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Drug Treatment of Vertigo

Timothy C. Hain, MD Please read our disclaimer Page last modified: November 12, 2014

This pharmacological  review is written at a continuing medical education level. An older version of this article can be found in print: (Yacovino and Hain, 2012). We also highly recommend the neuropharmacology review article written by Soto et al (2013).

Pharmacology

There are at least four major neurotransmitters of the vestibular system involved in the "three neuron arc" between the vestibular hair cells and oculomotor nuclei that drives the vestibulocular reflex. There are also a host of other neurotransmitters which modulate function.

Glutamate is the major excitatory neurotransmitter at vestibular afferents (Serafin et al, 1992) as well as with neurons of the vestibular nuclei (where they may also release aspartate). Glutamate interacts with several subreceptors including NMDA, AMPA, and KA, and metabotrophic receptors (Soto et al, 2013). The NMDA receptors determine the basal discharge and tonic response (Soto et al, 2013).

According to Soto et al (2013), hair cells and efferent neurons release numerous other neuroactive substances including CGRP, substance-P, opiod peptides, endocannabinoids, GABA, ATP, nitrous oxide, adenosine and histamine.

Acetylcholine (ACH) is both a peripheral and central agonist affecting muscarinic receptors, including the vestibular nucleus as well as efferent synapses (Soto et al, 2013). Receptors found in the pons and medulla, presumably those involved with dizziness, are almost exclusively of the M2 subtype (Barton et al, 1994). However there are also nicotinic receptors, as well as M1 and M5 (Soto et al, 2013).

Calcium channels: These are not neurotransmitters but rather are methods that neurotransmitter release is triggered. The subtypes of L, N and T are reportedly active in the vestibular system (Soto et al, 2013). In the CNS, the N or P/Q type are the ones that participate in neurotransmitter release. Because calcium channels are ubiquitous, then may affect both input and output to the vestibular system (Soto et al, 2013).

Gamma-aminobutyric acid (GABA) and glycine are inhibitory neurotransmitters found in connections between second order vestibular neurons and onto oculomotor neurons (Spencer et al, 1992). Stimulation of the two types of GABA receptors, GABA-A and GABA-B, have similar effects on vestibular pathways (Neerven et al, 1989), but specific GABA-B agonists, such as baclofen, decrease the duration of vestibular responses in animal models (Cohen et al, 1987). Glycine receptors colocate with GABA receptors (Soto et al, 2312).

The circuitry by which several other neurotransmitters affect vestibular responses is less well understood. Histamine (H1-H3) is found diffusely in central vestibular structures and centrally acting antihistamines modulate symptoms of motion sickness (Takeda et al, 1989). Both the H1 and H2 subtypes of histamine receptors affect vestibular responses (Serafin et al, 1992). The H3 receptor is an autoreceptor and thus affects H1 and H2. The H4 receptor affects primary vestibular neurons (Desmadryl et al, 2012).

Norepinephrine is involved centrally in modulating the intensity of reactions to vestibular stimulation (Wood, 1979) and also affects adaptation. Both alpha (1 and 2) and beta receptors are found in the vestibular nucleus.

Dopamine affects vestibular compensation, and serotonin is involved with nausea.

Nitric oxide is also produced in the vestibular nucleus, and may play a role in compensation (Soto, 2013).

Serotonin receptors are also found in the vestibular nerve and vestibular nucleus (5HT-1, 2 and 7, according to Soto et al, 2013), but the functional significance of this uncertain (Ahn and Balaban, 2010). CGRP co-localizes with 5HT1F (Soto et al, 2013). Withdrawall from serotonergic drugs, such as SSRI antidepressants, is commonly associated with vertigo, and serotonin depletion can cause severe dizziness (Soto et al, 2013). It has been speculated that this is due to loss of inhibition of glutamate -- in other words, increased vestibular responses as glutamate is excitatory (Smith PF, Darlington CL, 2010). There is some equivocal data suggesting that serotonin agonists such as are used for migraine can prevent motion sickness.

VESTIBULAR SUPPRESSANTS

Vestibular suppressant and antiemetic drugs are the mainstay of treatment of vertigo. The term "vestibular suppressant" is a vague one generally used to indicate drugs that reduce nystagmus evoked by a vestibular imbalance or which reduce motion sickness. Table 1 lists commonly used vestibular suppressants, which consist of three major drug groups, the anticholinergics, the antihistamines, and the benzodiazepines.

