Vertebral artery dissection ( VAD ) is a tear that resembles a flap in the inner lining of the vertebral artery, located at the neck and supplies blood to the brain. After tearing, blood enters the arterial wall and forms a blood clot, thickening of the artery walls and often blocking blood flow. Symptoms of vertebral artery dissection include head and neck pain and intermittent or permanent stroke symptoms such as speech impairment, impaired coordination and vision loss. Usually diagnosed with enhanced CT scan or MRI contrast.
Vertebral dissection may occur after a physical trauma to the neck, such as a blunt injury (eg a traffic collision), strangulation or manipulation, but may also occur spontaneously. 1-4% of spontaneous cases have a clear underlying connective tissue disorder affecting the blood vessels. Treatment is usually with antiplatelet drugs such as aspirin or with anticoagulants such as heparin or warfarin.
Vertebral artery dissection is less common than carotid artery dissection (major arterial surgery in front of the neck). Both conditions together account for 10-25% of non-hemorrhagic strokes in young and middle-aged persons. More than 75% recover fully or with minimal impact on function, with the rest having more severe disability and a very small proportion (about 2%) dying of complications. It was first described in 1970 by Canadian neurologist C. Miller Fisher.
Video Vertebral artery dissection
Classification
Vertebral artery dissection is one of two types of arterial dissection in the neck. Dissection of other types of carotid arteries, involving the carotid artery. Further vertebral arterial dissection is classified as traumatic (caused by mechanical trauma to the neck) or spontaneously, and may also be classified by the involved part of the artery: extracranial (intracranial) and intracranial (inner part) of the skull).
Maps Vertebral artery dissection
Signs and symptoms
Headache occurs in 50-75% of all cases of vertebral artery dissection. It tends to lie on the back of the head, either on the affected side or in the middle, and progresses gradually. It is boring or like pressure in character or pulsed. About half of those who suffer from VAD consider different headaches, while the rest have the same headache before. It is suspected that VAD with headache as the only symptom is quite common; 8% of all cases of vertebral and carotid dissection were diagnosed on the basis of pain alone.
The obstruction of blood flow through the affected vessel can cause dysfunction of the part of the brain supplied by the arteries. This occurs in 77-96% of cases. It may be temporary ("transient ischemic attack") in 10-16% of cases, but many (67-85% of cases) end up with a permanent deficit or stroke. The vertebral artery supplies the part of the brain located in the posterior fossa of the skull, and this type of stroke is called posterior circulating infarction. Problems may include speech or swallowing difficulties (lateral medullary syndrome); this occurs in less than one-fifth of cases and occurs due to brainstem dysfunction. Others may experience imbalances or lack of coordination due to small brain involvement, and others may experience visual loss (on one side of the visual field) due to visual cortical involvement in the occipital lobe. In the case of sympathetic channel involvement in the brainstem, partial Horner syndrome may occur; this is a combination of sagging eyelids, limited pupils, and sunken-looking eyes on one side of the face.
If arterial surgery extends to the portion of the artery located within the skull, subarachnoid hemorrhage may occur (1% of cases). This arises because of the rupture of the arteries and the accumulation of blood in the subarachnoid space. It may be characterized by different headaches, usually severe; it may also cause additional neurologic symptoms.
13-16% of all people with vertebral or carotid dissection have dissection in other cervical arteries. Therefore, it is possible for symptoms to occur on both sides, or for symptoms of carotid artery dissection occurring at the same time as vertebral artery dissection. Some give some veneer dissection dissection as high as 30%.
Cause
The causes of vertebral artery disorders can be grouped into two major, spontaneous and traumatic categories.
Spontaneous
Spontaneous cases are thought to be caused by intrinsic factors that weaken the arterial wall. Only a minority (1-4%) have an underlying connective tissue disorder, such as Ehlers-Danlos type 4 syndrome and, more rarely, Marfan's syndrome. Ehlers-Danlos syndrome type 4, caused by the mutation of the
There are also reports in other genetic conditions, such as osteogenesis imperfecta type 1, autosomal dominant polycystic kidney disease and pseudoxanthoma elasticum ,? 1 antitrypsin deficiency and hereditary hemochromatosis, but evidence for this association is weaker. Genetic studies on other connective tissue-related genes mostly produce negative results. Other disorders of the blood vessels, such as fibromuscular dysplasia, have been reported in the proportion of cases. Atherosclerosis does not seem to increase the risk.
There are many reports of risk factors for vertebral artery dissection; many of these reports suffer from methodological weaknesses, such as selection bias. Increased levels of homocysteine, often due to mutations in the MTHFR gene, appear to increase the risk of vertebral artery dissection. People with aneurysms from aortic roots and people with a history of migraine may tend to vertical dissection of the arteries.
Traumatic
Traumatic vertebral dissection may follow blunt trauma to the neck, such as in a traffic collision, direct blow to the neck, strangulation, or whiplash injury. 1-2% of those with major trauma may be injured in the carotid or vertebral artery. In many cases of vertebral dissection, people report recent mild trauma to the neck or sudden neck movement, for example in the context of playing sports. Others report recent infections, particularly respiratory infections associated with coughing. Trauma has been reported to occur within one month of dissection in 40% with nearly 90% of the time the trauma becomes small. It is difficult to prove the relationship of vertebral artery dissection with mild trauma and infection statistically. It is likely that many cases of "spontaneous" may actually be caused by a relatively minor insult in someone who tends to be exposed to other structural problems to the blood vessels.
