Mechanisms for chronic dizziness and motion intolerance?

— Begin quote from “rockyksmom”

HI
I haven’t read the links yet, but I will, and thanks for posting.
Dr. Staab, if memory serves, really believes in anxiety as the root of the dizziness. I am so tempted to believe that, as I never had any history of migraine…but I did get 2 visual auras, and that I guess is the defining YUP…sigh…
Kelley

— End quote

Hi Kelly,

This is basically right but I wanted to clarify one thing. I was a patient of Dr. Staab at the Mayo Clinic, and he said that there are two types of CSD: one is where there is no vestibular injury per se but the root cause is anxiety (as you mention above) and other is where there is some traumatic event such as a vestibular bacterial infection or virus that gives BPPV attacks followed by CSD. In the second case, the brain is overactive in trying to adjust to the vestibular event, and it continues to be overactive even when the vestibular function has healed. In both cases, the treatment is SSRIs/SSNRIs. Normally they start with Effexor, but in my case they started with Celexa.

I wish the doctors would develop some system for telling us which A-D would work best for us, prior to the trial-and-error!

I am looking further into the Smith and Darlington article, and this is a real gold mine of information. I believe that this research gives us some understanding about how migraine can cause both episodic and chronic vestibular symptoms.

“If a sudden change in serotonin levels in the VNC is the cause of dizziness following SSRI withdrawal, then there are several important implications for vestibular function. First, it suggests that in cases where the natural levels of serotonin in the brain are altered, such as in depression, the change in serotonin levels in the VNC may affect vestibular function. In fact, Soza Ried and Aviles [20] reported that patients with major depression who were not medicated exhibited a significant decrease in the slow phase velocity of the vestibulo-ocular reflex for rotation to the right side, suggesting hypoactivity of the right VNC.”

“Serotonin has been found in the peripheral vestibular system, in the vestibular labyrinth, although its function there is poorly understood (see Smith and Darlington [11] for a review). Serotonin is also known to be an important neurotransmitter in the brainstem vestibular nucleus, which along with the cerebellar flocculus, is the only area of the brain to receive direct input from the vestibular nerve carrying vestibular sensory information from the inner ear. Serotonin exists in high concentrations in the vestibular nucleus complex (VNC) and an important source of serotonergic projections to the VNC comes from the dorsal raphe nucleus”

“Interestingly, approximately one-eighth of the serotonergic dorsal raphe neurons projecting to the VNC also project into the central amygdaloid nucleus [13], suggesting a surprising connection between the vestibular system and anxiety.”

“Since glutamate is the major excitatory neurotransmitter in the VNC and the neurotransmitter mediating input from the vestibular nerve [11], this suggests that the impact of changes in serotonin levels on VNC neurons could be dramatic. Consistent with this evidence, 5-HT1F receptors have recently been reported to be co-localized with glutamate in the VNC [14].”

“the decrease in serotonin may result in the reduced activation of the 5-HT1F receptors, thereby increasing glutamate release by VNC neurons. If this happened bilaterally, as would be expected with a systemically administered drug, then both the left and right VNCs would send increased vestibular signals to the rest of the brain. This hypothesis would be consistent with the evidence that patients discontinuing SSRIs do not experience vertigo (which would require unilateral increased activation of the VNC) but only dizziness, and that the dizziness is exacerbated by head movement.”

Link: xa.yimg.com/kq/groups/1920818/73 … ziness.pdf

This article shows that the anxiety processing region of the brain and the vestibular processing portion of the brain share some common pathways in the dorsal raphe nuclei. The job of the dorsal raphe nuclei is to release serotonin into the brain. Since the raphe nuclei shares some pathways for the amygdala and the vestibular nucleus, we can derrive that low serotonin in the amygdala can cause low serotonin in the vestibular nucleus.

“These findings indicate that a subpopulation of serotonergic and nonserotonergic dorsal raphe nucleus cells may act to co-modulate processing in the vestibular nuclei and the central amygdaloid nucleus, regions implicated in the generation of emotional and affective responses to real and perceived motion.”

ncbi.nlm.nih.gov/pubmed/16600519

Wowza!! That’s a hell of an article and I find it amazing! Wish I understood it better. So finding a medicine that would increase serotonin would seemingly help, but since sero In other places in the body would just cause side effects. And!! A need to decrease glutamate, which is Prevelent throughout the body as well .
I am not near a computer for a few more days but really want to research this. Thanks for sharing
Kelley

— Begin quote from “ichbindarren”

This article shows that the anxiety processing region of the brain and the vestibular processing portion of the brain share some common pathways in the dorsal raphe nuclei. … Since the raphe nuclei shares some pathways for the amygdala and the vestibular nucleus, we can derrive that low serotonin in the amygdala can cause low serotonin in the vestibular nucleus.

— End quote

That’s interesting. I’ve observed how a little bit of sudden stress can immediately worsen my balance. However I may be mixing things up because I imagine serotonin doesn’t have an effect that quickly.