Facial sympatalgias

R. Bing combined a number of conditions similar in their clinical manifestations into a group of so-called facial sympathalgias. As a rule, they have a defined paroxysmal course; between attacks, the condition is satisfactory. The duration of attacks is from tens of minutes to a day (less often); they are manifested by a sharp, often unbearable, pain in the area of one half of the face of a burning, bursting, pressing, sometimes pulsating nature. An important pathognomonic clinical sign is vegetative disorders on the side of pain: lacrimation, reddening of the conjunctiva of the eyeball, discharge of fluid from one half of the nose and a feeling of congestion in it, swelling of the face. In general, the syndrome is much more common among men (we will discuss a possible reason for this a little later). Attacks occur acutely, mainly at night; the sharp pain forces the patient to move, since at rest the pain becomes even sharper.

Facial sympathetic pain, as has been clarified to date, is an expression of two fundamentally different forms of pathology:

1. sympathetic syndromes caused by damage to the autonomic peripheral nodes and nerves - nasociliary neuralgia (Charlin syndrome), pterygopalatine neuralgia (Sluder syndrome), neuralgia of the greater petrosal superficial nerve (Gartner syndrome);
2. vascular syndromes similar to migraine and designated as cluster headache, cluster effect, Horton's histamine migraine, Harris's migraine-like neuralgia. Glaser's carotid artery syndrome stands somewhat apart.

Thus, in the past, various diseases were united under the general term "facial sympathalgias", and the main motivating idea was to separate them from the group of facial (primarily trigeminal) neuralgias. True sympathalgic syndromes are extremely rare. Charlin's syndrome is characterized by herpetic rashes on the skin of the nose, keratitis or iritis, predominant localization of pain in the eye area with irradiation to the nose, and pain upon palpation of the inner angle of the orbit.

In Slader syndrome, pain is localized in the eye, jaw, teeth, and spreads to the tongue, soft palate, ear, and cervical-shoulder-scapular region. Sometimes there is a contraction of the soft palate muscles, which manifests itself as a characteristic clicking sound. After an attack, paresthesia 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 are much more common - in the overwhelming majority of patients with so-called facial sympathalgias; they manifest themselves in the attacks described at the beginning of the section, and are more common in men. Glaser's carotid artery syndrome develops rarely and, by analogy with the posterior sympathetic syndrome of Barre-Lieou, is designated by us as "anterior sympathetic syndrome".

[ 1 ], [ 2 ]

Pathogenesis

True sympathetic syndromes (Charlin and Sluder) are caused by the involvement of peripheral vegetative (nasociliary and pterygopalatine) nodes in the pathological process, their irritation. The nature is not clear enough. In connection with the presence of herpetic rashes in Charlin syndrome, one can think of herpetic ganglionitis of the nasociliary node. Pterygopalatine sympathalgia is associated with infectious processes in the sinuses (in particular, maxillary) and the involvement of the pterygopalatine node.

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

Differential diagnosis

Facial pain can be a manifestation of four processes:

1. neuralgia of the trigeminal and (less commonly) glossopharyngeal nerve;
2. facial forms of migraine, including cluster vascular pain;
3. Charlin's or Slader's sympathy;
4. psychogenic headaches.

Most patients with facial sympathalgia are first diagnosed with trigeminal neuralgia. However, neuralgia is characterized by the occurrence of short (seconds, minutes) pain attacks, manifested by sharp, shooting pains, provoked by chewing and talking. During an attack, patients freeze; there are "trigger" zones in the innervation of the II and III branches of the trigeminal nerve. Women predominate among patients. There are no vegetative manifestations characteristic of sympathalgia.

A syndrome close to neuralgia of the V nerve is described in case of malocclusion and involvement of the temporomandibular joint in the process (Costen's syndrome or syndrome of painful dysfunction of the temporomandibular joint). Charlin's syndrome should be differentiated from herpetic ganglionitis of the trigeminal (Gasserian) ganglion, which manifests itself with symptoms in the innervation zone of the first branch of the trigeminal nerve. It is also not characterized by a bright vegetative accompaniment.

Psychogenic facial pain is often bilateral in nature, combined with vivid emotional and personal symptoms, as well as with other psychogenic sensorimotor (functional-neurological) disorders.

Not the most striking, but quite a definite sign of facial sympathalgia is unilateral swelling of the face during an attack. This forces us to differentiate them primarily from angiotrophic edemas of the Quincke type. Typical localization is in the area of the lips, cheeks; often its bilateral nature does not cause diagnostic difficulties. More difficult is the diagnosis in case of local edemas of the same nature in the area of the orbital tissue, which manifest, in addition to edema, also as pain syndrome. Angiotrophic edemas in the area of the facial nerve canal lead to facial nerve insufficiency. Recurrent neuropathy of the VII nerve of this nature in combination with folded tongue, cheilitis is defined as Rossolimo-Melkersson-Rosenthal disease.

Treatment facial sympatalgias

Treatment of Charlin and Slader syndromes includes the use of vegetative drugs (N-anticholinergics, ganglionic 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. Complex treatment includes psychotropic drugs (tranquilizers and antidepressants). In acute situations, lubrication of the middle nasal passage with cocaine is effective (it is not used for a long time). Novocaine or lidocaine blockade of the vegetative nodes is indicated.