Thoracic Nerve Root Entrapment by Intrathecal Catheter Coiling: Case Report and Review of the Literature.

BACKGROUND: Intrathecal catheter placement has long-term therapeutic benefits in the management of chronic, intractable pain. Despite the diverse clinical applicability and rising prevalence of implantable drug delivery systems in pain medicine, the spectrum of complications associated with intrathecal catheterization remains largely understudied and underreported in the literature. OBJECTIVE: To report a case of thoracic nerve root entrapment resulting from intrathecal catheter migration. STUDY DESIGN: Case report. SETTING: Inpatient hospital service. RESULTS/ CASE REPORT: A 60-year-old man status post implanted intrathecal (IT) catheter for intractable low back pain secondary to failed back surgery syndrome returned to the operating room for removal of IT pump trial catheter after experiencing relapse of preoperative pain and pump occlusion. Initial attempt at ambulatory removal of the catheter was aborted after the patient reported acute onset of lower extremity radiculopathic pain during the extraction. Noncontrast computed tomography (CT) subsequently revealed that the catheter had ascended and coiled around the T10 nerve root. The patient was taken back to the operating room for removal of the catheter under fluoroscopic guidance, with possible laminectomy for direct visualization. Removal was ultimately achieved with slow continuous tension, with complete resolution of the patient's new radicular symptoms. LIMITATIONS: This report describes a single case report. CONCLUSION: This case demonstrates that any existing loops in the intrathecal catheter during initial implantation should be immediately re-addressed, as they can precipitate nerve root entrapment and irritation. Reduction of the loop or extrication of the catheter should be attempted under continuous fluoroscopic guidance to prevent further neurosurgical morbidity.

Central regulation of photosensitive membrane turnover in the lateral eye of Limulus, II: octopamine acts via adenylate cyclase/cAMP-dependent protein kinase to prime the retina for transient rhabdom shedding.

Why photoreceptors turn over a portion of their photoreceptive membrane daily is not clear; however, failure to do so properly leads to retinal degeneration in vertebrates and invertebrates. Little is known about the molecular mechanisms that regulate shedding and renewal of photoreceptive membrane. Photoreceptive cells in the lateral eye of the horseshoe crab Limulus turn over their photoreceptive membrane (rhabdom) in brief, synchronous burst in response to dawn each morning. Transient rhabdom shedding (TRS), the first phase of rhabdom turnover in Limulus, is triggered by dawn, but requires a minimum of 3-5 h of overnight priming from the central circadian clock (Chamberlain & Barlow, 1984). We determined previously that the clock primes the lateral eye for TRS using the neurotransmitter octopamine (OA) (Khadilkar et al., 2002), and report here that OA primes the eye for TRS through a G(s)-coupled, adenylate cyclase (AC)/cyclic adenosine 3',5'-monophosphate (cAMP)/cAMP-dependent protein kinase (PKA) signaling cascade. Long-term intraretinol injections (6-7 h @ 1.4 microl/min) of the AC activator forskolin, or the cAMP analogs Sp-cAMP[s] and 8-Br-cAmp primed the retina for TRS in eyes disconnected from the circadian clock, and/or in intact eyes during the day when the clock is quiescent. This suggests that OA primes the eye for TRS by stimulating an AC-mediated rise in intracellular cAMP concentration ([cAMP]i). Co-injection of SQ 22,536, an AC inhibitor, or the PKA inhibitors H-89 and PKI (14-22) with OA effectively antagonized octopaminergic priming by reducing the number of photoreceptors primed for TRS and the amount of rhabdom shed by those photoreceptors compared with eyes treated with OA alone. Our data suggest that OA primes the lateral eye for TRS in part through long-term phosphorylation of a PKA substrate.

Central regulation of photosensitive membrane turnover in the lateral eye of Limulus. I. Octopamine primes the retina for daily transient rhabdom shedding.

Limulus lateral eyes shed and renew a portion of their photosensitive membrane (rhabdom) daily. Shedding, in many species including Limulus, is regulated by complex interactions between circadian rhythms and light. Little is known about how circadian clocks and photoreceptors communicate to regulate shedding. Limulus photoreceptors do not contain an endogenous circadian oscillator, but rely upon efferent outflow from a central clock for circadian timing. To investigate whether the putative efferent neurotransmitter octopamine (OA) communicates circadian rhythms that prime the lateral eye for transient rhabdom shedding, we decoupled photoreceptors from the clock by transecting the lateral optic nerve (contains the retinal efferent fibers). Overnight (6 h) intraretinal injections of 40 microM OA restored transient shedding to lateral eyes with transected nerves to levels comparable to those of intact internal control eyes. To determine whether OA acts alone in communicating circadian rhythms that prime the lateral eye for transient shedding, we "primed" eyes with intact nerves for transient shedding with exogenous OA during subjective day. In nature, lateral eyes shed their rhabdoms only once a day at dawn following overnight efferent priming. Eyes in animals placed in darkness during subjective day, when the retinal efferents are quiescent, and injected for 6 h with 40 microM OA shed their rhabdoms in response to a second introduction to light. Untreated control eyes of the same animals did not. The same results were observed in vitro in lateral eyes treated similarly. Octopamine is the only efferent neurotransmitter/messenger required to make lateral eyes competent for transient shedding. Phentolamine, an OA receptor antagonist, reduced the number of photoreceptors primed for transient shedding and the amount of rhabdom shed in those photoreceptors suggesting that OA acts via a specific OA receptor.