No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Bilateral spontaneous internal carotid artery dissection with both early and very late recanalization: A case report
Abstract
Spontaneous bilateral internal carotid artery dissection has frequently been described in the literature as a cause of stroke. In more than half of the patients with internal carotid artery dissection, recanalization occurs early after the event and is unusual later than 6 months after onset of the dissection. We describe a patient with ischemic stroke due to left internal carotid artery occlusion in the extracranial segment. The patient was treated with anticoagulants and early vessel recanalization did not occur. Ten months later, he developed contralateral internal carotid occlusion in the intracranial tract, which was followed by early complete recanalization. Anticoagulation therapy was continued and, 16 months after the initial event, the left internal carotid artery unexpectedly also reopened.
... The treatment for ICAD consists of three possible approaches [29, 30]: conservative, endovascular or surgical. Conservative treatment consists of two steps: an acute anticoagulation with heparin followed by secondary prophylaxis by oral anticoagulation/antiplatelet that normally is sufficient for 3-12 months (however, delayed recanalization as described by Vicenzini et al. [10] can prolong this period). ...
... The natural course of ICAD seems to be composed of an acute phase during which conservative or more rarely endovascular/surgical treatments are undertaken followed by a chronic phase during which a recanalization occurs in the majority of patients during the following 6 months. Some have reported that delayed recanalization can occur after 16 months as well [10], a fact that might prompt individual consideration regarding the time for anticoagulation/antiplatelet therapy. ...
... ICAD can account for 10-25% of strokes in young patients [2, 8, 10, 11, 12] and is considered as one of the main causes for stroke recurrence [12]. Among 1-5% of all spontaneous ICAD cases, a heritable connective-tissue disorder can by identifiable and ∼5% may have one family member with spontaneous dissection of various arteries including the aorta or its main branches [13, 14, 15, 16]. ...
Emphasizing the therapeutic and diagnostic implications of concomitant inadequate collaterals from the circle of Willis in a rare case of spontaneous acute bilateral internal carotid artery dissection (BICAD) following 5 days of isolated rigorous cough (pertussis like).
A 45-year-old male has been referred to our department with rapid neurological deterioration consisting of dysarthria and severe left hemiparesis following 5 days of isolated rigorous cough. CTA demonstrated BICAD, a tiny anterior communicating artery and no bilateral posterior communicating artery. The patient had no personal or familial risk factors. Infectious, traumatic, vascular and connective tissue diseases were ruled out.
Neurological deterioration persisted despite immediate provision of continuous 'full-heparinization' with concomitant rigorous control of blood pressure. Endovascular treatment consisting of bilateral stenting was undertaken. Ten days later, the patient was discharged with mild hemiparesis and resuming normal activity after 3 months.
BICAD with concomitant inadequate collaterals from the circle of Willis may predispose to hypoperfusion which might not respond to the usual conservative treatment prompting for flow reestablishment. Moreover, isolated rigorous cough can cause acute spontaneous BICAD even among patients without any risk factors.
... Internal carotid artery dissection (ICAD) is a significant cause of ischemic stroke, and accounts for ≤25% of ischemic strokes in young and middle-aged patients (1). The majority (70%) of patients are reported to be <50 years old, with a slight predominance of male patients (2,3). ...
Internal carotid artery dissection (ICAD) is a major cause of ischemic stroke in young and middle-aged patients. Patients may be asymptomatic or present with symptoms ranging from headache and neck pain to severe cerebral ischemic events. Conventional treatment is medical anticlotting therapy or involves the use of interventional tools, such as endovascular treatment. Anticoagulation or antiplatelet therapy are the primary treatment modalities used to prevent thromboembolic complications from arterial dissections, however, they are unsuitable in certain cases of dissecting aneurysms. In the current study reports the case of a 52-year-old male patient presenting with the primary complaint of left limb weakness. Computed tomography angiography revealed a right ICAD located in the oropharyngeal segment. Subsequently, digital subtraction angiography was performed to assess the oropharyngeal segment. Antithrombotic therapy resulted in no improvement; therefore, endovascular treatment with the insertion of a Willis covered stent was performed, resulting in an improved outcome. © 2016, Experimental and Therapeutic Medicine. All rights reserved.
