What is SGB?
Stellate ganglion block (SGB), a cervical sympathetic injection.
The stellate ganglion block (SGB) is an anesthetic injection in a group of nerves in the neck that are called the stellate ganglion. The procedure has been used to treat chronic pain since 1925 and recent studies have demonstrated great promise as a successful intervention for PTSI.
The author reported the first successful treatment of PTSI through the use of SGB in 2008 (42). The subject of that report was a civilian robbery victim who presented for SGB treatment due to severe anxiety related to PTSI, two months post being robbed at gun-point. The patient experienced excellent response to SGB and reported significant resolution of hyper vigilance and anxiety.
Potential Complications of SGB
Stellate ganglion blockades carry a very small risk of infection. Using prophylactic antibiotics can reduce the slight risk of infection. Although rare, severe complications following SGB do include bleeding, seizures, pneumothorax and spinal cord trauma. A study of the incidence of severe complications was last undertaken in 1992 by German researchers Wulf and Maier, with a reported 1.7 complications per 1,000 blockades based on surveys completed by patients receiving a combined total of 45,000 blocks. No fatalities or persistent complications were reported (43). This survey was conducted prior to the use of fluoroscopic guidance where the stellate ganglion blocks were performed at the C7 level rather than C6. The current improvements in guidance technology and changing the needle location to C6 are likely to reduce the chance of complications.
Stellate Ganglion Block (SGB) and the treatment of PTSI, current evidence.
Stellate Ganglion Block has been used to treat PTSI since 2008. Dr. Navaie summarized available literature published between 2008 and 2013 on the use of SGB to treat PTSD (44). She indicates that: patients were predominantly male (n=21, 88%) and active duty military (n=14, 58%) or veterans (n=8, 33%) with combat-related PTSD. The average age was 40.5 years. All patients received more than 1 year of psychotherapy and pharmacotherapy before SGB. Seventeen patients (71%) received one SGB, seven (29%) received multiple SGBs. Clinically, meaningful improvements were observed in 75% (n=18) of patients after SGB, with significant differences in mean PTSD scores, pre and post treatment. In clinical case reports reviewed above, two have specific merit.
Dr. Alino reported; a patient with a 2 year history of suicidal ideation had become free of suicidal thought two days after SGB(45). Dr. Mulvaney reported that; two patients with severe PTSI were able to completely stop taking psychiatric medications after SGB (46). Recently, further validation of SGB efficacy has been published.
Dr. Mulvaney, in follow up to 2010 publication (46) observed that 166 service members with symptoms of PTSI that received SGB had clinically significant reductions in PCL scores. Specifically, 70% of those treated with SGB reported significant reductions in PCL scores and the effects were sustained three to six months post procedure (47). Further validation of SGB efficacy in 2014 came from Dr. Alkire. He presented an abstract titled: “Prolonged Relief of Chronic Extreme PTSI and Depression Symptoms in Veterans Following a Stellate Ganglion Block.” In this report, Dr. Alkire selected the most extreme PTSI cases in the veteran population and observed that SGB was greatly effective in helping 75% (9/12) of the subjects (48).
Proposed mechanisms for the clinical effect of SGB
The hypothesis for potential mechanism of action for SGB (or cervical sympathetic chain blockade) has been described in multiple peer-reviewed publications (31), (46), (47), (48), (49). The hypothesis rests on previously demonstrated evidence and was originally proposed by the author.
The first line of evidence in supporting the theory demonstrates a poly-synaptic neurological connection from stellate ganglion to the part of the brain associated with PTSI, the amygdala (39) (Figure #1). Specifically, Dr. Liberzon demonstrated increased activation of the amygdala in PTSI patients when compared to controls (50).
The second line of evidence relies on the nerve growth factor (NGF) increase observed as a physiological response to acute and chronic stress (51) (52). NGF increase is known to increase perivascular norepinephrine (NE). This has been demonstrated by direct intracerebroventricular brain infusion of NGF into adult rats (53). Stress-induced release of NE in amygdala and related structures has been shown to facilitate a number of anxiety-like behavioral responses that are mediated in these regions (54). Norepinephrine increase has been shown to be associated with PTSI in urine (33) and cerebrospinal fluid (34) as discussed previously. The NE increase is likely due to NGF increase in the stellate ganglion which in turn is caused by retrograde NGF transport from the intracerebral site to the stellate ganglion (55). NGF increase is also known to promote neurite outgrowth (sprouting) at the end terminals (56). The neurite outgrowth has been associated with NE increase (57) (Figure #2). Finally, local anesthetic injections are known to suppress NGF (58), leading to dying of new nerve outgrowth since maintenance of sprouting is dependent on the presence of NGF (59). As a result, it is hypothesized that the suppression of NGF would reduce NE levels and reverse the cascade of PTSI (31) (Figure #3).
The third and final line of evidence in support of the theory is based on EEG evaluation of rats following SGB. Dr. Jeong found that SGB with bupivacaine resulted in significantly decreased EEG activities in rats. These results suggest that SGB can induce a sedative effect in rats. The proposed mechanism of the effect described above was reduction in brain norepinephrine (60).
A possible new nomenclature for organization for PTSI etiology and treatment; based on the sympathetic system involvement. Complex regional pain syndrome (CRPS) and PTSI correlates.