Abstract In this report we compare a subintimal hemor-rhage of a dissected vertebral artery to a subadventitial he-morrhage of a dissected extracranial internal carotid artery.A subintimal hemorrhage compresses the lumen of theartery. Therefore, magnetic resonance imaging (MRI), an-giography and ultrasound are screening methods. For thesubadventitial hemorrhage, which does not really com-press the lumen but forms an aneurysmal dilatation, MRIis the only method of choice. We describe a case in whichvertigo, nausea and vomiting are the only symptoms of asubintimal vertebral artery dissection. In this case an in-farction of the cerebellar region supplied by the superiorcerebellar artery could be demonstrated. Our second casedemonstrates a palsy of the 10th, 11th and 12th cranialnerves, which is a less frequent symptom of internal arterydissections. The palsy of these cranial nerves seems to becaused by compression of the nerves or their nutritionalarteries close to the aneurysmal dilatation of the subad-ventitial dissected internal carotid artery. In both casesclinical symptoms were resolved after anticoagulation.

Keywords Spontaneous dissection of internal and vertebral arteries · Vertigo · Cranial nerve palsy · MRI

Introduction

In an artery dissection, circulating blood penetrates the ar-terial wall and splits the media, or there is a primary in-tramural bleeding of the vasa vasorum. Mostly the hemor-rhage is subintimal and compresses the lumen of the ves-sel. Less often, the intramural blood expands towards the

adventitia, not compressing the lumen, but forming a sub-adventitial aneurysmal dilatation [4]. Traumatic dissec-tions are reported after definite injury such as sudden neckmovement or chiropractic neck manipulations [25].

Spontaneous dissections occur without histories oftrauma or after trivial manipulations or activities, such ascoughing, straining [8], oesophagoscopy [19] or arteri-opathies such as fibromuscular dysplasia, Marfan syn-drome, Ehler Danlos syndrome type IV, autosomal domi-nant polycystic kidney disease, osteogenesis imperfectatype I or α1-antitrypsin deficit [2, 26].

Traumatic (68%) and spontaneous (80%) vertebralartery dissections occur in the age group between 30 and50 years. It is the most common cause of vertebrobasilarischemic strokes in this age group [13]. Spontaneous dis-section of the extracranial internal carotid artery affectsyoung and middle-aged adults as well [6, 21]. At least 5%of all ischemic infarcts in this age group can be explainedby this genesis [11]. The annual incidence of spontaneousvertebral artery dissection ranges from 1 to 1.5 per100,000 and of spontaneous carotid artery dissection from2.5 to 3 per 100,000 [26].

The most important clinical symptoms of a sponta-neous vertebral artery dissection are unilateral headacheand neck pain in 55 to 60% [12, 16]. In 23% to 43% [3,12], the symptoms are identical to those of Wallenbergsyndrome or lateral medullary syndrome (vertigo, ataxia,falling toward the side of lesion, dysphagia and typicalloss of sense of pain and temperature)

The main symptoms of spontaneous internal carotidartery dissection are ipsilateral headache or face pain in83% [17], ipsilateral cervical pain [7], ipsilateral Hornersyndrome in 40 to 50% [1, 4] and delayed focal cerebralsymptoms such as stroke or a transient ischemic attack.Cranial nerve palsy as a further symptom is less fre-quently described [9, 10]. A palsy of the hypoglossusnerve, which is almost invariably involved in the syn-drome of lower cranial nerve palsies, can be observed inonly 5% of all cases [9, 17].