Background:
Intra- and extracranial internal carotid artery dissections (ICD) are two different pathological conditions. Extracranial dissection is considered to be among the most frequent causes of stroke in the young and the segment generally reopens in 2 out of 3 cases, completely or partially, within 6 months. Intracranial ICD (IICD) is considered a rare occurrence in stroke and, accordingly, there are few systematic published data. However, it is a clinically significant condition that may cause severely disabling ischemic stroke or subarachnoid hemorrhage. In the past, sole availability of invasive imaging methods for its detection may have induced an underreporting. The aim of the study was to analyze ultrasound findings, timing and predictors of recanalization in patients with IICD.
Methods:
IICD acute patients admitted to our Stroke Unit were submitted to carotid sonographic seriated monitoring, daily for the 1st week after symptom onset, at day 14, at month 1 and every 3 months thereafter up to a follow-up of 4 years. Contrast carotid ultrasound was performed in patients with persistent occlusion after month 1.
Results:
Fourteen acute patients with IICD were enrolled. Extracranial internal carotid patency was observed in 8 patients at first ultrasound scans; all of these showed complete intracranial recanalization within the 1st week and oral anticoagulants were withdrawn after 6 months. Conversely, in 6 patients retrograde extracranial internal carotid thrombosis was immediately observed, since the first ultrasound scans. In 4 of these the occlusion persisted after 4 years while 2 of them had only a partial recanalization, with evidence at contrast ultrasound of still late remodeling processes in the extracranial thrombus up to 2 years after the first observation; for this reason, in these 2 patients anticoagulation was not discontinued, while in the 4 patients with persistent, stable, occlusion, therapy was suspended 1 year after the diagnosis.
Conclusions:
Identification of the site of dissection - i.e. extra- versus intracranial - is fundamental in clinical studies for outcome and prognosis evaluation. Carotid ultrasound strict surveillance is important to monitor eventual recanalization in patients with ICD, even in a late phase. Retrograde internal carotid thrombosis seems to be correlated with persistent occlusion and partial recanalization. Remodeling of thrombotic material in the internal carotid artery may, however, continue for up to 2 years. In these cases, contrast ultrasound evidence of thrombus morphological changes may support the decision to continue anticoagulation.
Several specialists use three-dimensional (3D) ultrasound as adjuvant imaging technique in their clinical practice. It has been applied to study carotid plaque morphology, surface and volume during atherosclerosis progression. Nonetheless, no papers have so far described the use of this technique in conditions different than carotid stenosis, such as bifurcation anatomy changes of the caliber and vessel course modifications.
Patients admitted to our ultrasound laboratory for vascular screening were submitted to standard carotid duplex and to 3D ultrasound reconstruction of the carotid bifurcation.
Forty normal subjects, 7 patients with caliber alterations (4 carotid bulb ectasia and 3 internal carotid lumen narrowing), 45 patients with course variations (tortuosities and kinking) and 35 patients with internal carotid artery stenosis of various degrees have been investigated.
3D ultrasound is a feasible technique. It can improve carotid axis imaging through a better presentation of caliber variations and vessel course 'at a glance'. 3D ultrasound from the inward flow can provide imaging of the stenosis, but stenosis quantification should always take into account the assessment of plaque morphology and vessel wall.
Internal carotid artery dissection has increasingly been reported as a cause of transient ischemic attack or stroke. However, scarce data exist on the natural history of the arterial lesions and the temporal profile of recanalization.
We followed 48 patients with 50 angiographically confirmed internal carotid artery dissections by sequential duplex Doppler studies in 2- to 4-day intervals during the first weeks after the onset of symptoms and after 4 weeks in 1- to 2-month intervals for up to 2 years. We assessed sonographic features as well as the frequency and time course of resolution.
