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B&B Part 1 > B&B Week 2 > Flashcards

B&B Week 2 Flashcards

1
Q

what is the spinal cord?

A

an extension of nerve tissue and support cells from the medulla segment of the brain

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2
Q

what are meninges?

A

covers the spinal cord

are continuous with the meninges associated with the brain

three layers–> dura, arachnoid and pia

dura–> single outermost layer; tough, thick, protective
arachnoid–> middle layer, lines dura underneath, bridges over sulci
pia–> innermost layer, most delicate; adheres tightly to spinal cord surface

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3
Q

what is the denticulate ligament?

A

thickening of the pia and glia

lateral “ribbon” between the dorsal and ventral roots

attaches spinal cord to the dura/arachnoid tube (suspends it within CSP in the subarachnoid space

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4
Q

what are the two enlargements of the vertebral column?

A

cervical (C4/5–> T1)

lumbosacral (L2–>S3)

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5
Q

what is the conus medullaris?

A

the tapered end of the spinal cord at L1-L2

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6
Q

what is the filum terminale?

A

the extension of pia and supporting cells which anchors the spinal cord to the dorsum of the coccyx

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7
Q

list 4 surface markings of the spinal cord

A

anterior median fissure–> anterior spinal artery runs along spinal cord

anterolateral sulcus–> ventral nerve roots exit

posterior median sulcus

posterolateral sulcus–> dorsal nerve roots enter

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8
Q

why do nerve root lengths have to travel further to exit through the appropriate intervertebral foramen as you move down the spinal cord caudally?

A

because the spinal cord ends at L1/2 so the nerve roots must travel down from here to exit at, for example, S3

thus, the lumbosacral roots are the longest and form the cauda equina that fills the lower part of the subarachnoid space

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9
Q

describe, from anterior to posterior, the surrounding osteology and ligamentous structures of the vertebral column

A

from anterior to posterior—>

anterior longitudinal ligament–>

vertebral body/intervertebral disc–>

posterior longitudinal ligament–>

vertebral canal (containing the spinal cord wrapped in meninges)–>

ligamentum flavum–>

spinous process–>

supraspinous ligament

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10
Q

what makes up the inner core of of the spinal cord?

A

grey matter

consists of NERVE CELL BODIES (soma) and processes, and NEUROGLIA (supporting cells)

divided into laters called “rexed’s laminae”

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11
Q

what are the layers of the grey matter of the spinal cord?

A

rexed’s laminae

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12
Q

what do you find in the posterior horn of grey matter in the spinal cord?

A

sensory

receives and processes sensory information (sensory cell body is in the dorsal root ganglion)

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13
Q

what do you find in the anterior horn of grey matter in the spinal cord?

A

motor

location of cell bodies of lower motor neurons (nerves innervating skeletal muscle)

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14
Q

what do you find in the lateral/intermediate horn of grey matter in the spinal cord?

A

aka intermediolateral cell column

T1-L2/3–> preganglionic SYMPATHETIC cell bodies (prominent)

S2-S4–> preganglionic PARASYMPATHETIC cell bodies (less prominent)

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15
Q

what is the central canal of the spinal cord?

A

becomes continuous with the 4th ventricle in the medulla

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16
Q

what surrounds the grey matter of the spinal cord?

A

white matter

consists of nerve processes (mainly axons) which form tracts, and neuroglia

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17
Q

what major tracts are found in the posterior (dorsal) column?

A
  1. fasciculus gracilis (present at all levels)

2. fasciculus cuneatus (present about T6)

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18
Q

what major tracts are found in the lateral column?

A
  1. lateral corticospinal tract
  2. rubrospinal tract
  3. spinocerebellar tracts (including the dorsal spinocerebellar tract and the ventral spinocerebellar tract which has minor importance)
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19
Q

what major tracts are found in the anterior column?

A
  1. spinothalamic tract (anterolateral system)
  2. vestibulospinal tracts (lateral and medial)
  3. reticulospinal tracts (lateral and medial)
  4. anterior corticospinal tract
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20
Q

what does the fasciculus cuneatus transmit?

A

ascending tract

discriminative touch

proprioception

upper limb

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21
Q

from what side of the body does the fasciculus cuneatus and gracilis detect sensation from?

A

the same side as where they are located

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22
Q

what does the fasciculus gracilis transmit?

A

ascending tract

discriminative touch

lower limb

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23
Q

what does the lateral corticospinal (pyramidal) tract transmit? (lateral column)

A

descending tract

from contralateral cerebral cortex–> SKILLED and WILLED movements to the same side of the body

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24
Q

what does the vestibulospinal tract transmit?

A

uncrossed

descending tract

stimulates extensors of trunk and lower limb and flexors of upper limb

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25
Q

what do the reticulospinal tracts transmit?

A

descending tract

crossed and uncrossed

UNSKILLED and INVOLUNTARY movements

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26
Q

what motor neurons are found in the ventral horn of grey matter?

A

limb muscles and trunk muscles

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27
Q

what does the spinothalamic tract transmit?

A

ascending pathway in the anterolateral system (anterior column)

simple touch (non-discriminative)

pain

temperature

opposite side of body

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28
Q

what does the ventral spinocerebellar tract transmit?

A

ascending tract in the lateral column

proprioception

both lower limbs

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29
Q

what does the dorsal spinocerebellar tract transmit?

A

ascending tract of the lateral column

proprioception of the lower limb of same side

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30
Q

is the spinothalamic tract ascending or descending?

A

ascending

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31
Q

where does the spinothalamic tract enter the spinal cord?

A

posterior horn

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32
Q

where do neurons in the spinothalamic tract synapse?

A

in the posterior horn, up or down 1-2 segments from where they enter

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33
Q

where do fibers of the spinothalamic tract cross the midline?

A

immediately after synapsing, in the anterior white commisure

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34
Q

where is the final destination for fibers of the spinothalamic tract?

A

VPL of thalamus then the primary sensory cortex of the cerebrum

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35
Q

what makes up the PCML?

A

fasciculus cuneatus (above T6) and gracilis

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36
Q

what does the PCML detect?

A

discriminative touch (as opposed to spinothalamic which is non-discriminative)

vibration

pressure

concious propropception

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37
Q

where does the PCML enter the spinal cord?

A

posterior horn

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38
Q

where do fibers in the PCML synapse?

A

nucleus cuneatus or gracilis of MEDULLA

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39
Q

where do fibers of the PCML cross the midline?

A

immediately after synapsing

they cross as INTERNAL ARCUATE FIBERS and from the medial lemniscus

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40
Q

where is the final destination for fibers from the PCML?

A

VPL of thalamus

then the primary sensory cortex of the cerebrum

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41
Q

where does the lateral corticospinal tract originate from?

