Laughing gas(nitrous oxide) misuse a 'growing concern' as doctors diagnose 18 people with neurological disorder

 Make sure your competent? doctor has EXACT PROTOCOLS on its' use! Oh, your doctor doesn't even know of the benefits? SOUNDS LIKE PURE INCOMPETENCE TO ME?

Nitrous oxide (3 posts to March 2016)

Laughing gas misuse a 'growing concern' as doctors diagnose 18 people with neurological disorder

Doctors at Tallaght University Hospital diagnosed 18 young people with a neurological disorder caused by inhaling nitrous oxide, or ‘laughing gas’, during a recent 20-month period.

The patients attended the hospital’s emergency department suffering from myeloneuropathy, a condition caused by damage to both the spinal cord and peripheral nerves.

They noted that many of the patients were using larger 580g or 640g canisters of nitrous oxide, rather than 8g ‘whippets’ that had originally been popular in the recreational setting.

Some of those admitted to the hospital reported using laughing gas for years, while others told doctors that it was their first time. 

The median length of stay at Tallaght University Hospital for the 18 patients was eight days, but discharge was delayed in some cases where patients required intensive rehabilitation due to 'significant functional disability'. File photo: Sasko Lazarov / RollingNews.ie

One said they had consumed 14 canisters a day for three weeks, while another had ‘binged’ six 580g canisters prior to admission.

Nearly all of the patients complained of a numb or tingling sensation on the skin, while 13 reported limb weakness, and eight were observed to have gait impairment.

The median length of hospital stay for the 18 patients was eight days, but discharge was delayed in some cases where patients required intensive rehabilitation due to “significant functional disability”.

Nitrous oxide can cause inactivation of vitamin B12 in the body, which in turn causes damage or loss of the protective layer around nerve fibres in the dorsal spinal column. Three of the patients had taken multivitamins or injected vitamin B12 in a bid to prevent this from happening.

All of the 18 patients who presented with these symptoms between October 2022 and July 2024 were treated with a high dose of vitamin B12 replacement, which the doctors said prevented life-changing disability in a cohort of previously healthy individuals.

“From a public health perspective, this case series demonstrates that nitrous oxide abuse remains a persistent source of concern for physicians and public health bodies in Ireland, despite repeated efforts at public education,” they wrote.

The authors of the study, published in the Irish Journal of Medical Science, said nitrous oxide poses a challenge from a legislative perspective, as it is used without restriction in the catering industry and can be imported for this purpose.

Nitrous oxide(laughing gas) promotes exploratory activity and stimulates neurogenesis in a male rat model of post-traumatic stress disorder

 Your competent? doctor started using this for your depression years ago, right? And with your risk of PTSD and needing neurogenesis, what's not to like?

Since there is a 23% chance of stroke survivors getting PTSD what is your doctor's prevention plan?

New Depression Treatment So Obvious You Won’t Believe It’s NEVER Been Tried Before - nitrous oxide(laughing gas)  February 2017 

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?

The latest here:

Nitrous oxide promotes exploratory activity and stimulates neurogenesis in a male rat model of post-traumatic stress disorder

Author links open overlay panel, , , , , 

https://doi.org/10.1016/j.neuroscience.2025.12.017Get rights and content

Highlights

• •
  SPS resulted in suppression of hippocampal neurogenesis.
• •
  Exposure to N2O reversed PTSD-induced anxiety-like behavior
• •
  N2O treatment markedly enhanced hippocampal neurogenesis in SPS rats.
• •
  N2O treatment did not alter glial activation, where optical intensity of Iba-1 (microglia) and GFAP (astrocytes) remained unchanged.

