Pica (disorder)

We reviewed 29 patients with vertebrobasilar dissections (VBD) to investigate the correlation between minor trauma and VBD and the clinical features of this trauma-related condition. Mean age was 43 years, with a male predominance (male/female ratio was 25/4). Seventeen patients presented with subarachnoid hemorrhage (SAH), and 12 with ischemic symptoms. Two patients presenting with ischemia had extracranial VBD (V3 segment). Angiographically, aneurysmal dilatation was observed in most SAH patients (13 patients) in contrast to narrowing or occlusion in most ischemic patients (10 patients). Among the 12 SAH patients treated with coil embolization or conservatively, five died, whereas all ischemic patients recovered well with anticoagulation and/or antiplatelet therapy. Seven patients had received minor or trivial head/cervical trauma, due to whiplash injury, minor fall, or during exercise, which were identified to precede with the lapse of some time (a few minutes or days) the onset of symptoms. All of these patients presented with ischemic symptoms, and they were younger than the other ischemic or SAH patients. The site of vertebral artery dissection was intracranial in four cases, extracranial in one case, and combined in two cases at the level of the V3 segment and the origin of the posterior inferior cerebellar artery. However, no SAH occurred. These clinicopathological findings, i.e. ischemia and angiographic narrowing/occlusion, suggest that dissections were subintimal. Therefore, it is believed that this minor or trivial trauma may primarily cause subintimal dissection with luminal compromise, leading to ischemic symptoms, rather than subadventitial or transmural dissection with aneurysmal dilatation, leading to SAH. This lesion may also occur in younger patients with a favorable outcome. Careful note should be made of patient for the early recognition of this disorder. (Neurol Res 2002; 24: 129-1381

Keywords: Vertebrobasilar dissection; minor trauma; subarachnoid hemorrhage; ischemia; clinical features

INTRODUCTION

Recently, dissections of the vertebrobasilar artery have been increasingly recognized. The clinical and radiological findings have been described in detail, and have focussed on the pathophysiology, causes, clinical course and management, and their early detection using imaging studies'-5. These dissections occur spontaneously or in association with head or neck trauma, and are termed spontaneous dissections when no obvious trauma has been identified. Traumatic dissections can be easily diagnosed with the clinical and radiological evidence of significant trauma . Vertebrobasilar artery dissection, however, is a well known complication of minor or trivial trauma to the neck and head, which can develop in exercise-related activities, minor fall or injury, or neck manipulation, but these traumatic events may be ignored by patients1,6. Though vertebrobasilar artery dissections have been reported frequently in association with trauma, few studies have focussed on intracranial dissections associated with apparently minor or trivial trauma"-8. The clinical characteristics of minor trauma-related intracranial dissections are little known compared with spontaneous dissection. It has been reported that traumatic lesions are less likely to resolve over time in extracranial internal carotid artery dissections9. Nonetheless, others are of the opinion that there is no difference between the lesions The purpose of this study was to investigate the correlation between minor or trivial trauma and vertebrobasilar dissection and to analyze its clinical features.

MATERIALS AND METHODS

The clinical features and radiological findings of 29 patients with a diagnosis of vertebrobasilar dissection, presented between 1992 and 1998 were reviewed retrospectively. The 29 patients studied comprised 25 males and four females, age range 4 to 67 years, with a mean age of 43 years. Diagnosis was made on the basis of angiographic findings in association with MRI and MR angiography and clinical features, such as subarachnoid hemorrhage or neurological manifestations related to the disturbance of vertebrobasilar circulation, including headache and vertigo. Seventeen patients presented with subarachnoid hemorrhage. The remaining 12 patients had a clinical presentation of ischemia in the vertebrobasilar territory. Patients' history was assessed in detail with regard to potential traumatic events. Seven cases were identified to be associated with minor or trivial trauma. The follow-up period ranged from 10 to 92 months, with a mean of 53 months.

RESULTS

Vertebrobasilar dissection with subarachnoid hemorrhage

Seventeen patients (13 males and 4 females) presented with sudden headache and/or an altered mental state resulting from subarachnoid hemorrhage. Patient age ranged from 18 to 67 years, with a mean age of 49 years. The clinical and radiological features of the patients are summarized in Table 1.

