KR20170003530A - Kits and methods for treating post traumatic stress disorder (ptsd) and hot flashes - Google Patents

Abstract

The present invention teaches kits and methods for the treatment of patients suffering from post-traumatic stress disorder (PTSD) and / or facial flushing by administering a mixture made with a combination of long-acting topical anesthetics in combination with clonidine . The combination of the two agents provides a significant increase in duration and onset rate of sympathicotomy, an increased intensity of sympathicotomy, as well as a local decrease in local anesthetic absorption. The combination significantly improves efficacy, onset rate and block strength of the right neck sympathetic ganglion (RCSGI), thereby increasing the resolution period of PTSD and flushing, as well as reducing the likelihood of complications associated with local anesthetic absorption.

Description

TECHNICAL FIELD [0001] The present invention relates to a kit and a method for treating post-traumatic stress disorder (PTSD) and facial flushing,

This application claims priority to U.S. Patent Application No. 61 / 889,895, filed October 11, 2013, to the extent permitted by law.

Field of invention

The present invention relates to a method for treating post-traumatic stress disorder (PTSD) and facial flushing by administering a right neck sympathetic ganglion injection (RCSGI) to deliver a long-acting anesthetic and an injectable clonidine mixture to a patient in need of PTSD treatment And a kit.

BACKGROUND OF THE INVENTION

Posttraumatic stress disorder (PTSD) is a complex pathological anxiety condition that adds tremendous damage, characterized by severe pain and mental and physical dysfunction. Symptoms typically include severe anxiety, excessive awakening, recall, and sleep disorders. The effects and consequences for individuals diagnosed with PTSD include depression, drug abuse, violence, inability to maintain close relationships, inability to maintain parental relationships, suicide, and premature death. PTSD is also a public health dilemma, because nearly 80% of the population experience traumatic events in their lifetime. Women may experience PTSD symptoms twice as often as men because of the spread of sexual abuse.

Individuals affected by PTSD require prompt medical intervention. The current standard of care for PTSD is pharmacotherapy and psychotherapy. The pharmacological treatment includes selective serotonin reuptake inhibitors [SSRIs]. Treatment of PTSD is considered successful if the severity, frequency and severity of symptoms decrease. Women tend to respond to psychotherapy and SSRI treatment, but many patients do not respond or only partially respond to these treatments, and there is no consensus on the most beneficial treatment measures for these patients.

Approximately 10% of PTSD patients seek treatment within 12 months for trauma events that stimulate PTSD. The decision to seek treatment is based on factors such as cost-benefit analysis, reluctance to psychotherapy, and side effects of SSRIs and other pharmacological agents (eg, nausea, tremor, nervousness and other side effects) .

The outbreak of PTSD in the US military has been a headline for newspapers for many years. There has been a notable increase in PTSD due to recent military operations. The number of veterans who commit suicide each day increased to 22 per day in the United States, compared to the previous rate of 18 cited by the Veterans Association. Possibly less than 30% returned veterans suffer PTSD, and more than 400,000 veterans receive disability benefits due to PTSD.

The cost of treatment should also be considered not only for the patient but also for the health care system and the community. The cost of medical insurance can range from $ 6,000 to $ 30,000 per year, and the estimated cost of a single disability claim for a veteran soldier is estimated to be $ 650 billion over the next 20 years. However, if the patient is untreated, these costs can not measure the potential loss of life through suicide and assault. The overall efficacy of PTSD treatment in soldiers (except SGB) is reported to be 25% (Hoge. C. W., Interventions for War-Related Posttraumatic Stress Disorder; Meeting Vetrans Where They Are, JAMA 2011: 306: 549-51].

