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Background: Patients presenting with bilateral trigeminal hypoesthesia may go on to have trigeminal isolated sensory neuropathy, a benign, purely trigeminal neuropathy, or facial-onset sensory motor neuronopathy (FOSMN), a malignant life-threatening condition. No diagnostic criteria can yet differentiate the two conditions at their onset. Nor is it clear whether the two diseases are distinct entities or share common pathophysiological mechanisms., Methods: Seeking pathophysiological and diagnostic information to distinguish these two conditions at their onset, in this neurophysiological and morphometric study we neurophysiologically assessed function in myelinated and unmyelinated fibres and histologically examined supraorbital nerve biopsy specimens with optic and electron microscopy in 13 consecutive patients with recent onset trigeminal hypoesthesia and pain., Results: The disease course distinctly differed in the 13 patients. During a mean 10 year follow-up whereas in eight patients the disease remained relatively stable, in the other five it progressed to possibly life-threatening motor disturbances and extra-trigeminal spread. From two to six years elapsed between the first sensory symptoms and the onset of motor disorders. In patients with trigeminal isolated sensory neuropathy (TISN) and in those with FOSMN neurophysiological and histological examination documented a neuronopathy manifesting with trigeminal nerve damage selectively affecting myelinated fibres, but sparing the Ia-fibre-mediated proprioceptive reflex., Conclusions: Although no clinical diagnostic criteria can distinguish the two conditions at onset, neurophysiological and nerve-biopsy findings specify that in both disorders trigeminal nerve damage manifests as a dissociated neuronopathy affecting myelinated and sparing unmyelinated fibres, thus suggesting similar pathophysiological mechanisms.

Objective: To assess whether pain in the anterior-lateral part of the thigh in women affected by endometriosis is due to femoral nerve invasion by endometriotic implants., Design: Case-control study., Setting: Hospital., Patient(s): We enrolled 30 patients with endometriosis and leg pain in the anterior-lateral part of the thigh and 30 healthy women., Intervention(s): Skin biopsy and neurologic examination for detection of neuropathy., Main Outcome Measure(s): Intraepidermal small fiber density reduction and positive neurologic examination agree with sensitive neuropathy., Result(s): Biopsy results showed no statistically significant difference between the case group and the control group. At neurologic examination nine patients in the study group (30%) showed positive results, none in the control group showed signs. These nine patients had reduced intraepidermal small fiber density, compared to the lower cutoff values of the control group, suggesting a sensitive neuropathy., Conclusion(s): When there is leg pain in women with endometriosis it is important to distinguish neuropathic from referred pain. Skin biopsy and neurologic examination should be introduced in the management of leg pain in endometriosis, due to their low invasiveness to diagnose a sensitive neuropathy. As a result early detection of nerve injury and planning for a prompt specific treatment would be possible., (Copyright © 2013 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.)

Neuropathic pain, i.e. pain arising as a direct consequence of a lesion or disease of the somatosensory system, affects about the 7 % of the general population. In this short review, we describe the most reliable laboratory tools for assessing neuropathic pain, such as quantitative sensory testing, laser-evoked potential recordings and skin biopsy, procedures that selectively assess nociceptive pathways.

Objective To investigate the cutaneous silent period (CSP), a spinal inhibitory reflex mainly mediated by A-delta fibres, in demyelinating and axonal polyneuropathy (PNP) and evaluate whether CSP parameters differ between patients with and without neuropathic pain. Methods Eighty-four patients with demyelinating PNP, 178 patients with axonal PNP and 265 controls underwent clinical examination, DN4 questionnaire, standard nerve conduction study, motor-root stimulation and CSP recordings from abductor digiti minimi. We calculated the afferent conduction time of CSP (a-CSP time) with the formula: CSP latency − root motor evoked potential latency. Results In the demyelinating PNP group the a-CSP time was significantly longer; in the axonal PNP group, CSP duration was shorter than the demyelinating group ( p = 0.010) and controls ( p = 0.001). CSP parameters were not different between patients with and without neuropathic pain. Conclusions The abnormality of a-CSP time in the demyelinating PNP group suggests the crucial role of A-delta fibres in the mechanism of CSP; the shorter CSP duration in the axonal PNP group supports the strong influence of the number of axons on this parameter. Our study suggests that neuropathic pain could be related to pathophysiological mechanisms differing from mere A-delta fibre loss. Significance CSP evaluation is effective in detecting A-delta fibre dysfunction in axonal as well as demyelinating PNP. [ABSTRACT FROM AUTHOR]

Abstract: In this clinical and neurophysiological study, we examined the clinical characteristics and underlying mechanisms of neuropathic pain related to multiple sclerosis. A total of 302 consecutive patients with multiple sclerosis were screened for neuropathic pain by clinical examination and the DN4 tool. In patients selected for having ongoing extremity pain or Lhermitte’s phenomenon, we recorded somatosensory evoked potentials, mediated by Aβ non-nociceptive fibres, and laser evoked potentials, mediated by Aδ nociceptive fibres. Of the 302 patients, 92 had pain (30%), and 42 (14%) neuropathic pain. Patients with neuropathic pain had more severe multiple sclerosis, as assessed by the expanded disability severity score, than those without pain. Whereas, in patients with ongoing neuropathic pain, laser evoked potentials were more frequently abnormal than somatosensory evoked potentials, we found the opposite in patients with Lhermitte’s phenomenon. Our data underline the clinical importance of pain in multiple sclerosis and indicate that a more severe disease is associated with a higher risk of developing neuropathic pain. The prevalence of pain that we found, which was lower than that reported in previous studies, may reflect the lesser disease severity in our patients. Neurophysiological data show that whereas ongoing extremity pain is associated with spinothalamic pathway damage, Lhermitte’s phenomenon is related to damage of non-nociceptive pathways. These findings may be useful in designing a new therapeutic approach to neuropathic pain related to multiple sclerosis. [Copyright &y& Elsevier]