A

primary motor cortex of the cerebrum

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42
Q

where do fibers in the lateral corticospinal tract cross the midline?

A

85% cross at the junction of the medulla and the spinal cord and go on to form the lateral corticospinal tract

15% descend as the anterior corticospinal tract and cross at the level at which they terminate

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43
Q

where is the location of synapse for fibres in the lateral corticospinal tract?

A

synapse with the LMNs in the anterior horn of the spinal cord

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44
Q

need to know blood supply to the spinal cord

A

look on page 24 of B&B notes and lab 5 from neuroanatomy

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45
Q

how many arteries supply the posterior of the spinal cord?

A

2–the posterior spinal arteries

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46
Q

how many arteries supply the anterior of the spinal cord?

A

1–the anterior spinal artery

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47
Q

name two branches of the internal carotid artery

A

middle cerebral and anterior cerebral arteries

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48
Q

what arteries make up the circle of willis?

A

posterior cerebral artery, posterior communicating artery (one on each side), anterior cerebral arteries and anterior communicating artery (which joins the anterior cerebral arteries)

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49
Q

in what fissure does the anterior spinal artery (ASA) run?

A

anterior median fissure

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50
Q

what makes up the ASA?

A

branches off each vertebral artery join to form the ASA

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51
Q

how are the spinal segments supplied by the ASA?

A

5-9 sulcal branches go to each spinal segment from the ASA

each branch supplies the anterior 2/3 of either the right or left side of the segment

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52
Q

what makes up the posterior spinal arteries?

A

arise from vertebral arteries or PICAs

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53
Q

what sulci do the posterior spinal arteries run in?

A

posterolateral sulci

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54
Q

how much of the spinal cord do they posterior spinal arteries supply?

A

posterior 1/3

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55
Q

what arteries give off the coronal arteries that form the corona around the spinal cord?

A

the ASA and PSAs give off branches (coronary arteries) that anastamose with each other and form the corona

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56
Q

what is the purpose of the radicular arteries?

A

circulation to the spinal cord is reinforced by radicular arteries which are branches from cervical, intercostal, lumbar and sacral arteries that arise segmentally, enter the vertebral canal at the intervertebral foramina, anastamose with coronal arteries and (from the lower cervical area down) with the ASA and PSAs

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57
Q

how does the major blood supply differ between the upper cervical and lower cervical and below regions of the spinal cord?

A

the ASA and PSAs provide the major blood supply to the upper cervical cord

beginning with lower cervical segments, large supply comes from the radicular arteries

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58
Q

what is the great radicular artery and where do you find it?

A

aka artery of Adamkiewicz

present at about T12

provides major supply for the lumbosacral spinal cord

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59
Q

where do the ASA and PSAs receive their blood supply from?

A
  1. vertebrobasilar system

2. segmental arteries

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60
Q

what is the major excitatory neurotransmitter involved in spinal cord function?

A

glutamate

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61
Q

what is the function of the neurotransmitter glutamate in spinal cord function?

A

at the AMPA receptor: glutamate acts by opening NA and K channels when glutamate binds–> this causes an EPSP

at the NMDA receptor: when the cell is already depolarized, this receptor allows Ca to permeate

good: calcium causes protein phosphorylation–> synaptic plasticity results–> LEARNING
bad: excitotoxicity and neuron death from too much CA influx

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62
Q

what are the major inhibitory neurotransmitters in spinal cord function?

A

glycine and GABA

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63
Q

does glycine act pre-synaptically or post-synaptically?

A

post-synaptically

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64
Q

does GABA act pre-synaptically or post-synaptically?

A

both

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65
Q

what is the function of glycine in spinal cord function?

A

inhibitory

involved in post-synaptic inhibition (i.e Cl- channels open and cause IPSP)

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66
Q

what is the function of GABA in spinal cord function?

A

inhibitory

get pre-synaptic inhibition by GABA-B receptors–> act by decreasing Ca in the presynaptic vesicales

also acts via GABA-A receptor to open chloride channels and cause post-synaptic inhibition

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67
Q

what is spastic paralysis? what type of lesions cause it?

A

UMN lesions

increased muscle tone AND hyper-reflexive below level of the lesion

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68
Q

why do you get spastic paralysis with UMN lesions?

A

because the inhibitory descending influences are lost with an UMN lesion

especially in the RETICULAR FORMATION in the brainstem, which gives rise to the reticulospinal tracts –> UMN lesion may cause loss of mostly-inhibitory reticulospinal influences (i.e increased gamma motor neuron activity) and therefore increased sensitivity to stretch in the muscle spindle

these inhibitory influences are responsible for modulation and control of downstream LMNs–> when they are absent, this control is lost and spasticity is produced

the pathophysiologic basis of spasticity is incompletely understood–there are some other theories as to why muscle becomes spastic in upper motor neuron lesions. The changes in muscle tone probably result from alterations in the balance of inputs from reticulospinal and other descending pathways to the motor and interneuronal circuits of the spinal cord and the absence of an intact corticospinal system

once spasticity is established, the chronically shortened muscle may develop physical changes such as shortening and contracture that further contribute to muscle stiffness

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69
Q

where do the reticulospinal tracts arise from in the CNS?

A

the reticular formation in the brainstem

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70
Q

what causes the increase in stretch reflexes seen in spasticity?

A

not well understood

unlike healthy subjects, in whom rapid muscle stretch does not elicit reflex muscle activity beyond the normal short-latency tendon reflex, patients with spasticity experience prolonged muscle contraction when spastic muscles are stretched

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71
Q

what fibers from the nocireceptors convey pain?

A

A-delta and C fibers (fast and slow)

respond maximally to intense stimuli

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72
Q

what happens when intense, repeated or prolonged stimuli are applied to damaged or inflamed tissues?

A

the threshold for activating primary afferent nocireceptors is lowered and the frequency of firing is higher for all stimulus intensities (i.e in sensitized tissues, normally innocuous stimuli can cause pain)

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73
Q

describe the path of the axons of primary afferent nocireceptors and then neurotransmitters they use at synapse

A

axons of primary afferent nocireceptors enter the spinal cord via the dorsal root and terminate in the dorsal horn of the spinal gray matter

they contact the spinal neurons that transmit pain signals to the brain sites involved in pain perception by releasing GLUTAMATE as a neurotransmitter as well as substance P and calcitonin gene related peptide which rapidly excites dorsal horn neurons

the axons of primary afferent nocireceptors contact many spinal neurons and each spinal neuron receives convergent inputs from many primary afferents (SPATIAL SUMMATION)

there is also temporal summation which occurs when the afferent signal frequency increases

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74
Q

what is the ASCENDING pathway for pain sensation?

