Nimodipine

Rhea

Member
Author
Apr 30, 2013
172
UK
Tinnitus Since
2004
Hey,

A person mentioned "Nimodipine" as a tinnitus treatment. I googled Nimodipine and it appears that it works by binding specifically to L-type voltage-gated calcium channels.

This sound similar to Autifony's approach with the calcium channels? Maybe not. I just thought it was interesting...

Rhea x
 
Autifony's AUT00063 is targeting potassium channels. I don't really know what potassium channels or calcium channels are though. Never heard of Nimodipine either. What's its original purpose?
 
If it's for high blood pressure it seems to me that it could be beneficial for pulsitate T only, but I have no idea. Looking at the links @Mpt provided, this could also make the T worse, so be careful if you gonna try it out. We better call in the science guys on this one: @jazz @Hudson @bill 112 @benryu what exactly is this?
 
Nimodipine acts as a calcium channel blocker, the direct effect is to lower blood pressure. As you said, this may work for some blood circulation problem tinnitus (pretty rare).

It can also help some other "regular" tinnitus because a low blood pressure deprive blood from oxygen. Less oxygen means the brain has less energy and the neuronal hyperexcitability is less important.

But let's be clear, this is A VERY BAD idea and this is only VERY SHORT TERM. Plus such as Aspirin that lower blood pressure too, this drug is likely to increase tinnitus, or the low oxygenation is also likely to create some yoyo effect.

Forget about this drug :)
 
Ironically I found this post about the drug the other day...

"I have very bad tinnitus likely due to my age 67. You mention no medication will help. That is not correct. I use nimodipine 30 mg capsules which does not eliminate the tinnitus but cuts it back from 50 -70%. I can sleep now and work well throughout the day. The best time is to take a pill about an hour before you go to sleep. There may or may not be some tinnitus in the morning when you wake up but it is under control. Also do not eat for at least 2 hours before taking the pill and not under one hour after taking the pill. Take the pill with a full glass of water."
 
I found something interesting here.

In an open study 30 patients with the symptome of tinnitus were treated for 12 weeks with nimodipin (Bay e 9736) 3 × 30 mg/die. 12 patients showed sudden deafness with a history of one day up to more than 20 years. In six cases we observed complete remission, in two cases remission up to 70-80 %, in two cases slight improvement. Four patients showed no side reaction to the treatment of nimodipin. Ten patients suffered from so-called degenerative inner ear deafness. 3 (n = 10) showed complete remission, one nearly 90 % improvement, another patient showed 60 % improvement, one slight improvement, in 4 patients tinnitus persisted.

Vertigo-Morbus Menière: 4 out of 30 patients were included with the diagnosis of Morbus Menière with tinnitus. 3 (n = 4) showed complete remission of tinnitus, normal hearing level and no more symptoms of vertigo after 12 or less weeks of treatment with nimodipin. In one case with an history over more than 20 years only the vertigo could be cured.

Traumatic inner ear deafness is not apt to be treated with an agent such as nimodipin.
 
From a Facebook group:

upload_2021-5-4_9-50-20.png
 
Calcium channel blockers (CCB) of the dihydropyridine type like Nimodipine seem pretty overlooked in the tinnitus community. Compared to other CCBs they have relatively high affinity for L-type calcium channels. Compared to the phenylalkylamines, like verapamil, the dihydropyridines have higher affinity for the blood vessels compared to the heart.

L-type calcium channel blockers are interesting for tinnitus and hyperacusis because, at the basolateral membrane of the outer hair cells, Cav1.3, an L-type calcium channel, is responsible for the influx of calcium ions which cause OHCs to release vesicles to Type II afferent boutons. Type II afferent spiral ganglion neurons are thought to be implicated in some forms of hyperacusis and tinnitus as well.

Does anyone have any experience with the following dihydropyridine drugs?
  • Amlodipine (Norvasc)
  • Aranidipine (Sapresta)
  • Azelnidipine (Calblock)
  • Barnidipine (HypoCa)
  • Benidipine (Coniel)
  • Cilnidipine (Atelec, Cinalong, Siscard) - not available in the US.
  • Clevidipine (Cleviprex)
  • Efonidipine (Landel)
  • Felodipine (Plendil)
  • Isradipine (DynaCirc, Prescal)
  • Lacidipine (Motens, Lacipil)
  • Lercanidipine (Zanidip)
  • Manidipine (Calslot, Madipine)
  • Nicardipine (Cardene, Carden SR)
  • Nifedipine (Procardia, Adalat)
  • Nilvadipine (Nivadil)
  • Nimodipine (Nimotop) - this substance can pass the blood-brain barrier and is used to prevent cerebral vasospasm.
  • Nisoldipine (Baymycard, Sular, Syscor)
  • Nitrendipine (Cardif, Nitrepin, Baylotensin)
  • Pranidipine (Acalas)
From a Facebook group:

View attachment 44787
Very cool. I wish there were more doctors that would and could concoct medicine and supplement combos like this, instead of cycling the patient through each drug one by one.
 
