Homotopic reduction in laser-evoked potential amplitude and laser-pain rating by abdominal acupuncture.

BACKGROUND: The neural mechanism underlying the analgesic effect of acupuncture is largely unknown. We aimed at investigating the effect of abdominal acupuncture (AA) on the laser-evoked potential (LEP) amplitude and laser-pain rating to stimulation of body parts either homotopic or heterotopic to the treated acupoint. METHODS: Laser-evoked potentials were recorded from 13 healthy subjects to stimulation of the right wrist (RW), left wrist (LW) and right foot (RF). LEPs were obtained before, during and after the AA stimulation of an abdominal area corresponding to the representation of the RW. Subjective laser-pain rating was collected after each LEP recording. RESULTS: The amplitude of the N2/P2 LEP component was significantly reduced during AA and 15 min after needle removal to both RW (F = 4.14, p = .02) and LW (F = 5.48, p = .008) stimulation, while the N2/P2 amplitude to RF stimulation (F = 0.94, p = .4) remained unchanged. Laser-pain rating was reduced during AA and 15 min after needle removal only to RW stimulation (F = 5.67, p = .007). CONCLUSION: Our findings showing an AA effect on LEP components to both the ipsilateral and contralateral region homotopic to the treated area, without any LEP change to stimulation of a heterotopic region, suggest that the AA analgesia is mediated by a segmental spinal mechanism. SIGNIFICANCE: Although abdominal acupuncture has demonstrated to be effective in the reduction in laser-evoked potential (LEP) amplitude and laser-pain rating, the exact mechanism of this analgesic effect is not known. In the current study, we found that treatment of an area in the "turtle representation" of the body led to a topographical pattern of LEP amplitude inhibition that can be mediated by a segmental spinal mechanism.

Abnormality of Auditory Mismatch Negativity in Depression and Its Dependence on Stimulus Intensity.

Mismatch negativity (MMN) is thought to reveal several abnormalities of cognitive functioning. Although depression often affects cognitive functioning, previous studies concerning MMN in depressed patients provided conflicting results. In recent reports, it has been suggested that depressed patients may show abnormal auditory response to regular auditory stimuli presented with at a relatively high intensity. We thus recorded acoustic MMN in 16 drug-free patients suffering from moderate depression and in 10 healthy subjects at 2 different stimulus intensities. Differences in MMN latency and amplitude between depressed patients and healthy subjects reached the significance level only for high intensity stimulation, and they were consistent with a dysfunction of frontal MMN subcomponents in depressed patients. This finding suggests that consistent MMN abnormalities can be observed in depressed patients by using high-intensity stimulation; moreover, it supports the hypothesis of disturbances of frontal networks in depression even in early stages of disease.

Patterns of habituation and clinical fluctuations in migraine.

BACKGROUND: Habituation deficit, suggesting a deregulation of cortical excitability, represents a typical hallmark of interictal stages of migraine. We previously demonstrated that several neurophysiological markers of altered cortical excitability are significantly correlated to spontaneous clinical fluctuations of migraine. We therefore aimed at verifying whether clinical fluctuations are correlated to specific patterns of somatosensory evoked potential (SEP) habituation. METHODS: We analyzed habituation after median nerve stimulation of both high-frequency oscillations (HFOs) and N20 SEP in 25 migraine patients and 18 healthy volunteers. Subjects underwent six consecutive series of 500 stimuli. RESULTS: Migraine patients as a whole showed a significant habituation deficit of the N20 response. Moreover, spontaneously worsening patients show a clear potentiation of this wave in the last block of stimuli, whereas in spontaneously improving patients the N20 amplitude remained stable. Presynaptic HFOs were smaller in worsening patients and larger in improving ones, but they did not undergo habituation in patients as well as in healthy subjects. CONCLUSIONS: Potentiation of the N20 response in spontaneously worsening migraineurs confirms that the reduction of the thalamocortical drive plays a major role in migraine pathogenesis. Moreover, the stable pattern we observed in spontaneously improving patients suggests that compensatory mechanisms can also play an important role. The normal response to repeated stimuli of HFOs in migraineurs might indicate that, although its initial amount depends on clinical conditions, high-frequency thalamocortical drive remains stable during the stimulation and probably reflects the activity of a buffer mechanism.

Bilateral thalamic stroke transiently reduces arousals and NREM sleep instability.

The vascularization of the human thalami is supplied by many perforating arteries, which exhibit complex distribution and many possible individual variations. One rare variant is the artery of Percheron that supplies the paramedian thalami bilaterally. Its ictal occlusion may result in a symmetric paramedian infarction, which generally leads to impairment of consciousness associated with hypersomnia. Our aim is to describe in detail sleep-wake schedules, sleep structure and microstructure in a 68-year-old patient with occlusion of Percheron's artery. EEG monitoring, performed 24 h after the onset of symptoms, showed severe disruption of the sleep-wake cycle, with episodes of sleep and wakefulness recurring irregularly during day and night. Thalamic nuclei are part of the human arousal system; medial thalamic nuclei play a pivotal role in sleep regulation at different levels. A diagnosis of paramedian thalamic infarction should be considered in patients who present with recurrent episodes of unresponsiveness.

Left thalamomegaly in a patient with partial epilepsy.

Temporal lobe epilepsy (TLE) is associated with modification in thalamic structure and function. In particular, thalamic atrophy and hypometabolism can occur, affecting ipsilateral, contralateral thalami or both. We describe a 28-year-old epileptic woman, who presented peculiar neuroimaging findings, with enlargement of the thalamus contralateral to the epileptic focus. The patient was born from dystocic delivery, she presented partial motor seizures in the left side of the body, followed by generalisation, and the EEG showed a right temporal epileptic focus. Serial CT and MRI scan, performed along 11 years, showed a non-evolutive left thalamomegaly. 18-FDG PET showed reduced metabolic activity in the upper right temporal gyrus and in the ipsilateral thalamus. Thalamic asymmetry in our patient could be an occasional finding.