A

SPINOTHALAMIC TRACT

axons enter the spinal cord from spinal ganglion then travel up or down 1-2 segments in LISSAUR’S tract

synapse in the posterior horn

axons of secondary neurons cross the midline in the ANTERIOR WHITE COMMISURE and ascend as the spinothalamic tract

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75
Q

what are the DESCENDING pathways for pain modulation?

A

inputs from the FRONTAL CORTEX and HYPOTHALAMUS activate cells in the MIDBRAIN that control spinal pain transmission via cells in the MEDULLA –> can either enhance or suppress pain

pain suppressing activities of this pathway is mainly via OPIOID receptors and endogenous opioid peptides like ENKAPHALINS and BETA-ENDORPHIN

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76
Q

name two endogenous opioid peptides the body uses in pain suppression

A

enkaphalins and beta-endorphins

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77
Q

what role do prostaglandins play in pain sensation?

A

prostaglandins sensitize afferent nerve terminal nociceptive receptors (stimulated by mechanical or chemical stimuli) to actions to mediators such as bradykinin and serotonin leading to the sensation of pain

inhibitors of the COX pathway thus produce analgesia

this is especially effective in treating mild to moderate pain conditions

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78
Q

is acetaminophen cox selective?

A

no it is NON cox selective

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79
Q

how does acetaminophen produce analgesia?

A

exact mechanism of action is unknown but it is known to mediate its actions CENTRALLY

thought to act primarily in the CNS and increase the pain threshold by inhibiting COX (and thus prostaglandin synthesis)

appears to be a potent inhibitor of both isoforms of COX (1 and 2) within the CNS

does NOT inhibit cox in peripheral tissues –> reason for its lack of peripheral anti-inflammatory effects

may also inhibit synthesis or actions of chemical mediators that sensitize the nocireceptors to mechanical or chemical stimulation

also has antipyretic activity

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80
Q

how do NSAIDs and acetaminophen differ in their site of function?

A

acetaminophen, unlike NSAIDs, does not inhibit cox in peripheral tissues (and thus acetaminophen does not have the same peripheral anti-inflammatory effects)

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81
Q

how does acetaminophen exert its anti-pyretic activity?

A

blocks the effects of endogenous pyrogen on the hypothalamic heat-regulating center by inhibiting prostaglandin synthesis

heat is dissipated by vasodilation, increased peripheral blood flow, and sweating

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82
Q

how do NSAIDs exert their analgesic and anti-pyretic activities?

A

most NSAIDs are NON-selective inhibitors of cox enzymes

anti-pyretic effects are mediated via inhibition of cox production of prostaglandins (PGE2) within the hypothalamus

anti-inflammatory action is mainly related to COX2 inhibition, while unwanted side effects are largely due to COX 1 inhibition (i.e GI disturbances, sin reactions and renal insufficiency)

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83
Q

how does ASA (aspirin) exert its analgesic effects?

A

NSAID

anti-inflammatory, analgesic and anti-pyretic

the antithrombotic actions of aspirin are primarily COX1-inhibition mediated as COX 1 normally produces TXA2 which promotes platelet aggregation

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84
Q

what type of receptors are opioid receptors?

A

7 transmembrane G protein coupled receptors

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85
Q

what is the MOA of opioids?

A
  1. post synaptic–> hyperpolarization of neurons by opening of K+ channels
  2. pre-synaptic–> reduction of excitatory transmitter release (i.e glutamate, peptides, tachykinin)
  3. activation of inhibitory enkephalin interneuron in the dorsal horn of the spinal cord
  4. activation of inhibitory descending pathway
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86
Q

what are the sites of action of opioids?

A

brain

brainstem

spinal cord

primary afferent neurons

medullary respiratory center

medullary chemoreceptor center

GI tract

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87
Q

what are the four opioid receptor types?

A

Mu1

Mu2

Delta

Kappa

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88
Q

what opioid acts at the Mu1 receptor? what is its action?

A

morphine

supraspinal analgesia

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89
Q

what opioid acts at the Mu2 receptor? what is its action?

A

morphine

respiratory depression

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90
Q

what opioid acts at the delta receptor? what is its action?

A

enkephalins

spinal analgesia

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91
Q

what opioid acts at the kappa receptor? what is its action?

A

dynorphin A

spinal analgesia and sedation

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92
Q

list 4 natural alkaloids extracted from opium

A

morphine

codeine

papaverine

thebaine

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93
Q

list 3 synthetic opioids

A

meperidine

fentanyl

methadone

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94
Q

list 3 endogenous opioid peptides

A

endorphins

enkephalins

dynorphins

*these are not used clinically

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95
Q

what does propriomelanocortin become? i.e what is a a precursor to

A

aka POMC

it is the precursor to beta-endorphin

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96
Q

list some of the characteristics of endogenous opioid peptides

A
  • mimic most effects of morphine
  • antagonized by naloxone
  • produce tolerance
  • produce physical dependence
  • participate in endogenous control mechanisms
  • modulate nocireceptive transmission
  • may be responsible for placebo effect
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97
Q

list the various modes of delivery for opioids (i.e systemic, neuraxial, local)

A
  1. systemic
    - oral
    - SC/IM/IV
    - IV via patient controlled analgesia (PCA) pump (i.e morphine, fentanyl, hydromorphone)
    - suppository (rectal)
    - nasal/oral mucosa
    - skin (i.e fentanyl transdermal patch)
  2. neuraxial
    - spinal (subarachnoidal)
    - epidural (i.e morphine…results in long acting 24 hours analgesia)
  3. local
    - intra-articular
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98
Q

describe the absorption of opioids. what is special about the absorption of

  1. morphine
  2. codeine
  3. heroin?
A

most opioids are absorbed readily (GI tract, SC/IM sites, mucosa, skin)

  1. morphine–> higher hepatic first pass metabolism and lower oral bioavailability (around 20-40% due to first pass metabolism)
  2. codeine–> higher oral bioavailability (around 60%)
  3. heroin–> high lipid solubility and BBB penetration
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99
Q

how is morphine metabolized?

A

hepatic conversion to morphine-6-glucoronide (ACTIVE METABOLITE) and morphine-3-glucoronide (which is excitatory and toxic… high concentrations cause myocloni and seizures)

100
Q

how is meperidine metabolized? what type of drug is it?

A

opioid

hepatic conversion to normeperidine (excitatory and toxic, can cause seizures)

101
Q

how are heroin and codeine metabolized?

A

conversion to morphine

102
Q

how is remifentanil metabolized?

A

rapid hydrolysis by nonspecific esterases–> useful for continuous, easily adjustable IV infusion in anesthesia

103
Q

how is morphine excreted?

