For individuals under 45 years old, vertebral artery dissection (VAD) is a known cause of stroke.
When the inner lining (intima) of the vertebral artery wall tears, blood can enter and split the layers of the vessel wall, a disease known as vertebral artery dissection.
The brain’s posterior circulation may constrict (stenosis), become completely occluded, or develop an aneurysmal dilatation as a result.
The subclavian arteries give rise to the vertebral arteries, which are paired vessels.
The basilar artery is formed when they rise via the transverse foramina of the cervical vertebrae (usually C6-C1) and reach the cranial cavity through the foramen magnum.
Dissections take place in the V2 (foraminal) and V3 (extradural, atlantoaxial) portions of the vessel, which are separated into four segments (V1-V4).
A false lumen is created when blood may pass through the layers of the artery wall due to an intimal tear.
Compression of the actual lumen may result in intramural hematoma development or impaired blood flow.
Posterior circulation ischemia can result from thrombus development in the false lumen embolizing distally.
Epidemiology
The extracranial cervical arteries are not dissected. Cervical artery dissections account for up to 25% of ischemic strokes in persons under 50, but only 2% of all ischemic strokes.
Vertebral artery dissection has a 3:1 female-to-male ratio. Men are somewhat more likely than women to have a stroke associated to cervical artery dissection, although women have these strokes earlier in life and at a higher peak age.
The average age of those diagnosed with cervical artery dissection is 45 years old.
With an average age of forty, VAD affects a considerably younger population than atherothrombotic disease of the vertebrobasilar circulation.
Anatomy
Pathophysiology
Hemorrhage into the artery wall and subarachnoid hemorrhage are destructive complications of VAD that are part of the pathophysiologic process underlying the illness.
The root lesion in VAD is a growing hematoma in the vessel wall. Via bleeding of the vasa vasorum within the vessel’s media, an intramural hematoma may develop spontaneously or as a later consequence of slight trauma.
The growing hematoma may obstruct the vertebral artery or one of its branches entirely or partially if the dissection is subintimal.
Subadventitial dissections frequently result in pseudoaneurysmal dilatation of the vertebral artery, which can compress nearby neural tissues.
Distal emboli may develop and spread because to the thrombogenic environment created by the intimal rupture and low flow conditions that occur in VAD.
Etiology
Individual comorbidities, genetic/congenital factors, environmental triggers, anatomical variables, and the dissection location are thought to interact in a complex way to produce cervical artery dissection.
A history of mild trauma is more common in VADs, while a recent systemic illness is more common in carotid artery dissections.
The phrase “spontaneous VAD” refers to any situation in which blunt or penetrating trauma is not a contributing factor.
Patients with a history of severe trauma, such as car crashes, falls, or piercing injuries, are eligible to get the diagnosis of traumatic VAD.
20-40% of patients with severe cervical trauma, such as fractures of the cervical spine or spinal cord injuries show traumatic occlusion when examined for vertebral artery damage.
Genetics
Prognostic Factors
If they survive the initial crisis, most patients who undergo extracranial dissection fare quite well. At follow-up, up to 88% of these patients show full clinical recovery.
In up to two thirds of these individuals, follow-up angiography shows spontaneous healing.
A more seriously impacted subgroup of all VAD patients is those who have intracranial vertebrobasilar dissection.
Rapidly worsening neurologic impairments, such as diminished awareness, are indicative of a dissection affecting the intracranial segment of the vertebral artery.
Individuals who survive the first crises perform exceptionally well (80-90%), and long-term consequences are uncommon.
Clinical History
Collect details including neurological symptoms, timeline pattern, past medical and risk factors of patients.
Small dissections remain clinically silent, delayed posterior circulation TIA or stroke
Differential Diagnoses
Hemorrhagic Stroke
Cervical Strain
Vertebrobasilar Atherothrombotic Disease
Subarachnoid Hemorrhage
Migraine Headache
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Treatment Paradigm:
Treat each patient according to their risk of ischemic stroke and cerebral bleeding. According to standards, anticoagulant medication and antiplatelet therapy are equally effective in lowering the risk of stroke.
When a person is at a higher risk of an ischemic stroke but has a low risk of cerebral bleeding, then consider parenteral and then oral anticoagulation.
If the patient satisfies other standard criteria in the most recent guidelines, intravenous thrombolysis (IVT) is a fair choice for patients with acute ischemic stroke with cervical artery dissection.
