Spinothalamic Lesion Research Articles

Cold-evoked potentials in clinical practice: A head-to-head contrast with laser-evoked responses.

Innocuous cooling of the skin activates cold-specific Aδ fibres, and hence, the recording of cold-evoked potentials (CEPs) may improve the objective assessment of human thermo-nociceptive function. While the feasibility of CEP recordings in healthy humans has been reported, their reliability and diagnostic use in clinical conditions have not been documented. Here, we report the results of CEP recordings in 60 consecutive patients with suspected neuropathic pain, compared with laser-evoked potentials (LEPs) which are the gold standard for thermo-algesic instrumental assessment. CEP recording was a well-tolerated procedure, with only ~15 min of surplus in exam duration. The reproducibility and signal-to-noise ratio of CEPs were lower than those of LEPs, in particular for distal lower limbs (LLs). While laser responses were interpretable in all patients, CEPs interpretation was inconclusive in 5/60 because of artefacts or lack of response on the unaffected side. Both techniques yielded concordant results in 73% of the patients. In 12 patients, CEPs yielded abnormal values while LEPs remained within normal limits; 3 of these patients had clinical symptoms limited to cold sensations, including cold-heat transformation. CEPs appear as a useful technique for exploring pain/temperature systems. Advantages are low cost of equipment and innocuity. Disadvantages are low signal-to-noise ratio for LL stimulation, and sensitivity to fatigue/habituation. Joint recording of CEPs and LEPs can increase the sensitivity of neurophysiological techniques to thin fibre- spinothalamic lesions, in particular, when abnormalities of cold perception predominate. Recording of cold-evoked potentials is a well-tolerated, inexpensive and easy-to-use procedure that can be helpful in the diagnosis of abnormalities in the thin fibre- spinothalamic pathways. Supplementing LEPs with CEPs allows consolidating the diagnosis and, for some patients suffering from symptoms limited only to cold, CEPs but not LEPs may allow the diagnosis of thin fibre pathology. Optimal CEP recording conditions are important to overcome the low signal-to-noise ratio and habituation phenomena, which are less favourable than with LEPs.

Do we activate specifically somatosensory thin fibres with the concentric planar electrode? A scalp and intracranial EEG study

Laser-evoked potentials (LEPs) are acknowledged as the most reliable laboratory tool for assessing thermal and pain pathways. Electrical stimulation with a newly developed planar concentric electrode, delivering stimuli limited to the superficial skin layers, has been suggested to provide selective activation of Aδ fibres without the inconveniences linked to laser stimulation. The aim of our study was to compare the scalp and intracranial responses to planar concentric electrode stimulation (CE-SEPs) with those of LEPs and standard somatosensory-evoked potentials (SEPs). Sixteen healthy subjects, 6 patients with intracortical electrodes, and 2 patients with selective lesions of the spinothalamic pathway were submitted to Neodymium:Yttrium-Aluminium-Perovskite laser stimulations, and electrical stimulations using standard electrodes or planar concentric electrodes (CE). In both healthy controls and epileptic implanted patients, CE- and standard SEPs showed significantly shorter latencies than LEPs. This is consistent with Aβ-fibre activation, peripheral activation time being unable to account for longer LEP latencies. In the patients with spinothalamic lesions, LEPs were absent after stimulation of the affected territory, while CE-SEPs were still present. For these 2 reasons, we conclude that the planar CE does not selectively activate the Aδ and C fibers, but coexcites a significant proportion of large myelinated Aβ fibres that dominate the ensuing cortical response. The use of CE-SEPs for the detection of spinothalamic system lesions is therefore not warranted; the planar electrode can, however, represent a useful tool to study nociceptive reflexes, which can be reliably elicited even in the presence of Aβ coactivation.

Pain as heralding symptom in multiple sclerosis

It is becoming recognised that neuropathic pain is among the major burdens of patients affected by multiple sclerosis (MS). Neuropathic pain may be an early symptom of the disease. Well known presentations are symptomatic trigeminal neuralgia and also pseudo-radicular pain due to lesions of the dorsal entry zone. Here we report two patients with visceral pain and three patients with pseudo-radicular pain due to spinothalamic lesion (central pain) caused by MS. The diagnosis was hampered and delayed by the absence of objective signs. In four patients the only abnormal clinical finding was spinothalamic hypoaesthesia. Pain may be one of the heralding symptoms of MS. In the present series it was severe, chronic and poorly responsive to treatment. A sensory examination is mandatory in all cases of complex pain syndromes of unidentified nature.

Central poststroke pain and Wallenberg's lateral medullary infarction: frequency, character, and determinants in 63 patients.

Central poststroke pain (CPSP) is an infrequently recognized complication of lateral medullary infarction (LMI). We determined the frequency, nature, and predictors of this complication in 63 patients with LMI. The hypothesis tested was that the degree of clinical sensory loss and extent of infarction seen on MRI, both graded by a predetermined scoring scale, would be predictive of CPSP. We also performed quantitative sensory testing (QST) of thermal and pressure sensation thresholds in a subgroup of 19 patients (nine with CPSP and 10 without) to analyze in detail the spinothalamic and trigeminothalamic systems mediating these modalities from both sides of the face and body. We analyzed these results for specific markers of CPSP. CPSP developed in 25% (16/63) of the patients, all within 6 months. This was constant and severe with frequent allodynia, but responded in all cases to amitriptyline and recurred promptly on attempted weaning. CPSP affected the ipsilateral peri-orbital region most commonly, either alone or in combination with the contralateral limbs. Ipsilateral neurotrophic facial ulceration developed in two cases. CPSP correlated significantly (Fisher's exact test, p < 0.0002) with the degree of clinical sensory loss but not with the size of infarction seen on MRI (Fisher's exact test, p = 0.7). QST revealed a highly specific (100%) and sensitive (89%) finding for CPSP-thresholds from the check contralateral to the LMI were normal in eight of nine cases with CPSP and abnormal in all of the 10 cases without CPSP. Abnormalities in the face contralateral to the infarct are referable to the crossed trigeminothalamic tract in the medullary reticular formation medial to the infarcted lateral medulla. We conclude that this argues for the theory that central pain is caused by denervation sensitivity of the "paleo"-reticulothalamic connections due to a selective "neo"-spinothalamic lesion.