Initial Doppler findings were abnormal in all patients, most of whom (68%) presented with a characteristic bidirectional high-resistance Doppler signal in the internal carotid artery. Gradual recanalization was found in 68% of the dissections after an average interval of 51 days. Changes of Doppler flow patterns in follow-up studies and features of intra-arterial angiography correlated with the development of internal carotid artery dissection and mirrored the recanalization process.
Our findings suggest that Doppler sonography provides early recognition of internal carotid artery dissection and monitoring of its resolution. Thus, ultrasound studies may guide clinical decisions according to the development of the dissection.
To evaluate long-term outcome after extracranial internal carotid artery dissection (eICAD) in consideration of the applied antithrombotic therapy.
Among 33 consecutive eICAD patients initially treated either with anticoagulation (n = 25) or with antiplatelets (n = 8), a standardized interview was performed after 28 +/- 22.1 months to analyze risks and benefits of both agents. Ischemic and hemorrhagic complications, occurrence of seizure and rates of arterial recanalization were compared and long-term clinical outcome was assessed using the modified Rankin Scale (mRS) and Barthel Index (BI).
Among anticoagulated patients, 1 died due to brain herniation. In 3 patients stroke (n = 2) or TIA (n = 1) recurred. In the antiplatelet group, none died and no subsequent ischemic events happened. Hemorrhagic complications were noted in neither treatment group. Functional outcome among anticoagulated patients was BI 92 +/- 21.6 and mRS 1.48 +/- 1.50, which did not differ from patients initially treated with antiplatelets (BI 89 +/- 18.9, mRS 1.50 +/- 1.41, p > 0.05). Four anticoagulated patients developed seizures, compared to 2 patients with antiplatelets (p > 0.05). Arterial recanalization occurred in 16 of 22 antico- agulated patients with ultrasound follow-up, compared to 6 of 6 patients with antiplatelets (p > 0.05).
In the absence of iatrogenic side effects, both anticoagulation and antiplatelets seem to be safe for eICAD. The rates for death and stroke were low and outcome ratings did not differ between both agents. These findings may indicate that a controlled randomized trial comparing anticoagulation and antiplatelets is ethically justified.
There is limited information about predictors of outcome and recurrence of ischaemic stroke affecting young adults.
To assess the predictive value of the presenting characteristics for both outcome and recurrence in young stroke victims.
Clinical and radiological data for 203 patients aged 16 to 45 years were collected prospectively; they comprised 11% of 1809 consecutive patients with ischaemic stroke. The National Institutes of Health stroke scale (NIHSS), the Bamford criteria, and the trial of ORG 10172 in acute stroke treatment (TOAST) classification were used to define stroke severity, subtype, and aetiology. The clinical outcome of 198 patients (98%) was assessed using the modified Rankin scale (mRS) and categorised as favourable (score 0-1) or unfavourable (score 2-6).
Stroke was caused by atherosclerotic large artery disease in 4%, cardioembolism in 24%, small vessel disease in 9%, another determined aetiology in 30%, and undetermined aetiology in 33%. Clinical outcome at three months was favourable in 68%, unfavourable in 29%, and lethal in 3%. Thirteen non-fatal stroke, two fatal strokes, and six transient ischaemic attacks (TIA) occurred during a mean (SD) follow up of 26 (17) months. High NIHSS score, total anterior circulation stroke, and diabetes mellitus were independent predictors of unfavourable outcome or death (p<0.0001, p = 0.011, and p = 0.023). History of TIA predicted stroke recurrence (p = 0.02).
Severe neurological deficits at presentation, total anterior circulation stroke, and diabetes mellitus predict unfavourable outcome. Previous TIA are associated with increased risk of recurrence.
