BELL’S PALSY PATHOPHYSIOLOGY The pathophysiology pathophysiology of Bell's Palsy is not entirely clear, but is most likely related to compression of the facial nerve due to demyelination, inflammation, or ischemia (inadequate blood supply). The facial nerve that is damaged is called the seventh cranial nerve (CN VII) . This nerve primarily moves the facial muscles, controls the salivary and tears glands, and enables the front part of the tongue to detect tastes. The paired seventh cranial nerve is located in the Fallopian canal in the skull, inferior to the ear and is connected to the muscles on the face bilaterally. As well as controlling facial muscles and some glands, it is also responsible for letting one open and close their eyes. Predisposing factors Age: risk increases with age (56 y/o) equal in men and Gender: women. Race: higher if in Japanese descent. Genetics: approximately approximately 4 % of cases.
It is thought that viral infections or damage to the myelin sheath of the seventh cranial nerve can bring on the disorder. disorder. Viral infections may lead to inflammation, which in turn places pressure on the Fallopian canal leading to an infarction. Damage to the myelin sheath of the nerve can cause the disruption disruption or slowing of signals from the brain to the facial muscles. It is also believed that the disorder can be brought on by patients with Lyme disease, diabetes, diabetes , high blood pressure, tumors, HIV, chickenpox, or even trauma to the face or skull near the nerve. Bell’s Palsy, but those primarily susceptible include pregnant women and those with with diabet diabetes es or upper upper resp respira irator tory y ailme ailment nts s such such as the the cold cold or flu. flu. Anecd Anecdota otally lly,, exposure to cold is a frequently cited cause – for example, driving with a car window open in frigid weather, or sleeping with the window open on a chilly night. Also, young and middle aged adults are more likely to be affected. It is quite uncommon to see a case in an individual ten or younger and sixty or older. Short Description of Pathologic Process From the course of the illness, it is presumed that the acute non-supportive inflammation of unknown etiology causes swelling and/ or edema and hyperemia of the the nerve nerve sheath sheath,, with with comp compres ressio sion n of the axons axons in the narro narrow w facial facial cana canal, l, thus thus strangulating them and inhibits appropriate neural stimulation. Pathophysiological Process 1. Inflammation - facial nerve becomes inflamed in reaction to the infection.
(Rub (Rubor or (redn (rednes ess), s), Calor Calor (hea (heat), t), Dolor Dolor (pain (pain), ), Tumor (swelling) and Function laesa (loss of function) Infl Inflam amma mato tory ry reac reacti tion on may may hind hinder er or bloc block k nerv nerve e conductions. Usually at the internal auditory meatus, •
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2. Compression - facial nerve is compressed against the skull’s hard bony surface
(because it passes through a narrow, bony canal called the Fallopian canal)
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The facial nerve courses through a portion of the temporal bone commonly referred to as the facial canal. The first portion of the facial canal, the labyrinthine segment, is the narrowest; the meatal foramen in this segment has a diameter of only about 0.66 mm. This is the only segment of the facial nerve that lacks anastomosing arterial cascades, making the area vulnerable to embolic phenomena, low-flow states, or vascular compression. Given the tight confines of the facial canal, it seems logical that inflammatory, demyelinating, ischemic, or compressive processes may impair the function of the facial nerve.
3. Infarction - the death of nerve cells due to insufficient blood oxygen and supply •
In some mild cases, there is damage only to the myelin sheath.
4. Interruption - damage to the myelin sheath of the nerve can cause the
disruption or slowing of signals or messages from the brain to the facial muscles. •
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The block inhibits appropriate neural stimulation to the muscle by the motor fibers of the facial nerve. As a result of its convoluted path through the temporal bone which is only slightly larger in diameter than itself, the 10,000 neurons that exist in the facial nerve are prone to impairment due to vascular congestion with secondary ischemia.
5. Facial weakness or paralysis •
Damage to one of two facial nerves can possibly result in temporary paralysis of the facial muscles, most often to only one side of the face and in rare cases, both sides.
Onset and Symptoms Within a day or two after exposure, there may be slight fever, pain behind the ear, and pain and stiffness in the neck. The onset is sudden or acute, and often, the patient awakens to find the face paralyzed. A feeling of stiffness and numbness but sensory testing is normal. About ½ of the cases attain maximum paralysis in 48 hours and practically all cases in 5 days.
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movement of facial expression muscles except jaw, close eyes, labial speech sounds.
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taste- anterior two third of tongue sensation to Pharynx
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secretion of saliva and tears.
Motor The classic presentation of Bell's palsy is weakness on one side of the face. The potential range of weakness is wide – it may range from difficulty blinking all the way to a complete paralysis on one side of the face with an inability to close the eye. Onset usually occurs acutely, but the weakness may worsen for 24 to 48 hours before stabilizing. Poor eyelid closure Brow droop Paralytic ectropion of the lower lid Mild, generalized mass contracture of the facial muscles, rendering the affected palpebral fissure narrower than the opposite one (after several months) Aberrant regeneration of the facial nerve with motor synkinesis Reversed jaw winking (ie, contracture of the facial muscles with twitching of the corner of the mouth or dimpling of the chin occurring simultaneously with each blink) Autonomic synkinesis (ie, crocodile tears-tearing with chewing)
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Sensory Alteration of taste (57%) or hearing is occasionally a symptom. People with Bell's palsy may describe the sensation of unilateral loss of facial movement as deadness, loss of feeling, or numbness, although the affected part of the face is neither asleep nor tingling. Aching of the ear or mastoid (60%)
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Parasympathetic Decreased tear output/poor tear distribution Excessive tearing Hypersalivation
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Medical Management
The objectives of management are to maintain facial muscle tone and to prevent or minimize denervation. Steroidal therapy may be initiated to reduce inflammation and edema, which reduces vascular compression and permits restoration of blood circulation to the nerve. Early administration of corticosteroids appears to diminish severity, relieve pain, and minimize denervation. Facial pain is controlled with analgesic agents or heat applied to the involved side of the face. Additional modalities may include electrical stimulation applied to the face to prevent muscle atrophy, or surgical exploration of the facial nerve. Surgery may be performed if a tumor is suspected, for surgical decompression of the facial nerve, and for surgical rehabilitation of a paralyzed face. •
Analgesics- to relieve pain
Steroids- to reduce facial nerve edema & improve edema & improve nerve conduction & blood flow Possible electrotherapy Surgery for persistent paralysis •
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Nursing Considerations Watch for adverse effects of steroids use Apply moist heat to the affected side of the face-to reduce pain • •
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Help the pt maintain muscle tone: massaging the face with a gentle upward motion 2-3xdaily x 5-10mins exercise by grimacing in front of a mirror
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Protect eyes, have pt cover eye w/ an eye patch
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Prevent excessive wt loss: have him chew on unaffected side of his mouth
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provide a soft, nutritionally balanced diet, eliminating hot foods & fluids apply a facial sling to improve lip alignment Provide frequent & complete mouth care
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Offer psychological support
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Gatera, Jad Paulo C.
