What is dissection of vertebral artery

Vertebral artery dissection. Reference article, Radiopaedia. Vertebral arterial dissection Vertebral dissection VA dissection. URL of Article. On this page:. Baumgartner RW. Handbook on cerebral artery dissection. S Karger Ag. Read it at Google Books - Find it at Amazon. Promoted articles advertising. Case 1 Case 1. Case 2: with thrombosis Case 2: with thrombosis. Case 3 Case 3. Case 4: on left Case 4: on left. Case 5: on right Case 5: on right.

Case 6: on right Case 6: on right. Case 7: bilateral Case 7: bilateral. Case 8 Case 8. Case 9 Case 9. Case 10 Case Case 11 Case Loading more images Close Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Loading Stack - 0 images remaining. By System:. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Case report. Key points. Conflicts of interest. Vertebral artery dissection: not a rare cause of stroke in the young.

Udayaraj Umasankar , Udayaraj Umasankar. Address correspondence to: U. Tel: Email: usankar68 hotmail. Oxford Academic. Timothy J. Adeyosola Famuboni. Mehool D. Ian D. Select Format Select format. Permissions Icon Permissions. Abstract We hereby describe a year-old lady who developed vertebral artery dissection following a head injury.

Open in new tab Download slide. Incidence and outcome of cervical artery dissection: a population-based study. Google Scholar Crossref. Search ADS. Headache and neck pain in spontaneous internal carotid and vertebral artery dissections. Vertebral artery dissection warning symptoms, clinical features and prognosis in 26 patients. Ophthalmic manifestations of vertebral artery dissection. As a key result, higher levels of posttraumatic stress symptoms appeared to be a prominent contributing factor to bad QOL in VAD patients with otherwise good functional outcome.

Cross sectional analysis of our baseline data displayed no significant group differences regarding sociodemographic variables. Likewise, mean values of pre-baseline total QOL were not significantly different.

Although there was a preponderance of atrial fibrillation in group I, no significant group differences of neurovascular risk factors were found in line with current knowledge about VAD characteristics [ 3 , 35 ]. The prevalence of Likewise, in concordance with the literature [ 5 , 6 , 36 ], functional outcome was good mRS0—2 in the majority of patients Published data about the possible impact of stenosis or occlusion of dissected vertebral artery to outcome have been rare and inconsistent so far.

The multivariate analysis of patients with carotid and vertebral artery dissections in a retrospective study design showed that the variables stroke and arterial occlusion were independent factors associated with a poor outcome [ 37 ]. Traenka et al. Furthermore, some recently published data suggested for the first time a role of VAD-accompanied atherosclerosis as additional putative contributing factor to functional outcome at three months in posterior circulation stroke PCS patients [ 39 ].

This may also refer to some of the older patients in our study though we have not examined them for arteriosclerosis in such detail. The method of evaluation, i. Because previous studies have shown no crucial role of neurovascular risk factors or sociodemographic factors for QOL of VAD patients, we focused our analysis of potential contributing factors for QOL on previously less investigated neurological, neurocognitive and psychological variables with special respect to the biopsychosocial model [ 12 ].

Psychological variables such as pre-baseline symptoms of anxiety and depression were not significantly different between our groups. There were significant more neurological impairments at baseline, that are higher scores of mRS for functional disability or NIH-SS for neurological deficit, in group D as well as I patients with ischemic stroke lesions compared to stroke mimics. Likewise, functional impairment measured by mRS at follow-up significantly correlated with reduced SS-QOL at follow-up in concordance with the results of the mixed cervical artery dissection series of Fischer et al.

Corresponding to their multivariate analysis, the NIH-SS score on admission was also found to be an independent predictor of QOL at follow-up in our univariate regression analysis. Finally, mRS scoring at baseline proved to be an independent predictor for SS-QOL at follow-up not only according to our univariate but also to our multivariate regression analysis model, explaining The MRI-based evaluation of white matter lesions WML was reported because of previously published data about their potential role for the functional outcome [ 40 ] and neuropsychological performance after stroke [ 41 ].

Kissela et al. Jokinen et al. Other published data remained inconsistent. Even if WML predominated in groups D and I compared to stroke mimics, they showed no significant inter-group difference.

