Copied from http://dcmsonline.org/, but now removed from that site.
Jacksonville Medicine, October, 1998
Duval County Medical Society, Jacksonville, FL 32204
Nerve blockade has widespread and diverse application in the field of pain management. The purpose of this article is to sensitize the practitioner to some of the indications for frequently employed blocks by pain medicine specialists. It is not intended to be inclusive of all possible blocks performed on the somatic and sympathetic nervous system. This form of therapy may be diagnostic or therapeutic, but it remains only a small part of a quality pain management practice.
All somatic nerves exit the spinal column as roots. Some of these nerves continue as individual nerves but many form plexi. There are four main plexi formed by spinal nerves. The upper cervical nerves combine to form the cervical plexus. The lower cervical and upper thoracic nerves unite to form the brachial plexus and innervate the upper limb. The lumbar and upper sacral plexus innervates the genitalia. The mid and lower thoracic nerves form individual intercostal nerves and innervate the chest and abdominal wall.
Individual nerves which are amenable to blockade (cranial to caudal listing) include occipital nerves (C2-4), suprascapular nerves (C5-6), brachial plexus (C4-T2), intercostal nerves (T1-12), lumbosacral plexus (T12-S3), and the sacral plexus (S4-5). These plexi or individual nerves formed by combinations of these segments can be blocked. Somatic nerves are selectively1 blocked for diagnostic and therapeutic purposes with short acting local anesthetic. This may allow surgeons to confine surgery to the affected levels causing pain. These nerves may on rare occasion also be blocked with neurolytic agents, cryotherapy, or radiofrequency lesioning.
Data estimate that facet joint pain is the primary problem in 20% of nonspecific low back pain.2 This is typically described as low back pain radiating into one or both gluteal regions, groin, hip, posterior or lateral thigh. It occasionally radiates below the knee but not into the foot. The pain is usually described as a deep dull ache. The pain is reproduced by anything that increases contact between the involved facet joints. This is typically associated with twisting, extension, or rotational movements. Typically there is no increased pain with maneuvers which increase intraspinal pressure. The pain may be more prominent in the morning or with inactivity, and it is usually improved with walking. Tenderness over the facet joints occurs (but this may be difficult to evaluate in heavier patients) and there is frequently associated muscle spasm. There are usually no associated objective neurologic findings, and usually no restrictions with flexion but muscle spasm may restrict some motion. Straight leg raising is negative for nerve root irritation or tension. The diagnosis is made when pain relief occurs with either direct facet injection or blocking the medial branch of the dorsal ramus of the spinal nerve supplying the involved facet. This only provides short term relief. Medial branch rhizotomy may provide long term treatment in 55% of patients responding to a diagnostic block.2,3
The cervical facet joints have been implicated in headache pain as well as upper, lower, and paracervical neck pain syndromes. The patients have pain to palpation directly over the facets as well as characteristic referral patterns.4 Patients frequently have a positive Spurling's sign on the affected side. This is an increase in the patient's pain with extension and lateral tilt of the head with pressure applied to the top of the head. Most diagnostic tests are nonspecific as facet joint changes are ubiquitous in adults. CT scanning may be helpful in diagnosing abnormalities such as narrowing, subchondral irregularities, and erosions. These abnormalities may correlate with clinical symptoms.5 The diagnosis is confirmed by pain relief with facet injection or medial branch blockade. Medial branch rhizotomy may provide long term treatment.
The administration of lumbar epidural blockade is useful in the treatment of a variety of chronic benign pain syndromes including low back pain with radiculopathy, some nonspecific low back pains, herpes zoster, post herpetic neuralgia, spinal stenosis, vertebral compression fractures, pelvic pain syndromes, abdominal pain syndromes, post laminectomy syndrome, diabetic polyneuropathy, chemotherapy related peripheral neuropathy, orchalgia, proctalgia, cancer related pain, and reflex sympathetic dystrophy. Blockade includes injecting a variety of medicines including local anesthetics, narcotics, steroids, neurolytic agents, alpha-2 agonists, NMDA antagonists, and many other medicines in the research literature.6
This technique is designed to deliver the medicine to the nerve roots, spinal cord, and perhaps the segmental nerves. Different sites, volumes, and medications make this form of therapy highly versatile. The components of the epidural space are composed of nerves and vessels, but the majority of the space is fat. This is especially true in the caudal canal. The fat solubility of medications may have important implications in this technique.
There is much controversy over the benefit of epidural steroid injections in the literature but there are over 50 studies showing beneficial results. The main indication for epidural steroid injections is the presence of pain related to nerve root pathology. Clinically, this is manifested as radicular pain. Patient selection for this technique is important. Pain related to acute disc protrusions do well.7 Chonicity and prior back surgery lower the success rates.8.9 Clinically, most patients do well with these injections, but for only short periods of time. Data exist showing that patients responding to early epidural steroid injection have a higher incidence of employment at six months (66% vs. 29%) and a marked reduction in pain medication use (52% vs. 36%).9 This data suggests early treatment successes may continue to do well and lead to functional improvement.
Any somatic nerve can become entrapped leading to chronic pain. This can contribute to headache pain, abdominal pain, or pelvic pain.