Radiologically dissections were located intracranially along the vertebrobasilar artery, but in one case involvement of the vertebral artery occurred between the V3 segment (between C2 and the dural penetration) and the origin of the posterior inferior cerebellar artery (PICA). Intracranial involvement was at the vertebral artery proximal to the origin of the PICA in one case, distal to the origin of the PICA in 10, at the vertebral artery near the origin of the PICA in three, and at the basilar artery in two cases. Angiographically aneurysmal dilatation was observed in 13 cases (76%), while occlusion was observed in one case and segmental narrowing or stenosis in three (Figure 1A,B). Aneurysmal dilatation usually took the form of fusiform aneurysm rather than pouch-like saccular aneurysm (Figure 2A,B). In one patient with segmental narrowing bilateral vertebral arteries were involved between the V3 segment and the origin of the PICA.

The initial Hunt and Hess grades were 1 in one, 2 in eight, 3 in six, and 4 in two patients. Focal infarction was observed on MRI in seven patients: at the cerebellum in four, at the thalamus in one, and at the pons in four, which included two patients with a basilar dissection. However, two patients had both subarachnoid hemorrhage and ischemic symptoms at the time of diagnosis. No patient had a history of preceding trauma. Six patients had a medical history of hypertension, and one had a polycystic kidney. Acute hydrocephalus, which was caused by rebleeding in four, developed in nine patients, and extraventricular drainage proved very effective for reducing intracranial pressure in this condition. Rebleeding occurred in four of 17 patients (24%), with an interval between the hemorrhagic episodes ranging from 1 to 10 days. Three patients had repeated hemorrhage before management at days 1 and 4 after the initial hemorrhage in one, at days 10, 11 and 14 in one, twice on day 1 in another patient. The remaining patient had rebleeding on day 9. All patients deteriorated rapidly and comatosed immediately after rebleeding, one led to respiratory arrest. Acute hydrocephalus following rebleeding was confirmed by computed tomography. All patients with rebleeding recovered rapidly with extraventricular drainage.

Five patients underwent surgery; proximal clip occlusion of the dissected artery was performed in four and aneurysmal neck clipping in one. Surgical outcome was excellent in all patients. Endovascular treatment using Guglielmi detachable coils was performed in seven patients: aneurysmal occlusion using coils was tried in four patients and proximal occlusion of the vertebral artery in three. The dissecting aneurysm was completely occluded in five patients. The remaining two showed partial filling of the lesion after procedure completion. Four of five patients with complete occlusion recovered well with an excellent outcome. Three of five patients treated conservatively were in an excellent condition during the follow-up.

There were five deaths in those with subarachnoid hemorrhage (Table 3). Two patients treated conservatively died on days 9 and 17 after the initial hemorrhage. Two patients treated incompletely with endovascular coils revealed progressive enlargement of fusiform aneurysms with recurrent hemorrhage, and died on days 16 and 39 after the initial hemorrhage (8 and 25 days after endovascular treatment). In the remaining patient with bilateral dissection of the vertebral artery, the proximal vertebral artery was occluded completely with endovascular coils, and he died 10 days later (at day 12 after the initial hemorrhage) with extension of the dissection on the contralateral vertebral artery. It was noteworthy that all patients died suddenly with fulminant signs of brain stem failure. Follow-up CT demonstrated infarction in some parts of the brain stem and/or cerebellum. All patients with recurrent hemorrhage died, though they showed clinical improvement after extraventricular drainage. CT showed no additional hemorrhage at the time of stem failure due to infarction.

Vertebrobasilar dissection with ischemic manifestations

Twelve male patients presented with ischemic symptoms and signs. Ages ranged from 4 to 58 years, with a mean age of 37 years. Clinical and radiological features of the patients are summarized in Table 2.

Radiologically dissection was located along the vertebral artery. The site of dissection was intracranial, near the origin of the PICA in eight cases, and extracranial dissection was located at the V3 segment in two cases. In two cases dissection was both intracranial and extracranial, from the V3 segment to the origin of the PICA, and from the V3 segment to the vertebrobasilar junction. Angiographically segmental narrowing or stenosis was observed in six cases (Figure IC,D), occlusion in three cases, and double lumen in one case, while aneurysmal dilatation was visualized in two cases: fusiform and dolichoectatic (Figure 2C,D).

