Spatial Normalization and Regional Assessment of Cord Atrophy: Voxel-Based Analysis of Cervical Cord 3D T1-Weighted Images

Valsasina, Paola; Horsfield, Mark A.; Rocca, Maria A.; Absinta, Martina; Comi, Giancarlo; Filippi, Massimo

doi:10.3174/ajnr.a3139

Cited by 37 publications

(54 citation statements)

References 32 publications

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“…Consistent with our findings, animal models of neuropathic pain show nerve injury evokes neuronal degeneration in the region of recipient primary synapse (Sugimoto et al, 1990;Azkue et al, 1998;Whiteside and Munglani, 2001;de Novellis et al, 2004;Scholz et al, 2005). This neuronal degeneration is thought to result from excessive, ongoing afferent excitation (Sloviter and Damiano, 1981;Coggeshall et al, 1993), a theory supported by reports that myelinated primary afferents in nerve-injured animals discharge ectopically at high frequencies, thus providing aberrant excitatory input (Khan et al, 2002;Chaplan et al, 2003;Amir et al, 2005) that in turn is responsible for the protracted induction of neuronal loss (Coggeshall et al, 1993;Scholz et al, 2005). Furthermore, the number of neurons in superficial laminae is reduced by ϳ22% at 4 weeks after injury, including a ϳ25% loss of GABAergic inhibitory interneurons .…”

Section: Discussionsupporting

confidence: 89%

“…Although a decrease in gray matter volume may result from neuronal loss, it may also result from shrinkage or atrophy of neurons or glia or synaptic loss (May and Gaser, 2006). In addition, MD and FA are markers of more subtle changes in tissue microstructure that may result from tissue shrinkage and dense packing of myelinated fibers as a result of neurodegeneration and gliosis (Sierra et al, 2011). Consistent with our findings, animal models of neuropathic pain show nerve injury evokes neuronal degeneration in the region of recipient primary synapse (Sugimoto et al, 1990;Azkue et al, 1998;Whiteside and Munglani, 2001;de Novellis et al, 2004;Scholz et al, 2005).…”

Section: Discussionsupporting

confidence: 85%

“…In addition, MD and FA are markers of more subtle changes in tissue microstructure that may result from tissue shrinkage and dense packing of myelinated fibers as a result of neurodegeneration and gliosis (Sierra et al, 2011). Consistent with our findings, animal models of neuropathic pain show nerve injury evokes neuronal degeneration in the region of recipient primary synapse (Sugimoto et al, 1990;Azkue et al, 1998;Whiteside and Munglani, 2001;de Novellis et al, 2004;Scholz et al, 2005). This neuronal degeneration is thought to result from excessive, ongoing afferent excitation (Sloviter and Damiano, 1981;Coggeshall et al, 1993), a theory supported by reports that myelinated primary afferents in nerve-injured animals discharge ectopically at high frequencies, thus providing aberrant excitatory input (Khan et al, 2002;Chaplan et al, 2003;Amir et al, 2005) that in turn is responsible for the protracted induction of neuronal loss (Coggeshall et al, 1993;Scholz et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…This inhibitory neuron loss is likely responsible for the observed decrease in dorsal horn postsynaptic inhibition (Moore et al, 2002). Dorsal horn neuronal degeneration appears to play an important role in the establishment of chronic pain because a reduction of this neuronal loss by administration of caspase apoptosis inhibitors reduces the occurrence of neuropathic pain-like behaviors in experimental animals (Whiteside and Munglani, 2001;Scholz et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…The trigeminothalamic tract conveys noxious orofacial information from the SpV to the cerebral cortex largely via the somatosensory thalamus (Craig, 2004). Although, in animal models, loss of primary afferent neurons (substance P immunoreactive fibers) and GABAergic interneurons in the dorsal horn have been shown (de Novellis et al, 2004;Scholz et al, 2005), the fate of ascending projection neurons originating in the dorsal horn has not been specifically investigated. Despite a reported loss of ϳ22% of dorsal horn neurons, our data suggest that these are not thalamic projecting neurons.…”

Section: Discussionmentioning

confidence: 99%

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Anatomical Changes at the Level of the Primary Synapse in Neuropathic Pain: Evidence from the Spinal Trigeminal Nucleus

et al. 2015

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Accumulated evidence from experimental animal models suggests that neuronal loss within the dorsal horn is involved in the development and/or maintenance of peripheral neuropathic pain. However, to date, no study has specifically investigated whether such neuroanatomical changes also occur at this level in humans. Using brain imaging techniques, we sought to determine whether anatomical changes were present in the spinal trigeminal nucleus in subjects with chronic orofacial neuropathic pain. In 22 subjects with painful trigeminal neuropathy and 44 pain-free controls, voxel-based morphometry of T1-weighted anatomical images and diffusion tensor images were used to assess regional gray matter volume and microstructural changes within the brainstem. In addition, deterministic tractography was used to assess the integrity of ascending pain pathways. Orofacial neuropathic pain was associated with significant regional gray matter volume decreases, fractional anisotropy increases, and mean diffusivity decreases within the spinal trigeminal nucleus, specifically the subnucleus oralis. In addition, tractography revealed no significant differences in diffusivity properties in the root entry zone of the trigeminal nerve, the spinal trigeminal tract, or the ventral trigeminothalamic tracts in painful trigeminal neuropathy subjects compared with controls. These data reveal that chronic neuropathic pain in humans is associated with discrete alterations in the anatomy of the primary synapse. These neuroanatomical changes may be critical for the generation and/or maintenance of pathological pain.

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