Mexiletine for thalamic pain syndrome

The thalamic pain syndrome, a rare sequelae of cerebrovascular event, is a severe and disabling form of central pain which treatment remains a major clinical problem. We present our results of a preliminary open label study using mexiletine, an orally active antiarrhythmic agent, in the management of thalamic pain in 9 patients. Using a dose of 10 mg/kg/day over a 4-week period, mexiletine produced improvement in pain in 8 of the 9 patients. Mexiletine was generally well tolerated with only two patients experiencing transient nausea and dizziness. Our findings suggest that mexiletine may be a safe and effective agent in the management of thalamic pain and possibly other paroxysmal pain syndromes of central origin.     

Evoked response studies of the thalamic pain syndrome

Human and animal studies have suggested that the occurrence of thalamic pain (hyperpathia) is not simply a manifestation of a functional deficit in the major lemniscal pathway mediated through the ventral posterior (VP) thalamic nucleus. More effective relief of this pain has occurred following stereotaxic lesions of the centromedianum (CM) than after lesions restricted to VP. Median nerve stimulation has evoked abnormal contralateral somatosensory evoked responses (SER) in patients with lesions of VP. In this study the SERs evoked by contra-lateral stimulation in two patients with thalamic pain secondary to infarction were normal. These results support the hypothesis that thalamic pain can be caused by thalamic lesions sparing VP. The minor change noted in the ipsilateral SER when the abnormal hand was stimulated was consistent with a lesion involving CM or adjacent nonspecific thalamic nuclei.     

Dorsolateral thalamic infarct syndrome with therapeutically modifiable pain crises

The Controlateral Pain Flexor Reflex (CPFR) is demonstrated by a case study of a thalamic syndrome with a typical thalamic hand, thalamic foot, and thalamic pain crisis. Mechanical triggering by a painful irritation on the healthy hand side leads to a stronger motoric-nocifensic reflex response of the contralateral extremities. On the other hand the healthy person would develop an ipsilateral nocifensic response only. In the case reported here, the electrically evoked CPFR led to the same result, and simultaneously caused disappearance of the thalamic pain, since this kind of management represents therapeutical approach via the endorphin system. In respect of the pathophysiological basis of the thalamic modified nocifensic reflex response, we are inclined to believe that painful stimulation evokes an accentuated flexor reaction if the thalamic-controlled influences are omitted by a lesion of the specific nuclei.     

Rapid relief of thalamic pain syndrome induced by vestibular caloric stimulation

Central post-stroke pain syndrome develops in a minority of patients following a stroke. The most usual causative lesion involves the lateral thalamus. The classic presentation is of severe, unrelenting pain that involves the entire contralateral half of the body. It is largely refractory to current treatments. We found that in two patients with this condition their pain was substantially improved by vestibular caloric stimulation, whereas placebo procedures had no effect. We proposed that this is because vestibular stimulation activates the posterior insula, which in turn inhibits the generation of pain in the anterior cingulate.     

Central pain from cerebral abscess: thalamic syndrome in AIDS patients with toxoplasmosis.

We describe two patients with acquired immunodeficiency syndrome (AIDS) who developed classic thalamic syndrome (TS) due to Toxoplasma abscesses in the thalamic region. Treatment with amitriptyline provided substantial relief in both patients. Postmortem examination in one case revealed a lesion in the internal capsule and thalamic reticular nucleus. These observations indicate that (1) TS can result from an isolated lesion in the internal capsule and reticular nucleus of the thalamus, (2) cerebral abscess can cause classic TS, (3) central pain can be added to the many pain syndromes that afflict AIDS patients, and (4) an analgesic response to amitriptyline is possible in these patients.     

Cheiro-oral-pedal syndrome in thalamic infarction

Sensory disturbance around the corner of the mouth, in the palm of the hand and in the foot on the same side (cheiro-oral-pedal syndrome) has been reported only in 2 patients with brainstem lesion. We report 2 cases of cheiro-oral-pedal syndrome; the causative lesion was revealed by magnetic resonance imaging to be in the ventral posterolateral and ventral posteromedial nuclei of the thalamus.     

Stereotactic mesencephalic tractotomy for thalamic pain

Forty years after its first reported use, stereotactic mesencephalic tractotomy remains effective in relieving thalamic pain. Twenty seven patients suffering central pain following cerebrovascular accidents were treated by this operation and twenty four were reviewed: sixteen (66.7%) reported long term relief. Fourteen underwent surgery at the original 'superior colliculus' target, nine out of twelve (75%) reporting significant relief. Thirteen had surgery at a revised 'inferior colliculus' target, seven out of twelve (58.3%) obtaining relief. Postoperative disorders of ocular movement were reduced from 83.3% to 20%, and significant problems of binocular vision from 50% to nil. The mortality rate was 7.4%.     

Brain glucose metabolism in thalamic syndrome.

Regional brain glucose metabolism was studied in a case of postischaemic thalamic syndrome. Despite a normal density of the thalamus on MRI and CT images, a 17% relative hypometabolism was found in the posterior thalamus on the affected side. This observation of functional anomalies in the posterior thalamic complex in case of thalamic syndrome is compatible with a deregulated processing of pain-related information at this level.     

Reversibility of Parinaud syndrome in thalamic hemorrhage

Parinaud syndrome, associated with a left thalamic hemorrhage, disappeared completely in a 57-year-old woman after ventriculoperitoneal shunt. The syndrome may be attributed to increased intracranial pressure owing to mass effect on the pretectal region and tectum, or to tightness in the incisura causing hydrocephalus secondary to aqueduct compression. The lesions responsible for the syndrome may not be irreversible.     

The syndrome of posterior thalamic hemorrhage

In six patients with CT evidence of posterior thalamic hemorrhage, we found the following signs: saccadic hypometria away from the lesion; defective pursuit toward the lesion with corresponding opticokinetic abnormalities; mild ipsilateral ptosis; ipsilateral miosis; unilateral sensory neglect; and sensorimotor hemiparesis. This distinct syndrome has a benign course and satisfactory recovery. It differs from the classic picture of thalamic hemorrhage, and can be called "the syndrome of posterior thalamic hemorrhage."     

Altered mesolimbocortical and thalamic dopamine in Tourette syndrome

We used [F-18]fallypride PET in six adults with Tourette syndrome and age-matched controls to assess extrastriatal dopamine 2 (D2) receptors. D2 receptor availability was significantly lower in the orbitofrontal cortex, primary motor cortex, anterior cingulate gyrus, mediodorsal nucleus of thalamus, and hippocampus, areas important for motivation and reward, sensory gating, movement, and attention. Altered dopaminergic function in mesolimbocortical systems and thalamus may contribute to increased motivational salience of tics.     

Plasmatic beta-endorphin levels and thalamic surgery for pain

Plasma beta-endorphin levels were found to be significantly lower in patients suffering from chronic pain of malignant etiology than in a control group. After a bilateral stereotactic cryothalamotomy in Centrum Medianum and Parafascicularis nuclei, a good clinical result and a significant increase in plasma beta-endorphin levels were obtained.