Tag: post traumatic stress injury

Brexpiprazole + Sertraline: A New Hope for PTSD Treatment

We’ve all seen it: PTSD that won’t budge. Patients try sertraline or paroxetine—the so-called “gold standards”—and walk away with little more than side effects and a sense of failure.

Enter a new contender: brexpiprazole + sertraline.

A recent Phase 3 randomized controlled trial might finally offer something real for those stuck in the PTSD trenches.

🚨 The Results

In a study across 86 sites with over 550 adults, adding brexpiprazole (2–3 mg) to sertraline (150 mg) led to a 5.6-point greater reduction on the CAPS‑5 (the gold-standard PTSD measure) compared to sertraline + placebo. That’s not a marginal win—it’s a clinically significant shift, especially in a treatment-resistant population.

Responder rates tell the story even clearer:

  • 68.5% of patients on the combo had ≥30% reduction in symptoms
  • Compared to 48.2% on sertraline alone
  • That’s a +20% absolute response rate boost

And the improvements weren’t just short-lived. Benefits held through 12 weeks, even during a post-treatment observation period. No relapse, no rebound—just stability.

🧩 More Than Symptom Checklists

It wasn’t just about PTSD symptoms. This combo also:

  • Improved psychosocial functioning (B-IPF scores)
  • Reduced anxiety and depression (HADS)
  • Lowered global illness severity (CGI-S)
  • Helped with all symptom clusters, including reexperiencing, avoidance, and hyperarousal

That’s rare. Most meds in psychiatry hit one or two domains and leave the rest hanging. This one made a dent where it counts: function, resilience, and real-world relief.

⚠️ What About Side Effects?

Brexpiprazole is still an atypical antipsychotic, so there’s baggage. But the trial data suggest it’s relatively well-tolerated:

  • Fatigue: 6.8%
  • Weight gain: 5.9%
  • Somnolence: 5.4%
  • Discontinuation due to AEs? Just 3.9%, vs 10.2% in placebo.

No new safety signals. No psychosis worsening. Not perfect, but not the metabolic disaster zone we see with other agents.

🚀 What’s Next?

The FDA is reviewing this combo

For those of us treating chronic PTSD, this may be a real tool—not just a shiny new molecule with good marketing.

Until then, it’s worth paying attention. Because when sertraline alone doesn’t cut it—and we know it often doesn’t—this combo could offer a lifeline.

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Clearing the Smoke: What We Know About Cannabis for Mental Health Treatment

Research into the therapeutic potential of cannabis for mental health disorders has grown in recent years, with mixed findings from randomized controlled trials (RCTs).

Anxiety Disorders

  • CBD (Cannabidiol) has shown promise in reducing anxiety symptoms in RCTs, particularly for social anxiety disorder (SAD). For instance, a small RCT found that a single dose of 300 mg of CBD reduced anxiety levels in participants undergoing a simulated public speaking test.
  • Some RCTs suggest that CBD may be anxiolytic without causing impairment or euphoria, making it preferable for anxiety compared to THC-dominant cannabis products, which may exacerbate anxiety in some users.

Post-Traumatic Stress Disorder (PTSD)

  • RCTs exploring THC and CBD combinations in PTSD have had mixed outcomes. Some studies indicate that THC may reduce nightmares and improve sleep in PTSD patients, though these findings are generally based on small sample sizes and short-term trials.
  • A recent RCT with a synthetic cannabinoid (nabilone) reported some symptom improvement in PTSD-related insomnia and nightmares. However, larger trials with longer follow-ups are necessary to clarify the efficacy and safety for PTSD.

Depression

  • Few RCTs show consistent evidence supporting cannabis (CBD or THC) as an effective treatment for major depressive disorder. Some trials indicate that CBD may have antidepressant-like effects, possibly due to serotonin receptor activity, but more robust and long-term studies are needed.
  • Concerns persist over THC’s potential to exacerbate depressive symptoms, particularly with regular or heavy use.

Schizophrenia and Psychotic Disorders

  • THC-dominant products have been associated with increased risk of psychosis and exacerbation of symptoms in people predisposed to psychotic disorders. This has led to caution against THC use in people with schizophrenia.
  • CBD has shown promise as an adjunctive treatment in some RCTs, with findings suggesting that it may have antipsychotic effects without the psychoactive effects of THC. For example, an RCT found that CBD reduced psychotic symptoms and improved cognitive function when added to standard antipsychotic treatment, though the effects were modest.

