"Nerve blocks have long been used to treat both acute and chronic pain. When performing
regional anesthesia procedures, clinicians realized that pain relief could be achieved not
only by blocking the afferent somatic nerves but also by anesthetizing the efferent nerves
of the sympathetic nervous system at sites containing regional collections of autonomic
ganglia.1
The sympathetic nervous system (SNS) is a key mediator of the “fight or flight” response. During periods of stress, pre-ganglionic, cholinergic nerves in the spinal cord fire, releasing the neurotransmitter acetycholine. Some of these pre-ganglionic neurons transmit directly to the adrenal medulla, causing bulk release of adrenalin and other stress-hormones. However, most pre-ganglionic SNS neurons synapse with peripheral neurons and release noradrenalin at nerve terminals, which induce stress-appropriate responses specific to the tissue involved.2 Masses of postganglionic, adrenergic neurons can be found in a chain of ganglia that lay along the spinal cord.
The stellate ganglion (SG) is the result of the fusion of the inferior cervical ganglion (C7) and the first thoracic ganglion into a single, star-shaped mass measuring about 1.5 cm3. It is normally situated lateral and posterior to the lateral edge of the longus colli muscle anterior to the first rib and posterior to the subclavian artery. About 80% of individuals will have fused anatomy, with the remaining 20% having unfused ganglia that lay in a similar area anterior to the transverse process of the C7 vertebra.3,4 All pre-ganglionic sympathetic nerves innervating the head and neck, as well as many to the upper extremity, either synapse here or pass through to more distal sites."
"Pharmacological complications are related to the dose, volume, type of local anesthetic and site of deposition of the solution. This includes hoarseness of voice due to paralysis of the recurrent laryngeal nerve. Additionally, phrenic nerve paralysis may lead to respiratory distress, especially if there is contralateral dysfunction of the phrenic nerve. Other adverse events may include seizures, loss of consciousness, profound hypotension due to a high spinal anesthetic blockade, air embolism, and loss of cardioaccelerator activity that may lead to various bradyarrhythmias and hypotension.
The sympathetic nervous system (SNS) is a key mediator of the “fight or flight” response. During periods of stress, pre-ganglionic, cholinergic nerves in the spinal cord fire, releasing the neurotransmitter acetycholine. Some of these pre-ganglionic neurons transmit directly to the adrenal medulla, causing bulk release of adrenalin and other stress-hormones. However, most pre-ganglionic SNS neurons synapse with peripheral neurons and release noradrenalin at nerve terminals, which induce stress-appropriate responses specific to the tissue involved.2 Masses of postganglionic, adrenergic neurons can be found in a chain of ganglia that lay along the spinal cord.
The stellate ganglion (SG) is the result of the fusion of the inferior cervical ganglion (C7) and the first thoracic ganglion into a single, star-shaped mass measuring about 1.5 cm3. It is normally situated lateral and posterior to the lateral edge of the longus colli muscle anterior to the first rib and posterior to the subclavian artery. About 80% of individuals will have fused anatomy, with the remaining 20% having unfused ganglia that lay in a similar area anterior to the transverse process of the C7 vertebra.3,4 All pre-ganglionic sympathetic nerves innervating the head and neck, as well as many to the upper extremity, either synapse here or pass through to more distal sites."
"Pharmacological complications are related to the dose, volume, type of local anesthetic and site of deposition of the solution. This includes hoarseness of voice due to paralysis of the recurrent laryngeal nerve. Additionally, phrenic nerve paralysis may lead to respiratory distress, especially if there is contralateral dysfunction of the phrenic nerve. Other adverse events may include seizures, loss of consciousness, profound hypotension due to a high spinal anesthetic blockade, air embolism, and loss of cardioaccelerator activity that may lead to various bradyarrhythmias and hypotension.
