Spontaneous Dissection of the Cervical Internal Carotid Artery Presentation With Lower Cranial Nerve Palsies Bahram Mokri, MD; Wouter I. Schievink, MD; Kerry D. Olsen, MD; David G. Piepgras, MD \s=b\ Spontaneous dissections of the internal carotid arteries but are not rare. They constitute a fairly common cause of ischemic stroke in young patients (young in terms of the age at which strokes generally occur). The common presenting manifestations are (1) unilateral headaches followed after a period of delay by focal cerebral ischemic symptoms or (2) unilateral headaches and ipsilateral incomplete Horner's syndrome. These may or may not be associated with subjective or objective bruits. In rare instances, spontaneous dissections of the internal carotid arteries may present as lower cranial nerve palsies and cause dysphonia, dysarthria, dysphagia, and numbness of the throat. Affected patients may initially present to the otolaryngologist or be referred to one. This article describes eight patients with spontaneous dissections of the internal carotid arteries and lower cranial nerve palsies, and the pertinent literature is reviewed. (Arch Otolaryngol Head Neck Surg. 1992;118:431-435) are uncommon of the internal carotid (ICAs) pro¬ duced by penetration of circulating blood the Dissections of the vessel. This extend for various distances the arteries manifestations include (1) unilateral headaches followed after a period of delay by focal cerebral ischemie symp¬ toms (transient ischemie attacks or stroke or both) or (2) unilateral headaches associated with ipsilateral incom¬ plete Horner's syndrome. The average age of patients is the early 40s. Spontaneous ICA dissection is a common cause of stroke in young patients (young in terms of the age at which strokes generally occur). Because of the nature of the presenting symptoms, af¬ fected patients often present to or are referred to the neurol¬ ogist or neurosurgeon. In some patients, spontaneous ICA dissection may manifest with lower cranial nerve palsies and cause dysphonia, dysarthria, and dysphagia. Such patients may initially present to the otolaryngologist or be referred to one by the primary or consulting physician. In this article we describe eight patients with sponta¬ neous ICA dissections who presented with lower cranial nerve palsies. We also review the pertinent literature. are into may graphie features of this entity.4-10 The common clinical wall along artery, often more distally than proximally. The intramural hematoma that is thus formed splits off the media and forms a false lumen. This may lie close to the intima and cause nar¬ rowing of the true lumen of the ICA, or sometimes it may expand toward the adventitia and cause an aneurysmal dilatation—a "dissecting aneurysm." At times the intramu¬ ral hematoma may rupture back into the original arterial lu¬ men and create a "double lumen."1 Some ICA dissections may occur spontaneously, whereas others occur after definite head or neck injury. In spontane¬ ous dissections, the role of minor or trivial trauma such as coughing, straining, and abrupt or exaggerated neck move¬ ments has not been entirely excluded.2 Some patients have evidence of primary arterial disease, which is thought to pre¬ dispose the vessel to spontaneous dissection. Internal carotid artery dissections are uncommon but are not rare. The first case was reported in 1954.3 Subse¬ quent sporadic reports were published. However, in the past two decades, several reports and series have ap¬ peared in the literature, and clinicians and radiologists have become more familiar with the clinical and angio- Accepted for publication October 17, 1991. From the Departments of Neurology (Dr Mokri), Neurologic Surgery (Drs Schievink and Piepgras), and Otorhinolaryngology (Dr Olsen), Mayo Clinic and Mayo Foundation, Rochester, Minn. Reprint requests to Department of Neurology, Mayo Clinic, 200 First St SW, Rochester, MN 55905 (Dr Mokri). REPORT OF CASES CASE 1. —A 57-year-old previouslyhealthy woman noted abrupt onset of dysphagia and nasal régurgitation and, subsequently, de¬ velopment of dysphonia. A pharyngoesophageal diverticulum was suspected, but at surgical exploration one was not found. The pa¬ tient was then referred to the Mayo Clinic, Rochester, Minn, 2 months after the onset of symptoms. She had a flaccid