Correct clinical diagnosis of dizziness in the ER could save $$ billions

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We have already blogged about the danger of escalating health costs in the USA.

The cost of emergency room visits for severe dizziness has grown exponentially in recent years, topping $3.9 billion in 2011 and projected to reach $4.4 billion by 2015.

Investigators from Johns Hopkins estimate that half a billion a year could be saved immediately if emergency room physicians stopped the routine and excessive use of head CT scans to search for stroke in dizzy patients, and instead used simple bedside physical exams to identify the small group of patients that truly needs imaging.

Click here to find out more about the Johns Hopkins study.

Click here to find out more about the hidden dangers of unnecessary CT scans.

Once they understand how inner ear disease can cause vertigo and nystagmus, any physician can use our simple clinical scheme to distinguish inner ear problems from more serious and rarer central causes like stroke in dizzy patients.  Click here to find out how.

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What causes vertigo and nystagmus?

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Dizziness is a vague term than different people use to indicate a variety of experiences including lightheadedness, unsteady gait and vertigo.

Vertigo is a more precise term, which indicates a sense of false movement – if feels like the world is moving (using spinning).

To understand what causes vertigo, you first have to understand the vestibular system, and the vestibular ocular reflex (VOR).

The vestibular system is made up of 2 systems of semicircular canals, within the inner ears (or labyrinths), designed to detect head position and movement:

inner ear

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Each semicircular canal works like a spirit level to determine head position in it’s plane:

spirit level

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The VOR is a connection between the vestibular system and the muscles that move the eyes, which allows us to seamlessly compensate for every little head movement.

Simple_vestibulo-ocular_reflex

Life without a normally functioning VOR would be something like this:

For the sake of simplicity, we’re just going to talk about the horizontal canals.

There is tonic input to the brain from each side at rest.

When the head moves to the right, input from the right side increases, input from the left side decreases, this creates a mismatch between the two sides, and brain knows the head is moving:

The VOR then provides a reflex corrective eye movement to the left, so that the eyes keep looking in the same direction to maintain fixation:

normal VOR

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Now, let’s say there’s a medical problem like a viral infection or a tiny stroke, that injures the L sided labyrinth, we call this labyrinthitis or acute labyrinthine failure.  This reduces tonic input from the damaged L side, and will lead to the same mismatch as if the head were turning to the right side:

labarynthitis

This, in turn, will:

1. Fool the brain into thinking the head is turning to the right side, creating an illusion of movement, “vertigo” .

2. Lead to unnecessary “corrective” eye movements to the L side, which (in the alert patient) will be followed by a voluntary eye movement back to the R to maintain fixation.  This combination of a slow drift of the eyes to the underactive side, and a rapid eye movement back to the middle is know as nystagmus.

Optokinetic_nystagmus

Nystagmus from L labyrinthine failure – slow eye drift to L, then rapid eye movement back to R side.

We can reproduce this phenomenon with the cold caloric – the cold water causes temporary vestibular hypofunction, vertigo and nystagmus:

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Ultimately, the brain will “reset” and the vertigo and nystagmus improve.  During this phase, stable visual input (which says the world is stationary) overcomes the abnormal vestibular input (which says the world is moving).  You are probably aware of this phenomenon from sea and car sickness –  You are less likely to get sick if you are on deck (looking at the horizon) or in the front seat of a car (looking out the window).