In cases of cervical artery dissection, antithombotic medication should be administered for three to six months.
When cervical artery dissection occurs with severe stenosis that compromises distal hemodynamics and subacute stenting may be considered for subsequent stroke prevention.
If there are no contraindications to the administration of thrombolytic drugs, they should be started as soon as possible for dissections that result in acute ischemia.
Antithrombotic therapy with antiplatelet or anticoagulant drugs is the standard treatment for verified or suspected spontaneous VAD in individuals who are not afflicted by the subarachnoid hemorrhage consequence.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Most dissections resolve over time with no lasting neurological deficits. It is crucial to note that when the dissection extends intracranially, the risk of subarachnoid hemorrhage significantly increases, making anticoagulation contraindicated. Endovascular or surgical interventions are reserved for patients with concurrent complications or those for whom maximal medical therapy proves unsuccessful.
Hospital admission is necessary for all patients with vertebral artery dissection, and close monitoring of neurological deficits is essential. Technological advancements have facilitated the use of endovascular therapies, although their role remains controversial, as most patients can be effectively managed with anticoagulation therapy.
Moreover, many dissections undergo spontaneous repair. Therefore, endovascular therapy is best suited for patients ineligible for thrombolytics or those experiencing subarachnoid hemorrhage.
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Use of non-pharmacological approach for Vertebral Artery Dissection
Avoid activities that raise intrathoracic pressure or heavy lifting since they might put stress on the artery wall.
Make ergonomic changes to workstations, monitors, and seats to maintain a neutral neck position both when at rest and when working.
Steer clear of extended uncomfortable neck postures and make use of pauses and reminders to restore your posture.
Minimize migraine triggers enough water, regular meals, and a suitable sleeping environment in individuals who also suffer from migraines.
Proper awareness about VAD should be provided and its related causes with management strategies.
Appointments with specialists and preventing recurrence of disorder is an ongoing life-long effort.
Use of Anticoagulants
Heparin:
It prevents a clot from reaccumulating following spontaneous fibrinolysis.
Warfarin:
For thromboembolic diseases, pulmonary embolism, and venous thrombosis prevention and therapy.
Use of Antiplatelet Agents
Aspirin:
It prevents cyclooxygenase from producing the powerful platelet activator thromboxane A2.
Use of Thrombolytics
Alteplase:
To convert plasminogen into plasmin, tissue plasminogen activator acts on the fibrinolytic system.
Surgery is saved for patients who are not candidates for endovascular treatments and whose symptoms are chronic and unresponsive to the most effective medicinal treatment.
Patients who continue to have ischemic episodes after taking antithrombotic medication are often the greatest candidates for surgical or endovascular correction of dissections.
In patients with persistent stenosis or dissecting aneurysm following acute extracranial artery dissection, the advantages and disadvantages of endovascular or surgical therapy are not well understood.
In acute phase, the goal is to stabilize the patient, prevent or limit ischemic injury, and relieve pain.
In long-term, the goal is to maintain vascular health and prevent recurrence.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
For individuals under 45 years old, vertebral artery dissection (VAD) is a known cause of stroke.
When the inner lining (intima) of the vertebral artery wall tears, blood can enter and split the layers of the vessel wall, a disease known as vertebral artery dissection.
The brain’s posterior circulation may constrict (stenosis), become completely occluded, or develop an aneurysmal dilatation as a result.
The subclavian arteries give rise to the vertebral arteries, which are paired vessels.
The basilar artery is formed when they rise via the transverse foramina of the cervical vertebrae (usually C6-C1) and reach the cranial cavity through the foramen magnum.
Dissections take place in the V2 (foraminal) and V3 (extradural, atlantoaxial) portions of the vessel, which are separated into four segments (V1-V4).
A false lumen is created when blood may pass through the layers of the artery wall due to an intimal tear.
Compression of the actual lumen may result in intramural hematoma development or impaired blood flow.
Posterior circulation ischemia can result from thrombus development in the false lumen embolizing distally.
The extracranial cervical arteries are not dissected. Cervical artery dissections account for up to 25% of ischemic strokes in persons under 50, but only 2% of all ischemic strokes.
Vertebral artery dissection has a 3:1 female-to-male ratio. Men are somewhat more likely than women to have a stroke associated to cervical artery dissection, although women have these strokes earlier in life and at a higher peak age.
