We conducted a literature search focusing on carotid dissection as a cause of severe dental pain; however, the search failed to reveal any similar occurrences. Dentists should be aware of the potential for dental pain to be associated with spontaneous dissection of the ICA. This could avoid inadvertent and potentially incorrect dental therapy that might result in delayed referral for evaluation and treatment to prevent irreversible neurological sequelae.

	REPORT OF A CASE

TOP ABSTRACT REPORT OF A CASE DISCUSSION CONCLUSION REFERENCES

 
The patient was a healthy 52-year-old man who developed pain in his right maxilla after a day of strenuous work around his home that involved hyperextension, flexion and rotation of the neck. He had no other complaints and no weakness. About 24 hours later, the pain became increasingly severe and localized in the maxillary right first molar; 10 years earlier, the patient had undergone endodontic treatment in this tooth, which included insertion of a post and a crown restoration.

The next morning, the patient visited one of us (T.R.), who performed a percussion test by using the flat handle of a mirror. She carried out the percussion test on tooth no. 3, the adjacent teeth and the contralateral molar. The dentist detected a positive response on tooth no. 3 only. She then referred the patient to an oral surgeon (L.S.) with a presumptive diagnosis of failed endodontic therapy and a suggestion that he undergo apical surgery or extraction.

The oral surgeon obtained panoramic and periapical radiographs (Figure 1, A and B), which were inconclusive and revealed no distinct periradicular disease that would signal the need for apical surgery or extraction. He referred the patient to the radiology department for sinus radiographs, as well as to an endodontist and an otolaryngologist. No maxillary sinus abnormality was detected, and the endodontist’s examination revealed no endodontic disease. The examination by the otolaryngologist was unremarkable, but because the pain was unremitting, the patient underwent magnetic resonance imaging (MRI) of the brain, which revealed the presence of multiple cerebral infarcts of the right hemisphere (Figure 2). The radiologist then performed magnetic resonance angiography (MRA) of the carotid arteries, which revealed complete occlusion of the right ICA secondary to an acute spontaneous dissection (Figure 3).

View larger version (66K): [in this window] [in a new window]   Figure 1. A. Panoramic radiograph shows no evidence of disease in the tooth or surrounding areas. B. Periapical radiograph reveals no evidence of periapical disease in tooth no. 3.

View larger version (85K): [in this window] [in a new window]   Figure 2. Axial diffusion-weighted magnetic resonance image at the level of the centrum semiovale demonstrates multiple areas of high signal (arrows) in the right centrum semiovale consistent with acute infarctions.

View larger version (85K): [in this window] [in a new window]   Figure 3. Magnetic resonance angiogram of the right side of the neck demonstrates acute tapering at the origin of the right internal carotid artery consistent with acute dissection and occlusion (arrow).

Approximately one year later, the patient was doing fine, and to date has had no neurological sequelae. His MRA showed no abnormalities (Figure 4). The dentist performed another percussion test on the tooth and obtained radiographs, neither of which revealed any significant findings.

View larger version (100K): [in this window] [in a new window]   Figure 4. Magnetic resonance angiogram 13 months after the acute dissection demonstrates complete reconstitution of flow in the right internal carotid artery (ICA), which now appears normal. The arrow points to the origin of the right ICA, which is widely patent and appears normal, compatible with recanalization.

	DISCUSSION

TOP ABSTRACT REPORT OF A CASE DISCUSSION CONCLUSION REFERENCES

Schievink¹ extensively reviewed spontaneous dissection of the carotid artery. He noted that this was thought to be a rare cause of stroke, with the diagnosis usually not made until the postmortem examination. Only in the last 20 years—with the advent of modern diagnostic approaches—has the diagnosis of dissection been made before death.¹

Carotid artery dissection can occur spontaneously (that is, no discernible inciting event), after trauma or as the result of underlying disease of the vessel (such as cystic medial necrosis, Marfan syndrome or fibromuscular dysplasia). Patients often reveal a history of minor trivial trauma, such as that resulting from chiropractic manipulation of the neck, coughing, vomiting, sneezing or painting a ceiling. These neck movements, especially if sudden, may injure the artery as a result of mechanical stretching.¹ Our patient was sticking his head out of windows and flexing, extending and rotating his neck as he replaced window screens.

