This is not an exhaustive overview of the muscles of the arm and forearm, but it demonstrates some of the tricky relationships that often catch people up. Some of the key points of compression are also noted and the muscles are coloured per their innervation. One thing not mentioned in the doodle that is important to notice is the way that the aponeurosis of the biceps veers medially (ulnarly) this is why it is also a supinator and not just an elbow flexor.
Category Archives: Anatomy
Peripheral nerve branches and compression neuropathy
The branches of the three main terminal branches of the brachial plexus can be difficult to remember. Even worse is trying to remember where all of those pesky compression points are and why it is that you get some symptoms with some and not others.
This diagram attempts to clarify the branches of the radial, median, and ulnar nerves and where they can get squished along the way. There are of course, slight anatomic variations, but this is a good starting point. I’ve even included where the famed Martin-Gruber anastomosis and the Riche-Cannieu anastomosis are, since they can make an otherwise (totally not) straightforward examination of a median or ulnar nerve palsy more muddied since both carry motor fibers between the two nerves.
Most interestingly is John Struthers, whose namesake structures compress the median nerve as a ligament and the ulnar nerve as an arcade.
Brachial plexus schematic with distal targets (printable diagram)
I’ve drawn the brachial plexus before showing more of its anatomical relationships (which is actually why the trunks and cords are named as they are). As I’m gearing up studying, I created this more schematic diagram of the plexus, including the distal targets (mostly the muscles but some sensory too).
Hopefully this will help you figure out “where is the lesion?” when you are faced with a brachial plexus question on your exams (and in life) as well.
I’ve also included a printable version for your printing and pasting-up-to-the-wall-to-passively-absorb pleasure.
Long thoracic: serratus anterior
Dorsal scapular: rhomboids, levator scapulae
Suprascapular: supraspinatus, infraspinatus, sensory to the AC & GH joints
Nerve to subclavius: subclavius
Lateral pectoral: pec major (clavicular head), sensation to pec
Superior subscapular: subscapularis (upper part)
Thoracodorsal (aka middle subscapular): lat dorsi
Inferior subscapular: subscapularis (lower part), teres major
Medial pectoral: pec minor, pec major (sternocostal head)
Medial cutaneous n. of arm: sensory to medial surface of arm (tiny area)
Medial cutaneous n. of forearm (antebrachial cutaneous): sensory to skin over biceps and medial forearm
Paracentesis: Anatomic Landmarks
Today’s post follows up on one of the first ones on this site, about abdominal paracentesis!
Paracentesis is the process of drawing out fluid from the peritoneum. It is useful for diagnosing ascites when its cause is unclear, and the procedure be used to therapeutically remove large volumes of ascites fluid.
While it is overall a quite safe procedure, the risks of paracentesis include: bleeding, bowel or bladder perforation, persistent ascites fluid leak, infection.
Paracentesis is usually done in a lateral decubitus position (or supine, for large volumes). The level of the ascites fluid is percussed and a needle is inserted in either in the midline (2-3 cm below umbilicus) or lateral lower quadrant (lateral to rectus abdominus muscle, 2-4 cm superomedial to anterior superior iliac spine). This positioning prevents puncture of the inferior epigastric arteries; visible superficial veins and surgical scars should be avoided too. To reduce risk of ascites fluid leak, the needle is inserted either with a z-tracking technique, or at a 45-degree angle.
- Lee SY, Pormento JG. 2009. Abdominal paracentesis and thoracentesis. Surgical Laparoscopy, Endoscopy & Percutaneous Techniques; 19:e32.
- McGibbon A, Chen GI, Peltekian KM, Veldhuyzen van Zanten S. 2007. An evidence-based manual for abdominal paracentesis. Digestive Disease Science; 52:3307.
- Thomson TW, Shaffer RW, White B, Setnik GS. 2006. Paracentesis. NEJM; 355:e21.
Jugular Venous Pulse (JVP)
The jugular venous pulse/pressure (JVP) is a favourite topic on the wards!
The jugular veins fill with blood and pulsate in relation to filling in the right atrium. Since the JVP correlates well with central venous pressure, it’s used as an indirect marker of intravascular fluid status.
Traditionally, the right internal jugular (IJ) vein is used in JVP measurement; it’s preferred since it is directly in line with the superior vena cava and right atrium. The external jugular (EJ) vein is not commonly used to assess the JVP because it has more valves and an indirect course to the right atrium, but EJ is easier to see than IJ, and JVP measurements from both sites correlate fairly well. The left-sided jugular veins are also uncommonly used, since they can be inadvertently compressed by other structures and thus be less accurate!
Learners on the ward are often asked how to identify the JVP and distinguish it from carotid artery pulsations. The mnemonic POLICE describes the distinguishing features of the JVP:
- Palpation: The carotid pulse is easy felt but the JVP is not.
- Occlusion: Gentle pressure applied above the clavicle will dampen the JVP but will not affect the carotid pulse.