L-type voltage-gated calcium channel is involved in the pathogenesis of acoustic injury in the cochlea

Excessive calcium entry into cells leads to cell death, and voltage-gated calcium channels (VGCCs) are responsible for the calcium entry in the central nervous system. VGCC blockers inhibit excessive calcium entry and protect the central nervous system against various types of injury. The purpose of the present study was to identify the type of calcium channels that is responsible for acoustic injury of the cochlea. The effects of L- and T-type VGCC blockers on acoustic injury were examined. Female ddY mice, at 8 weeks of age, were used in this study. The animals were subjected to a 4-kHz pure tone of 128-dB sound pressure level (SPL) for 4 hours through an open field system inside a sound-exposure box. A L-type or T-type VGCC blocker was administered immediately before acoustic overexposure. The hearing ability was evaluated using the auditory brainstem response (ABR). ABR is an electrical signal evoked from the brainstem by the sound. After the final ABR measurement at two weeks after acoustic overexposure, cell nuclei in the organ of Corti were stained with propidium iodide, and hair cell loss was calculated in a region 3.66 mm from the apex. Each of four L-type VGCC blockers tested, i.e. diltiazem, verapamil, nicardipine and nimodipine, significantly improved shifts of the ABR threshold from the pre-exposure levels. In addition, each L-type VGCC blocker consistently decreased hair cell loss, but not a given T-type calcium blocker. The present findings suggest that the L-type VGCC is involved in the pathogenesis of acoustic injury in the cochlea.
 
It was Pragma Therapeutics that was developing either an L or T type calcium channel blocker. Now it seems there is no information on them.
 
I'm a pharmacist and I find Nimodipine very interesting. I might discuss it with a few doctors.
If the results are positive, maybe these doctors can make some sort of recommendation letter for Nimodipine? I suppose it would make it easier for tinnitus patients to get Nimodipine prescribed if they can present their GP with that kind of letter.
 
I'm a pharmacist and I find Nimodipine very interesting. I might discuss it with a few doctors.
Did you have a chance to discuss this with doctors yet? Any thoughts?

Thank you!
L-type calcium channel blockers are interesting for tinnitus and hyperacusis because, at the basolateral membrane of the outer hair cells, Cav1.3, an L-type calcium channel, is responsible for the influx of calcium ions which cause OHCs to release vesicles to Type II afferent boutons. Type II afferent spiral ganglion neurons are thought to be implicated in some forms of hyperacusis and tinnitus as well.
And if type II afferents are nociceptors, you can add noxacusis.

Yes, this is VERY interesting.
Cp-PYT is so far the only compound with some evidence for Cav1.3-selectivity.
(Source)
Nimodipine blocks the neuronal L-type Ca2+ channels, CaV1.2 and CaV1.3
(Source)

Prof. Jos Eggermont got back to me and said he is using Amiodipine (Sandoz) but that must be a typo, and he meant Amlodipine.

However, Nimodipine might be more effective:
5.2.2. CCB Brain Drug Delivery

Brain permeation has been demonstrated for several approved DHP LTCC blockers in several species, including humans. An exception is amlodipine which does not efficiently cross the blood-brain barrier. Isradipine and nimodipine reach total brain concentrations [/B]that are similar to those in plasma but increasing the drug concentration in brain relative to plasma would be another strategy to reduce peripheral side effects and allow higher dosing to efficiently engage brain channels.
(Source)

But then again, we don't know much about the blood-labyrinth barrier.

What do you think, pharmacists? Amlodipine or Nimodipine?

I have an appointment on Tuesday with my GP.
 
Does anyone have experience taking Nimodipine?
I have for a while used 4 x 30 mg per day. Out of all the drugs I've tried, it has helped the most with stabbing hyperacusis pain, although I must mention that I was also and still am using 20 mg of Memantine per day, and occasionally 0.5 mg Clonazepam. I have also been following part of Ziem's neural protocol for 2 months now. The effect lasted for a couple of days before fading out, but was very noticeable. I don't think it affected my tinnitus.

Unfortunately, even though I repeatedly ask him for a higher dose, my current doctor has only prescribed me 30 mg Nimodipine per day.
 
I have for a while used 4 x 30 mg per day. Out of all the drugs I've tried, it has helped the most with stabbing hyperacusis pain, although I must mention that I was also and still am using 20 mg of Memantine per day, and occasionally 0.5 mg Clonazepam. I have also been following part of Ziem's neural protocol for 2 months now. The effect lasted for a couple of days before fading out, but was very noticeable. I don't think it affected my tinnitus.

Unfortunately, even though I repeatedly ask him for a higher dose, my current doctor has only prescribed me 30 mg Nimodipine per day.
Do you have TTTS, and if yes, has anything you have tried helped out with that?
 
I have experience with Amlodipine. It spiked my tinnitus a lot. I can't sleep now.
Sorry to hear that. I've heard from Dirk de Ridder that either N or T-type calcium channel blockers (I don't remember which one he said) can worsen tinnitus. Amlodipine also blocks N-type calcium channels so maybe the worsening is because of that.
Do you have TTTS, and if yes, has anything you have tried helped out with that?
I don't have TTTS.
 
Back from the ENT.

He suggested an MRI, a sleep specialist and CBT. Great.

I'm in pain for God's sake.

Does anyone know the difference between Nimodipine and Verapamil? I want to give it another try at the GP.
 

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