The use of metformin is associated with decreased lumbar radiculopathy pain.

Lumbar radiculopathy pain represents a major public health problem, with few effective long-term treatments. Preclinical neuropathic and postsurgical pain studies implicate the kinase adenosine monophosphate activated kinase (AMPK) as a potential pharmacological target for the treatment of chronic pain conditions. Metformin, which acts via AMPK, is a safe and clinically available drug used in the treatment of diabetes. Despite the strong preclinical rationale, the utility of metformin as a potential pain therapeutic has not yet been studied in humans. Our objective was to assess whether metformin is associated with decreased lumbar radiculopathy pain, in a retrospective chart review. We completed a retrospective chart review of patients who sought care from a university pain specialist for lumbar radiculopathy between 2008 and 2011. Patients on metformin at the time of visit to a university pain specialist were compared with patients who were not on metformin. We compared the pain outcomes in 46 patients on metformin and 94 patients not taking metformin therapy. The major finding was that metformin use was associated with a decrease in the mean of "pain now," by -1.85 (confidence interval: -3.6 to -0.08) on a 0-10 visual analog scale, using a matched propensity scoring analysis and confirmed using a Bayesian analysis, with a significant mean decrease of -1.36 (credible interval: -2.6 to -0.03). Additionally, patients on metformin showed a non-statistically significant trend toward decreased pain on a variety of other pain descriptors. Our proof-of-concept findings suggest that metformin use is associated with a decrease in lumbar radiculopathy pain, providing a rational for larger retrospective trials in different pain populations and for prospective trials, to test the effectiveness of metformin in reducing neuropathic pain.

Transcranial ultrasound (TUS) effects on mental states: a pilot study.

BACKGROUND/OBJECTIVE: Transcranial ultrasound (TUS) can modulate brain function. To assess possible TUS modulation of mental states, we investigated effects on subjective reports of pain and mood of sub-thermal TUS versus placebo applied to frontal scalp and brain of chronic pain patient volunteers. METHODS: With IRB approval and informed consent, subjects with chronic pain completed two visual analog scales for pain (NRS) and mood (VAMS/Global Affect), and their vital signs were recorded 10 min prior to, and 10 min and 40 min following exposure to either subthermal TUS (8 MHz) or placebo (in a double blind crossover study) using the 12L-RS probe of a LOGIQe ultrasound imaging machine (General Electric, USA). A physician, also blinded for TUS versus placebo, applied the probe (with gel) to scalp over posterior frontal cortex, contralateral to maximal pain, for 15 seconds. A second investigator operated the ultrasound machine, randomizing TUS versus placebo. The process was then repeated, applying the opposite modality (TUS or placebo). RESULTS: Subjective reports of Mood/Global Affect were improved 10 min (P = 0.03) and 40 min (P = 0.04) following TUS compared with placebo. NRS pain reports slightly improved following TUS (P = 0.07) at 40 min. CONCLUSION: We found improvement in subjective mood 10 min and 40 min after TUS compared to placebo. TUS can have safe neurophysiological effects on brain function, and is a promising noninvasive therapy for modulating conscious and unconscious mental states and disorders. We suggest TUS acts via intra-neuronal microtubules, which apparently resonate in TUS megahertz range.

Receptor specificity defines algogenic properties of propofol and fospropofol.

BACKGROUND: Propofol-evoked injection site pain is not observed with fospropofol. We hypothesized that unlike propofol, fospropofol does not activate the irritant receptor, transient receptor potential 1 (TRPA1). METHODS: We tested the hypothesis using electrophysiology and behavioral studies. RESULTS: Our data demonstrate that propofol (100 µM) evokes an inward current only in TRPA1-expressing neurons. However, fospropofol (100 µM and 1 mM) is unable to evoke depolarizing currents in either TRPA1-positive or TRPA1-negative neurons. Both propofol and fospropofol produced general anesthesia. CONCLUSIONS: The lack of algogenic activity in fospropofol is most likely the result of its inability to activate TRPA1 on nociceptors.

Peripheral nerve stimulation for trigeminal neuropathic pain.

