| Transcript |
So, today we're going to be talking about how I use tempo in the history to help differentiate things in the differential diagnosis. As you know, the differential diagnosis is always the same and you might have your own mnemonic that you're using; a popular one is "VINDITCH MD"-vascular, ischemic, neoplastic, demyelinating, infectious, traumatic, congenital, and hereditary, metabolic, dystrophic, degenerative. Whatever your little mnemonic is that's the differential we are starting with in every single case. And so, one of the important pieces of information is the tempo of whatever their complaint is. So, we'll just use decreased visual acuity or visual field in this example. So, we're going to take prototypes from each of these things and establish how the tempo will alter the differential diagnosis and how we think about this case. So, for example if it's a 25-year-old white female with acute unilateral loss of vision, and RAPD, and a normal fundus that is a duck that is quacking, flying, and looking like optic neuritis. So, in this 25-year-old female, if we have a hundred percent of our vision here, and zero percent of our vision here and time the tempo of that vision loss (so, normally patients who have optic neuritis, in this case the 25-year-old female, she will have degradation of her vision over time), it's usually sub-acute and then it either stays the same for a little bit if we give steroids or no steroids it doesn't matter because the vision will always get better. And this can be varying in severity: can be very severe, or not very severe, but the tempo is the same. They get worse sub-acutely and then over the next 14 days they get better with or without treatment: optic neuritis. However, if we change the age to a 45-year-old, acute unilateral loss of vision, RAPD but we have a swollen optic nerve and a small cup-to-disc ratio in the fellow eye, and is hypertensive, and diabetic that's going to be more in line with an ischemic optic neuropathy rather than optic neuropathy from demyelinating disease. And because the disc is swollen that's going to be anterior ischemic optic neuropathy. And because the patient's a forty-five-year-old with vasculopathic risk factors that's likely to be non-arteritic anterior ischemic optic neuropathy. What does that look like? Well, they get worse. There's no effective treatment they either stay the same or they might get a little bit better and then it stays the same; that is the tempo of NAION. But what if the person keeps getting worse like this? Well, that's not non-(NAION), that's too much decline. So, if you have a 45-year-old like female who presents with unilateral loss of vision, and it's just painless and progressive over weeks or painless and progressive over months to years, that is the stem for neoplasm. That's what a compressive lesion looks like-an optic nerve sheath meningioma. It's just slowly pressing, and it just keeps pressing until you do something about it. So, the course of neoplasm is a relentless, painless, and progressive course. If it's benign-months to years; if it's a malignancy, it'll go faster-weeks. So, now you see how we're using the tempo to differentiate between vascular, and ischemic things, neoplasms, demyelinating things. For trauma, the worst deficit is going to be usually right away, to varying levels of severity, and either it gets better and stays the same, or sometimes it just gets better completely. But most of the time the trauma causes the deficit and it just remains the same. If you've had a congenital or hereditary optic neuropathy it just starts off bad and it just doesn't change-you're born with it. So, if you're a congenital thing you're blind, you stay blind. If you have amblyopia-amblyopia at this level. What if you have amblyopia, and it get worse? Well, that doesn't occur in adulthood. Amblyopia from childhood just stays the same. So, congenital things you're born with them: con-genital, the genesis, "con-"-with birth. Hereditary things are similar but sometimes hereditary things that should occur, occur when you're an adult. So, Leber hereditary optic neuropathy can look superficially like optic neuritis: a 25-year-old white male presents with acute unilateral loss of vision, they have a central scotoma. You think they have optic neuritis, but you do an MRI scan-no enhancement, no lesion seen, but instead of the expected course of improvement the tempo was this: he just went down, it stayed count fingers and it stayed the same ever since, and now it's in my other eye. That's going to suggest that the patient has Leber hereditary optic neuropathy. And degenerative things like age-related macular degeneration, they normally follow a degenerative course. Neurodegenerative things follow a degenerative course. It's going to mimic compressive and neoplastic lesions: a slowly progressive loss over months to years. So, you need to know that when you're dealing with the differential diagnosis no matter what your mnemonic is- "VITAMIN", or "VINDITCH MD", or whatever, that list of etiologies has a tempo associated with it. You need to understand that tempo so that you can incorporate that information into your clinical practice by analyzing and synthesizing, and not just memorizing the course of each of these things. |