The most common symptom was occipital headache and/or posterior neck pain associated with vertigo. In one patient intracranial dissection of the vertebral artery was considered to be detected incidentally, because extracranial internal carotid artery dissection was combined, and acute symptoms of infarction in the middle cerebral artery territory developed without any symptoms or signs attributable to the posterior circulation: hemiparesis and aphasia. Among the other patients, six had hemiparesis due to the infarction at the brain stem and/or thalamus. Infarction was detected on MRI in nine patients; at the cerebellum in six, at the brain stem in five, at the thalamus in three, and at the high cervical cord in one. Vertebrobasilar transient ischemic attacks were observed in two patients without any definable infarction. Recurrent ischemic episodes occurred in two patients.

All patients except one were treated medically with anticoagulation and/or antiplatelet therapy. Surgical trapping of fusiform dissecting aneurysm was performed in one patient. Outcome was excellent in all patients. A dolichoectatic dissecting aneurysm enlarged slowly during the follow-up period, but symptoms subsided with no recurrence. Recurrent stroke occurred only in one patient after anticoagulation discontinued, but the recurred symptoms disappeared soon with retreatment. All patients presenting with ischemic symptoms had a favorable clinical course and there was no mortality (Table 3).

Vertebrobasilar dissection associated with trivial trauma

Seven male patients with vertebrobasilar dissection had a history of preceding trivial trauma. The ages ranged between 4 and 58 years and were less than 15 years in three patients. The clinical findings of each patient are summarized in Table 4. All patients presented with ischemic symptoms and signs. In patients presenting with subarachnoid hemorrhage no patient was identified to have a history of associated trauma. Infarction was detected on MRI at the cerebellum, thalamus, basal ganglia, and medulla. The ischemic symptoms with occipital headache were referable to the posterior circulation and infarction. In one patient (Case 2), dissection of the intracranial vertebral artery was simultaneously associated with internal carotid artery dissection. The clinical outcome with anticoagulation and/or antiplatelet therapy was excellent. There was no clinical feature distinct from dissection with ischemia.

Minor or trivial trauma was associated with vertebral artery dissection, as follows: rotation and/or flexion-- extension movement of the neck with activites such as Yoga (Case 1); neck rotation and head turning during exercise (Cases 2 and 4); head struck by fist (Case 3); light rear car collision (Case 5); and a minor fall with flexed neck from a chair and sofa (Cases 6 and 7). The time interval between the traumatic event and the ischemic episode ranged from a few minutes to one week. No other risk factor was detected.

The location of the dissection was intracranial in four cases, extracranial in one case, and both intracranial and extracranial in two cases. Segmental narrowing occurred in four cases, occlusion in one, double lumen in one, and dolichoectatic aneurysmal dilatation in one. Dissection with segmental narrowing was intracranial and/or extracranial (Figure ICD), and dissection with aneurysmal dilatation was intracranial (Figure 2C,[D).

DISCUSSION

Intracranial vertebral artery dissections have been reported to have two major types of presentation, focal neurological deficits due to vertebrobasilar circulation ischemia (transient ischemic attack or stroke) and subarachnoid hemorrhage'0-12. According to numerous reports on intracranial dissection, the incidence of the types is variable 4,13-16. The incidence seems to vary due to the under-evaluation of patients with ischemia for the further diagnosis of dissections, and the chosen admission department, neurosurgery or neurology. In our series, which included 17 patients with subarachnoid hemorrhage and 10 patients with ischemia, clinical presentation with subarachnoid hemorrhage was more frequent than ischemia (37%).

Dissections occur because of the intima tearing or hemorrhage from vasa vasorum, causing an intramural hematoma within a tissue plane of the arterial wall: subintima, media or subadventitia . Subintimal dissection extends inward, resulting in a narrowing of the arterial lumen or occlusion with progression. Subadventitial or transmural dissection results in aneurysmal dilatation of the outer wall, causing the dissecting aneurysm. The consequences of dissection vary depending on its location and extent . Subintimal dissections are usually associated with cases presenting with ischemia, while subadvantitial or transmural dissections may penetrate the adventitia and cause subarachnoid hemorrhage",'z,' 1,12,17,18

