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Some interesting notes I took from Sciatica and Chronic Pain by Robert Baloh I thought I'd share with you guys.

Here's the book if anyone wants it..
I read this the other day and learned a lot more about pain than I ever have off my doctors and other medical professionals. Here's some interesting notes I found throughout the book.
  • When the sciatic nerve is compressed in the pelvis the band of pain down the leg is much broader and often there is no associated back pain.
  • Vigorous early morning exercises, particularly weight lifting, could lead to a disc rupture as the vertical load on the disc exceeds the strength of the outer ligament.
  • Foramen stenosis refers to a narrowing of the bony canal where the spinal nerves exit the spine (Fig. 3.3c) and spinal stenosis refers to narrowing of the entire spinal canal. Both conditions tend to be aggravated by bending backward and relieved by bending forward and lying down.
  • As wallets have become stuffed with credit cards there are reports of sciatica being relieved by removing a bulging wallet from the back pocket, so-called credit-carditis. Presumably other objects such as tools or golf balls in the back pocket or prolonged sitting on a hard surface can also cause or aggravate sciatica due to entrapment of the sciatic nerve.
  • [Piriformis:] The typical symptom complex includes: pain in the mid-buttock, worsening of pain with outward rotation of the hip, tenderness at the back of the hip (in the so-called sciatic notch area), and worsening of pain with prolonged sitting.
  • After reviewing all of the medical studies available committees on guidelines around the world concluded that intensive diagnostic and management approaches in people with new onset sciatica such as CT, MRI, injections, and surgery may actually prolong disability compared to benign management approaches.
  • Regular use of pain medication may increase pain sensitivity
  • Sudden manipulations in chiropractic care can aggravate nerve damage
  • A course of oral corticosteroids is commonly used to treat new onset sciatica but studies have not found this treatment very helpful and prolonged use can lead to major systemic side effects including GI bleed and psychosis
  • If one can feel the spasm, placing a tennis ball on the floor and rolling back and forth on the ball over the muscle (like using a rolling pin) may relieve the spasm. It is important to avoid excessive heat or deep massage since it could injure the tissue and make the problem worse.
  • Although traction has been used for treating sciatic for hundreds of years there is little evidence that it works. A Cochrane Back Review Group analysis of controlled treatment trials for both mechanical and manual traction (just stretching the back), either alone or in combination with other treatments found that traction had little or no impact on pain intensity, functional status, global improvement and return to work among people with sciatica due to herniated discs.
  • In a similar review of controlled treatment trials, a structured exercise program with a physical therapist was found to be slightly better than just advice to remain active for reducing leg pain in the short term but no difference at intermediate and long-term follow-up between exercise and advice.
  • [Chiropractors] still treat patients with sciatica with manipulations even though there is no scientific evidence that “subluxations” of the spine can cause sciatica or that manual manipulation corrects the “subluxation” if such a thing exists. Furthermore there is a real danger that manipulations can aggravate the nerve injury causing sciatica.
  • Surgery is the only effective treatment of tumors and abscesses compressing spinal nerves or the sciatic nerve. These disorders get worse despite conservative non-surgical management. Progressive compression of the cauda equina with resulting lower extremity weakness and bladder and bowel dysfunction requires immediate surgical exploration regardless of the cause
  • Although both procedures show comparable complications and repeat herniation rates sequestrectomy has a higher satisfaction rate so it is the procedure of choice.
  • What patients and physicians should know when considering back surgery for a herniated disk:
. Herniated disks are common – lifetime prevalence of 1–2%
. More than 90% get better without surgery
. Only 2–4% of patients are candidates for surgery
. MRI will identify herniated disks in 20–30% of asymptomatic people under the age of 60 years
. Surgery improves short term outcome but probably not long term outcome
. Surgery is rarely indicated before 6 weeks of symptoms but should not be delayed beyond 3–4 months
. The disk will continue to degenerate with any form of treatment
. Scar tissue will form making future surgery more difficult
  • About a quarter of patients that suffer from chronic pain develop the chronic pain after surgery. Chronic pain can occur after any type of surgery although it is most frequent after operations lasting more than 3hrs and operations producing a great deal of tissue damage. The highest rates of postoperative pain are associated with cardiothoracic and spine surgeries and with amputations.
