Facial Paresthesias, Itching, and Dysesthesias

Facial paresthesia is a general term that can be applied to a variety of abnormal sensations occurring spontaneously. Paresthesias may be associated with many of the anesthetic and painful facial syndromes discussed in this chapter. The responsible lesion usually involves the nerve endings or the nerve trunk. Occasionally, the lesion is in the central nervous system. Itching represents an unusual form of paresthesia. Dysesthesias represent an abnormal perception of a common exteroceptive stimulus.

Itching

The common sensation of itching deserves mention in our discussion of the trigeminal sensory system. According to modern concepts based upon experimental observation, the sensation of itching is mediated by the same nerves as the sensation of pain. The difference between these two sensations is a function of the degree of stimulation. Itching results from a mild stimulus and pain from a more severe stimulus. According to Shelley and Arthur (1957), the sensation of facial itching is transmitted to the brain by impulses that travel centrally via afferent unmyelinated C fibers. These investigators believe that the stimulus that generates the sensation of itching is chemical in nature and commonly arises in the skin as the result of the action of proteinases on the fine nerve endings of afferent C fibers. Such proteinases may be derived from the epidermis, blood, dermal cells, infiltrates, and the surface microflora. Mechanical stimulation of the itch receptor produces a transitory sensation of itching lasting only a few seconds, but chemical stimulation by proteinases results in itching for a period of minutes. An itch point is a rich aggregate of fine fibers in the subepidermal tissue. Physiologically, this point is simply an area of low threshold to chemical, mechanical, thermal, and electric stimuli.

Arthur and Shelley (1959), in confirming that itch and pain are mediated by the same receptors, observed a number of patients in whom loss of touch had no effect on itch sensation. They also observed other patients in whom loss of pain was invariably associated with loss of itching. Rothman (1941) also concluded that pain and itch receptors are identical. He called attention to the observation that during periods of increasing and decreasing analgesia there are phases of hypalgesia in which pain stimuli do not elicit pain, but do cause itching.

Graham et al. (1950) showed that if itching occurred in a small area of skin, a stimulus from a pin pricked lightly into the surrounding skin could abolish itching for about 45 seconds. Since the slight pain from the pinprick completely faded within 10---15 seconds, they felt that cessation of itching could not be regarded as mere substitution of pain for itch. An area of potentially itchy skin surrounding a central focus of itching skin (e.g., an insect bite) coincides with the area in which the pinprick extinguishes the itch. Ayres (1964), in an article entitled "The Fine Art of Scratching," emphasized that scratching the area of potentially itchy skin around a mosquito bite gives almost as much relief as scratching over the bite itself.

Crosby et al. (1962) stated that fascicles associated with the lateral spinothalamic tract (and presumably the descending tract of the trigeminal nerve) carry impulses interpreted as itch. They noted that facial pain and itch sensations are both abolished by trigeminal medullary tractotomy. Patients with analgesia of the face from any cause cannot perceive the itching normally evoked by cowhage (itching powder).

White and Sweet (1955) performed bulbar tractotomy for the relief of itching that had been present for 15 ½ years in a patient who had had a compound fracture of the skull complicated by osteomyelitis of the underlying frontal bone. The patient's itching had caused him to scratch off all the hair from his left eyebrow and the anterior quadrant of his scalp. Supraorbital and supratrochlear neurectomy had provided only temporary relief with symptoms recurring following partial regeneration of the peripheral trigeminal axons. The patient experienced intense itching of his upper and lower eyelids and nose. Tractotomy alleviated his symptoms completely without producing undesirable neurologic sequelae.



Dysesthesia and Paresthesia From Specific Disorders

Trauma

Facial dysesthesia is common after partial injury or incomplete recovery of peripheral branches of the trigeminal nerve. Associated sensory loss in the area supplied by the injured nerve is common. Dysesthesia of the forehead and brow is a frequent sequel of trauma to the supraorbital nerve where the latter crosses the superior rim of the orbit. Although a painful neuroma may develop following trauma to the supraorbital notch (Sutula and Weiter, 1980), the associated symptoms do not compare in severity with those produced by the traumatic neuromas that develop in the stumps of amputated extremities.

Goldstein et al. (1963) emphasized the frequency of dental and oral trauma as a cause of mandibular and maxillary sensory neuropathy and paresthesia. Roberts and Person (1979) found maxillary and mandibular bone cavities at previous tooth extraction sites in 37 patients with mandibular and/or maxillary division pain and paresthesia. In all cases, the sensory neuropathy responded to curettage of the cavities and administration of systemic antibiotics.