Intracranial dissections differ clinically from extracranial lesions. Subintimal dissection between the internal elastic lamina and media is the most common location of the intramural hematoma19,20. Intracranial arteries have a thinner media and adventitia and a comparative lack of external elastic lamina compared to the extracranial arteries20,21. These structural differences allow intracranial dissection to proceed through the media to the adventitia and to take the form of aneurysmal dilatation with subadventitial or transmural dissection'"9. Intracranial dissection is subadventitial or transmural with aneurysmal dilatation, or subintimal with luminal compromise, causing subarachnoid hemorrhage in the former pattern or ischemia in the latter",12,17. Extracranial dissection is usually subintimal because the media and adventitia remain relatively thick and tight with the external elastic lamina, causing ischemia 12,20,22. Anticoagulation is recommended in extracranial dissections to reduce the risk of infarction, but contra-indicated in intracranial dissections to precipitate the subarachnoid hemorrhage 2'8,10,23. Extracranial dissection is spontaneous or traumatic, and more common than intracranial dissection, which is exclusively spontaneous10,11,24. In traumatic extracranial dissections of the vertebrobasilar arteries, all cases present with ischemia caused by subintimal dissection, and the preferred site of dissection is known to be the V3 segment with angiographic findings of narrowing or occlusion . Subadventitial dissection and aneurysmal dilatation can also be seen in the extracranial arteries25'27. In our series, most of the dissections were intracranial: 27 patients with intracranial dissection, including three with extension to the V3 segment. Only two patients presenting with ischemia had extracranial dissections involving the V3 segment. Among 27 patients with intracranial dissections, 17 presented with subarachnoid hemorrhage and 10 with ischemia. Although the reported incidence of subarachnoid hemorrhage is variable 4,13-16, subarachnoid hemorrhage occurs more frequently in studies involving larger groups of patients, with the incidence of up to 86%16. In our series, the incidence of hemorrhage was 63%, and dissections of the intracranial vertebral arteries associated with trivial trauma occurred exclusively in the less frequent cases, which presented with ischemia.

Diagnosis of vertebrobasilar artery dissections is made based on the characteristic radiological findings and the appropriate clinical presentation To,". MRI and MR angiography are also useful for detection and follow-- up as noninvasive methods4'28,29. Angiography, however, is still the mainstay of radiological diagnosis. The angiographic findings consist of narrowing, occlusion, double lumen, or pseudoaneurysm formation, and referred to as 'string sign' or 'pearl and string sign' with a distal site of dilatation2,30. Other findings such as intimal flap and stasis of contrast material in the late phase can be included15,16. Generally it is admitted that angiographic findings are subject to change depending on the pathological patterns of dissections: narrowing, or occlusion in the subintimal pattern, and aneurysmal striction in the subadbentitial pattern. Thus, the pathology of dissections, i.e. the patterns of dissections, can be estimated on the basis of clinical presentation and angiographic findings. Dissections with ischemia and angiographic findings of narrowing or occlusion may have the subintimal pattern, whereas dissections with subarachnoid hemorrhage and pseudoaneurysm tend to have the subadventitial or transmural pattern. These clinical findings correspond well with previous reports on intracranial vertebrobasilar artery dissections, especially those involving a large series of patients4,13-16,31,32. Yamaura et al.16 noted that all of 24 patients, consisting of 21 patients with subarachnoid hemorrhage and three with ischemia, had fusiform aneurysm. A previous report has described the angiographic findings consistent with clinical presentation in all cases31. Although these findings in ischemia patients were reported to vary somewhat, compatibility with clinical presentation was observed in the majority13-15. Only 7 of 22 patients with ischemia showed aneurysmal dilatation; narrowing or occlusion was not demonstrated in all of 16 patients with subarachnoid hemorrhage".

Aneurysmal dilatation was observed among some patients with asymptomatic dissections or ischemia The correlation between the patterns of dissections and clinical presentations was well documented by pathological investigations: the plane of dissection was subintimal in cases involving ischemia development, and subadventitial when subarachnoid hemorrhage had occurred11,12,17,18. In addition, this clinicopathological correlation was supported by the characteristic angiographic findings of narrowing or occlusion in the ischemic group and aneurysmal dilatation in the hemorrhage group11,12,17,18.

