Facial palsy
•
1 recomendación•1,598 vistas
Comunicazione presentata al simposio sul nervo facciale tenutosi a Roma nell'aprile 2009. Etiopatogenesi virale della paralisi del nervo facciale
![VIRAL ETIOLOGY ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
Recomendados
Recomendados
Más contenido relacionado
Similar a Facial palsy
Similar a Facial palsy (20)
Más de Giuseppe Attanasio
Más de Giuseppe Attanasio (13)
Último
Último (20)
Facial palsy
- 1. Herpes virus detection in Bell’s palsy R. Filipo G. Balsamo E. Covelli G. Attanasio O. Turriziani G. Antonelli
- 4. ANATOMY Gh. Lacrimale Ner. Lacrimale Gh. Sottomandibolare Gh. Sottolinguale N. linguale N. stiloioideo Corda timpani Stylomastoid foramen Parotide Forame ovale N. Grande petroso CUI Ganglio otico Geniculate ganglion Iatus petroso Mm. facciali Digastrico Stapedius Nervo vago Fibre secretorie (lacrimali e salivari) Fibre gustative dei 2/3 ant. della lingua N. vidiano Plesso carotideo I II III 74° 95-120° meatal foramen (mean diameter .68 mm)
- 8. MATERIAL AND METHODS 53 PATIENTS 94,4 % (50 pts) 3 pts
- 9. 63% right 27% left MATERIAL AND METHODS 53 PATIENTS
- 10. 53 PATIENTS MATERIAL AND METHODS
- 11. MATERIAL AND METHODS 53 PATIENTS
- 13. RESULTS Prevalence of Anti-HSV-1 antibody Prevalence of Anti-VZV antibody IgM+ Grey zone IgM+ IgG+ IgG+ IgM+ Grey zone IgM+ 8 pts 5 pts 50 pts 48 pts
- 14. RESULTS Prevalence of Anti-HSV-1 antibody Prevalence of Anti-VZV antibody IgM+ HSV-VZV 8% (4pts) 4 pts 1 pt
Notas del editor
- Although Bell’s palsy has been described as idiopathic facial paralysis, many evidence suggest a viral etiology. McCormick postulated the etiologic agent to be the herpes simplex virus in 1972. Studies by Murakami strongly suggest that herpes simplex virus type 1 (HSV-1) is active in cases of Bell’s palsy. In this study, endoneural fluid from 11 of 14 patients undergoing transmastoid decompression during the acute phase of the disease displayed DNA fragments of HSV-1 via the polymerase chain reaction (PCR). None from this surgical group displayed evidence of herpes zoster or Epstein Barr virus in the obtained samples. Again, finding of HSV-1 DNA in a temporal bone section of a patient dying six days after developing Bell’s palsy. An animal model for Bell’s palsy has been developed in which animals inoculated with HSV-1 demonstrate transient facial paresis, thus further supporting the idea that Bell’s palsy is the result of a viral inflammatory response that induces edema within the facial nerve.
- The meatal segment of the facial nerve and the nervus intermedius remain in the anterior-superior quadrant of the IAC and enter the fallopian canal at the meatal foramen, superior to the transverse crest and anterior to the vertical crest (Bill’s bar). Ge and Spector (14) have determined that the narrowest portion of the fallopian canal is located at the meatal foramen (mean diameter .68 mm). Thus, the size of the foramen coupled with a tight arachnoid band located at this segment contributes to the constriction of the facial nerve at this point in Bell’s palsy. The labyrinthine segment of the nerve, encased within the narrowest portion of the fallopian canal, courses 2-4 mm to the geniculate ganglion, where the nerve takes an acute turn at the external genu to enter the middle ear. The tympanic segment (horizontal segment) courses a total of 11 mm slightly above the cochleariform process and oval window and turns into the second turn (pyramidal turn) inferior to the lateral semicircular canal. The mastoid segment (vertical portion) then descends 13 mm to the stylomastoid foramen (2).
- Sunderland's classification describes five degrees of nerve injury. The first degree (neuropraxia) involves a localized conduction block in the nerve with the nerve fibers responding to electrical stimuli proximal and distal to the lesion, but not across the injured segment. Axonal continuity is preserved, wallerian degeneration does not occur, and recovery is usually complete. The second degree of nerve injury is called axonotmesis. This refers to disruption of the axon into proximal and distal portions with interrupted axoplasmic flow and Wallerian degeneration. The third, fourth, and fifth degree of nerve injury are grouped together as neurotmesis, and subdivided depending on the integrity of perineurium and epineurium. Wallerian degeneration occurs at the faster rate than axonotmesis and prognosis is the poorest. The rate of nerve degeneration in Bell’s palsy falls in between axonotmesis and neurotmesis. However, there is no electrical test to-date that can quantitatively differentiate the two subclasses of injury.
- The efficacies of oral prednisone and anti-viral agents have been studied extensively, yet there is no consensus among experts on ideal regimen and dosage.Adour, whose double-blind randomized controlled trial shows that the combined therapy of prednisone and acyclovir results in better return of muscle function and prevention of partial nerve degeneration.
- This result is challenged by another prospective trial by Kawaguchi who illustrates that valacyclovir plus prednisone have no advantage over prednisone alone.