Bipolar Disorder

  • Evidence from RCTs on the use of cannabis in bipolar disorder is sparse and generally negative. Some trials indicate that THC may worsen manic and depressive symptoms in bipolar patients, and there is little to no support for cannabis as a treatment for bipolar depression.

Sleep Disorders

  • Some RCTs have evaluated cannabinoids for sleep disturbances, with CBD showing potential for improving sleep quality. However, THC may reduce REM sleep, which could impact sleep architecture negatively over time.
  • For PTSD-related insomnia, cannabinoids like nabilone have shown some benefit, but the effects on sleep in general populations remain uncertain.

Limitations

  • Sample Sizes and Duration: Many RCTs are small and short-term, limiting the generalizability and understanding of long-term effects.
  • Dosing and Formulations: Variability in cannabinoid content (THC vs. CBD), formulations (edibles, oils, vapes), and dosages across studies makes comparison challenging.
  • Side Effects: Both CBD and THC can have side effects, though THC’s psychoactive properties can lead to cognitive impairment, addiction potential, and negative impact on mood in some patients.

While CBD shows some promise in anxiety, PTSD, and psychotic disorders, RCT evidence for other mental health conditions remains inconclusive or even negative, especially with THC. Further large-scale, long-term RCTs are needed to establish the efficacy and safety profile of cannabis-based treatments in mental health.

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Breaking the Trauma Cycle: Can We Prevent PTSD Before It Begins?

The use of hydrocortisone and propranolol in the prevention of post-traumatic stress disorder (PTSD) has been explored in several randomized controlled trials (RCTs). We always want to know does it work or is it just another interesting idea with little evidence to support its use

Hydrocortisone:

Hydrocortisone, a corticosteroid, has been investigated for its potential to modulate the stress response and prevent the consolidation of traumatic memories, which is thought to contribute to the development of PTSD.

  1. Mechanism: Hydrocortisone works by increasing cortisol levels, which can suppress the stress-induced overactivation of the hypothalamic-pituitary-adrenal (HPA) axis. Cortisol may reduce memory consolidation of trauma, thus decreasing PTSD risk.
  2. RCT Evidence:
    • Schelling et al. (2004) conducted a study on patients in the ICU, where hydrocortisone was used to treat septic shock. They found that patients who received hydrocortisone had a significantly lower risk of developing PTSD symptoms at follow-up compared to the placebo group. This suggested that hydrocortisone might have a protective effect in stress-related conditions.
    • Survivors of trauma: In a study by Zohar et al. (2011), trauma patients who received hydrocortisone in the immediate aftermath of the traumatic event had lower rates of PTSD symptoms compared to those who received placebo. The results suggested that hydrocortisone may reduce PTSD incidence when administered shortly after trauma exposure.
    • Critically ill patients: Schelling et al. (2001) showed that administering hydrocortisone to critically ill patients in the ICU reduced PTSD symptoms at follow-up, supporting the idea that early cortisol intervention can modulate the long-term psychological impact of traumatic experiences.
  3. Summary: Hydrocortisone has shown promise in reducing PTSD symptoms when administered during or soon after traumatic experiences, particularly in ICU patients or survivors of trauma. Its role appears to be in modulating the stress response and memory consolidation processes.

Propranolol:

Propranolol, a beta-blocker, is primarily used to treat cardiovascular conditions but has been studied for its effects on memory reconsolidation and emotional arousal, both of which are implicated in the development of PTSD.

  1. Mechanism: Propranolol reduces adrenergic activity by blocking beta-adrenergic receptors, potentially interfering with the emotional enhancement of traumatic memories, thus reducing their consolidation.
  2. RCT Evidence:
    • Pitman et al. (2002) conducted a double-blind, placebo-controlled trial in which trauma victims (e.g., car accident survivors) were given propranolol or placebo within a few hours of the event. At follow-up, patients who received propranolol had reduced PTSD symptoms compared to those given placebo, though the results were not statistically significant.
    • Brunet et al. (2008) performed a study on individuals with PTSD, where propranolol was administered before memory reactivation (i.e., recalling the traumatic event). The group that received propranolol showed reduced physiological responses to trauma reminders and decreased emotional impact, suggesting that propranolol may weaken the reconsolidation of traumatic memories.
    • Stein et al. (2007) did not find a significant reduction in PTSD incidence when propranolol was administered following trauma. This led to mixed conclusions regarding its preventive efficacy.
  3. Summary: The evidence for propranolol is more mixed. While some studies suggest it may reduce PTSD symptoms by weakening emotional memory consolidation, other trials have not demonstrated a significant reduction in PTSD development.

