No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Relief of Vascular Headache with Intravenous Lidocaine
Abstract
The effectiveness of intravenous lidocaine for relief of vascular headache was assessed using a single-blind protocol. Patients with acute pain due to common migraine or cluster headache were studied and compared with patients with cranial pain of other causes. Pain intensity was measured using a visual analog scale. In 13 headache patients, an intravenous injection of lido- caine (100 mg standard dose) produced rapid relief of clinical pain, with an associated significant change in visual analog scale scores (p < 0.001). Relief lasted approximately 20 min; in most patients the pain then returned to pretreatment levels. No significant side effects were reported by the subjects. This response may be the result of a direct, anesthetic action of lidocaine on trigeminal nociceptive afferents innervating cranial blood vessels.
(C) Lippincott-Raven Publishers.
... (4,5) However, its use on the treatment of cluster headache attacks was reported in a few papers, and remains largely unknown. (6,7) We describe a case of a refractory cluster headache patient, whose condition remitted after the use of intravenous lidocaine. ...
... (4,5) Although the results suggest a good response to intravenous lidocaine as an abortive therapy of SUNCT, its mechanisms of action are still unclear. (4) In 1988, Maciewicz (6) reported the use of intravenous lidocaine for treating migraine and cluster headache attacks. In this report, the author found a significant reduction in pain intensity reported by patients with cluster headache. ...
... In this report, the author found a significant reduction in pain intensity reported by patients with cluster headache. (6) He also suggested that the good result was due to the direct action of lidocaine in the trigeminal nociceptive input from local blood vessels. (6) Marmura, in 2009, (7) through a retrospective study on the use of intravenous lidocaine in 68 patients, two of whom were suffering from cluster headache, reported a 50% improvement of pain after administration of the anesthetic in these patients. ...
Cluster headache is a rare clinical condition, classified by the IHS as a trigeminal autonomic cephalalgia. Some known abortive treatments are inhaled oxygen, subcutaneous sumatriptan, intravenous dihydroergotamine and intranasal lidocaine. However, previous case reports suggest that intravenous lidocaine may play a role in the treatment of cluster headache attacks. We describe a patient with refractory cluster headache, whose condition remitted after the use of intravenous lidocaine. Therapy with lidocaine was conducted without harm, and the remission after a "single shot" suggested this approach to be safe and desirable to be tried in patients with cluster headache..
... Shortly thereafter, Rosner reported his observations on the efficacy of IV lidocaine in the treatment of headaches [18]. In 1988, Maciewicz et al. was the first group to evaluate the effectiveness of a single bolus dose of IV lidocaine in patients with "vascular headaches" [19]. In their study, a single injection of 100 mg lidocaine was found to produce a rapid, but transient reduction in acute pain in 13 patients with migraine or cluster headache. ...
... In their study, a single injection of 100 mg lidocaine was found to produce a rapid, but transient reduction in acute pain in 13 patients with migraine or cluster headache. The mechanism of analgesia was believed to be related to local inhibition of the nociceptive trigeminal afferents that are responsible for nociception [19]. ...
Purpose of Review
The purpose of this review is to discuss the available evidence and therapeutic considerations for intravenous drug therapy for refractory chronic migraine.
Recent Findings
In carefully monitored settings, the inpatient administration of intravenous lidocaine and ketamine can be successful in treating refractory chronic migraine.
Summary
Many patients with refractory chronic migraine have experienced treatment failure with the Raskin protocol. The use of aggressive inpatient infusion therapy consisting of intravenous lidocaine or ketamine, along with other adjunctive medications, has become increasingly common for these patients when all other treatments have failed. There is a clear need for prospective studies in this population comprised of patients who have largely been excluded from other studies.
... Intravenous lidocaine has been demonstrated to provide effective analgesia in a variety of acute and chronic pain states (14,15). It has been reported to be effective in several headache syndromes including trigeminal neuralgia (16), chronic migraine (17) and cluster headache (18). It has been proposed as treatment for status migrainosis (19) and chronic daily headache (20), although a brief infusion in migraine did not prove effective in one trial (21). ...
Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) is a primary headache syndrome that has been reported to be resistant to treatment with intravenous lidocaine. We report four cases of SUNCT in whom intravenous lidocaine (1.3-3.3 mg kg(-1) h(-1)) completely suppressed the headaches for the duration of the infusion. The headache returned after cessation of treatment. Two patients went on to have their symptoms controlled on topiramate (50-300 mg daily). One patient had typical migrainous aura in association with some of the attacks of pain but never migrainous headaches. These cases suggest that treatment with lidocaine can be considered when acute intervention is required to suppress a severe exacerbation of SUNCT, and further broaden the therapeutic and clinical background of this syndrome.