  • To avoid intraoperative nerve injury the surgeon should perform a careful dissection, minimize inflammation and of course use minimally invasive techniques whenever possible
  • Even when large nerves are not involved in the surgery, tissue retraction or cutting the skin or other tissues can damage sensory nerves and trigger chronic neuropathic pain.
  • There is convincing evidence that the longer pain persists the greater the chance of developing central sensitization to pain.
  • A subset of all patients who undergo surgery of any kind develop chronic pain with the lowest rate (5–30%) for simple procedures such as hernia repair and C-sections, an intermediate rate (30–60%) for chest and heart surgery and the highest rate (50–85%) for surgeries involving major nerves such as surgery for sciatica. Between 25% and 50% of patients who develop acute sciatica will go on to develop chronic sciatica whether or not they have surgery.
  • Following peripheral nerve injury structural and chemical changes occur in central pain pathways that can persist long after the injury has resolved. Just as in the primary pain neurons secondary pain neurons in the spinal cord can show increased spontaneous firing rates, decreased thresholds for firing and increased response to incoming pain signals.
  • A patient with long standing sciatica will report pain when the leg area of the somatosensory cortex is stimulated. Furthermore, stimulating the nearby area that normally just receives input from the arm will also trigger pain in the leg. The chronic pain signals not only change the response of the leg area of the somatosensory cortex but also the neighboring arm area.
  • The antiseizure drugs gabapentin (Neurontin) and pregabalin (Lyrica) that are widely used to treat chronic neuropathic pain work by blocking a subunit of calcium channels that are upregulated after nerve injury.
  • The hallmark of depression is a dysregulation of these neurotransmitters. As we will see in Chap. 8, drugs such as duloxetine and venlafaxine that increase brain norepinephrine and serotonin levels, treat both depression and chronic pain. Drugs and placebos that activate the opioid DPMS also treat both chronic pain and depression.
  • The primary neurons for the autonomic system are located in the hypothalamus, part of the limbic pain system pathway. The hypothalamus is the key brain neuroendocrine center and pain has the potential to affect all body organs through activation of the limbic system and release of a wide range of hormones.
  • Since pain normally signals impending danger or harm it is not surprising that patients with pain might avoid activities such as exercise that can induce or exacerbate pain. While this may be an appropriate reaction to acute pain, fear-avoidance behavior can lead to increased disability with chronic neuropathic pain. Muscles become weak, joints become stiff and bones become thinner. Fear of pain may be a better predictor of chronic disability than the degree of pain itself.
  • Sleep is a key issue in dealing with chronic pain. If patients have a good night sleep they often will have a good day in dealing with pain. On the other hand, the worst days come after a bad night sleep. Sleeping pills on a regular basis is not the answer since they become less effective after a few weeks. Occasional use for a bad night leads to better results. Regular daily exercise is key to living with chronic pain. Exercise not only improves sleep but also helps relieve pain by releasing endogenous opioids and enhancing the Descending Pain Modulatory System (DPMS).
  • Another area that requires constant effort is to avoid negative thinking. With a bad pain day it is natural to wander whether something new is happening. Even if patients are given a reasonable understanding of the mechanism of chronic pain it is common for them to wonder whether something changed or something new has happened. Catastrophising, always expecting the worst, increases the disability associated with chronic neuropathic pain. If one anticipates a catastrophic consequence of an activity such as exercise one will avoid the activity. Patients need constant reassurance that their activities are not causing the chronic pain.
  • Of all surgeries for sciatica, removal of a schwannoma from a lumbosacral spinal nerve has the highest risk for developing chronic neuropathic pain (>50%).
  • After nerve injury, the density of ion channels increases in the damaged nerve fibers and the channels have different pharmacologic and depolarization characteristics. This explains why many current drugs that block ion channels (e.g. seizure drugs and antidepressant drugs) are useful for treating chronic neuropathic pain.