Table 1: Vestibular Suppressants (order of preference)
Drug Dose Adverse Reactions Pharmacologic Class and Precautions Pregnancy Category
Meclizine (Antivert, Bonine) 25-50 mg q 4-6h sedating

antihistamine anticholinergic precautions if prostatic enlargement B
Lorazepam (Ativan) 0.5 mg BID mildly sedating benzodiazepine drug dependency  
Clonazepam (Klonopin) 0.5 mg BID mildly sedating benzodiazepine drug dependency  
Dimenhydrinate (Dramamine) 50 mg q 4-6h same as Meclizine antihistamine anticholinergic B
Diazepam(Valium) 2 bid PO

5 mg IV (1 dose)

sedating benzodiazepine drug dependency Precaution in glaucoma. D
Amitriptyline (Elavil) 10-50 hs sedating, in overdose cardiac arrhythmia anticholinergic tricyclic antihistamine  

Doses are all those used routinely for adults, and will generally not be appropriate for children. Pregnancy category varies from A (controlled human studies have failed to demonstrate a risk to the fetus) through D (there is positive evidence of human fetal risk, use only in a life-threatening situation or for a serious disease for which safer drugs cannot be used or are ineffective.

Anticholinergics which affect muscarinic receptors, such as scopolamine, increase motion tolerance. Anticholinergics also affect compensation, producing a reversible overcompensation if administered after compensation has been attained to a vestibular imbalance (Zee, 1988).

Agents with central anticholinergic effects are most important in treating vertigo, since anticholinergic drugs that do not cross the blood-brain barrier are ineffective in controlling motion sickness (Takeda et al, 1989). Unlike antihistamines which will be discussed subsequently, pure anticholinergics are ineffective if administered after symptoms have already appeared.

All anticholinergics used in the management of vertigo have prominent side effects of dry mouth, dilated pupils, and sedation. Scopolamine and atropine are nonspecific muscarinic receptor antagonists (Barton et al, 1994; Soto et al, 2013). Diphenidol (Vontrol), is also an anticholinergic, although little used in the US. There are also some reports of scopolamine inducing migraine, as well as a withdrawall syndrome. Cholinergic agonists that cross into the brain, such as physostigmine, can cause a motion-sickness syndrome (Soto et al, 2013). Cholinergic agonists that do not cross into the brain such as neostigmine, do not produce motion sickness. It is to be hoped that agents selective for vestibular subtypes of muscarinic receptors will eventually be developed or discovered among our presently available pharmacopoeia, as these agents may provide vestibular suppression with less side effects.

Addiction is possible to the anticholinergics. While this has only been described for scopolamine (Luetje and Wooten 1996), it seems likely that other anticholinergics may also have addiction syndromes.

Antihistamines. While the precise role of histamine in central vestibular processing is uncertain, there are data indicating that centrally acting antihistamines prevent motion sickness and reduce the severity of its symptoms even if taken after the onset of symptoms (Takeda et al, 1989). All the antihistamines in general use for control of vertigo also have anticholinergic activity. With the possible exception of astemizole (Hismanal) in Meniere's disease (Turner and Jackson, 1989), antihistamines that do not cross the blood brain barrier, are not used to control vertigo. Unfortunately, astemizole does not appear to be generally useful as it is ineffective in preventing motion sickness (Kohl et al, 1987) and because it has significant potential toxicity. There is evidence for involvement of several types of histamine receptors. Serafin and others (1993) reported that histamine increases firing in MVN cells, mediated through the H2 receptor. H1 receptors are present in guinea pig vestibular nucleus, but they don't seem to be relevant to vertigo, and it does not appear that the therapeutic effects of H1 receptor blockers can be attributed to blockate of H1 (Timmerman, 1994). H3 receptor agonists appear to cause the same result as blockade of H2 receptors. Most antihistamines also have calcium channel blocking effect (according to Timmerman, 1994).

Benzodiazepines are GABA modulators, acting centrally to suppress vestibular responses. They increase the affinity of chloride channel opening (Soto et al, 2013). There are differential effects across benzodiazepines on Gaba-A receptor subtypes. In small doses, these drugs are extremely useful. Addiction, impaired memory, increased risk of falling, and possibly impaired vestibular compensation are their main shortcomings.

