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Nerves Flashcards

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1
Q

What does the CNS consist of?

A
  • Brain and spinal cord
    • Terminates at L1
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2
Q

What does the PNS consist of?

A
  • ** Cranial ( 12 pairs)**
  • Spinal ( 31 pairs)
  • and peripheral nerves
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3
Q

What does the autonomic nervous system consist of?

A
  • Sympathetic and parasympathetic systems
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4
Q

What does the CNS control?

A
  • Somatic and visceral function
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5
Q

What does the PNS do?

A
  • relays information from the periphery to the brain and vice versa
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6
Q

What do afferent ( sensory) nerve fibres transmit?

A
  • Somatic and visceral information from the periphery to the brain
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7
Q

What do the efferent ( motor) nerves transmit?

A
  • Somatic and autonomic information from the brain to the periphery
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8
Q

What is the basic functional unit of a nerve?

A
  • Cell body
  • Axon
  • the axolemma ( cell membrane ) encloses the axoplasm ( cytoplasm)
  • Dendrites- branch out from the cell body and conduct impulses to other cell bodies
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9
Q

What is a nerve composed of?

A
  • Fascicles or bundles ( groups of sheathed axons) of nerve fibres
  • Endoneurieum
    • connective tissue covering the nerve fibres
    • longitudinally arranged collagen fibres, fibroblasts and blood vessels
  • Perineurieum
    • envelops the nerve fibre bundles -> a fascicle
    • consists of alternating layers of collagen and cell processes acting as a diffusion barrier
  • Epineurium
    • conists of collagen and fibroblasts acting as a supporting structure for nerve fasciles grouped into a nerve trunk
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10
Q

Describe the blood supply to neves?

A
  • Intrinsic plexus
    • ​distributed in longitudinal fashion in endoneurium, perineurium and epideneurium
  • Extrinsic plexus
    • vessels are segmental
    • found in the paraneurium ( layer external to the perineurium)
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11
Q

What is the neuron supported by in the Extracellular matrix?

What are these cells in the CNS?

A
  • Glial cells
  • Ogliodendrocytes ( responsible for myelination)
  • Astrocytes
  • Microglia
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12
Q

What is the myelin sheath made from?

A
  • Cytoplasmic extension of oligodendrocytes in CNS
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13
Q

What is different between myelin sheath of the PNS cf CNS?

A
  • Myelin sheath of CNS has no neurilemma
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14
Q

What is astrocytes role in CNS?

A
  • **Regulate extracellular potassium concentration & Neurotransmitters **
  • Storing and transfer metabolites from blood vessel to neurons
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15
Q

What is microglia role in CNS?

A
  • thought to play a phaogocytic role- defending the CNS from noxious stimuli
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16
Q

What are responsible for myelination in the PNS?

Where do they arise?

A
  • Schwann cells
  • Neuroectoderm
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17
Q

What determines myelination in the PNS?

A
  • The size of the axon
  • larger axons are invaginated into a series of schwann cells that lays down the myelin sheath in spiral layers => neurilemma
  • Each schwann cell contributes myelin to one segment ( internode) of the axon
  • At the end of each internode the axon has an increased diameter=> paranode
  • here the axon and myelin sheath are crenated with myelin lamellae, ending in terminal loops of schwann cell cytoplasm
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18
Q

What are the nodes of ranvier?

A
  • Gaps between adjacent shwann cell internodes along the myelinated axon
  • here the axon diameter is reduced slightly
  • the axon diameter is inversely proptional to the length of the node of ranvier
  • the concentration of Na channels is increased in this region to facilitate saltatory conduction
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19
Q

What is axonal transport important?

What drives it?

A
  • to maintain sturcture of nerve and supply neurotransmitters
  • ATP ( adenosine triphosphate) driven
  • can occur in an
    • antegrade ( microtubule/microfilaments components) /
    • retrograde fashion- neurotransmitter
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20
Q

what is the membrane potential?

A
  • -70 mV
  • the voltage difference between intracellular and extracellular
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21
Q

Why is there a membrane potential ?

A
  • Due to high concentration of K+ ions and low conc of Na + and CL- ions in the cell
  • In the extracellular space there is a low conc of K+ and high concn of NA+ and CL-
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22
Q

How is the membrane potential maintained?