Therapeutic Utility of SGB
NONPSYCHIATRIC CONDITIONS
SGB has been shown to have utility for diagnostic, therapeutic, and prognostic purposes for a variety of conditions, including: chronic regional pain syndrome types I and II to the upper extremities (CRPS I and II);; chronic and acute vascular insufficiency/occlusive vascular disorders of the upper extremities, such as Raynaud’s disease, intra-arterial embolization and vasospasm. SGB has also been found an effective treatment for poor lymphatic drainage and local edema of the upper extremity following breast surgery;; postherpetic neuralgia;; and phantom limb pain or amputation stump pain. Patients with quinine poisoning;; sudden hearing loss and tinnitus;; hyperhidrosis of the upper extremity;; cardiac arrhythmias and ischemic cardiac pain;; Bell’s palsy and a variety of orofacial pain syndromes, including neuropathic orofacial pain and trigeminal neuralgia;; vascular headache such as cluster and migraine headaches;; and neuropathic pain syndromes among cancer patients are all also candidates for SGB.
NONPSYCHIATRIC CONDITIONS
SGB has been shown to have utility for diagnostic, therapeutic, and prognostic purposes for a variety of conditions, including: chronic regional pain syndrome types I and II to the upper extremities (CRPS I and II);; chronic and acute vascular insufficiency/occlusive vascular disorders of the upper extremities, such as Raynaud’s disease, intra-arterial embolization and vasospasm. SGB has also been found an effective treatment for poor lymphatic drainage and local edema of the upper extremity following breast surgery;; postherpetic neuralgia;; and phantom limb pain or amputation stump pain. Patients with quinine poisoning;; sudden hearing loss and tinnitus;; hyperhidrosis of the upper extremity;; cardiac arrhythmias and ischemic cardiac pain;; Bell’s palsy and a variety of orofacial pain syndromes, including neuropathic orofacial pain and trigeminal neuralgia;; vascular headache such as cluster and migraine headaches;; and neuropathic pain syndromes among cancer patients are all also candidates for SGB.
SGB has also been recommended for improving blood flow to the cranium for angiography
and following stroke/cerebrovascular accident and hyperhidrosis to the upper
extremities.13,14 Additionally, SGB’s use has been reported in the treatment of Ménière’s
syndrome3 and hot flashes.17–19
PSYCHIATRIC CONDITIONS
It might seem counterintuitive that treating the peripheral nervous system could affect psychiatric conditions presumably mediated in the brain. Most psychiatrists, however, are probably familiar with the observation that vagal nerve stimulation improves depression.20 As early as 1947, reported cases of improvements in depression subsequent to SGB treatment began emerging in the literature.21 More recently, unexpected benefits of SGB have been reported for hallucinations in schizophrenia,22 and in “climacteric psychosis” (a term for mental illness associated with menopause).23
Although not specifically SGB, similar techniques of lesioning the sympathetic chain has been reported widely as a potential treatment for social phobia.24–26
In the case of social phobia, the mechanism is presumably because the techniques
prevent blushing. For patients with both blushing and social phobia, sympathectomy
proved as good as or better than sertraline in improving anxiety.27 Taken together, the
evidence suggests that techniques that influence the peripheral sympathetic nervous
system could potentially be used to treat psychiatric conditions."
PSYCHIATRIC CONDITIONS
It might seem counterintuitive that treating the peripheral nervous system could affect psychiatric conditions presumably mediated in the brain. Most psychiatrists, however, are probably familiar with the observation that vagal nerve stimulation improves depression.20 As early as 1947, reported cases of improvements in depression subsequent to SGB treatment began emerging in the literature.21 More recently, unexpected benefits of SGB have been reported for hallucinations in schizophrenia,22 and in “climacteric psychosis” (a term for mental illness associated with menopause).23
Although not specifically SGB, similar techniques of lesioning the sympathetic chain has been reported widely as a potential treatment for social phobia.24–26
"Cumulatively, the growing body of preliminary evidence about the potential therapeutic
benefits of SGB for PTSD is compelling. Starting in 2008, a series of case reports were
published in which SGB relieved symptoms of PTSD, even when co-occurring pain was
not present among patients in a private clinic practice.29–31 The effect was usually
immediate and often dramatic. SGB appeared to produce some form of a “calming effect”
that primarily impacted symptoms associated with avoidance and hyperarousal. However,
to experience sustained symptom relief, patients often required at least two SGB
injections over a short follow-up period (< 30 days).31 In some cases, radiofrequency
ablation of the SG was needed to prolong the duration of benefit.30 "
Psychiatric Annals
February 2013 - Volume 43 · Issue 2: 87-92
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