- Location: The IJ lies lateral to the common carotid, starting between the sternal and clavicular heads of the sternocleidomastoid (SCM), goes under the SCM, and when it emerges again can be followed up to the angle of the jaw. The EJ is easier to spot because it crosses SCM superficially.
- Inspiration: JVP height usually goes down with inspiration (increased venous return) and is at its highest during expiration.
- (Kussmaul’s Sign describes a paradoxical rise in JVP during inspiration that happens in right-sided heart failure or tamponade)
- Contour: The JVP has a biphasic waveform, while carotid pulse only beats once.
- Erection/Position: Sitting up erect will drop the meniscus of the JVP, while lying supine will increase filling of the JVP.
To measure the JVP, the patient lies supine in bed at a 30 – 45 degree angle, with their head turned slightly leftward and jaw relaxed. A hard light source (e.g., penlight) pointed tangential to the patient’s neck will accentuate the visibility of the veins. Once the highest point of JVP pulsation is seen, measure high how it is at its maximum, in terms of centimeters above the sternal angle (aka Angle of Louis, at the 2nd costal cartilage). The JVP normally is 4 cm above the sternal angle or lower; increased in fluid overload and decreased in hypovolemia.
- Beigel R et al. 2013. Noninvasive evaluation of right atrial pressure. Journal of the American Society of Echocardiography: 26;1033.
- Chua Chiaco JMS, Parikh NI, Fergusson DJ. 2013. The jugular venous pressure revisited. Cleveland Clinic Journal of Medicine. 80;638.
- Cook DJ, Simel DL. 1996. Does this patient have abnormal central venous pressure? Journal of the American Medical Association: 275;630.
- Vinayak AG, Pohlman AS. 2006. Usefulness of the external jugular vein examination in detecting abnormal central venous pressure in critically ill patients. Archives of Internal Medicine: 166;2132.
- Wang CS et al. 2005. Does this dyspneic patient in the emergency department have congestive heart failure? Journal of the American Medical Association: 294;1944.
Describing where things are on the hand
For being such a small anatomic location, people find it very difficult to describe where on the hand or digits things are actually happening when there is an injury.
I think part of it stems back to medical school when we are taught that the digits all have numbers, the thumb is D1, index D2 and so forth. The problem comes when people say “the 3rd finger” and all of the sudden one has no idea whether they are talking about the long finger (D3) or the ring finger (D4 but then, the thumb doesn’t count as a finger, does it?)
Which finger (digit?!) is which?
This is why it’s always best to call digits by their names, this even goes for metacarpals. It is totally OK, and generally less confusing to call a bone the index finger metacarpal.
- Thumb = D1
- Index = D2
- Long = D3
- Ring = D4
- Small = D5
Which side of the hand?
The same goes for which side of the hand the problem is on. There is no lateral or medial side to the hand. One could argue that it’s how someone is in anatomical position, so obviously the small finger side is medial, unfortunately very few people walk around in anatomic position and it’s their thumbs that point to the body.
So best to describe side by two things that stay put regardless of how someone has their hands in space: the radius and the ulna.
- Thumb side = RADIAL
- Small finger side = ULNAR
Finally for the top and bottom (or is it back and front) of the hands: use the terms DORSAL (where the nails are) and VOLAR (or palmar)
Amyotrophic Lateral Sclerosis (ALS) & the corticospinal tract
Amyotrophic Lateral Sclerosis (ALS) is a degenerative disease of the motor neurons in the brain and spinal cord. It progressively affects all the muscles in the body but there is no known cause and no treatment. Only about 5-10% of cases are inherited while the rest are sporadic.
The neurons ALS affects are primarily the upper motor neurons. These are the ones that originate in the brain and travel down the spinal cord. These neurons then synapse with the lower motor neurons in the ventral horn, and it is the lower motor neurons that go directly to the muscles.
In ALS there are both upper motor neuron and lower motor neuron symptoms. As the neurons die, a constellation of symptoms including numbness, weakness and paralysis emerge. Eventually the paralysis progresses leading to inability to speak, swallow and breath. There is no cure for ALS and treatments only help with the symptoms, they do not slow the progression of the disease.
So you may have seen a lot of ice bucket challenges over the last few weeks but please support this cause as it is a horrible disease that up until now had almost no recognition or support. So please donate to The ALS Association (alas.org).
And in case you get tired or jaded seeing your social media full of these videos, watch this one of my father doing it. He’s not an emotional guy, but he has lost more than his fair share of friends to this disease.
donate to help fund ALS research and support from Ali & Mike on Vimeo.
Scaphoid bone anatomy and fractures
The scaphoid bone is one of the eight carpal bones of the wrist (you can check out this doodle for a refresher).
The scaphoid is the most commonly fractured carpal bone, accounting for almost 70% of fractures. It tends to be young males who break their scaphoid this is both an anatomical thing: younger kids get ligament injuries and older folks break their distal radius and a lifestyle thing: falling on outstretched hands (skateboarding, snowboarding) or throwing a punch both place a lot of force across the scaphoid leading to fractures.
