Navigating Gabapentin Withdrawal: Symptoms, Timeline, and Treatment
Gabapentin, widely prescribed for seizures, neuropathic pain, and off-label uses such as anxiety, has become increasingly recognized not just for its therapeutic effects but also for its potential to cause dependence. As prescriptions rise, so do reports of challenging withdrawal experiences. For individuals seeking to taper off this medication, understanding the symptoms, timeline, and treatment avenues is essential to a safe and effective recovery process.
Gabapentin is a prescription medication primarily used to treat nerve pain and seizures, but it has also gained attention for non-medical use. Some individuals may misuse it in hopes of experiencing euphoria or sedation. Can Gabapentin get you high? While it is not typically classified as a recreational drug, high doses may produce feelings of relaxation or altered perception in some users, especially when combined with other substances. However, misuse can lead to unwanted side effects like dizziness, confusion, and dependency. It's important to use gabapentin only as prescribed to avoid potential health risks.
Understanding Gabapentin and Its Uses
What is Gabapentin?
Gabapentin, also marketed under the brand name Neurontin, is a synthetic analog of the neurotransmitter GABA (gamma-aminobutyric acid). Despite its structural similarity, it does not bind directly to GABA receptors. Instead, it modulates calcium channels in the central nervous system, thereby dampening excessive neuronal excitability.
Medical Conditions it Treats
Initially approved for epilepsy, gabapentin is now commonly used to alleviate nerve pain associated with shingles, diabetic neuropathy, and fibromyalgia. Off-label, it is often employed to treat anxiety disorders, restless leg syndrome, and even insomnia. This broad spectrum of applications has led to its proliferation in both primary care and psychiatric settings.
Why Gabapentin Withdrawal Occurs
Dependence and Neurological Adaptation
Gabapentin alters neural activity in a way that, over time, can lead to physical dependence. The brain, conditioned by the drug's dampening effect on excitatory signals, compensates by adjusting neurotransmitter levels. When gabapentin use is suddenly reduced or halted, this imbalance manifests as withdrawal.
Risk Factors for Withdrawal
Higher doses, prolonged use, and concurrent use of other CNS depressants such as opioids or benzodiazepines amplify the likelihood of withdrawal. Individuals with a history of substance use disorder are especially vulnerable. Additionally, abrupt cessation rather than a gradual taper significantly increases withdrawal severity.
Recognizing the Symptoms of Gabapentin Withdrawal
Physical Symptoms
The physical effects can be distressing. These often include sweating, nausea, headaches, dizziness, tremors, and palpitations. Some report flu-like symptoms, such as chills, body aches, and fatigue, mimicking opioid withdrawal.
Psychological and Neurological Effects
More insidious are the neuropsychological symptoms. Heightened anxiety, irritability, insomnia, and even paranoia can occur. In some cases, individuals experience seizures, particularly if gabapentin was initially prescribed for epilepsy. Cognitive fog and mood instability are also common during the withdrawal period.
The Timeline of Gabapentin Withdrawal
Acute Phase
Withdrawal typically begins within 12 to 48 hours after the last dose. The acute phase lasts approximately 3 to 7 days and is marked by the most intense symptoms—sleeplessness, anxiety, agitation, and gastrointestinal discomfort.
Subacute and Prolonged Symptoms
Though many physical symptoms subside within a week, some effects may linger. Mood disturbances, insomnia, and cognitive difficulties can persist for several weeks. In rare cases, individuals report a protracted withdrawal syndrome lasting several months, especially in those with long-term or high-dose use.
Effective Treatment Options for Withdrawal
Medical Detox and Tapering Strategies
The safest way to cease gabapentin use is under medical supervision. Tapering—gradually reducing the dose over weeks or months—helps mitigate the shock to the nervous system. Physicians may employ adjunct medications such as clonidine or propranolol to address specific symptoms like anxiety or hypertension.
Supportive Therapies and Holistic Approaches
Behavioral therapies, particularly cognitive behavioral therapy (CBT), can assist in managing psychological symptoms. Nutritional support, hydration, and sleep hygiene also play pivotal roles. Alternative treatments, including acupuncture and mindfulness-based interventions, may provide additional relief during recovery.
Preventing Gabapentin Misuse and Relapse
Monitoring Prescriptions
Clinicians should exercise caution when prescribing gabapentin, particularly to individuals with a history of substance misuse. Prescription monitoring programs (PMPs) can help track usage patterns and flag potential abuse.
Education and Support Networks
Patient education is vital. Understanding the risks of long-term use and the importance of adherence to tapering schedules can reduce misuse. Support groups, both in-person and online, offer encouragement, accountability, and shared wisdom from others navigating similar challenges.
