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Neuroscience > Injury, Recovery, Plasticity > Flashcards

Injury, Recovery, Plasticity Flashcards

1
Q

What structures are affected in the PNS?

A

NM jxn, axon, cell body, myelin

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2
Q

What can cause NM jxn disorders?

A

Myasthenia Travis, botulinum toxin, alcohol, nerve blocks

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3
Q

What are disorders that cause damage to axons?

A

Trauma, diseases scar tissue

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4
Q

Disorders that cause cell body damage

A

Viruses (polio), trauma

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5
Q

Disorders that cause myelin damage

A

MS, guillain-barre, carpal tunnel

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6
Q

What is the clinical relevance for understanding PNS damage?

A

Weakness, paralysis, sensory change, paresthesia, wounds, abn tone, abn reflexes, pain

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7
Q

What cause cause CNS damage?

A

Laceration, impact injury, pressure (mass/tumors), circulatory (infarcts, CSF, O2 deprivation), poison Hg, alcohol, pharm, degeneration, genetic programming (Huntington’s), excitotoxicity (synaptic neurons die from excess glutamate)

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8
Q

What’s the clinical relevance of CNS damage

A

Loss of fxn (motor, sens, cog) depending on lesion location/disease type

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9
Q

How do we learn anything new

A

Neuroplasticity

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10
Q

What does the PNS consist of

A

All neural structures distal to spinal nerves (axons of sens, motor, autonomic neurons, specialized sens endings, post gang ANS neurons)

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11
Q

Spinal are…

A

Roots DRG spinal nerves

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12
Q

Spinal damage can cause

A

Sensory motor ANS loss in Kyoto all or dermatology pattern

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13
Q

Peripheral neurons location is considered…

A

After spinal nerve

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14
Q

Damage to peripheral neurons would cause

A

Sensory motor ANS loss in peripheral nerve distribution

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15
Q

Dorsal ramus

A

Skin paravertebral muscle sof back, posterior parts of vertebrae

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16
Q

Ventral ramus

A

Some branches form plexuses to arms legs pelvis ant trunk

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17
Q

What are the layers of peripheral connective tissue

A

Mesoneurium- surrounds epineurium
Epineurium- most ext cover holding multiple fascicles together
Perineurium- connective tissue sheath aroudn a bundle of nerve axons (fascicles)
Endometrium- CT around indiv axons

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18
Q

Classifications of neuropathies

A

Mononeuropathy
Multiple mononeuropathies- asymm of 1+ nerve
Polyneuropathy-generalized, distally, symm

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19
Q

What classification would neurapraxia fall under

A

Mononeuropathy

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20
Q

What is neurapraxia

A

Demyelination with temp conductionblock (traumatic myelinopathy)

  • interfere w fxn of larger diameter nerves (motor, discrim touch, proprio)
  • focal compressions/repeated mech stress (stretch, vibration)
  • nerve entrapment
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21
Q

Neurapraxia- complete or incomplete recovery

A

Complete due to demyelination

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22
Q

What is axonotmesis

A

Axons damaged but endometrial tubes intact (traumatic axonopathy)

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23
Q

Axonotmesis- wallerian degeneration occurs where

A

Below injury and above next node of rancher or higher, some muscle denervation

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24
Q

Axonotmesis can affect all size axons t/f

A

True

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25
Q

Whats a common cause with axonotmesis

A

Crush injuries of nerve secondary to dislocations or closed fx

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26
Q

Neurotmesis

A

Endoneural tubes and surrounding perineurium disrupted (severance)

27
Q

Neurotmesis wallerian degeneration starts when

A

3-5 days after lesion
Rare to have full recovery
Need surgical intervention

28
Q

Multiple mononeuropathy: ______ causing ______ pattern of nerve fxn

A

Ischemia, irregular

29
Q

What happens with DM

A

High blood sugar levels destroy nerves (affects transmitter production and release, damages small blood vessels to the nerve, inflamm, oxidative stress)

30
Q

What are other examples of multiple mononeuropathy

A

Vasculitis
Infections (Lyme, HIV)
Bacterial infection of nerves (leprosy attacks Schwann cells and perineurium)

31
Q

How does polyneuropathy progress

A

Distal to proximal

32
Q

Wallerian/anterograde degeneration

A

Distal end of neuron/ proximal end to 1st node, demyelination

33
Q

Retrograde degen

A

Proximal nerve- cell body

34
Q

PNS axons regenerate at a sad rate of..

