Post-traumatic stress disorder (PTSD) is a chronic anxiety disorder caused by seeing or experiencing traumatic events that are exceptionally threatening or catastrophic nature, and likely to cause pervasive distress in almost anyone. PTSD does not, therefore, develop following those upsetting situations that are described as 'traumatic' in everyday language, for example, divorce, loss of job, or failing an exam. The symptoms of PTSD include re-experiencing the event through flashbacks or nightmares, avoidance of stimuli which remind the victim of the traumatic event, and increased arousal, such as anxiety, anger or hypervigilance. A formal diagnosis of PTSD requires these symptoms to persist for at least a month and to cause significant disruption in one’s personal and/or professional life. The person with PTSD has clinically significant distress and/or functional impairment. PTSD is a disorder that can affect people of all ages. Around 25–30% of people experiencing a traumatic event may go on to develop PTSD.
Post-traumatic stress disorder (PTSD) develops following a stressful event or situation of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone. PTSD does not develop following those upsetting situations that are described as ‘traumatic’ in everyday language, for example, divorce, loss of job, or failing an exam. PTSD is a disorder that can affect people of all ages. Around 25–30% of people experiencing a traumatic event may go on to develop PTSD. The most characteristic symptom of PTSD is re-experiencing symptoms. Stellate ganglion block is an innovative management option for PTSD. Although stellate ganglion block’s precise mechanism of action in PTSD remains elusive, a growing number of case reports and case series have been published on its use for treatment-refractory cases of PTSD. However there is lack of randomised controlled trials and further research is needed to know which patients would benefit from this treatment, how many injections are needed and whether bilateral injections should be performed?
The earliest description of PTSD in the modern era was from the Civil War (1861–1865): ‘‘irritable heart’’ or ‘‘soldiers’ heart’’ (Da Costa, 1871). According to a paper published in 1876 by Mendez DaCosta, MD, Civil War combat veterans with ‘‘soldiers’ heart’’ had startle responses, hyper-vigilance, and heart arrhythmia, thus the first modern description of PTSD had a physiologic description. Current term PTSD was introduced in the 1980s in the United States and Western Europe. In DSM-III, multiple terms were applied to what is now called PTSD, many of which allude to a stress reaction and the biological effects on the heart, and presumably, the brain.
Individuals responding to a traumatic event may develop PTSD. This involves having experienced, witnessed, or been confronted with an event or events involving actual or threatened death or serious injury, or a threat to the physical integrity of self or others. Moreover, their response must have involved intense fear, helplessness, or horror. Symptoms can develop within weeks but according to the 10th Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) (WHO 2010) onset is almost always within six months. It may take months or even years for individuals to present to services. Delayed presentation is common but there is also some evidence that PTSD may have a delayed onset (Andrews et al. 2007).
According to DSM-IV (APA 1994) the symptoms are grouped into three clusters:
For a diagnosis of PTSD, symptoms must have been evident for more than one month and must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
Post-traumatic stress disorder (PTSD) is a debilitating mental health condition that is triggered by a distressing event. It is common for people to struggle with a variety of overwhelming symptoms of PTSD, which can prevent them from embarking on everyday activities and could potentially damage relationships with their loved ones.
Some people with PTSD can also adopt unhealthy coping mechanisms, as they might be unsure how to manage their emotions and negative thoughts, and they might be ashamed to seek help for the disorder.
A few of the more common causes of PTSD include:
PTSD can develop immediately after someone experiences a disturbing event, or it can occur weeks, months or even years later.
PTSD is estimated to affect about 1 in every 3 people who have a traumatic experience, but it’s not clear exactly why some people develop the condition and others do not.
People with PTSD can develop a wide range of symptoms after the event – this can happen instantly or even take a few years for symptoms to develop. The symptoms are wide-reaching and can affect people differently. The main symptoms of PTSD include:
These are just a few of the more common symptoms but there are many more. These symptoms can interfere with all areas of your life which is why you hear of so many people with PTSD who struggle to hold down a job or struggle to maintain relationships. This some-times leads people to take their own lives. PTSD can be hard to live with and interfere with many areas of your life, but it is important to know that there are effective treatment options available and many people go on to lead happy lives.
While PTSD symptoms can often vary between people, re-experiencing is one of the most common issues connected with the disorder. It occurs when a person both vividly and involuntarily relives a trauma through flashbacks, nightmares, physical sensations, or distressing images.