Lorazepam is a particularly useful agent because of its effectiveness and simple kinetics. Addiction, the biggest problem, can usually be avoided by keeping the dose to 0.5 mg BID or less. Other problems include higher incidence of car accidents (risk x1.5), and hip fractures (risk x 1.8) (Ray, Griffin et al. 1987; Ray, Fought et al. 1992). Fall risk is increased in the elderly by roughly the same proportions.

Nevertheless, low doses of diazepam (Valium) (2 mg) can be quite effective for dizziness. Clonazepam (Klonopin), is as effective a vestibular suppressant as lorazepam (Ganaca et al, 2002). The author prefers to avoid use of alprazolam (Xanax) for vestibular suppression, because of the potential for a difficult withdrawal syndrome. Long acting benzodiazepines are not helpful for relief of vertigo. Diazepam does not delay vestibular compensation in the cat (Bernstein et al, 1972), but logically GABA would be expected to delay or stop compensation.

Antiemetics: Table 2 lists the drugs that are commonly used for control of nausea in vertiginous patients. Relatively new are the 5HT3 agents (Zofran, Kytril). In theory, these agents might not be ideal for emesis related to vestibular imbalance. The choice of agent depends mainly on considerations of the route of administration and the side effect profile. The oral agents are used for mild nausea. Suppositories are commonly used in outpatients who are unable to absorb oral agents because of gastric atony or vomiting. Injectables are used in the emergency room or inpatient settings. The new agents are used when all else fails.

Some antihistamines commonly used as vestibular suppressants have significant antiemetic properties (e.g. meclizine). When an oral agent is appropriate, this agent is generally the first to be used, because it rarely causes adverse effects any more severe than drowsiness. Phenothiazines, such as prochlorperazine (Compazine) and promethazine (Phenergan), are effective antiemetics, probably because of their dopamine blocking activity, but they also act at other sites. For example, promethazine is also an H1 blocker. Because these drugs can induce significant side effects, such as dystonia, they are considered second-line drugs whose use should be brief and cautious.

Table 2: Antiemetics
Drug Usual Dose (Adults) Adverse Reactions Pharmacologic Class Pregnancy Category
granisetron(Kytril) 1 mg PO BID 10 ug/kg IV daily

headache

sedation

5HT3 antagonist  
meclizine (Antivert, Bonine) 12.5-25 mg q4-6h PO sedating Precautions in glaucoma, prostate enlargement antihistamine anticholinergic B
metoclopramide(Reglan) 10 mg PO TID or 10 mg IM restlessness or drowsiness extrapyramidal dopamine antagonist stimulates upper gastrointestinal motility B
ondansetron (Zofran) 4-8 mg PO TID

32 mg IV one dose

precaution in hepatic dysfunction 5HT3 antagonist B
perphenazine(Trilafon) 2 - 4 mg PO, up to QID or 5mg IM, up to TID sedating extrapyramidal phenothiazine  
prochlorperazine(Compazine) 5 mg or 10 mg IM or PO q6-8 hr.

25 rectal q12h

sedating extrapyramidal phenothiazine C
promethazine(Phenergan) 12.5 mg PO q6-8h or 12.5 mg IM q 6-8h sedating extrapyramidal phenothiazine  
trimethobenzamide(Tigan) 200 mg IM TID extrapyramidal sedating similar to phenothiazine  
thiethylperazine(Torecan) 10 mg PO, up to TID or 2 ml IM, up to TID sedating extrapyramidal phenothiazine  

Doses are all those used routinely for adults, and will generally not be appropriate for children. Pregnancy category varies from A (controlled human studies have failed to demonstrate a risk to the fetus) through D (there is positive evidence of human fetal risk, use only in a life-threatening situation or for a serious disease for which safer drugs cannot be used or are ineffective.

Drugs that speed gastric emptying, such as metoclopramide (Reglan) and powdered ginger root may be helpful in managing emesis (Grontved et al, 1988). Metoclopramide, a dopamine antagonist and a potent central antiemetic, is ineffective in preventing motion sickness (Kohl, 1987).  Domperidone (Motilium) is an antiemetic that does not cross the blood brain barrier and thus has less side effects. Although droperidol has been used in the past, it is no longer recommended.

