kind of defect?

A

postsynaptic –> pool of immediately releasable vesicles is depleted –> less ACh release and more failure of postsynaptic muscle –> normally this doesn’t happen because there is sufficient ACh released to stimulate the postsynaptic muscle

231
Q

What constitutes a motor neuron pool?

A

many motor neurons, each of which innervates a motor unit with the muscle

232
Q

Where are vesicles produced?

A

In NMJ, empty vesicles are made in the cell body (which for LMN is in the spinal cord) –> transported to the end of axons

233
Q

Where are vesicles in the NMJ filled with neurotransmitter?

A

At the end of the axon –> ACh-H exchanger proton pump ensure inflow of ACh

234
Q

T/F ACh is the only neurotransmitter to connect nerve and muscle.

A

T

235
Q

T/F Vesicles made in the cell body have a higher pH than the cell body of the neuron.

A

F –> a lower pH ensures the ACh-H exchanger can function to fill the vesicle

236
Q

3 stores of vesicles

A
  1. primary/immediate - 1000 vesicles at the presynaptic membrane 2. secondary/mobilization - 10,000 vesicles that can replenish the primary store 3. tertiary/reserve - 100,000 vesicles in the axon
237
Q

T/F ACh is the neurotransmitter involved in the synapse between preganglionic sympathetic and parasympathetic neurons with corresponding postganglionic neurons.

A

T

238
Q

What are the neurotransmitters employed in the junctions between postganglionic parasympathetic and sympathetic neurons and end organs?

A

ACh and norepinephrine

239
Q

How do immediate store vesicles interact with the cell membrane?

A

nerve terminal has syntaxin and SNAP25, both t-snares that attach to synaptotagmin and synaptobrevin (vsnares) on the vesicle –> nsec1 dissociates from syntaxin allowing the bonds to form into a tertiary complex

240
Q

3 main SNAREs involved in vesicle-membrane interaction

A

synaptobrevin (vesicular) + SNAP25 and syntaxin

241
Q

To what molecule does calcium bind to trigger vesicle release?

A

synaptotagmin

242
Q

T/F All immediate store vesicles are released upon activation.

A

F –> Under normal physiologic conditions, only 20% of primary store vesicles are released

243
Q

T/F each ACh receptor binds 1 molecule of ACh

A

F –> each binds 2 which are both necessary for activation –> opening of selective cation channel

244
Q

How many subunits form an NMJ nicotinic ACh receptor?

A

4

245
Q

T/F the ACh receptor involve different subunits resulting in different receptor pathologies in different age groups.

A

T

246
Q

Which associated ACh receptor protein is vulnerable to auto-antibodies?

A

MuSK –> muscle specific tyrosine kinase

247
Q

Safety factor formula

A

resting membrane potential - stimulation (endplate potential) -30 = safety factor

248
Q

Compound Muscle Action Potential

A

sum of voltage of muscle action potentials of all lower motor neurons stimulated at one time

249
Q

Botulism - clinical presentation

A

fluctuating weakness from face that descends to limbs and respiratory muscles

250
Q

How do tetanus and botulinum toxins differ?

A

Botulinum reduces vesicle release at the NMJ and tetanus toxin reduces vesicle release at inhibitory spinal interneurons

251
Q

Organophosphorous Gases

A

synapse related –> reacts with AChesterase –> continual stimulation of receptor –> initial uncontrolled muscle contraction and subsequent paralysis (diaphragm)

252
Q

Physostigmine, Neostigmine, Pyridostigmine

A

organophosphorous analogs that are reversible –> transient inhibition of AChesterase

253
Q

In what NMJ condition does increased stimulation not prevent worsening of symptoms?

A

myasthenia gravis –> fluctuating skeletal muscle weakness/fatigue that worsens over time

254
Q

Paralytics used in anesthesia

A
  1. Succinylcholine –> depolarizing NMJ blocker –> raises muscle contraction and subsequently induces paralysis 2. pancuronium –> selective competitive antagonist to ACh
255
Q

2 types of synapses

A
  1. Electrical: fast, direct, all or nothing excitation via ion channels 2. Chemical: flexible, plastic, excitatory/inhibitory, amplifiable, via neurotransmitters in a cleft
256
Q

Ionotropic transmission

A

ligand-gated ion channels: 1. excitatory = cation selective (Glutamate and ACh) 2. inhibitory = anion selective (GABA and glycine)

257
Q

How is receptor diversity in ligand-gated ion channels generated?