  • More recently, ketamine in smaller doses has been found to be effective for treating a range of refractory chronic pain conditions including chronic neuropathic pain, phantom limb pain, and causalgia (now called chronic regional pain syndrome – CRPS type II). In one small study, ketamine induced coma for 5 days in patients with refractory chronic pain lead to significant improvement in the chronic pain. This suggests the intriguing possibility that a complete shut down of pain pathways for a few days may “break the cycle” of chronic pain.
  • The inhibitory neurotransmitter GABA is released by interneurons throughout the central pain pathways including the inhibitory “gate” neurons in the dorsal horn of the spinal cord. Drugs that mimic GABA, so-called GABA agonists, decrease pain transmission but also decrease overall brain activity. High doses are typically required for pain control, however, and as with the AMPA and NMDA blockers sedation and memory loss are bothersome side effects. Development of tolerance and dependency is also a problem.
  • Although opioids are the most potent activator of the descending pain modulatory system (DPMS) surprisingly they are not very effective for treating chronic neuropathic pain such as chronic sciatica. This may be in part because opioid receptors are down regulated after nerve injury decreasing opioid inhibition via the DPMS. Not only are opioids not very good for treating chronic neuropathic pain, in some cases they may actually worsen chronic pain producing so-called opioid-induced hyperalgesia (OIH). With this condition, patients receiving opioids for treating chronic pain become more sensitive to pain.
  • Overall drugs that increase noradrenalin neurotransmission decrease pain transmission and are effective in controlling chronic pain. TCAs that inhibit the reuptake of norepinephrine or both norepinephrine and serotonin, such as amitriptyline and desipramine, have demonstrated efficacy in the treatment of chronic pain conditions such as diabetic neuropathy, fibromyalgia, chronic headaches, and post-herpetic neuralgia
  • Serotonin is clearly involved in pain control but its role is complicated and it can inhibit or facilitate pain transmission. In rodent animal models injecting serotonin into the spinal fluid attenuates pain transmission at the dorsal horn in normal animals but has relatively little effect on chronic neuropathic pain.
  • As a general rule, drugs that increase serotonin levels decrease pain transmission but serotonin may play multiple potentially conflicting roles in pain perception depending on which neurons and which receptors are activated.
  • The level of expression of dopamine receptors in the net- work determines ones ability to feel pleasure and pain. Dysfunction in the motivation/reward dopamine network is associated with a variety of clinical syndromes including mood disorders, neuropsychiatric disorders and chronic pain. Furthermore baseline activity in the neuronal centers of the network effects the magnitude of opioid induced analgesia via the DPMS.
  • A wide variety of neurotransmitters are involved in pain transmission. As a general rule, drugs that block glutamate transmission and drugs that enhance GABA, opioid, noradrenalin, serotonin and dopamine transmission decrease pain perception. The effect is more prominent for chronic pain than for acute pain. However, there are exceptions to this general rule particularly with regard to serotonin and dopamine and all of these neurotransmitters play multiple potentially conflicting roles in pain perception depending on which neurons and which receptors are activated. Considering the widespread distribution of these neurotransmitters and their receptors in the brain and spinal cord the fact that drugs that modulate the level of these neurotransmitters have troubling side effects is not surprising.
  • Anti-epileptic drugs work at least in part by blocking sodium channels thereby decreasing neuronal excitability. All of them are associated with serious side effects including Stevens-Johnson syndrome and idiosyncratic blood dyscrasias such as aplastic anemia and agraulocyto- sis but side effects are less common with oxcarbazepine and lamotrigine than with phenytoin and carbamazepine. These drugs have important interactions with many other drugs so physicians must be aware of these interactions before prescribing the drugs.
  • Overall, the different tricyclic amines have been about equally effective in clinical trials for neuropathic pain and all have bothersome side effects including sedation, weight gain, dizziness, constipation, urinary retention and sexual dysfunction. These drugs should be used with caution in patients with coronary artery disease, heart arrhythmias, known seizures, urinary retention, and glaucoma. A big problem with the tricyclic amines is potential drug interactions. They should not be used with other drugs that elevate brain serotonin and noradrenalin levels such as the selective serotonin and noradrenalin reuptake inhibitors and tramadol and they should be used with caution in patients taking NSAIDs and warfarin (can increase the risk of bleeding).
