The first manifestation of MS is very often an optic neuritis (ON); but it is known that "temporary or permanent blindness is a very rare complication of pertussis; it can be associated with signs indicating optic neuritis and retinal ischaemia, or it can be secondary to cerebral damage ^{( see note 1 )} ". The optic nerve anatomy ^{( see note 2 )} explains its frequent involvement in MS. In fact: the tortuosity of the ophtalmic artery and vein, the length of the nerve and of its blood vasa (rather greater than the distance between optic foramen and rear pole of the glene), the disposition of ciliary and of retinal vasa, the path of the nerve in an inextensible canal (optic canal), make the post-capillary venules of the optic nerve a vasal net with very slow flow (ulteriorly slowed down by the movements of the glene, during which the curves of the italic-S of the nerve narrow). In the immune circulating complexes (ICC) precipitation we have ^{( see notes 3, 4 )}:

• leucocytes and plasmocytes aggregation, capillary necrosis, haemorrhages, anaphilotoxins and cytokines release;
• in reply to the bacterial stimuli (LPS) and per cytokines action, the vasal endothelium exposes the adhesion molecules ^{( see note 5 )}, which "hook" the fimbrial adhesins, always associated ^{( see note 6 )} with the LPF pertussis toxin;
• infiltration of ICC under the endothelium (that is, serious alteration of Haemato-Encephalic Barrier, HEB) ^{( see notes 7, 8 )}. The initial lesion of the optic nerve is due to type III immunoreactions;

Adhesion molecules ^{( see note 5 )} are normally generated by the vasal endothelium in reply to bacterial stimulus (LPS) and/or per cytokines action. They constitute "adhesion receptors" to which phagocytes "adhere", having become "sticky" for chemiotactic stimulus. The quick transition from "adherence" to "non-adherence" allows the immunocompetent cells to carry out the double role of surveillance and reply (adherence) or non-reply (non adherence), depending on local necessities. The adhesion receptors are expressed not only by the immune system but also by other systems, including the CNS ^{( see note 5 )}. Adhesion molecules always intervene in the ICC precipitation; but, in MS, the pathologic process is precipitated by the activation of the immunocompetent cells operated by Bordetella toxins. Adhesion molecules are a physiologic aspect of the type III immune reaction, that damages the HEB; they are "effect", not "cause". About the role of astrocytes, I think it`s sufficient to remember that in cerebral vasa the adventitia is not composed of connective tissue but of astrocytes, that are therefore integral part of the vasal wall. In MS the initial damage to haemato-encephalic barrier and to the perivenous nervous tissue is due to ICC precipitation into the small cerebral vessels; only after these lesions, T-limphocytes and macrophages, preliminarily activated and made autocytotoxic by Bordetella toxins, get in touch with cerebral antigens; but, it is important to know that, if lesions were not too much serious and if ICC production ceases, lesions regress and they tend to disappear completely ^{( see note 4 )} (frequent restitutio ad integrum, in O.N.).