Facial sympathy

A number of similar in their clinical manifestations of states R. Bing combined in the group of so-called facial sympathy. As a rule, they have a defined paroxysmal course; between attacks the state is satisfactory. Duration of attacks from tens of minutes to days (less often); they are manifested by the sharpest, often intolerable, pain in the field of one half of the face of a burning, bursting, pressing, sometimes pulsating character. An important pathognomonic clinical sign are vegetative disorders on the side of pain: lacrimation, reddening of the conjunctiva of the eyeball, separation of fluid from one half of the nose and a feeling of stuffiness in it, swelling of the face. In general, the syndrome is much more common among men (a possible reason for this will be discussed later). Attacks occur acutely, mainly at night; the sharp pain makes the patient move, because at rest the pain becomes even more acute.

Facial sympathy, as it was possible to clarify by now, is an expression of two fundamentally different forms of pathology:

1. sympathetic syndromes, caused by affection of vegetative peripheral nodes and nerves, - nosoresnichnaya neuralgia (Charlene's syndrome), pterygoal neuralgia (Slader's syndrome), neuralgia of the large stony surface nerve (Gartner's syndrome);
2. cardiovascular syndromes close to migraine and labeled as headache, cluster effect, Horton's histamine migraine, migraine-like neuralgia of Harris. Somewhat apart is Glyzer's carotid artery syndrome.

Thus, under the general term "facial sympathy" in the past, various diseases were combined, and the main incentive was to separate them from the group of facial (trigeminal first) neuralgia. True sympathetic syndromes are extremely rare. Charlene syndrome is characterized by herpetic eruptions on the skin of the nose, the phenomenon of keratitis or iritis, the predominant localization of pain in the eye area with irradiation in the nose, tenderness in palpation of the inner corner of the orbit.

In Slader's syndrome, the pain is localized in the eye, jaw, teeth, extends to the tongue, soft palate, ear, cervico-shoulder-scapula. Sometimes there is a contraction of the muscles of the soft palate, which is manifested by a characteristic clinking sound. After an attack, paresthesias in the face and noise in the ear are noted.

Naturally, in both cases the pain is accompanied by characteristic unilateral vegetative manifestations (see above). Vascular syndromes occur much more often - in the vast majority of patients with so-called facial sympatalgia; they are manifested by attacks described at the beginning of the section, they are more common in men. The syndrome of Glyzer's carotid artery develops rarely and, by analogy with the posterior sympathetic syndrome of Barre-Lieu, is designated by us as "anterior sympathetic syndrome".

[1], [2]

Pathogenesis

The true sympathetic syndromes (Charlina and Sladera) are caused by the involvement of peripheral vegetative (naso-ciliary and pterygopic) nodes in the pathological process, their irritation. Nature is not clear enough. In connection with the presence of herpetic rashes with Charlene's syndrome, one can think of a herpetic ganglionitis of the nosoresnichnogo node. Pterygoal sympathaly is associated with infectious processes in the sinuses (in particular, the maxillary sinus) and involvement of the pterygoid node.

Anterior sympathetic Glaser syndrome is caused by irritation of the sympathetic plexus surrounding the carotid artery, as a result of vascular pathology or involvement in the pathological process of the upper sympathetic ganglia.

Differential diagnosis

Face pain can be manifested in four processes:

1. neuralgia of the trigeminal and (more rarely) glossopharyngeal nerve;
2. facial forms of migraine, including beam vascular pain;
3. sympalgia of Charlene or Slader;
4. psychogenic headaches.

Most patients with facial sympathologies are primarily diagnosed with trigeminal neuralgia. However, neuralgia is characterized by the emergence of short (seconds, minutes) painful attacks, manifested by sharp, shooting algism, provoked by chewing and talking. During the attack, the patients froze; there are "trigger" zones in the innervation of the II and III branches of the trigeminal nerve. Women predominate among the patients. Characteristic for sympathetic vegetative manifestations does not exist.

Close to neuralgia of the V nerve, the syndrome is described in the pathology of the occlusion and involvement of the temporomandibular joint in the process (Kosten's syndrome or the pain of dysfunction of the temporomandibular joint). Charlene syndrome should be differentiated from herpetic ganglionitis of the trigeminal (gasser) node, which manifests itself in the innervation zone of the first branch of the trigeminal nerve. For him also uncharacteristically bright vegetative accompaniment.

Psychogenic facial pains are more often bilateral, combined with bright emotional-personal symptoms, as well as with other psychogenic sensorimotor (functional-neurological) disorders.

Not the most striking, but rather definite sign of facial sympathy is one-sided edema of the face during the seizure. This makes them differentiate primarily from angiotrophic edema of the Quincy type. Typical localization in the area of the lips, cheeks; often its bilateral nature does not cause diagnostic difficulties. It is more difficult to diagnose a local edema of the same nature in the field of cellulose orbit, which, in addition to edema, manifests itself, in addition, with pain syndrome. Angiotrophic edema in the area of the canal of the facial nerve leads to insufficiency of the facial nerve. Recurrent neuropathy of the nerve VII of this nature, combined with a folded tongue, cheilitis, is defined as the Rossolimo-Melkersson-Rosenthal disease.

Treatment of the facial sympatagy

Treatment of Charlene and Slader syndromes includes the use of vegetotrophic drugs (H-cholinolytics, ganglion blockers - gangleron, pachycarpine, alpha-adrenoblockers - pyrroxane), which have a denervating effect on the affected node. As with all paroxysmal conditions, carbamazepines (tegretol, finlepsin) are used. The complex treatment includes psychotropic drugs (tranquilizers and antidepressants). Effective in acute situations, cocaine lubrication of the middle nasal passage (not used for a long time). Novocaine or lidocaine blockade of vegetative nodes is shown.