
Animal models of dysesthesias have been established, and reveal the following major points. Dysesthesias of peripheral nerve or dorsal root origin have a central neural cause. Chronic dysesthesias of spinal origin have a cause which resides in the brain. The origins of these effects are lesions in the spinothalamic system. The causes of these effects are abnormal functionings among opiate, catecholamine, and purine pathways. Denervation supersensitivity is suggested.
Fourteen patients with secondary generalized epilepsy suffering from multiform seizures (MS) not amenable to medication were submitted to partial section of the corpus callosum. In all patients, there was a partial disruption of the previous generalized bilateral synchronous epileptiform discharges (GBSD). The electroencephalographic findings after callosal section are discussed with respect to their implications in furthering our understanding of the mechanisms subserving the organization of GBSD.
This chapter discusses the importance of reflex activity. The reflex responses of skeletal muscle to stretch are best understood because they are most easily investigated. The main stretch reflexes are negative feedback responses of two types—extension of the receptor opposes extension in one and tension of the receptor opposes tension in the other. The tendon jerk or pluck reflex is a brief short latency contraction of an abruptly stretched muscle most easily elicited from the antigravity muscles but not confined to them. The excitability of the stretch reflex arcs is modified by the balance of facilitatory and inhibitory impulses acting at the somadendritic region of their motoneurons. Proprioceptive signals from receptors in the ligaments and joints of the first three cervical vertebrae ascend and cross in the medulla oblongata to the contralateral vestibular nucleus and the medial longitudinal bundle. These signals act in combination with signals from the labyrinth to maintain ocular stability during simultaneous head and neck movements and to adjust the postural muscles to maintain the upright posture during axial rotation.
16 subjects with severe spasms secondary to traumatic and nontraumatic myelopathy underwent epidural spinal cord stimulation. 4 patients had a complete motor and sensory spinal cord lesion. 6 of the subjects with an incomplete spinal cord lesion were ambulatory. All patients had previously undergone extensive trials with medications and physical therapy. All 14 subjects in whom a satisfactory placement of the electrode could be obtained had a reduction in the severity of the spasms. In 6 patients, the spasms were almost abolished. Extremity, trunkal and abdominal spasms were affected. Clonus in the upper extremities was consistently reduced. Marked improvement in bladder and bowel function was observed in each of 2 subjects. In over 1-year follow-up, 5 subjects show persistence of the results, with less stimulation required to maintain the therapeutic effects. No neurological deterioration occurred following the procedure or after long-term spinal stimulation. 1 patient showed after several months of continuous stimulation increased voluntary motor control present only when spinal cord stimulation was activated. Complications included 1 system infection, 1 electrode migration, 1 wire breakage and skin breakdown at a connector site, development of high impedance in 1 electrode and 1 skin breakdown over the lead.
The purpose of this study was to assess the biochemical mechanisms underlying spinal cord stimulation (SCS). Seventeen patients with chronic pain were investigated by measuring cerebrospinal fluid concentrations of endogenous opioids and biogenic amines before and during dorsal column stimulation. Basal cerebrospinal fluid beta-endorphin levels were below the normal range. No significant change of norepinephrine, epinephrine, dopamine, beta-endorphin, beta-lipotropin, or adrenocorticotropic hormone levels were found after SCS. A 50% increase of cerebrospinal beta-endorphin and beta-lipotropin levels occurred in 6 out of 16 patients, namely those where SCS gave the major pain relief. These data confirm the derangement of the endogenous opioid system in chronic pain conditions and suggest that the beta-endorphin response to SCS could have clinical value in predicting the success of treatment.
The method of radiofrequency heat lesion generation is reviewed with specific reference to the dorsal root entry zone. Experimental data on the impedance of electrolytic media as a function of temperature are reported, and their relation to what should be observed during radiofrequency lesioning in the body is commented upon. The future utility of impedance monitoring is discussed as well as possible implications of bipolar lesion electrode systems.
A patient developed continuous patterned involuntary movements of abduction-adduction, flexion-extension of his right lower extremity following surgical placement of spinal dorsal root entry zone lesions for the treatment of phantom limb pain. The stereotype movements were monitored by video and electromyographic recording of quadriceps femoris and hamstring muscles. Administration of para-chlorophenylbutyric acid (baclofen) dramatically stopped the involuntary movements and electromyographic silence ensued. Voluntary muscle movements were preserved. The theoretical implications of this unique movement disorder and central patterning of motor activity within the spinal cord are discussed.