Abstract

Neurogenesis in the adult brain is a precisely regulated process that remains highly sensitive to intrinsic and extrinsic influences. Among the external factors are psychological conditions, such as post-traumatic stress disorder (PTSD), which arises after exposure to trauma such as war, accidents, violence, or natural disasters. PTSD, as well as other disorders like stress and depression, has been linked to diminished hippocampal neurogenesis. In this study, we utilized the single prolonged stress (SPS) model to induce PTSD-like behavior in male rats, demonstrating its suppressive effects on hippocampal neurogenesis and on exploratory behavior. Recent research has explored the potential of nitrous oxide gas (N2O), an anesthetic and analgesic used in medical procedures, as a potential treatment for depression. Accordingly, we propose nitrous oxide exposure as a therapeutic intervention for PTSD-like to counteract its adverse effects on neurogenesis and anxiety-related behavior. Our results showed that SPS-exposed rats exhibited reduced exploratory performance in the Y-maze test and increased anxiety behavior in the elevated plus maze. Furthermore, BrdU tracing revealed decreased neurogenesis in these rats compared to sham. Remarkably, exposure to nitrous oxide reduced anxiety-related symptoms of SPS-exposed rats and enhanced neurogenesis. This aligns with prior research, highlighting nitrous oxide as a promising therapeutic avenue for addressing PTSD and other psychological disorders. We propose nitrous oxide as a therapeutic approach for treating cognitive and anxiety-related symptoms of PTSD through its effects on hippocampal neurogenesis. However, further comprehensive research is essential to understand the potential benefits, risks and long-term impacts associated with this treatment approach.

Introduction

In light of recent global stressful events, such as the COVID 19 pandemic, earthquakes, and ongoing conflicts, post-traumatic stress disorder (PTSD) has emerged as a serious mental health concern (Chamaa et al., 2021, Mann et al., 2024). The prevalence of PTSD cases resulting from either a single or multiple traumatic events has markedly increased in recent years (Zhai and Du, 2024). The psychological burden of these traumatic events is profound and warrants greater emphasis on prioritizing mental health (Hoppen et al., 2021). PTSD symptoms include hyperarousal, an overgeneralized threat response to safe environments, and involuntary reliving of traumatic events through flashbacks or distressing thoughts (Hammell et al., 2020).

PTSD is particularly debilitating as it is characterized by a pathological endurance of memories, manifesting as either vivid involuntary flashbacks or disorganized voluntary recollections of the traumatic event (Brewin, 2011). This is attributed to dysfunction in mechanisms that regulate memory storage and expression (Pitts et al., 2022). Given the pivotal role the hippocampus has in memory formation and storage and mediating responses to stress and fear, it has an established direct pathophysiological involvement in PTSD (Zilcha-Mano et al., 2023). Studies have shown that PTSD patients exhibit reduced hippocampal volume, with smaller volumes correlating with more severe symptoms (Hinojosa, 2022, O'Doherty et al., 2015). Additionally, spatial working memory, a hippocampal related function, has been linked to re-experiencing of symptoms in PTSD (Mathew et al., 2022).

The dentate gyrus (DG) of the hippocampus harbors one of the two neurogenic niches in the adult brain (Kempermann et al., 2015). Within this region, the process of neurogenesis is highly sensitive and can be influenced by a variety of intrinsic and extrinsic factors that may either promote or inhibit the generation of new neurons. Factors such as stress, infections, and inflammation can lead to suppression of neurogenesis (Darwish et al., 2019, Darwish et al., 2022), with chronic stress particularly affecting the proliferation of neural progenitor cells in the DG (Gould and Tanapat, 1999). This decline in neurogenesis linked to chronic stress is suspected to be primarily due to elevated glucocorticoid levels, which interfere with the survival and proliferation of neural stem cells (Shin et al., 2024). Additionally, this phenomenon may involve other mechanisms, including increased apoptosis, oxidative stress, inflammation, and autophagy (Kohda et al., 2007, Liu et al., 2016). In contrast, several antidepressants have been shown to enhance hippocampal neurogenesis, highlighting their therapeutic potential in the treatment of stress-related disorders (Santarelli et al., 2003). Furthermore, invasive approaches such as deep brain stimulation and kainic acid stimulation, have also been reported to boost hippocampal neurogenesis (Chamaa et al., 2022, Chamaa et al., 2016, Zhang et al., 2014). However, the clinical applicability of these methods is limited due to their invasive nature.

