Cutaneous Sensibility Changes in Bell’s Palsy Patients

Palacio, Carlos Andrés Cárdenas; Galarza, Francisco Alejandro Múnera

doi:10.1177/0194599817690107

Cited by 5 publications

(3 citation statements)

References 39 publications

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“…Nevertheless, it is unlikely that any sensory abnormality is restricted to only a part of the paralyzed hemiface. This fits with a recent study analyzing six areas of the faces of patients with Bell's palsy that did not reveal any differences between the areas ( 27 ). We had to limit the assessment to one well-defined spot in the midface, mainly for practical reasons.…”

Section: Discussionsupporting

confidence: 93%

“…From today's perspective, these studies do not fulfill the high standards for a reliable measurement of facial sensibility. In a recent study, Cárdenas Palacio et al examined the facial sensibility with pressure threshold and two-point discrimination in six areas of the face in 12 patients with Bell's palsy over a 2- to 6-week period (three or four patients per timepoint) ( 27 ). Significant differences were observed between both sides of the face with a two-point discrimination test on eyelid, cheek, and lip.…”

Section: Discussionmentioning

confidence: 99%

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Sensory function in the faces of patients with facial palsy: A prospective observational study using quantitative sensory testing

et al. 2022

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Objectives/HypothesisTo determine the sensory function of both sides of the face in patients with acute or chronic facial palsy.Study designProspective observational study.MethodsThe standardized quantitative sensory testing (QST) protocol of the German Research Network on Neuropathic Pain (DFNS), including thermal or mechanical stimuli (touch, pain, vibration, and pressure), was used to investigate somatosensory function in the faces of patients. A patient-reported outcome measures for the assessment of disturbed facial comfort or facial pain, the facial Clinimetric Evaluation Scale (FaCE) Facial Comfort Subscale, and the 36-Item Short Form Survey (SF-36) pain subdomain were used.ResultsA total of 29 patients (22 female, median age of 48 years; 7 acute palsy; 22 chronic palsy; House-Brackmann grade II–VI) were included. The median FaCE Facial Comfort Subscale score and the median SF-36 pain subdomain score were 50 and 100, respectively. Most patients had, at an individual level, a normal sensory function in all or most tests. On average, the frequencies for all parameters were not different between the paretic side and the contralateral side (all p > 0.05). Additionally, when z-scores were used to compare our patient sample with healthy controls from the DFNS reference database, there was no difference between the paretic side and the contralateral side (all p > 0.05). Furthermore, there were no differences between patients with acute facial palsy and those with chronic facial palsy (all p > 0.05). The FaCE Facial Comfort Subscale score and the SF-36 pain subdomain score did not correlate with the QST parameters (all p > 0.05).ConclusionPatients with acute or chronic unilateral peripheral facial palsy had normal sensory function on the paretic and contralateral sides compared with the reference values of healthy controls, and there was no significant difference between the sides. The numbness frequently felt in the affected hemiface is not related to a peripheral sensory disorder and is most likely a manifestation of an unsolved cortical somatosensory-motor mismatch.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Sensory function in the faces of patients with facial palsy: A prospective observational study using quantitative sensory testing

et al. 2022

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“…First, the unilaterally impaired sensation in the face is well-known in patients with prior isolated facial nerve dysfunction, as in Bell's palsy ( 11 , 12 ); this is probably due to impairment of visceral efferent fibers of the facial nerve. Another possible explanation for the sensory symptoms in facial nerve palsy is impaired processing of the facial somatosensory information ( 11 ).…”

Section: Discussion/conclusionmentioning

confidence: 99%

Case report: Bitter vertigo

Goldschagg

Brem²,

Strupp³

2022

Front. Neurol.

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BackgroundThere are many causes of episodes of vertigo and very few causes of episodes of changes in taste, and the combination of the two is very rare. Here, we describe a patient with recurrent short episodes of vertigo in combination with simultaneous episodes of recurrent paroxysmal dysgeusia and altered feeling on the left side of face. The symptoms were caused by compression of the vestibulocochlear nerve and the facial nerve due to dolichoectasia of the basilar artery.MethodsThe patient was diagnosed in our routine clinical practice and underwent a complete neurological and neuro-otological examination, including video head impulse test, caloric irrigation, ocular and cervical vestibular evoked myogenic potentials, acoustic-evoked potentials, neuro-orthoptic examination, cranial MRI, and MR angiography. The patient was seen twice for follow-up.CaseA 71-year-old patient primarily presented with a 2-year history of recurrent short episodes of spinning vertigo. Each of the episodes began with an altered feeling on the left side of the face, followed by a bitter taste on the left half of the tongue, and subsequently vertigo lasting for up to 15 s. The frequency of the attacks was high: up to 80 times per day. Laboratory tests revealed signs of a peripheral vestibular deficit on the left side. There were no signs of sensory or motor deficits or of altered taste between the episodes. An MRI of the brain showed an elongated basilar artery leading to an indentation of the facial and vestibulocochlear nerves on the left side.ConclusionWe propose a neurovascular compression in the proximal part of two cranial nerves because of pulsatile compression by the elongated basilar artery with ephatic discharges as the cause of the recurrent episodes. Consistent with the theory of ephatic discharges, treatment with the sodium channel blocker lacosamide for over six months with a final dosage of 200 mg per day p.o. led to a significant reduction of the attack frequency and intensity. This treatment option with a sodium channel blocker should therefore not only be considered in vestibular paroxysmia but also in cases of paroxysmal dysgeusia.

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