Larynx, secondary paralysis

  1. GASTROEPATO
  2. Neurology
  3. Larynx, outline of anatomy and pathophysiology
  4. Larynx, secondary paralysis
  5. Cerebral stroke, stroke or apoplexy
  6. Hemorrhagic stroke
  7. Occlusive pathology of cerebral arteries
  8. How to evaluate a patient with stroke
  9. Cerebral embolism of cardiac origin
  10. Why coma

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La vocalizzazione
afasia
Noduli delle corde vocali e polipi
Anatomia della laringe
Anatomia della laringe fisiopatologia
Paralisi della laringe,anatomia
Paralisi della laringe, classificazioni
Paralisi della laringe, secondarie

The real clinical case.

A gentleman, a heavy smoker, had begun to present symptoms characterized by dysphonia and then by frank aphonia and spitting of blood. The specialist otolaryngologist who had consulted, had prescribed a cure based on aerosols, cortisone drugs, vitamin B12 parenterally. The clinical condition of the patient, despite the therapies practiced, worsened. The patient, who was an old and dear friend of mine, contacted me, although I was still a very young and inexperienced doctor. I decided to check his vocal cords, suspecting a tumor. One of the two vocal cords was paralyzed and my friend could not pronounce the letter "E" on my invitation. The diagnosis was made after the CT that documented a lung tumor with recurrent nerve palsy.

Peripheral laryngeal palsies are due, in most cases, to injuries of the recurrent nerve (recurrent paraphyses). In some cases they are caused by lesions of the vagus or of the accessory: given the close relationships that these nerves contract, just emerged from the endocranium, with hypoglossal, with the glossopharyngeal and with the cervical sympathetic, it is almost always laryngeal paralysis associated with the impairment of other organs and functions. They will therefore be taken into consideration later. Recurrent paralysis are more frequent on the left than on the right, because the left recurrent has a longer course and also comes in contact with organs contained in the thorax. Accidental traumas of the recurrent nerve are very rare; more frequent are the surgical traumas that can occur in the interventions on the cervical esophagus, on the thyroid and on the cervical lymph nodes. Most of the laryngeal paralysis is due to the compression and stretching of the applicant. This event can occur on the left for: aneurysm of the aorta; pericarditis; congenital heart disease acquired with dilatation of the left atrium; tracheobronchial adenopathy from a systemic process (leukemia, lymphogranuloma), metastatic (pulmonary tumor), inflammatory (pulmonary tuberculosis); malignant neoplasm of the trachea, cancer of the esophagus, thyroid cancer. Given the close relationships that the right-hand applicant contracts with the ipsilateral pleural dome, the right-sided tuberculous processes with reactive pleurisy are one of the most frequent causes of paralysis of this nerve.

Other causes of laryngeal paralysis

B base della lingua -L laringe -T trachea - E esofago- A arco dell'aorta -S arteria succlavia - C arteria Carotide Comune - G vena giugulare interna-  L nervo laringeo superiore con il suo ramo esterno ed il suo ramo interno 2) nervo vago destro. 3) nervo ricorrente destro 4 nervo vago sinistro. 5 nervo ricorrente sinistro. 6) ansaanatomica di Galeno

