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M Lacerenza

Publications and source records attributed to M Lacerenza.

14 recordsLinked to original sources

Iatrogenic painful neuropathic complications of surgery in cancer.

It is estimated that at least one out of four patients with cancer complains of pain originating from nerve injury. Nerve injury may result from direct invasion/compression by tumour, or by remote effect of the cancer such as paraneoplastic polyneuropathy. In many cases, the nerve injury is caused by medical therapy, or surgical interventions. Pain generated by drugs or medical acts is called iatrogenic. A common iatrogenic neuralgia is chemotherapy induced painful polyneuropathy. This neuropathy typically affects mostly the small myelinated and unmyelinated nerve fibres. Surgical and anaesthesiological interventions also frequently cause direct nerve stretch or section. Some interventions, particularly those requiring extended resection, have a higher incidence of painful sequelae. Limb and colon amputation, nerve dissection, mastectomy and thoracotomy are the most common interventions for cancer known to cause nerve injury. As pain clinicians, we focus attention on the painful consequences of surgical interventions because there is evidence that a more accurate surgical approach and possibly a prophylactic prevention of the neuralgia may reduce the painful sequelae of nerve injury.

Humans↗

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.

Analgesics↗

Sympathetically maintained pain.

Reflex sympathetic dystrophy (RSD) is a controversial condition, redefined in 1996 by an ad hoc International Association for the Study of Pain (IASP) task force. One of the strongest critiques against the entire concept of sympathetic-dependent pain is that patients labeled as having RSD harbor in reality a somatoform disorder. Here clinical cases are described to prove that other organic medical conditions may exist other than RSD and still present the clinical picture of pain, sensory, and vasomotor disorders and trophic changes. The analysis of each patient illustrates how the inappropriate diagnosis of RSD may lead to increased worsening of pain intensity, or delay the proper diagnosis, and consequently the appropriate treatment.

Adolescent↗

Injured nerve block alters adjacent nerves spinal interaction in neuropathic rats.

Baseline activity and responses to simultaneous saphenous stimulation of pairs of neurones recorded from sciatic (L5-6) and saphenous (L2) spinal cord segments, in rats with thermal hyperalgesia following sciatic constriction, were analysed before, during and after a sciatic nerve block with a local anaesthetic. In sciatic neurones, during the block, reductions of baseline activity (p < 0.001), increases in threshold of saphenous electrical stimulation (p < 0.01) and reductions of responses to electrical and to natural noxious saphenous stimuli (p < 0.001) were consistently found. The neuronal baseline and evoked activities remained unmodified in saphenous neurones. The contribution of input from injured periphery to central neurone circuitry mechanisms underlying the unmasking of improper afferents is discussed.

Afferent Pathways↗

Evidence of peripheral axonal neuropathy in primary restless legs syndrome.

Restless legs syndrome (RLS) is a well-defined clinical entity characterized by an unpleasant creeping sensation arising in the legs with an irresistible need to move them. The trouble is more pronounced when the affected people lie in a prolonged rest position and try to fall asleep. It is known that RLS may be consequent to systemic disorders and to diseases affecting the central or peripheral nervous system. The International Classification of Sleep Disorders states that peripheral neuropathy should be ruled out by medical history and clinical grounds before diagnosing primary RLS (pRLS). The present study extended peripheral nerve investigation in eight consecutive pRLS patients with normal neurological examination results and showed that all patients exhibited two or more electrical, psychophysiological, and/or morphological features of peripheral axonal neuropathy. Morphometric analysis of sural nerve showed a significant reduction in myelinated fiber density and g ratio (axon diameter/fiber diameter) in the pRLS group compared with eight control biopsy specimens. These results suggest that axonal neuropathy is often present in patients with RLS. A comprehensive peripheral nerve investigation should be considered in RLS patients.

Adult↗

Different time-courses of i.v. lidocaine effect on ganglionic and spinal units in neuropathic rats.

The effect of intravenous lidocaine (4 mg kg-1) on ganglionic and spinal neuronal hyperactivity following sciatic chronic constriction injury (CCI) was studied in anaesthetized and curarized rats. A significant difference in the time course and magnitude of the lidocaine effect on the two neuronal populations was found. Longer lasting and more potent inhibitory effects on the dorsal horn neurones in comparison with ganglionic neurones were observed. By contrast the magnitude and time course of the inhibitory effects were highly comparable in dorsal horn neurones before and after acute rhizotomy. The results indicate that peripheral and central effects of lidocaine are not sequentially related. The likelihood that lidocaine inhibition at central sites may have a role in its analgesic effect, at least in the neuropathic model, is discussed.

