Thursday, 17 May 2012

Following a tutorial Prof. Giovannoni gave in his clinic last week I would like to share an excellent link about eye movements. Tutis Vilis of the Department of Physiology, University of Western Ontario has developed a flash tutorial explaining many normal and abnormal eye movements, which can be found here:

There are a few points to develop around the link, once you've worked through it:

1) The accommodation reflex or near response comprises three movements - the first two are mentioned in the eye movement tutorial:
  • both eyes rotate medially towards the target  - vergence
  • the ciliary muscle contracts, causing the lens to be come more spherical/convex - accommodation
  • the pupils constrict
Why do the pupils need to constrict? The quality of the lens results in spherical aberration - light passing through the edge of the lens will be focussed more poorly onto the retina, reducing the quality of the image. Pupillary constriction prevents light from passing through the edges of the lens and ensures the eye can produce a sharp image on the retina. In a given light level, a near object will reflect more light onto the retina than one further away, so the pupillary constriction does not typically impair vision by inadequate illumination.

2) Humans have 6 extraocular muscles which are responsible for positioning the eye and one which elevates the eyelid (levator palpebrae superioris). Cows (for example) manage with just four muscles to rotate the globe. Why does Man need two more?

This image of the right orbit (from above) shows the origins and insertions of the orbital muscles.The orbit is cone shaped and this cone is externally rotated by about 20 degrees. The rectus (straight) muscles all originate from a common point at the back of that cone - the common tendinous ring (also known as the Annulus of Zin). Due to the cone's shape and position, the rectus muscles act not only in the direction they are named, but also cause rotation in other axes.

For example superior rectus (in the middle of the image above) when contracting rotates the globe upwards (elevation) but also has some internal rotation (intorsion) and medial rotation (adduction). The inferior rectus (not seen on the illustration) causes not only depression of the eye but extorsion and adduction. With only four muscles, there would be no control over in- and ex-torsion of the globe. Our bovine friends do not encounter this problem due to the shape of their orbits - presumably the tendinous ring lies deep to the centre of the globe, so their rectus muscles pull straight, as the name "rectus" would normally suggest.

The addition of two oblique (slanted) muscles allows for control over intorsion and extorsion. Superior oblique acts to intort, depress and abduct the eye. Some use the acronym SO-LID as a reminder - Superior Oblique Lateral rotation, Intorsion, Depression. The muscle is of interest as it originates in the common tendinous ring, then passes through a sling or pulley attached to the superio-medial orbit before attaching at the superior posteriolateral segment of the globe (see below):

Inferior oblique acts to extort, elevate and abduct the eye; this muscle does not arise from the common tendinous ring, but instead from the maxillary component of the anterior orbit and attaches to the inferior posteriolateral globe, see below, deep to the inferior rectus:

3) Why do we examine eye movements in an "H" shape?

Although above I have talked about eye movements from the neutral position, in clinical practice it is not possible to ask a patient to contract, for example, only their superior oblique muscle. If we examined simply elevation/depression and adduction/abduction, we would get a mixed picture of which muscle was acting. The picture below is of the right eye movements in a patient, as observed by the examiner, i.e. lateral rectus abducts the eye:

By examining in an "H" pattern, we can isolate the action of individual muscles. This image is also of right eye movements in a patient, as observed by an examiner. For the muscles in the left eye, simply consider a mirror image.

You'll note that even though the action of the superior rectus is elevation, intorsion and adduction, once the eye is already abducted by lateral rectus, superior rectus acts solely to elevate the eye. This is because once the eye is abducted, the other eye elevator - inferior oblique - becomes slightly slack and is unable to contribute to elevation.

Similarly even though the action of inferior oblique is extortion, elevation and abduction, once the eye is adducted by medial rectus, the superior rectus is unable to act as it now is slack, leaving inferior oblique as the only muscle able to elevate the eye.

The previous two paragraphs probably do not make much sense unless you've understood the attachments and direction of rotation caused by each muscle earlier in this post. Please feel free to ask questions or for clarification below!

Next time from me: what happens when these movements go wrong...

Spurious Elevations of Vitamin B12 with Pernicious Anemia

Yang DT, Cook RJ. Spurious elevations of vitamin B12 with pernicious anemia. N Engl J Med. 2012 May 3;366(18):1742-3.

Level 2

Have you ever seen a patient with pernicious anemia with spuriously elevated levels of vB12? 

This report of 2 cases, of pernicious anaemia, highlights an important the problem of false normal results for vitamin B12 levels generated by automated analysers when the serum of patients with pernicious anaemia are evaluated. The results have been attributed to high levels of intrinsic factor–blocking antibodies that interfere with the assay.

Subacute combined degeneration of the spinal cord due to vB12 deficiency.
Teaching point: If you have a high-index of suspicion that a patient has vB12 deficiency please check plasma levels of homocysteine and methylmalonic acid and screen the serum for anti-intrinsic factor–blocking antibodies and antiparietal-cell antibodies. Or you can do the methionine loading test. 

Smooth red tongue due to vB12 deficiency 

Sunday, 6 May 2012

TED Talk: Oliver Sacks

If you are not a convert already can I suggest watching TED talks; I am an addict! 

