Central pain syndrome: elucidation of genesis and treatment.

Central pain (CP), namely, pain or allied symptoms that follow damage to the CNS, has remained an obscure neurological syndrome with no explanation or effective treatment since Edinger's description in 1891. Once believed to be rare, CP is now known to affect several millions of people worldwide, making it at least as frequent as, for example, Parkinson's disease. It follows such common entities as stroke, spinal cord injury and multiple sclerosis, but also many other conditions, including neurosurgical procedures on the brain and spine. A disturbance of thalamocortical transmission is now acknowledged to be the main engine of CP. When drugs fail, neuromodulation, both electrical and chemical, provide relief to many drug nonresponders. A small stereotactic lesion deep in the subparietal white matter promises complete relief, without the ravages of neuroablation as performed widely in the past.

Extradural cortical stimulation for central pain.

Central pain results from a central nervous system injury and represents a challenge for the pain therapist. Human studies have shown that motor cortex stimulation (MCS), i.e. the placement of a stimulating plate on the dura overlying the motor cortex can relieve brain central pain. Studies suggest that MCS directly affects activity in the first and second order somatosensory areas, thalamic nuclei and also inhibits spinal primary afferents and spinothalamic tract neurons. The following factors have been found to predict analgesia by MCS: intact or almost intact corticospinal motor function, mild or negligible sensory loss, absence of thermal sensory threshold alteration within the painful area, positive response to the barbiturate and/or ketamine test, positive response to the propofol test, positive response to transcranial magnetic stimulation (TMS). The targeting of the cortical area is made by anatomical localization by computed tomography (CT), magnetic resonance imaging (MRI), neuronavigation, intraoperative neurophysiological recordings, functional MRI (fMRI), and intraoperative clinical assessment. We perform the procedure under local anaesthesia. We describe in detail our surgical technique and stimulation protocol. Furthermore, we review the most important studies with respect to their results, the observed side effects and complications. The future prospects and likely developments of MCS for central pain are also discussed.

Extradural cortical stimulation for movement disorders.

Extradural cortical stimulation is a recent addition to the armamentarium of operative neuromodulation. Motor cortex stimulation (MCS) is offered by positioning a stimulating plate extradurally on the primary motor cortex. It is a minimally invasive technique that was originally proposed for the control of central neuropathic pain. Currently, its use has been extended to patients with movement disorders. The need for minimally invasive therapies, with low morbidity-mortality which can be applied to patients who are excluded from deep brain stimulation (DBS), led to the first attempt of MCS in Parkinson's disease (PD). Following the demonstration that transcranial magnetic stimulation (TMS) is beneficial in PD, we attempted direct extradural MCS on patients with advanced PD not meeting the criteria for DBS. The mechanisms of action may include "hyperdirect" motor cortex-subthalamic nucleus (MI-STN) input, inhibition, resynchronisation, plasticity changes, interhemispheric transfer of inhibition/excitation and modulation of other cortical areas. In this article, we review the mechanism of action of MCS in movement disorders, the predictive factors of MCS efficacy in PD, the indications, particularly in the elderly who are not suitable for DBS, the adverse effects, and the technique for localization of the central sulcus and for performing the procedure. The future prospects and developments are also discussed.

Intravenous subhypnotic propofol in central pain: a double-blind, placebo-controlled, crossover study.

OBJECTIVE: To validate IV subhypnotic propofol, a gamma-aminobutyric acid A (GABA-A) agonist, as a diagnostic test for central pain. METHODS: The efficacy of systemic propofol (0.2 mg/kg IV bolus) was evaluated in a double-blind, placebo-controlled and crossover fashion on both spontaneous ongoing pain and allodynia in 44 patients with chronic central pain of both brain and cord origin. RESULTS: Propofol was significantly superior to the placebo (Intralipid, Kabi Pharmacia) in reducing the intensity of spontaneous ongoing pain for up to 1 hour after the injection: 24 of 44 patients (55%) receiving propofol showed a significant reduction in spontaneous pain, whereas only 6 patients showed this after the placebo. Propofol also significantly reduced the intensity of both mechanical and cold allodynia. In a few cases, only the evoked components were abolished but not the spontaneous pain. In general, the side effects were minimal and consisted mainly of transitory burning upon injection of both propofol and placebo and slight lightheadedness in a few cases. CONCLUSIONS: Systemic propofol induces analgesic effects on all studied components of central pain and highlights the key role of GABA modulation in central pain.

