Ketamine Treatments: Side Effects & Addiction Risks Unveiled

Have you spotted advertisements for ketamine treatments in your city? Initially designed as an anesthetic and animal tranquilizer, ketamine has experienced a rise in popularity due to its potential in treating depression, anxiety, and chronic pain. This has resulted in its adoption as a wellness therapy in medical clinics.

Nonetheless, it's essential to know the potential side effects and addiction risks linked to ketamine use. In this article, we will offer a comprehensive examination of ketamine's side effects and delve into the possibility of addiction.

What is Ketamine?

Ketamine is a dissociative anesthetic, primarily used in veterinary medicine but also employed in human medicine for anesthesia and analgesia. In recent years, research has demonstrated its potential for treating various mental health disorders and chronic pain conditions, such as major depressive disorder, anxiety, post-traumatic stress disorder (PTSD), and fibromyalgia. This has led to the rise of wellness clinics offering only ketamine treatments, often in the form of intravenous (IV) infusions.

Side Effects of Ketamine

While ketamine may offer relief for some patients, it is crucial to understand the potential side effects that can arise from its use. The severity and duration of these side effects may vary depending on the individual and the dosage administered. Some common side effects include:

Dissociative Effects 

Ketamine can cause a range of dissociative symptoms, such as out-of-body experiences, feelings of detachment, and hallucinations. These effects typically last for the duration of the treatment and may persist for several hours afterward.¹ This dissociative state may be related to the inhibition of N-methyl-D-aspartate (NMDA) receptors in the brain, which can disrupt normal cognitive function and perception. ²

Dizziness and Loss of Coordination 

Some patients may experience dizziness, loss of balance, and difficulty with motor skills during and after ketamine treatments.¹ These effects may be attributed to the drug's interference with the functioning of the cerebellum, a region of the brain responsible for coordinating movement. ³

Nausea and Vomiting 

Ketamine can cause gastrointestinal discomfort, leading to nausea and vomiting in some individuals.¹ The precise mechanism for these side effects is not entirely understood but may involve the stimulation of certain receptors in the brain and gastrointestinal tract responsible for regulating nausea and vomiting.⁴

Blurred Vision and Involuntary Eye Movements

Patients may experience blurred vision and rapid, involuntary eye movements (nystagmus) during ketamine treatment.¹ These effects are likely due to the drug's action on specific neurotransmitter systems in the brain, including the cholinergic and dopaminergic systems. ⁵

Increased Heart Rate and Blood Pressure 

Ketamine can cause a temporary increase in heart rate and blood pressure, which may be problematic for individuals with pre-existing cardiovascular issues.⁶ The exact mechanism behind this effect is not completely understood, but it may involve activating the sympathetic nervous system and the release of stress hormones such as epinephrine and norepinephrine.⁷

Cognitive Impairment

Ketamine can potentially cause cognitive deficits, such as memory, attention, and problem-solving, particularly with long-term use.⁸ This cognitive impairment may be due to the drug's disruptive effects on glutamate signaling in the brain, which plays a crucial role in cognitive processes. ⁹

Urinary Issues 

Long-term ketamine use has been linked to urinary problems, including cystitis, bladder inflammation, and kidney damage.¹⁰ The exact mechanism behind these side effects is not well understood, but it may involve the toxic effects of ketamine and its metabolites on the urinary tract.¹¹

Potential for Addiction from Ketamine Treatments

The potential for addiction with ketamine treatments is a crucial concern for both patients and healthcare providers. Although ketamine has therapeutic benefits, it is essential to understand its addictive potential and monitor its use closely.

Ketamine is classified as a dissociative anesthetic and has a history of recreational use due to its hallucinogenic and dissociative effects.¹ It acts on various neurotransmitter systems in the brain, including the glutamate and dopamine systems, which are known to play a role in the development of addiction.^{12, 13} The drug's ability to induce euphoria, dissociation, and relief from negative emotions can make it appealing for abuse and increase the risk of addiction.

The risk of developing an addiction to ketamine depends on various factors, including the individual's genetic predisposition, the frequency of use, the dosage administered, and the presence of other mental health or substance use disorders.¹⁴ Generally, the risk of addiction increases with the frequency and amount of ketamine use. While some patients might not develop an addiction even after using ketamine multiple times, others may become addicted after just a few uses.

