Abolished laser-evoked potentials and normal blink reflex in midlateral medullary infarction

Abstract

IntroductionThe clinical diagnosis of Wallenberg's syndrome is based on classical features such as loss of pain and temperature sensation on the ipsilateral face and contralateral body and limbs, ipsilateral Horner's sign, dysphagia, dysphonia, gait ataxia, and nystagmus [26]. The variability of the clinical pattern, however, is much greater than was initially described [4,14,21] due to the variable arterial supply of the affected region [6,7].We investigated laser-evoked (LEP) and electrically evoked somatosensory (SSEP) potentials, magnetically evoked potentials (MEP), and the blink reflex and examined the correlation between lesion topography and brainstem function in two patients with dissociated hemianalgesia and a sensory level on the contralateral side due to ventrolateral medullary infarction. Material and methodsLaser-evoked potentials Painful stimuli were generated by an infrared thulium laser (wavelength = 2.01 µm, energy 540 mJ for the hand and 600 mJ for the foot; duration 3 ms; diameter 5 mm beam). Perception and pain thresholds were determined by the method of limits using three ascending and descending energy series. LEP after stimulation of two skin Abstract We investigated two patients presenting with the rare finding of almost isolated hemianalgesia with a sensory level on the contralateral side sparing the face. Clinical findings, electrophysiological studies (absent laser-evoked pain-related somatosensory potentials, normal electrically evoked somatosensory potentials, magnetically evoked potentials, and blink reflexes), and magnetic resonance imaging showed the ventrolateral medullar tegmentum containing the spinothalamic tract to be affected by lacunar infarction. The blink reflex R2 component was unimpaired in both patients.

Brain-evoked potentials as a tool for diagnosing neuropathic pain

“…Laser-evoked potentials have proved useful in the functional assessment of the nociceptive system in clinical conditions characterized by hypalgesia, such as syringomyelia [80,81] and Wallenberg's syndrome [82,83]. It is reasonable that when there is damage of the nociceptive pathways leading to a reduction of the pain perception, the brain responses generated by nociceptive inputs are abnormally modified (delayed in latency and/or reduced in amplitude or even absent).…”

“…In Wallenberg's syndrome, LEPs are abnormal (either absent, reduced in amplitude, or delayed in latency) in response to stimulation of the affected side, in spite of normal SEPs and blink reflex recording [64], and in the brainstem lacunar infarctions LEPs sometimes represent the only objective instrumental tool for documenting the lesion [82,108].…”

Neurophysiological studies of pain pathways in peripheral and central nervous system disorders

“…In patients with lacunar infarctions in the ventrolateral medullary tegmentum that spare the spinal trigeminal tract and nucleus (Fig. 4), impaired LEPs sometimes are the only objective functional sign for the lesion of the spinothalamic tract [90].…”

“…Laser evoked potentials were normal on the unaffected right hand and grossly deformed on the hypoalgesic left hand. From Urban [90], with permission tains some nociceptive neurons [42], cortical lesions most often do not change pain sensitivity. There is some evidence that lesions in the fronto-parietal operculum may be associated with a reduced pain sensitivity [27].…”

Abnormal sudomotor skin responses to temperature and pain stimuli in syringomyelia

“…The fact that similar results were obtained from the evaluation of LEPs and laser-induced SSR in all patients locates the dysfunction in the thermoalgesic tract at a point before it activates the sudomotor sympathetic reflex circuits. The circuit of laser-induced SSR is thought to begin in the activated pain receptors, follow the Ad and C fibers travelling in the peripheral nerves, enter the spinal cord by the dorsal root, cross the midline near the anterior white commissure, and ascend towards the central nervous system by way of the spinothalamic, spino-reticular, spino-mesencephalic and other ascending tracts [23,26,29]. The lesion in syringomyelia usually begins at the central canal and extends into the commissures and the grey substance, probably damaging the spinothalamic tract at that level.…”