Conclusion:

  • Hydrocortisone has more consistent evidence supporting its role in preventing PTSD, particularly when administered soon after trauma.
  • Propranolol shows mixed results, with some evidence suggesting it may reduce emotional memory consolidation and PTSD symptoms, though its effectiveness in preventing PTSD development is less conclusive.

Both treatments hold potential, but more research is needed to establish their routine use in PTSD prevention.

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Unlocking Relief: Can Prazosin Power Up Depression Treatment?

The evidence for the use of prazosin in major depressive disorder (MDD) comes mainly from smaller studies or trials focusing on its off-label use, as prazosin is primarily an alpha-1 adrenergic antagonist used to treat hypertension and PTSD-related nightmares.

Clinical Rationale

The theoretical rationale for prazosin in MDD is based on its ability to block alpha-1 adrenergic receptors, which may help reduce the hyperactivity of the norepinephrine system—a pathway implicated in stress and depression.

Randomized Controlled Trials (RCTs)

RCT evidence for prazosin in treating MDD is limited compared to other antidepressants, but a few studies have explored its potential benefits:

  1. Prazosin as Adjunctive Treatment for MDD (2009):
    A small pilot RCT assessed prazosin as an add-on therapy for MDD in patients who were already on standard antidepressants. The results showed modest improvements in depressive symptoms when prazosin was combined with SSRIs or SNRIs, particularly in patients with high anxiety or sleep disturbances.
  2. Prazosin for PTSD and MDD Comorbidity:
    Some RCTs conducted in patients with PTSD (a condition often comorbid with MDD) showed improvements in both PTSD and depressive symptoms. For example, a trial published in 2015 demonstrated that prazosin led to a significant reduction in depressive symptoms in veterans with PTSD and depression. While the trial primarily focused on PTSD, the secondary outcomes regarding depression were positive.
  3. Prazosin and Treatment-Resistant Depression (TRD):
    Some trials have explored prazosin’s efficacy in treatment-resistant forms of depression, hypothesizing that its ability to reduce stress-related symptoms could augment antidepressant efficacy. However, these trials have generally been small, and results have been inconsistent or not statistically significant in terms of primary depressive outcomes.

Limitations

  • Sample Sizes: Most studies are small and underpowered.
  • Population: Most studies have focused on patients with PTSD, rather than pure MDD.
  • Adjunctive Use: Prazosin has mostly been tested as an adjunctive treatment, not as monotherapy for depression.

While prazosin has shown some promise in improving depressive symptoms, particularly related to sleep disturbances and anxiety, larger RCTs specifically targeting MDD are needed to establish its efficacy.

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Transforming Pain Into Strength 

Many people spend their entire lives holding themselves back, often because they’re unconsciously addicted to the pain they cause themselves. When trauma hits, especially early in life, it has a way of sticking with us. In many ways, that pain shapes who we are, and the thought of letting it go feels like losing a part of ourselves. It can become a form of behavioral addiction.

But what if we could use that pain as fuel to push ourselves forward, to become the best version of who we are? It’s hard, especially when you’ve been picked on, or felt like you don’t fit in. We all just want to live authentically, to be true to ourselves.

I get it—I’ve been there too. If I can push through, so can you. It’s never easy, especially in tough times. But if there’s one thing I know, I’m not giving in.

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PTSD by Any Other Name: Rethinking the Label to Break the Stigma

An advocacy group has proposed changing the name of post-traumatic stress disorder (PTSD) to post-traumatic stress injury (PTSI) for inclusion in the DSM-5 TR. However, in November 2023, the APA steering committee rejected the proposal, citing insufficient evidence to support the change. Advocates argue that the term “disorder” is both imprecise and carries stigma, which can discourage people from seeking timely care. This delay or avoidance of care can lead to serious consequences, including suicide attempts. The term “disorder” has long been controversial in psychiatry, and I’ve always favored the use of “disease” to help distinguish between true disease processes and challenges of living. I also believe that people may be more likely to seek help if they view the issue as a disease or injury. While this change may not happen soon, maintaining open dialogue about how to encourage treatment is essential.


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