dysphonia and weakness and fasciarlations of the right side of the tongue. The right eye had been amblyopic since childhood. A small indentation at the level of the tracheopharyngeal muscle (noted on esophagoscopy) was dilated. She returned home and began to complain of pain in the right jaw. Extraction of the right upper teeth did not help. Six months later she returned to our institution complaining also of right facial numbness. Neurologic examination showed mild right pterygoid and right tongue weakness, mild weakness of the right sternocleidomastoid muscle, and a right carotid bruit and subjective sensory loss at the distribution of the first division of the right trigeminal nerve. Results of computed tomography (CT) of the head were normal. Electromyographic examination showed evidence of right trigeminal nerve involvement. Overall, the history and findings pointed to involve¬ ment of cranial nerves XII, XI, X, IX, and V. Arteriography showed dissection of the right ICA leading to occlusion just above the bi¬ furcation (Fig 1). No particular treatments were advised. Seven months later the patient was hospitalized elsewhere for sudden decrease of vision in her amblyopic right eye. Arteriog¬ raphy showed that the ICA occlusion had not changed. Explo¬ ration of the carotid artery revealed that the occluded vessel ap¬ peared normal exteriorly, and no other lesions were seen. A treatment trial with prednisone did not help. The visual loss was concluded to be related to an ischemie optic neuropathy. Her fa¬ cial pain required analgesics. On follow-up her vision had not improved and there was pallor of the right optic disc. Downloaded From: http://archotol.jamanetwork.com/ by a Oakland University User on 06/03/2015 Fig 1. Case 7. Right carotid arteriogram showing occlusion of right internal carotid artery with "flamelike" configuration (arrow) result¬ ing from dissection of the internal carotid artery. Fig 2.— Case 3. Left carotid arteriogram demonstrating a loop ofthe cervical internal carotid artery just proximal to the base of the skull with an associated aneurysm (arrow); slight luminal irregularities of the artery can be seen proximal to the aneurysm. CASE 2.—A 44-year-old previously healthy man noted tongue weakness associated with an unusual sensation of the left side of the tongue, drooping of the left upper eyelid, and dysarthria. Two days later he was hospitalized, and at that time left partial Horner's syndrome and paralysis of the left side of the tongue were noted. Results of CT of the head were normal. Arteriography showed narrowing of the left ICA. Anticoagulation therapy with heparin sodium and subsequently with warfarin sodium (Coumadin) was given. The patient's symptoms and signs grad¬ ually improved over 6 weeks. Three months later he was seen at the Mayo Clinic. Results of a neurologic examination were normal except for mild left ptosis and miosis. Dysarthria and paralysis of the left tongue had resolved. Results of a general medical examination were normal. Review of the patient's arteriograms showed a dissection of the left ICA extending from the C-2 level to the horizontal portion of the carotid canal. There was a high degree of stenosis. Intravenous dig¬ ital subtraction angiography showed residual stenosis related to the dissection. No aneurysms were seen. Administration of warfarin was discontinued and aspirin was given. and periauricular headache developed Case 3. —Left in a 41-year-old man. Two days later he experienced tongue weakness associated with dysarthria. During the next few days a mild dysphagia also developed, and, later, dysphonia and weakness of some of the muscles of the left shoulder developed. The patient's otolaryngologist noted a left vocal cord paralysis and manifestations of paresis of cranial nerves IX through XII on the left. Results of magnetic resonance imaging of the head and base of the skull were thought to be normal. The patient was subsequently referred to the Mayo Clinic. Examination showed flaccid dysarthria and dysphonia, devi¬ ation of the uvula to the right, deviation of the protruded tongue to the left, furrowing of the left side of the tongue, and decreased sensation of taste over the left posterior aspect of the tongue. The gag reflex was decreased on the left, and left vocal cord paraly¬ sis and mild weakness of the