In a report of 10 patients with spontaneous dissection of the ICA, Chaves and colleagues² noted that nine patients experienced a stroke, while one patient experienced only transient ischemic attacks. The most common initial clinical symptom was severe retro-orbital or temporal headache, followed by contralateral hemiparesis. In contrast, our patient experienced only acute dental pain and had no neurological sequelae, except for the oculosympathetic palsy.

Konzelman and colleagues³ reported a number of obscure syndromes that can mimic dental or jaw pain in the absence of pathological findings within these structures. They presented case reports of carotidynia, temporal tendinitis, pre-trigeminal neuralgia and complex regional pain syndrome, but they did not mention spontaneous dissection of the ICA.

Ophthalmological signs and symptoms. On admission to the hospital, our patient had oculosympathetic palsy. Kerty⁴ reviewed the ophthalmological signs and symptoms of carotid dissection. Of 28 patients with spontaneous dissection of the ICA who underwent a neuro-ophthalmological examination, 23 had oculosympathetic paresis. A plexus of nerves arises from the sympathetic cervical ganglion on the surface of the carotid artery on its path to the eye. These sympathetic fibers innervate the tarsal muscles of the eyelid. Thus, a patient with Horner’s syndrome experiences a mild droop of the eyelid. Another abnormality that occurs with Horner’s syndrome is miosis, in which the pupil is smaller on the side of the dissection. However, both of these findings are difficult to detect. Unless one is specifically searching for a subtle ptosis, it can be missed. Similarly, miosis is difficult to detect in a brightly lit examining room because both pupils will be small.

Facial anhidrosis (a lack of facial sweating), the third component of the "typical" case of Horner’s syndrome, is not present in these patients, because the sympathetic plexus surrounding the external carotid artery innervates the facial sweat glands. (However, we should note that in our review of the literature, we found that most clinical articles use the term "Horner’s syndrome," whereas the ophthalmological literature uses the term "oculosympathetic palsy" or "partial Horner’s syndrome" in reference to patients with dissection of the ICA.

Prognosis for patients. Our patient’s only neurological sequela was the oculosympathetic palsy. We found the literature to be divided about the prognosis for patients with spontaneous dissection of the ICA. In his review of the literature, Schievink¹ reported that the patient’s prognosis is related to the severity of the initial ischemic injury and the extent of collateral circulation. He noted that the reported death rate is less than 5 percent and that approximately three-fourths of patients who have had a stroke experience a good functional recovery. This is in sharp contrast to the study findings of Milhaud and colleagues,⁵ who compared the prognosis for 73 patients with ICA occlusion due to dissection with that for 81 patients with ICA occlusion due to atherothrombosis. They reported that patients who experienced dissection had more severe clinical impairment—with a higher frequency of decreased consciousness and poorer outcomes at one month—than did patients who experienced atherothrombosis.

Schievink¹ reported that the annual incidence of spontaneous carotid artery dissection ranged from 2.5 to 3 per 100,000. This condition accounted for only 2 percent of all ischemic strokes, but it was an important etiologic factor (10 to 25 percent of cases) in ischemic stroke in young and middle-aged patients.

MR techniques. Conventional angiography has long been the gold standard in the diagnosis of arterial dissection, because it can demonstrate the arterial lumen and allow characterization of the carotid dissection. However, MR techniques are replacing conventional angiography in the diagnosis of dissection, because the resolution of MRA approaches that of conventional angiography, and MRI can demonstrate the intramural hematoma noninvasively. Carotid ultrasonography and transcranial Doppler ultrasonography, though less effective for the initial detection of dissection of ICA, are excellent noninvasive methods for evaluating the resolution of the dissection, which may occur over weeks to months.¹

The major goal of treatment is to prevent thromboembolic complications. Anticoagulation with intravenous heparin therapy followed by oral warfarin therapy has been recommended. Most dissections heal spontaneously¹ (Figure 4).

	CONCLUSION

TOP ABSTRACT REPORT OF A CASE DISCUSSION CONCLUSION REFERENCES

 
We have presented the first case report, to our knowledge, of spontaneous dissection of the ICA manifesting initially as dental pain in an endodontically treated maxillary molar. Our primary purpose is to alert dentists to this possibility so that they will not perform inappropriate aggressive therapy on a tooth for which it is not indicated. Clinicians need to refer patients to a physician for prompt evaluation and treatment to prevent irreversible neurological sequelae.