The syndrome of isolated disturbance of the tympanic nerve.

In a patient with cerebrocranial trauma that resulted in a fracture of the pyramid of temporal bone, disappearance of neurologic and otologic symptoms was followed for a long period by an isolated disturbance of the tympanic nerve, in the form of the postdenervation syndrome of a parotid gland and, in particular, of the atropine sulfate salivatory paradox.

Salivatory responses to classical and nontraditional parasympatholytic agents in human subjects: critical comments.

Both classical (atropine, scopolamine) and nontraditional (pirenzepine, telenzepine) cholinolytic agents themselves cause no salivation in human subjects. Ordinarily, they block salivation caused by pilocarpine. Conversely, they all stimulate intense salivatory response in the chronically denervated human parotid gland. The author presents critical comments on the concept that cholinolytic agents cause salivation by suppression of the mechanism of presynaptic autoinhibition. An alternative explanation of the initial cholinomimetic effect of cholinolytic agents is suggested.

Syndromes of a complex lesion of greater and lesser superficial petrosal nerves (paradoxical facial hyperaemia, salivation, lacrimation and mucus excretion).

After closed cranial trauma with paralysis of the facial nerve, a patient had a fracture into the petrosus apex with a bony bridge over the nerve, and a subdural haematoma, which were dealt with during an operation for nerve decompression. Examination of the patient 2.5 years later revealed the presence of the crocodile tears syndrome, mucus secretion and the salivary atropine paradox, i.e. severe hyperaemia of the paretic half of the face during intense salivation in response to atropine. Other patients who suffered similar trauma but had no operation demonstrated the same syndrome. The crocodile tears syndrome is considered to be a result of an ephaptic union of the central portion of the damaged lesser superficial petrosal nerve (SPN) with the peripheral portion of the greater SPN. The salivary atropine paradox is then due to the loss of the peripheral portion of the former nerve combined with denervation of the salivary parotid gland. Facial hyperaemia during intense salivation after atropine administration is explained as a result of the intensified release of vasoactive intestinal polypeptide from the gland, stimulated by atropine, into the blood circulation.

On stages of postdenervational disturbances in functioning of the human salivary parotid gland (a concise report).

The author presents an original classification of the muscarinic cholinoreceptor subpopulations in the human salivary parotid gland in normal condition or following parasympathetic denervation. The criteria characterizing each stage of the postdenervational syndrome and the general scheme of their occurrence and restoration both reflect the stages of evolutionary transformations in cholinergic receptors. Assessment of salivation rate and volume, observed as the effect of vegetotropic agents, and of electrolyte contents in saliva provide the above scheme of 3 stages of the postdenervational syndrome.

Synchronous facial vascular vasodilation and salivatory response to atropine in the parasympathetically denervated human salivary parotid gland.

Hypersalivation and facial skin hyperemia that simultaneously emerge in response to atropinization have been observed in patients who suffered trauma to the skull base combined with damage of the parasympathetic secretory and vasodilatory fibers in the greater and lesser petrosal nerves at the tip of the temporal bone pyramid. The study was facilitated by special vacuum capsules applied to both outlet ducts of the parotid glands. Hyperemia and hyperthermia of the face were evaluated visually, by thermometer readings, and color photography. The events described are distinct from those reported in the literature (i.e., paradoxical disturbances of facial and salivary gland innervation). This study analyzes the mechanism of initiation and the manifestations of this complex syndrome.

Salivatory effects induced by pirenzepine, atropine, metacine and hexamethonium in preganglionar chronically denervated human parotid gland.

Both classical (atropine) and non-traditional (pirenzepine, metacine) antagonists of the muscarinic cholinoreceptors induce, rather than block, an intense and prolonged salivary response in chronically denervated human parotid glands and thus are capable of discriminating between neuronal and aneuronal receptors. Hexamethonium (benzohexonium) a ganglion-blocking agent (0.4 mL, 2.5%) completely inhibits this paradoxical salivation to atropine, benzilylcholine (metacine) and pirenzepine in the chronic preganglionically denervated human parotid gland. The authors discuss the essence of the revealed paradoxical phenomena.

The concept of fillet flaps: classification, indications, and analysis of their clinical value.