Occipital neuralgia originates as the sensory branches of C2 and C3. Symptoms are pain in the occipital region which may extend to the top of the head. The diagnosis is made by complete pain relief with local anesthetic blockade of the occipital nerve. Injections of steroids or cryoneurolysis may provide prolonged analgesia.
Abdominal cutaneous nerve entrapment syndrome can be caused by anything which stretches, torses, compresses, or lyses nerves. This may be secondary to trauma, infection, pregnancy, surgery, or possible unknown factors. It has been described in the surgical literature since 1972.10 The ilioinguinal nerve has been linked to pelvic pain and successfully treated with local anesthetic somatic blockade in women.11 The iliohypogastric nerve has been implicated as causing pain by compression and stretching during the classic Pfannensteil incision, use of retractors, and laparoscopy. Pudendal neuropathy has been associated with difficult delivery (large fetus or prolonged second stage), chronic constipation, endometriosis, and the trauma of surgery. Neuralgia of the genital branch of the genitofemoral nerve is frequently described as pain starting in the low back or abdomen which migrates into the groin. The pain is frequently accentuated with movement involving the lower abdominal and upper quadriceps muscle groups. The pain is often incapacitating and occurs in sharp repeated attacks.
Neuralgia of the infrapatellar branch of the saphenous nerve occurs weeks to years after blunt injury to the tibial plateau or following total knee replacement. It is manifested as dull pain below the knee joint and achiness below the knee. Physical exam reveals pain with digital pressure between the lateral malleolus and extensor retinaculum.
Superficial and deep peroneal neuralgia may occur in diabetics who are vulnerable to compression injury. It is less commonly associated with a blunt injury to the dorsum of the foot. A dull pain in the great toe made worse with prolonged standing is described. Physical examination demonstrates pain with digital pressure between the first and second metatarsal heads.
Superior gluteal neuralgia results from a lifting injury involving the lower back and hip. There is a shearing of the nerve between the gluteal musculature with forced external rotation of the leg and extension of the hip under mechanical load. Rarely, this occurs with forced extension of the hip from head on automobile collision as the knee extends in anticipation of impact. The clinical presentation demonstrates a sharp pain in the low back, dull pain the buttock, and a vague pain in the popliteal fossa. The pain is aggravated with prolonged sitting, leaning forward, or twisting to contralateral side. A giving way of the leg is sometimes described. The patients tend to position themselves so as to minimize their weight on their contralateral buttock.
Supraorbital neuralgia typically results from a deceleration injury as may occur with the head striking an automobile windshield. It presents as a throbbing frontal headache. Associated symptoms are blurred vision, nausea, and photophobia. The pain typically worsens with time. It is confused with frontal sinusitis.
Infraorbital neuralgia may be caused by trauma of the zygoma. This pain is exacerbated by smiling and laughter. The pain is referred to the teeth. It is confused with maxillary sinusitis.
Mandibular neuralgia may be caused by hypertrophy of the pterygoids or loss of oral cavity vertical dimension.
Auriculotemporal neuralgia causes temporal pain and retroorbital pain. This frequently is manifested as referred pain to the teeth. Patients awaken at night with temporal headache. The pain is described as throbbing, aching, or pounding. The pain can be bilateral. It is associated with bruxism and temp-oramandibular disorders. One must be careful to exclude temporal arteritis as a disease which can mimic this neuralgia.
Posterior auricular neuralgia is typically caused by blunt injury to the mastoid. A scenario may occur in abused women having left ear pain resulting from a blow from a right handed male. It is described as a pain in the ear with a feeling of fullness and tenderness. It is frequently misdiagnosed as a chronic ear infection.
The ANS is divided into a sympathetic and parasympathetic component which function physiologically as opposites. The sympathetic nervous system has been implicated in maintaining a number of pain states.12 The central components of the sympathetic nervous system are the hypothalamus, midbrain, pons, medulla, and lateral columns of the spinal cord extending from T1 to L2. Peripherally, the sympathetic nervous system consists of preganglionic and postganglionic efferents innervating deep somatic structures, the viscera and skin. Preganglionic nerves leave the spinal nerve as white rami communicantes to rejoin the spinal nerve and eventually innervate their respective viscera. Usually there are three paired cervical ganglia, twelve paired thoracic ganglia, four paired lumbar ganglia, four paired sacral ganglia, and a single ganglion impar.13
A stimulated sympathetic nervous system or direct nerve injury can lead to a burning painful condition. The classic terminologies for these conditions were Reflex Sympathetic Dystrophy and Causalgia. These conditions are now known as Complex Regional Pain Syndromes Type I and Type II. CRPS Type I is "a syndrome that usually develops after an initiating noxious event, is not limited to the distribution of a single peripheral nerve, and is apparently disproportionate to the inciting event. It is associated at some point with evidence of edema, changes in skin blood flow, abnormal sudomotor activity in the region of the pain, or allodynia or hyperalgesia."14
The presentation typically involves trauma to an extremity which may be minor such as an innocuous ankle sprain. It may also involve visceral events like a stroke or myocardial infarction. The pain is typically burning in quality and follows a nondermatomal distribution. It frequently results in immobility, discoloration, swelling, temperature changes, mottling of skin, rubor, cyanosis, hyperhidrosis, hair, nail, and skin changes in the involved extremity. Extension proximal to the inciting lesion frequently occurs. Motor manifestations may include tremor, weakness, and dystonia. Dissociation of the extremity from the rest of the body is a common description of the involved extremity late in the disease. For example, a patient may refer to his affected hand as "the hand."15
CRPS Type II is a syndrome defined as "burning pain, allodynia, and hyperpathia usually in the hand or foot after partial injury of a nerve or one of its major branches."14 CRPS Type II differs in that there is a direct neural injury. There is extension of the disease beyond the distribution of the injury manifested as burning discomfort, hypersensitivity, and allodynia. Edema, discoloration, and motor dysfunction may also be present.