INTRODUCTIONCarotid and vertebral artery dissections are potentially disabling and yet probably under-diagnosed, and mainly seem to affect young and middle-aged people (Bogousslavsky et al. 1987). Our review focuses on the mechanisms, possible underlying causes, clinical manifestations, diagnostic tools, treatment and prognosis of both carotid and vertebral dissection.EPIDEMIOLOGYCervical artery dissection accounts for up to 20% of strokes in patients under 30 years of age (Bogousslavsky et al. 1987). The incidence of carotid dissection is about 2–3 per 100 000 per year (Schievink et al. 1993; Giroud et al. 1995); the incidence of cervical dissection must be higher because these figures do not take into account vertebral dissection (about 25% of all dissections), dissections without ischaemic events (20% of extracranial dissections) or asymptomatic dissections. Furthermore, dissections may be overlooked because the clinical manifestations resolve spontaneously and are not necessarily familiar to many emergency physicians. Most studies report either
To the Editor:
We congratulate Nedeltchev and coworkers for their meritorious report1 on recanalization of spontaneous internal carotid artery dissection. The strengths of this work are a fairly large patient population compared with most previous reports and the repeated ultrasound examinations of the vasculature at 1, 3, 6, and 12 months. Recanalization always occurred within 6 months, but not later. We, having similar experience, currently repeat vascular imaging only at 6 months.
Nedeltchev et al discuss that they did not detect any beneficial effect of complete recanalization and refer to 2 articles that do not directly support their view; of these, one is a small study on 60 cervical artery dissection patients treated with anticoagulants2 and the second3 is a review in Spanish …
Cervical-artery dissection (CAD) is a major cause of cerebral ischaemia in young adults and can lead to various clinical symptoms, some of which are benign (eg, headache, neck pain, Horner's syndrome, and cranial-nerve palsy), but most patients have a stroke or transient ischaemic attack. In addition to trauma to the neck, other risk factors have been suggested, such as infection, migraine, hyperhomocysteinaemia, and the 677TT genotype of the 5,10-methylenetetrahydrofolate reductase gene (MTHFR 677TT), although evidence is sparse. An underlying arteriopathy, which could in part be genetically determined, is believed to have a role in the development of CAD. Importantly, both research on and optimum management of CAD strongly rely on diagnostic accuracy. Although the functional outcome of CAD is good in most patients, socioprofessional effects can be important. Incidence of the disorder in the general population is underestimated. Mortality and short-term recurrence rates are low but possibly also underestimated. Further research is warranted to improve our understanding of the underlying pathophysiology, to assess the long-term outcome, and ultimately to provide treatment and prevention strategies.
We set out to investigate the predictors and time course for recanalization of spontaneous dissection of the cervical internal carotid artery (SICAD).
We prospectively included 249 consecutive patients (mean age, 45+/-11 years) with 268 SICAD. Ultrasound examinations were performed at presentation, during the first month, and then at 3, 6, and 12 months, and clinical follow-ups after 3, 6, and 12 months.
Of 268 SICADs, 20 (7.5%) presented with <or=50% stenosis, 31 (11.6%) with 51% to 80% stenosis, 92 (34.3%) with 81% to 99% stenosis, and 125 (46.6%) with an occlusion. Antithrombotic treatment included anticoagulation in 174 (67%) patients, aspirin in 64 (24%) patients, and aspirin followed by anticoagulation or vice versa in 22 (8%) patients. Follow-up ultrasound showed normal findings in 160 (60%), <or=50% stenosis in 27 (10%), 51% to 80% stenosis in 4 (1%), 81% to 99% stenosis in 26 (10%), and occlusion in 51 (19%) vessels. The rate of complete recanalization was 16% at 1 month, 50% at 3 months, and 60% at 6 and 12 months. Initial occlusion of the dissected vessels reduced the odds of recanalization (OR, 4.0; 95% CI, 2.2-7.3; P<0.001), whereas the occurrence of local symptoms and signs only at presentation were independently associated with complete recanalization (OR, 0.4; 95% CI, 0.2-0.8; P=0.048).