Tissue of amputated or nonsalvageable limbs may be used for reconstruction of complex defects resulting from tumor and trauma. This is the "spare parts" concept. By definition, fillet flaps are axial-pattern flaps that can function as composite-tissue transfers. They can be used as pedicled or free flaps and are a beneficial reconstruction strategy for major defects, provided there is tissue available adjacent to these defects.From 1988 to 1999, 104 fillet flap procedures were performed on 94 patients (50 pedicled finger and toe fillets, 36 pedicled limb fillets, and 18 free microsurgical fillet flaps). Nineteen pedicled finger fillets were used for defects of the dorsum or volar aspect of the hand, and 14 digital defects and 11 defects of the forefoot were covered with pedicled fillets from adjacent toes and fingers. The average size of the defects was 23 cm2. Fourteen fingers were salvaged. Eleven ray amputations, two extended procedures for coverage of the hand, and nine forefoot amputations were prevented. In four cases, a partial or total necrosis of a fillet flap occurred (one patient with diabetic vascular disease, one with Dupuytren's contracture, and two with high-voltage electrical injuries).Thirty-six pedicled limb fillet flaps were used in 35 cases. In 12 cases, salvage of above-knee or below-knee amputated stumps was achieved with a plantar neurovascular island pedicled flap. In seven other cases, sacral, pelvic, groin, hip, abdominal wall, or lumbar defects were reconstructed with fillet-of-thigh or entire-limb fillet flaps. In five cases, defects of shoulder, head, neck, and thoracic wall were covered with upper-arm fillet flaps. In nine cases, defects of the forefoot were covered by adjacent dorsal or plantar fillet flaps. In two other cases, defects of the upper arm or the proximal forearm were reconstructed with a forearm fillet. The average size of these defects was 512 cm2. Thirteen major joints were salvaged, three stumps were lengthened, and nine foot or forefoot amputations were prevented. One partial flap necrosis occurred in a patient with a fillet-of-sole flap. In another case, wound infection required revision and above-knee amputation with removal of the flap.Nine free plantar fillet flaps were performed-five for coverage of amputation stumps and four for sacral pressure sores. Seven free forearm fillet flaps, one free flap of forearm and hand, and one forearm and distal upper-arm fillet flap were performed for defect coverage of the shoulder and neck area. The average size of these defects was 432 cm2. Four knee joints were salvaged and one above-knee stump was lengthened. No flap necrosis was observed. One patient died of acute respiratory distress syndrome 6 days after surgery. Major complications were predominantly encountered in small finger and toe fillet flaps. Overall complication rate, including wound dehiscence and secondary grafting, was 18 percent. This complication rate seems acceptable. Major complications such as flap loss, flap revision, or severe infection occurred in only 7.5 percent of cases. The majority of our cases resulted from severe trauma with infected and necrotic soft tissues, disseminated tumor disease, or ulcers in elderly, multimorbid patients. On the basis of these data, a classification was developed that facilitates multicenter comparison of procedures and their clinical success. Fillet flaps facilitate reconstruction in difficult and complex cases. The spare part concept should be integrated into each trauma algorithm to avoid additional donor-site morbidity and facilitate stump-length preservation or limb salvage.

Effect of denervation on parotid gland function.

In 110 subjects with traumatic severance of secretory nerves, salivation was studied to determine the effect of denervation on gland function. A sequence of responses was found in which an initial hyperpositive response to cholinergic agents was blocked by atropine (stage I); this effect was reversed and increased salivation occurred in both latent (stage II) and overt (stage III) forms of the atropine paradox. The hypothesis suggested is that chemoreceptive cells of parotid membranes include a minimum of five populations of cholinergic receptors which respond differentially to parasympathetic agonists and antagonists.

Comparison of paradoxical salivatory responses to chlorosyle and atropine in a denervated human parotid gland.

In the case of the denervated human parotid gland, atropine is a cholinopositive agent that causes an extremely intense and prolonged (up to 3-5 h) salivation. An attempt was made to find out the extent to which the "weight increase" principle had an effect on such a gland, i.e. whether larger analogues of atropine which has a relative molecular mass of 289.4 would stimulate or inhibit the paradoxical salivation. The studies involving chlorosyle of a mass of 355.89 were carried out in seven subjects during the last three years. The cholinopositive activity of chlorosyle, as a ligand with increased weight on both poles, on a denervated gland, was several times lower than that of atropine. With the increase of the ligand's dosage, the cholinoexciting activity of chlorosyle decreased sharply and was just restricted by the initial cholinomimetic excitement transforming into a blockade, which may be compared with the action of depolarizing myorelaxants. The data obtained may provide a foundation for conceptualization of the expansion of a response-active cholinopositive zone in a cholinoreceptor deprived of nervous control, which, probably, results from relocation of hydrophobic segments to the macromolecular periphery or, more precisely, to the synthesis of receptors with another part of the zone. The chlorosyle radicals with increased length and weight, while contacting the hydrophobic segments, conditioned the occurrence of cholinoblocking activity and inhibition of the cholinoexciting effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Dualism in the effect of cholinolytics upon the human parotid gland deprived of parasympathetic control.

Dualism in the effects of atropine, and metixene upon the denervated human parotid salivary gland is demonstrated by the fact that they suppress pilocarpine secretion while themselves causing an extremely intense and prolonged salivation. A still stronger cholinolytic, chlorosyle, although causing salivation, blocks paradoxical salivation initiated by atropine and metacine. With respect to the latter ligands, chlorosyle acts as a partial agonist. Dualism in the cholinolytics' effect is conditioned by generation, following chronic enervation of the gland, of cholinoreceptor subpopulations of different functional significance and evolutional maturity. Depending on the length of the cholinoreceptor reactive zone, cholinolytics initiate blockade of some receptors and excitement of others.

Dissociation of the functioning of a human parotid gland following trauma of the tympanic nerve (a pseudocolchicine phenomenon).

In a group of patients with break-up of the tympanic nerve, restitution of unconditioned reflexes in a denervated parotid gland was accompanied with both an increased sensitivity to cholinergic agonists and a sharply perverted paradoxal secretory response to antagonists (atropine, scopolamine, metacine, chlorosile). The above phenomenon is similar to the syndrome resulting from the effect of colchicine on the nervous-muscle connection when, mediatory transmission remaining intact, a post-denervational increased sensitivity to mediators of cholinergic excitation is observed.

[Syndromes of combined damage to the greater and lesser superficial petrosal nerves (paradoxical phenomena of hyperemia of the face, salivation, lacrimation and mucus secretion)]. / Sindromy sochetannogo povrezhdeniia bol'shogo i malogo poverkhnostnykh kamenistykh nervov (paradoksal'nye fenomeny giperemii litsa, sliuno-, slezo-, slizeotdeleniia).

Combined damage to the large and small superficial petrosal nerves is associated with paradoxical phenomena: face hyperemia, profuse salivation from the parotid gland, lacrimation and mucus secretion from the nose. Face hyperemia and salivation develop following atropine administration (an atropine salivatory paradox) while lacrimation and mucus secretion at the impaired side usually develop during eating. The above is explained by the development of ephaptic ("false") relation between the damaged nerves.