Overcoming addiction requires not only determination but also the right medical support to ease withdrawal symptoms and promote healing. For individuals seeking a quicker path to sobriety, rapid medical detox offers a controlled and supervised method to cleanse the body of harmful substances. Unlike traditional detox programs, this approach accelerates the process using medications and close monitoring, often within a hospital or clinical setting. It's designed for those who need immediate relief from the physical effects of addiction. While not suitable for everyone, this method can be the first crucial step toward a stable and long-term recovery.
Conclusion
Gabapentin withdrawal is a complex and often underestimated process. While the medication serves a legitimate and valuable purpose for many, its potential for dependence necessitates cautious use and informed discontinuation strategies. With proper guidance, individualized treatment, and robust support, individuals can successfully navigate the withdrawal process and restore neurochemical equilibrium.
TIME BUSINESS NEWS
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Newsweek
04-08-2025
- Newsweek
PTSD Drug Discovery May Help Patients Let Go of Trauma
Based on facts, either observed and verified firsthand by the reporter, or reported and verified from knowledgeable sources. Newsweek AI is in beta. Translations may contain inaccuracies—please refer to the original content. A promising new drug could help people living with post-traumatic stress disorder (PTSD) finally let go of trauma. This is the discovery of scientists at the Institute of Basic Science (IBS) and Ewha Womans University in South Korea who have identified a new brain mechanism driving the mental health condition—and a drug with the potential to counteract its effects. The team has shown for the first time that "excessive" gamma-aminobutyric acid (GABA)—the brain's primary neurotransmitter—produced by star-shaped support cells in the brain known as "astrocytes" impairs the brain's ability to extinguish fear memories. This inability to forget traumatic memories even after a long period of time is distinct to PTSD and has posed a major hurdle for treatment. Current medications targeting serotonin receptors offer limited relief for only a subset of patients, the authors said. "Current FDA-approved treatments for PTSD are mainly SSRIs, which focus on reducing general symptoms like anxiety and mood instability," study author Dr. Woojin Won told Newsweek. "However, only about 20–30 percent of patients achieve full remission, which is often unsatisfactory. Our approach is fundamentally different." Woman with head in hands in dark room. Woman with head in hands in dark room. Domepitipat/Getty Images Won continued: "While prefrontal cortex (PFC) dysfunction has been consistently reported in PTSD, the role of GABAergic mechanisms in this dysfunction has not been fully explored." The researchers found that a brain-permeable drug called KDS2010, which selectively blocks an enzyme called 'monoamine oxidase B' (MAOB) responsible for this abnormal GABA production, can reverse PTSD-like symptoms in mice. "It targets the pathological reactive astrocyte-derived GABA at the source," said Won. "Unlike traditional MAO inhibitors, which can have off-target effects and are irreversible, KDS2010 is highly selective, reversible, and brain-penetrant, making it safer and more targeted." They report the drug has already passed Phase 1 safety trials in humans, which makes it a "strong candidate" for future PTSD treatments. GABA can be a positive thing, helping to regulate motor function, sensory processing and emotional stability. It can also offer calming effects, including helping to reduce anxiety and stress by controlling overactive neurons. "However," Won explained, "GABA does not act uniformly across the brain, and its outcome varies depending on the target circuit. "While GABA is generally calming, in this context [of the researcher's findings], it was silencing a circuit that the brain needs to overcome fear. This highlights that the effect of GABA is not simply good or bad, but it critically depends on where it acts and what neural circuits are involved." Digital illustration showing brain waves and activity. Digital illustration showing brain waves and activity. selvanegra/Getty Images The study focused on the medial prefrontal cortex (mPFC), a region of the brain critical for regulating fear. It found that PTSD patients had unusually high levels of GABA and reduced cerebral blood flow in this area, based on brain imaging studies of more than 380 participants. On the other hand, GABA levels decreased in patients who showed clinical improvement, suggesting the chemical has a central role in recovery. To unearth the origin of the excess GABA, the researchers examined postmortem human brain tissue and used PTSD-like mouse models. They discovered that astrocytes, not neurons, were producing abnormal amounts of GABA via the MAOB enzyme. This astrocyte-derived GABA impaired neural activity, blocking the brain's ability to forget traumatic memories. "This inspired us to investigate astrocytic GABA dysregulation as a potential driver of PTSD pathology, and ultimately, as a novel therapeutic target," said Won. Explaining further how "excessive" GABA in PTSD is produced, he added: "Trauma and stress might increase putrescine metabolism, which raises the levels of MAOB's presubstrate, leading