The average age of those diagnosed with cervical artery dissection is 45 years old.
With an average age of forty, VAD affects a considerably younger population than atherothrombotic disease of the vertebrobasilar circulation.
Hemorrhage into the artery wall and subarachnoid hemorrhage are destructive complications of VAD that are part of the pathophysiologic process underlying the illness.
The root lesion in VAD is a growing hematoma in the vessel wall. Via bleeding of the vasa vasorum within the vessel’s media, an intramural hematoma may develop spontaneously or as a later consequence of slight trauma.
The growing hematoma may obstruct the vertebral artery or one of its branches entirely or partially if the dissection is subintimal.
Subadventitial dissections frequently result in pseudoaneurysmal dilatation of the vertebral artery, which can compress nearby neural tissues.
Distal emboli may develop and spread because to the thrombogenic environment created by the intimal rupture and low flow conditions that occur in VAD.
Individual comorbidities, genetic/congenital factors, environmental triggers, anatomical variables, and the dissection location are thought to interact in a complex way to produce cervical artery dissection.
A history of mild trauma is more common in VADs, while a recent systemic illness is more common in carotid artery dissections.
The phrase “spontaneous VAD” refers to any situation in which blunt or penetrating trauma is not a contributing factor.
Patients with a history of severe trauma, such as car crashes, falls, or piercing injuries, are eligible to get the diagnosis of traumatic VAD.
20-40% of patients with severe cervical trauma, such as fractures of the cervical spine or spinal cord injuries show traumatic occlusion when examined for vertebral artery damage.
If they survive the initial crisis, most patients who undergo extracranial dissection fare quite well. At follow-up, up to 88% of these patients show full clinical recovery.
In up to two thirds of these individuals, follow-up angiography shows spontaneous healing.
A more seriously impacted subgroup of all VAD patients is those who have intracranial vertebrobasilar dissection.
Rapidly worsening neurologic impairments, such as diminished awareness, are indicative of a dissection affecting the intracranial segment of the vertebral artery.
Individuals who survive the first crises perform exceptionally well (80-90%), and long-term consequences are uncommon.
Collect details including neurological symptoms, timeline pattern, past medical and risk factors of patients.
Small dissections remain clinically silent, delayed posterior circulation TIA or stroke
Hemorrhagic Stroke
Cervical Strain
Vertebrobasilar Atherothrombotic Disease
Subarachnoid Hemorrhage
Migraine Headache
Treatment Paradigm:
Treat each patient according to their risk of ischemic stroke and cerebral bleeding. According to standards, anticoagulant medication and antiplatelet therapy are equally effective in lowering the risk of stroke.
When a person is at a higher risk of an ischemic stroke but has a low risk of cerebral bleeding, then consider parenteral and then oral anticoagulation.
If the patient satisfies other standard criteria in the most recent guidelines, intravenous thrombolysis (IVT) is a fair choice for patients with acute ischemic stroke with cervical artery dissection.
In cases of cervical artery dissection, antithombotic medication should be administered for three to six months.
When cervical artery dissection occurs with severe stenosis that compromises distal hemodynamics and subacute stenting may be considered for subsequent stroke prevention.
If there are no contraindications to the administration of thrombolytic drugs, they should be started as soon as possible for dissections that result in acute ischemia.
Antithrombotic therapy with antiplatelet or anticoagulant drugs is the standard treatment for verified or suspected spontaneous VAD in individuals who are not afflicted by the subarachnoid hemorrhage consequence.
Most dissections resolve over time with no lasting neurological deficits. It is crucial to note that when the dissection extends intracranially, the risk of subarachnoid hemorrhage significantly increases, making anticoagulation contraindicated. Endovascular or surgical interventions are reserved for patients with concurrent complications or those for whom maximal medical therapy proves unsuccessful.
Hospital admission is necessary for all patients with vertebral artery dissection, and close monitoring of neurological deficits is essential. Technological advancements have facilitated the use of endovascular therapies, although their role remains controversial, as most patients can be effectively managed with anticoagulation therapy.
Moreover, many dissections undergo spontaneous repair. Therefore, endovascular therapy is best suited for patients ineligible for thrombolytics or those experiencing subarachnoid hemorrhage.
Avoid activities that raise intrathoracic pressure or heavy lifting since they might put stress on the artery wall.
