Davis PT Collection. Murtagh Collection. About Search. Enable Autosuggest. You have successfully created a MyAccess Profile for alertsuccessName. Previous Chapter. Next Chapter. Beal, M. Flint, and Stephen L. Larry Jameson, et al. Harrison's Principles of Internal Medicine, 20e.
McGraw Hill; Accessed November 14, Clinical experience and studies from China and elsewhere have shown that the earlier to start acupuncture treatment the better. Although in some cases the facial deviation may get worse after the first one or two sessions of acupuncture, it is most certainly not caused by acupuncture but the condition itself still being in the developing stage.
Some TCM practitioners may use other therapies such as tuina massage, moxibustion, or Chinese herbal medicine. It is more common in elderly people, with the average age of onset being in the 50ss. Women are nearly twice as likely to suffer from TN comparing to men. The cause of TN is still an area of discordance among the medical professionals. Most of them believe that the deterioration of the myelin protective coating of the nerve allows the transmission of abnormal messages of pain.
The damage of the myelin sheath may be caused by pressure from blood vessels or arteries, tumours, multiple sclerosis, injury to the nerve, consequences of shingles, or just the aging process.
When trigeminal neuralgia develops in a young adult or is bilateral, multiple sclerosis MS is a key consideration, and in such cases the cause is a demyelinating plaque at the root entry zone of the fifth nerve in the pons; often, evidence of facial sensory loss can be found on careful examination.
Cases that are secondary to mass lesions—such as aneurysms, neurofibromas, acoustic schwannomas, or meningiomas—usually produce objective signs of sensory loss in the trigeminal nerve distribution trigeminal neuropathy, see later in the chapter. An ESR is indicated if temporal arteritis is suspected. In typical cases of trigeminal neuralgia, neuroimaging studies are usually unnecessary but may be valuable if MS is a consideration or in assessing overlying vascular lesions in order to plan for decompression surgery.
Most patients require a maintenance dose of mg qid. Dizziness, imbalance, sedation, and rare cases of agranulocytosis are the most important side effects of carbamazepine.
If treatment is effective, it is usually continued for 1 month and then tapered as tolerated. Oxcarbazepine — mg bid is an alternative to carbamazepine, has less bone marrow toxicity, and probably is equally efficacious.
If these agents are not well tolerated or are ineffective, lamotrigine mg daily or phenytoin, — mg daily, are other options. Baclofen may also be administered, either alone or in combination with an anticonvulsant.
The initial dose is 5—10 mg tid, gradually increasing as needed to 20 mg qid. If drug treatment fails, surgical therapy should be offered. The most widely used method currently is microvascular decompression to relieve pressure on the trigeminal nerve as it exits the pons. This procedure requires a suboccipital craniotomy. In a small number of cases, there is perioperative damage to the eighth or seventh cranial nerves or to the cerebellum, or a postoperative CSF leak syndrome. Highresolution magnetic resonance angiography is useful preoperatively to visualize the relationships between the fifth cranial nerve root and nearby blood vessels.
Gamma knife radiosurgery is also utilized for treatment and results in complete pain relief in more than two-thirds of patients and a low risk of persistent facial numbness; the response is sometimes long-lasting, but recurrent pain develops over 2—3 years in half of patients.
Compared with surgical decompression, gamma knife surgery appears to be somewhat less effective but has few serious complications. Another procedure, radiofrequency thermal rhizotomy , creates a heat lesion of the trigeminal gasserian ganglion or nerve.
It is used less often now than in the past. Postoperatively, partial numbness of the face is common, masseter jaw weakness may occur especially following bilateral procedures, and corneal denervation with secondary keratitis can follow rhizotomy for first-division trigeminal neuralgia.
A variety of diseases may affect the trigeminal nerve Table Most present with sensory loss on the face or with weakness of the jaw muscles. Deviation of the jaw on opening indicates weakness of the pterygoids on the side to which the jaw deviates.
