Stellate Ganglion Block: Effects

The most common indication for stellate ganglion block is complex regional pain syndrome of the upper extremity. Additional indications for stellate ganglion blockade include: neuropathic pain of the hand or arm, symptoms of menopause, refractory ventricular tachycardia, cardiac electrical storm, vascular insufficiency, hyperhidrosis, among others. 

The stellate ganglion is formed by the fusion of the inferior cervical ganglion and first thoracic ganglion, normally located at the level of cervical vertebral body, C7.  The target stellate ganglion blockade is most commonly the transverse process of C6 (Chassaignac's tubercle). Needle placement occurs at the level of C6 to avoid side effects of pneumothorax, nerve root injury and vascular injection. 

Common side effects of stellate ganglion block are: Horner’s Syndrome (ptosis, miosis, anhidrosis, enophthalmos), Hoarseness (Recurrent Laryngeal Nerve), as well as Hemidiaphragm (Phrenic Nerve). Horner’s syndrome is by far the most commonly encountered side effect and is considered by some practitioners to be an indicator of successful blockade.

Post Herpetic Neuralgia

Post herpetic neuralgia (PHN) is a sequelae of herpes zoster infection. Herpes zoster infection typically begins with flu like prodromal symptoms and progresses to a rash of grouped vesicles on an erythematous base as the reactivated virus replicates and spreads to dermoepidermal junction. Herpes zoster most often affects thoracic dermatomes in 50% of cases followed by the face in 10-20% of cases. Diagnosis of herpes zoster is made clinically with history and symptomatic dermatomal rash not crossing the midline. Risks factors for herpes zoster include older age and immunosuppression, greater severity of acute pain, presence of painful prodrome, greater rash severity. Treatment of herpes zoster rash with antiviral therapy has been shown to decrease acute and chronic pain and should be initiated within 72 hours of rash onset if possible. Herpes zoster treatment should also include effective multimodal pain therapy which may decrease the risk of PHN. Herpes zoster vaccination in adults is recommended in healthy adults 50 years and older with live attenuated vaccine or the new recombinant zoster, which is preferable.

Herpes zoster pain can precede or accompany the rash and mostly resolves as the rash resolves. When persistent pain results, it can be defined as post herpetic neuralgia if the pain that persists for more than 90 to 120 days after rash onset. Risk of PHN after herpes zoster varies from 5% to more than 30% worldwide depending on the study.

Treatment of postherpetic neuralgia is mostly pharmacological with a limited role of interventional and alternative modalities. Anticonvulsants, tricyclic antidepressants, serotonin norepinephrine reuptake inhibitors, opioids, and topical modalities are often used. Anticonvulsants are first line therapies and include gabapentin and pregabalin. Tricyclic antidepressants are also effective in PHN and act by inhibiting reuptake of norepinephrine and serotonin and sodium channel blockade. Opioids are effective, however, adverse effect profile must be considered including nausea, sedation, urinary retention, pruritis, constipation, immune suppression, hypogonadism, as well as tolerance, dependence and opioid induced hyperalgesia. Topical therapies including lidocaine and capsaicin are also attractive therapy in the older patients who are sensitive to side effects. Interventional therapies including nerve blocks, neuraxial blockade, dorsal root ganglion pulsed radiofrequency ablation, botulism injection, and sympathetic nerve blocks have been performed for PHN.

Phantom Limb Pain: Treatment

Post amputation pain (PAP) is a challenging constellation of painful disease states caused by the surgical or traumatic removal of a limb or appendage.  The most common causes are vascular disease and trauma.  The two most common causes of PAP are residual limb pain and phantom limb pain.  Residual limb pain is often referred to as stump pain.  This is pain which can be localized to the residual appendage after an amputation.  There are multiple causes which include infections, soft tissue injuries, bony injuries, nerve lesions or neuromas, hematomas, and even local ischemia or poor healing.  The treatment for stump pain is often treating the underlying cause.  When identifiable anatomic pathology is identified, surgical exploration can be helpful.  Also, neuroma injections have shown anecdotal benefit.  Often times, this pain can be resolved by reviewing the fit of a prosthesis or through exercise based physical therapy.  Often times, musculoskeletal issues can arise due to gait changes and prosthetic devices can cause irritation at the stump site which can be extremely uncomfortable.  

