Neurophysiology Flashcards
Parts of neuron
Dendrites, axons, soma, synaptic terminal
Neuron types: type, examples, describe
Multipolar: motor neurons, interneurons -1 axon, many dendrites Bipolar: special senses neurons -1 axon process, one drenditic process Pseudounipolar: somatic, visceral sensory neurons -1 process but brances
Graded membrane potentials - where?
- graded in amplitude, proportional to intensity (stronger stimulus fires STRONGER signal)
- in dendrites and body
- sensory neuron: receptor potentials (Stimulus > receptor activated > Na+ influx in sensory neuron > potential that is graded
- synaptic neurons: synaptic potentials
Action Potential - where? characteristics?
- fixed amplitude
- in axons
- used for propagation
- frequency proportional to intensity: stronger stimulus fires MORE
- communication over long distance bt neurons
- all or none
- spike initiation zone
- unidirectional (b/c of refractory periods)
Axonal transport: anterogrde vs retrograde
- Fast anterograde - soma > synapse. transport NTs, macomolecules in vesicles long KINESIN
- Slow anterograde - diffusion of cytosolic proteins
- Fast retrogrde - nerve terminals > soma. along DYNEIN. surplus materials, endocytocized materials, infections
What does dendrites have that axons don’t
- multiple branching
- RIBOSOMES!
- graded potentials
resting membrane potentil
- 70mV due to higher K+ permeability > leaks OUT = inside more negative then outside
- maintain by Na/K/ATPase: pumps K+ in and Na+ out
Relationship bt receptor potential and APs
-RPs in large > initiate APs
-
Factors for conduction velocity
- increase size (decrease resistance)
- myelination (decrease capacitance)
- distance
Myelination
- lipid insulator > faster AP conduction
- PNS: Schwann cells, CNS: oligodendrocytes
- Nodes of Ranvier: AP leap bt nodes = saltatory conduction
Demyelination
-diseases?
> Conduction block
-AP can’t reach next patch of N channels
ex: MS - demylenation of central axons
Guillin-Barre: peripheral
Local anesthetics and pain
- block what?
- ex?
- blocks Na+ chnnels from inside. no Na+ influx > no AP
- targets small-diameter, unmyelinated fibres because can access more Na+ channels to block
ex: cocain, lidocaine
Why use NCS and EMG?
- localize lesion
- distinguish bt axonal loss vs demylination
- assess severity and prognosis
- asses age of lesion
- nerogenic vs myopathic
* *PNS nor CNS test
Timelines of nerve lesion: acute, subacute, chronic
Acute 1-2wk
Subacute 4-8 wks
chronic months-yr
Describe nerve conduction studies
- motor and sensory
- particularly for myelinated fibres, large d
- axonal loss: lower amplitude (takes few days after injury to happen, mimics conduction block. Test 7-10 days fter injury)
- delymination: slower conduction, lower amplitude only for proximal test
What are the electro signs of delymination?
- sign. prolongation of distal latency
- sign. slowing
- conduction block (distal ok, proximal test have lowered amplitude)
Recovery timelines for nerve damage?
Demylination: usually complete recovery 1-3 months
Axonal loss: longer, incomplete b/c regeneration is slow
What is EMG?
-needle electrode examination
-test at rest and during voluntary movement
-only MOTOR
-Abnormal:
fibrillation potentials at rest = axonal loss
change in motor unit potentials (MUP): long and high indicates re-innervation = chronic lesion
recruitment of motor units
1. reduced: neurogenic
2. early: myogenic
What is neurogenic lesion?
- nerve issue: fever motor units available to recruit
- fire faster
- reduced recruitment
What is myogenic lesion?
- muscle issue: smaller units
- need to recruit early
