In a case of long lasting severe neglect resulting from a large right parieto-temporo-occipital infarct, vestibular stimulation produced a temporary reduction of the motor deficit and disappearance of the somatoparaphrenic delusion, in addition to the already reported improvement of extrapersonal and personal neglect and anosognosia. These data open new perspectives in the understanding of the neglect syndrome and of functional involvement of the parietal lobe in space representation.
A 48 year old woman developed an acute vestibular syndrome associated with upside down vision a few hours after minor cervical trauma. Magnetic resonance imaging showed an ischaemic lesion in the territory of the medial branch of the posterior inferior cerebellar artery. An arteriogram showed a dissection of the left extracranial vertebral artery.Since the advent of CT small cerebellar strokes are known to present as isolated vestibular, syndromes."5 The pathophysiology of these labyrinthine-like syndromes has recently been clarified from the results ofmagnetic resonance imaging (MRI) and pathological studies.'7 In most cases they result from infarction associated with the medial branch of the posterior inferior cerebellar artery.67 We report a case of such a stroke due to dissection of a vertebral artery after a closed head injury.
Nociceptive flexion reflexes (RIII response) of the lower limbs were recorded after unilateral cervico-thoracic anterolateral cordotomy (ALC) in 7 patients. Pre-operative recordings were also obtained in 1 patient and follow-up observations in 3 patients. Flexion reflexes ipsilateral to cordotomy remained normal after surgery. Conversely, responses contralateral to the cordotomy exhibited two consistent postoperative changes: first, the RIII reflex was always dissociated from subjective pain, i.e., it appeared in the absence of any pain sensation, and, second, the RIII was depressed in the limb contralateral to ALC in 5 of 7 patients. RIII attenuation ranged from slight reduction to total abolition, and proved to be reversible in 2 of 3 patients tested during the follow-up. The reappearance of withdrawal reflexes was never accompanied by a recovery of pain sensation in the stimulated limb. We conclude that the dissociation between flexion reflexes and pain sensation, which was evidenced even in case of depressed RIII responses, should be attributable to the surgical lesion of spinothalamic fibers. Dissociation between RIII and subjective pain is a landmark indicating a lesion of the spinothalamic fibers, and may be used for the clinical assessment of spinothalamic dysfunction. Conversely, RIII depression after ALC does not depend upon the surgical lesion to the spinothalamic axons, but may be secondary to interruption of ascending spinoreticular fibers in the anterolateral quadrant, and/or of descending excitatory axons in the ventral cord.
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