Another health concern that causes considerable discomfort in many women is the occurrence of facial flushing. The cause of facial flushing is not well known, but it happens when the blood vessels on the skin surface are enlarged to cool the object. Facial flushes can be accompanied by sweating, fast heart rate or chills. The severity of the symptoms may vary from woman to woman, especially throughout the menopause, and several factors may trigger symptoms such as caffeine, alcohol, tight clothing, spicy foods and stress,

In addition to some lifestyle adjustments that avoid triggering and maintain, for example, coolness and include exercise on a daily basis, patients with facial flushing can be treated with drugs, such as birth control pills, blood pressure drugs, antidepressants, and other hormone therapy Can be treated. All of these treatments have the risk of side effects such as blood clotting, cancer, headache, nausea, anxiety, drowsiness, tremor, diarrhea, constipation, and reproductive side effects. Due to the negative side effects of current treatment, many women choose to be untreated and even have facial flushing symptoms for years.

As noted above, current treatments of PTSD and facial flushes are not effective and can not exaggerate the need to improve treatment access, participation by patients, adherence to treatment protocols, and tolerability of treatment .

Gist of invention

The methods and kits of the present invention include administering RCSGI to deliver a long acting anesthetic and a mixture of injectable clonidine to a patient in need of PTSD or facial flushing to treat post-traumatic stress disorder (PTSD ) And a method and kit for the treatment of facial flushing.

The kit of the present invention comprises at least the therapeutically active ingredient of the present invention including anesthetics and clonidine which act for a long time. Long-lasting anesthetics and clonidine can be present as two separate vials of solution that are not mixed in the kit or as precipitates that dissolve in situ before administration. Long-lasting anesthetics and clonidine can also be present in a mixed solution as a single vial or as a precipitate that dissolves in situ prior to administration. The kit may optionally include a package insert on a paper or package insert on a data storage device. The kit may optionally include at least one syringe. The kit may optionally include at least one blue towel.

1 is a perspective view showing the nerve and needle positions of various vertebrae and necks for right neck sympathetic ganglion injection (RCSGI).
Fig. 2 shows the connection from the stellate ganglion to the brain. The most relevant is the connection of the amygdala, which is part of the brain that is mainly active in PTSD from the stellate ganglion. The constellation is also connected to the temperature-regulating hypothalamus.

details

Stellate ganglion blockade (SGB) and right neck sympathetic ganglion injection (RCSGI) provide new treatment options for PTSD or facial flushing. SGB is a commonly used anesthetic technology that is traditionally administered for pain relief. Local anesthetic injections with these nerves block the impulses, which in turn can reduce pain, swelling, pigmentation, and sweating in the upper limb and can improve mobility. Astigmatic ganglion blockade is known as part of the treatment of reflex sympathetic dystrophy (RSD), sympathetic dystrophy, complex site pain syndrome (CRPS) and shingles (thigh herpes) associated with the head and face and / or upper extremities. Depending on the practice, SGB is an injection of the cervical sympathetic ganglia at C7 and T1 levels, SGB is administered to the left and / or right side of the neck, and the anesthetic volume used for SGB varies from 5cc to 25cc.

The Chicago Block (CB) was used for the pre-treatment of PTSD by use of the right cervical sympathetic ganglion injection (RCSGI), and the right cervical sympathetic ganglion block at the C-6 neck level used for PTSD treatment, Gt; of 7 < RTI ID = 0.0 > cc < / RTI > CB is different from SGB because CB is not just C7 but right on C6. Long-acting anesthetics are not used to control pain in CB procedures. This use is referred to as the "para anestheic" application of sympathetic blockade. In short, the abbreviation RCSGI will be used later in the specification.

Bupivacaine and lopivacaine were used in the Chicago blockade procedure. Most were positive and the first placebo controlled trial was performed by the Navy and demonstrated no difference between RCSGI and placebo. This study used ultrasound guidance rather than lobyvacin and x-ray induction. Stellate ganglion blockers seemed promising, but were considered to be merely placebo effects by studies conducted by the Navy. Preliminary data from the Navy led to a positive study.