Angiographic features of arterial dissection vary because arterial dissection, which may follow a healing process following the tissue injury of an arterial wall, is a dynamic condition. The pathological features cannot be evaluated appropriately with the characteristic findings of dissection in the acute or delayed phase . Subtle changes of arterial lumen or segmental narrowing at the initial angiography can progress to an aneurysmal dilatation; this was observed particularly in some patients with subarachnoid hemorrhage of unknown etiology32,36,37. Abnormal findings changed in a majority of cases during the follow-up examinations; usually narrowing or occlusion either subsided or improved, and aneurysmal dilatation usually remained unchanged10,25,31,13,11 . The timing of angiographic examinations is important in terms of reflecting the pathological status, because of these temporal changes. Considering temporal evolution and that pseudoaneurysm formation can also cause ischemia with luminal compromise or thrombosis, a small number of cases with narrowing or occlusion in the hemorrhage group and aneurysmal dilatation in the ischemic group seem to be acceptable. In our series, 13 of 17 cases with hemorrhage showed aneurysmal dilatation; the remaining four showed narrowing or occlusion. Ten of 12 cases with ischemia showed narrowing or occlusion, and the remaining two showed aneurysmal dilatation. These angiographic features supported the evaluation of the clinicopathological correlation of dissections. The true incidence of intracranial dissections remains unknown. Intracranial dissections of the vertebrobasilar arteries have been reported to be associated with trauma, especially minor or trivial trauma, in a small number of studies2-4,6-8. However, the frequency of traumatic dissections seems to be under-appreciated, particularly in association with minor or trivial trauma. In cases reported previously2-4,6-8, all patients presented with ischemia. In one of these studies, narrowing was observed in all of two patients with intracranial or combined dissection . In another study, three of four cases showed narrowing, and aneurysmal dilatation in the remaining ones. Among 12 patients with ischemia in our series, two patients had extracranial dissection in the V3 segment with narrowing or occlusion, and one of these two cases was related to minor trauma. Six of the remaining 10 cases with intracranial or combined dissection, i.e. intracranial and V3 segment, were related with minor or trivial trauma. Of them, four showed narrowing or occlusion: aneurysmal dilatation in one, and double lumen in one. Thus, it is suggested that minor or trivial trauma may be related to dissections, which can occur intracranially and/or extracranially, usually presenting with ischemia caused by subintimal dissection and showing the angiographic findings of narrowing or occlusion. It is presumptive to provide this clinicopathological correlation without the pathological evidence, however, the clinicoradiological features of dissections support this correlation. The angiographic feature of aneurysmal dilatation in one case was dolichoectatic. Fragmentation of the internal elastic lamina, instead of its widespread disruption, with multiple dissection of a thickened intima, and organized thrombus are common findings in this type of aneurysm38. These aneurysms can grow to a giant size before rupture due to the mesh structure of the internal elastic lamina and also show symptoms in the early stage. It is more likely that this type of aneurysm is related with subintimal dissection rather than subadventitial dissection.

Vertebral artery dissection is reported to be a well-- known complication of neck and/or head trauma1. Minor trauma, including exercise-related activities, or trivial trauma such as head turning or neck flexion/ extension are also well-described precipitating factors of arterial dissection'6. A wide spectrum of types of minor or trivial trauma have been reported to precede this dissection and may be causative, and include chiropractic manipulation1,6,23,26,27,39,40. Close questioning is required to determine the history of trauma, because these types of trauma are usually not considered to be significant when they occur. Additionally, considering these events as potential causative factors is only based on temporal relationships. According to previous studies, generally the time interval between these traumatic events and the onset of symptoms ranges from the immediate to one week 2,25,36,41 . The delayed onset of symptoms has also been reported to be sometimes later than one week; in some cases symptoms and signs have developed several months or one year later possible mechanism, by which dissection may occur following minor or trivial trauma, is believed to be due to a rotational or flexion/extension movement of the neck. Movement may cause vertebral artery dissection by direct injury or stretching injury. Stretching of the vertebral artery is most commonly induced at the level of Cl-2, by a downward and forwards motion of the atlas relative to the axis on the side away from which the head is turned . Studies in cadavers and clinical settings support this phenomenon by providing evidence of occlusion at this level44,46. Although dissection occurs along the vertebral artery, the V3 segment is known to be the preferred site10,24,25. Dissection may also be attributed to stretching of the vertebral artery at the site of dural penetration, where the artery is fixed around the dura mater4. Dissection may extend both proximally and distally, involving the V3 and V4 segments. It is suggested that dissection related to head turning or neck movement may be attributed to compression of the vertebral artery at or near the origin of the posterior inferior cerebellar artery, which is the most common site of intracranial dissection 2. Nevertheless, we found only a small number of cases of intracranial dissection related to minor or trivial trauma in several reports2-46-8. In our seven patients that were found to have had a minor or trivial trauma event, these were characterized by head turning (yoga, exercise), unusual head position (head struck by a fist, minor fall from chair or sofa) or flexion/ extension of the neck (car accident). In six patients, symptoms began within a few minutes or 1-2 days, whereas symptoms developed one week after yoga in one patient. The flexion/extension of the neck caused by a car accident was a typical whiplash injury, and neurological deficits with pain began within minutes of the accident in this case. Minor or trivial trauma, including whiplash injury, was identified to be causative in our cases. Of seven cases, the intracranial artery was involved in six: the V4 segment in four, the V3 and V4 in two, and the V3 in one. Thus, minor or trivial trauma is also related to intracranial vertebral artery dissection.