Facial pain is a complex disease with a number of possible etiologies. Trigeminal neuropathic pain (TNP) is defined as pain caused by a lesion or disease of the trigeminal branch of the peripheral nervous system resulting in chronic facial pain over the distribution of the injured nerve. First line treatment of TNP includes management with anticonvulsant medication (carbamazepine, phenytoin, gabapentin, etc.), baclofen, and analgesics. TNP, however, can be a condition difficult to adequately treat with medical management alone. Patients with TNP can suffer from significant morbidity as a result of inadequate treatment or the side effects of pharmacologic therapy. TNP refractory to medical management can be considered for treatment with a growing number of invasive procedures. Peripheral nerve stimulation (PNS) is a minimally invasive option that has been shown to effectively treat medically intractable TNP. We present a case series of common causes of TNP successfully treated with PNS with up to a 2 year follow-up. Only one patient required implantation of new electrode leads secondary to electrode migration. The patients in this case series continue to have significant symptomatic relief, demonstrating PNS as an effective treatment option for intractable TNP. Though there are no randomized trials, peripheral neuromodulation has been shown to be an effective means of treating TNP refractory to medical management in a growing number of case series. PNS is a safe procedure that can be performed even on patients that are not optimal surgical candidates and should be considered for patients suffering from TNP that have failed medical management.

Transforaminal blood patch for the treatment of chronic headache from intracranial hypotension: a case report and review.

This case report describes the successful treatment of chronic headache from intracranial hypotension with bilateral transforaminal (TF) lumbar epidural blood patches (EBPs). The patient is a 65-year-old male with chronic postural headaches. He had not had a headache-free day in more than 13 years. Conservative treatment and several interlaminar epidural blood patches were previously unsuccessful. A transforaminal EBP was performed under fluoroscopic guidance. Resolution of the headache occurred within 5 minutes of the procedure. After three months without a headache the patient had a return of the postural headache. A second transforaminal EBP was performed again with almost immediate resolution. The patient remains headache-free almost six months from the time of first TF blood patch. This is the first published report of the use of transforaminal epidural blood patches for the successful treatment of a headache lasting longer than 3 months.

Severe methemoglobinemia detected by pulse oximetry.

An elderly surgical patient acquired a life-threatening methemoglobinemia as a result of topical benzocaine spray to the oropharynx in preparation for awake endotracheal intubation. A new multiwavelength pulse oximeter, the Masimo Rad-57, detected this methemoglobinemia an hour before it was confirmed by laboratory CO-oximetry. The Rad-57 monitored the patient's methemoglobin levels during diagnosis and treatment with methylene blue, and the values it provided (as high as 33%) were very close to those of the laboratory CO-oximeter. The new pulse oximeter gave continuous readings of methemoglobin level at the bedside, whereas the laboratory values were delayed by up to an hour. This case demonstrates the clinical application of a multiwavelength pulse oximeter in the diagnosis and treatment of a life-threatening dyshemoglobinemia.

Subdural intrathecal catheter placement: experience with two cases.

BACKGROUND: Subdural migration of epidural catheters is well known and documented. Subdural placement of intrathecal catheters has not been recognized. Two cases of sudural placement of intrathecal catheters are presented. OBJECTIVE: The possibility of subdural migration of epidural catheters and its manifestations has been well documented. The following 2 cases demonstrate that intrathecal catheters can enter the subdural space upon placement. CASE REPORTS: The first case is a 52-year-old male with multiple sclerosis receiving a pump for intrathecal baclofen. It worked well for 10 years, but after 2 months of inadequate relief despite a 2-fold increase in baclofen, the catheter was imaged. The catheter pierced the arachnoid in the lower thoracic spine and tunneled subdural. It then pierced the arachnoid again, re-entering the cerebrospinal fluid (CSF) in the cephalad portion of the thoracic spine. Over time, the tip became covered with tissue, preventing direct CSF communication and causing subdural drug sequestration. The second case is a 54-year-old male with chronic bilateral lower extremity pain having a pump placed for pain control. Because of inadequate relief after implantation, the catheter was imaged. It pierced the arachnoid at L4-L5 but became subdural at T12-L1. At the time of surgical revision, the catheter was pulled back to L2. Repeat imaging showed it to be entirely subarachnoid, and analgesia was restored. CONCLUSIONS: These cases differ from others in the literature because the catheter was apparently subdural at the time of initial implantation. As these 2 cases demonstrate, this placement may manifest immediately, but it may remain undetected for a prolonged period. Initial subdural placement should be considered along with catheter migration into the subdural space in the differential of a malfunctioning pump.