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Normally, blood that enters the inner ear has the same density as the endolymphatic fluid that is normally contained within the inner ear compartments. The main sensory organ of the inner ear called the cupula is responsible for spatial orientation by informing the brain when a head rotation/movement has occurred. With a normally functioning inner ear, the cupula is stimulated ONLY when it is "pushed" by the surrounding endolymphatic fluid when the body moves/turns (watch video demonstrating this).
However, this delicate balance between the cupula and endolymphatic fluid is altered when alcohol is present.
When alcohol enters the bloodstream, it literally makes the blood less dense given alcohol's lower specific gravity. When the alcohol infused blood enters the inner ear, the alcohol first rapidly diffuses into the inner ear cupula because of the proximity of this structure to blood capillaries and only slowly diffuses into the surrounding endolymph.
All of a sudden, the cupula now becomes less dense than the surrounding endolymphatic fluid when normally it should be the same density. Because of the cupula's lower density, it will "float" relative to the endolymph and with this movement, the inner ear sends an erroneous signal to the brain that a head rotation/movement has occurred. Remember, in the normal situation, the cupula ONLY moves when head movement occurs, but now cupula movement occurs due to a density change. Furthermore, cupula movement occurs due to any change in gravity's relative orientation to the head as long as the cupula "floats" in its lower density bath of endolymphatic fluid.
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Recall that alcohol rapidly diffuses into the cupula from the blood, but only slowly into the endolymph. As such, assuming the consumption of alcohol has stopped, an equilibrium of sorts is achieved about 3 hours later when the alcohol concentration in the endolymph catches up to the alcohol concentration found in the blood. When this occurs, there is no difference in density between the cupula and endolymph resulting in restoration of "normal" balance. This is the honeymoon period signaling the end of PAN 1 and the start of PAN 2.
Unfortunately, as blood alcohol levels start to fall, the reverse situation occurs with the cupula becoming "heavier" than the surrounding endolymph (alcohol concentrations fall more quickly in the blood due to liver metabolism and alcohol more slowly diffuses out of the endolymphatic fluid back into the blood). The heavier cupula now "sinks" relative to the surrounding fluid resulting in a movement which again erroneously signals the brain that a turn/movement has occurred.
Because the cupula deflection is now in the opposite direction, the spins from the perspective of the intoxicated person is now in the opposite direction from the spins experienced earlier in their drunken state.
Eventually, alcohol concentrations drop back down to zero both in the blood (cupula) and endolymph resulting in normal balance restoration due to equivalent densities of the cupula and surrounding endolymph. With this normalization, PAN 2 has now ended.
The overstimulation of the inner ear during PAN I and PAN II is associated with the unsteadiness, nausea, and vertigo felt by intoxicated individuals. PAN I is associated with positional problems (e.g. standing and walking) while PAN II is associated with hangover effects.
So now you know... This explanation is also known as the "Buoyancy Hypothesis."
Positional alcoholic nystagmus (PAN) in man following repeated alcohol doses. Acta Otolaryngol Suppl. 1975;330:15-29.
Heavy water nystagmus and effects of alcohol. Nature. 1974 Feb 8;247(5440):404-5.