The most common disorder of the facial nerve is acute idiopathic facial paralysis or Bell’s palsy and there may be significant morbidity or incomplete recovery associated with severe cases. Individuals may report other symptoms, including a headache, tearing, changes in the amount of saliva and tears, drooling, difficulty eating and drinking, change in facial appearance, impairment of taste, and hearing loss. Unclear causes lead to unidentified treatments. Incidence for facial palsy was 8.6/100,000/children/year. A relationship between each meteorological variable and the incidence of BP was investigated by applying (Χ2) test on data from 13 contingency tables. Still, herpes simplex virus (HSV) has become accepted as the likely cause of Bell’s palsy. The intraoperative swelling of geniculate ganglion of facial nerve was found in 78% of patients with enhanced facial segment in MRI (p = 0.01).
Treatment of Bell’s Palsy is designed to decrease swelling and restore circulation around the nerve, so that the nerve fibers may again function normally. Bell’s palsy accounts for 80% of all peripheral facial palsies diagnosed annually and it is known to occur in 20 – 30 people per 100,000 per year. You have a facial nerve (also called the seventh cranial nerve) on each side of your face. Herpes zoster oticus, caused by varicella zoster virus (VZV) in the geniculate ganglion (Hunt, 1907), yields more severe symptoms of facial palsy and higher risk of complete nerve degeneration. The purpose of this study was to investigate the correlation between the swelling of the facial nerve and visualization of an enhanced segment by MRI. Acute paralysis or weakness on one side of your face Facial droop and difficulty with facial expressions. Because of possible drug interactions, individuals should always talk to their doctors before taking any over-the-counter medicines.
MRI scan was taken in all patients to exclude other pathology. The male-to-female ratio was 7:6 and the average age was 47 years old. There were 5 cases of right side palsy and 8 cases with the left side. Seven patients were diagnosed with Bell’s palsy and 6 patients with Ramsay Hunt syndrome. All patients underwent facial nerve decompression via the middle cranial fossa approach (MCFA) with any of following conditions; no symptomatic improvement despite medical treatment, degeneration ratio more than 90% by electroneuronography (ENoG), or no evidence of recovery upon facial electromyography. Most people who have Bell’s palsy recover completely, without treatment, in 1 to 2 months.footnote 1 This is especially true for people who can still partly move their facial muscles. Let the doctor know if you recently hit your head.
Age, sex, the degree of facial palsy on admission, the time interval between the symptom onset and the MRI scan, the enhanced facial nerve on MRI, the time interval between the symptom onset and the surgery and intraoperative finding of the facial nerve were analyzed in all patients. During surgery, the surgeon determined the swelling of facial nerve under operating microscope. The intraoperative swelling of facial nerve was determined by the extension of swelling beyond facial canal or the degree of bulging through the incision in the nerve sheath. These symptoms may include twitching, weakness, or paralysis on one or rarely both sides of the face. Call me vain, but I’m a young female and figured I had many years before getting the usual wrinkles and age spots. People report a sensitivity to sound, pain in or near the ear, and sometimes headaches. Patients with other diseases or conditions (eg, Lyme disease) sometimes develop a peripheral facial nerve palsy, but these are not classified as Bell’s palsy (see Differentials).
The analysis of time versus degree of nervous swelling and its correlation to other factors was done with a Fisher’s exact test. All 13 patients showed at least a H-B grade IV facial palsy upon admission, within which there were 10 cases with grade V and 1 case with grade VI. Some cases of Bell’s palsy are mild and do not require treatment because the symptoms the persons is experiencing subside on their own within a couple of weeks. Here, the amplitude of the recorded potential correlates (positively) with the number of functioning neurones and may have prognostic value. As a result, physical therapy is often necessary to keep the facial nerve stimulated and maintain muscle tone. Enhancement of the intracanalicular and geniculate ganglion were seen in 9 cases, and enhancement in the tympanic segment, and mastoid segment were also noted (). The use of antiviral medications such as acyclovir, often in addition to prednisone, is somewhat controversial.
Intraoperative findings of the facial nerve change demonstrated edema of the labyrinthine segment in all patients with enhanced facial nerve in MRI and hemorrhage in one case of Ramsay Hunt syndrome. The frequency of occurrence for edema decreased toward the geniculate ganglion and distal portion of the tympanic segment (). shows the MRI and operative findings in a patient with Ramsay Hunt syndrome. The enhanced area of facial nerve correlated with the swollen area during surgery. The relationship between the MRI findings and the degree of intraoperative facial nerve edema was that all patients with enhancement of the labyrinthine segment in MRI had intraoperative edema at the labyrinthine segment of the facial nerve except for the two cases that did not show enhancement of facial nerve in MRI. Facial nerve edema was also seen in the two patients without enhancement on MRI. Of the 9 cases that had enhanced MRI of the geniculate ganglion, the edema of the facial nerve was actually seen in 7 patients.
