Altered somatosensory processing in trigeminal neuralgia

Abstract

Trigeminal neuralgia (TN) is a pain state characterized by intermittent unilateral pain attacks in one or several facial areas innervated by the trigeminal nerve. The somatosensory cortex is heavily involved in the perception of sensory features of pain, but it is also the primary target for thalamic input of nonpainful somatosensory information. Thus, pain and somatosensory processing are accomplished in overlapping cortical structures raising the question whether pain states are associated with alteration of somatosensory function itself. To test this hypothesis, we used functional magnetic resonance imaging to assess activation of primary (SI) and secondary (SII) somatosensory cortices upon nonpainful tactile stimulation of lips and fingers in 18 patients with TN and 10 patients with TN relieved from pain after successful neurosurgical intervention in comparison with 13 healthy subjects. We found that SI and SII activations in patients did neither depend on the affected side of TN nor differ between operated and nonoperated patients. However, SI and SII activations, but not thalamic activations, were significantly reduced in patients as compared to controls. These differences were most prominent for finger stimulation, an area not associated with TN. For lip stimulation SI and SII activations were reduced in patients with TN on the contra- but not on the ipsilateral side to the stimulus. These findings suggest a general reduction of SI and SII processing in patients with TN, indicating a long-term modulation of somatosensory function and pointing to an attempt of cortical adaptation to potentially painful stimuli.

Quantitative sensory testing in classical trigeminal neuralgia—a blinded study in patients with and without concomitant persistent pain

“…However, Geber et al 8 only found a weak correlation between the degree of hypoesthesia and pain intensity or duration, but supported the hypothesis of pain-induced central plasticity rather than acute nociceptive stimulation as an underlying mechanism, supported by similar findings in a TN study. 4 Additionally, TN patients with subclinical hypoesthesia on the asymptomatic side reported higher mean pain intensity ratings compared with the group with none, supporting the hypothesis of pain-induced hypoesthesia.…”

Cortical processing of facial tactile stimuli in temporomandibular disorder as revealed by magnetoencephalography

“…Several functional neuroimaging studies have been performed to investigate cortical function in patients suVering from orofacial pain, including positron emission tomography (PET) (Derbyshire et al 1994;Hagelberg et al 2003;Kupers et al 2000Kupers et al , 2004 and functional magnetic resonance imaging (fMRI) Blatow et al 2009;Borsook et al 2003;DaSilva et al 2007DaSilva et al , 2008de Leeuw et al 2005de Leeuw et al , 2006Jantsch et al 2005;Jiang et al 2006;Morelli et al 2008;Nash et al 2007). It has been found that SI and SII participate in the perception of sensory features of pain, together with other cortical areas (Apkarian et al 2005;Bushnell et al 1999).…”

“…In contrast, the perigenual cingulate cortex showed signiWcantly decreased signal intensity (Nash et al 2007). Blatow et al (2009) tested whether pain is associated with an alteration in somatosensory function in patients with trigeminal neuralgia (TN) using fMRI. A tactile non-painful stimulus was delivered in the lips and Wngers.…”

“…With respect to lip stimulation, SI and SII showed a reduced activation on the contralateral but not on the ipsilateral side to the stimulus application. This reduced activation probably reXects reduced neural processing, due perhaps to long-term adaptation to painful stimuli (Blatow et al 2009). Jiang et al (2006) compared the brain activation patterns after evoked clenching, among three groups of subjects, namely patients with atypical facial pain, patients who had occlusal treatment for synovitis pain of temporomandibular disorder (TMD), and normal subjects.…”

Reorganization in Secondary Somatosensory Cortex in Chronic Low Back Pain Patients

“…The ROI analysis for S1 comprised the probability maps in the medial portion of the hemispheric central region, including the mesial wall and the subareas BA3a, BA3b, BA1, and BA2, as described in the study by Eickhoff et al, 13 and for S2 in the parietal opercular region (OP) covering the subregions OP1, OP2, OP3, and OP4. [13][14][15] Statistical map threshold was set at P <0.05 and corrected for multiple comparisons (family-wise error correction, FWE). Estimation of statistical power was not possible due to a lack of prior data.…”