These results suggest that recanalization of SICAD occurs mainly within the first 6 months after the onset of symptoms. Initial occlusion reduces the likelihood of complete recanalization, whereas presentation with local symptoms and signs only increases it.
Neurovascular ultrasound (nUS) is widely used as a screening and monitoring tool in patients with spontaneous cervical artery dissection (sCAD). The aim of the study was to describe the sonographical course of the affected arteries in patients with a MRI-proven sCAD by repetitive nUS.
Thirty-seven consecutive patients aged<60 years with 1.5 T MRI-proven sCAD were prospectively investigated by nUS, and within 48 hours after admission before MRI. The patients were re-investigated after 6 months and again after a period>12 months.
Forty-nine sCAD were detected in 37 patients; 24 lesions (49%) were located in the internal carotid arteries (ICA), and 25 (51%) in the vertebral arteries (VA). An arterial occlusion was found in 13 arteries (27%). The recanalization rate of occluded arteries was 62%. Regression of stenosis/occlusion within the first 6 months was found in 34 (69%) of the affected arteries, while between 6 and >12 months, the improvement rate was lower (19%). A complete recanalization without residual stenosis after 6 months was found in 39%. In only one artery, initial high grade ICA stenosis progressed to complete persistent occlusion (2%).
The course of arterial stenosis or occlusion caused by sCAD is highly dynamic during the first 6 month after the event. The vast majority of arteries show regression of stenosis or recanalization of initial occlusion. Only a minority of patients experience a persistent deterioration of the vessel status.
Dissection of the cervicocranial arteries is becoming more frequently recognized as a cause of neurological disorders. Typical clinical features seen with dissection include unilateral headache, oculosympathetic palsy, amaurosis fugax, and symptoms of focal brain ischemia. The diagnosis of carotid or intracranial dissection is usually best confirmed by angiography, although magnetic resonance imaging and computed tomography have been shown to visualize intimal dissection. The prognosis in cases of spontaneous dissection is generally benign unless the initial manifestation involves infarction with substantial deficit. The best approach to treatment appears to be the administration of the anticoagulant, heparin, followed by warfarin or antiplatelet therapy. Surgical intervention is reserved for cases of progressive or recurrent ischemic complication that occurs despite the administration of adequate doses of anticoagulants.
Extracranial and transcranial Doppler and duplex sonographic findings in six patients with internal carotid artery dissection proven by angiography is reported. Extracranial Doppler analysis showed occlusion without a recordable signal from the internal carotid artery at any level or stenosis with accelerated flow in the high cervical segment. Transcranial Doppler findings demonstrated the hemodynamic consequences of the internal carotid artery occlusion or stenosis with collateral flow across the circle of Willis and also showed the dampened pulse wave of the middle cerebral artery ipsilateral to the dissection. In duplex sonography, the indirect signs indicating internal carotid artery dissection were a patent carotid bifurcation and proximal internal carotid artery segment but with no or only a short systolic flow signal. Atherosclerotic wall changes were absent, an important finding that suggests nonatherosclerotic stenosis or occlusion. Direct signs making the diagnosis likely were a tapering of the internal carotid artery lumen distal to the bulb, an irregular membrane crossing the vessel lumen, and the demonstration of a true lumen with flow and a false one without flow. While cerebral angiography is still considered the gold standard, ultrasound may become the primary modality for early diagnosis. Doppler and duplex examinations help to indicate angiography and are the methods of choice for follow-up investigations. They clearly demonstrate spontaneous recanalization with normalization of carotid circulation or, in case of persistent occlusion, improvement of collateral blood supply. Sequential examinations may prove helpful to determine the duration of anticoagulant treatment.