A

90% as glucoronides in the urine

10% unchanged in bile, feces

104
Q

list the central effects of opioids (10)

A
  1. analgesia
  2. hyeralgesia (at high doses)
  3. cough suppression
  4. euphoria (also dysphoria)
  5. sedation
  6. respiratory depression (decreased resp rate)
  7. nausea and vomiting
  8. pruritus (itching)
  9. miosis (pupillary constriction)
  10. truncal rigidity
  11. convulsions
105
Q

list the peripheral effects of opioids (6)

A
  1. constipation
  2. urinary retention
  3. constriction of the sphincter of Oddi (increased biliary colic)
  4. histamine release (direct mast cell degranulation)
  5. bradycardia (no other significant effects on the heart)
  6. hypotension (due to vasodilation)
106
Q

what are some therapeutic uses for opioids (general classes)?

A

analgesia
cough suppression
antidiarrheal therapy
acute pulmonary edema

107
Q

in what types of cases would you use opioids for analgesia?

A
  1. acute pain (moderate to severe i.e acute MI, acute post-op pain)
  2. cancer pain (i.e oral morphine)
  3. anesthesia (blunt hemodynamic response to intubation and surgery)
108
Q

what opioids might you use as cough suppressants?

A

codeine or dextromethorphan

109
Q

what opioids might you use as antidiarrheal therapy?

A

loperamide

diphenoxylate

110
Q

what opioids might you use in the setting of acute pulmonary edema? why?

A

IV morphine

to increase pulmonary vasodilation

111
Q

list the therapeutic principles that govern clinical opioid use

A
  1. individualize route, dosage and schedule
  2. administer analgesics regularly (not PRN) if pain is present most of the day
  3. become familiar with dose and time course of several strong opioids
  4. follow patients closely, particularly when beginning or changing analgesic regimens
  5. when changing to a new opioid or different route, use an equianalgesic dosing table to estimate the new dose–> modify the estimate based on clinical situation
  6. recognize and treat SEs
  7. be aware of the potential hazards of meperidine and mixed agonist-antagonists, particularly pentazocine
  8. do not use placebos to assess the nature of pain
  9. watch for the development of tolerance and treat appropriately
  10. be aware of the development of physical dependence and prevent withdrawal
  11. do not label a patient “addicted” (psychologically dependent) if you merely mean physically dependent on or tolerant to opioids
  12. be alert to the psychological state of the patient
112
Q

what is tolerance (with regards to opioids)? when does it begin in opioid use? what physiological effects of opioids do not develop tolerance?

A

it is defined as an incraese in dose required to produce a given pharmacological effect

begins with the FIRST opioid dose

NO tolerance to miosis or constipation

cross tolerance among opioids

113
Q

define dependence (i.e on opioids)

A

defined by the occurrence of withdrawal symptoms (physical) and/or craving for the drug (psychological)

114
Q

list two opioid receptor antagonists

A

naloxone and naltrexone

115
Q

how do the opioid receptor antagonists naloxone and naltrexone act?

A

antagonists at Mu, delta and kappa opioid receptors

almost do effects when given in the absence of agonists (therefore there is little risk to giving them to a patient if you suspect an opioid overdose, even if it turns out they are not actually overdosing)

rapid reversal of agonist effects (i.e reversal of respiratory depression, sedation, miosis, analgesia)

NO TOLERANCE

potential to PRECIPITATE WITHDRAWAL sx in dependent patients

116
Q

how would an opioid overdose present?

A

clinical triad of:
COMA
MIOSIS
RESPIRATORY DEPRESSION

117
Q

what is the treatment for an opioid overdose?

A

general measures: maintain/monitor ABCs, 100% oxygen

specific measures: naloxone IV

118
Q

what are some contraindications or cautions for opioid use?

A
  1. respiratory disease (i.e COPD, obstructive sleep apnea due to risk of respiratory arrest)
  2. drug interactions (i.e meperidine and MAO inhibitors can cause hyperpyrexic coma; opioids and sedatives/ethanol can cause increased CNS depression leading to pulmonary aspiration and respiratory depression)
  3. pregnancy (physical dependence of fetus)
  4. use of pure agonists with agonist-antagonists (decreases analgesia and may cause withdrawal)
119
Q

what other drug is contraindicated for use with the opioid meperidine?

A

MAO inhibitors

can cause hyperpyrexic coma

120
Q

what general class of drug is contraindicated for use with opioids in general?

A

sedatives/ethanol

increases CNS depression can potentially lead to pulmonary aspiration and respiratory depression

121
Q

how many sphincters make up the anal sphincter?

A

2–internal and external

122
Q

what type of muscle is found in the internal anal sphincter?

how much is the internal anal sphincter responsible for the anus’ resting tone?

A

smooth muscle (involuntary)

accounts for 85% of resting tone

123
Q

what innervates the internal anal sphincter?

A

innervated by intestinal MYENTERIC PLEXUS (sympathetic and parasympathetic, both of which are INHIBITORY) which keeps the sphincter in a constant state of contraction

parasympathetic supply is from the NERVI ERIGENTES (S2, 3, 4)

sympathetic innervation is from the L1-3 via the PREAORTIC PLEXUS

124
Q

what type of muscle is found in the external anal sphincter?

how much is the external anal sphincter responsible for the resting tone of the anus?

A

skeletal muscle, voluntary

15% of resting tone

125
Q

which sphincter–internal or external–is responsible for the voluntary squeeze pressure of the anus?

A

external (100%)

126
Q

what innervates the external anal sphincter?

A

pudendal nerve (S2, 3, 4)–voluntary

127
Q

describe the process of defecation and the reflexes involved

A

it is a complex mechanism that is not clearly understood–> anal sphincter function as a unit with levator ani, puborectalis and rectum

periodically, the internal sphincter relaxes and allows the rectal contents to drop down into the anal canal where it is sensed by the anoderm

in response, the external sphincter contracts and the contents is pushed back up into rectum

this “sampling reflex” (aka the “rectoanal inhibitory reflex”) occurs up to 7 times a day

progressive distension of the rectum causes continuous inhibition of the anal sphincter, and relaxation of the external sphincter, resulting in an urge to defecate

when one wishes to defecate, sitting/squatting position is assumed, valsalva maneuver is initiated, puborectalis relaxes, and reflex relaxation of internal sphincter occurs

128
Q

describe the sacral reflex pathway associated with the bladder and bladder function. How does this differ between infants and adults?

