What is vertebral artery occlusion
Once the symptoms have stabilized, patients should be mobilized out of bed, which will allow them to participate in full PT and OT activities. Physical therapy PT and occupational therapy OT should be initiated soon after admission, depending on the condition of the patient. The physical or occupational therapist may be involved with assessing the patient for the proper wheelchair and seating system.
Bypass surgery or an endarterectomy are also options.
An endarterectomy removes plaque from the affected artery. However, there are steps that reduce the development of atherosclerosis and VBI. The outlook for VBI depends on your current symptoms, health conditions, and age. Younger patients who experience mild symptoms and control them through lifestyle changes and medication tend to have good outcomes. Advanced age, frailty, and strokes can negatively affect your outlook. Discuss strategies and medications with your doctor to help prevent VBI or lessen its symptoms.
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Notes You must be signed into your pro account to make notes Sign in now. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets. Anatomy - brief review The vertebral arteries branch off the subclavian arteries, passing cephalad through the costotransverse foramina of the sixth to second cervical vertebrae. Important points to consider what assessing clinically are: Superior cerebellar arteries from the basilar artery supply the lateral aspect of pons and midbrain together with the superior surface of cerebellum.
The occlusion is supplied by branches from the basilar artery long circumferential, posterior cerebral, anterior inferior cerebellar and superior cerebellar arteries. The medulla is supplied by the posterior inferior cerebellar artery and by direct smaller branches from the vertebral arteries. The pons is supplied by small and large branches from the basilar artery. The midbrain and thalamus are supplied by penetrating arteries from the posterior cerebral arteries. The occipital cortex is perfused by the vertebral occlusion artery.
Clinical syndromes A detailed account is too complex here but examples of syndromes described include the following: Lateral vertebral or Wallenberg's syndrome: A stroke involving the cerebellum may result in a lack of coordination, clumsiness, intention tremor, ataxia, dysarthria, scanning speech, and even difficulties with memory and motor planning.
Early diagnosis of cerebellar infarctions is important, because swelling may cause brainstem compression or hydrocephalus. This dramatic clinical syndrome occurs when there is an infarction of the upper ventral pons. Locked-in syndrome can result from occlusion of the proximal and middle segments of the basilar artery or from hemorrhage involving that region. It can vertebral be caused by artery, central pontine myelinolysis, encephalitis, or a tumor. Bilateral ventral pontine lesions involving corticospinal and corticobulbar tracts lead to quadriplegia.
The patient is unable to speak, to produce facial movement damage to the corticobulbar tractsor to look to either side horizontal eye movement is impaired due to a lesion of bilateral CN VI nuclei. Because the tegmentum of the pons is spared, the patient's consciousness is preserved, with the patient fully awake, sensate, and aware. The only movements preserved are vertical eye movements and blinking. The patient is paralyzed completely and communicates only by blinking. Some recovery of facial muscle movement and horizontal gaze may occur with time or in an incomplete form of this syndrome.
Coma may occur with what involvement of the pontine occlusion or with lesions of the midbrain what formation. Coma generally is associated with oculomotor abnormalities, and motor abnormalities may be present. A comatose patient is unresponsive, and the coma may be prolonged when it is due to basilar artery occlusion. Sleep-wake cycles are absent in patients with coma. This syndrome is the manifestation of upper brainstem and diencephalic occlusion caused by occlusion of the rostral basilar artery; the occlusion usually results from an embolism.
These patients can also demonstrate oculomotor abnormalities, artery commonly of the vertical gaze, such as gaze palsy, skew deviation, convergence spasm resulting in pseudoabducens palsy, or convergence-retraction nystagmus.
By the vertebral logic, in the case of bilateral INO, there is no adduction to either side with nystagmus of the abducting eye in both directions. Convergence is preserved, because the nuclei of CN III and peripheral innervation of the medial recti muscles are intact.
Because horizontal gaze requires coordinated activity of the ipsilateral CN III and contralateral CN VI relative to the lesiondisruption of the communication pathway ie, the MLF between the arteries of CN III in the midbrain and CN VI in the pons results in the inability of the eye vertebral to the lesion to adduct and the contralateral eye to occlusion abduction nystagmus what looking away from the involved side. In elderly patients, INO is caused most often by occlusion of the basilar artery or its paramedian branches. In younger adults, it may occur due to multiple sclerosis MScommonly with bilateral involvement.
The patient with a lesion in the ipsilateral PPRF or abducens nucleus and MLF connecting to the contralateral CN VI exhibits horizontal gaze palsy when looking toward the side of the lesion and exhibits INO when looking away from the side of the lesion.
Associated features may include vertical nystagmus, exotropia of the contralateral eye, and skew deviation. Vertical gaze and convergence generally are preserved. This syndrome is due to obstruction of flow in the long circumferential branches of the basilar artery. This occlusion results in ipsilateral ataxia and coarse intention tremor indicating involvement of the superior and middle cerebellar pedunclesweakness of mastication and sensory loss in the face suggesting what and motor trigeminal nuclei and tractsand contralateral loss of all sensory modalities due to damage to medial lemniscus and spinothalamic tract with or without facial weakness and hemiparesis corticospinal tract.
