Acute Onset Facial Droop

Case Study

The bedside nurse initiated a rapid response event for a patient because of acute onset left-sided facial droop that was noted by the physical therapist, who was evaluating the patient for his morning therapy session. On arrival of the rapid response team, the patient’s nurse informed the team that the patient is a 63-year-old male with a history of hypertension and gout that is post-operative day one of a right total knee replacement. The patient’s nurse reported that he did not have a facial droop when she saw him 2 h ago.

Vital Signs

Temperature: 98.3 °F, axillary
Blood Pressure: 132/76 mmHg
Heart Rate: 81 beats per min – normal sinus rhythm on telemetry
Respiratory Rate: 11 breaths per min
Pulse Oximetry: O ₂saturation of 99% on room air

Focused Physical Examination

A quick exam revealed a well-built middle-aged man in no acute distress resting comfortably in his bed. Upon auscultation, his lungs were clear, and his heart sounds were regular. There was a pronounced left-sided facial droop. The patient was not able to raise his left eyebrow. The left eye did not fully close when the patient was instructed to close his eyes tightly. There was an absence of wrinkles noted on the left side of the forehead. The remaining cranial nerve testing did not reveal any abnormalities. He was alert and orientated, had full strength in his upper extremities and left lower extremity. His right lower extremity demonstrated 4/5 strength that was limited secondary to pain. Finger-nose-finger testing was intact. He denied any headaches, vision problems, or dizziness. He reported that he had some eye dryness and irritation over the last two days, but he attributed this to being in the hospital and undergoing his knee replacement. His National Institutes of Health (NIH) score was three.

Interventions

Given the neurological exam findings, a stroke alert was called, and expert stroke team consultation was sought. A stat computed tomography (CT) of the head was done, which did not show any acute hemorrhage. Stat magnetic resonance imaging (MRI) of the brain was obtained and was negative for any acute infarcts. A presumptive diagnosis of Bell palsy was made, and the patient was started on 60 mg of oral prednisone; he received his first dose after the imaging had been reported. Due to the patient being unable to close his left eye fully, artificial tears and an eye patch were ordered to prevent ocular injury.

Final Diagnosis

Bell palsy.

Bell Palsy

The facial nerve (cranial nerve VII) has a complex anatomy and a wide distribution. It has four broad functions: somatic motor, somatic sensory, visceral motor, and visceral sensory.

The motor portions of the facial nerve arise from the facial nerve nucleus located in the pons. The facial nerve’s sensory portions are derived from the superior salivatory nuclei and the solitary nucleus in the pons. The motor and sensory nerves travel individually through the temporal bone, where they come together as a single nerve in the geniculate ganglion. While in the temporal bone, the facial nerve gives off the greater petrosal nerve, which will provide parasympathetic innervation to the lacrimal glands, the nerve to the stapedius, which is a motor nerve that innervates the stapedius muscle of the inner ear, and the chorda tympani, which provides sensory fibers to the anterior two-thirds of the tongue, and the submandibular and sublingual glands.

The extracranial portion of the facial nerve begins just posterior to the mastoid process, where it quickly distributes three branches. The first branch is the posterior auricular nerve, and it supplies motor control to some of the muscles around the ear. The nerve to the digastric muscle and the nerve to the stylohyoid are the other two branches. The facial nerve then travels to the level of the parotid gland and branches into its five terminal branches (temporal, zygomatic, buccal, marginal mandibular, and cervical), which innervate the muscles of facial expression around the forehead, cheek, mouth, and neck (platysma) ( Fig. 42.1 ).

Having a sound understanding of neuroanatomy can help understand Bell palsy’s pathogenesis. The forehead musculature is supplied by motor neurons from both the left and right temporal branches, which ultimately are derived from each side of the pons. At their origin, a portion of these motor fibers ultimately crosses sides to provide bilateral innervation to the forehead musculature. Because of this crossing over, an upper motor lesion, such as a stroke, will not completely eliminate the motor fibers from the unaffected pons allowing the patient to raise his eyebrows and causing wrinkles of the forehead. However, since Bell palsy is a lower motor lesion, motor innervation of the forehead musculature from both temporal branches is affected. This causes the patient to have paralysis of the forehead muscles, resulting in the inability to raise his eyebrow and loss of the forehead’s wrinkles. See Table 42.1 for differences between upper versus lower motor neuron lesions of the facial nerve.

Table 42.1

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