to more GABA production. "At the same time, the enzyme that breaks down GABA, ABAT, is reduced. Together, this combination causes the accumulation of astrocytic GABA and excessive tonic inhibition in key brain regions like the PFC." When the team administered KDS2010, "a highly selective, reversible MAOB inhibitor" developed at IBS, the mice showed normalized brain activity and were able to extinguish fear responses. The promising drug reduced GABA levels, restored blood flow in the mPFC, and re-enabled memory extinction mechanisms. This confirms astrocytic MAOB as a central driver of PTSD symptoms and MAOB inhibition as a viable therapeutic path. The researchers flagged a major challenge of the study was linking clinical findings in humans with cellular mechanisms in the lab. They addressed this by applying a "reverse translational" strategy, beginning with clinical brain scans and moving backward to identify the cellular source of dysfunction. They then confirmed the mechanism and tested drug effects in animal models. This led to a new understanding of how glial cells—non-neuronal cells long thought to be passive—actively shape psychiatric symptoms. Would this type of drug be used alongside other methods like talking therapy for PTSD? "DS2010 alone has a strong potential to restore brain function by normalizing astrocytic GABA and improving fear extinction. However, we think that combining it with psychotherapy, especially exposure-based therapy, could create even greater synergy. By reducing abnormal inhibition in fear extinction circuits, KDS2010 may help the brain become more responsive to therapeutic input," Won explained. How would it be administered? "KDS2010 is an orally available small molecule. In preclinical and early-phase clinical studies, it has been administered once daily in capsule or liquid form. This makes it highly feasible for long-term outpatient use, similar to antidepressants." What about side effects? "In the Phase 1 clinical trial, KDS2010 was found to be well tolerated, with no serious adverse effects reported, even at higher doses. This safety is largely due to its selectivity for MAOB and its reversible mechanism, which avoids the long-term enzyme compensation seen with older MAO inhibitors. Nevertheless, larger trials in PTSD patients will be needed to fully assess tolerability and any rare side effects." Won said the drug is currently undergoing Phase 2 trials for other neurological disorders, which means its safety profile is already being tested extensively in patients. "Because of this, we believe it could reach the public faster than many other new drugs. If future trials for PTSD are successful and regulatory steps proceed smoothly, it could become available within a few years. Importantly, KDS2010 is part of a broader platform that may also be useful for treating other disorders involving astrocytic dysfunction, such as Parkinson's and Alzheimer's disease." Do you have a tip on a health story that Newsweek should be covering? Do you have a question about PTSD? Let us know via health@ Reference Yoon, S., Won, W., Lee, S., Han, K., Ha, E., Lee, J., Hyeon, S. J., Joo, Y., Hong, H., Lee, H., Song, Y., Park, K. D., Huber, B. R., Lee, J., Edden, R. A. E., Suh, M., Ryu, H., Lee, C. J., & Lyoo, I. K. (2025). Astrocytic gamma-aminobutyric acid dysregulation as a therapeutic target for posttraumatic stress disorder. Signal Transduction and Targeted Therapy, 10(1), 240.
New York Post
22-07-2025
- New York Post
The ‘very potent' supplement once given to Soviet cosmonauts can curb anxiety
Houston, we have a chill pill. Back in the 1960s, Soviet scientists developed a sweet little supplement that they stocked in the space kits of cosmonauts — the Russian version of an astronaut — to keep them cool under pressure. Still a popular over-the-counter option in Russia today, the drug promises to curb anxiety, cure insomnia, manage alcohol withdrawal and PTSD and promote clear thinking. Advertisement 3 Back in the 1960s, Soviet scientists developed a sweet little supplement that they stocked in the space kits of cosmonauts — the Russian version of an astronaut — to keep them cool under pressure. Gamma-Keystone via Getty Images It can even give you a bit of a high — but experts are warning that phenibut can also be a Red Scare in disguise. Utah recently classified it as a Schedule I controlled substance, placing it among the 'most dangerous drugs with no accepted medical use.' Phenibut's soothing properties come from its ability to mimic GABA — the neurotransmitter that mellows out brain activity — which makes it not dissimilar to benzodiazepines like Xanax and Valium. Advertisement Writer Delynn Willis started taking phenibut, sold under the brand names Anvifen, Fenibut and Noofen, precisely because she wanted to avoid the potentially addictive properties of benzos. A friend told her the Russian drug was dependence-free. 3 Phenibut's soothing properties come from its ability to mimic GABA — the neurotransmitter that mellows out brain activity — which makes it not dissimilar to benzodiazepines like Xanax and Valium. terovesalainen – Advertisement However, things quickly went south. 'After I had been using it for a few weeks, I started to notice I needed higher and higher doses to get the same effect,' she told Discover Magazine. When she tried to wean herself off the drug, the withdrawal symptoms were out of this world. Advertisement 'My anxiety skyrocketed, my temper shortened and I experienced dizzy spells,' she said. 