Technique and technical problems

Adams, Joseph E.; Hosobuchi, Yasuhiro

doi:10.1097/00006123-197709000-00017

Cited by 27 publications

(8 citation statements)

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“…DBS has produced therapeutic effects in patients with pain [1,22], hemiparesis, dystonia, torticollis, tremor, speech impairment and epilep sy. The history of 6 consecutive patients will be summarised briefly.…”

Section: Clinical Resultsmentioning

confidence: 99%

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Reversibility of Chronic Neurologic Deficits. Some Effects of Electrical Stimulation of the Thalamus and Internal Capsule in Man

Cooper

Upton

Amin

1980

Stereotact Funct Neurosurg

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Stimulation of the thalamus and internal capsule with Medtronic® deep brain stimulation electrodes produced improvement in pain, hemiparesis, dystonia, torticollis, tremor, speech impairment and epilepsy. Stimulation at voltages above or below clinically effective levels (e.g., 6 V, 0.3 ms, 74 Hz) resulted in a loss of clinical efficacy. Somatosensory evoked responses (short and long latency) and depth electrode recordings were helpful in localisation and ‘biocalibration’ of electrical stimulation.

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Section: Clinical Resultsmentioning

confidence: 99%

“…The Medtronic DBS electrode [1,22] consists of platinum wires with four bare areas varying from 2.5 (deepest) to 4.6 mm2 (most superficial). We calculated that maximum charge densities were 20 nC/cmVphase, but the stimulus had ramped …”

Section: Dbs Electrodesmentioning

confidence: 99%

Reversibility of Chronic Neurologic Deficits. Some Effects of Electrical Stimulation of the Thalamus and Internal Capsule in Man

Cooper

Upton

Amin

1980

Stereotact Funct Neurosurg

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“…Previous studies have reported that stimulation‐produced analgesia could be evoked from the hypothalamus (Carstens et al,1982; Aimone et al,1988; Morgan et al,1989) and that microinjection of lidocaine into the RVM resulted in increased stimulation thresholds in the hypothalamus for inhibition of the tail flick reflex (Aimone et al,1988). In addition, it has been reported that systemic naloxone will inhibit the analgesic effect of the stimulation of the caudal hypothalamus in humans (Adams and Hosobuchi,1977). Our results provide the anatomical evidence that EM‐2 may mediate, at least in part, the analgesia produced by stimulation of the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

Endomorphin‐2‐immunoreactive fibers selectively appose serotonergic neuronal somata in the rostral ventral medial medulla

Wessendorf²

2007

J of Comparative Neurology

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The rostral portion of the ventral medial medulla (RVM) is a crucial site for the supraspinal antinociceptive actions of opioids. Previous studies have reported that serotonergic antagonists block the analgesia induced by microinjection of morphine into the RVM (Hammond and Yaksh [1984] Brain Res 298:329-337) and that spinally projecting serotonergic RVM neurons express mu-opioid receptors (MOR) (Kalyuzhny et al. [1996] J Neurosci 16:6490-6503; Wang and Wessendorf [1999] J Comp Neurol 404:183-196). In addition, axons immunoreactive for the endogenous MOR ligand endomorphin-2 (Tyr-Pro-Phe-Phe-NH2) (EM-2) have been reported to be in the RVM (Martin-Schild et al. [1999] J Comp Neurol 405:450-471; Pierce and Wessendorf [2000] J Chem Neuroanat 18:181-207). In the present study we examined the relationship of EM-2-immunoreactive (EM-2-ir) axons to serotonergic and nonserotonergic RVM neurons in rats, including neurons projecting to the dorsal spinal cord. We also examined the origins of EM-2-ir in the RVM. Using unbiased methods we estimated the total number of cells in the RVM to be 1.50 x 10(4) and of these up to 70% were retrogradely labeled from the dorsal spinal cord. EM-2-ir fibers apposed both serotonergic and nonserotonergic RVM neuronal profiles. However, serotonergic profiles were significantly more likely to be apposed than nonserotonergic profiles. Thus, although serotonergic neurons comprise a minority of RVM neurons (23% of the total RVM neurons), they appear to be selectively apposed by EM-2-ir fibers. We also found that hypothalamic EM-2-ir neurons, but not EM-2-ir neurons, in the nucleus of the solitary tract projected their axons to the RVM.

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“…Information about previous pain surgery appeared in half of the reported series [25,26,28,30,35,36,[43][44][45][48][49][50]. However, the criteria used to diagnose painful disorders were not comparable among different studies [11,20,25,26,34,36,41,49,61,62,70,81]. Only four groups of investigators defined how they diagnosed peripheral or nociceptive pain versus neuropathic or deafferentation pain [25,26,28,30,36].…”

Section: Case Selection Diagnosis and Dbs Targetsmentioning

confidence: 99%

Deep Brain Stimulation for Chronic Pain: Results of Two Multicenter Trials and a Structured Review

2001

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Objectives. A U.S. Food and Drug Administration ruling required clinical trials to evaluate the safety and efficacy of deep brain stimulation devices, thereby limiting treatment to the investigational setting. Introduction. As an investigator in two clinical trials of deep brain stimulation, I sought to determine why pain remained an unapproved indication despite regulatory approval of the same device for tremor. Methods. The results of two multicenter trials of deep brain stimulation for pain were analyzed, and the pertinent literature was reviewed using published guidelines for the evaluation of clinical trial reports. Results. The first‐generation Model 3380 lead trial enrolled 196 patients; the current Model 3387 trial enrolled 50 patients. Prospectively defined criteria for success included at least half of patients reporting 50% pain relief at 1 year. Manufacture of the Model 3380 lead was discontinued, and the 3387 trial closed early because of slow enrollment, high attrition, and low efficacy. When results were analyzed according to the study plan, neither trial was successful. Consequently, deep brain stimulation has not been approved for pain control by the U.S. Food and Drug Administration. Conclusions. Deep brain stimulation has not been shown to produce effective long‐term pain relief. Future studies of motor cortex stimulation and similar therapies will require appropriate control groups and accepted methods of data collection and analysis to support claims that predictable and reliable analgesic effects are produced in humans.

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Technique and technical problems

Cited by 27 publications

References 0 publications

Reversibility of Chronic Neurologic Deficits. Some Effects of Electrical Stimulation of the Thalamus and Internal Capsule in Man

Reversibility of Chronic Neurologic Deficits. Some Effects of Electrical Stimulation of the Thalamus and Internal Capsule in Man

Endomorphin‐2‐immunoreactive fibers selectively appose serotonergic neuronal somata in the rostral ventral medial medulla

Deep Brain Stimulation for Chronic Pain: Results of Two Multicenter Trials and a Structured Review

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