Other causes are to be found in the aneurysms of the right subclavian and in the malignant thyroid neoplasms and of the carcinoma of the cervical esophagus. In other cases the recurrent paralysis may be due to a toxic neuritis (saturnin intoxication, diabetes) or infectious (typhoid, diphtheria, flu: in the flu the right recurrent seems to be mainly affected). Finally, there are cases related to a dysergic-hyperergic pathogenesis, similar to that which determines the "frigore" paralysis of the facial nerve. In unilateral forms (laryngeal hemiplegia) the vocal cord is very rarely fixed on the midline; more often it assumes a "paramedian" position or a "cadaveric" position, intermediate between adduction and abduction. For the processes of muscular atrophy the vocal cord becomes thinner than the contralateral, with a concave edge. In the phonation the healthy vocal cord tends to cross the median line to approach the contralateral cord, in an attempt to perform often insufficient functional compensation. The symptomatology is essentially represented by dysphonia, because even in cases where the paralyzed vocal cord is fixed on the midline, the abduction of the healthy vocal cord is sufficient to guarantee the passage of a sufficient quantity of air.
The extent of dysphonia is related to the position assumed by the paralyzed vocal cord: of limited entity when the vocal cord is fixed in the middle position, it tends to progressively increase as the distance between the midline and the position assumed by the string increases. paralyzed. The dysphonia of these patients has a particular character, for which it is referred to as diplofonia. Bilateral forms (laryngeal diplegia) include a type (ZlEMSSEN syndrome) in which the two vocal cords are fixed in abduction (so called phonatory diplegia, and a type (RlEGEL syndrome) in which the vocal cords are fixed in adduction on the line median (so called respiratory diplegia.) Symptomatology will be constituted in the first case by aphonia, in the second by dyspnea.

A laryngoscopic and symptomatological picture very similar to the one found in RlEGEL syndrome, is also obtained in cases where the paralysis occurred exclusively in the posterior crico-arytenoid muscles. This type of incomplete bilateral paralysis is one of the most important symptoms of the dorsal tabe and is linked to a process of meningo-radicolonevrite luetica which affects the roots of the eleventh pair of cranial nerves containing the fibers destined for the posterior crico-arytenoid muscles. In GERHARDT syndrome the two vocal cords are in paramedian position separated from each other by a space of 1 -2 mm; during the phonation, since the adduction movements are preserved, the vocal cords are supported. In the inhalation they are aspirated, brought down and in, with a consequent, further narrowing of the already reduced glottal space; the exhaled air pushes them away passively from one another by 1-2 mm). Laryngeal insiprenous dyspnea is the essential symptom of RlEGEL and GERHARDT syndrome, whereas vocal function does not appear to be compromised.

The differential diagnosis should be essentially set up with crico-arytenoid ankylosis. Among the incomplete bilateral paralysis must be remembered those due to lesion of the superior laryngeal, which are sometimes of diphtheria origin. The vocal cords, due to the insufficiency of the crico-thyroid muscle, which has a tensor function, have a wavy appearance; the voice is veiled and the patients experience considerable difficulty in the emission of acute sounds. In these cases the concomitant laryngeal hypoesthesia may cause serious broncho-pulmonary complications by inhalation of food material.

Therapy

The therapy is related to the cause that caused paralysis: a possibility of effective treatment is unfortunately missing in many cases. In the paralysis of toxic neuritis a causal treatment must always be established; in the "cold" and infective neuritis forms, the early, intense and prolonged corticosteroid therapy, associated with the administration of antibiotics (tetracyclines), will give excellent results. A complementary vitamin treatment (vitamins B12 and B6) will complete the general therapy. In bilateral abduction paralysis, it is possible to try to reduce the glottic space by median tyrotomy and internal subperiodal grafting of fragments of auricular cartilage or acrylic resin. Bilateral paralysis in adduction often requires tracheotomy to ensure respiratory function. In order to decannulate the patient numerous surgical interventions have been proposed aimed at expanding the lumen of the glottic space. The aim can be achieved either with the unilateral or bilateral resection of the arytenoid, or by fixing, with appropriate expedients, the arytenoid in abduction position (arithenopedic). The enlargement of the glottal space that is obtained allows in many cases a natural breathing, with a reduced but sufficient phonatory function. The close relationships between the vagus and the accessory contract at the base of the skull and in the superior cervical region with the glosso-pharyngeal, hypoglossal and oculo-pupillary sympathetic fibers justify the existence of posterior associated paralytic syndromes that may occur due to thrombophlebitis post-otitic of the jugular, for resection of the internal jugular carried out in the latero-cervical ganglionic emptying, by penetration of projectiles, by metastatic adenopathy of the lymph node of KRAUSE and CUNEO from rhinopharyngeal neoplasm, for neoplastic processes starting from the rhinopharynx or the tympanic paraganglio - jug that extend along the base of the skull.

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