Low-rate repetitive TMS allays central pain.

Only about 50% of central pain patients respond to motor cortex stimulation in the long run. There is a need for prognostic factors. Here we show that propofol test and TMS both predict short-term effect in nine patients with central pain. This may help reduce the number of failures.

Neuromodulation for central pain.

Central pain, which follows brain and spinal cord injury remains an ill-treated entity affecting approximately 1-2 million people worldwide. When oral drugs fail, either immediately or in the long run, the only therapeutic option is neuromodulation, via either electrical or chemical means. The whole spectrum of neuromodulatory techniques for central pain is poorly appreciated by pain therapists. Results of all these techniques provide rational guidelines for the treating physician and are detailed in this review. Reviewed techniques include cortical, deep brain and spinal cord stimulation, transcutaneous electrical nerve stimulation, electroconvulsion, and pump infusion of intrathecal drugs.

The important role of pain in neurorehabilitation. The neurosurgeon's approach or (neurorehabilitation: the neurosurgeon's role with special emphasis on pain and spasticity).

Pain syndromes due to peripheral or central nervous system damage, or both, may hinder neurorehabilitation. Control of pain may be obtained by ablative or augmentative procedures. Of the ablative modes only DREZ and Cordectomy are still being employed in cases of pain due to Brachial Plexus Avulsion and conus and cauda damage at T9-L1: in both pain is not simply due to "deafferentiation". The augmentative procedures include spinal cord, deep brain and cortical stimulation. Subarachnoid infusion of drugs (midazolam, clonidine, baclofen, etc.) is a new avenue open to control pain. Indications, results and mechanisms of action of those procedures in neuropathic pain are discussed on the basis of literature and personal experience.

Transcranial magnetic cortical stimulation relieves central pain.

Extradural cortical stimulation for neurogenic pain is a recent addition to the field of functional neurosurgery. About 50% of patients with central pain draw benefit in the long run. However, there is an urgent need for prognostic factors in order to cut the costs of the procedure. In this paper we report a statistically significant correlation between the subhypnotic propofol test, transcranial magnetic cortical stimulation (TMS) and the actual short-term outcome of extradural cortical stimulation in 9 patients. The propofol test and TMS appear to predict short-term effects of extradural cortical stimulation.

Reversible central pain.

We report two cases of central pain which receded completely after treatment of the inciting lesion. These cases highlight the intrinsic reversibility of central pain and the focal nature of central pain mechanisms.

Disappearance of central pain following iatrogenic stroke.

An exceptional case of long-standing central pain temporarily relieved by a focal stroke in the primary somatosensory area is reported. This case highlights the focal nature of central pain mechanisms and the possible value of selective subparietal leukotomies in the management of central pain.

Peri- and postoperative pain valutation in carpal tunnel release of median nerve compression.

We analysed 108 patients, operated on day surgery, for carpal tunnel release of median nerve compression, to evaluate peri- and postoperative pain. We made in all cases a short intertenarian incision (25 mm) with microsurgical technique and local anaesthesia using mepivacaine 2% without vasoconstrictor. We evaluated pain for local anaesthetic infiltration as VRS (Verbal Rating Scale) 6,3 median-time to the first possible analgesic assumption (in all cases paracetamol 500 mg), total analgesic assumption, pressure algometry (to evaluate "allodiny") after the first 48 hours and subjective pain intensity by a numerical pain scale. Pain intensity on first drug assumption (after a mean time of 7 hours from the end of surgery) had a mean VAS value of 2,15; while after a second assumption of analgesic (after a mean time of 15 hours from surgery) had a mean VAS value of 2. Mean total analgesic assumption was 1,64 tablets of paracetamol 500 mg. From these data we may deduce that peri- and postoperative pain following median nerve decompression with this technique and anaesthesia, has a moderate intense peak of brief duration, for local anaesthetic infiltration (that seems to be the most painful event) and modest and not constant pain in the postoperative time (more evident 7 and 15 hours from the end of surgery). It may be useful association with mepivacaine bicarbonate solutions or injecting less painful local anaesthetic.

Painful supernumerary phantom arm following motor cortex stimulation for central poststroke pain. Case report.

In this report, the authors describe a case in which the patient began to experience a supernumerary phantom arm after she received motor cortex stimulation for central pain. The patient had a history of right thalamocapsular stroke. It is speculated that the motor cortex activation triggered a response in the patient's parietal lobe, precipitating perception of the phantom limb. To the authors' knowledge this is the first reported case of its kind.