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migliorando la situazione ipossica legata sia alla compressione arteriosa sia, soprattutto, alla stasi

venosa. Non va dimenticata, infine,l’azione reflessoterapica (“agopuntura chimica”) capace di

interrompere la catena del dolore cronico attraverso lo stimilo di meccanismi antalgici di tipo

antinocicettivo.

Introduction

Per fornire delle ipotesi valide sul meccanismo farmacologico grazie al quale l’ozono agisce sul

dolore da ernia discale (19,28), è premessa fondamentale l’analisi del sintomo dolore da conflitto

disco-rdicolare.

Root pain is commonly linked to nerve compression (disc-root or spine-root conflict). However,

there is much evidence in clinical practice that the cause-effect ratio of root pain is not as

straightforward as is generally thought (24). For example, we know that many people live normal

lives despite a disc herniation disclosed by chance during neuroradiological investigation of the

spine for reasons other than disc disease. In addition, patients with known disc herniation live with

the lesion in between pain attacks, even though the morphology of the disc lesion and consequent

nerve root compression remain unchanged on CT and MR scans.

Another common finding in a fair number of patients is the success of medical management or

micro-invasive surgery such as intramuscular or intradiscal oxygen-ozone injection, in resolving

pain without affecting the morphology of the herniation, i.e. with no structural change to the disc

lesion.

Lastly, although disc compression is corrected by surgery, many patients continue to feel pain,

either attenuated or even exacerbated, irrespective of the structural changes to the disc herniation

disclosed by neuroradiological scans after the operation (26).

These findings led us to investigate the mechanisms responsible for root pain related to the

pharmacological basis of ozone action in herniated disk.

Pathogenesis of root pain

Reviewing the literature, we can distinguish two broad categories of pathogenetic mechanisms:

mechanical and inflammatory, a cui va aggiunta l’amplificazione del dolore stesso legata alla sua

cronicità (24,26).

1.Pathogenetic components of root pain:mechanical pressure.

The mechanical factors responsible for pain are linked to the mass effect of the herniated disc

material. In turn, these can be divided into:

• Direct mechanical factors : given the absence of nociceptors in the nerve bundle, these are linked

in order of importance to:

• Compression of the spinal ganglion, possible in intraforaminal and extraforaminal herniation

(22)

• Deformation and flattening of the ligaments and annulus, location of the afferent nociceptors

to Luschka’s nerve of the posterior root of the spinal nerve;

• Deformation and flattening of nerve fibres disrupting the myelin nerve sheath with possible

major conduction abnormalities.

• Indirect mechanical factors : globally defined as vasculomediated and divided into:

• “ischaemic” vasculomediated factors with trophic nerve impairment due to compression on

the arterial afferents and microcirculation of the nerve bundle and secondary anoxic

demyelination of the nerve fibres;

• vasculomediated factors “due to venous stasis with oedema and trophic nerve impairment

caused by partial or total blockage of venous reflux (especially in intraforaminal

herniations); this seems to be the most important mechanical factor responsible for root pain

because of its effects on the spinal ganglion due to the anatomical relations between the

intraforaminal vessels and spinal ganglion

2. Pathogenetic components of root pain: inflammation.

Neural and perineural inflammation plays a major role in the origin of root pain (note the frequent

beneficial effects of corticosteroid therapy) (2, 10, 23). Speculative evidence of the importance of

inflammatory factors is that higher levels of antibodies anti-pso P27 (markers for inflammatory

process, particularly of autoimmune origin) are found in CSF from patients with low back pain and

sciatica (11).

They include:

• Immune-mediated inflammatory reaction: experimental and other evidence shows that disc

protrusion causes immune inflammatory events. The most likely hypothesis (albeit not universally

accepted) to account for this behaviour is that the adult intervertebral disc is segregated from a

humoral standpoint with respect to the immune system as long as it is confined within the

fibrocartilaginous structure of the annulus. Once the disc is herniated, it is recognised as “non self”

by the immunocompetent system, triggering a cell-mediated reaction in other tissues. The presence

of peridiscal inflammatory tissue is confirmed by the CT and MR finding of peripheral

enhancement of the disc fragment after i.v. contrast administration (21)

In addition to the findings of Zwarth et Al. (29), further experimental evidence of the autoimmune

component of peridiscal inflammation is the finding of macrophages with IL 1β gene expression

characteristic of autoimmune reactions (22) and the reduction of mechanical hyperalgesia following

drug-induced leucopenia under experimental conditions (15).

• Inflammatory reaction due to biohumoral factors linked to disc tissue (21): experimental evidence

in this field includes:

• Phospholipase A2 (PLA2): the herniated disc material contains very high levels of PLA2

enzyme activity. PLA2 is a potent inducer of the inflammatory reaction since its enzymatic

activation to arachidonic acid leads to the production of major chemical mediators of inflammation

such as prostaglandins and leucotrenes. In addition, PLA2 may directly damage nerve fibres by

attacking perineural and neural membrane phospholipids (14);

• Matrix metaloproteinases (MMPs): there is a significant production of these enzymes

which enhance the inflammatory reaction by attacking disc tissue;

• Prostaglandin E2 (PGE2): PGE2 is produced directly by the disc tissue as well as by the

enzymatic intervention of PLA2 which is known to be a potent inducer of inflammation; the same

applies to interleukin 6 (IL6) (7, 3);

Ongoing studies are currently investigating a recently identified glycoprotein, YKL-40

produced in abundance following joint lesions, including degenerative disease, which could be one

of the main mediators of the inflammatory reaction in disc disease (13).

3. Pathogenetic components of root pain: Amplificazione sintomatologica da dolore cronico.

Per amplificazione sintomatologica da dolore cronico si intende quel meccanismo per il quale la

stimolazione cronica, meccanica ed infiammatoria, della radice comporta una sensibilizzazione dei

nocicettori gangliari e perigangliari (prevalemtemente di tipo C, polimodali) responsabili

dell’iperalgesia, una condizione nella quale si osserva allodinia, cioè una riduzione della soglia del

dolore, ed un aumento dell’intensità del dolore anche per stimoli sottoliminali, sino ad attivare, in

qualche caso, scariche algiche spontanee (3).


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DESCRIZIONE DISPENSA

La dispensa fa riferimento alle lezioni di Neuroradiologia, tenute dal Prof. Leonardi nell'anno accademico 2012.
Il documento è dedicato all'ozonoterapia.
Tra gli argomenti affrontati: ernia discale, dolore radicolare, ozono, infiammazione bioumorale, basi farmacologiche, ossigeno.


DETTAGLI
Corso di laurea: Corso di laurea magistrale in medicina e chirurgia (ordinamento U.E. - a ciclo unico) (magistrale europea)
SSD:
Università: Bologna - Unibo
A.A.: 2012-2013

I contenuti di questa pagina costituiscono rielaborazioni personali del Publisher Atreyu di informazioni apprese con la frequenza delle lezioni di Neuroradiologia e studio autonomo di eventuali libri di riferimento in preparazione dell'esame finale o della tesi. Non devono intendersi come materiale ufficiale dell'università Bologna - Unibo o del prof Leonardi Marco.

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