The present invention details the efficacy of RCSGI for the treatment of PTSD based on synaptic neurological connections from the stellate ganglion (SG) to parts of the brain associated with PTSD, mainly amygdala and hypothalamus, as shown schematically in Figure 2 do. The stellate ganglion junctions in the intracerebral structures were demonstrated by the use of Schwannoma virus vaccination (Westerhaus and Loewy, 2001). These viruses enable the identification of one to three synaptic nerve pathways away from the injection site (where there are stellate ganglia).

Additional evidence of sympathetic ganglia and cerebral connections was reported in the rat model. In these experiments, certain cholinotoxins are injected from the hippocampus (HP), causing HP cholinergic neurons and resulting in the final growth of the peripheral sympathetic nerve fibers derived from the superior cervical ganglion to HP (Harrell LE). Thus, the present inventors have found that modulation of the SG can modify the amyloid activity and ultimately the PTSD symptoms by the reported pathways.

The second set of reports focus on nerve growth factor (NGF) as a physiological response to stress. This is due to chronic stress (Smith. 1996], and reported by Aleva et al. To acute stress (Alleva et al., 1996). NGF is the most well understood member of the neurogenic class and its function is to regulate a variety of signaling events, such as cell differentiation and neuron survival and apoptosis (Snider, 1994). Increased stress-regulated NGF is considered to activate the cascade of events that eventually lead to increased levels of norepinephrine (NE) and lead to an increase in the PTSD symptoms hypothesized by Lipov in 2009 (Lipov, The description is summarized below.

Increased NGF in the brain showed an increase in NGF concentration in the SG due to the retrograde movement of NGF from the intracerebral region to the SG (Johnson et al., 1987). Next, the increase in NGF in the stellate ganglion has been shown to cause germination at the sympathetic nerve end (new neuronal growth), which is NGF dependent (Chen et at, 2001), which in turn increases the level of norepinephrine . This cascade appeared in the rat model, where injection of NGF into the rat brain causes an increase in NE (Isaacson and Billieu, 1996). Evidence points out that NE is involved in PTSD, where the urine level of NE is known to increase in PTSD (Kostcn et al., 1987). Thus, trauma has been shown to trigger a neurobiological cascade that ultimately leads to PTSD.

We contemplate that this cascade is reversed by the application of topical anesthetic with the stellate ganglion to the ultimate reduction of NE. This view is supported by the fact that local anesthetics inhibit nerve growth factor-mediated neurite proliferation that reverses this process (see Takatori T). The present inventors' theory is further supported by a report by Dr. Masataka, in which serum NE was reduced after SGB in non-PTSD setting (Masataka Y, 2 patients with post-SGB PTSD NE is significantly decreased urinary (see Lipov). Thus, since local anesthetics are applied to SG, PTSD symptoms can be solved. Perhaps, as more NGF is reduced, more neurites will be removed to a greater extent after reversal of PTSD, and brain changes will occur. Finally, the effect of sympathetic blockade in PTSD becomes stronger if the SG more strongly blocks the sympathetic nerve for longer periods of time. A mixture of local anesthetics and clonidine is notable in the present invention and is known to cause more potent and prolonged sympathetic blockade.

The mixture is considered to have a more profound effect on the inhibition of nerve growth factor-mediated neurite outgrowth, the more powerful reduction or elimination of neurite outgrowth, and the decrease in NE levels in the brain in a more effective treatment of PTSD and facial flushing .

The following are the injections (injected material) used in SGB and RCSGI:

Local anesthetics;

Sympathetic ganglion block was performed using local anesthetics. Usually, long-acting anesthetics were used to perform extended sympathetic nerve resection (or sympathetic effect). Epinephrine may be used in conjunction with topical anesthetics to reduce local absorption of local anesthetics and to increase duration of effect. This approach has the theoretical problem of epinephrine acting on the sympathetic nerve effect because epinephrine is one of the sympathetic nervous system agents.

phenol:

Sympathetic ganglion block was performed using phenol, which is a more permanent way to block or block ganglion neurons, but it has been associated with significant common complications, such as persistent Horner's (tired eyes) It is associated with complications that may be permanent as well as nerve trauma.

