Tuesday, December 8, 2015

New Facial Droop

New Facial Droop

A 43-year-old female presents to the emergency department with a concern that she is having
a stroke. She notes left facial weakness, pain in her left ear, and that whenever she drinks water it spills out the left side of her mouth. The symptoms have progressed over the past 24 hours. The photograph demonstrates the patient when she is asked to “smile and look up.”
Lower motor facial palsy CN VII

Question: In the patient with this condition, which of the following medical treatments should be considered?

A. Prednisone
B. Gammaglobulin
C. Thrombolytics
D. Heparin
E. Edrophonium

Answer: A
Diagnosis: Bell ’ s palsy
Discussion: The patient pictured has Bell ’ s palsy. Note the ptosis of the left eye and the weakness of the orbicularis muscles on the left side of the face. Also note the absence of wrinkling to the forehead on the affected left side. Bell ’ s palsy is the most common disorders affecting the facial nerve. It is an abrupt, isolated, unilateral, peripheral facial paralysis without detectable causes. While the actual pathophysiology is unknown, the mostwidely accepted theory postulates infl ammation of the
facial nerve causing it to be compressed as it courses through the temporal bone. 

 It occurs equally in men and women, most commonly between ages 10 and 40 years.
Clinical conditions associated with Bell ’ s palsy include pregnancy (especially the third trimester), immunocompromised states, and diabetes. Patients may present with a concern that they have suffered a stroke. Other common symptoms include pain in or behind the ear, numbness
on the affected side of the face, a recent upper respiratory infection, drooling, alteration in taste, and hyperacusis. The classic defi nition describes a lower motor neuron defi cit of the facial nerve, manifesting as weakness of the entire face (upper and lower) on the affected side. This is
in contradistinction to upper motor neuron lesions such as a cortical stroke, where the upper third of the face is spared while the lower two - thirds are paralyzed. While considered to be an idiopathic facial paralysis, there is signifi cant evidence to support an infectious cause. 

Herpes simplex virus (HSV - 1) has been isolated in many patients and is the most likely infectious agent, although there are likely other etiologic agents with a shared common pathway leading to facial nerve dysfunction.

No specifi c laboratory tests exist to diagnose Bell ’ s palsy. Clinical suspicion helps to direct what tests may be of value, and may include thyroid function studies and Lyme titer. One can also consider obtaining (if clinically suspected) a Rapid Plasma Reagin or a Venereal Disease Research Laboratory test for syphilis, as well as a human immunodeficiency virus test. There is no evidence to
support emergent imaging studies with Bell’s palsy. 

The primary treatment in the emergency department is with pharmacologic management. The remainder of care focuses on patient education as to the course of the disease and eye care instructions. While considered by some to be controversial, treatment with steroids remains common
if the patient presents within 7 days of symptom onset.

The postulated mechanism of action is in reducing facial nerve swelling. Current data supports using steroids as a means to improve outcomes, and earlier treatment is preferred (i.e., prednisone at 40–60 mg per day for 7–14 days).

Some recent evidence supports HSV as the presumed cause in more than 70% of cases; therefore, antiviral agents have been a logical choice for pharmacologic management. Recommendations include acyclovir 400–800 mg five times a day for 10 days, or valcyclovir 1 g three times
a day for 10 days. It should be noted, however, that recent literature has challenged this traditional treatment, and many practitioners are no longer using it. 

The eye on the affected side is potentially at risk for corneal drying and foreign body exposure, as the lid may not close completely, especially when the patient is asleep. This is generally managed with artificial tears and some form of eye protection (patch or glasses during the day, taping the eye shut at night). The vast majority (85% or more) of patients recover without any cosmetically obvious deformities. Ultimately, 10% will have some residual asymmetry of the facial muscles, and 5% will suffer from significant facial nerve deficits. In most cases, recovery begins 3 weeks after symptom onset, but it may take up to a year for complete resolution. Patients with incomplete facial nerve involvement have a more favorable prognosis than those with a complete deficit.


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