No abstract

Analysis of the authors' experience over the last 10 years has indicated that excellent pain control has rarely been obtained by thalamic relay nucleus stimulation in patients with thalamic pain. In the present study, 11 patients with thalamic pain were treated by chronic stimulation of the precentral gyrus. In eight patients (73%), the stimulation system was internalized since excellent pain control was achieved during a 1-week test period of precentral gyrus stimulation. In contrast, no clear effect was noted or the original pain was even exacerbated by postcentral gyrus stimulation. The effect of precentral stimulation was unchanged in five patients (45%) for follow-up periods of more than 2 years. In the remaining three patients, the effect decreased gradually over several months. This outcome was significantly better than that obtained in an earlier series tested by the authors with thalamic relay nucleus stimulation (p < 0.05). The pain inhibition usually occurred at intensities below the threshold for production of muscle contraction (pulse duration 0.1 to 0.5 msec, intensity 3 to 8 V). When good pain inhibition was achieved, the patients reported a slight tingling or mild vibration sensation during stimulation projected in the same area of distribution as their pain. The authors discuss the possibility that, in deafferentation pain, sensory neurons below the level of deafferentation cannot exert their normal inhibitory influences toward deafferented nociceptive neurons because of the development of aberrant connections. Thus, while stimulation of the first- to third-order sensory neurons at the level of the thalamic relay nucleus or below cannot bring about good pain inhibition in patients with thalamic pain, activation of hypothetical fourth-order sensory neurons through precentral stimulation may be able to inhibit deafferented nociceptive neurons within the cortex. None of the patients developed either observable or electroencephalographic seizure activity.

All forms of therapy, including chronic stimulation of the thalamic relay nucleus, can provide satisfactory pain control in only 20%-30% of cases of thalamic pain syndrome. In order to develop a more effective treatment for thalamic pain syndrome, we investigated the effects of stimulation of various brain regions on the burst hyperactivity of thalamic neurons recorded in cats after deafferentiation of the spinothalamic pathway. Complete, long-term inhibition of the burst hyperactivity was induced by stimulation of the motor cortex. Based on this experimental finding, we treated seven cases of thalamic pain syndrome by chronic motor cortex stimulation employing epidural plate electrodes. Excellent or good pain control was obtained in all cases without any complications or side effects. During the stimulation, an increase in regional blood flow of the cerebral cortex and thalamus, a marked rise in temperature of the painful skin regions, and improved movements of the painful limbs were observed. These results suggest that thalamic pain syndrome can be most effectively treated by chronic motor cortex stimulation.

In an attempt to clarify the neurochemical background of central post-stroke pain and to undertake a pharmacological analysis, the basic pharmacological characteristics of this intractable pain syndrome were investigated by the morphine, thiamylal and ketamine tests. In addition, the correlation between the pharmacological characteristics and the effects of chronic motor cortex stimulation therapy was examined. The study employed 39 central post-stroke pain patients who had intractable hemibody pain associated with dysesthesias, and radiologically demonstrated lesions in the thalamic area (thalamic pain, n = 25) or suprathalamic area (suprathalamic pain, n = 14). The pharmacological evaluations showed that definite pain reduction occurred in eight of the 39 cases (20.5%) by the morphine test, in 22 of the 39 cases (56.4%) by the thiamylal test, and in 11 of 23 cases (47.8%) by the ketamine test. Based on these pharmacological assessments, there was no obvious difference between thalamic and suprathalamic pain. A comparison of the long-term follow-up results of chronic motor cortex stimulation therapy revealed that thiamylal and ketamine-sensitive and morphine-resistant cases displayed long-lasting pain reduction with chronic motor cortex stimulation therapy, whereas the remaining cases did not show good results. We conclude that pharmacological classification of central post-stroke pain by the morphine, thiamylal and ketamine tests could be useful for predicting the effects of chronic motor cortex stimulation therapy. It has recently been suggested that excitatory amino acids may be involved in the development of central post-stroke pain. However, the fact that only 23 of the present 39 cases (59.0%) of thalamic and suprathalamic pain were sensitive to the thiamylal or ketamine test reflects the complex pharmacological background and the difficulties associated with treating central post-stroke pain.

Intravascular volume expansion in the presence of excessive natriuresis requires a large sodium and water intake and is often associated with hyponatremia. Inhibition of natriuresis with fludrocortisone can effectively reduce the sodium and water intake required for hypervolemia and prevent hyponatremia at the same time.