Facial paresthesias may occur in patients who undergo either differential section of the trigeminal root or percutaneous radiofrequency trigeminal rhizotomy for trigeminal neuralgia (see the section on "Trigeminal Neuralgia" in this chapter). Although complete or partial section of the trigeminal root is no longer used for relief of facial pain, in cases where it has been performed, paresthesias after operation usually included crawling or drawing sensations and occurred in 56% of the cases reported by Peet and Schneider (1952). White and Sweet (1969) emphasized the problem of continuous paresthesias following percutaneous radiofrequency trigeminal rhizotomy. A few of their patients considered these sensations as intolerable as the pain of the neuralgia for which the procedure was performed. White and Sweet also noted a distressing tendency of some patients to scratch the itching, paresthetic skin (which is also anesthetic), until they tore away a portion of the face, usually in the region of the nostril. Howell (1962) as well as Cliff and Demis (1967) have described similar cases. Apfelbaum (1977) reported anesthesia dolorosa in 6 of the 48 patients (12.5%) in whom he performed percutaneous radiofrequency trigeminal rhizotomy and stated that a number of other patients had "mild dysesthesias." Burchiel et al. (1981) performed radiofrequency rhizotomy on 78 patients with trigeminal neuralgia of whom 3 (3.8%) developed anesthesia dolorosa and 11 (14.1%) complained of paresthesias in the area affected by the lesion. Tew (1977) reported a 2% incidence of anesthesia dolorosa in his series of patients. Drs. A.E. Maumenee and F.B. Walsh evaluated a patient who destroyed her eye and most of the skin of her cheek and nostril because of constant, postoperative facial paresthesias.


Toxic Reactions

Itching and burning paresthesias of the skin of the eyelids and cheeks have occurred as a complication of the fumes of trichloroacetic acid (Adams and Victor, 1981) and of hydroxystilbamidine isethionate (stilbamidine) therapy for trigeminal neuralgia (Arai and Snapper, 1947). This drug causes a specific sensory neuropathy of the trigeminal nerve. Only rarely does it involve other sensory nerves of the neck and trunk. Goldstein et al. (1963) commented that the paresthesia that their patients experienced tended to be stereotyped. They would complain of numbness of both sides of their face, by which they meant a wooden or dead feeling, and crawling or tingling sensations. Symptoms usually last for many months or several years and are refractory to all conservative forms of therapy.


Diabetes Mellitus

Diabetes mellitus is another cause of facial paresthesia. We have seen these symptoms in several diabetic patients who developed ocular motor nerve palsies. Their complaints of paresthesia in some cases were preceded by severe neuralgic pains in the distribution area of one or more divisions of the trigeminal nerve. In other cases, ill defined paresthesias (usually in the maxillary as well as the ophthalmic division) were the only clinical evidence that an ipsilateral sensory neuropathy accompanied the more obvious motor neuropathy of the abducens or oculomotor nerve. One of our patients with a typical diabetic oculomotor palsy had been annoyed for almost 9 months with a constant sensation on the ipsilateral side of his face that made him think that "ants were crawling" over his cheek and under his eyelids. Another elderly diabetic patient recalled that she had a peculiar itching sensation on one side of her face that persisted for almost 3 weeks and then went away. Two months later, she developed a typical ischemic oculomotor neuropathy.

  Miscellaneous Causes

Aneurysm is a rare cause of facial paresthesia and associated signs of sensory neuropathy. We have seen several patients with aneurysms of the intracavernous portion of the internal carotid artery who complained not only of diplopia from ocular motor nerve palsies but also of ill defined crawling or tingling sensations of the ipsilateral portion of the face innervated by the ophthalmic division of the trigeminal nerve. Höök et al. (1963) reported a 47-year-old woman in whom intermittent and sudden attacks of prickling in the eyelids and blurred vision recurred repeatedly over a 3-year period. The symptoms were produced by a large aneurysm of the midsegment of the basilar artery. Goldstein et al. (1963) mentioned two patients with symptoms of trigeminal neuropathy evoked by aneurysm. One patient had a fusiform aneurysm of the internal carotid artery; the other had a large basilar artery aneurysm that occupied the cerebellopontine angle.

Viral infections (herpes simplex and herpes zoster) may cause facial paresthesias. Other causes include tumors of the Gasserian ganglion or nasal sinuses (Hodgkin's disease, carcinoma, etc.), pontine tumor, and syringobulbia. Intermittent attacks of facial paresthesia are an infrequent manifestation of vertebral basilar insufficiency.
 

 

 

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