A

different combinations of different subunits in the formation of the ion channel

258
Q

Metabotropic transmission

A

g-coupled receptors: modulate synaptic input (amplifiable)–> different post-synaptic effects

259
Q

Which kind of neuronal chemical transmission is faster?

A

ionotropic

260
Q

Which kind of neuronal chemical transmission is more sustained?

A

metabotropic

261
Q

How is receptor diversity in metabotropic receptors generated?

A

monomers but have different structural subtypes

262
Q

Ex. 3 AA neurotransmitters

A

Glutamate, GABA ,Glycine

263
Q

Ex. small molecule transmitter

A

Acetylcholine

264
Q

Ex. biogenic amine neurotransmitter

A

Catecholamines, 5-HT, Histamine

265
Q

Glutamate

A

major CNS excitatory neurotransmitter –> ionotropic and metabotropic –> reuptake by neurons and glia –> learning and memory

266
Q

What are some excitotoxic effects of gluatamate?

A

seizures, hypoglycemia, ischemia, hiv

267
Q

4 glutamate receptors

A
  1. NMDA - postsynaptic ionotropic gated with Ca and Na 2. AMPA - postsynaptic ionotropic gated with NA 3. Kainate - pre/post synaptic ionotropic gated with NA 4. mGluRs - pre/post synaptic metabotropic with increased PI hydrolysis and reduced cAMP
268
Q

Glutamate NMDA receptor

A
  1. most common; slow and sustained currents -> minimal desensitization 2. permeable to Ca –> EPSP increase intracellular Ca that can act as second messenger 3. Glycine co-agonist 4. Mg plug –> blocks pore at hyperpolarized; open at depolarized
269
Q

Glutamate AMPA receptor

A

primary mediator of fast response –> desensitize with repeated stimulation

270
Q

Glutamate Kainate receptor

A

primary mediator of fast response –> desensitize with repeated stimulation

271
Q

3 GABA receptors

A

main inhibitory transmitter in the brain (vs. glycine in the spinal cord) 1. GABAa - ionotropic (Cl) 2. GABAc - ionotropic (Cl) retina 3. GABAb - metabotropic

272
Q

GABAa receptor

A
  1. principal mediator of fast synaptic inhibition in the brain 2. multiple subunits; gated with Cl- 3. allosteric modulators (benzodiazepine, barbituate, steroid)
273
Q

How do benzodiazepines affect GABAa receptors?

A

increase the frequency with which the receptor opens

274
Q

How do barbituates and steroids affect GABAa receptors?

A

increase affinity for GABA and increase channel conductance

275
Q

GABAb receptor

A
  1. slow long lasting currents 2. metabotropic pre/post synaptic (K+ and Ca+) 3. baclofen treats spasticity, ecstasy, GHB
276
Q

Acetylcholine

A

major excitatory transmitter in the PNS (but also widespread in the CNS) 1. ionotropic nicotinic receptor 2. muscarinic metabotropic receptor

277
Q

Nicotinic acetylcholine receptor

A

ionotropic with neuron-type R –> expressed in the CNS early in life and decline with age

278
Q

What kind of receptor is linked with Parkinson’s and Alzheimer’s disease?

A

Nicotinic and muscarinic ACh

279
Q

Which systems do cholinergic systems regulate?

A

dopaminergic

280
Q

Biogenic Amines

A
  1. serotonin –> both types of receptors; depression 2. catecholamines –> metabotropic (dopamine, norepinephrine, epinephrine)
281
Q

Where is norepinephrine made?

A

locus coeruleus

282
Q

Where is serotonin made?

A

Raphe nuclei

283
Q

Where is dopamine made?

A

substantia nigra and ventral tegmental area

284
Q

Where is acetylcholine made?

A

pontomesencephalotegmental complex, septal nuclei, and nucleus basalis

285
Q

In the corticospinal tract, where do the fibers destined for the arms or upper limbs travel?

A

medially –> peel off and synapse with LMN earlier (remember, the corticospinal tract is on the edge of the spinal cord

286
Q

In the corticospinal tract, where do the fibers destined for the legs or lower limbs travel?

A

laterally

287
Q

Where do spinothalamic tract axons cross?

