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Biomedical subjects

V Bonicalzi

Publications and source records attributed to V Bonicalzi.

At least 19 recordsLinked to original sources
PubMed2002

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.

Electric Stimulation Therapy↗
PubMed2001

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.

Cysts↗
PubMed2001

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↗
PubMed2000

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.

Anesthesia, Local↗
PubMed1999

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.

Cerebrovascular Disorders↗
PubMed1998

The neurochemistry of central pain: evidence from clinical studies, hypothesis and therapeutic implications.

Recent evidence suggests that central pain, i.e., pain due to central nervous system damage, may be due to a deranged neurotransmission between the sensory thalamus and sensory cortical areas. Central pain can be controlled either by opposing glutamate neurotransmission or potentiating GABAergic transmission. It is speculated that a relative hypofunction of the GABAergic inhibition both at thalamic and cortical levels leads to a sectorial excitatory hypertonus in those same areas. A blend of the two should mark each patient. A pharmacological dissection approach is provided that should optimize the treatment, up to now globally poor, of central pain.

Anesthetics, Intravenous↗