Early treatment includes sympathetic and somatic nerve blocks in combination with physical therapy involving desensitization, active range of motion, and work hardening.
Cell bodies for the head and neck originate from nerves in the first and second thoracic spinal cord segments and those to the upper extremity originate from segments T2 to T8 or T9. Then these synapse at the inferior (stellate), middle, or superior cervical ganglion. All preganglionic nerves however pass through or synapse in the stellate ganglion allowing successful interruption of the head, neck, and most of the upper extremity with blockade here. Inconstant contributions are from T2 and T3 which may miss the stellate ganglion innervating distal structures in the upper extremity.16
Blockade has been found useful in circulatory problems in the upper extremity such as Raynaud's disease, arterial embolism, accidental intraarterial injection of drugs, and Meniere's syndrome associated with vascular disease. It is also beneficial in the treatment of acute herpes zoster and palliation of postherpetic neuralgia of the face, lower cervical, and upper thoracic dermatomal distributions. It is classically performed for CRPS Types I and II. It has been indicated as immediate therapy for pulmonary embolus.17
Preganglionic fibers arise from the greater (T5-10), lesser (T10-11), and least (T11-12) splanchnic nerves. This celiac plexus lies at the level of L1 anterior or anterolateral to the aorta and below the level of the celiac artery. Post ganglionic fibers innervate the distal esophagus, stomach, duodenum, small intestine, ascending and proximal transverse colon, adrenal glands, pancreas, spleen, liver, and biliary system.
Celiac plexus block is used to differentiate visceral sympathetic pain in the flank, retroperitoneum, or upper abdomen pain from somatic pain.18 This procedure has been shown to produce palliation of pain and reduction of morbidity and mortality associated with acute pancreatitis.19,20 It has been shown to reduce the acute pain of arterial embolization of the liver for cancer therapy and to reduce abdominal "angina" associated with visceral arterial insufficiency.21 Malignancies of the retroperitoneum and abdomen, and chronic pancreatitis in selected patients may respond to neurolytic blockade.12,22
The cell bodies responsible for vasoconstriction in the lower limbs are in the lower three thoracic and first three lumbar segments. These synapse in ganglia located at the anterolateral portion of the spinal column at the level of the L2-3 and L4-5 discs. Therefore classic technique describes blockade at the L2, L3, and L4 levels.
Sympathetic blockade may be therapeutic, and function as an analgesic in circulatory insufficiency, renal colic, CRPS (Types I and II), urogenital pain, amputation stump pain, phantom pain, frostbite, phlegmasia alba dolens, erythromelalgia, and trench foot, and may be therapeutic in acrocyanosis and hyperhidrosis. It may also be diagnostic in differentiating between pain which is sympathetically maintained or sympathetically independent.
Composed of the lumbar sympathetic chains, branches of the aortic plexus and parasympathetic fibers of the S2-S4 roots, the superior hypogastric plexus innervates the ureteric, testicular or ovarian plexuses, the sigmoid colon and a plexus that surrounds the common and internal iliac arteries. It is blocked just anterior to the L5 vertebral body. The inferior hypogastric plexus is blocked by proximal blockade of the superior hypogastric plexus.
SHPB is used to treat intractable visceral pelvic pain of both neoplastic and nonneoplastic origin. Visceral pelvic pain is usually described as vague, poorly localized, dull, crampy, pulling, squeezing, or colicky. A diagnostic block may help distinguish between visceral and somatic pain.
The paired paravertebral sympathetic chains terminate at the single Ganglion of Walther. This ganglia is blocked just anterior to the sarococcygeal junction.
Intractable neoplastic visceral perineal pain of sympathetic origin are responsive to this procedure. This tends to be a vague, poorly localized pain with sensations of burning or urgency. This blockade may also help distinguish between visceral and somatic pain.
Basic research provides many exciting developments in the field of pain medicine. The development of long-acting local anesthetics, diffusion modifiers (liposomes, microspheres, particulates, cyclodextrin), nonlocal anesthetic blocking agents, NK-1 antagonists, tumor necrosis factor antagonists), and advancement of the techniques for neurolysis make long term blockade of individual nerves or the plasticity of an abnormal nervous system possible in the future. Abolition of pain, reduction in medications, and improved lifestyle are real possibilities. Proof of these methods requires further study.