Local anesthetics and steroids Combined water:

The regretful implementation of the combination of steroids and local anesthetics continues without medical reasons for this. This practice is associated with stroke and should not be sustained.

Local anesthetics mixed with clonidine:

The duration and magnitude of vasodilatory effects induced by sympathicotomy were studied by adding different concentrations of clonidine versus mefavacaine. The mean arterial blood pressure (MAP), heart rate (HR), and right brachial artery blood flow (BABF) were measured before and after stellate ganglion block (SGB) used as sympathetic block in dogs. The experimental protocol was designed as follows: 1) Group 1: left SGB (n = 6) using 1 ml of 0.5% mefenacaine, 2) Group 2: 0.5 ml of 0.5% Left SGB (n = 6), 3) Group 3: Left SGB (n = 6) using the addition of 5 μg of clonidine to 1 ml of 0.5% mepivacaine.

RESULTS: MAP did not show any significant changes during the study in groups 1 and 2. In group 3, MAP was lower than group 1. HR did not show any significant change in the three groups during the study. The left BABF was significantly increased after the left SGB in three groups. The duration of the increased BABF in group 2 is the longest, the shortest among them in group 3. Right-side BASF was significantly reduced in the three groups during the post-SGB post-SGB study, and the decrease in BABF in group 3 was the highest. Studies have concluded that sympathetic blockade with clonidine in local anesthetics increases both the duration and magnitude of its vasodilatory effect. However, sympathetic blockade with the addition of a higher dose of clonidine to local anesthetics may induce a shorter duration and a smaller size of vasodilatation effect compared to a local anesthetic alone.

Although clonidine has been shown to extend analgesia in central nervous system blockade, its use in peripheral nerve block is controversial. Current systematic phylogenetic evaluation was performed to determine the benefit of clonidine addition to peripheral nerve block.

A systematic qualitative assessment of a double-blind randomized trial of the benefits of clonidine as an adjunct to peripheral nerve block was performed. The study was published in PubMed (www.ncbi.nlm.nih.gov/entrez) and EMBASE (www.embase.com) database (July 1999 - 2006) for terms related to clonidine as an adjunct to peripheral nerve block October). The study has been classified as supporting the use of clonidine for reduced pain and total analgesic consumption, or for prolonged interruption periods, when compared to being negative, when found to be no difference. We identified 27 studies that met inclusion criteria. Five studies included systemic controls. The total number of patients evaluated was 1,385. The dose of clonidine varied from 30 to 300 μg. A total of 15 studies supported the use of clonidine as an adjunct to peripheral nerve blockade in 12 studies, and 12 studies failed to show benefit. On the basis of qualitative analysis, clonidine was shown to prolong analgesia when added as an intermediate-acting topical anesthetic for axillary and peritoneal blockage. Clonidine improves analgesia and duration of anesthesia for several peripheral nerve blockages when used as an adjunct to a mid-acting topical anesthetic. Side effects are limited to doses of 150 mug or less. There is insufficient evidence to use clonidine as an adjunct to topical anesthetics in the case of continuous catheterization. Further studies are required to examine the peripheral analgesic mechanism of clonidine.

In another study, 12 to 15 ml of a 0.5% volume bicin cervical sympathetic nerve block (bulimicin, clonidine) solution containing 50 mcg of clonidine for cervical sympathetic block was administered in a single shot. It is not clear from the literature that a clonidine mixture with a local anesthetic has a clinical effect.