It is also likely people will endure negative thoughts after the event, as they might continually ask themselves various questions, which can prevent them from moving on from the distressing experience. For example, they might wonder if there were any actions they could have taken to have stopped it or may struggle to understand why the experience happened to them, which can result in feelings of shame or guilt.
People living with PTSD will likely want to do everything in their power to avoid reminders of the trauma. Consequently, they might avoid key people in their lives or places that could trigger a flashback. They also are likely to dismiss talking about an event or will aim to push it from their mind by focusing on their career or pastimes.
Post-traumatic stress disorder can lead to severe anxiety and can make it challenging for people to relax. The traumatic event could also make a person easily startled or more afraid of potential threats, which is known as hyperarousal. As a result, they might struggle with:
Although it takes time to develop PTSD, symptoms typically start within a month of a trauma. However, it is possible they will not occur until many months or years later. Those living with the disorder could experience lengthy periods when their symptoms might not be noticeable to their family members or friends, but it is likely they will endure periods when their symptoms will grow.
PTSD can, however, lead to some people consistently struggling with severe symptoms, including anxiety disorders, which can impact every aspect of their daily lives. For example, it could impair their ability to complete normal tasks, destroy their career, and prevent them from embarking on social activities.
People who repeatedly experience traumatic situations, such as severe neglect, abuse or violence, may be diagnosed with complex PTSD.
Complex PTSD can cause similar symptoms to PTSD and may not develop until years after the event. It is often more severe if the trauma was experienced early in life, as this can affect a child’s development.
Complex PTSD is thought to be more severe if:
As it may take years for the symptoms of complex PTSD to be recognised, a child’s development, including their behaviour and self-confidence, can be altered as they get older.
Adults with complex PTSD may lose their trust in people and feel separated from others.
The symptoms of complex PTSD are similar to symptoms of PTSD, but may include:
The PTSD Checklist (PCL) is a 17-item self-report measure reflecting DSM-IV symptoms of PTSD (Blanchard et al. 1996). The PCL has a variety of clinical and research purposes, including:
The PCL-C (civilian) asks about symptoms in relation to generic “stressful experiences” and can be used with any population. This version simplifies assessment based on multiple traumas because symptoms are not attributed to a specific event. The response options are: not at all (scored 1), a little bit (2), moderately (3), quite a bit (4), and extremely (5). A total symptom severity score (range = 17–85) can be obtained by summing the scores from each of the 17 items listed below. There are a number of ways of scoring the PCL.
A positive screen may be defined as a score of 50 or more, together with endorsement of the DSM-IV criteria, identified as positive responses to at least one B item (questions 1–5 on re-experiencing symptoms), three C items (questions 6–12 on avoidance and numbing), and two D items (questions 13–17 on hyperarousal symptoms).
Below is a list of problems and complaints that individuals sometimes have in response to stressful life experiences. Please read each one carefully, and indicate how much you have been bothered by that problem in the last month:
Please click below to complete a PTSD checklist:
It is never too late to seek treatment for post-traumatic stress disorder. After PTSD diagnosis, there are so many treatment options available out there to help you overcome the disorder. A mental health professional might recommend one of three psychological therapies to treat PTSD, in addition to medication management.
Conventional PTSD treatment comprises 3 complementary strategies:
Cognitive behavioral therapy (CBT) can change how a patient both acts and thinks each day. A therapist may force a person to confront any traumatic memories and can ultimately change the way they view a negative event. For example, they could stop a person from feeling as if they are to blame for an accident or disaster.
Another option is eye movement desensitization and reprocessing (EMDR), which requires a patient to make side-to-side movements by following a therapist’s moving finger while discussing a traumatic experience. Other EMDR methods can include playing a tone or tapping a finger, which has proved effective for changing the way a person perceives a distressing event.
It might also be helpful for some people living with PTSD to talk about their experience with others. Group therapy could, therefore, serve as an effective treatment method, as it can help a person to manage their symptoms and learn more about their disorder.
Depending on a patient’s symptoms, a doctor may prescribe adults with antidepressant medications. However, many doctors will often only provide the medication if a patient has experienced next to no benefit from psychological treatment or if they are struggling with an underlying condition, such as depression.
Primarily indicated to address mood disorders, the SSRIs increase the amount of serotonin circulating in the brain but they have been shown to be helpful in mediating PTSD symptoms. However, side effects include sexual dysfunction (Balon, 2006), somnolence (Giner et al., 2005), and an increased risk for suicide (Giner et al., 2005). Four SSRIs have undergone clinical trials for efficacy in treating PTSD; these include citalopram, fluoxetine, paroxetine, and sertraline.