Oliver Sacks is a British trained neurologist and a gifted writer and storyteller. He is well known as a writer and you will a learn a lot of neurology from reading his books:
  1. Migraine (1970) London: Faber and Faber; Berkeley: University of California Press
  2. Awakenings (1973) London: Duckworth; New York: Doubleday
  3. A Leg to Stand On (1984) London: Duckworth; New York: Summit Books
  4. The Man who Mistook his Wife for A Hat (1985) London: Duckworth; New York: Summit Books
  5. Seeing Voices: A Journey into the World of the Deaf (1990) Berkeley: University of California Press; London: Picador
  6. An Anthropologist on Mars (1995) New York: Alfred A. Knopf; London: Picador
  7. The Island of the Colorblind (1996) New York: Alfred A. Knopf; London: Picador
  8. Uncle Tungsten: Memories of a Chemical Boyhood (2001) New York: Alfred A. Knopf; London: Picador
  9. Oaxaca Journal (2002) Washington DC: National Geographic Directions
  10. Musicophilia: Tales of Music and the Brain (2007) New York: Alfred A. Knopf; London: Picador
  11. The Mind’s Eye (2010) New York: Alfred A. Knopf; London: Picador
I would recommend starting with "The man who mistook his Wife for a Hat"

Saturday, 5 May 2012

Case study: ascending motor weakness

Ms SE a 26-year old single woman presents with an acute ascending motor weakness. On examination she has a lower motor neurone pattern of weakness and areflexia. She had recent diarrhoeal illness 2 weeks ago. At present she is unable to walk due to lower limb weakness and has mild distal weakness in her hands that is limiting her ability to perform fine motor tasks. Her vital capacity is normal, she has full control of her bladder and bowel and there is no evidence of autonomic dysfunction. General examination is unremarkable with no evidence of systemic disease.

Teaching points:

Level one

Areflexia: What is a reflex? What does areflexia mean?
What is a lower motor neurone weakness?
Differential diagnosis of acute ascending weakness?
How do you differentiate a motor neuropathy from acute spinal cord pathology?

Level two

What do you expect the nerve conduction study results to show?
How do you monitor respiratory function in patients with neurological disease? At what level do you admit a patient to ITU for monitoring?

Level three

What findings on the nerve conduction studies support a diagnosis of demyelination?
Apart from nerve conduction studies what other investigations would you do an why?
The consultant recommending treating this patient with IVIG. How do you use IVIG? What are the complications of using IVIG?


Friday, 4 May 2012

Clinical skills: Hoffman's reflex

Level 1
The test involves tapping the nail or flicking the terminal phalanx of the middle or ring finger. A positive response is seen when terminal phalanx of the thumb flexes. A positive Hoffman's reflex indicates an upper motor neuron lesion or a pyramidal sign. 

In my experience Hoffmann's reflex are often symmetrically positive in normal people, particularly in subjects with brisk reflexes, which is why I seldom use this test myself. An asymmetrically positive Hoffmann's sign is more worrying and is likely to be pathological.

Hoffman's reflex is similar to a deep tendon reflex and is mediated by spindle fibres and is therefore a monosynaptic reflex pathway. In other words it should be interpreted as you do tendon reflexes. In comparison, the plantar or Babinski's reflex is not a deep tendon reflex and hence is always considered pathological in adults.

Other relevant posts of interest: Babinski's sign, tendon reflexes

History of neurology: Johann Hoffmann (March 28, 1857 – November 1, 1919, Heidelberg) was a German neurologist remembered for describing the reflex above and Werdnig-Hoffmann disease (infantile spinal muscular atrophy or SMA).

Thursday, 3 May 2012

Lecture Halls without Lectures — A Proposal for Medical Education

If you are a medical educationalist or are interested in medical education you should read this article:

Prober & Heath. Lecture Halls without Lectures — A Proposal for Medical Education. | N Engl J Med 2012;366:1657-1659.

Some extracts:

"It’s time to change the way we educate doctors. Since the hours available in a day have not increased to accommodate the expanded medical canon, we have only one realistic alternative: make better use of our students’ time."

"As Sir William Osler aptly said, “He who studies medicine without books sails an uncharted sea, but he who studies medicine without patients does not go to sea at all.” Yet conversations with medical students about the first-year medical curriculum reveal that about half of lectures proceed without even the briefest example involving patients."

".... rather than a standard lecture-based format, the instructors provided short online presentations. Class time was used for interactive discussions of clinical vignettes highlighting the biochemical bases of various diseases. The proportion of student course reviews that were positive increased substantially from the previous year. And the percentage of students who attended class shot up from about 30% to 80% — even though class attendance was optional."

"I am an old convert! Lectures are the worst platform for teaching; they encourage passive learning and turn medical students into zombies. When I was a 3rd year medical student I got so despondent with my pathology lecturer, who essentially was rehashing what he had written in his published book of pathology lecture notes, that I stopped going to pathology lectures. I spent the time learning pathology myself in the library using a text book and other sources. This made me an active learner. When something interested me, for example the pathology of the thymus, I asked the pathology tutors to show me thymic sections in our pathology practicals; pathology of the thymus was not in our syllabus. I won the pathology prize that year, with a mark that was nearly 10% higher than the second best student. After my pathology viva the head of pathology summoned me to a meeting to find out why I had done so well in my pathology exams and to encourage me to do an intercalated BSc in pathology, with a further option of a follow-on intercalated PhD. Needless to say I did not take up his offer, but I did stop going to medical school lectures. Not attending lectures turned me into an active learner, which was the main reason I did well at medical school.  I only attended lectures when the lecturer had an established reputation for giving inspirational talks; these were few and far between." 

"In short  this paper suggests doing away with classic lectures and using the time instead to encourage active, rather than passive, learning, around clinical cases. Becoming an active learner and putting patients at the center of your learning experience will change your life. It will also make you a neurophile. Try it!"