A

in the ventral white commisure near their level of entry

288
Q

Where do spinothalamic tract 2nd order axons terminate?

A

in the contralateral ventroposterolateral thalamus

289
Q

In what tract do spinothalamic tract 1st order axons travel before synapsing in the dorsal horn?

A

Lissauer’s tract

290
Q

Where do axons from the nuclei gracilis and cuneatus terminate?

A

in the ventroposterolateral thalamus

291
Q

In the dorsal column system, where do 1st order axons run?

A

in the ipsilateral fasciculi gracilis and cuneatus

292
Q

Which spinal tracts cross in the lower medulla?

A

The medial lemniscal/dorsal column and the corticospinal/motor tract

293
Q

Where do sympathetic fibers run?

A

ipsilaterally to the T1-L2 spinal nerves

294
Q

Horner’s syndrome symptoms

A

ptosis, miosis, anhydrosis

295
Q

Where do sympathetic fibers arise?

A

hypothalamus

296
Q

What is the effect of cocaine on the eye?

A

blocked reuptake of norepinephrine –> makes the pupil large (unless sympathetic system is interrupted)

297
Q

Where are afferent cell bodies related to bladder control located?

A

stretch receptors in smooth muscle wall of bladder send sensory input via S2-S4 dorsal roots

298
Q

Where are efferent cell bodies related to bladder control located?

A

cell bodies in gray matter of S2-S4 –> parasympathetic stimulation causes contraction of detrusor

299
Q

Where do parasympathetic axons controlling bladder function arise?

A

pontine micturition center

300
Q

What happens once parasympathetic axons involved in the bladder response are myelinated?

A

you gain control over bladder emptying

301
Q

Where do corticospinal axons cross?

A
  1. 90% at the pyramidal decussation –> lateral corticospinal tract 2. continue as anterior corticospinal tract and decussate in anterior white commissure near level of termination
302
Q

What is the consequence of a lesion above the pons on bladder control?

A

infantile bladder (fill/empt cycley)

303
Q

What is the consequence of a lesion above the conus and below the pontomesencephalic micturition center on bladder control?

A

acute: acontractile bladder chronic: spastic bladder secondary to loss of inhibitory influence on the detrusor –> incontinence

304
Q

What is the consequence of a lesion of sacral dorsal roots, cauda equina, and conus medullaris on bladder control?

A

atonic bladder, flaccid, loss of sensation (dribbling)

305
Q

What is the blood supply of the spinal cord?

A

Anterior 2/3 = anterior spinal artery from vetebral artery Posterior 1/3 = paired posterior spinal arteries

306
Q

What is the watershed zone of the spinal cord?

A

midthoracic region –> least vascularized and vulnerable to infarct

307
Q

What is the largest branch of the posterior artery system?

A

Artery of Adamkiewicz (T9-T12)

308
Q

Slowness and stiffness are symptoms of UMN/LMN.

A

UMN –> increased tone/spasticity, hyperactive reflexes, pathologic reflexes

309
Q

Weakness and cramps are symptoms of UMN/LMN.

A

LMN –> weakness, atrophy, fasiculations, decreased tone, decreased reflexes

310
Q

What term refers to the loss of sensation at or below a dermatome?

A

sensory level

311
Q

What term refers to loss of sensation in adjacent dermatomes with preservation above and below that level?

A

segmental sensory loss

312
Q

Weakness in the extensors of the arms and the flexors of the legs indicate UMN/LMN.

A

UMN

313
Q
A
  • Motor: loss of all motor function below lesion
  • Sensory: loss of all modalities below lesion
  • Autonomic: bowel and bladder dysfunction
  • Causes: trauma, compression, inflammatory myelitis
  • Outcome:
    • C1-C3 = ventilatory support
    • C4 = partial ventilatory independence
    • spared C7 = independent elbow –> live on own
314
Q

T/F Bowel and bladder control can be lost with unilateral spinal cord injury.