The CBT component of treatment helps the client change how he or she thinks about the traumatic event and the response to that event. Using exposure therapy, the client is reintroduced to portions of the traumatic event in a controlled, safe environment. The typical CBT course is three months with one to two visits per week. Alternatives with potentially similar efficacy include eye movement desensitization and reprocessing (EMDR).
The sympathetic nervous system (SNS) is part of the autonomic nervous system. Its role is to mobilize body’s resources under stress, to induce the fight-or-flight response. It is also constantly active at a basal level in order to maintain homeostasis. In PTSD, the SNS is known to be chronically activated over the normal baseline levels (Lemieux and Coe 1995; Krystal et al., 1989). In large part, the activation of the SNS is accomplished by the increase of catecholamines, mainly epinephrine and norepinephrine. The role of norepinephrine in the brain is that of a neurotransmitter leading to arousal, selective attention, and vigilance which has been demonstrated in preclinical studies (Southwick et al., 1999). Specifically, elevated urinary norepinephrine has been identified among patients with PTSD (Mason et al., 1988). Similarly, norepinephrine concentrations in cerebrospinal fluid (CSF) are significantly higher in subjects with PTSD than among healthy controls and have been correlated with the severity of PTSD symptoms (Geracioti et al., 2001). Such notable increases in noradrenergic activity among subjects with PTSD suggest that reducing CNS noradrenergic activity could be effective, especially for arousal symptoms such as nightmares and startle reactions (Taylor et al., 2006). Orally active noradrenergic blocking or deactivating agents that have been used to moderate an over-active SNS include clonidine and prazosin.
The stellate ganglion block (SGB) is an anesthetic injection in a group of nerves in the neck, called the stellate ganglion. The procedure has been used to treat chronic pain since 1925 and recent pilot studies have demonstrated great promise as a successful intervention for PTSD, among other indications. The first documented use of SGB for psychiatric effect was its use in the resolution of depression by bilateral SGB as noted by clinicians at the Cleveland Clinic in 1947 (Karnosh and Gardner, 1947).
The first case study of successful use of the SGB to treat PTSD was reported in 2008 (Lipov et al., 2008). The patient was a civilian and victim of a violent crime who experienced an excellent response to SGB with marked resolution of PTSD symptoms. This was followed by a publication by Dr. Sean Mulvaney and his team at Walter Reed Army Medical Center, where a significant resolution of PTSD symptoms in two Operation Iraqi Freedom veterans was reported over one year (Mulvaney et al., 2010)
The best-understood member of the neurotropic family, nerve growth factor (NGF) regulates a variety of signalling events such as cell differentiation and survival, growth cessation, and apoptosis (death) of neurons (Snider, 1994). The body responds to chronic stress by increasing NGF levels (Smith, 1996) and NGF is also known to be elevated immediately prior to soldiers’ first parachute jump (Alleva et al., 1996) thus demonstrating a connection between NGF, stress and possibly PTSD. Further studies have demonstrated intracerebral NGF increase leading to retrograde transport of NGF from the intracerebral site to the stellate ganglion (Johnson et al., 1987). Next, NGF concentration increase at the stellate ganglion has been shown to lead to sprouting (a new nerve growth) at the sympathetic end terminals which is NGF dependent (Chen et al., 2001), which, in turn, causes increased norepinephrine (NE) levels. More evidence points to NE being involved in PTSD where urine levels of NE are known to increase in PTSD (Kosten et al., 1987). Thus, it appears that trauma triggers a neurobiological cascade that ultimately leads to PTSD. The reversal of this cascade possibly occurs following the application of a local anaesthetic to the stellate ganglion due to a reduction of NGF that is essential for the maintenance of sprouting, since sprouting is NGF dependent(Takatori et al., 2006). This NGF decrease leads to the death of new nerve shoots (Gatzinsky et al., 2004).
In non-medical terms, it works by dulling down a person’s fight or flight mechanism, which can help them to eliminate various symptoms associated with the disorder, and it can ultimately support other PTSD therapies, such as medication and cognitive-behavioural therapy (CBT).
Some patients (up to 50% in our experience) will have almost immediate relief from some PTSD symptoms after receiving the SGB injection. While the benefits are not typically permanent, it could help people to take greater control of the disorder, and quickly move on from a distressing experience. For example, it could lift a person’s anxiety, and help them to feel like themselves.
