Scientific understanding of the neurobiological changes occurring during PTSD onset shows memory consolidation appears particularly vulnerable to disruption in the first six hours after trauma, making this a crucial period for intervention for prevention of PTSD. This technical commentary presents the evidence on pharmaceutical interventions administered during this period. Please also see the psychotherapy for prevention of PTSD topic.

What is the evidence on medications for the prevention of PTSD?

Hydrocortisone is a glucocorticoid, which attenuates heightened fear response through increased removal of fear-inducing memories. Moderate to low quality evidence found a medium to large, reduced risk of PTSD within 3-6 months post-trauma in people with severe physical illness or injury receiving hydrocortisone post-trauma. Risks were not assessed in these samples, so contraindications need checking.

There was no benefit of hydrocortisone over placebo after 6 months post-trauma. There were also no benefits of propranolol, oxytocin, gabapentin, fish oil, dexamethasone, escitalopram, imipramine, or chloral hydrate for preventing PTSD at any time frame. Studies are few and small.

August 2021

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Several beneficial treatments for PTSD are available, including pharmaceutical and psychological approaches. Treatment guidelines typically recommend psychological therapies as first-line PTSD treatment. However, some antidepressants in particular may also be used as first-line treatment. It remains uncertain whether benefit increases when combining pharmacological and psychological treatments. This topic presents the evidence for all pharmaceutical treatments compared to all psychosocial and combination therapies for PTSD.

What is the evidence on pharmaceutical versus psychological and combination interventions for PTSD?

Moderate to low quality evidence found large improvements in PTSD symptoms by last follow-up with psychotherapy and with psychotherapy + medication compared to medications alone. There were no differences between these three treatment options immediately following treatment, and no differences between combined and psychological therapies at last follow-up. There were no differences in drop-outs rates, indicating similar tolerability of all treatments.

Note that last follow-up time frames were not reported in the reviewed evidence, and treatments were not all necessarily maintained to last follow-up, so these results must be interpreted with caution.

August 2021

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Alpha blockers, such as prazosin, are medications that work as alpha-adrenergic receptor antagonists. They cross the blood-brain barrier, antagonise the alpha receptors in the central nervous system, and block the stress response. Higher than normal nocturnal central nervous system adrenergic activity that occurs in PTSD contributes to the disruption of normal rapid eye movement sleep. Prazosin reduces this adrenergic activity and therefore could be effective in treating posttraumatic arousal symptoms such as sleep disturbances and nightmares.

What is the evidence on prazosin for PTSD?

Moderate quality evidence found medium to large improvements in PTSD symptoms, nightmares, and sleep disturbances with prazosin than with placebo when compared at treatment endpoint. When comparing baseline to endpoint improvements over time, there was also a large reduction in nightmare frequency, and a trend, medium-sized improvement in PTSD symptoms with prazosin. However, there were no significant differences in sleep quality between prazosin and placebo, suggesting the placebo group may have had more sleep disturbances at baseline (the two reviews in this topic included mostly the same studies).

Prazosin resulted in more dry mouth than placebo, with no differences in dizziness, headache, nausea, lack of energy, muscle weakness or asthenia, drowsiness or somnolence, syncope, nasal congestion, or palpitations.

August 2021

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Anticonvulsants are primarily used to treat epilepsy, but may also be effective for some mental disorders. Anticonvulsant medications influence the actions of neurotransmitters including glutamate and GABA, leading to a decrease in brain cell (neuron) excitability. Anticonvulsant medications for PTSD symptoms assessed in this topic include topiramate, tiagabine, and divalproex.

What is the evidence on anticonvulsants for PTSD?

Moderate quality evidence found topiramate improved symptom response more than placebo. Tiagabine showed less symptom improvement than the antidepressant phenalzine, and divalproex showed less symptom improvement than the antidepressants phenelzine, paroxetine, and desipramine. There were more dropouts due to adverse events with topiramate than with the antidepressant brofaromine.

No other significant differences were found in response, symptom improvement or adverse effects between anticonvulsants and other pharmaceutical agents (antidepressants and antipsychotics).

August 2021

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Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), have been found to be efficacious in the treatment of depression and anxiety. PTSD was originally classed as an anxiety disorder. Antidepressants may work for PTSD by correcting imbalances in neurotransmitters thought to play a role in causing and/or maintaining symptoms.

What is the evidence on antidepressants for PTSD?