The ASAM Handbook on Pain and Addiction provides clinical guidance to health care professionals who treat patients with co-occurring pain and addiction. Produced by the largest medical society dedicated to the improvement of addiction care, the handbook takes an evidence-based approach. Its advice is based on the current scientific literature and the advice of well-regarded organizations and government agencies, including NIDA, CDC, SAMHSA, PCSS-O, and ASAM itself. The ASAM Handbook is organized in five sections, which cover the core concepts of pain and addiction; diagnosis and treatment; treating pain in patients with, or at risk for, addiction; treating substance use disorders (SUD) and addiction in patients with co-occurring pain; and adapting treatment to the needs of specific populations. Each chapter concludes with suggestions for further reading on the topics discussed. The Handbook is ideal for primary care practitioners, mental health clinicians, addiction clinicians, and pain clinicians who wish to bridge the knowledge gap related to treating patients suffering from both pain and addiction.
Lidocaine and mexiletine are class 1B antiarrhythmic drugs that act on sodium channels. Lidocaine is also an important anesthetic and topical agent that is useful in the treatment of multiple pain disorders, and mexiletine is commonly used for neuropathic pain and myotonia. Both intravenous lidocaine and mexiletine are increasingly used to treat pain syndromes and appear to be particularly effective in neuropathic pain. This suggests a role for these agents in patients with headache disorders. This article describes the role of intravenous lidocaine and mexiletine in the management of headache and trigeminal autonomic cephalalgias based on the published literature to date and provides practical guidelines for their use.
Lidocaine has been used in treatment of patients with refractory headache. Personal observations of neuropsychiatric toxicity in these patients led us to review our cases and the literature systematically for lidocaine side-effects, especially neuropsychiatric symptoms. In our series of 20 patients, side-effects were observed in all, the most frequent being neuropsychiatric (75%) and cardiological (50%). When reviewing published series on intravenous lidocaine use, reports of side-effects range from 0 to 100%, with neuropsychiatric symptoms being reported in 1.8-100%. Thirty-six case reports of lidocaine-induced psychiatric symptoms were also analysed. Psychiatric symptoms of toxicity were similar in most patients, despite their differing ages, pathologies, co-therapies and lidocaine dosages. In conclusion, lidocaine neuropsychiatric toxicity has a well-recognized stereotypical clinical presentation that is probably unrecognized in headache series. As lidocaine represents an emerging alternative therapy in headache, particularly in short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing, clinicians and patients should be aware of the extent of this problem.
Systemic application of lidocaine in rats suppressed ectopic impulse discharge generated both at sites of experimental nerve injury and in axotomized dorsal root ganglion (DRG) cells. ED50 for DRGs was significantly lower than for the injury site. Lidocaine doses effective at blocking ectopic discharge failed to block the initiation or propagation of impulses by electrical stimulation, and only minimally affected normal sensory receptors. This selectivity may account for the effectiveness of systemic local anesthetics and other drugs that share the same mechanism of action (notably certain anticonvulsants and antiarrhythmics), in the management of neuropathic paresthesias and pain. In addition, it may account for the prolonged analgesia sometimes obtained using regional local anesthetic block.
Ten patients with organic nerve injury causing chronic neuropathic pain were tested for the effects of intravenous lidocaine versus saline upon psychophysical somatosensory variables. The variables assessed were the subjective magnitude of pain, area of mechanical hyperalgesia and presence and magnitude of thermal heat/cold hyperalgesia. The study methods applied to evaluate these conditions were the conventional testing of somatosensory submodalities with area mapping and the subjective magnitude estimation of spontaneous pain. It was found that spontaneous pain and mechanical hyperalgesia were consistently improved, transiently, by intravenous administration of lidocaine in all 10 patients; areas of hyperalgesia which extended beyond the territory of the nerve also improved transiently. Spontaneous pain and mechanical hyperalgesia, but not hypoesthesia, were transiently improved by injection of saline in only 1 of the 10 patients. This outcome is probably due to a placebo effect. This improvement is in keeping with the inhibition of anomalous neural impulses which can be generated anywhere along the sensory channels responsible for generating spontaneous pain and hyperalgesia. Thus, intravenous lidocaine is proposed as a diagnostic aid in the examination of patients complaining of complex sensory disorders associated with nerve injury. The transient pain relief may allow a fuller identification of the area of sensory loss.
