Painful neuralgia of the trigeminal nerve results in the clinical syndrome of tic douloureux or trigeminal neuralgia. y The paroxysmal disorder presents as excruciating, lancinating painful spasms affecting one or more divisions of CN V. Trigeminal neuralgia is unilateral and usually affects the second or third division of CN V (3rd>2nd>1st). In less than 5 percent of cases V1 is affected, whereas V3 is affected in more than 70 percent of cases. y Rarely, pain may occur bilaterally, although simultaneous bilateral spasms are quite atypical. The pain occurs spontaneously as brief lightning-like spasms lasting seconds to minutes, or pain may be precipitated by cutaneous or auditory stimuli. In many instances, there is a demonstrable trigger point that can reproduce pain, and some patients may be unable to chew, eat, drink, shave, or brush their teeth for fear of triggering a spasm. y Paroxysms recur throughout the day and night. Between attacks, there are no symptoms, but the patient is usually anxious about having another attack. Objective sensory or motor deficits are not a feature, although a subjective report of hypesthesias over the face may be reported. Often there is a temporal summation of stimuli necessary to invoke a response. The pain is reported as lancinating, stabbing, searing, burning, or electrical, and the intensity is such that the patient often winces or grimaces in a tic-like fashion. Trigeminal neuralgia affects approximately 155 people per million population and has a slight female predominance (3:2). It is the most common neuralgia, and its incidence peaks in middle age. The age of onset is important, however, because the appearance of trigeminal neuralgia in a young patient should raise the suspicion of demyelinating disease such as multiple sclerosis y , y or another structural brain stem disorder. y y
Pathological analyses of trigeminal biopsy specimens taken during vascular decompression have described focal demyelination but no inflammatory cells. y y Abnormal ephaptic nonsynaptic neurotransmission between demyelinated trigeminal axons within the nerve root, ganglion, or spinal trigeminal nucleus may provide the physiological substrate for the paroxysmal pain characteristic of trigeminal neuralgia, especially if initiated by cutaneous stimuli.
On physical examination, objective neurological deficits are not present. The patient, however, may appear emaciated if, for example, a trigger point is initiated during chewing, or males may appear disheveled if shaving induces a spasm. Laboratory study results are normal. Careful inspection and palpation of the teeth, gums, nares, nasal sinuses, palate, and pharynx should be performed because disease processes such as infections or inflammatory disorders in these regions can cause significant facial pain. MRI of patients with trigeminal neuralgia may be helpful in identifying other etiologies or associated disorders.
The diagnosis of tic douloureux can usually be made by history alone, but the disorder must be distinguished from other causes of facial pain syndromes such as glossopharyngeal neuralgia, which can be confused with tic douloureux that involves the third division of CNV. Herpes zoster or post-herpetic neuralgia may also provide some diagnostic confusion. Tumors or vascular lesions of the cerebellopontine angle y or within the trigeminal ganglion itself may induce pain similar to that of trigeminal neuralgia, although these disorders can be distinguished by findings of trigeminal sensory loss, atrophy of facial masticatory muscles, diminished corneal reflexes, and involvement of other adjacent brain stem structures that are not characteristic of trigeminal neuralgia. The nature of the pain in these cases is also distinct from that of trigeminal neuralgia in that it is often continuous and unremitting rather than episodic.
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