Chronic low back pain is a common condition with diverse etiologies. It is a major cause of functional impairment and disability. In recent years, our understanding of the pathophysiology of low back pain has improved significantly especially in regard to the contribution of dorsal root ganglia and pain mediators.
Botox injections can be beneficial in management of chronic back pain, especially of myofascial origin. Botox is not only an excellent muscle relaxant but can also work against neuropathic pain. Botox injections are generally safe and can provide sustained pain relief in some patients. However it is important to note that in some cases injection treatment may not provide the desired results or the pain relief may not be sustained. At Pain Spa Dr Krishna is very experienced in performing botox injections. Dr Krishna always performs botox injections under ultrasound guidance for greater accuracy and improved safety.
The treatment of chronic low back pain is challenging. The vast majority of cases of LBP are self-limiting and resolve within a few weeks. However, up to 5% to 10% of individuals can have persistent symptoms associated with psychological illness and disability (Manchikanti 2009). Several treatment options are available, yet despite this, many individuals are unable to attain adequate relief and seek different therapeutic modalities.
One such option is intramuscular botulinum neurotoxin (BoNT) injections. Freeze-dried BoNT is reconstituted with saline solution and injected multiple times intramuscularly into the posterior lumbar region. The erector spinae muscle is the most superficially accessible muscle in this area and is located roughly 2 cm from midline of the lumbar spine on either side. Multiple injections on the affected side into the muscle at L1, L2, L3, L4, L5, or a combination of sites, are administered to encompass all or part of the entire mass of muscle. If pain involves the sacral region, injections can also be administered into the paraspinal sacral muscles.
The lumbosacral area contains a number of muscles arranged at different levels. These muscles stabilize the spine and allow movement of the low back in different directions (flexion, extension, rotation).
Erector spinae (ES) are the most superficial of the low back muscles. At lumbar region, the Erector spinae consists of a single muscle mass with three distinct groups: medially located spinalis, laterally located iliocostalis, and longissimus between the two. Rostrally, the three muscles separate from each other approximately at L1–T12 vertebral level. The fi bers of iliocostalis attach to T7–T12 ribs. The fibers of lumbar spinalis and longissimus attach rostrally to the transverse and spinal processes of lumbar and thoracic vertebrae.
Quadratus lumborum (QL) and multifi dus muscles are located deeper than Erector spinae muscles. Quadratus lumborum is often implicated in low back pain. Quadratus lumborum is rostrally attached to the lower level of the 12th rib and the transverse processes of the first four lumbar vertebrae. Its fibers end distally via aponeurosis to the lumboinguinal ligaments and attach to the medial part of iliac crest. Unilateral contraction of Quadratus lumborum produces ipsilateral flexion of lumbar spine, whereas bilateral contraction helps with extension of the spinal column. Quadratus lumborum is innervated by the ventral rami of the 12th thoracic and upper three or four lumbar spinal nerves.
Multifidus muscle fills up the groove in either side of the spinal processes of the vertebrae from the sacrum to the coccyx. In the lumbar region, its fibers attach to mamillary processes of all lumbar vertebrae. Multifidus muscles, like facet joints, are innervated by the medial branch of the dorsal ramus of the spinal nerves.
Muscle strain and disturbance play a major role in the pathophysiology of mechanical low back pain. Major low back muscles such as Erector spinae and Quadratus lumborum are richly innervated. Irritation of nerve endings may lead to accumulation of pain mediators (glutamate, calcitonin gene-related peptide, and substance P) at the periphery causing peripheral sensitization. In patients with anatomically tight compartment for ES muscles, the compressed muscle can cause pain and discomfort especially during exercise, the lumbar compartment syndrome.
Recently, the role of dorsal root ganglia (DRG) in chronic disc disease leading to low back pain has attracted much attention. It has been shown that DRG is very sensitive to pressure, and even light compression can cause long periods of repetitive firing (5–25 min) in DRG neurons. The ruptured disc material, due to proximity to DRG, can influence DRG neurons and upregulate expression of pain mediators and inflammatory agents to produce or enhance pain.
The role of sympathetic nervous system in maintaining pain and its chronicity has long been suspected based on anatomical studies showing massive sprouting of sympathetic fibers into DRG after peripheral injury. Normally no sympathetic fibers are inside DRG, and noradrenergic innervation is present only in the adjacent blood vessels. Following peripheral injury, inflammation develops in DRG and sympathetic ganglia with influx of macrophages and T cell lymphocytes into DRG. This leads to the release of cytokines and increases discharge of DRG neurons. Sympathectomy or removal of sympathetic ganglia decreases the influx of macrophages and T cells into DRG and, consequently, decreases the magnitude of inflammation. In chronic low back pain caused by root or DRG injury, sympathetic nervous system hyperexcitability may play a role in the maintenance of pain (sympathetically maintained pain).
In chronic pain states, peripheral sensitization (PS) due to accumulation of pain mediators and inflammatory agents leads to central sensitization (CS) that is believed to contribute to pain chronicity. This central sensitization occurs at multiple levels of CNS starting with the spinal cord neurons and followed by the brain stem, thalamic, and cortical levels. There is evidence from molecular biology, electrophysiological investigations, and neuroimaging studies that pathological conditions associated with chronic low back pain are capable of inducing central sensitization. In conditions such as herniated disc or trauma, DRG and spinal nerve injuries lead to the generation of ectopic discharges in DRG neurons causing hyperexcitability of spinal cord sensory neurons. Functional MRI of patients with chronic low back pain compared to asymptomatic age matched volunteers has shown augmented activation in premotor, supplementary motor, insula, and anterior cingulate cortex in patients with chronic low back pain.
