With the symptoms of fever, headache, confusion, diplopia, and signs of neck stiffness, intracranial infection was firstly considered. Furthermore, increased intracranial pressure, normal glucose, monocytic pleocytosis, increased protein concentration, increased IgA and IgG concentration of CSF suggested viral inflammatory reaction although the immunological reactions and polymerase chain reactions for some common viruses were negative. Consequently, our case was initially diagnosed as brainstem encephalitis. However, resolution of confusion and diplopia in several hours, and the findings of left lateral medullary infarction on the DWI MRI indicated otherwise. Subsequent DSA suggested dissection of the left vertebral artery involving V4 segment proximal to PICA. As the patient had fever, headache, neck stiffness and inflammatory CSF, the diagnosis of VAD accompanied by viral meningitis was preferred.
VAD was once considered to be a rare event, but recently it has been recognized as an important cause of ischemic stroke in middle-aged adults (10–25% of these cases) [1
]. About 60% of VAD patients have symptoms of vertebrobasilar circulation ischemia, such as vertigo, hoarseness, dysphagia and cerebellar dysfunction [5
]. Occipital headache and neck pain are common symptoms and occur in 70% of patients with VAD [6
]. The acute onset of occipital headache in our patient was thought to result from VAD. The normal MRI signs of the midbrain and pons suggested that the transient confusion and diplopia were due to ischemia rather than brainstem encephalitis. The development of intramural hematoma due to the dissection resulted in narrow lumen and hypoperfusion of vertebrobasilar system. With recanalization or reperfusion, the patient’s consciousness recovered rapidly. Since ipsilateral PICA was usually not well compensated, infarction of left lateral medullary developed, and the patient experienced dysphagia, ataxia and numbness of left face and right extremities. The other possible mechanism might be related to transient embolization of vertebrobasilar system from the VAD, or related to a combination of embolization and local occlusion [7
The pathogenesis of VADs is actually not completely understood now. In the past, it was believed that mild or severe neck trauma caused mechanical stretching and compression of the vessel resulting in intimal disruption and intramural hemorrhage [5
]. However, mechanical stress tends to affect extracranial segments, including V1 to V3, because of its mobility and prone to be damaged by bony structures [7
]. Recent histopathological studies of both internal carotid artery dissection (ICAD) and VAD revealed that there was no mechanical damage being observed [8
]. In our case, only the intracranial segement of the vertebral artery was involved, and the patient had no history of trauma, even a possible damage from coughing or sneeze. We therefore believe that the patient’s VAD was associated with viral meningitis. There was an inflammation-associated injury of the arterial wall that led to weakness of vessel wall and subsequent dissection. The leucocytosis and elevated hs-CRP were indicative of this proposed inflammatory process. Furthermore, significantly elevated WBCs and protein level in CSF confirmed the inflammatory reaction of central nervous system.
Recent observations showed that infections may play an important role in both ICAD and VAD [3
]. Microbial agents themselves may cause substantial damage to the vascular wall, as destructive changes after infection have been shown to be centered in the tunica media where dissections occur [11
]. Different viruses and bacteria were suspected as being the responsible agents but previous studies failed to prove a common microbe [1
]. Although some authors attributed the association between infection and dissection to mechanical stress (e.g., coughing, sneezing and vomiting) [11
], the multivariate analysis in Grau’s study confirmed that the dissection was independently associated with a diagnosis of recent infection rather than mechanical factors occurring during the infection [10
]. Latest data showed persistently elevated hs-CRP values in ICAD and VAD patients, and elevated WBCs and CRP in spontaneous dissections as compared to traumatic dissections [16
]. These findings may indicate that the inflammatory response is more likely responsible for dissections [15