A

when stretch receptors in the bladder wall are activated, the afferent fibers go via the pelvic nerve to the sacral cord (S2, 3, 4)–> parasympathetic nerve cell bodies are activated–> contraction of detrusor muscle

in infants, this is the only pathway controlling urinary voiding (no control over external sphincters)

in adults, the external sphincter is under somatic control through the pudendal nerve

129
Q

describe the neural process/pathway of bladder voiding in the adult

A

in adults, the external sphincter is under somatic control through the pudendal nerve:

  • awareness of bladder fullness is relayed to the cortex and the PAG
  • when it is socially acceptable to void, the pontine micturition center is activated through both the cortex and the PAG
  • this activation of the PMC excites the parasympathetics (S234) causing the detrusor muscle to contact
  • at the same time, the sympathetics (T12 and L1) are inhibited and the internal sphincter is relaxed
  • in addition, the somatic control for the external sphincter via the pudenal nerve is inhibited (via Onuf’s nucleus at S234)
130
Q

what is the role of the pontine micturition center in bladder voiding?

A

when stimulated by both the cortex and the PAG, the PMC inhibits the sympathetics (T12, L1) that innervate the internal sphincter, excite the parasympathetics that innervate the detrusor muscle (S234) and inhibits Onuf’s nucleus (S234)

131
Q

what is the role of Onuf’s nucleus in bladder control and voiding?

A

most of the time, Onuf’s nucleus keeps the external sphincter contracted and thus closed to prevent involuntary urination (pudenal/S234)

when it is inhibited by the pontine micturition center, the external sphincter relaxes

132
Q

what tell the cortex and PAG that you need to urinate?

A

mechanoreceptors in the bladder than sense distension

133
Q

what afferent pathways (nerves and tracts) are involved in erection (and lubrication) sexual responses?

A

genital stimulation

touch/rub–> pudendal nerve–> S234–> spinothalamic tract and dorsal columns

deep pressure/visceroreceptive–> pelvic and hypogastric nerves–> thoracolumbar roots

134
Q

what efferent pathways (nerves) are involved in psychogenic erection?

A

sympathetic and other fibers carried in T10-L3

135
Q

what efferent pathways (nerves) are involved in reflex erection?

A

parasympathetic and motor fibers carried in S234

136
Q

how does the innervation for the efferent pathways differ between psychogenic and reflex erections?

A

psychogenic: sympathetic and other fibers in T10-L3
reflex: parasympathetic and motor fibers in S234

137
Q

what is the afferent pathway (nerves and tracts) involved in ejaculation?

A

somatic stimulation–> pudendal nerve–> S234–> cross somewhere between T10 and S4–> SPINOTHALAMIC TRACT

138
Q

what are the efferent pathways involved in ejaculation? differentiate between stage 1 (seminal emission) and stage 2 (spasmodic contraction and ejection)

A

stage 1: seminal emission

  • sympathetic (T10-12)
  • responsible for sperm transport, seminal fluid formation

stage 2: spasmodic contraction and ejection

  • parasympathetic (S234)–> contraction of the seminal vesicles, prostate and urethra
  • sympathetic (S234)–> contraction of the levator ani, bulbospongiousus, ischiocavernosus, related muscles
139
Q

what are the afferent pathways involved in genital orgasm?

A

genital/body stimuli–> SPINOTHALAMIC TRACT

cerebral stimuli also play a role

140
Q

what is the efferent pathway involved in genital orgasm?

A

CORTICOSPINAL TRACT

141
Q

what two tracts (one ascending and one descending) are involved in genital orgasm?

A

ascending–> spinothalamic

descending–> corticospinal

142
Q

what is the etiology of central cord syndrome (small lesion)?

A

TRAUMA with UNDERLYING spinal stenosis, intramedullary tumour or syringomyelia

143
Q

what is central cord syndrome (small lesion)? what fibers/tracts are affected? what are symptoms?

A

damage to SPINOTHALAMIC FIBERS crossing in the anterior white commisure

results in SUSPENDED sensory loss to pain and temperature (i.e cape distribution if lesion is in the cervical cord)

144
Q

what is central cord syndrome (large lesion)? what are symptoms of different lesions?

A
  1. anterior horn cells damaged–> LMN deficits at the level of the lesion
  2. corticospinal tract affected–> UMN signs (spasticity, hyerpreflexia, increased deep tendon reflexes)
  3. anterolateral spinothalamic tracts affected–> near complete loss of pain and temperature EXCEPT FOR SACRAL SPARING
  4. posterior columns may be affected–> loss of vibration and position sense
145
Q

what is the etiology of central cord syndrome (large lesion)?

A

NONtraumatic or POSTtraumatic syringomyelia

146
Q

what is a syringomyelia?

A

Syringomyelia (sear-IN-go-my-EEL-ya) is a disorder in which a cyst forms within the spinal cord. This cyst, called a syrinx, expands and elongates over time, destroying a portion of the spinal cord from its center and expanding outward. As a syrinx widens it compresses and injures nerve fibers that carry information from the brain to the extremities. Damage to the spinal cord often leads to progressive weakness in the arms and legs, stiffness in the back, shoulders, arms, or legs, and chronic, severe pain.

147
Q

what is the etiology of complete cord injury?

A

trauma, cord compression by tumor or abscess, transverse myelitis, MS

148
Q

what are the symptoms/presentation of complete cord injury?

A

loss of all motor, sensory and sphincter function below the level of the lesion

spinal shock is common–> hypotonia, hyporeflexic (loss of supraspinal descending input) below lesion lasting days to weeks

149
Q

what is another name for Brown Sequard Syndrome? (i.e what is the abnormality)

A

spinal cord hemisection

150
Q

what is the etiology of spinal cord hemisection/brown sequard syndrome?

A

penetrating cord injury (stab or gun wound), lateral compression from extrinsic cord lesions (Schwannoma tumor/disc), blunt spinal cord trauma laterally, MS

151
Q

what are the symptoms of spinal cord hemisection?

A
  1. lateral corticospinal tract affected–> UMN weakness ipsilateral to side of lesion
  2. posterior column affected–> IPSILATERAL loss of vibration and position sense
  3. lateral spinothalamic tract affected–> CONTRALATERAL loss of pain and temperature sensation

**loss of contralateral pain and temp sensation often begins slightly below the lesion since the fibers ascend 2-3 segments as they cross the anterior white commissure

**may be some strips of IPSILATERAL loss of pain and temp due to damage to posterior horn cells before their spinothalamic axons have crossed over

152
Q

what is the etiology of anterior cord syndrome?

A

anterior spinal artery infarct due to thrombosis, embolism, surgery on descending aorta (artery of adamkiewicz usually arising on the L between T9-L2), trauma, MS

153
Q

what are the symptoms of anterior cord syndrome?

A
  1. anterolateral pathways damaged–> loss of pain and temp sensation below lesion
  2. damage to anterior horn cells–> LMN deficits at level of lesion
  3. lateral corticospinal tracts affected–> UMN signs (spasticity, hyperreflexia)

**INCONTINENCE commonly involved because of descending tracts controlling sphincter function are more VENTRALLY located

154
Q

what bodily function is often affected in anterior cord syndrome? why?