A
  • Lipid membrane- prevents passage of water-soluble ions
  • Selective permeable ion channels
  • a metabolically active Na/K+ exhange pump
  • Donnan equilibrium
    • ​irregular distribution of permant ions across an impermenant membrane when a large impermeable organic ion is present on one side
  • Cl- ions diffuse out of cell thru the lipid membrane
  • the Na/K+ xchange pump maintains a high concentration of K+ in the cell and high Na extracellularly
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23
Q

What is the threshold stimulus?

A
  • is the minimum stimulus intensity needed to produce an action potential
  • A subthreshold stimulus will not produce a stimulus
  • however summation of a subthreshold stimulus maybe enough to stimulate a response
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24
Q

Describe an action potential?

A
  • occurs when a neuron is stimulated
  • -> opening of Na+ channels ( dependent on O2/ ATP)
  • IN rush of Na+ into cell
  • ->Depolaristion of membrane resting potential from -70 mV due to ionic conductance
  • polarity across cell = positive
  • This triggers the opening of more Na+ channels
  • The channels stay open for 1ms before closing
  • For a few milliseconds after closing they cannot reopen ( refractory period)- limiting the no of stimuli to which a nerve can respond
  • Repolarisation then occurs= passage of K+ ions out of cell thru K= channels
  • Electrical potential falls to below the orginal -70mV resting potential due to the delay in closure of the K+ channel & time taken for Na+ channels to convert from an inactive to a resting state.
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25
Q

How is the action potential propagated?

How does this occur in myelinated axons?

A
  • Local change in potential of an area of the nerve fibre membrane cf with an adjacent area at resting potential=> a current
  • At the nodes of ravier the action potential jumps - ‘Saltatory conduction’
  • this increases the efficiency of the cell=> fast conduction with minimal metabolic activity
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26
Q

How do neurons communicate?

A
  • Via synapses
    • chemical or electrical
    • in humans chemical predominate
  • Synapse pccur between terminal branch of one axon and the cell body dendrites of another axon
  • an action potential causes the release of neurotransmitters from synaptic vesicles
  • the NT diffuses across the synaptic cleft to the postsynaptic membrane which it either excites ( excitatory postsynaptic membrane) or inhibits ( inhibitory postsynaptic potentials)
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27
Q

Name some examples of neurotransmitters?

A
  • Acetylcholine ( preganglionic synpases, parasympathetic postganglionic synapses
  • adrenaline ( sympathetic post ganglionic synapses)
  • noradrenaline ( sympathetic postganglionic synapses
  • serotonin
  • histamine
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28
Q

When do the spinal nerve divide close to the spinal cord what do they form?

A
  • Sensory dorsal root
  • motor ventral root
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29
Q

What can superifical sensory receptors be divided into?

A
  • Mechanoreceptors
  • Thermoreceptors
  • Nociceptors
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30
Q

What does a merkel cell respond to?

A
  • Sustained pressure
  • inervated by fast myelinated Aß
  • Slowly adapting receptor status
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31
Q

What does a meissner corpsule respond to?

A
  • Changing stimuli
  • innervated by fast myelinated Aß
  • rapidly adapting receptor
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32
Q

What does a ruffini’s corpusle respond to?

A
  • innervated by fast myelinated Aß
  • Slowly adapting receptor status
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33
Q

What does a pacinian corspule inervated by

A
  • fast myelinated Aß
  • Rapidly adapting
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34
Q

what is a hair follicle innervated by?

A
  • Fast myelinated Aß and Aσ
35
Q

What are the different types of thermoreceptors?

A
  • Cooling receptors
  • warming receptors
  • detect changes in environmental temperature
  • Innervated by Myelinated fast Aß and unmyelinated slow C fibres
36
Q

What do nociceptors respond to ?

A
  • Noxious stimuli
  • consist of
    • mechanical
    • thermal
    • mechanothermal
    • polymodal receptors
  • ​Myelinated fast Aß and unmyelinated slow C fibres innervate these receptors
37
Q

What do deep sensatio from muscles/ligaments /tendons adn joints occur via what?

