Giant cystic sacral schwannoma mimicking tarlov cyst: a case report.

PURPOSE: To present a rare case of a giant schwannoma of the sacrum mimicking a Tarlov cyst. METHODS: A 58-year-old woman had a 1-year history of low back pain. MRI revealed a large cystic mass in the sacral canal with bony erosion. Radiological diagnosis of Tarlov cyst was made. RESULTS: The patient underwent surgical treatment for the lesion, which revealed a solid mass. Histopathological examination of the tumor confirmed the diagnosis of schwannoma. The postoperative course was uneventful and the patient has had significant improvement in her pain 1 month postoperatively. CONCLUSION: Giant cystic schwannoma of the sacrum is a very rare diagnosis overlooked by practitioners for more common cystic etiologies, but its treatment is significantly different. Care should be taken to include this diagnosis in a differential for a cystic sacral mass.

Sustained neuronal hyperexcitability is evident in the thalamus after a transient cervical radicular injury.

STUDY DESIGN: This study used extracellular electrophysiology to examine neuronal hyperexcitability in the ventroposterolateral nucleus (VPL) of the thalamus in a rat model of painful radiculopathy. OBJECTIVE: The goal of this study was to quantify evoked neuronal excitability in the VPL at day 14 after a cervical nerve root compression to determine thalamic processing of persistent radicular pain. SUMMARY OF BACKGROUND DATA: Nerve root compression often leads to radicular pain. Chronic pain is thought to induce structural and biochemical changes in the brain affecting supraspinal signaling. In particular, the VPL of the thalamus has been implicated in chronic pain states. METHODS: Rats underwent a painful transient C7 nerve root compression or sham procedure. Ipsilateral forepaw mechanical allodynia was assessed on days 1, 3, 5, 7, 10, and 14 and evoked thalamic neuronal recordings were collected at day 14 from the contralateral VPL, whereas the injured forepaw was stimulated using a range of non-noxious and noxious mechanical stimuli. Neurons were classified on the basis of their response to stimulation. RESULTS: Behavioral sensitivity was elevated after nerve root compression starting at day 3 and persisted until day 14 (P < 0.049). Thalamic recordings at day 14 demonstrated increased neuronal hyperexcitability after injury for all mechanical stimuli (P < 0.024). In particular, wide dynamic range neurons demonstrated significantly more firing after injury compared with sham in response to von Frey stimulation (P < 0.0001). Firing in low threshold mechanoreceptive neurons was not different between groups. CONCLUSION: These data demonstrate that persistent radicular pain is associated with sustained neuronal hyperexcitability in the contralateral VPL of the thalamus. These findings suggest that thalamic processing is altered during radiculopathy and these changes in neuronal firing are associated with behavioral sensitivity. LEVEL OF EVIDENCE: N/A.

Salmon and human thrombin differentially regulate radicular pain, glial-induced inflammation and spinal neuronal excitability through protease-activated receptor-1.

Chronic neck pain is a major problem with common causes including disc herniation and spondylosis that compress the spinal nerve roots. Cervical nerve root compression in the rat produces sustained behavioral hypersensitivity, due in part to the early upregulation of pro-inflammatory cytokines, the sustained hyperexcitability of neurons in the spinal cord and degeneration in the injured nerve root. Through its activation of the protease-activated receptor-1 (PAR1), mammalian thrombin can enhance pain and inflammation; yet at lower concentrations it is also capable of transiently attenuating pain which suggests that PAR1 activation rate may affect pain maintenance. Interestingly, salmon-derived fibrin, which contains salmon thrombin, attenuates nerve root-induced pain and inflammation, but the mechanisms of action leading to its analgesia are unknown. This study evaluates the effects of salmon thrombin on nerve root-mediated pain, axonal degeneration in the root, spinal neuronal hyperexcitability and inflammation compared to its human counterpart in the context of their enzymatic capabilities towards coagulation substrates and PAR1. Salmon thrombin significantly reduces behavioral sensitivity, preserves neuronal myelination, reduces macrophage infiltration in the injured nerve root and significantly decreases spinal neuronal hyperexcitability after painful root compression in the rat; whereas human thrombin has no effect. Unlike salmon thrombin, human thrombin upregulates the transcription of IL-1ß and TNF-α and the secretion of IL-6 by cortical cultures. Salmon and human thrombins cleave human fibrinogen-derived peptides and form clots with fibrinogen with similar enzymatic activities, but salmon thrombin retains a higher enzymatic activity towards coagulation substrates in the presence of antithrombin III and hirudin compared to human thrombin. Conversely, salmon thrombin activates a PAR1-derived peptide more weakly than human thrombin. These results are the first to demonstrate that salmon thrombin has unique analgesic, neuroprotective and anti-inflammatory capabilities compared to human thrombin and that PAR1 may contribute to these actions.

The roles of mechanical compression and chemical irritation in regulating spinal neuronal signaling in painful cervical nerve root injury.

Both traumatic and slow-onset disc herniation can directly compress and/or chemically irritate cervical nerve roots, and both types of root injury elicit pain in animal models of radiculopathy. This study investigated the relative contributions of mechanical compression and chemical irritation of the nerve root to spinal regulation of neuronal activity using several outcomes. Modifications of two proteins known to regulate neurotransmission in the spinal cord, the neuropeptide calcitonin gene-related peptide (CGRP) and glutamate transporter 1 (GLT-1), were assessed in a rat model after painful cervical nerve root injuries using a mechanical compression, chemical irritation or their combination of injury. Only injuries with compression induced sustained behavioral hypersensitivity (p≤0.05) for two weeks and significant decreases (p<0.037) in CGRP and GLT-1 immunoreactivity to nearly half that of sham levels in the superficial dorsal horn. Because modification of spinal CGRP and GLT-1 is associated with enhanced excitatory signaling in the spinal cord, a second study evaluated the electrophysiological properties of neurons in the superficial and deeper dorsal horn at day 7 after a painful root compression. The evoked firing rate was significantly increased (p=0.045) after compression and only in the deeper lamina. The painful compression also induced a significant (p=0.002) shift in the percentage of neurons in the superficial lamina classified as low- threshold mechanoreceptive (sham 38%; compression 10%) to those classified as wide dynamic range neurons (sham 43%; compression 74%). Together, these studies highlight mechanical compression as a key modulator of spinal neuronal signaling in the context of radicular injury and pain.