The incidence of bilateral vertebral artery dissection is reported to range from 30% to 60% and that of coexistent vertebral artery and internal carotid artery dissection from 8% to 26%10'2,zz,zs,a. In our series, bilateral involvement was seen in only one case, and both the vertebral artery and the extracranial internal carotid artery were also involved in one case, related to trivial trauma.

A predisposing arteriopathy, like fibromuscular dysplasia, Marfan syndrome, type IV Ehlers-Danlos syndrome, and cystic medial necrosis, is reported to be associated with arterial dissection in the majority1,19,25,48. Risk factors, like diabetes mellitus, hypertension, migraine, smoking, and oral contraceptive pills, are also described for this lesion1,2,10,49. In our patients presenting with subarachnoid hemorrhage, polycystic kidney was found in one patient, and six patients had hypertension. Polycystic kidney is thought to be a predisposing condition associated with dissection as in the previous report5. Hypertension is not suggested to be one of the risk factors, because the incidence is less common than in previous studies4,20. Risk factors were not detected in our cases with ischemia or related to minor or trivial trauma. In our series, the mean age was 43 years, which is similar to prior reports. The age is reported to be lower in patients with intracranial dissection than in patients with extracranial dissection 3'8,",19. Furthermore, one previous report noted in intracranial dissection that patients with ischemia are younger than those with subarachnoid hemorrhage . In our series, the mean age of patients with subarachnoid hemorrhage or ischemia was 49 or 37 years. Patients with ischemia were younger than those with subarachnoid hemorrhage, including three patients below 15 years of age, all of which were associated with minor or trivial trauma. The ratio of male and female was 25/4. Male predominance was noted as reported in previous stud ies4,11,16,20,30.

The clinical features in our patients substantiate findings of previous studies. However, it is still noteworthy that rebleeding, high mortality and the extension of the dissection can be serious problems related to intracranial dissection with subarachnoid hemorrhage, and attention should be paid to these clinical features. Previous studies have shown that recurrent hemorrhage occurred in between 21% and 30%, resulting in a high mortality, ranging from 80% to 100%13-16,51. In one previous study, the rate of rebleeding was as high as 71.4%, and the mortality was 46.7%32. Additionally, recurrent hemorrhage usually occurred during the acute stage, within one or two weeks after the initial bleeding, and more than half the cases reported rebled within one or three days . In our series, recurrent hemorrhage occurred in 4 of 17 patients (24%), within two weeks. Of these four patients, three rebled two or three times before endovascular therapy. The interval between the hemorrhagic episodes was between 1 and 10 days in all of four patients. Of 17 patients, five died (mortality 29%), including all of the four patients with recurrent hemorrhage. Nevertheless, extension of the dissection was believed to cause all deaths, because patients showed sudden deterioration with signs of brain stem failure and brain stem and/or cerebellar infarction. This extension took place after the incomplete occlusion of dissecting aneurysms by endovascular therapy in two patients; coexistent dissection extended from the contralateral side after the complete occlusion of the ipsilateral dissection in one; and dissection extended with conservative management in two. Possible causes such as rebleeding, hydrocephalus, and vasospasm, were ruled out because patients showed no clinical or radiological evidence relevant to these causes. Until the sudden deterioration, they remained stable or had improved with extraventricular drainage, even after a previous hemorrhage. Some authors advocate the clinical importance of the extention of dissection, and this can be suspected when there is a progression or recurrence 13,16. The true frequency of this condition, however, remains unknown. Notably, a propensity for recurrent hemorrhage during the acute stage, and extension of the dissection support the notion that dissections with subarachnoid hemorrhage may have a progressive course. Because of the poor prognosis after rebleeding during the acute stage or the risk of extension, early surgical or endovascular treatment is recommended to prevent these as insisted by several previous authors' Spontaneous regression, and good outcome, has also been reported . We observed that three patients recovered well with conservative management, but none of these had the angiographic finding of aneurysmal dilatation: two patients had segmental narrowing, and one, diagnosed as basilar artery dissection, had an occlusion.

