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Neuroscience > Injury, Recovery, Plasticity > Flashcards

Injury, Recovery, Plasticity Flashcards

(63 cards)

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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
Whats a common cause with axonotmesis
Crush injuries of nerve secondary to dislocations or closed fx
26
Neurotmesis
Endoneural tubes and surrounding perineurium disrupted (severance)
27
Neurotmesis wallerian degeneration starts when
3-5 days after lesion Rare to have full recovery Need surgical intervention
28
Multiple mononeuropathy: ______ causing ______ pattern of nerve fxn
Ischemia, irregular
29
What happens with DM
High blood sugar levels destroy nerves (affects transmitter production and release, damages small blood vessels to the nerve, inflamm, oxidative stress)
30
What are other examples of multiple mononeuropathy
Vasculitis Infections (Lyme, HIV) Bacterial infection of nerves (leprosy attacks Schwann cells and perineurium)
31
How does polyneuropathy progress
Distal to proximal
32
Wallerian/anterograde degeneration
Distal end of neuron/ proximal end to 1st node, demyelination
33
Retrograde degen
Proximal nerve- cell body
34
PNS axons regenerate at a sad rate of..
1mm/day :(
35
Regeneration of long nerves may have complete regeneration BUT
Target organ may not be the same or contacted fully
36
You have greater success with ________ because _________
Crush injuries, atonal structures are approximated and distal segments provide a guide for regeneration
37
What do schwann cells emit to encourage axonal sprouting?
Neuronal Growth Factor
38
What is neuroma?
Entanglement of nerve sprouts and Schwann cells
39
Collateral sprouting damages
Presynaptic
40
Regenerative sprouting damages
Postsynaptic
41
If you do dermatology testing, are you testing CNS or PNS
PNS- via peripheral nerve pattern, you can determine if central cause (SC) vs peripheral
42
What is nerve conduction velocity?
Testing sensory, | Diff in amplitude vs diff in speed (myelin vs axon damage)
43
PNS testing for motor
DTR, myotomes, MMT, hyporeflexive vs hyperreflexive (UMN vs LMN), nerve conductionvelocity (motor), EMG
44
What is habituation
Decreased neuronal response to repeated benign stim
45
Repeated stim results in
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
If theres a short break in stimulation (habituation) If persistent,
Rxn returns Permanent reduction in synaptic connections Allows other types of learning to occur, focus attn to impt stim (tune out irrelevant)
47
Desensitization
Sensory defensiveness- someone hypersensitive to touch can use theres intervention to keep stimulating to desensitize
48
What’s the theoretical basis of desensitization
Sensory integration
49
What’s good about TENS for pain reduction
Pain reduction is greater with adjusting pulse amplitudes vs constant If use same amplitude, pt will habituated. alternating amps prevents habituation.
50
Who can you use desensitization for?
Nystagmus positionally- expose pt to that position to habituate
51
What is long term potentiation
Long term strengthening of synapse between 2 neurons that are activated simultaneously Synaptic plasticity is the underlying memory and learning**
52
Where is primarily located?
Hippocampus but also motor, ss, visual, auditory cx
53
What can cause LTP
High frequency stimulation- Post synapticnneuron becomes depolarizer following sustained activation of its AMPA receptors (allows Na and K)
54
LTP- what does depolarization allow
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
What does this increase concentration of Ca in dendrites cause?
Increased Ca sets off several biochemical rxns that make this synapse more efficient for extended Pd.
56
When would LTP not work?
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
How long does the insertion of AMPA last?
Several hours
58
What can cause a more permanent change?
Increase in synapse size and numbers are due to changes in gene expression from higher Ca2+ post synaptiaclly- makes new proteins.
59
Long term depression
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
What happens to the brain when you lose a finger?
Digital amputation can lead to reorganization of SS cx where adjacent digits fill in cortical map
61
What can cause the SScx to reorganize?
Repetitive behavioral task. Heavily used digits have greater representation
62
Contra coup injuries
Hit one side, rebound hits the other side
63
What happens when you deprive your brain of O2?
Neurons die such as lesions, stroke or traumatic

Neuroscience (6 decks)

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