Animals↗

Diverse modulation by systemic lidocaine of iontophoretic NMDA and quisqualic acid induced excitations on rat dorsal horn neurons.

The effects of systemic lidocaine (3-4 mg/kg) on the responses of 60 wide dynamic range neurons (WDR) to iontophoretically applied N-methyl-D-aspartic acid (NMDA) and quisqualic acid (QUIS) were studied in anesthetized, paralysed rats. The results show that lidocaine induced (i) potentiation of the NMDA excitation, reversible by 7-chloro-kynurenate (7-Cl-KYNA), a selective antagonist of the glycine binding site on the NMDA receptor; (ii) reduction of the QUIS excitation, reversible by strychnine (STRYCH), a glycine antagonist at its receptor. These findings, supporting a glycine-like action of lidocaine, are discussed together with data on the role of excitatory amino acids (EAAs) and the analgesic effect of lidocaine on neuropathic pain.

Animals↗

Effect of systemic lidocaine on dorsal horn neuron hyperactivity following chronic peripheral nerve injury in rats.

Systemic lidocaine (3-4 mg/kg) was tested for its effect on identified spinal cord wide-dynamic-range (WDR) neurons in rats with a unilateral chronic neuropathy induced by two different peripheral nerve injuries (section or compression by ligatures). In both cases, neurons on the side ipsilateral to the injuries showed a spontaneous firing frequency higher than that of the opposite intact side (23.5 +/- 3.4 vs 4.2 +/- 1.5 spikes/sec). The hyperactivity was not affected by a sensory block of the peripheral receptive field. It was consistently found that lidocaine suppressed or reduced the spontaneous neuronal hyperactivity on the ipsilateral side, whereas it had no effect on the normal spontaneous activity of the neurons on the intact side. In all recordings, the hyperactivity returned to the prelidocaine injection rates within 20 min. These results indicate a preferential action of subanesthetic doses of lidocaine on the hyperactive WDR neurons. Such preferential action is related to a susceptibility acquired by WDR neurons of the peripherally injured side and is not simply attributable to the increased frequency of firing.

Animals↗

Selective inhibition by systemic lidocaine of noxious evoked activity in rat dorsal horn neurons.

The effect of systemically injected lidocaine (3-4 mg kg-1) on the responses to noxious and non-noxious stimuli on 28 wide dynamic range (WDR) neurons in the dorsal horn was studied in anesthetized and curarized rats. It was consistently found that lidocaine reduced or suppressed the responses to noxious stimuli whereas it did not act on the responses to non-noxious stimulation and on the spontaneous activity. Furthermore the noxious stimuli were completely ineffective from 10-15 min following the lidocaine injection while the non-noxious stimuli maintained their efficacy. The control responses, in all the cases, returned within 20 min. The results suggest that lidocaine exerts a selective inhibitory effect on nociceptive transmission at the spinal level.

Animals↗

The objective assessment of visual contrast sensitivity by pattern reversal visual evoked potentials in diabetes.

Recent studies have described abnormalities of visual evoked potentials and pattern electroretinography in diabetics without retinopathy. The visual contrast sensitivity, determined by psychophysical tests, has proved to be abnormal in diabetic patients with and without clinical retinopathy. In this study we evaluated contrast sensitivity function using both electrophysiologic and psychophysical methods. The objective assessment of functional visual contrast sensitivity was superior to psychophysical evaluation in the detection of contrast sensitivity alterations. No relationships were found between contrast sensitivity dysfunction and abnormalities of pattern electroretinography or fluorescein angiography. Our data suggest that functional visual deficits might precede background retinopathy and that the involvement of foveal function is early and very frequent in diabetic patients, even if they have normal visual acuity.

Adolescent↗

Sensitized nociceptors in reflex sympathetic dystrophies.

Painful neurogenic syndromes commonly diagnosed as reflex sympathetic dystrophy (RSD) may not be the consequence of sympathetic dysfunction. Recent experimental data on the mechanism of hyperalgesia indicate that the primary pathophysiological mechanism of RSD may be sensitization of either peripheral nociceptors, or central neurons, or both. The sympathetic system might be involved in maintaining this condition, but this is not always the case. This presentation is an attempt to interpret clinical neuropathic syndromes on the basis of new scientific knowledge.

Humans↗