Previous reports have noted that vertebral artery dissection typically presented with posterior neck pain/ occipital headache and/or focal neurological defiCitS2,39-11,25,30 . Approximately 70% of our patients in the ischemic group suffered pain/vertigo, and this frequency is similar to that found previously2,10,48. Intracranial dissection may have a progressive course, or lead to hemorrhage afterwards, even when presenting with ischemia. In the case of ischemia, however, it has been generally reported to have a benign or favorable course 11, 13,14, 6. Anticoagulation therapy is not indiGated in subarachnoid hemorrhage or hemorrhagic infarction 2,8,10,22,23,34, but is still controversial for the management of intracranial dissection with ischemia, because of the probability of provoking intramural dissection'0,34. Anticoagulation therapy has been advocated for intracranial dissection to prevent symptoms in the ischemic group as well as for extracranial dissection2,3,8,10,14. In our series, all patients were successfully treated with anticoagulation and/or antiplatelet therapy; two showed recurrent ischemic attacks, but all subsequently recovered well and there was no case of bleeding or worsenign of symptoms. Intracranial dissection is reported to be more often associated with major sequelae and brain stem stroke than extracranial dissection3. This difference in the clinical features was not noted in our ischemic series. There was no difference between cases related to minor or trivial trauma and other ischemic cases.

The configuration of dissections is known to change 2-3 months after the initial diagnosis, because reparative changes in the vessel wall take place within that time8,15,34. Spontaneous resolution is observed in a high proportion of stenotic or occlusive dissections, whereas regression of aneurysmal dilatation is unusual and more commonly persistent at follow-up angiography 10,25,31,33,34. Based on these circumstances and clinicoradiological correlation, the angiographic findings at the initial diagnosis should be considered together with the initial presentation as one of the major determinants of the clinical course to decide upon the appropriate treatment. It is believed that the angiographic findings may also reflect the pathological status of arterial dissection, which can determine the clinical characteristics.

CONCLUSION

Intracranial vertebral artery dissection, in isolation or combined with extracranial extension, can be associated with minor or trivial trauma caused by whiplash injury, minor fall, and exercise, as can extracranial dissection. Intracranial dissection associated with these events was not presented with subarachnoid hemorrhage, but with ischemia in all cases. Angiographic findings demonstrating narrowing or occlusion in most cases were also supportive of this clinical feature. Despite the absence of pathological data, these findings suggest that this dissection is subintimal. Thus, it is conceived that these minor or trivial trauma may for the main part cause subintimal dissection with luminal compromise, leading to ischemic symptoms, rather than subadventitial or transmural dissection with aneurysm al dilatation, leading to subarachnoid hemorrhage. Additionally, this lesion has a favorable outcome with medical therapy, and may occur in younger patients, inclusive of children, than other intracranial and extracranial dissections. Careful history taking is important for the early recognition of this disorder. Further detailed studies, including pathological investigations, must be made on a large number of patients to clarify this hypothesis.

ACKNOWLEDGEMENTS

The present paper was supported by grants from the Seoul National University Hospital.

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Young-Seob Chung and Dae-Hee Han

Department of Neurosurgery, Seoul National University College of Medicine, Seoul, Korea

Correspondence and reprint requests to: Dae-Hee Han, MD, Department of Neurosurgery, Seoul National University Hospital, 28 Yongondong, Chongno-gu, Seoul 110-744, Korea. [daehan@snu.ac.kr] Accepted for publication September 2001.

Copyright Forefront Publishing Group Mar 2002
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