Sensorimotor and Pain Modulation Brain Abnormalities in Trigeminal Neuralgia: A Paroxysmal, Sensory-Triggered Neuropathic Pain

Abstract

ObjectiveIdiopathic trigeminal neuralgia (TN) is characterized by paroxysms of severe facial pain but without the major sensory loss that commonly accompanies neuropathic pain. Since neurovascular compression of the trigeminal nerve root entry zone does not fully explain the pathogenesis of TN, we determined whether there were brain gray matter abnormalities in a cohort of idiopathic TN patients. We used structural MRI to test the hypothesis that TN is associated with altered gray matter (GM) in brain areas involved in the sensory and affective aspects of pain, pain modulation, and motor function. We further determined the contribution of long-term TN on GM plasticity.MethodsCortical thickness and subcortical GM volume were measured from high-resolution 3T T1-weighted MRI scans in 24 patients with right-sided TN and 24 healthy control participants.ResultsTN patients had increased GM volume in the sensory thalamus, amygdala, periaqueductal gray, and basal ganglia (putamen, caudate, nucleus accumbens) compared to healthy controls. The patients also had greater cortical thickness in the contralateral primary somatosensory cortex and frontal pole compared to controls. In contrast, patients had thinner cortex in the pregenual anterior cingulate cortex, the insula and the orbitofrontal cortex. No relationship was observed between GM abnormalities and TN pain duration.ConclusionsTN is associated with GM abnormalities in areas involved in pain perception, pain modulation and motor function. These findings may reflect increased nociceptive input to the brain, an impaired descending modulation system that does not adequately inhibit pain, and increased motor output to control facial movements to limit pain attacks.

Thickening of the somatosensory cortex in migraine without aura

“…First, a number of activation studies using positron emission tomography and functional MRI have highlighted the role of brainstem structure, not the SSC, in the generation of migraine headache, indicating the brainstem as the key region specific to migraine (1). Second, it is noteworthy that such thickening of the SSC has also been observed in other forms of chronic pain disorders, including trigeminal neuralgia (34), temporomandibular disorder (35) and chronic low back pain (36). Moreover, a significant positive correlation was found between the SSC thickness and disease duration in patients with cluster headache, a distinct headache syndrome from migraine (37).…”

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

“…Neuroplastic changes in the grey matter have been reported in patients suffering from chronic pain (Desouza et al, 2013). Sub-cortical structures such as the anterior cingulate cortex and the insular cortex are important in modulating the sensory and affective aspects of pain Xie et al, 2009).…”

Pathophysiological implication of CaV3.1 T-type Ca2+channels in trigeminal neuropathic pain

“…There is increasing evidence that TNP is associated with anatomical and biochemical changes in the thalamus (14)(15)(16). Moreover, patients with TNP display significant reductions in thalamic volume and neural viability (15), indicating that altered thalamic anatomy, physiology, and biochemistry may result in disturbed thalamocortical oscillatory properties.…”

“…Abnormal thalamic activity has been investigated in patients with neuropathic pain (3-7, 10-13, 17, 18), including TNP (14)(15)(16). Furthermore, the potential role of thalamic burst firing in abnormally increased low-frequency oscillations has been proposed as a pathophysiological mechanism (2,12).…”