A

INCONTINENCE commonly involved because of descending tracts controlling sphincter function are more VENTRALLY located

155
Q

what is the etiology of posterior cord syndrome?

A

vitamin B12 deficiency (subacute combined degeneration), trauma, extrinsic compression from posteriorly located tumors, MS, tabes dorsalis (tertiary neurosyphilis)

156
Q

what are the symptoms of posterior cord syndrome?

A
  1. posterior column and spinocerebellar lesions–> loss of vibration and conscious proprioception below the level of the lesion
  2. possible involvement of lateral corticospinal tracts–> UMN weakness
157
Q

what is the etiology of cauda equina syndrome?

A

large central disc herniation, L spine # or sublux, epidural metastatic tumor, hematoma or abscess

158
Q

what are the symptoms of cauda equina syndrome?

A

LMN features –> impaired function of multiple nerve roots below L1/2

saddle anesthesia–> S2-S5–> decreased sensation

159
Q

contrast apoptosis to ischemic damage. what histological features are shown by neurons experiencing apoptosis and/or ischemic damage?

A

apoptosis is:

  1. programmed cell death
  2. due to external causes (i.e cytokines, physical and chemical agents)
  3. single cell death
  4. initially nuclear (the nucleus dies first)

ischemic damage is:

  1. accidental cell death
  2. due to an external cause which is ISCHEMIA (vascular in origin)
  3. clusters of cell die
  4. initially mitochondrial (mitochondria die first)

both apoptotic and ischemic neurons exhibit the same histological features:

  1. acutely angulated cell body
  2. pyknotic nucleus –> karyorrhexis (fragmentation of the nucleus)
160
Q

what is excitotoxicity?

A

the role of neuronal excitation in ischemic cell death

ischemia–> glutamate release–> activation of glutamate receptors–> influx of Na+–> activation of voltage dependent Ca2+ channels–> influx of Ca2+–> neuronal injury

**some neurons appear to be more vulnerable to ischemia than others (i.e those with glutamate receptors or those with increased intracellular calcium (neurons that have just fired an AP)

161
Q

what is neuronal loss?

A

reduced numbers of neurons in the absence of frank tissue destruction

can be due to a variety of causes (nonspecific)

162
Q

list 4 type of neuronal inclusions

A

neuromelanin (normal inclusion)

lipofuscin (due to aging)

degenerative inclusions

viral inclusions

163
Q

what is neuromelanin?

A

a normal neuronal inclusion

a by product of catecholamine synthesis

found in neurons of SUBSTANTIA NIGRA, LOCUS CERULEUS and DORSAL MOTOR NUCLEUS OF VAGUS (which are the catecholamine producing neurons)

different than skin melanin–> found exclusively in neurons

164
Q

what is lipofuscin?

A

a neuronal inclusion due to aging

found mainly in neurons

also found in other cell types in the body

165
Q

what are some degenerative inclusions?

A

neuronal inclusions

of various types

may or may not be specific for a given disease

i.e Parkinson’s patients have Lewy body neuronal inclusions in the substantia nigra

166
Q

what are some viral inclusions?

A

neuronal inclusions

nuclear and/or cytoplasmic

for example: Cowdry Type A viral inclusions in nuclei found in herpes simplex encephalitis

167
Q

what types of inclusions may be found in patients with parkinsons?

A

degenerative–> lewy bodies in neurons in substantia nigra

168
Q

what types of inclusions may be found in patients with herpes simplex encephalitis?

A

Cowdry Type A viral inclusions

169
Q

how does the axon respond to axonal transection?

A
  1. wallerian degeneration (distal change)
    - degeneration of the distal fragment of the axon–> AXONOLYSIS (phagocytosis of the axon by macrophages) and MYELINOLYSIS (phagocytosis of the myelin by macrophages)
  2. central chromotolysis
    - swollen cell body, displaced nucleus and dispersed Nissl substance –> increased mRNA synthesis–> increased protein synthesis–> transported down the axon in an attempt to repair the transection (in the CNS this is futile as axons do not regenerate. In the PNS this may be effective)
  3. axonal “retraction balls” (proximal change)
    - damming up of organelles conveyed by axonal transport to proximal stump of axonal transection site
170
Q

how does the axon respond to axonal degeneration?

A

axonal spheroids (degenerating organelles)

  • seen in “neuroaxonal dystrophies” which are a group of diseases thought to be due to primary degeneration of axons, usually inherited
  • seen in certain locations in aging (i.e spinal cord posterior columns)
  • similar to axonal retraction balls on light microscopy, but ultrastructurally different
171
Q

what happens if there is an abnormality in the number, size, or shape of dendritic spines?

A

mental retardation (of various causes) and epilepsy can result

172
Q

what is the function of oligodendrocytes?

A

generation and maintenance of myelin

173
Q

how do the oligodendrocytes respond to axonal damage?

A
  1. primary demyelination–> macrophage removes myelin, axon remains relatively intact
  2. remyelination–> focal regeneration of myelin, occurs in both the CNS and PNS. the new myelin is thinner and has more nodes of Ranvier (i.e a shorter internodal distance)
  3. hypomyelination–> diffuse regeneration of myelin–> the new myelin is thinner and has more nodes of ranvier (as above)
  4. partial demyelination–> thinned myelin (often varies in thickness
174
Q

what is the function of astrocytes?

A

they are the “SCAR” cells of the CNS

have a SUPPORTIVE and STRUCTURAL component

forms a syncytium (multinucleated cell) throughout the CNS

undergo glycolysis for energy

GLUTAMATE and GABA uptake

pH regulation

regulation of osmolarity

spatial buffering of K+

glutamine for glutamate synthesis

part of the BBB (processes extend and latch onto blood vessels via foot processes)

175
Q

what are the types of astrocytes?

A
  1. protoplasmic–> in grey matter (thicker processes)

2. fibrous–> in white matter (long, skinny processes)

176
Q

how do astrocytes respond to axonal damage?

A

astrocyte SWELLING

GLIOSIS–> early changes involve hyerplasia, hypertrophy, upregulation of GFAP (glial fibrillary acidic protein)–> this makes the astrocytes look plump

astrocyte INCLUSIONS–> rosenthal fibers (linear/corkscrew hyaline inclusions which occur in long standing gliosis)

CORPORA AMYLACEA–> round inclusions of g;ycoprotein in astrocytic foot processes, particularly around blood vessels or near surfaces of the CNS

177
Q

what are ependymal cells?

A

form the lining of ventricles

178
Q

how do ependymal cells respond to damage?