Nonetheless, enhancing neurogenesis has been associated with improved stress coping, enhanced fear extinction, reduced anxiety-like behavior, and behavioral recovery in animal models of stress and trauma-related disorders (Schoenfeld et al., 2019). Such findings suggest that stimulating hippocampal neurogenesis may represent a promising avenue for mitigating PTSD-related symptoms. Till now, a substantial number of PTSD patients do not respond to cognitive behavioral therapy nor pharmacological treatments such as SSRIs (selective serotonin re-uptake inhibitors) or tetracyclic antidepressants (Burback et al., 2024, Williams et al., 2022). Therefore, there is an urgent need for innovative and fast-acting therapeutic interventions, as the incidence of diagnosed and undiagnosed PTSD continues to rise. Boosting hippocampal neurogenesis might stand as a potential therapeutic option. We have previously shown that exposure to nitrous oxide (N2O), an NMDA receptor antagonist, can significantly enhance the proliferation of hippocampal neural stem cells (NSCs) (Chamaa et al., 2018). NMDA receptor antagonists, such as ketamine, have gained attention as rapid-acting antidepressants, with evidence suggesting they can boost hippocampal neurogenesis through mechanisms that enhance synaptic plasticity and neurotrophic signaling (Yamada and Jinno, 2019, Zanos and Gould, 2018). Nitrous oxide has been explored as a treatment for PTSD in war veterans, yielding promising results (Varias et al., 2020). It has also demonstrated efficacy and safety for treatment-resistant depression in randomized controlled trials. Given the modulatory effect of nitrous oxide on hippocampal NSCs proliferation and the pivotal role of the hippocampus in PTSD, we propose that 70 % nitrous oxide can reverse the suppressed neurogenesis observed in the single prolonged stress (SPS) model of PTSD-like in rats. Therefore, in this study, we will investigate the mechanisms and effects of nitrous oxide exposure in treating memory and anxiety-related PTSD-like symptoms in the SPS rat model, suggesting nitrous oxide as a promising therapeutic approach to improve PTSD-like symptoms.

Access through your organization

Nitrous oxide speeds the reduction of distressing intrusive memories in an experimental model of psychological trauma

Would this be useful in stopping negative ruminations from the stroke event? and maybe lessen the  effects of 23% of survivors getting PTSD?

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=10208909&fileId=S003329171600026X

R. K. Das^a1 c1, A. Tamman^a1, V. Nikolova^a1, T. P. Freeman^a1, J. A. Bisby^a4, A. I. Lazzarino^a2a3 and S. K. Kamboj^a1 c1

^a1 Clinical Psychopharmacology Unit, UCL, London, UK
^a2 London School of Hygiene & Tropical Medicine, London, UK
^a3 Department of Epidemiology and Public Health, UCL, London, UK
^a4 Institute of Cognitive Neuroscience, UCL, London, UK

Abstract

Background Post-traumatic stress disorder (PTSD) involves maladaptive long-term memory formation which underlies involuntary intrusive thoughts about the trauma. Preventing the development of such maladaptive memory is a key aim in preventing the development of PTSD. We examined whether the N-methyl d-aspartate receptor (NMDAR) antagonist gas nitrous oxide (N₂O) could reduce the frequency of intrusive memories by inhibiting NMDAR-dependent memory consolidation in a laboratory analogue of psychological trauma.
Method Participants were randomized to inhale N₂O (N = 25) or medical air (N = 25) after viewing a negatively valenced emotional film clip (‘trauma film’). Participants subsequently completed a daily diary assessing frequency of intrusive thoughts relating to the film clip. A week later, participants completed an explicit memory recall task related to the film.
Results Post-encoding N₂O sped the reduction in intrusive memory frequency, with a significant reduction by the next day in the N₂O group compared to 4 days later in the air group. N₂O also interacted with post-film dissociation, producing increased intrusion frequency in those who were highly dissociated at baseline. Sleep length and quality the night after viewing the film did not differ between the groups.
Conclusion N₂O speeds the reduction of intrusive analogue trauma memory in a time-dependent manner, consistent with sleep-dependent long-term consolidation disruption. Further research with this drug is warranted to determine its potential to inoculate against enduring effects of psychological trauma; however, caution is also urged in dissociated individuals where N₂O may aggravate PTSD-like symptomatology.