In this report, we describe uncommon symptoms suchas vertigo in a dissection of the vertebral artery or cranial

Victor Bonkowsky · Silke Steinbach · Wolfgang Arnold

Vertigo and cranial nerve palsy caused by different forms of spontaneous dissections of internal and vertebral arteries

Eur Arch Otorhinolaryngol (2002) 259 :365–368DOI 10.1007/s00405-002-0460-3

Received: 18 December 2001 / Accepted: 15 February 2002 / Published online: 5 July 2002

MISCELLANEOUS

Dedicated to Professor Dr. W. Schwab for his 80th birthday

V. Bonkowsky (✉ ) · S. Steinbach · W. ArnoldDepartment of Otolaryngology, Technical University of Munich,Klinikum rechts der Isar, Ismaningerstr. 22, 81675 Munich, Germany e-mail: V.Bonkowsky@lrz.tum.deTel.: +49-89-41402389, Fax: +49-89-41404853

© Springer-Verlag 2002

nerve palsy in dissection of the extracranial internalcarotid artery. We also show the screening method for di-agnosis.

Case reportsCase 1

A 40-year-old pharmacist, without any remarkable past medical his-tory of trauma or unusual manipulation, complained of severe ver-tigo, nausea and vomiting. The sudden onset of vertigo followed a 3-h interval of playing tennis. The man could not remember any his-tory of trauma while playing tennis. A right horizontal-rotatoryspontaneous nystagmus was demonstrated combined with a severepostural imbalance to the left. All other findings of either otolaryn-

gological, ophthalmological or physical examination were withinnormal limits. Pure-tone audiometry, tympanometry, acoustic reflexesand auditory brain-stem response measurements were normal. Thediagnostic impression was one of peripheral vestibulopathy.

The patient’s symptoms were treated by the intake of antiemet-ics and fluid hydration. He was kept under observation. After 48 h,the symptoms did not really improve, and he was still unable towalk alone. A magnetic resonance image (MRI) was performed,which revealed an infarction of the territory of the left superiorcerebellar artery and a cerebellar edema (Fig.1a). MRI-angiogra-phy demonstrated an intramural thrombus causing a stenosis of theleft vertebral artery at the C2 level (Fig.1b). Therefore, the diag-nosis of a dissection of the left vertebral artery was consistent. Thepatient was heparinized for 21 days, and the vertigo resolved. A control MRI after a period of 6 months did not show any re-maining stenosis of the left vertebral artery.

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Fig.1 a Axial T2-weightedmagnetic resonance imagine(MRI) showing an infarct ofthe left cerebellum in distribu-tion of the left superior cere-bellar artery. b Left MRI-arte-riogram showing segmentalnarrowing of the left vertebralartery at the C2 level

Fig.2 a Subadventitial hemor-rhage of a dissected extracra-nial internal carotid artery onleft side in a T2-weighted axialMR imagine. b Same dissec-tion as in (a) 3 months afterheparinization. The subadven-titial hemorrhage is almost re-solved, but a new subintimaldissection of the left vertebralartery is observed

Case 2

Three weeks prior to hospitalization, a 36-year-old, healthy com-puter scientist reported a spontaneous, 4 h-long loss of visualfields, aphasia and paresthesia of the right arm. On the next day, hedeveloped feelings of a globus and hoarseness. Ten days after on-set, he visited an otolaryngologist, who observed a paralysis of theleft vocal cord and 1 week later a palsy of the left hypoglossalnerve. The patient could not remember a remarkable trauma. WithMRI, a hyperintense intramural thrombus of the left internalcarotid artery could be demonstrated, consistent with an artery dis-section from the plane of the left jaw to the base of the skull, wherethe hypoglossal and vagal nerves are located (Fig.2a).

The comparison of the internal diameter of the left and right in-ternal carotid artery showed almost identical sizes. A duplex ultra-sound investigation showed physiological blood flow in both theleft and right carotid arteries. These findings were consistent witha subadventitial dissection of the left internal carotid artery. Thepatient was treated with anticoagulation therapy.

After 3 months, a control MRI demonstrated a regressive intra-mural thrombus of the left internal carotid artery, but now showedan intramural thrombus of the left vertebral artery consistent with adissection of this artery from level C6 to C2 (Fig.2b). The compar-ison of the external diameter of the left and right vertebral arteryshowed almost no measurable differences. These findings wereconsistent with a subintimal hemorrhage of the left vertebral artery.