left sternocleidomastoid and trapezius muscles were noted. Computed tomographic scans re¬ vealed an enhancing mass at the base of the skull on the left adjacent to the carotid canal and jugular foramen, and there was thickening of the neighboring carotid sheath. Arteriography demonstrated a dissection of the left ICA manifested by slight luminal irregularities from the C-2 level to the base of the skull and a 15-mm aneurysm at the skull base associated with a loop of the carotid artery (Fig 2). The remainder of the cervical and intracranial circulation was normal. On follow-up examination 1 month later the patient's voice and swallowing had markedly improved, and only a mild resid¬ ual dysfunction of cranial nerves IX through XII on the left was noted. Arteriography showed no change in the size or shape of the aneurysm, but the luminal irregularities of the ICA had re¬ solved. Antiplatelet therapy with aspirin and neurologic follow-up were recommended. Case 4. —Left occipital headache, hoarseness, and dysphagia de¬ veloped in a 47-year-old man. He also had intermittent nausea and — occipital Downloaded From: http://archotol.jamanetwork.com/ by a Oakland University User on 06/03/2015 light-headedness. He was found to be hypertensive and was treated with a diuretic for the hypertension and with analgesics for the headache. Dysphagia and dysphonia became pronounced, and 2 weeks later, drooping of the left upper eyelid was noted. Results of a head CT scan, metrizamide cisternography, and jugular venography were normal. Arteriography showed bilateral ICA disease. The patient was referred to the Mayo Clinic. Examination showed left Horner's syndrome, left vocal cord paralysis, and weakness of the tongue, palate, and sternocleidomastoid muscle on the left. The findings were those of involvement of oculosympathetic fibers and cranial nerves LX through XII on the left. Review of the patient's arteriograms demonstrated bilateral dissections of the cervical ICAs at their distal portions. On the left there was luminal stenosis associated with a small dissecting aneurysm (Fig 3). On the right the ICA was dilated and tortuous and there was a small aneurysm. Results of vertebral angiography were normal. On surgical exploration, the clinically involved cranial nerves were grossly normal. The patient began to show improve¬ ment. Within 2 months, the headaches resolved. The ptosis and the dysphonia completely disappeared within 8 months. The patient has remained asymptomatic 7 years after the onset of symptoms. Interestingly, his father also had sponta¬ neous ICA dissection.11 Case 5.—A 40-year-old previously healthy woman noted sudden onset of light-headedness, visual blurring, left upper extremity weakness and clumsiness, pronounced dysarthria, dysphagia, and trouble with chewing or moving the food in her mouth with her tongue; later, decreased sensation in her left side was noted. A head CT scan obtained the next day showed an area of infarction in the right posterior frontal region. When the patient was seen at the Mayo Clinic 10 days later, her symptoms had resolved and the results of her neurologic examination were normal. The lesion seen on head CT did not appear to explain the patient's initial pronounced dysarthria and dysphagia. Arteriography showed intimai irregularities with mild stenosis in the proximal right ICA; these findings were compatible with a resolving ICA dissection. The left carotid and the vertebral basilar systems were normal. The carotid artery dissection was concluded to have caused the cerebral infarction as well as the lower cranial nerve palsies, which led to the mixed clinical picture of unilateral lower cranial nerve palsies and con¬ tralateral weakness and numbness. The patient was treated with dipyridamole as an antiplatelet agent. She had no further cere¬ bral ischemie events. Case 6. —A 48-year-old man had sudden development of a left temporal headache. In 10 minutes there was also pain in the left orbital-periorbital region and in the left posterior area of the neck. A milder pain was present in the right temporal region. Four days later, weakness of the left side of the tongue associ¬ ated with dysarthria and numbness of the left side of the throat was noted. Arteriography demonstrated a dissecting aneurysm of the left ICA at the level of the C-l vertebral body. The patient was treated with an anticoagulant (warfarin) and analgesics for the pain. Six weeks later, when the patient was first seen at the Mayo Clinic, the dysarthria and the throat numbness and tongue weakness on the left had resolved. Anticoagulation therapy was continued for another few months. Cerebral arteriography per¬ formed elsewhere, 8 months after the first study, showed no change in the appearance of the dissecting aneurysm. About 20 months after the dissection, the patient was reevaluated at the Mayo Clinic. There were no new neurologic devel¬ opments. Case 7.