Infection-Associated Cervical Artery Dissection
Background The pathogenesis of cervical artery dissection remains unknown. Infection-mediated damage of the arterial wall may be one contributing mechanism. We present three male patients with respiratory infection prior to cervical artery dissection.
Case Descriptions Case 1: During an upper respiratory tract infection, a 49-year-old patient developed bilateral carotid and vertebral artery dissection with complete vessel restitution. Case 2: Within 3 years, a 40-year-old patient experienced two episodes of bilateral internal carotid artery dissection, both preceded by febrile upper respiratory tract infection. Case 3: A 52-year-old patient developed right-sided and, 2 years later, left-sided internal carotid artery dissection, each following upper respiratory tract infection.
Conclusions Infection may be a trigger factor in the pathogenesis of cervical artery dissection.
Acute infectious disease can lead to considerable vascular injury. In 1906, Wiesel1 published a study on blood vessels from 300 patients who died after infectious disease. He typically found focal destruction of smooth muscles and elastic fibers in the tunica media of larger arteries, which either healed or transformed into fibrous scars. Inflammatory infiltrates were seldom present, and the intima was involved only in the most severe cases. Recent infection is presently discussed as a risk factor for cerebrovascular ischemia. Injury to the arterial wall may be one pathogenetic pathway in infection-associated stroke. In a recent case-control study, four of five patients with cervical artery dissection (CAD) had definite or probable infection within 1 week before stroke.2 We describe three patients with infection-associated CAD, one with four-vessel dissection and two with recurrent infection-associated dissection.
Ten days before admission, a 49-year-old male teacher developed sore throat, rhinitis, and subfebrile temperature (37.5°C). His general practitioner diagnosed tonsillitis and initiated antibiotic treatment. Tonsilar swab cultures revealed Staphylococcus aureus. The patient denied coughing. Two days after onset of symptoms, he developed pulsatile tinnitus and ptosis of the left side and increasing pain in the right neck and occiput. On the day of admission, he noticed fluctuating dizziness and left-sided hemisensory loss. Other than hypertension, his past history was unremarkable. Previous trauma was denied. The neurological examination revealed Horner's syndrome, mild sensorimotor hemiparesis, and hemiataxia, all on the left. Cranial CT was unremarkable. Cerebral angiography showed four-vessel dissection (Fig 1⇓). Superior mesenteric and renal arteries were unremarkable. Cervical MRI showed hyperintense signal of the vessel walls, indicating intramural hematoma. Erythrocyte sedimentation rate was slightly increased (18 mm/h), but other laboratory tests, including vasculitis and syphilis screening parameters, were unremarkable. The patient was treated conservatively. He was discharged with a mild residual hemisensory disturbance. Four-vessel angiography 5 months later revealed complete vascular restitution (Fig 2⇓).
In summer 1992, a 40-year-old male patient developed respiratory infection with cough, purulent sputum, rhinitis, sore throat, and fever up to 39°C. These symptoms resolved 1 week later, but pulsatile tinnitus and earache on the left developed. These symptoms were not continuously present and mainly appeared during physical activity. A neurologist consulted found increased flow velocity in both distal extracranial internal carotid arteries (ICAs) by Doppler ultrasound. MRI of the neck showed irregular narrowing and a hyperintense signal in the wall of both ICAs, indicating dissection. The patient had no vascular risk factors or recent trauma. Neurological examination on admission was unremarkable. Routine biochemical and hematological serum parameters were normal. Angiography of both carotid arteries revealed slight narrowing of the left subpetrous ICA and a small pseudoaneurysm of the right ICA just below the skull base. Findings on Doppler sonography normalized 6 months later.
At the end of a febrile infection with cough and general malaise in summer 1995, the patient developed right-sided pulsatile tinnitus. He presented at our hospital 2 weeks later. Neurological examination revealed normal findings. Doppler ultrasound indicated a stenosis in the submandibular portion of the left ICA. MRI of the neck showed mural hematoma in both ICAs and a marked narrowing of the right ICA, indicating new dissection. Follow-up with Doppler ultrasound showed a regression of the left-sided ICA stenosis.
In summer 1994, a 52-year-old patient suffered from an infection with fever and sore throat that was treated with penicillin. On the third day of infection, a Horner's syndrome on the right was diagnosed. Cervical MRI revealed a hyperintense signal in the wall of the right ICA, indicating dissection. Cerebral angiography 4 months later was normal. In summer 1996, the patient again had an episode with fever (38.5°C) and sore throat; his general practitioner diagnosed angina and pharyngitis and started antibiotic treatment. Two days later, the patient developed problems moving his tongue. On admission, neurological examination was normal except for left-sided hypoglossus palsy and preexisting right-sided Horner's syndrome. Hyperintense signal in the left ICA wall on cervical MRI indicated dissection. Routine blood analyses were normal other than slight leukocytosis (10.4/nL). The patient's history is unremarkable with the exception of common migraine. He denied coughing or vomiting in both episodes of infection. He reported no trauma before the first dissection but a fall and minor costal contusion 1 week before the second dissection.
Although increasingly diagnosed through modern neuroradiological techniques, nontraumatic CAD remains an enigmatic disease. Bilateral CAD is common, but simultaneous dissection of four cervical arteries, as in our first patient, appears to be unusual. Recurrent CAD is also rare,3 particularly when previously dissected arteries are affected again, as in our second patient. The low recurrence rate and the common observation of simultaneous multivessel dissection support the hypothesis that transiently active trigger mechanisms might contribute to the pathogenesis of nontraumatic CAD. Infection may be one such mechanism. During the past 5 years we observed three patients with recurrent CAD: the two patients described here and one female patient in whom one of the episodes was associated with respiratory infection. Some reports in the literature mention “flulike” syndromes,4 febrile illnesses,5 6 or increased inflammatory parameters7 in patients with CAD. Mechanical stress by vomiting or cough may explain the association of infection and CAD. However, only our second patient reported such symptoms. Alternatively, injury to the arterial wall by microbial agents or inflammatory mechanisms may also contribute to dissection during infection. Destructive changes after infection are centered in the tunica media,1 where dissection occurs, and such vessel wall injury may trigger dissection in predisposed patients. Cellular inflammation is usually not observed in CAD, but eosinophilic infiltrates frequently accompany spontaneous coronary artery dissection.8 This disease often leads to sudden cardiac death and hence to early histological examination, whereas death or vascular surgery early after CAD is rare. In CAD, cellular infiltration may be a short-lasting phenomenon, or humeral factors, not detected by conventional histology, may cause vascular injury. Renal artery dissection can accompany CAD5 7 ; however, it is unknown how often there is clinical or subclinical involvement of other than cervical arteries during CAD.
Future studies may determine whether infection contributes to the pathogenesis of CAD and whether a more generalized arteriopathy is frequently associated with CAD.
- Received July 26, 1996.
- Revision received October 24, 1996.
- Accepted October 25, 1996.
- Copyright © 1997 by American Heart Association
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