The bad thing about scaphoid fractures is that the blood supply (from a branch of the radial artery) comes from distal to proximal. Since most fractures happen at the waist of the scaphoid the likelihood of having poor blood supply to the fracture site is quite high. It doesn’t help matters that around 80% of the scaphoid is articular surface (joint surface), so if it doesn’t heel well, it can lead to problems with arthritis of the wrist later on.
Scaphoid fractures present with a pretty classic story and the person is usually swollen and bruised and will have tenderness in their “snuffbox.” So even if the x-ray doesn’t show a fracture, it’s best to treat with a cast for comfort and safety and then recheck them in 2 week’s time (this will be discussed in a separate post).
Brachial Plexus Part 1 – anatomical relations
The brachial plexus is the bane of many med students’ existence during any sort of neuro block. So many nerves, so many connections, so many seemingly arbitrary names of different sections. It’s just a woven mess of misery. (especially when they start getting into the “where is the lesion” questions)
Thus I’ve decided to have a couple posts about the brachial plexus, hopefully demystifying it to some extent. This first doodle is about the brachial plexus and its anatomical relationship to some of the structures that show why anatomists who named the parts weren’t as crazy as they seem.
Important structures to remember because they explain why parts are named the way they are:
- Anterior and posterior scalene muscles
- Subclavian artery
- The arm (in its anatomical position)
Vertebrae: There are 7 cervical vertebrae and 12 thoracic vertebrae. To make things confusing the cervical spinal nerves exit ABOVE their named vertebrae (except for C8) while the thoracic, lumbar and sacral exit BELOW. This messes up the whole numbering system because there are SEVEN cervical vertebrae but there are EIGHT cervical spinal nerve roots. The brachial plexus generally includes the nerve roots C5-T1*
* I say generally because there’s are anatomical variations such as a “prefixed” plexus that goes from C4-C8 and a “postfixed” plexus that goes from C6-T2
Scalene Muscles: The brachial plexus is nestled between the scalenes in the neck. At this point the plexus is oriented up and down and therefore the trunks are superior (closest to your noggin), middle, and inferior.
Subclavian Artery/Anatomical Position: The artery is in front of the plexus at the level of the trunks and then the plexus starts to wrap around it (or at least seems to because we don’t keep our arms straight out to our sides in “anatomical position” at all times). The cords are named for their relationship to the artery. One is lateral (again, if the arm was held out to the side), one is posterior and one is medial (think closest to armpit).
Subdivisions of the Brachial Plexus
The parts are: Roots/Trunks/Divisions/Cords/Branches or, as I remember them being a classy east coast Canadian: Real/Truckers/Drink/Cold/Beer
Then you might think, “But how do I remember which of the terminal branches comes off where?” For that I think of the two “M” branches being on the M: Musculocutaneous, Median and (M)Ulnar and that the whole thing together can just be said as “MARMU” Pick the mnemonics you want, the brachial plexus is rife with them. I personally just like the sound of the word marmu.
Internuclear opthalmoplegia (INO) is an impairment in lateral conjugate gaze (both eyes looking toward one side), caused by a lesion in the medial longitudinal fasciculus (MLF), and associated with multiple sclerosis.
Lateral conjugate gaze requires coordination of adduction (medial rectus muscle, CN III) in one eye and abduction (lateral rectus muscle, CN VI) in the other eye. These movements are coordinated by the paramedian pontine reticular formation (PPRF), also known as the pontine gaze centre. The pathway is as follows:
- To look to the left, the right frontal eye field (FEF) sends a signal to the left PPRF.
- The left PPRF innervates the left abducens (CN VI) nucleus, which controls the left lateral rectus muscle and causes the left eye to abduct (gaze to the left).
- Additionally, the left CN VI nucleus innervates the right oculomotor (CN III) nucleus, which controls the right medial rectus muscle and causes the right eye to adduct (gaze to the left). The MLF is the tract connecting the CN VI nucleus to the contralateral CN III nucleus.
In INO, there is damage to the MLF, giving a deficit in adduction of the corresponding eye during conjugate lateral gaze, but convergence (eye crossing) is classically preserved because that is controlled by a different pathway. In very mild cases of INO, the only deficit is a slowed velocity of the affected eye. For naming, a right INO (as in the sketch) involves damage to the right MLF, which means that the right eye can’t adduct to look to the left, but can abduct to look to the right.
INO may also be associated with gaze abnormalities such as nystagmus, skew deviation, and even abduction or convergence deficits.
The causes of INO include: multiple sclerosis, pontine glioma, and stroke.
- Flaherty AW, Rost NS. 2007. Eyes and vision. In: Massachusetts General Hospital Handbook of Neurology. Lippincott Williams & Wilkins.
- Frohman EM, Frohman TC, Zee DS, McColl R, Galetta S. 2005. The neuro-opthalmology of multiple sclerosis. The Lancet Neurology; 4:111.
- Ropper AH, Brown RH. 2005. Disorders of ocular movement and pupillary function. In: Adams and Victor’s Principles of Neurology. McGraw-Hill.
- Wilkinson I, Lennox G. 2005. Cranial nerve disorders. In: Essential Neurology. Blackwell.