One week before the control MRI, the patient complainedabout spontaneously starting cervical pain, which can be explainedby the new MRI findings. After 6 months of anticoagulation ther-apy, the clinical symptoms were resolved, and the patient got aprophylactic antiplatelet therapy. A control MRI revealed com-pletely normal findings after 18 months.

Discussion

The patient we present in case 1 is the typical, middle-aged adult suffering from a spontaneous vertebral arterydissection. In accordance with the literature [5, 18, 22],our patient’s only symptoms were vertigo and posturalimbalance. This made the discrimination between centraland peripheral vertigo extremely difficult. But a lack ofneurologic symptoms such as ataxia, dysphagia, headacheor neck pain should never exclude a central pathogenesis.

Even when a peripheral vestibulopathy is suspected,but the vertigo does not improve after 48 h, a MRI of thebrain is highly recommended to exclude a central etiologyof the symptom. When we did a MRI in our patient after48 h, we could observe an infarction of that part of thecerebellum that was supplied by the superior cerebellarartery. To discover the pathomechanism of the cerebellarinfarct, a MRI-angiography is indicated. In our case, astenosis of the left vertebral artery was present at levelC2, which was interpreted as a subintimal dissection ofthe left vertebral artery. The intracranial part of the verte-bral arteries are fixed by the dura mater [12].

Stretching of the vertebral artery may result in a tear ofthe intima layer at the ending of the vertebra canal levelC2 and in blood penetration, subintimal hemorrhage andcompression of the lumen. Since the superior cerebellarartery is a branch of the basilar artery, which arises fromthe left and right vertebral artery, a thromboembolism ofthe left superior cerebellar artery is most likely to explainthe infarct in our case. This is the first case report aboutvertigo, vertebral artery dissection and infarction of theblood supply area of the superior cerebellar artery.

Vertebral artery dissections can be treated by anticoag-ulation, as in our case, or by antiplatelet therapy. The du-ration of the therapy must be based on clinical symptomsand the restoration of the intraluminal blood flow aschecked by MRI, MRI-angiography or Doppler ultra-sound. More than 70% of spontaneous vertebral arterydissections show complete recovery [13, 20].

In case 2 we report about cranial nerve palsy caused bydissection of the extracranial part of the internal carotidartery, a rather rare pathomechanism [9]. A subadventitialhemorrhage was the exact diagnosis, since the lumen of theartery as shown by MRI and the blood flow as proven byduplex ultrasound were unchanged. In this type of dissec-tion, angiography or duplex ultrasound would not lead tothe right diagnosis. Therefore, MRI is the method of choice,allowing visualization of the subadventitial hemorrhage andits extension into the axial and longitudinal planes.

Most often, as in our case, the dissection starts 2 to 3 cm distal to the carotid bulb, extending cranially andshowing a maximal distension at the C1 or C2 vertebrallevel [23]. At this plane there is a close relationship be-tween the internal carotid artery and the 9th, 10th, 11th and12th cranial nerves as well as the sympathetic trunk [23].If there is an aneurysmal dilatation caused by subadventi-tial hemorrhage, these nerves can be compressed, leadingto dysfunction. Cranial nerves 10 and 12 have the longestanatomic relationship to the internal carotid artery [17].

Another possibility for cranial nerve palsy is a compro-mise of the nutrient arterial supply to the nerves. The nu-trient arteries are too small to be exactly visualized on an-giograms, and therefore this is difficult to document [14].

It is very important that all arteries are checked on aMRI. Dissections can occur in multiple arteries of thesame patient [16, 24], but it is uncommon that they repeatat the same artery [15]. Besides checking a vasculitis orarteriopathy, a regular screening of those patients and alife-long antiplatelet therapy are indicated.

Acknowledgements The authors are very grateful to Traute Kim-mich and Herbert Stimmer, who is from the Department of Radi-ology at the Technical University of Munich, for their support.

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