There is a possible role for new antiemetics which are a 5-HT3 antagonists (ondansetron, Zofran; granisetron, Kytril) used in treating the nausea associated with chemotherapy and post-operative nausea and vomiting. The high cost of these agents presently limits their usefulness in the treatment of vertigo, but they are reasonable agents to try in situations where the more usual agents are ineffective or contraindicated. These agents do not appear to be helpful in preventing motion sickness (Stott et al, 1989). In theory, these agents might be less effective for vestibular elicited emesis than agents with other pharmacologic actions.

Agents whose whose role is presently uncertain.

Mechanisms of effect of antidepressants for dizziness

Antidepressants.

All antidepressants increase ataxia and many cause nausea as well as hypotension. Thus one would think that their role would be limited. However, the ability of antidepressants to manage the psychological fallout from dizziness is often helpful (Horii, Mitani et al. 2004) Horii, A., K. Mitani, et al. (2004). Some antidepressants such as amitriptyline have strong anticholinergic properties which can be of use in managing dizziness. There are several reports of a positive effect, lacking an explanation (e.g. Grubb et al, 1996)

Calcium channel blockers are the most promising agents in this group. More detail about these drugs can be found here.

Calcium channel blockers, such as flunarizine and cinnarizine, are popular antivertiginous agents outside of the U.S. (Rascol et al, 1989). Flunarizine however is also a dopamine blocker, and cinnarizine an antihistamine. Some calcium channel blockers, such as verapamil, have quite strong constipating effects, which may be helpful in managing diarrhea caused by vestibular imbalance. However, calcium channel blockers often have anticholinergic and/or antihistaminic activity and the relative importance of calcium channel blocking associated activity for vestibular suppression has not been determined (Rascol et al, 1989). Another problem is that almost all antihistamines have calcium-entry blocking capacity and/or calmodulin blocking properties, making it difficult to ascertain the mechanism of action (Timmerman, 1994).

According to Soto et al (2013), Cinnarizine also blocks pressure sensitive potassium channels, which may provide it with a separate mechanism for treatment of hydrops.

Calcium channel blockers may be effective in "vestibular Menieres", or "benign recurrent vertigo", as persons with this diagnosis have a high prevalence of migraine (Rassekh and Harker, 1992), for which calcium channel blockers can be very effective. According to Soto et al (2013) the most commonly used calcium channel blockers for vertigo are nimodipine, nitrendipine (long lasting) and verapamil. Other long lasting dihydropyridines such as amlodipine, felodipine, nicardipine and nifedipine are seldom used.The author has found daily verapamil to be helpful in a roughly 1/3 of his patients with classic Menieres, causing amelioration or suppression of attacks as long as a reasonable dose is taken. This use of verapamil for vertigo has not been studied or approved in the US. Nimodipine, however, has recently been reported to be effective as prophylaxis of Menieres.In the US, our experience is that only verapamil is used to any great extent.

Gabapentin is also a calcium channel blocker (it is not a GABA agonist in spite of the name).

Diuretics

Carbonic anhydrase inhibitors such as acetazolamide, topiramate, and combinations such as HCTZ-Triamterine are commonly used to treat Meniere's disease. They may also have some efficacy in migraine and episodic ataxia.

A potassium channel blocker, 3-4 DAP (diaminopyridine) as well as its close relative, 4AP, has been reported useful for persons with ataxia and downbeating nystagmus.

This drug is sometimes used for fatigue in MS, as well as for a rare neuromuscular disorder (Eaton Lambert). Side effects include headache, fatigue perioral and/or distal paraesthesia 30-60 minutes after a dose, difficulty in sleeping. Excessive dosage can lead to seizures. The typical starting dose is 10 mg three times/day. 4-AP is a similar agent that has better CNS absorption. We have had no success with this drug at all in treating suitable patients in our clinical practice, and while we continue to be hopeful. Note that the brand-name version of 4AP is priced about 20 times higher than the compounded version of the same chemical.

A sodium channel blocker, phenytoin (Dilantin), has also been reported to be protective against motion sickness (Knox et al, 1994). We have not found this useful.

The author of this review has had no success in limited trials in patients with severe motion sickness unresponsive to the usual agents. Gabapentin (Neurontin), carbamazepine (Tegretol) and oxcarbazepine (Trileptal) are also sometimes successfully used in treatment of vertigo, although their use has not been studied extensively. Gabapentin has also been successfully used to suppress certain types of central nystagmus (Stahl et al, 1995). As these agents affect GABA, which is important in vertigo, an antivertigo effect is reasonable.

