Gray Matter Changes Following Limb Amputation with High and Low Intensities of Phantom Limb Pain

Preißler, Sandra; Feiler, Johanna; Dietrich, Caroline; Hofmann, Gunther O.; Miltner, Wolfgang H. R.; Weiß, Thomas

doi:10.1093/cercor/bhs063

Cited by 73 publications

(79 citation statements)

References 127 publications

(162 reference statements)

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“…The left posterior cingulate (x = -16.91, y = -25.36, z = 40.01) and right insula (x = 38.7, y = 17.8, z = 7.22) coordinates were used from Preißler et al (2013) after a validated Lancaster Talairach to MNI space transform was applied. White-matter coordinates for the left and right pyramids, posterior limb of the internal capsule and insula were extracted from the ICBM-DTI-81 atlas, as done previously (Freund et al, 2011).…”

Section: Methodsmentioning

confidence: 99%

Specific brain morphometric changes in spinal cord injury with and without neuropathic pain

Mole

MacIver²,

Sluming

et al. 2014

NeuroImage: Clinical

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Why only certain patients develop debilitating pain after spinal chord injury and whether structural brain changes are implicated remain unknown. The aim of this study was to determine if patients with chronic, neuropathic below-level pain have specific cerebral changes compared to those who remain pain-free. Voxel-based morphometry of high resolution, T1-weighted images was performed on three subject groups comprising patients with pain (SCI-P, n = 18), patients without pain (SCI-N, n = 12) and age- and sex-matched controls (n = 18). The SCI-P group was first compared directly with the SCI-N group and then subsequently with controls. Overall, grey and white matter changes dependent on the presence of pain were revealed. Significant changes were found within the somatosensory cortex and also in corticospinal tracts and visual-processing areas. When the SCI-P group was directly compared with the SCI-N group, reduced grey matter volume was found in the deafferented leg area of the somatosensory cortex bilaterally. This region negatively correlated with pain intensity. Relative to controls, grey matter in this paracentral primary sensory cortex was decreased in SCI-P but conversely increased in SCI-N. When compared with controls, discrepant corticospinal tract white matter reductions were found in SCI-P and in SCI-N. In the visual cortex, SCI-N showed increased grey matter, whilst the SCI-N showed reduced white matter. In conclusion, structural changes in SCI are related to the presence and degree of below-level pain and involve but are not limited to the sensorimotor cortices. Pain-related structural plasticity may hold clinical implications for the prevention and management of refractory neuropathic pain.

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Section: Methodsmentioning

confidence: 99%

Specific brain morphometric changes in spinal cord injury with and without neuropathic pain

Mole

MacIver²,

Sluming

et al. 2014

NeuroImage: Clinical

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“…Other areas, such as the thalamus, amygdala, motor cortex, and cerebellum, etc., also showed a decrease of grey matter depending on the type of chronic pain and disability the patients have [31][32][33] . The decreased grey matter was reversible in some cases after the pain was gone or was successfully treated 28,30,34 .…”

Section: Morphological Changes In Painmentioning

confidence: 86%

Comorbidity of Depression and Pain: a review of shared contributing mechanisms

Li¹

2017

J Neurol Neuromedicine

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Pain and depression are two major health issues that we are currently facing. Chronic pain is the main reason that people seek medical care; and numerous people commit suicide each year because of depression. These two pathological conditions often coexist. Chronic pain patients are more likely to develop major depressive symptoms, while depressed patients reported more pain symptoms than normal healthy population. Understanding the common mechanisms associated with depression and pain is important for developing the effective strategy to treat this comorbidity. In this review, the potential mechanisms that contribute to both depression and pain are discussed from four perspectives, the morphological changes in the brain, monoamine deficiency, brain-derived neurotrophic factor (BDNF) reduction in the hippocampus, and the hypothalamicpituitary-adrenocortical (HPA) axis dysfunction.

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“…67 Although our analysis limited our ability to stratify pain vs no pain groups after 1 year, decreased insular volume has been shown in amputees with high intensities of phantom limb pain vs low phantom limb pain. 61 Additionally, cognitive capacity (ie, visual learning, visuospatial logic) may affect outcomes following nerve repair, which may also be associated with cortical plasticity and variability in patient outcomes. 65 There are certain limitations associated with the present study, including the small sample size and multiple statistical Red circles indicate patients that have mild/moderate pain at time 2 ($3 pain intensity score), light green circles indicate patients with low/no pain at time 2 (#1 pain intensity score), and black circles indicate patients that were not tested at follow-up.…”

Section: Discussionmentioning

confidence: 99%

A longitudinal study of pain, personality, and brain plasticity following peripheral nerve injury

Goswami

Anastakis

Katz

et al. 2016

Pain

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We do not know precisely why pain develops and becomes chronic after peripheral nerve injury (PNI), but it is likely due to biological and psychological factors. Here, we tested the hypotheses that (1) high Pain Catastrophizing Scale (PCS) scores at the time of injury and repair are associated with pain and cold sensitivity after 1-year recovery and (2) insula gray matter changes reflect the course of injury and improvements over time. Ten patients with complete median and/or ulnar nerve transections and surgical repair were tested ∼3 weeks after surgical nerve repair (time 1) and ∼1 year later for 6 of the 10 patients (time 2). Patients and 10 age-/sex-matched healthy controls completed questionnaires that assessed pain (patients) and personality and underwent quantitative sensory testing and 3T MRI to assess cortical thickness. In patients, pain intensity and neuropathic pain correlated with pain catastrophizing. Time 1 pain catastrophizing trended toward predicting cold pain thresholds at time 2, and at time 1 cortical thickness of the right insula was reduced. At time 2, chronic pain was related to the time 1 pain-PCS relationship and cold sensitivity, pain catastrophizing correlated with cold pain threshold, and insula thickness reversed to control levels. This study highlights the interplay between personality, sensory function, and pain in patients following PNI and repair. The PCS-pain association suggests that a focus on affective or negative components of pain could render patients vulnerable to chronic pain. Cold sensitivity and structural insula changes may reflect altered thermosensory or sensorimotor awareness representations.

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Gray Matter Changes Following Limb Amputation with High and Low Intensities of Phantom Limb Pain

Cited by 73 publications

References 127 publications

Specific brain morphometric changes in spinal cord injury with and without neuropathic pain

Specific brain morphometric changes in spinal cord injury with and without neuropathic pain

Comorbidity of Depression and Pain: a review of shared contributing mechanisms

A longitudinal study of pain, personality, and brain plasticity following peripheral nerve injury

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