A

when destroyed, they are not replaced with other ependymal cells

form subventricular glial nodule–> (“granular ependymitis”) which is a non specific reaction of subventricular astrocytes to ependymal injury/loss–> astrocytes proliferate and intrude into ventricle

179
Q

what are microglia?

A

CNS cells originally derived from bone marrow

function is to phagocytose and present antigens

180
Q

how do microglia respond to damage?

A

mature into ACTIVATED MICROGLIA in response to CNS injury in the ABSENCE of parenchymal destruction

retain morphology of the resting state

secrete cytokines

express markers (i.e class II MHC, CD4, CD45, cell adhesion molecules, amyloid precursor protein)
----

mature into MACROPHAGES in response to CNS injury WITH parenchymal involvement

transform into macrophage morphology

secrete cytotoxic substances (NO, cytokines, enzymes)

express markers (class II MHC, complement receptors, IgG-Fc receptors)

perform phagocytosis

181
Q

what is meant by the term “immunological privilege of the CNS”?

A

activated T cells are able to BREACH the BBB (“trafficking”)

unactivated T cells do not traffic through the CNS

an immune response in the CNS will only result from a trafficking T cell if:

  1. the T cell receptor recognizes a specific T cell antigen
  2. the antigen is presented in the context of MHC to the T cell (the CNS normally has very few APCs to present antigens to T cells)
182
Q

in terms of imaging the spinal cord, what is one
1. advantage
2. disadvantage
for using RADIOGRAPHS?

what are the mostly used for?

A
  1. simple
  2. ionizing radiation and low resolution/detail

used for analyzing alignment (scoliosis and kyphosis) and for flexion, extension and bending views

183
Q

in terms of imaging the spinal cord, what is one
1. advantage
2. disadvantage
for using CT?

what are the mostly used for?

A
  1. fast, accessible
  2. ionizing radiation

used to look at cortical bone (in the case of trauma), check hardware position after surgery, and to look at calcifications and bone pathologies

184
Q

in terms of imaging the spinal cord, what is one
1. advantage
2. disadvantage
for using MRI?

what are the mostly used for?

A
  1. no radiation
  2. 30-90 min, less accessible, contraindicated: pacemaker, ocular foreign body, patient body habitus, claustrophobia

used to look at the marrow, soft tissues, spinal cord, infections

185
Q

when would you use a therapeutic epidural injection?

A

spinal stenosis–> inject steroids and local aneasthetic

CSF leak–> inject autologous blood patch

186
Q

when would you use a nerve root block?

A

confirm site of pathology

relieves radiculopathy from weeks to months as a temporizing measure

187
Q

what is a facet block/rhizotomy?

A

diagnostic and therapeutic steroid injection

destroys the nerve that innervates the facit with RF ablation

188
Q

when would you do a biopsy?

A

mets, infection

189
Q

when would you use a vertebroplasty?

A

acute osteoporotic compression fractures not responsive to conservative management

treatment of vertebral haemangiomas and palliation of mets

190
Q

when would you do a spinal angiogram?

A

to detect suspected vascular abnormality or tumor (i.e AV malformation)

re-embolize a known vascular abnormality or tumour (i.e renal cell mets to bone)

191
Q

when would you do myelography?

A

rare–> involves doing LP with injection of radiopaque dye

192
Q

what are the symptoms and signs of a complete cord transection?

A

NO motor, sensory or SPHINCTER function below the level of the lesion

193
Q

what is the etiology of complete cord transection?

A

trauma to spinal cord

cord compression (i.e tumour)

194
Q

what is the neuropathology of a complete cord transection?

A

hemorrhage into grey matter

white matter axon disruption

195
Q

what are the symptoms and signs of brown sequard syndrome?

A

pain and temperature loss on CONTRALATERAL side

light touch, vibration and position sense loss on IPSILATERAL side

motor loss on IPSILATERAL side

hyperreflexia bilaterally

196
Q

what is the etiology of brown sequard syndrome?

A

schwannoma (benign tumour)

penetrating injury (i.e gun shot wound)

blunt spinal cord trauma

197
Q

what is the neuropathology of brown sequard syndrome?

A

spinal cord hemisection

198
Q

what are the signs and symptoms of central cord syndrome?

A

pain and temperature sensation loss below the level of the lesion (some spared)

light touch, vibration and position sense NORMAL

deep tendon reflexes are absent at affected levels, increased below

motor –> weakness at affected levels

(arms usually more affected than legs)

199
Q

what is the etiology of central cord syndrome?

A

trauma

syringomyelia

tumour in central cord

200
Q

what is the neuropathology of central cord syndrome?

A

sacral sparing because sacral fibers are most peripheral in the spinal cord

201
Q

what are the signs and symptoms of anterior spinal artery infarct?

A

paralysis and areflexia below the lesion

pain and temperature loss below lesion

light touch, vibration and position sense are NORMAL

202
Q

what is the etiology of anterior spinal artery infarct?

A

thrombosis, embolism

surgery on descending aorta

203
Q

what is the neuropathology of anterior spinal artery infarct?

A

infarction of anterior 2/3 of the cord

204
Q

what are the signs and symptoms of subacute combined degeneration?

A

pain and temperature are not affected until later on

light touch, vibration and position sense are ABSENT below the lesion

weakness has a gradual onset

gait ataxia and positive ROMBERG test

205
Q

what is the etiology of subacute combined degeneration?

A

vitamin B12 deficiency

206
Q

what is the neuropathology of subacute combined degeneration?

A

demyelination of posterior and lateral columns (corticospinal tract and spinocerebellar tracts)

grey matter is SPARED

207
Q

what are the signs and symptoms of acute cauda equina compression?

A

RAPID onset of leg weakness, numbness, sphincter disturbance

ALL sensory modalities are affected

decreased rectal tone

208
Q

what is the etiology of acute cauda equina compression?

A

central disc herniation (L4/L5)

lumbar fracture

epidural tumour, hematoma

209
Q

what is the neuropathology of acute cauda equina compression?

A

herniated disc compresses cord

210
Q

what are the ventricles in the nervous system?

A

cavities in the CNS lined with EPENDYMAL cells (a thin layer of epithelial cells)

CSF circulates within the ventricles and flows out through the apertures to fill the subarachnoid space

211
Q

what produces CSF?

A

the choroid plexus and overlying choroid ependymal cells are responsible for the production of CSF

the choroid plexus is found in all 4 ventricles

212
Q

what forms the choroid ependymal/plexus?