Because data on the potential impact of infarct volume to outcome and QOL in VAD patients have been lacking so far, we used at least a very arbitrary method for semiquantitative evaluation of the extension of infarct lesions and were not able to ascertain any statistical association. Apart from the limits of our measurement method, we assumed that the neuroanatomical function of the affected stroke area was much more important than the extension.

The finding of more neurocognitive impairments in form of lower mean values in cognitive measures in patients with ischemic lesions of both group D and group I patients did not reach significance. Previous studies described poststroke cognitive decline by global cognitive screening such as MMSE and more recently and more sensitively by MoCA [ 42 ]. While the mean group values of MMSE around 28 out of 30 were within normal range, only the group of stroke mimics showed a normal mean value of Mean MoCA values of group D They most probably reflected stroke lesion-associated cognitive impairments whereas stroke mimics without any lesions did show normal scores.

Although MMSE and MoCA significantly correlated to our cognitive composite score CCS , further analysis of neurocognitive domain deficits by neuropsychological test battery yielded only some trends of mean group values, without statistical significance. The mean group values of single tests as well as of CCS showed at least clear trends of stronger cognitive impairments in group D and group I patients than stroke mimics regarding the following cognitive domains: Divided and selective attention TAP , combined attention and executive function TMT A and B , mental rotation LPS-7 , and spatial cognitive function FPT.

These findings corresponded widely to findings of Gottwald et al. This profile of cognitive dysfunction was related to predominance of cerebellar stroke lesions in both group D and group I. The findings were in line with modern concepts of cerebellar cognitive function [ 44 ] and also in accordance to previous data on cognitive impairments in patients with cerebellar stroke lesions, for example by Exner et al. Speck et al. Their mixed series included about two third of patients with spontaneous internal carotid artery dissection ICAD and one third with VAD.

Ischemic stroke was found in only Thirty-one of 62 study participants completed Because only three of them showed any signs of cognitive impairment, the authors argued that deficits were unlikely responsible for the reduced QOL. Apart from severity of neurological disorders , as scored by mRS, and impaired neuropsychological performance at baseline , as measured by global cognitive screening in form of MMSE, elevated posttraumatic stress symptoms levels , as assessed by Post-Traumatic Stress Syndrome Questions Inventory PTSS , proved to be an independent predictor for reduced QOL at follow-up in group D patients after VAD according to multivariate regression analysis.

It showed a high validity [ 47 ] against the Posttraumatic Diagnostic Scale PDS [ 48 ] as longer established item self-report measure. Czechowsky et al. Fischer et al. Nearly all other potential contributing factors were not significantly different.

Elevated levels of posttraumatic stress symptoms, as evaluated by PTSS scoring in our study, are in line with recent reports on the prevalence of posttraumatic stress disorder PTSD after stroke, even after minor stroke [ 49 ] or transient ischemic attack [ 50 ].

While post-stroke anxiety [ 9 ] and depression [ 10 ] have been described already earlier, even depression in stroke patients treated and non-treated with intravenous thrombolytic therapy [ 51 ], posttraumatic stress disorder has been coming to attention more recently. They assessed, partly retrospectively two months to five years, partly prospectively one month after dissection, the presence of PTSD by using the Posttraumatic Diagnostic Scale PDS as self-rating questionnaire.

Their series comprised physically less affected patients, two-third after ICAD and one-third after VAD, with ischemic stroke in form of mainly small lesions in about one-third of cases only. Their high PTSD prevalence might be overestimated because physically less affected people voluntarily participating in their study might have tended to mention more mental problems when asked by self-rating PDS.

Previous data [ 52 ], however, have already stressed that even subsyndromal scores may be of relevance, as can be assumed for our thirteen subgroup D patients with elevated PTSS levels and bad QOL despite good functional outcome. In this context the following aspects seem to be worthy to note: First, elevated scores of stress symptoms were also found in patients without any stroke lesion in our study in line with other study results [ 50 ].

Second, apart from elevated scores of stress symptoms, significantly higher scores of pre-baseline symptoms of anxiety were found which might be indicative for a predisposing vulnerability for anxiety disorders and subtypes like subthreshold posttraumatic stress disorder. Fourth, maladaptive coping strategies were significant predictors for and associated with posttraumatic stress disorder in patients with cervical artery dissection in the study of Speck et al. We think increased PTSS levels were neither decisively stroke unit-related, as they were less frequent in comparison group I and M patients who were also treated on the stroke unit, nor disease-specific, as they were also present in group I and M.