Of the 7 cases that had enhanced MRI of tympanic segment, the edema of the facial nerve was seen in only 3 patients. Thus, there was a statistically significant correlation between the enhancement of the facial nerve and the actual site of nerve edema with Fisher’s exact test (p = 0.01) (). This process continues until no further changes occur in the centers . (A) Axial contrast enhanced T1 image demonstrates enhancement from the lateral canalicular to the proximal tympanic segment of right facial nerve (arrow). (B) Coronal T1 weighted … The time interval between the symptom onset and surgery illustrates that the labyrinthine segment swelling was mainly seen in cases where the surgery was performed within 3 weeks, while change of the labyrinthine, geniculate ganglion and tympanic segment were in cases in which surgery was performed 3 to 9 weeks after the symptom onset. In the patients whose surgery was performed 9 weeks after symptom onset, changes in the labyrinthine segment and geniculate ganglion only were observed ().
However, some tests are done in some situations. The meatal foramen, which connects the internal auditory canal to the facial canal, is the narrowest portion of the facial nerve and as such is subject to high pressure, even if the degree of inflammation change is the same. As a result, decompression of this portion of the facial nerve is mandatory when performing facial nerve decompression.14 Therefore, in cases where surgical decompression is needed, decompression via MCFA is more effective than the transmastoid approach commonly performed during the early stages. For this reason, we performed facial nerve decompression via MCFA in all patients with surgical needs. In all patients, edema and swelling was observed in the labyrinthine segment of the facial nerve. The change in the nerve decreased towards the geniculate ganglion or distal portion of the tympanic segment. Yanagihara et al.
observed changes in the facial nerve in Bell’s palsy and Ramsay Hunt syndrome patients over time.15,16 They reported that facial nerve edema lasted longer and was more severe in Ramsay Hunt syndrome than in Bell’s palsy, but in all patients, the edema proceeded from the geniculate ganglion towards the peripheral area as time progressed and the facial nerve edema decreased. As for the intraoperative finding according to symptom onset, the edema of the labyrinthine segment was mainly observed, and the tympanic segment edema was seen in the subacute phase, 3 to 9 weeks after symptom onset. However, as time progressed, the edema remained only in the labyrinthine and geniculate ganglion. Some authors reported a correlation between enhancement and prognosis,3,4 while others reported the opposite.5,6 Absence of contrast enhancement can also be observed, and in our study, contrast enhancement could not be seen in 2 cases. This is thought to be due to the progression of swelling of the nerve, which disturbs the circulation around the nerve, which in turn decreases the diffusion of the contrast around the nerve. These various opinions are bounded by the clinical limitations of MRI, but in this study, enhancement of the labyrinthine segment was seen in all patients but two. Comparing the MRI findings with the actual intra-operative findings, the edema of labyrinthine segment of the facial nerve was seen in all patients with enhancement of the labyrinthine segment.
As for the geniculate ganglion, edema was seen in 78% of the patients with enhanced MRI. This test can determine the extent of nerve damage, as well as its location. My smile was still at about 75% of what it used to be on the right side (same goes for raising my eyebrows), but I knew there was some time to go as the doctor’s told me it’s a 6-month to a year or more healing process. One possible explanation is that the tympanic segment has a greater amount of normal arterio-venous plexus than the labyrinthine or geniculate ganglion, so that even without the presence of nerve edema, enhancement can be observed. Considering the etiologies of Bell’s palsy and Ramsay Hunt syndrome, the labyrinthine segment is influenced the most because it is located at the meatal foramen which is the narrowest part, and therefore enhancement is easily found in MRI and edema noted. However, as the time interval between MRI scan and the diagnosis varies along with the time interval from the diagnosis to the surgery, these differences may effect the changes in the lesion. In general, the continuation of contrast enhancement lasts longer than the clinical recovery, which is a limitation of the study.22 In addition, steroids can affect contrast enhancement but we did not control the role of steroid therapy.
The small population in this study warrants a larger work to confirm our results. Despite these limitations, we were able to identify the enhanced nerve segment on temporal MRI scans in Bell’s palsy and Ramsay Hunt syndrome and compared it with the actual injured facial nerve segment observed upon performing facial nerve decompression via the middle cranial fossa approach. Cases of Bell’s palsy and Ramsay Hunt syndrome treated with facial nerve decompression showed frequent enhancement of the labyrinthine segment on MRI scans. In all cases with enhancement in MRI, the edema of the actual labyrinthine segment of the facial nerve was observed. Subsequently, we believe that MRI scan is feasible in demonstrating the changes of the facial nerve, and the decompression of the labyrinthine segment during surgery is essential.