While over 90% of patients do experience phantom sensations after an amputation, only about 80% experience phantom limb pain.  This is described as dysesthesia in the absent part of the affected limb.  While phantom limb pain is extremely common in this population, it is also extremely difficult to treat.  While examination can rule out stump pain causes, it is rarely helpful in pointing to a cure of this disease.  Many neuropathic pain medications such as tricyclic antidepressants, gabapentinoids, NMDA antagonists, and calcitonin have shown promise in the treatment for this disease. 

Psychologic therapies such as cognitive behavioral therapy (CBT), hypnosis, and mirror therapy have shown some benefit for patients with this condition.  TENS therapy has also been found to be effective.  When conservative treatment have failed, interventional procedures like neuromodulation can be effective.  Dorsal column stimulation has been shown effective in case series and other anecdotal data.  More recently, dorsal root ganglion stimulation and peripheral stim is being studied specifically for phantom limb pain.  While these technologies are exciting, we are still awaiting true, concrete evidence. 

Ketamine – Effects

The action of ketamine involves multiple mechanisms with multiple receptors. Ketamine is noncompetitive, reversible N-methyl-D-aspartate (NMDA) channel blocker which blocks the excited nerves, potentiates delta and mu opioid agonism and opioid potentiation, alters the nitric oxide guanosine monophosphate system, changes in cholinergic activity, and central dopamine and noradrenaline release.  The NMDA channel blockade is especially unique to the mechanism of action of ketamine. This leads to quick onset of action (less than 5 minutes) and a short duration of activity when given in a single shot.

Indications of ketamine include anesthetic induction, maintenance, and perioperative pain management especially in patients with opioid tolerance, dependence or patients at risk of opioid related respiratory depression. Subanesthetic ketamine infusion are routinely used to treat complex regional pain syndrome and other causes of neuropathic pain. Ketamine has multiple systemic effects including central nervous system, cardiovascular system pulmonary system including the airways, and hepatic system. Side effects include nausea, headache, fatigue, dysphoria as well as dissociative experiences such as hallucination, delusion, or out of body experiences.  These central nervous system side effects may be mitigated with use of benzodiazepine prior to ketamine use.


Fibromyalgia is a challenging medical condition with multiple core symptoms including multifocal pain, fatigue, insomnia, cognitive or memory problems, and psychological stress. Multiple disorders coexist with fibromyalgia including regional musculoskeletal pain syndromes, chronic fatigue syndrome, irritable bowel syndrome, irritable bladder syndrome or interstitial cystitis, headaches, vulvodynia, and pelvic pain. Pathophysiology of fibromyalgia is attributed to decreased descending analgesic activity and increased wind-up or temporal summation. 

Diagnosis of fibromyalgia as defined by ACR requires widespread pain index (WPI) greater than or equal to 7 and symptom severity scale (SSS) score greater than or equal to 5 or WPI 4-6 and SSS score greater than 9, generalized pain of at least 4 out of 5 regions, duration of at least 3 months, no other diagnostic explanation for symptoms. Differential for fibromyalgia is hypothyroidism, polymyalgia rheumatica, autoimmune disorders (rheumatoid arthritis, SLE), Sjogren’s syndrome as well as less common disorders including hepatitis C, sleep apnea, Chiari malformation, celiac sprue.

Pharmacological treatments of fibromyalgia include tricyclic antidepressants (amitriptyline, nortriptyline), serotonin-norepinephrine reuptake inhibitors (duloxetine, venlafaxine), alpha 2 delta ligands (pregabalin, gabapentin). Non pharmacological treatments of fibromyalgia are also key to sustained remission including low intensity, low impact exercise programs, behavioral medicine programs including cognitive behavior therapy and psychological support. FDA approved drugs are pregabalin (lyrica), duloxetine (Cymbalta), and Milnacipran [SNRI] (Savella). Glutamate is increased in this patient population secondary to wind up.

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