A
  • free nerve endings and receptors such as
  • Muscle spindles
    • intrafusal nuclear bag fibres
    • nuclear chain fibres
    • innevated by myelinated afferent sensory A alpha fibres and efferent Ay fibres
  • Golgi tendon organs
    • near neuromuscular junctions
    • small bundles of tendon fibres enclosed in a capsule of concentric cytoplasmic sheets
    • capsule peirced by A alpha nerve fibres that divide and wrap around tendon faciculi
    • activated by passive stretch
    • important in prioprioception
  • Paciniform receptors
    • smaller than pacinain corpsules
    • rapidly adapting low threshold mechanoreceptors found in joint capsule
    • supplied by myelinated A alpha afferent fibres
38
Q

In the motor system transmission of impulses to muscles is via what?

A
  • Motor end plate
  • consists of neural endong and a muscle sole plate
  • 2 type of neural ending
    • extrafusal A alpha ( en plaque)
    • intrafusal A gamma ( plate ) ending
  • Muscle action potential is initated by acetylcholine release at nerve endings
39
Q

What can the autonomic nervous system be divided into?

A
  • Sympathetic
  • parasympathetic
  • Central and Peripheral components
40
Q

What does the sympathetic NS control?

A
  • Sweating
  • vasoconstriction
  • erector pilae
  • spincteric contraction
  • bronchial dilation
  • papillary dilation
  • reduction of gut motility
  • cardiac stimulation
41
Q

What does the sympathetic ns consist of?

A
  • preganglionic myelinated efferent axons from grey matter of the T1 to L2 of spinal cord
  • the axons emerge from the spinal cord thru ventral spinal roots before passing via the white comminicantes to synapse in the paravertebral or axial ganglia
  • the ganglia function as relay stations, where axons traverse or synapse with other axons, allowing amplication and dissemination of signals
42
Q

How do the post ganglionic neurons reach their target?

A
  • Pass directly to viscera
  • pass directly to adjacent blood vessels
  • pass via grey rami commiucantes, the axons return to their orginating spinal nerve and on to blood vessels, erector pilae and sweat glands
  • pass along sympathetic trunk to another level
43
Q

What do the parasympathetic nervous system consist of?

A
  • Efferent myelinated preganglionic fibres from the nuclei in the brain
    • via the oculomotor, facial , glossopharyngeal, vagus and accessory nerves and 2-4th spinal nerves
44
Q

What do the peripheral ganglia of the parasympathetic system include?

A
  • cranial ganglia
    • ciliary
    • pterygopalatine
    • submandicular
    • otic
  • which are efferent
  • afferent and postganglionic parasympathetic fibres also pass thru these ganglia but don’t synapse within them
45
Q

What is the cause of nerve injury?

A
  • Physical - trauma, injection, thermal,
  • Inflammation
  • infection
  • ischaemia
  • pharmacological
  • tumour
  • systemic disease
  • iatrophic
46
Q

What is the mechanism for nerve injury?

A
  • open/closed injuries
  • acute/chronic injuries
  • single/continuing/repeated injuries
  • whole/part of a nerve
  • depth of lesion
  • nerve state
47
Q

Name one classification of nerve injury?

A
  • Seddon 1943
  • Neurapraxia
  • Axonotmesis
  • Neuronotmesis
48
Q

What is neurapraxia?

A
  • transient concussion/crushing of the nerve
  • no wallerian degeneration
  • local conduction block to flow of nerve impulses
  • nerve and axons in continutity
  • on histology segemental demyelination
  • favourable outcome if source of injury removed
49
Q

What is axonotmesis?

A
  • A degenerative lesion- manifests as a progressive loss of all peripheral funciton
  • axon disrupted the endoneurium/perineurium and basal lamina intact
50
Q

What is neuronotmesis?

A
  • Loss of continiuity of all elements of the nerve
  • poor recovery if any
  • only repair of the nerve gives any useful chance of recovery
51
Q

Can you describe any other classificaiton system?