Make ergonomic changes to workstations, monitors, and seats to maintain a neutral neck position both when at rest and when working.
Steer clear of extended uncomfortable neck postures and make use of pauses and reminders to restore your posture.
Minimize migraine triggers enough water, regular meals, and a suitable sleeping environment in individuals who also suffer from migraines.
Proper awareness about VAD should be provided and its related causes with management strategies.
Appointments with specialists and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Heparin:
It prevents a clot from reaccumulating following spontaneous fibrinolysis.
Warfarin:
For thromboembolic diseases, pulmonary embolism, and venous thrombosis prevention and therapy.
Emergency Medicine
Aspirin:
It prevents cyclooxygenase from producing the powerful platelet activator thromboxane A2.
Emergency Medicine
Alteplase:
To convert plasminogen into plasmin, tissue plasminogen activator acts on the fibrinolytic system.
Emergency Medicine
Surgery is saved for patients who are not candidates for endovascular treatments and whose symptoms are chronic and unresponsive to the most effective medicinal treatment.
Patients who continue to have ischemic episodes after taking antithrombotic medication are often the greatest candidates for surgical or endovascular correction of dissections.
In patients with persistent stenosis or dissecting aneurysm following acute extracranial artery dissection, the advantages and disadvantages of endovascular or surgical therapy are not well understood.
In acute phase, the goal is to stabilize the patient, prevent or limit ischemic injury, and relieve pain.
In long-term, the goal is to maintain vascular health and prevent recurrence.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
For individuals under 45 years old, vertebral artery dissection (VAD) is a known cause of stroke.
When the inner lining (intima) of the vertebral artery wall tears, blood can enter and split the layers of the vessel wall, a disease known as vertebral artery dissection.
The brain’s posterior circulation may constrict (stenosis), become completely occluded, or develop an aneurysmal dilatation as a result.
The subclavian arteries give rise to the vertebral arteries, which are paired vessels.
The basilar artery is formed when they rise via the transverse foramina of the cervical vertebrae (usually C6-C1) and reach the cranial cavity through the foramen magnum.
Dissections take place in the V2 (foraminal) and V3 (extradural, atlantoaxial) portions of the vessel, which are separated into four segments (V1-V4).
A false lumen is created when blood may pass through the layers of the artery wall due to an intimal tear.
Compression of the actual lumen may result in intramural hematoma development or impaired blood flow.
Posterior circulation ischemia can result from thrombus development in the false lumen embolizing distally.
The extracranial cervical arteries are not dissected. Cervical artery dissections account for up to 25% of ischemic strokes in persons under 50, but only 2% of all ischemic strokes.
Vertebral artery dissection has a 3:1 female-to-male ratio. Men are somewhat more likely than women to have a stroke associated to cervical artery dissection, although women have these strokes earlier in life and at a higher peak age.
The average age of those diagnosed with cervical artery dissection is 45 years old.
With an average age of forty, VAD affects a considerably younger population than atherothrombotic disease of the vertebrobasilar circulation.
Hemorrhage into the artery wall and subarachnoid hemorrhage are destructive complications of VAD that are part of the pathophysiologic process underlying the illness.
The root lesion in VAD is a growing hematoma in the vessel wall. Via bleeding of the vasa vasorum within the vessel’s media, an intramural hematoma may develop spontaneously or as a later consequence of slight trauma.
The growing hematoma may obstruct the vertebral artery or one of its branches entirely or partially if the dissection is subintimal.
Subadventitial dissections frequently result in pseudoaneurysmal dilatation of the vertebral artery, which can compress nearby neural tissues.
Distal emboli may develop and spread because to the thrombogenic environment created by the intimal rupture and low flow conditions that occur in VAD.
Individual comorbidities, genetic/congenital factors, environmental triggers, anatomical variables, and the dissection location are thought to interact in a complex way to produce cervical artery dissection.
A history of mild trauma is more common in VADs, while a recent systemic illness is more common in carotid artery dissections.
The phrase “spontaneous VAD” refers to any situation in which blunt or penetrating trauma is not a contributing factor.
Patients with a history of severe trauma, such as car crashes, falls, or piercing injuries, are eligible to get the diagnosis of traumatic VAD.
20-40% of patients with severe cervical trauma, such as fractures of the cervical spine or spinal cord injuries show traumatic occlusion when examined for vertebral artery damage.
