Sensory function after cavernous haemangioma: a case report of thermal hypersensitivity at and below an incomplete spinal cord injury

Abstract

Study design: Case report of a 42-year-old woman with non-evoked pain diagnosed with a cavernous C7-Th6 spinal haemangioma. Objectives: To assess the effect of intramedullary haemorrhage (IH) on nociception and neuropathic pain (NP) at and below an incomplete spinal cord injury (SCI). Setting: Sensorimotor Function Group, Hospital Nacional de Parapléjicos de Toledo (HNPT). Methods: T2*-susceptibility weighted image (SWI) magnetic resonance imaging (MRI) of spinal haemosiderin and a complete pain history were performed 8 months following initial dysaesthesia complaint. Thermal pain thresholds were assessed with short 1 s stimuli, while evidence for central sensitization was obtained with psychophysical electronic Visual Analogue Scale rating of tonic 10 s 3 1C and 48 1C stimuli, applied at and below the IH. Control data were obtained from 10 healthy volunteers recruited from the HNPT. Results: Non-evoked pain was present within the Th6 dermatome and lower legs. T2*-SWI MRI imaging detected extensive haemosiderin-rich IH (C7-Th5/6 spinal level). Cold allodynia was detected below the IH (left L5 dermatome) with short thermal stimuli. Tonic thermal stimuli applied to the Th6, Th10 and C7 dermatomes revealed widespread heat and cold allodynia. Conclusion: NP was diagnosed following IH, corroborated by an increase in below-level cold pain threshold with at-and below-level cold and heat allodynia. Psychophysical evidence for at-and below-level SCI central sensitization was obtained with tonic thermal stimuli. Early detection of IH could lead to better management of specific NP symptoms, an appreciation of the role of haemorrhage as an aggravating SCI physical factor, and the identification of specific spinal pathophysiological pain mechanisms.

Bioinformatics Genes and Pathway Analysis for Chronic Neuropathic Pain after Spinal Cord Injury

“…According to the statistics of the GoPubMed website ( http://www.gopubmed.org/web/gopubmed/ ), the molecular mechanisms of NP following SCI remain elusive. NP in SCI can be classified as “at-level” pain [ 2 – 4 ], “below-level” pain [ 2 , 3 ], and “above-level” pain [ 5 – 7 ]. According to the International Spinal Cord Injury Pain Classification system [ 8 ], pain experienced at or within three dermatomes below the neurologic level of injury is considered at-level neuropathic pain, while pain that is present more than three dermatomes below the level of injury is classified as below-level neuropathic pain.…”

Treatment with albumin-hydroxyoleic acid complex restores sensorimotor function in rats with spinal cord injury: Efficacy and gene expression regulation

“…SCI involves several changes in sensorimotor function below the injury level, including varying degrees of paralysis, and the development of debilitating symptoms and spasticity [ 22 – 26 ]. In addition, spinal injury can cause changes in pain processing, some of which are generated by local pathophysiological mechanisms [ 27 – 30 ]. Taken together these symptoms interfere with successful rehabilitation of residual voluntary motor function following incomplete spinal cord injury [ 31 ] and lead to lower quality of life [ 25 , 27 – 32 ].…”

A preclinical model of hyperalgesia following spinal stenosis/compression

“…Injury to the grey matter establishes abnormal spontaneous activity, hypersensitivity to afferent input among surviving spinal neurons near the injury (Hao et al., ; Yezierski and Park, ; Drew et al., ), and abnormal sympathetic activation (Vierck et al., ). Late development of hyperalgesia and chronic pain appears to be predisposed particularly by a combination of increased neuronal excitability at the site of injury plus interruption of the spinothalamic tract (Vierck and Light, ; Finnerup et al., 2003a,b; Siddall et al., ; Gomez‐Soriano et al., ; Zeilig et al., ).…”