A
  • Birch and Bonney 1998
  • Transient conduction block ( non degenerative)
    • neurapraxia
  • Prolonged conduction block ( non degenerative)
    • neurapraxia
  • Degenerative favourable prognosis
    • axonometesis
    • axonal distruption; intact endo/perineurieum and basal lamina
  • Degenerative ( intemediate)
    • axonomesis
    • axonal disruption; basal lamina adn endoneurium damaged
  • degenerative unfavourable prognosis
    • axonomesis
      • axonal disruption, endoneurium and perineurium damaged, epi intact
  • Degenerative unfavourable prognosis
    • neuronotmesis
      • loss of continuity of nerve
52
Q

What is wallerian degeneration?

A
  • distal degeneration of the nerve axon occured with later regeneration of the neural tissue from the proximal stump
53
Q

What happens when a neve is sectioned?

A
  • the axon atrophies proximally
  • cell body dendrites retract and the axon distal to the site of injury degenerates
  • cell body role changes from neurotransmission to production of compoents for nerve regeneration
  • cell nucleus migrates to the periphery of the cell and chromatolysis occurs
  • the cell vol increases and production of RNA and regeneration enzymes increases
  • distal to the site of injury the myelin sheath degenerates, a haematoma forms and the macrophages are stimulated to remove the axonal debris
  • Schwann cells start to proliferate and migrate forming columns ( bands of Bunger)
  • the mitotic activity of the Schwann cell increases, and the cell starts to produce growth factors as it phenotypically changes and becomes non myelinating
  • axon proximal to site of injury=> mutliple axon sprouts with a growth cone situated at tip of each sprout
  • Filopodia in the growth cone use contact guidance for fibronectin and laminin in the schwann cell basement lamina to facilitate regeneration at a rate of 1mm/day
54
Q

How can regeneration of a nerve be followed ?

A
  • By advancing Tinel’s sign
55
Q

What factors determine the prognosis of the nerve injury?

A
  • Violence of injury
    • high energy- worse prognosis
  • Delay between injury and repair
    • due to time-dependent degeneration of the target organs
  • age
    • better prognosis with younger patients
  • Gap between nerves
    • larger the gap worse the prognosis
  • Level of injury
    • repair better prognosis at distal level ( PIN ) cf proximal site ( radial nerve in axilla)
  • Condition of nerve ends:
    • a tidy knife end better than untody crush
  • Assoc with arterial/bony injury
    • nerve inj assoc w bone have worse prognosis
  • type of nerve
    • those that innervate one/ 2 muscles better than those with mixed cutaneous and muscle innervation
56
Q

What are the different type of neuropathic pain?

A
  • Post-traumatic neuralgia
    • pain after nerve injury with no sympathetic involvement
    • pain expressed in territory of nerve
    • tx is to repair the nerve
  • Neurostenalgia
    • pain caused by perisistent neve compression/distortion/ischaemia
    • pain usually confined to territory of the nerve
    • tx of cause -> gd prognosis
  • Causalgia/chronic regional pain syndrome- type 2
    • burning pain with allodynia, hyperpathia , distribance of skin colour, altered temp adn sweating.
    • often seen with partial division of nerve
    • pain intense extends beyond territory of damaged nerve
    • sympathetic involvement is characteristic
  • Central pain
    • caused by root avulsions
    • constant crushing pain or burning pain felt within the anaesthetic part and a sharp shooting pain within the dermatone of the affected nerve
57
Q

What is parathesia?

A
  • spontaneous abnormal sensation
58
Q

What is dysaethesia?

A
  • unpleasant spontaneous normal sensation
59
Q

What is allodynia?

A
  • pain from stimulation that does not normally cause pain
60
Q

what is hyperalgesia?

A
  • Increased response to a stimulus that is normally painful
61
Q

What is hypersensitivity?

A
  • Over reaction sensitivity of regeneration
62
Q

What is hyperpathia?

A
  • deep seated , poorly localised fiery pain radiating throughout the limb that is induced by palpation of the muscles
63
Q

How can the diagnosis of nerve injury be supplemented?

A
  • Nerve conduction studies (NCS)
  • Elecromyography (EMG)
64
Q

How does the NCS work?

A
  • utilises an electrode to stimulate large, fast myelinated conducting fibres and a recording electrode to measure the motor or sensory action potentials
  • measurements of latency. ampitude and conduction velocity can then be made
65
Q

What is latency?