'The drug has very potent psychoactive properties,' University of Michigan psychiatrist Edward Jouney told the outlet at the time. 'There's evidence it can cause addiction.' Jouney noted that it's possible that phenibut could be used as an effective treatment for anxiety under strict medical supervision. 3 While low doses — under a gram — might be safe, side effects can include vomiting, nausea, diarrhea, insomnia, depression, hallucinations, tremors and difficulty breathing. LIGHTFIELD STUDIOS – While it is technically legal in most of the US and sold online for as little as $50, buying phenibut this way is a dubious prospect. Telehealth companies aren't held to the same quality assurance standards as doctors, who can't prescribe it because it's not approved by the Food and Drug Administration for medical use. Advertisement Poison control centers have been flooded with phenibut-related calls since 2015, according to the Centers for Disease Control and Prevention, with reports describing agitation, heart irregularities, confusion — and even coma. In 2019, the FDA sent warning letters to three companies in the US for marketing phenibut as a 'dietary supplement.' Alabama took matters into its own hands and classified it as a Schedule II controlled substance in 2021, making it illegal. As of May, it is also illegal to possess, distribute or manufacture phenibut in Utah. Advertisement While low doses — under a gram — might be safe, side effects can include vomiting, nausea, diarrhea, insomnia, depression, hallucinations, tremors and difficulty breathing. It can be easy to become dependent, which can lead to death. 'The reported adverse events of phenibut are just scratching surface of a largely unregulated online drug market with no standards of quality assurance,' pharmacologists Janet Cheung and Jonathan Penm wrote in The Conversation. 'So for those students seeking the competitive edge, it looks like those extra marks are not worth it after all.'
Yahoo
18-07-2025
- Yahoo
Dementia Linked With Treatment For Chronic Lower Back Pain
A drug widely used to treat nerve pain and epilepsy has been linked with an increase in cases of dementia and mild cognitive impairment. A team from Case Western Reserve University School of Medicine, Arizona State University, and the MetroHealth Medical Center in the US crunched the numbers on 26,416 records of patients with chronic lower back pain, looking at the relationship between prescriptions for the anticonvulsant gabapentin and dementia diagnoses. Having six or more gabapentin prescriptions was linked to a significant increase in dementia risk and mild cognitive impairment (MCI), the data showed: those in that group were 29 percent and 85 percent more likely to be diagnosed with dementia and MCI respectively, within 10 years. Related: Massive Study Links 15 Factors to Early Dementia Risk The increase was higher among patients aged between 35 and 49, and also rose with the number of prescriptions given, the researchers found. Though the study can't establish a cause for the increase, physicians are encouraged to keep a close eye on patients taking the drug. "Gabapentin prescription in adults with chronic low back pain is associated with increased risk of dementia and cognitive impairment, particularly in non-elderly adults," write the researchers in their published paper. "Physicians should monitor cognitive outcomes in patients prescribed gabapentin." Sold under brand names including Neurontin, gabapentin has proved to be less addictive than opioids, making it more likely to be prescribed in recent years. The drug does have some known side effects though, including extreme moods and allergic reactions. This isn't the first time researchers have examined associations between gabapentin and dementia, but previous studies haven't agreed on whether or not concerns are warranted. One of the study's strengths is the relatively large sample size of its participants, though the sample largely consisted of just one group of people – those with chronic lower back pain. A study published in 1997 found no link between gabapentin and cognitive decline in people with epilepsy, so it's important to continue to widen the data set. These conflicting results could suggest unique mechanisms among patients with the type of backpain that leads to a gabapentin prescription that also increases their risk of dementia, like a certain type of location of inflammation. But gabapentin works by dampening some of the brain's key communication channels, in order to provide relief from pain or make seizures less likely. So the worry is that it could also be damaging links between neurons in ways that might lead to dementia – a concern backed up by this latest study. Dementia is a challenging condition to study with so many potential factors to account for, but each study gets us closer to the full picture of how the brain breaks down over time. "We hope the current study promotes further research to delineate whether gabapentin plays a causal role in the development of dementia and the underlying mechanisms of this relationship," write the researchers. The research has been published in Regional Anesthesia & Pain Medicine. Related News 8 Babies Born in UK Using Radical 'Three Parent' IVF Technique These 4 Simple Exercises Could Help Break Your Insomnia Energy Drinks Seen Fuelling Cancer, But There's a Strange Catch Solve the daily Crossword