We report on the analgesic efficacy of intrathecal infusions of opioids alone or in combination with bupivacaine in 16 nonmalignant pain patients with implanted pumps. Three patients had nociceptive pain, five had neuropathic pain, and 8 had mixed pain syndromes. Infusional therapy was delivered over a combined monthly total of 445 mo of therapy (mean, 27.8 mo). Dose requirements appeared to be stable with a mean dose increase of 0.26 mg/mo. Bupivacaine was added to the opioid to enhance pain control in 13 patients who received combination therapy for an average of 11.7 mo/patient. Thirteen patients (81%) reported good to excellent results with opioid alone or opioid combined with bupivacaine. The addition of bupivacaine improved analgesia in two of three patients with nociceptive pain (66.7%), compared to eight of ten patients with a pure or mixed neuropathic component to their pain (80%). We conclude that intrathecal opioids alone or in combination with bupivacaine are efficacious for the treatment of nonmalignant pain states and are relatively free of significant side effects or tolerance.
Local anesthetics administered to block nerve conduction for surgical anesthesia and to provide analgesia in management of acute pain have become a standard of anesthesiology practice. These drugs have had an important role in the multimodality management of chronic pain as well, and this role is expanding since the revival of systemic administration. Local anesthetics are analgesics, albeit not in the traditional clinical and pharmacologic sense. Evidence suggests that intravenous administration is an effective treatment in chronic neuropathic pain syndromes. There is also evidence that intravenous local anesthetics can relieve acute pain. Furthermore, the novel idea that acute procedural and postprocedural pain control with local anesthetics could prevent the development of chronic pain syndromes, including chronic neuropathic pain syndromes, adds another important potential dimension to the role of local anesthetics in pain management.
We report the case of a 39-year-old man with severe pain due to unresectable squamous-cell carcinoma of the maxillary sinus that had invaded cranial bone and had metastasized to the cervical spine. Tolerance to opioids had developed, and high doses of transdermal, continuous intravenous, and epidural opioids did not control his pain. An acute episode of extremely severe head pain was immediately controlled with a subanesthetic dose of ketamine after failure of a stress dose of corticosteroid and intravenous lidocaine. Because the patient was terminally ill and invasive procedures were not options, we controlled his pain using a low-dose ketamine infusion until his death 13 days later. Ketamine may be a good co-analgesic for breakthrough pain and for severe pain caused by terminal cancer when invasive techniques are inappropriate. Its mechanism of action may include reversal of opioid tolerance in addition to an inherent analgesic effect.
Cancer presents itself in numerous ways, adding to the complexity of any pain syndrome with which it is associated. Neuropathic pain, unlike many other pain syndromes, is difficult to treat even in the absence of cancer. The combination results in a heterogeneous group of patients with a complex set of symptoms. This makes the assessment of pain, classification of syndromes, and clinical study a challenge. If the disease is nonprogressive, general principles of care are essentially the same as in those without cancer. In patients with progressive disease and more refractory painful conditions, spinal anesthetic and neurosurgical therapies must often be considered. Under such circumstances, caregivers are forced to carefully balance uncertain benefits and risks, often without the luxury of time. More careful observation and controlled trials in these patients help facilitate this challenging process.
This study investigated the effect of intravenous lidocaine at two doses (1 mg/kg and 5 mg/kg over 2 hours) and an intravenous saline placebo on the pain and allodynia of postherpetic neuralgia (PHN). Twenty-four patients were studied using a randomized, double-blind, within-patient crossover design. Each patient received normal saline, lidocaine 0.5 mg/kg/h, and lidocaine 2.5 mg/kg/h for a 2-h period. The McGill Pain Questionnaire Short Form, visual analogue scores (VAS), and area of allodynia were measured at intervals during the infusions. Free plasma lidocaine levels were also measured. The results were statistically analyzed using Student's t-test for paired data. The VAS for ongoing pain showed a significant reduction after all the infusions (P < 0.05). For dynamic pressure-provoked pain, the VAS was unaffected by placebo but showed a reduction at an equal level of significance with both lidocaine infusions (P < 0.05). The area of allodynia of PHN, as mapped by brush stroke, declined in association with intravenous lidocaine (0.5 mg/kg/h = P < 0.05; 2.5 mg/kg/h = P < 0.001). Placebo had no significant effect on the area of allodynia. These findings demonstrate a positive effect on pain and allodynia following a brief intravenous infusion of lidocaine. The higher dose infusion may produce plasma levels in the toxic range, with no significant clinical increase in response.
The trigeminal autonomic cephalgias include cluster headache, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT). The evidence for the current treatment options for each of these syndromes is considered, including oxygen, sumatriptan, and verapamil in cluster headache, indomethacin in paroxysmal hemicrania, and intravenous lidocaine and lamotrigine in SUNCT. Some treatments such as topiramate have an effect in all of these, as well as in migraine and other pain syndromes. The involvement of the hypothalamus in functional imaging studies implies that this may be a substrate for targeting treatment options in the future.
ResearchGate has not been able to resolve any references for this publication.