The anesthetic of the present invention may be any short or long acting local anesthetic, or an amide or ester thereof. A short-acting anesthetic may have an anesthetic effect ranging from several minutes to several hours in anesthetized subject. Long acting anesthetics may have anesthetic effects ranging from several minutes to several months in anesthetized subjects. Local anesthetics include short acting esters such as chloropropacaine, procaine, novocaine, short acting amides such as lidocaine, prilocaine, and mepivacaine; Long-acting esters such as tetracaine and amethocaine; Long acting amides such as, for example, bupivicaine, levobupivacaine, lopivacaine, dibucaine and etidocin; Or atypical anesthetics such as benzocaine, cocaine, cyclomethicaine, dimethokine, laurocaine, piperocaine, propoxycaine, proparacaine, trimecaine, and combinations thereof. Clonidine is used as an alpha-2-adrenergic agonist, but other active agents may also be used in admixture with anesthetics. Other alpha-2-adrenergic agonists that may be used as a mixture of the present invention include guanaxan, guanabenz, guanoxabenz, guanethidine, xylazine, tizanidine, methyldopa, paradomidine, dexmedetomidine and It is a combination of them.

Generally, to produce an active pharmaceutical ingredient for administration, at least one long-lasting anesthetic is mixed with clonidine in 0.9% physiological saline without preservatives. Upon mixing of the active pharmaceutical ingredients, the solution is passed through a 22 micron filter and brought to the desired volume with 0.9 sterile saline without preservatives.

The present invention can be prepared using standard techniques in the art, from solubilization and mixing to delivery of active pharmaceutical ingredients. However, by way of example, formulations can be formulated in a Class 5 sterile environment or in a better environment using aseptic techniques. The desired amount of clonidine and a long-acting topical anesthetic (e.g., bupivacaine) powder is weighed and dissolved in a small amount of antiseptic-free sterile water. A sufficient amount of 0.9% preservative-free (PF) sterile saline will reach 90% of the desired volume. The resulting solution can be passed through a suitably sized 0.22 micron filter to accommodate the final volume, which is made into a sterile syringe used to redistribute the final volume into the final preparation vessel (s). An additional volume of 0.9% preservative-free physiological saline can be passed through the same filter to establish 100% of the desired volume. A new new filter can be used to redistribute the pharmaceutical mixture into the new syringe or final formulation vessel (s). The mixture can be transferred into a sterile vial or syringe, sealed, and suitably labeled.

The kit of the present invention may comprise a single vial, which dissolves, mixes, filters and makes one vial volume of the active pharmaceutical ingredient. In another embodiment, the active pharmaceutical ingredient may be provided as a separate vial in solution or lyophilized form, as a precipitate, to provide reconstitution or dissolution, filtration and administration to the site or even to a volume at other locations.

The vial of the kit, the housing of the active pharmaceutical ingredient can be glass, clear glass, amber or any other vial used in the art. The active pharmaceutical ingredient may be housed in a sterile syringe prepared for a surgical forum or in any other housing known in the art.

The kit may optionally include an empty syringe or a filled syringe known in the art for use in a surgical forum. By way of example, the syringe can be a 22 g quince needle 3½ inches, a 1.0 cc syringe labeled DYE, a 10 cc syringe labeled mixture, a 10 cc syringe labeled topical 2 18 gauge 1 inch needle, a 1 25 gauge 1½ inch needle, have.

The kit may also include package inserts in any form, such as paper, or in a data storage device, which may include instructions for pharmaceutical ingredients, dosage formulations, dosage variations, storage instructions, administration instructions, Side effects, contraindications for administration, stability data related to the use of the invention for patient protection, or any other information, or medical staff information. The kit may also include a blue towel or other device to maintain sterility. The kit may further include manuals before and after the injection to screen for PTSD and facial flushing diagnoses. In PTSD, psychological devices, such as PCL M and non-military, as well as similar devices can be used. A psychological device for facial flushing, for example, a Sloan scale or equivalent, as well as a screening device for sleep disorders can be used.