We studied 36 patients (21 women and 15 men) with spontaneous dissection of the internal carotid arteries. The ages of these patients ranged from 21 to 63 years. Focal unilateral headache was the most common symptom. Other common clinical manifestations (in decreasing order of frequency) included focal cerebral ischemic symptoms, oculosympathetic paresis, bruits, light-headedness, and neck pain. Less common symptoms were syncope, amaurosis fugax, scalp tenderness, swelling in the neck, and dysgeusia. Common angiographic manifestations (in decreasing order of frequency) were elongated, irregular, and frequently tapered narrowing of the lumen; abrupt luminal reconstitution (often at the carotid canal); aneurysms; intimal flaps; slow internal carotid artery--middle cerebral artery flow; tapered occlusion; and distal branch occlusions. The incidence of hypertension in these patients was considerably higher than that in the general population. Angiographic evidence of fibromuscular dysplasia was found in 14% of the patients, but atherosclerotic changes were uncommon. Follow-up ranged from 14 to 140 months (mean, 58.5 months). Twenty-three patients with 29 dissected internal carotid arteries were also restudied angiographically. The stenosis of the internal carotid artery either completely resolved or substantially improved in more than 85% of the dissected vessels. About two-thirds of the dissecting aneurysms either resolved or decreased in size. Clinically more than 85% of the patients had an excellent or complete recovery. Recurrence of the dissection or rupture of a dissecting aneurysm was not noted. Despite their disconcerting appearance on angiography, spontaneous dissections of the internal carotid arteries are often associated with a good prognosis.
The authors report a young woman with bilateral internal carotid artery occlusion shown by carotid angiography. There was spontaneous bilateral recanalization demonstrated radiographically. The possible causes, e.g. the intake of oral contraceptive drugs, a spontaneous intimal dissection and other etiological features are discussed and the literature is reviewed.
To analyze the value of ultrasound for early diagnosis and follow-up of internal carotid artery dissection.
The carotid arteries were evaluated in 43 consecutive patients using extracranial and transcranial pulsed-wave Doppler and duplex sonography.
Ultrasound examination was performed, on average, 7.7 days after the first symptoms. The dissections subsequently were verified by MRI (16 patients), angiography (13 patients), or both (14 patients) on average 4.4 days later. The overall sensitivity of the combined examination was 95% (93% for extracranial Doppler, 86% for transcranial Doppler, and 79% for duplex sonography). All three methods detected occlusions or high-grade stenoses in 100% of patients and moderate- or low-grade stenoses in 80% (combined methods), 70% (extracranial Doppler), 40% (transcranial Doppler), and 20% (duplex) of the patients. The findings in 33 patients with an occlusion or high-grade stenosis according to neuroradiology were as follows: absent flow signal in the internal carotid artery (100%) and biphasic (stump) flow in its bulb (86%), high-resistance flow pattern of the ipsilateral common carotid artery (91%), signs of collateral flow across the circle of Willis (97%), and low flow in the middle cerebral artery (79%) on transcranial insonation. In seven patients, a moderate stenosis of the high cervical carotid segment was found because of a retromandibular high-velocity signal. In five of them this was the only abnormal finding. Duplex examination was helpful because it confirmed absent internal carotid artery flow or stump flow in the case of occlusion or high-grade stenosis (100%) and excluded an atherosclerotic origin by demonstrating a patent bulb (100%) and the absence of plaques (95%). Follow-up studies showed recanalization in 63% of patients, occurring at variable intervals. Occlusion persisted in 37%.
Ultrasound performed within the first weeks can corroborate a clinically suspected carotid dissection in up to 95% of patients. Repetitive follow-up studies in most cases are sufficient to monitor evolution.