—A 48-year-old woman noted a sudden roaring noise and pain in the left ear and a kaleidoscopic flashing light in the left eye, particularly when she stood up. A left ptosis, weakness of the left side of the tongue, and mild weakness of the distal aspect of the right lower extremity were also present. Arterio¬ graphy showed dissection of the left ICA manifested by a tapered and narrowed segment of the artery high in its extracranial portion. The right carotid and vertebral arteries were normal. Fig 3. —Case 4. Left carotid arteriogram demonstrating dissection of internal carotid artery, manifested by a small aneurysm (open arrowhead), stenotic segment distal to the aneurysm (arrow), and a fairly abrupt reconstitution of the lumen at the carotid canal. The patient was treated with warfarin. Speech returned to normal within 1 week. The left ptosis improved and the weak¬ ness of the right lower extremity resolved. Six months later, the only abnormalities on neurologic examination were mild left ptosis and mild weakness of the right extensor hallucis longus. Carotid ultrasonography showed no flow within the left ICA, a finding consistent with occlusion. However, clinically the pa¬ tient was asymptomatic, had very minimal signs, and was back to full-time work as a secretary. No further investigation was recommended and anticoagulation therapy was discontinued. CASE 8.—A 48-year-old right-handed college professor had development of left facial weakness, dysarthria, a feeling of thickness of the left side of the tongue, left upper limb numb- Downloaded From: http://archotol.jamanetwork.com/ by a Oakland University User on 06/03/2015 Summary of Reported Cases of Lower Cranial Nerve Palsies Related to Dissection of the Internal Carotid Artery* Sex/Age, y Cranial Nerve OSP Headache Lane et al,13 1980 F/55 Lt IX, XII + + Bradac et al,5 1981 M/58 Lt IX-XII + + M/41 Lt XII + + Havelius et al,141982 M/44 Rt IX-XII Goodman et al,151983 M/59 RtXII + + + + Source, y Goldberg et al,161986 M/49 Lt IX-XII Lieschke et al,'71988 M/42 Rt X, XII + Waespe et al,181988 M/41 Lt IX-XII + Bradac et al,191989 M/28 Rt X, XII F/41 Lt XII M/53 Lt XII M/58 Lt IX-XII M/45 M/54 RtXI, XII Lt IX, X, XII M/36 Rt IX-XII M/53 Lt IX, X, XII M/48 Lt XII + + Schievink and Limburg,231990 Hess et al,241990 M/54 Lt IX, X, XII + + M/41 Rt IX-XII Present series, 1991 F/57 Rt IX-XII M/44 Lt XII M/41 Lt IX-XII + M/47 Lt IX-XII + Dal Pozzo et al,201989 Panisset and Eidelman,21 1990 Vighetto et al,221990 + CI + + + + + + + + F/40 Rt IX, X, XII M/48 Lt IX-XII + F/48 LtXII + M/48 Lt XII OSP indicates oculosympathetic palsy; CI, cerebral ischemia; Lt, left; Rt, right; plus sign, present; and minus sign, absent. swishing noise in the right ear, and severe right-sided headache. He was referred to the Mayo Clinic. Neurologic examination revealed blindness of the left eye (dating back to a trauma at age 13 years), left ptosis, mild left hemiparesis, dys¬ arthria, and weakness of the left side of the tongue. There were no bruits. Head CT showed a low attenuation area high in the watershed zone of the right parietal region. Arteriography showed dissection of the right ICA in the neck above the carotid bifurcation and a dissecting aneurysm in the upper cervical por¬ tion of the left ICA. Weakness of the left side of the tongue and dysarthria were thought to be related to the left ICA dissection, and the other symptoms were thought to be due to the right ICA dissection. Anticoagulant therapy with warfarin was started. When the patient was rechecked 6 months later, he had no major problems and was working full-time. He reported that his speech sometimes slurred after long lectures. Neurologic examination showed residual mild left hemiparesis. Arteriography showed