Among infectious causes, herpes zoster and leprosy should be considered. Tumors of the middle cranial fossa meningiomas , of the trigeminal nerve schwannomas , or of the base of the skull metastatic tumors may cause a combination of motor and sensory signs. Lesions in the cavernous sinus can affect the first and second divisions of the trigeminal nerve, and lesions of the superior orbital fissure can affect the first ophthalmic division; the accompanying corneal anesthesia increases the risk of ulceration neuro keratitis.
Loss of sensation over the chin mental neuropathy can be the only manifestation of systemic malignancy. Rarely, an idiopathic form of trigeminal neuropathy is observed. It is characterized by numbness and paresthesias, sometimes bilaterally, with loss of sensation in the territory of the trigeminal nerve but without weakness of the jaw.
Gradual recovery is the rule. Tonic spasm of the masticatory muscles, known as trismus , is symptomatic of tetanus or may occur in patients treated with phenothiazine drugs. The sensory component is small the nervus intermedius ; it conveys taste sensation from the anterior two-thirds of the tongue and probably cutaneous impulses from the anterior wall of the external auditory canal.
The motor nucleus of the seventh nerve lies anterior and lateral to the abducens nucleus. After leaving the pons, the seventh nerve enters the internal auditory meatus with the acoustic nerve. The nerve continues its course in its own bony channel, the facial canal, and exits from the skull via the stylomastoid foramen. It then passes through the parotid gland and subdivides to supply the facial muscles. A, B, and C denote lesions of the facial nerve at the stylomastoid foramen, distal and proximal to the geniculate ganglion, respectively.
Green lines indicate the parasympathetic fibers, red line indicates motor fibers, and purple lines indicate visceral afferent fibers taste.
A complete interruption of the facial nerve at the stylomastoid foramen paralyzes all muscles of facial expression. The corner of the mouth droops, the creases and skinfolds are effaced, the forehead is unfurrowed, and the eyelids will not close.
The lower lid sags and falls away from the conjunctiva, permitting tears to spill over the cheek. Food collects between the teeth and lips, and saliva may dribble from the corner of the mouth.
The patient complains of a heaviness or numbness in the face, but sensory loss is rarely demonstrable and taste is intact. If the lesion is in the middle-ear portion, taste is lost over the anterior two-thirds of the tongue on the same side. Patients will be unable to wrinkle their forehead, tightly close their eye, or smile on the affected side. This distinction can aid in localizing the lesion to the appropriate place in the nervous system, thereby narrowing the differential diagnosis.
A The innervation to the muscles of the upper face originates on both sides of the brain, whereas the innervation to the muscles of the lower face comes from the opposite side of the brain only. Illustration Brook Wainwright Designs. The symptoms may also develop at night while the patient is sleeping, making them seem more acute. Facial weakness typically recovers—partially or fully—within six months.
Specific clinical features include: weakness raising the eyebrow and furrowing the brow; difficulty or inability to close the eye; weakness in grimacing and smiling; and flattening of the nasolabial fold. In some cases antiviral therapy may also be prescribed. A Normal anatomic landmarks during smiling and raising the eyebrows.
B On the left, the nasolabial fold is flat and the mouth is turned down but the forehead wrinkles are intact and the palpebral fissures are symmetric. C On the left, the nasolabial fold is flat, the mouth is turned down, the forehead is not wrinkled and the palpebral fissure is widened. Acute Stroke Acute ischemic stroke is due to an occlusion of an artery supplying the brain. Deficits are abrupt in onset and typically reach maximum severity within seconds to minutes.
In stroke, the pattern of symptoms is determined by the arterial supply of the affected blood vessel and should therefore correspond to a known vascular distribution in the brain or brainstem. Facial weakness can be caused by strokes in many different locations in the brain and brainstem. Strokes involving the brain typically cause central facial weakness that involves the mouth and spares the eye and forehead.
Strokes involving the brainstem can sometimes cause weakness of the mouth, eye and forehead—mimicking a peripheral lesion.
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