Two studies published from the Walter Reed Army Medical Center (WRAMC) first addressed the issue of BoNT efficacy, tolerability, safety, and quality of life in chronic LBP. The first study was double blind and placebo controlled (Foster et al. 2001). The second one was open label and prospectively assessed multiple treatment results (every 4 months) over a period of 14 months (Jabbari et al. 2006). Both studies used a similar protocol in respect to technique, dosing, and rating scales. The technique was based on the hypothesis that treatment results may not be optimal unless the whole length of erector spinae (ES) muscles in the lumbar region is exposed to and influenced by BoNT therapy. Hence, regardless of the location of pain or tender/trigger points (if present), injections were performed at five lumbar paraspinal levels (into lumbar ES) with a total dose of 200 units for unilateral LBP (blinded study) and 400–500 units for bilateral LBP (open study). Both studies used onabotulinumtoxinA (onaA). The third study performed by a different group reported on efficacy of aboA in a group of patients with chronic low back pain due to myofascial pain syndrome.
Study 1 concluded that paraspinal administration of onabotulinumtoxinA at five lumbar levels into ES is safe and can relieve pain and improve the quality of life in patients with predominantly unilateral chronic low back pain.
There is very low quality evidence that Botulinum toxin injections are better than corticosteroid injections for reducing pain intensity in chronic LBP in the short term. There is no evidence on inter- mediate or long-term improvement in pain intensity. There is no evidence on the effects of Botulinum toxin injections compared to corticosteroid injections for functional improvement in patients with LBP.
There is very low quality evidence that Botulinum toxin A injections are better than acupuncture for reducing pain intensity in chronic LBP in the intermediate-term. There is no evidence on the short or long-term improvement in pain intensity with the use of Botulinum toxin A injections compared to acupuncture for LBP. There is also very low quality evidence that Botulinum toxin A injections improved function better than acupuncture in the intermediate-term.
The exact mode of action of botulinum toxin A in chronic low back pain still remains to be determined. Based on animal and human research data, several plausible mechanisms exist:
In muscles, both A and B toxins produce relaxation via inhibiting the release of acetylcholine in the neuromuscular junction. This could explain some of the pain relief especially when low back pain is associated with muscle spasms. Furthermore, decreased muscle tone is often associated with a reduction in muscle bulk as well documented when BoNTs are used in hyperactive movement disorders. This decrease in muscle bulk (especially in the ES muscle) may be helpful when back pain is attributed to anatomically tight compartment (lumbar compartment syndrome).
Many causative factors, especially protruded disc, produce marked accumulation of pain mediators (CGRP, substance P) and inflammatory agents (cytokines) in DRG causing its hyperexcitability and leading to peripheral sensitization (PS). In animal studies, peripherally injected rimabotulinumtoxinB blocks release of substance P from DRG and dorsal horn neurons and reduces dorsal horn neuronal activation (c-Fos) evoked by formalin injection.
It has been shown that both development of inflammation in DRG and increased pain mediators within it are enhanced by extensive sprouting of sympathetic fibers into DRG after peripheral nerve injury. Peripheral injection of onabotulinumtoxinA impairs sympathetic transmission and, hence, has the potential to reduce pain mediators and inflammatory agents.
Botulinum toxin can all reduce central sensitization (CS) via their primary suppressing effect on peripheral sensitization (PS). Moreover, intramuscular administration of onaA may reduce central sensitization via its suppressing effect on muscle spindle discharge. Muscle spindles are one of the major sources of non-nociceptive input to the central nervous system reporting muscle length to CNS. In chronic pain disorders with established CS, wide range function spinal cord neurons perceive non- nociceptive stimuli as nociceptive. Reducing the input from muscle spindles can reduce central sensitization.
Botulinum toxin can all reduce central sensitization (CS) via their primary suppressing effect on peripheral sensitization (PS). Moreover, intramuscular administration of Botulinum toxin A may reduce central sensitization via its suppressing effect on muscle spindle discharge. Muscle spindles are one of the major sources of non-nociceptive input to the central nervous system reporting muscle length to CNS. In chronic pain disorders with established CS, wide range function spinal cord neurons perceive non- nociceptive stimuli as nociceptive. Reducing the input from muscle spindles can reduce central sensitization.
Although the investigators were worried about possible weakening effects of onaA in applied doses, none of the studied subjects in either of the two studies (blinded and open) complained of muscle weakness or impaired ambulation. However, the studied population in the WRAMC protocol included many (almost half) younger, muscular, and otherwise healthy military subjects with mechanical chronic low back pain. Therefore, the safety data in this study may not necessarily apply to older, thin, and fragile subjects with chronic low back pain; when treating such older, fragile patients, initial approach should be more conservative. The positive effect of WRAMC protocol was rated as C level of evidence (possibly effective) by AAN assessment subcommittee.
At Pain Spa we offer botox injections for management of various chronic pain conditions including low back pain. Dr Krishna performs botox injections under real time ultrasound guidance to ensure accurate placement and minimize any side effects.