A

F. Requires bilateral injury

315
Q
A
  • Motor:
    • ipsilateral weakness below lesion
    • segmental LMN and sensory signs
  • Sensory:
    • contralateral loss of pain/temp –> 1/2 levels below lesion
    • ipsilateral proprioception loss below lesion
  • Causes: trauma or compression by extrinsic lesion/rare intramedullary lesion
316
Q
A
  • Motor: anterior horn cells at the level of lesion with LMN findings
  • Sensory (first affected): crossing fibers of spinothalamic fibers –> bilateral capelike loss of pain/temperature
  • Autonomic: no bladder/bowel dysfunction
  • Causes: syringomyelia (assoc. with Chiari malformation, congenital, or tumor), hematomyelia, intramedullary tumor
317
Q

Chiari malformation

A

congenital malformation leading to partial herniation of the cerebellar tonsils through the foramen magnum that may be isolated or associated with syrinx or more severe malformation –> Central Cord Lesion

318
Q
A
  • Sensory: vibration/proprioception –> sensory ataxia that is worse in the dark –> + Romberg sign
319
Q

Syphilitic posterior column syndrom/tabes dorsalis

A
  • “great imitator”
  • lancinating pains in legs
  • no leg reflexes
  • sphincter dysfunction
  • blindness from optic atrophy
  • deficits irreversible with penicillin
320
Q
A
  • Motor: spasticity and hyperactive reflexes with Babinsky sign
  • Sensory: loss of proprioception and vibration –> sensory ataxia and + Romberg
  • Causes: B12 deficiency
321
Q
A
  • Motor: LMN findings at affected segment
    • atrophy
    • fasciculations
    • weakness
  • Causes: SMA, Polio, WNV, Entero 71, Coxsackie A/B, Echovirus, Monomelic amyotrophy (benign)
322
Q
A
  • Motor: UMN and LMN findings (not visible on MRI)
323
Q
A
  • Motor: initial flaccid weakness below lesion but spastic chronic parapersis (corticospinal) + LMN abnormalities at the level of the lesion
  • Sensory: loss of pain and temperature sensation below the lesion
  • Autonomic: loss of bowel and bladder control
324
Q

Intramedullary lesion

A
  • initial symptoms reflect parenchymal damage –> involvement with segmental sensory and motor findings too –> leading to complete cord compression
  • ex. ependymoma, astrocytoma, glioblastoma, myelitis, abscess
325
Q

Intradural extramedullary lesion

A
  • initial symptoms are extraparenchymal and may reflect root compression –> LMN symptoms
  • increasing tumor size –> myelopathy
  • schwannoma and meningioma
326
Q

Extradural lesion

A
  • initial symptoms extraparenchymal –> reflect root compression –> later myelopathy
  • disc disease, epidural metastasis, primary bone tumor, lymphoma, epidural abscess
327
Q

Most common herniations

A
  • C7 –> Cervical Myelopathy
  • L5 –> LMN lesion compressed nerve roots
    • dermatomal sensory loss
    • depression of reflexes at affected level
    • radicular pain
    • no bowel/bladder involvement
328
Q

T/F You can have a cord syndrome with disc herniation at L5.

A

F –> cord ends at L2

329
Q

Findings in Mild Cord Compression

A

radicular symptoms (e.g. touch hypersensitivity, pain in opposite limbs, girdle sensations, pain increased with coughing)

330
Q

Findings in Moderate Cord Compression

A

ipsilateral UMN findings (spasticity and plantar extension) + contralateral pain/temperature loss

331
Q

Findings in Severe Cord Compression

A

complete cord transection

332
Q

Absent reflexes and muscle atrophy suggest UMN/LMN.

A

LMN

333
Q

The presence of prolonged distal motor latencies and slowed conduction velocities is most consistent with what kind of neuropathy?

A

Demyelinating

334
Q

Loss of motor amplitudes with sparing of conduction velocities is most consistent with what kind of neuropathy?

A

Axonal

335
Q

Anterior horn cell abnormalities tend to spare what organ?

A

eyes

336
Q

Normal nerve conduction studies, normal EMG, and abnormal repetitive stimulation studies localize a lesion to what?

A

NMJ

337
Q

T/F A normal CK level rules out myopathic disease.

A

F.

338
Q
A
339
Q
A
340
Q

In what conditions are NCS abnormal?

A

Peripheral nerve and sometimes NMJ

341
Q

In what conditions does an EMG demonstrate fibrillation?

A

Peripheral nerve and anterior horn cell

342
Q

T/F approximately 40-50% of mass of the adult human body is composed of muscle tissue.

A
343
Q

What is the origin of the muscles of the limb and body?

A

The somite

344
Q

Muscles of the back arise from which lip of the dermamyotome?

A

medial lip = epaxial muscle

345
Q

Muscles of the back arise from which lip of the dermamyotome?