Moderate quality evidence found the antidepressants phenelzine (large effect), desipramine (medium-sized effect), paroxetine, venlafaxine, fluoxetine, and sertraline (all small effects) were more effective for PTSD symptoms than placebo. Phenelzine was more effective for PTSD symptoms than the antidepressants citalopram, bupropion, sertraline, and imipramine. Phenelzine was also more effective than the anticonvulsants divalproex and tiagabine, the alpha blocker prazosin, and the adrenergic receptor agonist guanfacine. Paroxetine and desipramine were more effective for PTSD symptoms than citalopram, divalproex, and prazosin. Venlafaxine and fluoxetine were more effective for PTSD symptoms than citalopram and prazosin. Citalopram was less effective for PTSD symptoms than the antidepressant mirtazapine and the antipsychotic olanzapine. There were fewer dropouts due to adverse events with the antidepressant brofaromine than with the antidepressants sertraline and paroxetine, and the anticonvulsant topiramate.

Moderate to low quality evidence found no differences between paroxetine or sertraline plus prolonged exposure vs. paroxetine, sertraline, or prolonged exposure alone. There were no differences in PTSD relapse rates after discontinuation of antidepressants or placebo. Moderate to high quality evidence found no influence of baseline PTSD symptom severity on efficacy of paroxetine and sertraline after 12 weeks of treatment.

August 2021

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While most pharmacological guidelines suggest first-line pharmacotherapy should include selective serotonin reuptake inhibitor (SSRI) antidepressants, some people with PTSD do not adequately respond to this treatment. There are also high prevalence rates of PTSD symptoms in people with psychosis, particularly in hospitalised patients. Antipsychotics are effective for the symptoms of psychosis and have also been investigated in people with a primary diagnosis of PTSD.

What is the evidence on antipsychotics for PTSD?

Moderate to high quality evidence found a small improvement in PTSD symptoms with risperidone or olanzapine than with placebo. Olanzapine was also more effective for symptom improvement than the antidepressant citalopram.

There were no significant differences between antipsychotics and placebo in treatment dropouts due to adverse events, however there was more weight gain with antipsychotics.

August 2021

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Benzodiazepines are implemented to treat insomnia, irritability, and anxiety, which are common symptoms in people with PTSD. While benzodiazepines may diminish these symptoms, they may worsen other features, such as promoting avoidance in the long term. They are also associated with well-established patterns of tolerance and dependence, so they are prescribed with caution.

What is the evidence on benzodiazepines for PTSD?

Moderate quality evidence found a small effect that benzodiazepines can have an adverse impact on the prevention and treatment of PTSD.

August 2021

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Glutamate receptor modulators have been suggested as an adjunctive treatment to psychological exposure therapies when individuals have sub-optimal responses to these therapies. D-cycloserine is a partial N-methyl-D-aspartate (NMDA) agonist that stimulates NMDA glutamate synapses involved in emotional learning and strengthens the fear extinction learning that takes place in exposure-based treatments.

What is the evidence on D-cycloserine for PTSD?

Moderate to low quality evidence finds no significant improvement in PTSD symptoms with D-cycloserine plus exposure-based treatment compared to placebo plus exposure-based treatment. There may be some improvement in people on serotonin reuptake inhibitor (SSRI) antidepressants, in people with co-occurring anxiety disorders, in people receiving more therapy sessions, and in people given earlier and greater D-cycloserine doses.

August 2021

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Countries are increasingly allowing cannabinoids (tetrahydrocannabinol [THC] and cannabidiol [CBD]) to be made available for medicinal purposes, including for the treatment of mental disorders. Medicinal cannabis refers to any part of the cannabis plant, such as flowers, buds, leaves, or full plant extracts. Pharmaceutical cannabinoids refer to pharmaceutical-grade medicinal extracts with defined and standardised THC, CBD, or a combination of both and synthetic cannabinoid derivatives.

What is the evidence regarding cannabinoids for PTSD?

Moderate to low quality evidence finds no consistent improvement in PTSD symptoms with cannabinoids. There may be more adverse events with cannabinoids than with a placebo. Few trials have been conducted to date.

August 2021

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Oxytocin is a neuromodulatory neuropeptide that is important for processing emotional stimuli in a social context. It is known for its role in facilitating trust and attachment between individuals as well as its involvement in behaviours such as mother-infant bonding, theory of mind, and empathic abilities. The impact of oxytocin may be moderated by features of the social environment or individual differences.

What is the evidence on oxytocin for PTSD?

Moderate to low quality evidence found intranasal oxytocin may enhance cognitive and empathic abilities but has no effect on PTSD symptoms. Intranasal oxytocin may be effective for the regulation of sympathetic nervous tone and cortisol reactivity.

August 2021

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