A

1mm/day :(

35
Q

Regeneration of long nerves may have complete regeneration BUT

A

Target organ may not be the same or contacted fully

36
Q

You have greater success with ________ because _________

A

Crush injuries, atonal structures are approximated and distal segments provide a guide for regeneration

37
Q

What do schwann cells emit to encourage axonal sprouting?

A

Neuronal Growth Factor

38
Q

What is neuroma?

A

Entanglement of nerve sprouts and Schwann cells

39
Q

Collateral sprouting damages

A

Presynaptic

40
Q

Regenerative sprouting damages

A

Postsynaptic

41
Q

If you do dermatology testing, are you testing CNS or PNS

A

PNS- via peripheral nerve pattern, you can determine if central cause (SC) vs peripheral

42
Q

What is nerve conduction velocity?

A

Testing sensory,

Diff in amplitude vs diff in speed (myelin vs axon damage)

43
Q

PNS testing for motor

A

DTR, myotomes, MMT, hyporeflexive vs hyperreflexive (UMN vs LMN), nerve conductionvelocity (motor), EMG

44
Q

What is habituation

A

Decreased neuronal response to repeated benign stim

45
Q

Repeated stim results in

A

Decreased intra-cellular Ca2+, decreasing amount of NT release

In order for NT to get release, has to have influx of Ca to send to NT thru vesicles

46
Q

If theres a short break in stimulation (habituation)

If persistent,

A

Rxn returns

Permanent reduction in synaptic connections

Allows other types of learning to occur, focus attn to impt stim (tune out irrelevant)

47
Q

Desensitization

A

Sensory defensiveness- someone hypersensitive to touch can use theres intervention to keep stimulating to desensitize

48
Q

What’s the theoretical basis of desensitization

A

Sensory integration

49
Q

What’s good about TENS for pain reduction

A

Pain reduction is greater with adjusting pulse amplitudes vs constant

If use same amplitude, pt will habituated. alternating amps prevents habituation.

50
Q

Who can you use desensitization for?

A

Nystagmus positionally- expose pt to that position to habituate

51
Q

What is long term potentiation

A

Long term strengthening of synapse between 2 neurons that are activated simultaneously

Synaptic plasticity is the underlying memory and learning**

52
Q

Where is primarily located?

A

Hippocampus but also motor, ss, visual, auditory cx

53
Q

What can cause LTP

A

High frequency stimulation-

Post synapticnneuron becomes depolarizer following sustained activation of its AMPA receptors (allows Na and K)

54
Q

LTP- what does depolarization allow

A

Allows Mg to withdraw from NMDA receptors and allow large numbers of Ca ions to enter cell

(NMDA receptor blocked by Mg at resting potential)

55
Q

What does this increase concentration of Ca in dendrites cause?

A

Increased Ca sets off several biochemical rxns that make this synapse more efficient for extended Pd.

56
Q

When would LTP not work?

A

In the presence of NMDA antagonists

-so if there’s things that inhibit activation of NMDA- then glutamate will not bind to NMDA receptors and Ca channels willl not open.

57
Q

How long does the insertion of AMPA last?

A

Several hours

58
Q

What can cause a more permanent change?

A

Increase in synapse size and numbers are due to changes in gene expression from higher Ca2+ post synaptiaclly- makes new proteins.

59
Q

Long term depression

A

Less stimulus= less receptor sites for glutamate to bind and less LTP

AMPA receptors go back in cleft (weaker connection)

Seen in hippocampus and cerebellum

60
Q

What happens to the brain when you lose a finger?

A

Digital amputation can lead to reorganization of SS cx where adjacent digits fill in cortical map

61
Q

What can cause the SScx to reorganize?

A

Repetitive behavioral task. Heavily used digits have greater representation

62
Q

Contra coup injuries

A

Hit one side, rebound hits the other side

63
Q

What happens when you deprive your brain of O2?

A

Neurons die such as lesions, stroke or traumatic

Neuroscience (6 decks)

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