com¬ plete resolution of the right ICA dissection. On the left, however, the dissecting aneurysm had persisted. Warfarin therapy had been discontinued 1 week earlier and was not restarted. ness, a COMMENT Clinical and artériographie features as well as the outcome in spontaneous ICA dissections have been described by us and by other investigators.1,2'4~10'12 Clinically, headache is the most common manifestation.12 This is often unilateral and focal and frequently occurs in the frontal, orbital, and periorbital regions. Sometimes there may be unilateral focal pain deep in the ear, mastoid region, angle of the mandible, or temporal or occipital region.10 Contrary to what might be ex¬ pected, neck pain is much less frequent than headache. Other symptoms and signs, in decreasing order of fre¬ quency, include focal cerebral ischemie symptoms (transient ischemie attacks or stroke, or both), oculosympathetic palsy (incomplete Horner's syndrome manifested by ptosis and miosis but without a change in sweating of the face), bruits, neck pain, syncope, amaurosis fugax, scalp tenderness, neck swelling, dysgeusia, and lower cranial nerve palsies.12 Occasionally, spontaneous ICA dissections may be asymp¬ tomatic and are detected incidentally during workup of spontaneous vertebral artery dissections or contralateral ICA dissection. Spontaneous ICA dissections are bilateral in about a third of patients. The common artériographie features, in decreasing or¬ der of frequency, include luminal stenosis (often elon¬ gated, irregular, and tapered), abrupt reconstitution of the stenosed lumen (usually at the carotid canal), aneurysms, intimai flaps, slow internal carotid artery-middle cerebral artery flow, occlusion (often tapered to a point with a "flame shape" or "radish tail" configuration), and distal branch occlusions due to distal embolization.9 The most common clinical syndromes include (1) uni¬ lateral focal headaches followed after a period of delay of several minutes to a few weeks by focal cerebral ischemie Downloaded From: http://archotol.jamanetwork.com/ by a Oakland University User on 06/03/2015 symptoms (transient ischemie attacks or stroke or both) and (2) unilateral headaches and ipsilateral oculosympa- thetic palsy. These may be accompanied by subjective or objective bruits. Sometimes the combination of these two syndromes is noted. Uncommonly, the spontaneous ICA dissections may present as lower cranial nerve palsies. Among some 120 patients with spontaneous ICA dissec¬ tions whom we have seen, the eight described herein presented with lower cranial nerve palsies. Only two of these patients (cases 5 and 7) also had focal cerebral ischemie symptoms in the distribution of the same vessel. Case 8 had bilateral ICA dissection and did have cerebral ischemie symptoms, but not in the distribution of the ar¬ tery ipsilateral to the lower cranial nerve palsy. Most of the patients actually presented with lower cranial nerve palsies, which in turn led to the referral to or consultation from an otolaryngologist. Sporadic cases of lower cranial nerve palsies related to ICA dissection have been reported in the past decade (Table).513"24 The mechanisms for symptoms and signs associated with carotid artery dissection have been postulated. Cerebral is¬ chemie symptoms may be embolie, caused by distal embolization from thrombus within the false lumen or the dissect¬ ing aneurysm, or they may be hemodynamic, resulting from decreased blood flow related to narrowing of the lumen of the ICA. The oculosympathetic palsy results from involve¬ ment of the periarterial sympathetic plexus by the arterial dissection. The Homer syndrome is incomplete in that the sympathetic fibers that accompany the ICA (internal carotid plexus) are involved, whereas the sympathetic fibers of the external carotid plexus that subserve sweating of the face are spared. The association of unilateral headache and face pain with carotid artery disease is also well known. By electrical stimulation of the wall of the carotid artery at its bifurcation, Fay25 produced ipsilateral head, neck, and face pain. The ex¬ act mechanism of the lower cranial nerve palsies, however, is less clear. Compression of the lower cranial nerves below the jugular foramen by the dissected carotid artery has been proposed as the mechanism by most investigators