A

at certain locations, the ependyma-pia complex invaginates into the ventricles together with capillaries travelling in the subarachnoid space

here, the ependymal layer becomes cuboidal, forming the choroid ependymal–> this structure is secretory

213
Q

describe the flow of CSF through the ventricles

A

CSF moves from the lateral, to the third, to the fourth ventricles, pushed along by the newly formed CSF

CSF can then move…

  1. into the central canal via the OBEX located in the base of the fourth ventricle
  2. out of the fourth ventricle via two lateral foramina–> foramina of LUSCHKA, or through a central foramen of MAGENDIE into the subarachnoid space

CSF moves through the subarachnoid space until it reaches the ARACHNOID GRANULATIONS or smaller arachnoid villi, which protrude primarily into the superior sagittal sinus (intracranial venous structure)

214
Q

how does CSF move across the arachnoid granulations and villi?

A

movement across the arachnid granulations and villi is passive, driven by the difference in hydrostatic pressure between the subarachnoid space and the superior sagittal sinus

transcytosis may be involved

the granulations and villi act as one way valves, preventing the fluid from returning from the venous system into the subarachnoid space

215
Q

name 4 types of glia

A

oligodendrocyte
microglia
ependyma
microglia

216
Q

can you distinguish between apoptotic neurons and ischemic neurons histologically?

A

no

217
Q

in what cases do you see neuronal cell body vacuolation?

A

cytotoxic ededma

prion diseases (CJD)

218
Q

what are neuroaxonal dystrophies?

A

a group of diseases thought to be due to a primary degeneration of axons, often inherited

219
Q

where are microglia derived from?

A

they are CNS cells originally derived from bone marrow

phagocytic function and antigen presenting

220
Q

name an autoimmune disorder of the CNS myelin sheath

A

MS (it is presumed to be autoimmune)

the initiation and extension of the actively demyelinating plaque in MS is thought to be orchestrated by CD4 T cells in the perivascular spaces in the lesion

there is considerable upregulation of class II MHC on microglia and macrophages

CD4 T cells recruit macrophages to carry out the demyelination

cytotoxic T cells and IgG from B cells also probably have roles in pathogenesis

antigens are not known

221
Q

define pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

  • *pain is ALWAYS subjective
  • pain is that experience we associate with actual or potential tissue damage
  • experiences which resemble pain but are not unpleasant (i.e pricking) should not be called pain

**if the patient regards their experience as pain and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain (even in the absence of clinically observable tissue damage)

222
Q

define analgesia

A

absence of pain in response to a stimulus that would normally be painful

223
Q

list drugs used in acute pain

A

acetaminophen

ASA and other NSAIDs

combination preparations (i.e acetaminophen with codeine)

local anesthetics

other drugs (clonidine, ketamine)

opioid analgesics

224
Q

define narcotics

A

drugs that produce sleep

225
Q

define opiates

A

drugs that are derived from opium

226
Q

define opioids

A

drugs that bind to the OPIOID RECEPTOR

227
Q

what is the best imaging tool to look at the spinal cord?

A

MRI

i.e MS, tumours, myelopathy, syringomyelia, cord compression

228
Q

list complications of LPs

A

infection

headache

CSF leak

epidural hematoma

229
Q

what is Klippel-Feil syndrome?

A

failure of segmentation of the vertebrae, resulting in fusion of the vertebrae

230
Q

how does the anterior longitudinal ligament attach to the vertebral body?

A

sharpey’s fibers

231
Q

what is the function of spinal interneurons? where are they found?

A

they are the building blocks of spinal reflexes

confined to spinal cord and influence nearby neurons

can span spinal segments (propriospinal interneurons)

have excitatory or inhibitory connections (can form patterns)

232
Q

what type of connections (inhibitory or excitatory) are found between peripheral afferents and the CNS?

A

ALL the connections between peripheral afferents and CNS neurons are EXCITATORY

CNS is always receiving excitatory input

this requires balance, then, by CNS inhibition –> processing often removes unwanted inputs

233
Q

which is more selective: pre or post synaptic modulation? why?

A

presynaptic

it is selective inhibition that decreases the effectiveness of one or a few inputs to a neuron

it does NOT affect other inputs or the post-synaptic membrane potential–> postsynaptic effects will affect ALL inputs to a neuron because of changes in the membrane potential

234
Q

what is the major neurotransmitter in presynaptic inhibition?

A

GABA

GABAa receptors–> Cl- conductance and shunting of AP

GABAb receptors–> G protein coupled modulation of K+ and CA2+ channels

235
Q

what is the transmitter at the neuromuscular junction?

A

Ach

activates Renshaw cells

236
Q

what are renshaw cells?

A

Renshaw cells are inhibitory interneurons found in the gray matter of the spinal cord, and are associated in two ways with an alpha motor neuron.

They receive an excitatory collateral from the alpha neuron’s axon as they emerge from the motor root, and are thus “kept informed” of how vigorously that neuron is firing.
They send an inhibitory axon to synapse with the cell body of the initial alpha neuron and/or an alpha motor neuron of the same motor pool.
In this way, Renshaw cell inhibition represents a negative feedback mechanism. A Renshaw cell may be supplied by more than one alpha motor neuron collateral and it may synapse on multiple motor neurons.

237
Q

how is local control in the spinal cord achieved?

A

recurrent inhibition and renshaw cells –> autoregulation of motor neurons firing

glycine is the dominant transmitter, with GABA

238
Q

what are the major mediators of postsynaptic inhibition in the spinal cord?

A

glycine receptors

tetanus is the result of dysfunction of glycinergic recurrent inhibition

239
Q

what does the reticulospinal tract do?

A

activity controls posture and strength of reflexes

interruption in pathways leads to deficits

240
Q

what two types of neuronal damage may result from a CNS lesion?

A
  1. neuronal cell death (at site of lesion and in close proximity)
  2. isolation of interneural function resulting from interruption of activity in neural networks (this process causes a much greater initial loss of function than could be accounted for by the loss of neurons)
241
Q

what happens when a CNS lesion interrupt descending input to the interneurons?

A

“releases” spinal interneurons–> as many are inhibitory, this “release” results in unrestricted flow of excitation reaching motor neurons unchecked–> hyperreflexia

242
Q

in what muscles does spasticity tend to be more pronounced?

A

in the anti-gravity muscles

243
Q

how does benzodiazepine diazepam (Valium) exert anti-spastic action?

A

by increasing the frequency of GABAa receptor channel openings and thus enhancing POSTsynaptic inhibition in the spinal cord

244
Q

how does Baclofen (Lioresal) reduce spasticity?

A

by activating PREsynaptic GABAa receptors and thus inhibiting glutamate release from afferent fibers

245
Q

list mechanisms of neuronal recovery

A
  1. changes in synaptic contact
    - unmasking–> reveal previously “silent” connections
    - sprouting–> growth of new synapses
    - transplantation
  2. neuromodulators of morphological changes

B&B Part 1 (4 decks)

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