Vertebral artery dissection has also been reported to be associated with some form of neck manipulation. There is significant controversy about the stroke risk rate of neck manipulation. Perhaps the manipulation may lead to dissection, or perhaps dissection already exists in some people seeking manipulative treatment. At the moment, conclusive evidence does not exist to support a strong relationship between neck and stroke manipulation, or no relationship.
Mechanism
The vertebral artery arises from the subclavian artery, and travels through the transverse foramen of the upper six vertebrae. After exiting at the level of the first cervical vertebra, its direction changes from vertical to horizontal, and then enters the skull through the foramen magnum. Inside the skull, the arteries combine to form the basilar artery, which joins the Willis circle. In total, three-quarters of the arteries are outside the skull; it has a high mobility in this area due to rotational motion in the neck and is therefore prone to trauma. Most dissections occur at the first and second vertebral levels. The vertebral artery supplies a number of vital structures in the posterior cranial fossa, such as the brain stem, the cerebellum and the occipital lobe. The brainstem stores a number of vital functions (such as respiration) and controls the facial and neck nerves. Cerebellum is part of a diffuse system that coordinates movement. Finally, the occipital lobe participates in the sense of vision.
Dissection occurs when blood accumulates in the walls of blood vessels. This is most likely caused by a tear in the intima tunica, allowing blood to enter the tunica medium, although another line of evidence suggests that blood may arise from vasa vasorum, a small blood vessel that supplies the outer layers of the larger blood vessels. Various theories exist concerning whether the person maintaining carotid and vertebral artery dissection, even if not suffering from connective tissue disorders, has an underlying susceptibility. Biopsy samples of the skin and other arteries indicate that this may be a possibility, but no genetic defects in collagen or elastin genes have been shown to be convincing. Another study showed inflammation of blood vessels, as measured by highly sensitive C-reactive proteins (hsCRP, inflammatory markers) in the blood.
After the dissection occurs, two mechanisms contribute to the development of stroke symptoms. First, the flow through the blood vessels can be disrupted due to accumulation of blood beneath the blood vessel wall, which causes ischemia (inadequate blood supply). Second, irregularities in blood vessel walls and turbulence increase the risk of thrombosis (formation of blood clots) and emboli (migration) of these brain clumps. From various paths of evidence, it appears that thrombosis and embolism are the main problems.
Subarachnoid haemorrhage due to arterial rupture usually occurs when the dissection extends into the artery V4 section. This can be explained by the fact that the artery walls are thinner and do not have any number of structural supporters in this section.
Diagnosis
Various diagnostic modalities exist to show blood flow or absence in the vertebral artery. The gold standard is cerebral angiography (with or without digital reduction angiography). This involves puncture of a large artery (usually a femoral artery) and advancing the intravascular catheter through the aorta to the vertebral artery. At that time, the radiocontras were injected and the downstream stream was captured on fluoroscopy (continuous X-ray imaging). The vessels may appear stenotik (narrowed, 41-75%), clogged (blocked, 18-49%), or as aneurysm (dilated area, 5-13%). Refinements can be described as "rat tail" or "string sign". Cerebral angiography is an invasive procedure, and requires a large volume of radiocontrast that can cause complications such as kidney damage. Angiography also does not directly show blood in the walls of blood vessels, as compared to a more modern modality. Use of angiography is left only when endovascular treatment is contemplated (see below).
More modern methods involve computed tomography (CT angiography) and magnetic resonance imaging (MR angiography). They use contrast in smaller amounts and are not invasive. CT angiography and MR angiography are more or less equivalent when used to diagnose or exclude vertebral artery dissection. CTAs have the advantage of showing certain abnormalities before, tend to be available outside of office hours, and can be done quickly. When MR angiography is used, the best results are achieved in the T 1 setting using a protocol known as "fat suppression". Doppler ultrasound is less useful because it gives little information about the part of the artery close to the base of the skull and in the vertebral foramen, and any abnormalities detected on ultrasound will still require confirmation by CT or MRI.
Treatment
Treatment is focused on reducing stroke episodes and damage from the distended arteries. Four modalities of treatment have been reported in the treatment of vertebral artery dissection. Two main treatments involve medications: anticoagulants (using heparin and warfarin) and antiplatelet drugs (usually aspirin). Less frequently, thrombolysis (a drug that dissolves blood clotting) can be given, and sometimes obstruction can be treated with angioplasty and stenting. No randomized controlled trials were performed to compare different treatment modalities. Surgery is used only in exceptional cases.
