1) A short 🧵 looking at median nerve palsy (MNP) and some useful tips to help differentiate the site of its lesion.
2) In terms of its anatomy. It is composed of two sections, the lateral cord (C5-7) which innervates proximal muscles and provides sensory innervation to thenar eminence and the radial 3.5 digits. The medial cord (C8-T1) is purely motor.
3) 1st if we start with the carpal tunnel (CT) which accounts for most MNP’s. An easy way to determine whether the lesion is proximal, is if the pt is c/o paraesthesia in the thenar eminence as this is innervated by the palmar cutaneous branch found 2 inches proximal to wrist.
4) Useful clues to help determine CT vs C5/6 radiculopathy would be; a) +’ve flick sign, +’ve phalens & tinels, often nocturnal paraesthesia and wrist flexion + triceps would be normal!
5) If there has been a lesion proximal to the elbow (e.g supracondylar #) we will lose all MN innervation. Easiest way to spot this is that the forearm will be supinated with an inability to pronate due to denervation of pronator teres & quadratus.
6) If we have an anterior interosseous lesion (albeit rare) this will only affect the medial cord and therefore we are presented with motor deficits. Inability / weakness with pincer grip / performing an OK sign is an easy way to assess FPL and IF flexors.
7) Another sign of AIN is the Hand of Benediction. We will see natural flexion of our ulnar sided digits. Whereas denervation of FPL, FDS and FDP will mean the thumb, IF & MF rest in an extended position.
8) Finally, with more chronic issues, denervation of the APB will mean the hand appears more flattened as the thumb will naturally lie in a more adducted position.
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Always keep on the radar 🚨 in any adolescent presenting with acute pelvic pain OR recalcitrant Sx which are not responding to conservative efforts
2) They account for approx 3-5% of adolescent injuries involve the groin (Di Maria et al., 2022). Avulsion fractures typically occur w forceful contraction +/- passive stretching & this is due to secondary ossification centres being weaker than the MTU
3) This table by Schiller et al., (2017) highlights the ages where ossification centres fuse.
▪️Females tend to be 1-2yrs sooner vs male counterparts.
Note how ASIS & ischial tuberosity may not ossify until as late as 25yrs
These are the most common 🚩 of the spine. But what are some of the risk factors which ⬆️ likelihood⁉️
2) Typically affects the thoracolumbar spine (as seen). Be mindful a large % are asymptomatic & picked up incidentally during other investigations (e.g CXR)
Some features
▪️Localised pain & tenderness
▪️Pain supine & sitting hard chair
▪️+’ve percussion
▪️⬇️ ROM
3) Henschke et al., (2009) in a primary care cohort illustrated 4 key features which raised suspicion of it
1. Female sex 2. Age > 70yrs 3. Prolonged steroid use 4. Trauma (minor in elderly)
Glucocorticoids was enough to ⬆️ post-test probability by 25%
1) Approx. 5-11% of patients undergoing MRI for suspected Cauda Equina Syndrome (CES) will have it confirmed (Metcalfe et al., 2023) 💡
Once differentials are ruled out 🕵️♂️
The remaining % are then considered to be ‘Scan-Negative CES’. But what does this actually mean?
2) Scan-Negative CES ‼️
Pt’s have 1+ symptoms suggestive of CES, yet without the radiological evidence of compression. One possible cause is that it may occur secondary to an almost functional neuro disorder 🧠
3) Pt’s in this subgroup tend to present with more of the following…
▪️Psychiatric diagnoses
▪️Pre-existing B/B disorder
▪️Non-cardiac chest pain
▪️Higher % are female
▪️IBS
▪️FM (Hoeritzauer et al., 2018)
1) A whistle stop tour of muscle cramps. How can we tell if they are idiopathic vs something more systemic?
2) Thought to be influenced by both the PNS (weighted more heavily) and the CNS. Majority of them are benign
3) The most common we see in clinic, these are some simple ways of helping to highlight to patients they are no cause for concern. Rather than ‘drink more’