  • Of the SSNRIs only venlafaxine and duloxetine have been studied and found to be effective in controlled treatment trials for chronic neuropathic pain. The main side effects include somnolence, constipation, nausea, dizziness, dry mouth, increased sweating and headache. Combined SSRIs and SNRIs should be used with great caution in patients with high blood pressure or in patients taking other drugs that increase serotonin including tricyclic amines and tramadol. They are contraindicated in patients with severe liver or kidney impairment.
  • During the [Electric Pulse Stimulator] trial period, that can last a few days to a few weeks, different pulse durations and amplitudes are tried and pain relief and functional activities are monitored with the goal of obtaining at least 50% relief of pain. If the trial is successful the electric pulse stimulator is implanted under the skin under local anesthesia where it can be programmed for the best results. To date nerve and spinal cord electrical stimulation has proved most helpful for treating chronic radicular pain such as chronic sciatica. It has been particularly effective for treating so-called failed back surgery syndrome (FBSS), where patients have undergone multiple surgeries for sciatica but continue to have chronic pain.
  • Further, with the discovery of medications for treating chronic pain, the risk associated with ablative procedures was difficult to justify. However, as imaging and surgical techniques dramatically improved in the late twentieth century there was a renewed interest in the use of ablative procedures for treating chronic neuropathic pain. Needles and endoscopes can be more accurately guided so that selective ablation can be achieved with minimal risk to surrounding tissue. Due to the problems with current medications described earlier in this chapter, pain management centers are increasingly returning toward a procedural based approach. The problem is we have very little information on the long-term effectiveness of these procedures for treating chronic sciatica.
  • With lack of activity, joints become stiff and bones become thinner and patients can become invalids.
  • Why did my pain become more pronounced after stopping pregabalin? Pregabalin blocks a sub-unit of a calcium channel that is critical for release of excitatory neurotransmitter throughout the brain and spinal cord. Nerve cells respond by increasing the production of the calcium channels in an attempt to overcome the pharmacological block. You require more and more medication to maintain the same benefit over time (called tolerance).
  • "I learned to expect occasional bad days and overall I found that the less pain medication I took the bet-ter I did in the long run. I also found that regular exercise was a key to living with the chronic pain. Sometimes there was a paradoxical increase in pain after vigorous exercise but I found that overall I did much better with a daily exercise routine." [Author also shared his story in the book]
  • Release of Nerve Growth Factor (NGF) with tissue and nerve injury leads to a cascade of events that cause chronic neuropathic pain. Skin injection of NGF in rodents and humans produces hypersensitivity to pain within a few hours.
  • Indeed when capsaicin is placed on the skin it initially causes burning pain but with time the burning disappears and the area becomes less sensitive to pain as the TRPV1 channels become desensitized. By applying a local anesthetic to the painful area prior to topical application of capsaicin the initial burning pain can be prevented.
  • One compound in particular, Sativex marketed by GW Pharmaceuticals has shown promise in treating chronic neuropathic pain. Sativex, which is administered as an oral-mucosal spray, combines THC and CBD in a 1:1 ratio along with several other minor cannabis substances.
  • Drugs that block AMPA or NMDA receptors prevent the development of central sensitization to pain after nerve injury but since there are multiple subtypes of these recep- tors and different subtypes are expressed throughout the central nervous system side effects are common, particularly sedation and memory impairment. For example the AMPA receptor blocker, NBQX, is a better sedative than a pain medication. The potent NMDA blocker, ketamine produces a trance-like state, sedation and memory loss after intravenous injection.
  • Long-term regular use of opioids or any other pain medication should be avoided. Over prescribing of opioids for back pain and sciatica is a major contributor to the current opioid crisis in the United States. With chronic neuropathic pain regular daily use of pain medications may actually aggravate the problem. In this case medications that stabilize damaged nerves such as antiepileptic and antidepressant drugs are more useful.
  • Manipulations followed by an audible snap or pop as the lateral articulation returns to its normal position leads to a dramatic cure and the kind of testimonial that assures a steady flow of patients. But this approach does not work with sciatica. Patients with nerve compression can have worsening of symptoms and signs after manipulation.
submitted by bgechc to ChronicPain

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