A

later lip = hypaxial muscle

346
Q

What are the two most important signals in somite division and differentiation?

A

Wnt and Shh

347
Q

Muscle of the head (but not the tongue) arise from what?

A

pre-chordal mesoderm

348
Q

Which muscle receptor acts as a voltage sensor?

A

the dihydropyridine receptor

349
Q

Which muscle receptor undergoes a confromormational change to release calcium upon voltage changes?

A

ryanidine receptor

350
Q

T/F There is no active muscle breakdown or ongoing regeneration in congenital myopathies.

A

T –> they are not muscular dystrophies and can show clinical improvement and/or stable course

351
Q

4 classical congenital myopathies

A
  1. nemaline myopathy
  2. centronuclear/myotubular myopathy
  3. central core disease
  4. multi/minicore myopathy
352
Q

T/F congenital myopathies are degenerative.

A

F –> this would be a muscular dystrophy

353
Q

What are red staining inclusions in muscle called in relation to congenital myopathy?

A

nemaline rods –> threads in the muscle

354
Q

What are the two most important genes implicated in nemaline myopathy?

A
  1. Nebulin
  2. Actin

All genes related to nemaline myopathy have to do with the thin filament.

355
Q

T/F All nemaline myopathy genes are to do with the thin filament.

A

T

356
Q

3 key histological findings in muscular dystrophy

A
  1. degeneration
  2. regeneration
  3. connective and fatty tissue infiltration
357
Q

Why are smooth muscle and cardiac muscle spared in nemaline myopathy?

A

different structure and isozymes related to the thin filament

358
Q

During skeletal muscle regeneration, why does the nucleus move to the center of the cell?

A

b/c satellite cells fuse with the muscle to make up losses

359
Q

Duchenne muscular dystrophy

A
  • 1:3500 boys
  • 2-4 year onset
  • wheelchair <12 years
  • lifespan now into 3rd decade
  • proximal progressive weakness, pseudohypertrophy, elevated CK
  • complications of cardiomyopathy, respiratory insufficiency, scoliosis
360
Q

T/F Duchenne muscular dystrophy is x-linked.

A

T

361
Q

Why do some muscles appear grossly larger in Duchenne’s?

A
  1. hypertrophy of remaining fibers
  2. infiltration of fatty tissue and connective tissue
362
Q

What clinical sign is used to demonstrate proximal muscle weakness?

A

Gowers’ maneuver

363
Q

What clinical sign demonstrates hip abductor weakness?

A

Stair climb with Trendelenburg sign

364
Q

3 important late complications of Duchenne’s

A
  1. scoliosis
  2. respiratory insufficiency
  3. cardiomyopathy
365
Q

Becker muscular dystrophy

A
  • 1:30,000 males
  • variable onset and severity
  • wheelchair >15 years
  • CK elevated
  • cardiomyopathy still important (even when pt is ambulant)
366
Q

T/F Only the full-length form of dystrophin can prevent muscular dystrophy.

A

T

367
Q

T/F Duchenne’s is associated with increased autism risk.

A

T

368
Q

What does dystrophin do in the muscle?

A
  • dystrophin holds the muscle protein complex to the membrane –> when dystrophin is malfunctioning, the muscle complex will not function
369
Q

Revertant fibers

A

muscles in which dystrophin is restored by a somatic mutation in the reading frame

370
Q

T/F Most mutations in dystrophin are deletions.

A

T

371
Q

What kinds of deletions are most common in DMD?

A

out of frame deletions –> truncated and degraded protein

372
Q

What kind of deletions are most common in BMD?

A

in frame deletions –> preservation of reading frame

373
Q

Frame restoration

A

removable of extra exons to turn DMD into BMD as a therapeutic approach

374
Q

Which gene therapy vector is being studied for therapy of DMD and what is its main limitation?

A

Recombinant Adeno-associated virus –> has a size limit for the genes that can fit inside it

375
Q

Where is CSF found in the CNS?

A

Ventricles and subarachnoid space

376
Q

What color is blood on a CT?

A

white

377
Q

What color is CSF on a CT?

A

black

378
Q

What color is bone on a CT?

A

white

379
Q

In an axial T1 MRI, what color is CSF?

A

black

380
Q

In an axial T2 MRI, what color is CSF?

A

white

Brain and Behavior (5 decks)

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