Anticoagulants and aspirin
From the analysis of existing small trial trials from cervical artery dissection (carotid and vertebral) it appears that aspirin and anticoagulation (heparin followed by warfarin) are equally effective in reducing the risk of stroke or further death. Anticoagulation is thought to be stronger than antiplatelet therapy, but anticoagulation may increase the size of the hematoma and worsen the obstruction of the affected artery. Anticoagulation may be relatively insecure if a large stroke has occurred, since the hemorrhagic transformation is relatively common, and if the dissection extends to V4 (carries the risk of subarakhnoid hemorrhage). Anticoagulation may be appropriate if there is rapid blood flow (via a very narrowed vessel) in transcranial doppler despite aspirin use, if there is a completely blocked vessel, if there is a recurrent stroke-like episode, or if a free-splitting blood clot is seen on a scan. Warfarin usually lasts for 3-6 months, because during this time the flow through the arteries usually improves, and most strokes occur within the first 6 months after development of dissection. Some consider 3 months as sufficient.
Professional guidelines in the UK recommend that patients with a VA dissection should be enrolled in clinical trials comparing aspirin and anticoagulants if possible. The American Guide states that the current anticoagulant benefits have not been established.
Thrombolysis, stenting and surgery
Thrombolysis, stenting and surgery are not widely used such as anticoagulant drugs or antiplatelets. This treatment is invasive or more risky, and is usually reserved for situations where symptoms worsen despite medical treatment, or where medical care may be unsafe (eg unacceptable bleeding tendencies).
Thrombolysis is the enzymatic destruction of blood clots. This is accomplished by administration of drugs (such as urokinase or alteplase) that activate plasmin, an enzyme that occurs naturally in the body and digests clots when activated. Thrombolysis is the accepted treatment for heart attacks and strokes unrelated to dissection. In cervical artery dissection, only small series of cases are available. Thrombolytic drugs are administered either intravenously or during cerebral angiography via a catheter directly to the affected artery. Data show that thrombolysis is safe, but its place in VAD treatment is uncertain.
Stenting involves the catheterization of the affected arteries during angiography, and the insertion of a mesh-like tube; this is known as "endovascular therapy" (in the blood vessels). This can be done to allow blood to flow through a very narrow vessel, or to close aneurysm. However, it is unclear whether the technical success of the procedure was translated into better results, since in both cases the problem often disappears spontaneously over time. Stenting, and insertion of coils by means of angiography, may be performed if there is aneurysm and/or extension of dissection to the artery V4 section.
Surgery carries a high risk of complications, and is usually offered only if there is damage or contraindication that can not be bargained on any other treatment. Various arterial repair procedures have been described.
Prognosis
The prognosis of spontaneous cervical arterial dissection involves neurological and arterial outcomes. The overall functional prognosis of individuals with stroke due to cervical arterial dissection does not seem to vary from young people with stroke due to other causes. The survival rate with good results (modified Rankin score 0-2) is generally about 75%, or perhaps slightly better (85.7%) if antiplatelet drugs are used. In anticoagulant and aspirin studies, combined mortality with one treatment was 1.8-2.1%.
After the initial episode, 2% may experience further episodes within the first month. After this, there is a risk of recurrence of 1% per year. Those who have high blood pressure and dissection in some arteries may have a higher risk of recurrence. Further episodes of cervical artery dissection are more common in younger individuals, have a family history of cervical artery dissection, or have a diagnosis of Ehlers-Danlos syndrome or fibromuscular dysplasia.
Epidemiology
The annual incidence is around 1.1 per 100,000 annually in population studies from the United States and France. From 1994 to 2003, incidents increased threefold; this has been attributed to the wider use of modern imaging modalities than the correct increase. Similarly, those living in urban areas are more likely to receive appropriate investigations, accounting for an increased diagnosis rate in those living in cities. It is estimated that the proportion of cases in people with mild symptoms remains undiagnosed.
There is controversy over whether VAD is more common in men or women; aggregate of all studies showed that incidence was slightly higher in men (56% versus 44%). Men averaged 37-44 years of age at diagnosis, and women 34-44. While the dissection of the carotid and vertebral arteries accounts for only 2% of stroke (which is usually caused by high blood pressure and other risk factors, and tends to occur in the elderly), they cause 10-25% of strokes at young and middle aged. people.
Vertebral artery aneurysm surgery is 4% of all cerebral aneurysms, and is therefore a relatively rare but important cause of subarachnoid haemorrhage.
History
Spontaneous vertebral artery dissection was described in the 1970s. Prior to this, there were isolated case reports of carotid surgery. In 1971, C. Miller Fisher, a Canadian neurologist and stroke physician working at Massachusetts General Hospital, first noted a "string sign" disorder in the carotid artery in the cerebral angiogram of stroke patients, and later found that the same disorder may occur in the arterial vertebral. He reported the discovery in a paper in 1978.
Famous cases
Australian cricketer Phillip Hughes died on November 27, 2014 after developing a vertebral artery dissection as a result of being hit on the side of the neck by a cricket ball during a Sheffield Shield game on 25 November 2014. The ball hit Hughes at the skull base just behind his left ear causing vertebral artery dissection complicated by subarachnoid hemorrhage.
References
External links
- Disease of Arterial Cervix and Ischemic Stroke Patients, international research collaboration into cervical artery dissection
Source of the article : Wikipedia
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