The sodium channel blockers Tegretol and Trileptal are particularly useful in paroxysmal disorders such as microvascular compression syndrome, and neuritis of the vestibular nerve. They are also occasionally used for tinnitus. Because the both lower serum sodium, they are also sometimes used for treatment of hydrops.

Recent agents have been developed  for epilepsy which are glutamate antagonists, but at this writing, they have not been tried as treatments of vertigo.

Another Gaba agonist, Baclofen (Lioresal) has shown some promise in reducing vestibular asymmetry. A human trial indicated that it is not useful in speeding up vestibular compensation (de Valc et al, 2009), but nevertheless this agent may have other uses. GABA would be more likely to slow down compensation. This agent might be suitable for patients with uncompensated vestibular asymmetries. In our clinical practice, we use Baclofen very rarely.

Dopamine blockers:

There are a large assortment of dopamine blockers mainly used for emesis. These drugs may also treat migraine (as they are often effective migraine abortive drugs). All are limited by their propensity to cause movement disorders (such as drug induced parkinsonism) as well as others. In our view, these drugs should be "last resort" for treatment of chronic vertigo conditions. We are, for example, against the use of Stugeron (cinnarizine) for any chronic condition. These drugs are generally considered acceptable for acute use however.

Histamine agonists:

This is an interesting group that has been poised to move from the uncertain role category to the more conventional category for decades. Whereas the antihistamines used in treating vertigo are usually centrally acting histamine H1-receptor antagonists, in some parts of the world an H1+H2-receptor agonist and H3-H4 antagonist, Serc (betahistine), is used. According to Timmerman quoting Laurikainen, H1 receptors do not appear to be important at all in vestibular function and the antivertiginous effects of antihistamines are mediated either through non-H1 receptors or other effects of the drugs. Also, the H1 (and H2 effects) are minor. Accordingly, Serc's effects might occur through H2 agonism or H3 antagonism (Timmerman, 1994). H3 is an autoreceptor that modulates H1/H2 as well as potentially other neurotransmitter systems.

In the rat brainstem, betahistine produces a slight excitatory response in MVN neurons, and it reduces the excitatory effect of histamine (Soto et al, 2013).

Recently a 4th histamine receptor (H4) has been identified. H4 antagonists are reported to suppress rat primary vestibular neuron firing (Desmadryl et al, 2012). Also, according to these authors, betahistine does not have a significant effect on the H4 receptor in reasonable doses.

Pragmatically, a betahistine dose of 16 mg twice to three times/day is usually prescribed, although greater effect is obtained for doses as high as 48 mg (Strupp,et al. 2008). The rationale for this use is that betahistine is said to increase circulation to the inner ear (Halmagyi, 1992) or affect vestibular function in some through activity of H3 receptors (Kingma et al, 1997; Timmerman, 1994). It is difficult to see why vasodilation should improve vertigo, as vasodilation/constriction are side effects of many medications that have no effect at all on vertigo. At this writing, as H2 agonism would be stimulatory, it appears most likely that Serc acts through the H3 receptor.

Serc is not fully approved by the FDA in the US but it can be obtained through compounding pharmacies. Histamine is sometimes prescribed as sublingual drops or subcutaneous injections. It is the authors opinion that sublingual or subcutaneous histamine is a placebo as it is rapidly degraded. Nevertheless, in the authors experience, Serc is moderately effective in suppressing symptoms of Meniere's disease, for uncertain reasons. Following the pharmacological discussion above, Serc might be expected to be effective in any peripheral vestibular disorder, not merely Meniere's disease.

Opiods

Opiods often cause constipation, and drugs that cause constipation usually also reduce dizziness. Droperidol (a dopamine blocker) combined with fentanyl (a powerful opiate) was reported to be effective for acute attacks of Meniere's disease (Soto et al, 2013). Our thought is that these drugs are far too dangerous to use for this purpose, and that there are much easier ways to stop Meniere's attacks (e.g. lorazepam and ondansetron together).

Steroids for vestibular disorders.

Corticosteroids such as decadron have been advocated both for treatment of Meniere's disease and Vestibular neuritis, in both cases, in an attempt to reduce the duration of a vertiginous episode. They are also commonly used for sudden hearing loss. Data concerning efficacy for dizziness is presently conflicted (see here for a review of data). There are many possible mechanisms of efficacy -- modulation of compensation (Cameron et al, 1999), reduction of immune responses in the inner ear (see here), reduction of swelling of the vestibular nerve (Strupp et al, 2004), reduction of emesis (Wattwil et al, 2003), increased activity promoting better recovery through a general effect on the sensation of wellbeing. (See here for the references).