We reviewed the medical records of 60 consecutive patients (28 men and 32 women; aged from 13 to 63 years) with the diagnosis of dissection of the internal carotid artery (ICA), and with available clinical and neurosonological follow-up. Ten cases occurred after trauma and 50 cases were spontaneous. Angiographic evidence of fibromuscular dysplasia of the ICA was found in 23% of the cases. Unilateral headaches or neck pain associated with focal cerebral ischemic symptoms or oculosympathetic palsy were the most common findings. Less frequent symptoms such as isolated cranial nerve palsies and pulsating bruits were also observed. Follow-up ranged from 3 to 144 months (mean, 37.5 months). A favourable outcome occurred in 73.7% of the cases with a follow-up of 6 months or more, and seemed to depend on the severity of the ischemic cerebral deficit associated with the ICA dissection. 68% (41/60 cases) of our patients developed stroke and 18% (11/60 cases) experienced a transient ischemic attack, which occurred as the initial manifestation of the ICA dissection in 28.8% (15/52 cases) of the cases, and with a delay (more than 24 hours) in the other cases. Evidence of embolization in the cerebral arteries was found in 36% of the cases with stroke (15/41 cases). Anticoagulant therapy, given in 34 of our patients, seems to be justified by the fact that a considerable risk exists for cerebral emboli in association with ICA dissections; no serious neurological complications were observed in our series as a result of this anticoagulant therapy. Doppler sonography follow-up diagnosed a recanalization in 67.8% of the stenotic or occlusive dissections, most of them being completed within the first 6 months (92%). Recurrence of ICA dissection is exceptional but occurred in one of our 60 cases, 2.5 years after the first event.
When a tear occurs in one of the major arteries in the neck and allows blood to enter the wall of the artery and split its layers, the result is either stenosis or aneurysmal dilatation of the vessel. This process was long thought to be a rare cause of stroke, particularly in the absence of trauma, and the diagnosis was usually not made until the postmortem examination.1–3 It was not until the late 1970s, when Fisher et al.1 and Mokri et al.2 described dissections of carotid and vertebral arteries as detected by modern diagnostic approaches, that dissections began to . . .
To determine the 3-year outcome in 287 young adults (15 to 45 years old) consecutively admitted between 1992 and 1996 for an ischemic stroke.
Follow-up was obtained with clinical examinations or telephone interviews, and data were recorded about risk factors, associated disorders, causes of stroke, and current treatments. Functional outcomes were classified with the modified Rankin Scale (mRS). Endpoints were stroke recurrence, myocardial infarction, epileptic seizures, and death.
After a mean follow-up of 3 years, no patient was lost to follow-up; 25.4% of the follow-up visits were performed by telephone interview. The authors found 1) an annual mortality rate of 4.5% during the first year and then of 1.6%; 2) an annual stroke recurrence rate of 1.4% during the first year and then of 1.0%; 3) a 0.2% annual rate of myocardial infarct; 4) epileptic seizures occurring in 6.6% of patients, during the first year in most patients; 5) independence (mRS = 0 to 2) in 94.0% of patients; 6) 4.2% of patients lost their job after stroke despite an mRS score of < or =1; 7) 7.0% of patients reported divorce; and 8) only 22.2% of smokers gave up smoking.
Although young patients who experience ischemic strokes have a low risk of stroke recurrence and myocardial infarction, some patients do not regain independence.
Internal carotid artery dissection (ICAD) is a frequent etiology of stroke in the young. Immediate anticoagulation with unfractionated heparin is the most frequent treatment. A theoretical side effect of unfractionated heparin is an increase in the intramural hematoma resulting in hemodynamic cerebral infarction. We studied 20 patients with ICAD. All patients were immediately treated with unfractionated heparin. Activated partial thromboplastin time (aPTT) ratios were measured twice daily. We prospectively monitored the course of ICAD with repeated ultrasound in hospital. Unexpectedly, delayed ICA occlusion was noted in 5 patients under treatment. One of these developed a watershed infarct. We then analyzed the aPTT ratios over the first 6 days after diagnosis. Patients with delayed occlusion had significantly higher aPTT ratios (2.6 +/- 0.4 vs. 2.0 +/- 0.5, p < 0.05). Within the limits of a partially retrospective design, our study seems to support the notion that unfractionated heparin can increase the intramural hematoma. Our findings further justify a randomized clinical trial to resolve the anticoagulant/antiplatelet debate.