A
  • **Measures the time between onset of the stimulus and the response **
  • milliseconds (ms)
66
Q

What is the amplitude?

A
  • Measure the size of the response in microvolts (µV) or millivolts (mV)
67
Q

What is velocity?

A
  • Distance between the stimulating and recording electrodes divided by the time, measured in metres per second (m/s)
68
Q

What does the amplitude indicate?

A
  • The Quantity of the axons contributing to the action potential
69
Q

What does the latency and velocity indicate ?

A
  • The Quality of the action potential
70
Q

What is the motor unit action potential?

A
  • The supramaximal stimulation of the motor nerve
  • hence the amplitude mV of the MUAP = the number of functioning motor units
  • the latency (ms) of the MUAP= the time taken from motor nerve stimulation to muscle response and includes synaptic transmission and muscle depolarisation
71
Q

How is the conduction velocity calculated?

A
  • by stimulating the motor unit at 2 different sites
  • the distance between the distal stimulation site and the recording electrode is substracted from the distance beween proximal stimulation site and the recording electrode
  • the distance is then divided by the distal latency substracted from the proximal latency to give the velocity of the motor nerve
72
Q

How are sensory nerve action potentials measured?

A
  • stimulating and recording at separate sites along the same sensory nerve
  • the recording electrode is the more proximal of the 2 with the SNAP recorded for antidromic ( distal to proximal) conduction
  • ampitude and latency can be measure directly
73
Q

How would you measure motor studies in carpal tunnel syndrome?

A
  • A stimulating electrode placed over median nerve proximal to carpal tunnel
  • a recording electrode placed over a muscle in the hand suplied by median nerve APB
  • an indifference electrode placed a few cm away
  • a ground electrode place over an inactive muscle
74
Q

What is the normal velocity of upper limb nerves?

A
  • 50-70 m/s ( cf 40-50m/s in lower limb)
75
Q

To measure the proximal nerve what is used?

A
  • Late responses such as the F response ( wave) or H reflex are measured
  • these are low amplitude responses with long latencies including conduction in the proximal and distal sections of a nerve
76
Q

What does the F response measure?

A
  • The antidromic conduction of an impulse from a peripheral nerve to the anterior horn cells along with reflex orthodromic conduction down the motor nerves to the muscles
  • It does not cross any synapses so can be thought of as an echo.
  • useful in dectection early proximal lesions
  • a prolonged F response latency with normal peripheral motor nerve conduction would imply slowing over proximal motor fibres at the plexus / root level
  • muscles are innervated by mutliple roots so an abnormal F response is present only with mutiple severe root compromise ( guillane barre) extensive proximal neuropathies ( plexopathies)
77
Q

What is the H reflex?

A
  • A electophysiological equivalent of a deep tendon reflex
  • elicited by a submaximal stimulation of A alpha afferent fibres from muscle stretch receptors that enter the dorsal horn and synapse with alpha motor neurons, resulting in a motor response on the completion of the monsynaptic reflex arc
78
Q

What is seen on SNAP and EMG with conduction block neurapraxia?

A

SNAP

  • Reduced amplitude proximally
  • normal distally
  • conduction velocity- conduction block at site, preserved below

EMG

  • No sparse fibrillations
  • MUAP firing at rapid rates
  • reduced interference pattern
79
Q

What is seen on SNAP and EMG with degenerative lesion. favourable prognosis axonomesis?

A

SNAP

  • absent or reduced
  • conduction velocity absent or normal if present

EMG

  • fibrillations
  • reduced interference pattern
  • increased firing rate of MUAP
80
Q

What is seen on SNAP and EMG with degenerative lesion, unfavourable prognosis neuronomesis?

A
  • SNAP
    • Absent
  • Conduction velocity
    • absent
  • EMG
    • fibrillations
    • no voluntary MUAP
81
Q

What is the normal amplitude for emg testing of motor median and ulna nerves?

A
  • >5 mV
82
Q

What is the normal amplitude for snap testing of sensory median and ulna nerves?

A
  • >5µV
83
Q

What is the normal latency for motor median and ulna nerves?

A
  • median <4 ms
  • ulna <3ms

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