Storage instructions provided for the present invention and for selective inclusion in the kit of the invention are as follows: 15 to 30 캜 Storage at room temperature for up to 24 hours; 2 to 8 ° C refrigerated for 3 days or less; Or freezing for less than 45 days (-20 to -40 < 0 > C). Long acting anesthetics typically have a long shelf life, often less than two years, and clonidine should be stored at room temperature away from direct sunlight and moisture. The clonidine and bulkbicain mixtures are typically stable for at least 90 days at room temperature.

In an embodiment of the present invention, the long-lasting anesthetic of the present invention is a volatile, white crystalline powder, which is well soluble in 95% ethanol, water-soluble and slightly soluble in chloroform or acetone.

With respect to dosing, the dosage administered will depend on the needs of each individual patient. However, long-acting local anesthetics may range from 0.005 μg / cc to 40 μg / cc. In one embodiment, the anesthetic concentration may vary from 0.01% to 2% per cc. The dose of clonidine may range from 0.5 μg / cc to 1000 μg / cc. In one embodiment, the clonidine is 0.5 [mu] g / cc. The volume of dose administered to the patient may range from 2 to 50 cc. The dosage administered may be approximately 7 cc. If the patient's body weight is between 70 and 100 lb, the dose may be approximately 6 cc. If the patient's weight is between 50 and 70 lbs, the dose may be approximately 5 cc. The number of doses may vary, but the minimum dose to find effective results to eliminate or minimize PTSD symptoms or flushing is a single dose. Additional doses may be administered at intervals between doses of 1 to 50 days.

By way of example and without limitation, the formulation of the invention is administered at the C-6 cervical level as an injectable, right neck sympathetic ganglion block. Administration may also be left cervical sympathetic ganglion block at the C-6 neck level, as illustrated schematically in Fig. Administration of the present invention may be administered and administered at a higher level than C-6, for example, at C-3, on the right or left side. Administration of the present invention may also be lower than C-6, for example, right or left at C-7. Administration of the present invention may be in a multi-necked target in the same administration case. The active pharmaceutical ingredient may be administered via other routes of administration known in the art such as intracerebral, epidural, topical, intestinal, parenteral, intramuscular, intradermal, intravenous, subcutaneous, intrathecal, and the like.

In this study, patients with PTSD are given a dose of bovine cicin and clonidine as RCSGI. The first three injections did not have clonidine. The fourth included clonidine. Clonidine interception begins to execute within a 5 minute procedure and has a very strong effect.

A 43-year-old female patient was treated with CB with either clonidine or clonidine present and reported significantly more effective results using clonidine than local anesthetics alone.

In pediatric applications, an 11-year-old woman was first given an intended injection to alleviate PTSD-related symptoms. The procedure included local anesthetics mixed with clonidine delivered by shot to the patient's neck with a similar procedure given epidurally to the woman in labor. Anesthetic mixture blocks substances referred to as nerve growth factor, which is considered an increase in PTSD patients. Such conditions then cause excessive release of hormones that trigger a "fight or flight" reaction in the brain. Thus, blocking nerve growth factors can calm PTSD patients, which allows the patient to pass the basic survival response, and to better deal with life. The effect on the patient was immediate. These patients were afraid of being chartered before, but after such treatment, they went to the car and slept like a house. Previously, the patient reported that he thought he was not in a safe place, but after treatment he reported no further worries. The purpose of the treatment is to allow the patient to sleep well and decrease the mental illness medication, and the medicament allows her to receive psychotherapy and psychotherapy to be more effective. All these objectives were carried out after administration of the therapeutic agents of the present invention.

Another patient who was a shoot survivor responded to treatment described in the present invention. The shooting was a point blank range, and she showed fear with PTSD and remembers as if she was being traced and shot again. She received a ganglionic block procedure known as Chicago blockade, injected with a dose of local anesthetics in 1 minute, which is a mixture of bulk bicin and clonidine. The patient reported that she could talk about the horrific event when she was shot.

Also in another patient, a 54-year-old postmenopausal woman immediately and significantly improved her facial flushes after SOB treatment. A mixture of bupivacaine and clonidine was also used in these patients.