Studies on the addictive potential of ketamine are still limited, and it is difficult to pinpoint exactly how quickly a patient can become addicted. In a study by Morgan et al,⁸ frequent ketamine users experienced significant cognitive and psychological impairments, suggesting a higher risk of developing an addiction. Moreover, withdrawal symptoms, such as anxiety, agitation, and craving, have been reported in chronic ketamine users who stopped using the drug abruptly. ¹⁵

It is essential to recognize that the risk of addiction with ketamine treatment in a controlled clinical setting may be lower than with recreational use. Medical professionals typically administer ketamine at lower doses and on a limited basis to minimize the risk of addiction.¹⁶ In such circumstances, patients are closely monitored for signs of misuse or addiction, and alternative treatments can be considered if necessary.

To minimize the risk of addiction, it is crucial for healthcare providers to evaluate patients' risk factors, educate them about the potential dangers of ketamine use, and monitor their progress during and after ketamine treatments. Proper assessment and follow-up can help ensure the safe and effective use of ketamine for its therapeutic benefits while mitigating the risk of addiction.

Citations

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2. Krystal JH, Karper LP, Seibyl JP, Freeman GK, Delaney R, Bremner JD, Heninger GR, Bowers MB Jr, Charney DS. Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses. Arch Gen Psychiatry. 1994 Mar;51(3):199-214. doi: 10.1001/archpsyc.1994.03950030035004. PMID: 8122957.
3. Miyazaki T, Takase K, Nakajima W, Tada H, Ohya D, Sano A, Goto T, Hirase H, Malinow R, Takahashi T. Disrupted cortical function underlies behavior dysfunction due to social isolation. J Clin Invest. 2012 Jul;122(7):2690-701. doi: 10.1172/JCI63060. Epub 2012 Jun 18. Erratum in: J Clin Invest. 2014 Jun 2;124(6):2807. PMID: 22706303; PMCID: PMC3387818.
4. Sigtermans M, Dahan A, Mooren R, Bauer M, Kest B, Sarton E, Olofsen E. S(+)-ketamine effect on experimental pain and cardiac output: a population pharmacokinetic-pharmacodynamic modeling study in healthy volunteers. Anesthesiology. 2009 Oct;111(4):892-903. doi: 10.1097/ALN.0b013e3181b437b1. PMID: 19741495.
5. Li D, Vlisides PE, Mashour GA. Dynamic reconfiguration of frequency-specific cortical coactivation patterns during psychedelic and anesthetized states induced by ketamine. Neuroimage. 2022 Apr 1;249:118891. doi: 10.1016/j.neuroimage.2022.118891. Epub 2022 Jan 8. PMID: 35007718; PMCID: PMC8903080.
6. Kaushal RP, Vatal A, Pathak R. Effect of etomidate and propofol induction on hemodynamic and endocrine response in patients undergoing coronary artery bypass grafting/mitral valve and aortic valve replacement surgery on cardiopulmonary bypass. Ann Card Anaesth. 2015 Apr-Jun;18(2):172-8. doi: 10.4103/0971-9784.154470. PMID: 25849685; PMCID: PMC4881645.
7. Yanagihara Y, Ohtani M, Kariya S, Uchino K, Hiraishi T, Ashizawa N, Aoyama T, Yamamura Y, Yamada Y, Iga T. Plasma concentration profiles of ketamine and norketamine after administration of various ketamine preparations to healthy Japanese volunteers. Biopharm Drug Dispos. 2003 Jan;24(1):37-43. doi: 10.1002/bdd.336. PMID: 12516077.
8. Morgan CJ, Muetzelfeldt L, Curran HV. Consequences of chronic ketamine self-administration upon neurocognitive function and psychological wellbeing: a 1-year longitudinal study. Addiction. 2010 Jan;105(1):121-33. doi: 10.1111/j.1360-0443.2009.02761.x. Epub 2009 Nov 17. Erratum in: Addiction. 2010 Apr;105(4):766. PMID: 19919593.
9. Olney JW, Labruyere J, Price MT. Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs. Science. 1989 Jun 16;244(4910):1360-2. doi: 10.1126/science.2660263. PMID: 2660263.
10. Chu PS, Ma WK, Wong SC, Chu RW, Cheng CH, Wong S, Tse JM, Lau FL, Yiu MK, Man CW. The destruction of the lower urinary tract by ketamine abuse: a new syndrome? BJU Int. 2008 Dec;102(11):1616-22. doi: 10.1111/j.1464-410X.2008.07920.x. Epub 2008 Aug 1. PMID: 18680495.
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