If they survive the initial crisis, most patients who undergo extracranial dissection fare quite well. At follow-up, up to 88% of these patients show full clinical recovery.
In up to two thirds of these individuals, follow-up angiography shows spontaneous healing.
A more seriously impacted subgroup of all VAD patients is those who have intracranial vertebrobasilar dissection.
Rapidly worsening neurologic impairments, such as diminished awareness, are indicative of a dissection affecting the intracranial segment of the vertebral artery.
Individuals who survive the first crises perform exceptionally well (80-90%), and long-term consequences are uncommon.
Collect details including neurological symptoms, timeline pattern, past medical and risk factors of patients.
Small dissections remain clinically silent, delayed posterior circulation TIA or stroke
Hemorrhagic Stroke
Cervical Strain
Vertebrobasilar Atherothrombotic Disease
Subarachnoid Hemorrhage
Migraine Headache
Treatment Paradigm:
Treat each patient according to their risk of ischemic stroke and cerebral bleeding. According to standards, anticoagulant medication and antiplatelet therapy are equally effective in lowering the risk of stroke.
When a person is at a higher risk of an ischemic stroke but has a low risk of cerebral bleeding, then consider parenteral and then oral anticoagulation.
If the patient satisfies other standard criteria in the most recent guidelines, intravenous thrombolysis (IVT) is a fair choice for patients with acute ischemic stroke with cervical artery dissection.
In cases of cervical artery dissection, antithombotic medication should be administered for three to six months.
When cervical artery dissection occurs with severe stenosis that compromises distal hemodynamics and subacute stenting may be considered for subsequent stroke prevention.
If there are no contraindications to the administration of thrombolytic drugs, they should be started as soon as possible for dissections that result in acute ischemia.
Antithrombotic therapy with antiplatelet or anticoagulant drugs is the standard treatment for verified or suspected spontaneous VAD in individuals who are not afflicted by the subarachnoid hemorrhage consequence.
Most dissections resolve over time with no lasting neurological deficits. It is crucial to note that when the dissection extends intracranially, the risk of subarachnoid hemorrhage significantly increases, making anticoagulation contraindicated. Endovascular or surgical interventions are reserved for patients with concurrent complications or those for whom maximal medical therapy proves unsuccessful.
Hospital admission is necessary for all patients with vertebral artery dissection, and close monitoring of neurological deficits is essential. Technological advancements have facilitated the use of endovascular therapies, although their role remains controversial, as most patients can be effectively managed with anticoagulation therapy.
Moreover, many dissections undergo spontaneous repair. Therefore, endovascular therapy is best suited for patients ineligible for thrombolytics or those experiencing subarachnoid hemorrhage.
Avoid activities that raise intrathoracic pressure or heavy lifting since they might put stress on the artery wall.
Make ergonomic changes to workstations, monitors, and seats to maintain a neutral neck position both when at rest and when working.
Steer clear of extended uncomfortable neck postures and make use of pauses and reminders to restore your posture.
Minimize migraine triggers enough water, regular meals, and a suitable sleeping environment in individuals who also suffer from migraines.
Proper awareness about VAD should be provided and its related causes with management strategies.
Appointments with specialists and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Heparin:
It prevents a clot from reaccumulating following spontaneous fibrinolysis.
Warfarin:
For thromboembolic diseases, pulmonary embolism, and venous thrombosis prevention and therapy.
Emergency Medicine
Aspirin:
It prevents cyclooxygenase from producing the powerful platelet activator thromboxane A2.
Emergency Medicine
Alteplase:
To convert plasminogen into plasmin, tissue plasminogen activator acts on the fibrinolytic system.
Emergency Medicine
Surgery is saved for patients who are not candidates for endovascular treatments and whose symptoms are chronic and unresponsive to the most effective medicinal treatment.
Patients who continue to have ischemic episodes after taking antithrombotic medication are often the greatest candidates for surgical or endovascular correction of dissections.
In patients with persistent stenosis or dissecting aneurysm following acute extracranial artery dissection, the advantages and disadvantages of endovascular or surgical therapy are not well understood.
In acute phase, the goal is to stabilize the patient, prevent or limit ischemic injury, and relieve pain.
In long-term, the goal is to maintain vascular health and prevent recurrence.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and surgical interventional procedures.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
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