Some patients may have a slower onset and experience improvement in their symptoms after 48 hours to 72 hours or even after a couple of weeks. Some patients (30-40% or even higher) may not respond to the SGB injections at all.
It is essential to note that the SGB injection will not help people forget any memories associated with their traumatic experiences. Instead, it could help a person live a calmer, less anxious lifestyle, so they can change the way they react to their thoughts and improve how they respond to other forms of PTSD therapy.
SBG injections can be a fantastic treatment solution but it is important to note that the SGB is not a cure for PTSD and you are strongly advised to keep working/engaging with a mental health professional to move forward. The injection will not erase memories of the traumatic incident but the fact that it can alleviate symptoms and bring calmness can make managing these memories much easier and help with other treatment solutions, such as CBT.
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Alkire, M. T., Hollifield, M., Khoshsar, R., Nguyen, L., Alley, S. R., & Reist, C. (2015). Neuroimaging suggests that stellate ganglion block improves post-traumatic stress disorder (PTSD) through an amygdala mediated mechanism. In American Society of Anesthesiology annual meeting. American Psychiatric Association: The Diagnostic and Statistical Manual of Mental Disorders, Ed 4, Text Revision. Washington, DC, American Psychiatric Association, 2000.
Ferrada‐Noli M., Asberg M., Ormstad K., Lundin T., & Sundbom E. (1998). Suicidal behavior after severe trauma. Part 1: PTSD diagnoses, psychiatric comorbidity, and assessments of suicidal behavior. Journal of Traumatic Stress: Official Publication of The International Society for Traumatic Stress Studies, 11(1), 103-112.
Geracioti T.D. Jr, Baker D.G., Ekhatur N.N., et al: CSF norepinephrine concentrations in posttraumatic stress disorder. Am J Psychiatry 2001; 158: 1227–30.
Hanling S. R., Hickey A., Lesnik I., Hackworth R. J., Stedje-Larsen E., Drastal C. A., & McLay R. N. (2016). Stellate ganglion block for the treatment of posttraumatic stress disorder: A randomized, double-blind, controlled trial. Regional anesthesia and pain medicine, 41(4), 494-500.
Hickey A. H., Navaie M., Stedje-Larsen E. T., Lipov E. G., & McLay R. N. (2013). Stellate ganglion block for the treatment of posttraumatic stress disorder. Psychiatric Annals, 43(2), 87-92.
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Karnosh L.J., Gardner W.J. (1947) The effects of bilateral stellate ganglion block on mental depression; report of 3 cases. Cleve Clin Q 14: 133-138. (http://www.ncbi.nlm.nih.gov/pubmed/20250097).
Lipov E. G., Joshi J. R., Lipov S., Sanders S. E., & Siroko M. K. (2008). Cervical sympathetic blockade in a patient with post-traumatic stress disorder: a case report. Annals of Clinical Psychiatry, 20(4), 227-228.
Lipov E. G., Navaie M., Brown P. R., Hickey A. H., Stedje-Larsen E. T., & McLay R. N. (2013). Stellate ganglion block improves refractory post-traumatic stress disorder and associated memory dysfunction: a case report and systematic literature review. Military medicine, 178(2), e260-e264.
Lipov E. G., Joshi J. R., Sanders S., & Slavin K. V. (2009). A unifying theory linking the prolonged efficacy of the stellate ganglion block for the treatment of chronic regional pain syndrome (CRPS), hot flashes, and posttraumatic stress disorder (PTSD). Medical hypotheses, 72(6), 657-661.
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Mulvaney S.W., Lynch J.H., Hickey M.J., et al. Stellate ganglion block used to treat symptoms associated with combat-related post-traumatic stress disorder: a case series of 166 patients. Mil Med. 2014;179(10):1133–40.
This is the largest publication so far on the use of SGB in military PTSD. Takano M., Takano Y., Sato I. (2002) Unexpected beneficial effect of stellate ganglion block in a schizophrenic patient. Can J Anaesth 49: 758-759.
(http://www.ncbi.nlm.nih.gov/pubmed/12193502). Takatori M., Kuroda Y., & Hirose M. (2006). Local anesthetics suppress nerve growth factor-mediated neurite outgrowth by inhibition of tyrosine kinase activity of TrkA. Anesthesia & Analgesia, 102(2), 462-467.
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