PTSS levels have been still prevalent in group D which might be explained by the stress-vulnerability model [ 53 ]. According to modern stress concepts, situations that in particular include unpredictability and uncontrollability can trigger stress [ 54 ].

Both conditions fit if someone is suffering from a spontaneous artery dissection as well as subarachnoid hemorrhage in contrast to ischemic stroke caused by vascular risk factors which can be treated. Noble et al. Importantly, our study cohort of VAD patients appeared to be not significantly biased by exclusion of eight patients, whose features and mean age of More importantly, however, our study showed also several limitations.

First of all, the study cohort showed an unusual high percentage of elderly VAD patients mean age Cervical artery dissection is commonly considered to be underdiagnosed [ 3 , 57 , 58 , 59 ]. Grond-Ginsbach et al. In addition, differentiation of dissection from rupture of atheroma in the context of arteriosclerosis may be difficult so that Ahl et al.

Over the last years, cervical artery dissection has been increasingly diagnosed due to improved neuroimaging methods [ 58 ]. That is in particular striking regarding VAD.

Ahl et al. They finally hypothesized that the rate of incidence must be equal throughout life. The overrepresentation of elderly patients in our study may be most probably explained to some extent by a hospital-based selection bias: 1 Patients were recruited when referred to the supraregional stroke unit of our teaching hospital.

Despite obvious overrepresentation of elderly VAD patients and the need for confirmation of our results by larger studies, the main findings are in line with all three younger aged study cohorts that were previously examined for health related QOL after cervical artery dissection as discussed above: 1 Significant percentage of patients with bad QOL SS-QOL scoring despite good functional outcome mRS sccoring - Fischer et al.

The senior age of VAD patients may have several important implications for social life. Knecht et al. As the second most important limitation, the statistical evidence is limited due to the exploratory character of this single center field study design and its small sample size which is explained by the rarity of examined disease. Thus, the present investigation has to be characterized as an explorative study. Third, psychological condition was not examined at baseline.

It was only asked for affective symptoms of anxiety and depression pre-baseline and at follow-up there has been only exploration for stress symptoms but not for symptoms of anxiety and depression. Furthermore, there was no physical follow-up examination conducted, only a follow-up assessment by questionnaire.

Neurocognitive domain assessment at baseline was dichotomized into normal versus pathological values based on a difference of more than one standard deviation.

Therefore, pathological alterations might have been either too subtle for detection, the applied neuropsychological tests not sensitive enough, or the study cohorts too heterogenous. Finally, additional potential outcome-relevant lifestyle-factors such as nutrition and sports activity as well as social factors such as social networks and social support were not taken into account of this study.

It leads to a reduced QOL in a significant percentage of patients despite good functional outcome. Our data suggest that posttraumatic stress symptoms are of significant importance for the QOL after VAD, in particular in patients with reduced QOL despite good functional outcome. For both future research and clinical treatment, our data favor a multidimensional monitoring after VAD, with special focus on neuropsychiatric sequelae.

Psychometric self-rating tools, as used in this study, may enable timely detection of such sequelae and facilitate therapeutic intervention. The datasets used and analysed during the current study are available from the corresponding author on reasonable request.

Incidence and outcome of cervical artery dissection: a population-based study. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. Vertebral artery dissection: presenting findings and predictors of outcome. Leys D, Debette S. Long-term outcome in patients with cervical-artery dissections: there is still a lot to know. Cerebrovasc Dis. Czechowsky D, Hill MD. Neurological outcome and quality of life after stroke due to vertebral artery dissection.

Quality of life in survivors after cervical artery dissection. J Neurol. Measuring quality of life in a way that is meaningful to stroke patients. Bonita R, Beaglehole R. Recovery of motor function after stroke. Impact of anxiety on health-related quality of life after stroke: a cross-sectional study. Arch Phys Med Rehabil.

Factors affecting the quality of life after ischemic stroke: young versus old patients. J Clin Neurol. The role of cognitive impairment in the quality of life after ischaemic stroke. Engel GL. The clinical application of the biopsychosocial model. Am J Psychiatry. Craniocervical arterial dissection: spectrum of imaging findings and differential diagnosis.