The drug is used to treat addiction, especially to alcohol, like Acamprosate. (The latter was also tested on tinnitus.) Naltrexone helps with addiction by affecting dopamine. And dopamine pathways are implicated in tinnitus. But note Naltrexone helps with tinnitus distress, not volume. However, it is possible that by favorably affecting mood, you will be able to habituate. Some people do habituate to loud tinnitus, though most people--myself included--believe this must be very difficult.
Med Hypotheses. 2005;65(2):349-52.
Tinnitus dopaminergic pathway. Ear noises treatment by dopamine modulation.
Lopez-Gonzalez MA1, Esteban-Ortega F.
Abstract
To date, the neurophysiological model has been used to explain the complexity of tinnitus. However from now on, the tinnitus dopaminergic pathway opens new horizons for ear noises management. Tinnitus perception takes place in prefrontal, primary temporal and temporo-parietal associative areas, as well as the limbic system. Dopaminergic neurotransmitters go through prefrontal, primary temporal, temporo-parietal associative areas and the limbic system. Tinnitus perception and dopaminergic pathway share the same cerebral structures, which control attention, stress, emotions, learning, memory and motivated behavior. Distress of tinnitus emanates from these same cerebral functions. The dopaminergic pathway can be modulated by agonists and antagonists of their receptors and can reduce the perception of tinnitus, such as sulpiride, amisulpride, olanzapine, quetiapine, ziprasidone, zuclopenthixole and aripiprazole, still under investigation, that together with sound treatment as the Sequential Sound Therapy, and a personal contact with the patient, constitute a tinnitus integral treatment.
Sulpiride also affects dopamine and, taken with melatonin, has been studied as favorably reducing tinnitus perception:
J Otolaryngol. 2007 Aug;36(4):213-9.
Sulpiride and melatonin decrease tinnitus perception modulating the auditolimbic dopaminergic pathway.
Lopez-Gonzalez MA1, Santiago AM, Esteban-Ortega F.
OBJECTIVES:
Sulpiride and melatonin decrease dopamine activity. Sulpiride, a D2 antagonist of dopamine receptors, and melatonin, a pineal substance with antidopaminergic action, are administered to tinnitus patients to decrease tinnitus perception.
DESIGN:
A prospective, randomized, double-blinded, placebo-controlled study was done.
SETTING:
General otorhinolaryngologic consultation for 2002-2004 in Seville, Spain.
METHODS:
One hundred twenty patients consulted for subjective tinnitus. They were included randomly in four groups of 30. One group took sulpiride (50 mg/8 h) alone, the second group took melatonin (3 mg/24 h), the third group took the same doses of sulpiride (50 mg/8 h) plus melatonin (3 mg/24 h), and the fourth group took placebo (lactose 50 mg/8 h), all for 1 month. Ninety-nine patients completed the study.
MAIN OUTCOME MEASURES:
Clinical history, tonal audiometry, tympanometry, and tinnitometry were done at the beginning and end of the study. Subjective grading of tinnitus perception and a visual analogue scale (0-10) were done for evaluation of results.
RESULTS:
Based on the subjective grading, tinnitus perception diminished by 56% in patients treated with sulpiride, by 40% in patients treated with melatonin, by 81% in patients treated with sulpiride plus melatonin, and by 22% in patients treated with placebo. Based on the visual analogue scale, tinnitus perception diminished from 7.7 to 6.3 in patients treated with sulpiride, to 6.5 in those treated with melatonin, to 4.8 in patients treated with sulpiride plus melatonin, and to 7.0 in those treated with placebo.
CONCLUSIONS:
Sulpiride and melatonin reduce tinnitus perception, decreasing dopamine activity. The tinnitus auditolimbic dopaminergic pathway has broad therapeutic implications. [emphasis added]
Some people my also find this article interesting, but it does not refer to tinnitus. However, the article does refer to chronic pain:
Pleasure in the brain is primarily mediated through the neurotransmitter dopamine. Neurons in the ventral tegmental area (the starting post for those dopamine tracts I talked about a few days ago) respond to sex, drugs, rock n' roll, food, and communicate with some other neurons in the nucleus accumbens, and a third neural network in the amygdala and the ventromedial prefrontal cortex. These are all segments of the "medial dopamine tracts" I reviewed at some length a few days ago. It may be of interest that those of you who derive pleasure from other people's pain (schadenfreude) experience your mischievous pleasure here as well.
Pain is experienced in the aptly named "cortical pain network," which are regions of the brain a little separated from the pleasure centers. The different areas of the pain network collect sensory pain (such as a splinter in one's finger) and emotional pain. Typically, experiments used to isolate pain circuitry in the brain involve "aversive stimuli" such as electric shock.
So it turns out that social pleasure and pain have hijacked these evolutionary circuits of pleasure and pain, so that if you score a date with that hot chick and share a high five with your frat brothers, or you get arrested for that meth lab you are running in the basement of the chemistry building at school, you will experience the pleasure and pain in the same areas of the brain that you experience sex and electric shock. It hurts to be human, sometimes. If you feel that you are fairly treated and are feeling cooperative, your pleasure centers are stimulated. If you grieve the loss of a loved one, your cortical pain network lights up.
And what about opiates or wheat exorphins or binge eating? Turns out those activities stimulate the dopamine reward centers of the nucleus accumbens. That new weight loss drug is a combination of two older drugs, naltrexone and buproprion (wellbutrin). Naltrexone is a straight-up opiate blocker. It is FDA-approved to reduce cravings for alcohol, but to be honest I use it more often for people trying to kick an oxycodone or heroin habit. You have to be off opiates for a couple weeks or risk an exceedingly uncomfortable precipitated withdrawal, and once you are on naltrexone, your opiate tolerance will drop like a rock, so if you go back to using like you used to, you could easily overdose. But naltrexone isn't a controlled substance, and if you take your medicine as prescribed and try to use opiate drugs on top of it, those drugs won't work. There's nothing like a pharmacologic lock on the opiate system to help out an opiate addict. Naltrexone has been studied in binge eating and in gambling, and for some people, it seems to help. I've used it on a couple of occasions for sleep eating with extreme carb (grain) cravings with some success, also in patients with celiac who can't seem to kick the wheat habit. Naltrexone use requires monitoring of the liver, and typical side effects include upset stomach. But both of those are less noxious than a heroin habit in my opinion, but every case is different and risks and benefits must be discussed for each situation. [emphases added]
For further reading on naltrexone and dopamine--specifically as applied to alcoholism--please see this article:
References:
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