Steroids are commonly used to treat acute flareups of Meniere's disease. The author will occasionally use a few day course of decadron (4 mg qd) or a medrol dose pack, when faced with a severe and unremitting vertigo attributed to Menieres disease. The author routinely uses steroids in acute vestibular neuritis, when there is no serious coincident medical disorder (such as diabetes). All steroids are pregnancy category C, but they are generally felt to be safe during the third trimester.

More about oral steroids can be found here, and steroids injected through the ear drum, here.

Sympathomimetics.

These include ephedrine and the amphetamines. Sympathomimetics may increase alertness and thereby counterbalance the sedative effects of vestibular suppressants. Sympathomimetics also may increase compensation. However, if used for this purpose, the combination of a vestibular suppressant with a drug targeted to increase compensation seems somewhat illogical. Amphetamines are little used because of their addiction potential. Sympathomimetics are generally pregnancy category C.

Dopamine agonists reduce firing rate in the frog hair cells and also reduces resposne to glutamine (the excitatory transmitter) (Soto et al, 2013). On the other hand, dopamine antagonists are uncommonly used to treat vertigo (e.g. Droperidol, phenothiazines), suggesting that the net effect is against using dopamine agonists.

 

Acetyl-leucine.

This medication is marketed and largely used in France (Rascol et al, 1995). It is claimed to exert a rapid antivertiginous effect when administered intravenously in humans and also to act as a vestibular suppressant. It is not used in the US for vertigo. The evidence for it working is not the best.

Ginkgo Biloba.

This extract is widely used in France, but its efficacy is in question (Rascol et al, 1995). It has been reported to suppress vertigo and to enhance vestibular compensation in animals. See here for more information.

Selective ACH antagonists.

The ACH receptor has numerous subtypes, and it would seem reasonable that a selective antagonist to the M2 receptor might cause vestibular suppression without many of the untoward side effects of the more general anti-ACH agents. Unfortunately, little research has been pursued in this direction at the present time.

Alternative medicine agents.

Cocculus is advocated for the temporary relief of lightheadedness. For-HEEL and Vertigo-HEEL is also suggested for vertigo. See here for more about these agents.

Various individual agents, best avoided.

Varenicline (Chantix).

This drug, approved by the FDA for smoking cessation, has recently been reported useful for treatment of cerebellar ataxia (Zesiewicz et al, 2009). It is extremely surprising to find an agent that will ameliorate disorders caused by genetic damage to neurons. It is also disturbing that the number of individuals in the trial (7) was exactly the same as the number of authors on the study. In other words, it would seem to us that if this drug was effective, the number of subjects should be larger as patients with cerebellar disorders are common. We are frankly very dubious. We have never encountered a patient who responded to this mediation (who wasn't attempting to stop smoking).

Trimetazidine

This drugs is a medication developed for angina (cardiac disturbance). It has been reported useful in diverse disorders (Soto et al, 2013), including Meniere's disease. The evidence for this drug working is presently weak. For example, it is reported to be "as effective" as betahistine. Trimetazidine can also induce a myriad of CNS disorders, largely similar to those produced by dopamine antigonists (i.e. similar to haloperidol -- Haldol).

Memantine

This drug is mainly a glutamate blocker (NMDA), and thus might be a vestibular suppressant. It was approved in the US for prevention of progression of Alzheimer's disease. It also is reported to act on 5HT3, D2, and various cholinergic receptors (Soto et al, 2013). We have never encountered a dizzy patient who responded to memantine. We have also never encountered a patient whose pendular nystagmus responded to memantine. This is hardly suprising as it is a low-affinitive NMDA antagonist. A similar drug is caroverine, that is a glutamate AMPA receptor antagonist.

Hallucinogenic NMDA drugs (antagonists)

These include MK-01, phencyclidine (PCP, "angel dust"), and ketamine ("special K") among others. Of course, side effects and abuse are a problem. Ketamine produces a general "lack of responsive awareness", as well as dizziness (Soto et al, 2013).


REFERENCES

 

Copyright November 12, 2014 , Timothy C. Hain, M.D. All rights reserved. Last saved on November 12, 2014