TUTORING QUESTIONS

PAIN

LOL this was the most painful (lol geddit) thing to study. We still talk about how annoying this was lol

Overall don’t stress about this too much, its very detailed + has not been examined in the past

Nevertheless, heres an explanation below!

- Descending and ascending tracts

- Just confused on how to interpret these slides

This is a cross section of a spinal cord showing how nerve fibers run in bundles together
(tracts) depending on where they come from and go. The tract names help understanding
the origin and termination of the nerves i.e. spinothalamic comes from spinal cord and goes
to thalamus. DW about remembering where all these tracts are right now, youll cover them
again in neuro block at the end of the year.

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- This diagram is an attempt to simply the pathway of how pain is sensed by our brain.
- Essentially it shows how pain is first perceive by a peripheral nerve (FON aka first order
neuron, pseudounipolar, has its nucleus in the dorsal root ganglion) which then synapses in
the dorsal horn with another neuron, SON (ignore the excitatory interneuron bs). SON then
crosses the spinal cord from dorsal horn and travels up the lateral spinothalamic tract to the
thalamus (mainly). Pain in perceived mainly in the thalamus but this info also gets relayed to
the cortex, hypothalamus and reticular formation/insula as many areas of the brain are
involved in not only noticing pain, but also understanding it, responding to it, attaching
emotion e.g. fear to it, and switching to a state of alertness to anticipate more pain.
OVERALL just keep this simple: FON -> SON -> Thalamus+ via lateral spinothalamic tract
 This is where it gets cooked
Basically our brain has this way that lets us adapt to pain sometimes. This phenomenon can
be called ‘antinociception’. It works via 3 descending pathways:
A: gate control theory (theres actually an interneuron between FON and SON that when
stimulated, can stop FON from transmitting pain signal to SON)
(https://www.youtube.com/watch?v=hw-vHF1LrqY&ab_channel=DrMatt%26DrMike)
B: direct inhibition of FON via 5-HT/NA released from a descending neuron coming from PAG
matter/raphe nucleus
C: our body has endogenous opiates that act on the synapse between FON&SON to stop the
the pain signal (https://www.youtube.com/watch?v=tJHndCJq7TY&ab_channel=DrMatt
%26DrMike)

NERVE

Overall, don’t worry about these obstetric presentations right now. You can double check with nikki
but pretty sure she said these were non-assessable for us when we learnt it. Focus more on the basic
common presentations for brachial plexus injuries… dirty medicine vids have a great vid on it
(https://www.youtube.com/watch?v=Orr4KPUr9Ck)

- Klumpke
o Regarding Klumpke is the flexion of the hands due to the paralysis of the lumbricals
when it says intrinsic hand muscles?
o Why is it weakened wrist and finger flexion if the baby is only able to keep their
fingers flexed? Would it not just be only weakened wrist and finger extension since
they are unable to extend their fingers/wrist?
 o Klumpke Palsy is an proximal ulnar nerve injury… like any ulnar n injury, itll present
as claw hand! Below you can see the m innervation of ulnar n, tho I think just focus
on these two:
o Lumbricals weakness  persistent flexion of IP joints + extension of the MCP joints
o FCU weakness  difficulty flexing wrist… wrist extension (not an obvious finding)

o
- Erb
o What nerve is actually damaged in erb palsy?
o How does this palsy result in the following presentation (waiters tip)?

MUSCLES

- Confused about the relevance of Fused and complete tetanus?

- Its just describing one type of muscle contraction. Basically complete tetanus is the strongest
type of muscle twitch/contraction possible. In healthy states its useful for simple things like
lifting a heavy box and can even be progressed e.g. Olympic lifting. But in pathological states,
this type of contraction is obviously quite severe. This Wikipedia article (lol) helps
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