To evaluate the usefulness of various sonographic criteria for detecting a dissection of the internal carotid artery (ICA).
Twenty-three consecutive patients displaying typical clinical symptoms of ICA dissection were identified. The diagnosis of dissection in these cases was confirmed by MRI/MRA or arteriography. The sonographic examination was the first technical investigation and involved the combined use of Doppler and duplex sonography. The value of different sonographic criteria was evaluated for the identification of ICA dissection: 1) Morphological criteria: intramural haematoma or double lumen. 2) Haemodynamic findings of distal stenosis/occlusion in combination with suddenly appearing clinical signs of a space-occupying lesion in the respective region (Horner's syndrome, lower cranial nerve palsies). 3) Haemodynamic signs of distal stenosis/occlusion with ensuing recanalisation within a few weeks.
Morphological criteria alone allowed detection of a dissection in 47,8 % of patients. By the combined use of morphological and haemodynamic criteria ICA dissections were identified on admission in 73.9 % and after an average of 4.5 weeks (at the latest after 6 weeks) in 91.3 % of the patients.
ICA dissections can be identified sonographically with high sensitivity. In some of the cases, however, definite diagnosis can only be provided by follow-up evaluation.
Bilateral internal carotid artery dissections have been reported, but spontaneous bilateral dissections are rare. Internal carotid artery dissection can present with a spectrum of symptoms ranging from headache to completed stroke. Two cases of spontaneous bilateral carotid artery dissection are presented, one with headache and minimal symptoms and the other with a stroke syndrome. No cause could be found in either case, making the dissections completely spontaneous. Bilateral internal carotid artery dissection (ICAD) should be considered in young patients with unexplained head and neck pain with or without focal neurological symptoms and signs. The increasing availability of imaging would sustain the higher index of suspicion.
Antithrombotic therapy in patients with cervical artery dissection (CAD) is empiric rather than evidence based. The routine use of anticoagulants in each CAD patient cannot be recommended. A randomized controlled trial comparing antiplatelets with anticoagulation is clearly needed. However, due to the large sample size, which is required to gather meaningful results, such a trial is a huge venture. Thus, the matter of antithrombotic treatment in CAD is not expected to be solved in the near future. What should clinicians do in the meantime? There are several pathophysiological arguments in favor as well as against anticoagulants or antiplatelets. Until more data are available, it is our personal recommendation that treatment decisions should be geared to several clinical and paraclinical features of individual patients. The chapter compiles putative arguments in favor versus against immediate anticoagulation and may be helpful for individually tailored antithrombotic treatment decisions in CAD patients.
Background and purpose:
The widespread preference of anticoagulants over antiplatelets in patients with cervical artery dissection (CAD) is empirical rather than evidence-based. Summary of Review- This article summarizes pathophysiological considerations, clinical experiences, and the findings of a systematic metaanalysis about antithrombotic agents in CAD patients. As a result, there are several putative arguments in favor as well as against immediate anticoagulation in CAD patients.
Conclusions:
A randomized controlled trial comparing antiplatelets with anticoagulation is needed and ethically justified. However, attributable to the large sample size which is required to gather meaningful results, such a trial represents a huge venture. This comprehensive overview may be helpful for the design and the promotion of such a trial. In addition, it could be used to encourage both participation of centers and randomization of CAD patients. Alternatively, antithrombotic treatment decisions can be customized based on clinical and paraclinical characteristics of individual CAD patients. Stroke severity with National Institutes of Health Stroke Scale score > or =15, accompanying intracranial dissection, local compression syndromes without ischemic events, or concomitant diseases with increased bleeding risk are features in which antiplatelets seem preferable. In turn, in CAD patients with (pseudo)occlusion of the dissected artery, high intensity transient signals in transcranial ultrasound studies despite (dual) antiplatelets, multiple ischemic events in the same circulation, or with free-floating thrombus immediate anticoagulation is favored.