who have published reports on this subject. Cranial nerves IX through XII are located in the retrostyloid space immediately adjacent to the ICA. Lateral expansion of the ICA could compress these nerves. Because cranial nerves X and XII have the long¬ est anatomic relationship to the ICA, involvement of these nerves would be more common. Another proposed mech¬ anism has been compromise of an anomalous artery origi¬ nating from the petrous or extrapetrous ICA in the neck and providing vascular supply to the nearby cranial nerves or compromise of an anomalously arising ascending pharyngeal artery from the cervical ICA supplying the lower cranial nerves. Despite their disconcerting artériographie features, spon¬ taneous ICA dissections are associated with a good progno¬ sis. In our experience, more than 85% of patients have com¬ plete or excellent clinical recovery. We have not noted an in¬ stance of rupture of an extracranial ICA dissecting aneurysm or recurrence of dissection in the same vessel. On follow-up arteriography, 90% of the stenoses have completely or par¬ tially resolved and 63% of the aneurysms have resolved or become smaller.1012 For spontaneous ICA dissections, no in¬ fallible method of management has emerged. This is an un¬ common disease, and, to our knowledge, there are no col¬ laborative or controlled studies. Immediate mortality from massive cerebral infarction and edema has been reported, but this occurs uncommonly. Enthusiasm for a surgical ap- proach has substantially decreased, owing in part to the usual extent of the process to the skull base and also because of the overall favorable prognosis in most patients treated conservatively. Some of the surgical approaches that have been tried include removal of intramural hematoma, resec¬ tion of the involved segment of the artery and interposition of vein graft, graduated dilation, ligation, and superficial temporal artery-to-middle cerebral artery bypass. One com¬ monly advocated and practiced approach has been antico¬ agulant therapy for 3 to 4 months followed by antiplatelet therapy for a similar period. If a residual dissecting aneurysm produces symptoms due to its mass effect (a most unusual occurrence), or if it becomes a source of embolization, it should be resected when technically possible. References 1. Mokri B. Dissections of cervical and cephalic arteries. In: Sundt TM Jr, ed. Occlusive Cerebrovascular Disease: Diagnosis and Surgical Management. Philadelphia, Pa: WB Saunders Co; 1987:38-59. 2. Hart RG, Easton JD. Dissections of cervical and cerebral arteries. Neurol Clin. 1983;1:155-182. 3. Jentzer A. Dissecting aneurysm of the left internal carotid artery. 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Cervical internal carotid artery dissecting hemorrhage: diagnosis using MR. Radiology. 1986;158:157-161. 17. Lieschke GJ, Davis S, Tress BM, Ebeling P. Spontaneous internal carotid artery dissection presenting as hypoglossal nerve palsy. Stroke. 1988;19:1151-1155. 18. Waespe W, Niesper J, Imhof H-G, Valavanis A. Lower cranial nerve palsies due to internal carotid dissection. Stroke. 1988;19:1561-1564. 19. Bradac GB, Riva A, Stura G, Doriguzz C. Spontaneous ICA dissection presenting with 12th nerve palsy: clinical and radiological considerations. J Neuroradiol. 1989;16:197-202. 20. Dal Pozzo G, Mascalchi M, Fonda C, Cadelo M, Ronchi O, Inzitari D. Lower cranial nerve palsy due to dissection of the internal carotid artery: CT and MR imaging. J Comput Assist Tomogr. 1989;13:989-995. 21. Panisset M, Eidelman BH. Multiple cranial neuropathy as a feature of internal carotid artery dissection. Stroke. 1990;21:141-147. 22. Vighetto A, Lisovoski F, Revol A, Trillet M, Aimard G. Internal carotid artery dissection and ipsilateral hypoglossal nerve palsy. J Neurol Neurosurg Psychiatry. 1990;53:530-531. 23. Schievink WI, Limburg M. Dissectie van cervicale arteri\l=e"\nals oorzaak van hersenischemie of uitval van hersenzenuwen. Ned Tijdschr Geneeskd. 1990;134:1843-1848. 24. Hess DC, Seithi KD, Nichols FT. Carotid dissection: a new false localising sign. J Neurol Neurosurg Psychiatry. 1990;53:804-805. 25. Fay T. Atypical facial neuralgia, a syndrome of vascular pain. Ann Otol Rhinol Laryngol. 1932;41:1030-1062. Downloaded From: http://archotol.jamanetwork.com/ by a Oakland University User on 06/03/2015