We have found dorsal root entry zone (DREZ) lesions to be an effective treatment of chronic deafferentation pain in patients who have had avulsions of the dorsal rootlets from the spinal cord. Eight patients were operated in whom chronic pain of the lower extremity resulted from dorsal root avulsions from the conus medullaris. In 7 of the 8 patients, the mechanism of injury was a motor vehicle accident; all 7 sustained severe pelvic trauma. Seven of the 8 patients remained pain-free, off all narcotics, with an average follow-up of 33 months. All patients had DREZ lesions of the conus performed by radiofrequency techniques.
This chapter focuses on homoeostasis and general responses to stress. The hypothalamus is the homologue of the somatic righting reflexes control system—balancing the output of lower level hormonal, autonomic, and somatic efferent systems and controlled by goal-seeking cortex and paleocortex with ultimate frontal lobe control. The general category of response appears to differ according to whether an electrical stimulus is applied anteriorly or posteriorly in the hypothalamus of experimental animals, including the higher primates. The suprachiasmatic control is modulated by serotonin ascending from the raphe nuclei. Cholinergic stimulation of the hypothalamus elicits the drinking response. The ventromedial nucleus of the hypothalamus has been implicated in behavioral mechanisms, including evidence of satiety for food, water, and procreation. Stimulation of the posterior hypothalamus elicits continuing visceral and somatic responses appropriate to the alert state with preparation for rapid muscular activity.
This chapter discusses a special feature of the excitable cells—nerve and muscle—that is, the permeability that can be changed by processes that either increase or decrease the potential difference. Membrane permeability decreases during the outward flow of potassium current and increases with inward flow. Although the evidence is less satisfactory, it is likely that a similar voltage-dependent gate is opened at the internal end of the potassium channel. The node of Ranvier of the mammalian myelinated nerve fiber is believed to have many sodium but few potassium channels. The facility with which ions cross the membrane determines its electrical resistance. There is experimental evidence that glial cells are not necessary for production of action potentials by neurons, but it has been suggested that they act as a buffering mechanism to limit local concentrations of K+ outside nerve membranes producing action potentials, and at the same time, they accumulate potassium that would otherwise diffuse away from the nerve cell.
The dorsal horn region of the spinal cord, particularly the dorsal root entry zone (DREZ), represents the first central integration center for nociceptive afferent impulses. Here, the excitatory neurotransmitters/modulators, products of the primary sensory neurons, are released, the segmental interneuronal influences pertain, and the descending bulbospinal tracts terminate. A vast variety of compounds are thus involved in the processing of nociceptive information in these areas, among which are the ‘classical’ neurotransmitters and the more recently described neuropeptides. A continued vast interest exists concerning the chemistry of the dorsal horn/DREZ region. The current developments and understanding regarding the pharmacology of this region are presented. Particular emphasis is given to the interactions among the various compounds, the coexistence of some of these within single neuronal populations, the importance of the opiate receptor subtypes, and the actions and localizations of some of the newly discovered neuropeptides.
The spinal cord dorsal horn has been implicated in the generation of pain and dysesthesias following nerve and nerve root damage and/or avulsion, as well as following damage in adjacent spinal cord regions. Alterations in the functional properties of dorsal horn neurons occur after deafferentation and may underlie the occurrence of abnormal sensations referred to the denervated body part. Abnormal activity following deafferentation has also been noted at thalamic and cortical levels. Some of these post-denervation functional changes, determined anatomically and/or electrophysiologically, are reviewed as well as the results of behavioral studies of the deafferentation syndrome in the rat.
This paper details the long-term results in patients treated with dorsal root entry zone (DREZ) lesions for the treatment of pain following brachial plexus avulsion, spinal cord injury, and herpes zoster. With our current operative technique, 82% of patients with brachial plexus avulsion injuries were afforded long-term pain relief. Patients with pain confined to dermatomes just below the level of spinal injury also did well with DREZ lesions, although the results were less good in patients with diffuse pain or with sacral pain. The postoperative results in patients with postherpetic pain were disappointing.