The treatment of the present invention involves the nerve growth factor, or NGF, level spike, when a person experiences significant anxiety. These growth factors cause the nerve cells on the right side of the stellate ganglion-tree to stimulate an increase in the production of norepinephrine-stress hormone in the body, resulting in "struggle or escape" in the body. Anesthetics in the Chicago block seem to stop the overproduction of NGF in the body. When nerve growth slows and the body stops stress hormones and production, it changes the human body's response.

While preferred embodiments of the disclosure are illustrated and described in connection with specific features and formulations, the invention may be adapted for use with a wide variety of anesthetics and pharmaceutical actives. Other aspects and equivalents are envisioned within the scope of the claims. Various features of the disclosure have been particularly shown and described in connection with the illustrated embodiments. It should be understood, however, that the specific embodiments are illustrative of the invention only, and that the invention is to be interpreted as completely as possible within the scope of the claims.

Claims (25)

Administering an injection of a topical anesthetic and an alpha-2-adrenergic agonist. 3. The composition of claim 1, wherein the topical anesthetic is selected from the group consisting of chloroprocaine, procaine, novocaine, tetracaine, amethocaine, lidocaine, prilocaine, mephavacaine, bupivicaine, levobupivacaine, Wherein the method is selected from the group consisting of cine, ethidocin, benzocaine, cocaine, cyclomethicaine, dimethocaine / laurocaine, piperocaine, propoxycaine, proparacaine, trimecaine and combinations thereof. The method of claim 1, wherein said alpha-2-adrenergic agonist is selected from the group consisting of guanabenz, guanoxbenz, guanethidine, xylazine, tizanidine, methyldopa, clonidine, paradomidine, dexmedetomidine ≪ / RTI > and combinations thereof. 2. The method of claim 1, wherein the local anesthetic is mixed with the alpha-2-adrenergic agonist in solution. 8. The method of claim 1, wherein the topical anesthetic is a vapiconic. 2. The method of claim 1, wherein the alpha-2-adrenergic agonist is clonidine. 2. The method of claim 1, wherein said injection is administered as a right neck sympathetic ganglion injection. 2. The method of claim 1, wherein said injection is administered as a left cervical sympathetic ganglion injection. 2. The method of claim 1, wherein the injection is administered to the cervical vertebra. 2. The method according to claim 1, wherein the injection is administered to the cervical vertebra. 2. The method of claim 1, wherein said injection is administered to a cervical vertebra. 2. The method of claim 1, wherein the local anesthetic is administered in the range of 0.005 / / cc to 40 / / cc. 3. The method of claim 1, wherein said alpha-2-adrenergic agent is administered in the range of 0.5 to 1000 micrograms / cc. 3. The method of claim 1, wherein said injection is administered to treat a patient having post-traumatic stress disorder. 3. The method of claim 1, wherein said injection is administered to treat a patient having facial flushing. 3. The method of claim 1, wherein administration of said injection is intracerebral, epidural, topical, intestinal, parenteral, intramuscular, intradermal, intravenous, subcutaneous or intrathecal. A kit comprising the local anesthetic and the alpha-2-adrenergic agonist of claim 1, comprising at least one vial. 18. The kit of claim 17, further comprising at least one syringe. 18. The kit of claim 17, further comprising at least one needle. 18. The kit of claim 17, further comprising a package insert. 18. The kit of claim 17, further comprising a manual before and after the injection screening for PTSD and facial flushing diagnoses. A method of treating a patient suffering from post-traumatic stress disorder or facial flushing, comprising administering a cervical sympathetic ganglion injection comprising a long-lasting local anesthetic and a combination of clonidine. 24. The method of claim 22, wherein the long-lasting topical anesthetic is a volatile. 23. The method of claim 22, wherein the combination is produced in a preservative-free sterile saline solution. Wherein the combination is administered to the patient via injection with the cervical sympathetic ganglia.

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