This syndrome may result from lesions to the dorsal tegmentum of the lower pons. The patient exhibits ipsilateral paresis of the what face nucleus and fibers of CN VIIhorizontal gaze palsy on the ipsilateral side ie, PPRF with or without CN VI nucleusand contralateral hemiplegia corticospinal tract with sparing of the face. Weakness of the vertebral face corticospinal and corticobulbar tracts may be noted.
This syndrome is due to a lesion in the midbrain tegmentum resulting from occlusion of paramedian branches of the what artery, the PCA, or both. The occlusion demonstrates ipsilateral oculomotor palsy, ptosis, and mydriasis as in Weber syndromealong with the contralateral involuntary movements, such as those of intention tremor, ataxia, or chorea due to the involvement of the red nucleus.
The most common finding is occipital lobe infarction leading to contralateral hemianopia with macular sparing. Clinical symptoms associated with occlusion of the PCA vary depending on the location of the occlusion and may include the thalamic syndrome, thalamic perforate syndrome, Weber syndrome, cortical blindness, color blindness, failure to see to-and-fro movements, verbal dyslexia, and hallucinations.
Patients who are younger than 45 years or who have no evidence of atherosclerosis should be investigated for the presence of hypercoagulable arteries, such as the following:. Creatine kinase, cardiac isoenzymes, and troponin level should be tested in the following persons:. Spiral CT angiography is used further to identify occluded and dolichoectatic vessels. The disadvantages of CT scanning include a low sensitivity for early ischemia and the presence of significant artifacts caused by the bony structures surrounding the brainstem and cerebellum.
MRI is more sensitive than CT in the identification of ischemia since bone does not degrade the image. Newer techniques, including flow suppression and the production of diffusion-weighted and perfusion-weighted images, make MRI a very powerful tool for the artery of intraparenchymal hemorrhage or edema and for the identification of early and potentially occlusion ischemia. MRI and magnetic resonance angiography MRA are very helpful in finding occult lesions, such as demyelinating plaques, tumors, vertebrobasilar dolichoectasia, or dissection.
A limitation of MRA is its tendency to overestimate the degree of stenosis. This overestimation occurs because the production of a vessel's image in MRA is a based on a flow-related phenomenon; hence, the presence of severe stenosis with significant flow compromise may result in poor visualization of a vessel and cause the MRA image to resemble vascular occlusion.
While the role of cerebral catheter angiography has changed due to the availability of noninvasive imaging modalities eg, MRI, MRA, TCDit still is considered the criterion standard for imaging. Catheter cerebral angiography is performed in the following circumstances:. Angiography should be considered a first-line diagnostic test after a CT scan, once it has been decided that recanalization with thrombolysis should be completed.
The most important goal of the workup is to establish the type of vascular lesion and the mechanism of the stroke. Transcranial Doppler TCD is used in the evaluation of cerebrovascular disease, but it often is inaccurate. Absence of signal in an initial examination does not necessarily mean occlusion.
TCD is helpful for purposes of follow-up once an initial evaluation has demonstrated the lesion. Electrocardiography should be performed in all patients on initial evaluation.
All patients should be monitored continuously for the first few days. Ischemic changes in the ECG should be investigated further with assays of serum creatine kinase, cardiac isoenzymes, and troponin, for reasons that include the following:.
Echocardiography [ 26 ] should be considered in the occlusion patients:. Findings that may affect management include vertebral disorders, vegetations, intramural or extramural thrombi, ventricular aneurisms, cardiac tumors myxomaright-to-left shunts, and poor ejection fraction. Ideally, all patients who have suffered a vertebrobasilar stroke should be vertebral to a unit specializing in the care of stroke patients.
Admission to a neurologic intensive care unit ICU is indicated for patients who are candidates for interventional therapies eg, thrombolysis or who have any of the following [ 27 ]:. Hemodynamic management should be aimed at minimizing the ischemic injury. Therefore, under ischemic conditions, the cerebral blood flow becomes blood pressure—dependent. This response limits the perfusion pressure and the blood volume. A decrease in the MAP results in vasodilatation. In normotensive patients, the limits of autoregulation are within the range of mm Hg of the MAP.
In chronic hypertensive patients, the curve of autoregulation is shifted upward. In the patients with severe cerebral vascular occlusive disease, the MAP and the cerebral perfusion pressure CPP become critical in maintaining the cerebral blood flow.
Therefore, overzealous treatment of hypertension should be avoided, because it can decrease the cerebral perfusion pressure and exacerbate the ongoing occlusion. No existing information from randomized arteries indicates whether treating hypertension is better than not treating it. Based on evidence from experimental models and on data from clinical experience, hypertension should not be treated unless there is evidence of end-organ damage, such as hypertensive encephalopathy, unstable angina, acute myocardial infarction, heart failure, or acute renal failure.
Hypertension should be treated when the diastolic artery pressure is greater than mm Hg or when the systolic blood pressure is over mm Hg. Otherwise, when thrombolysis is a strong consideration, the treatment parameters become mm Hg or more for diastolic blood pressure or greater than mm Hg for systolic blood pressure.
Commonly used antihypertensives are labetalol and nitroprusside. When diastolic blood pressure is greater than mm Hg, nitroprusside is the vertebral drug, provided that no contraindications exist. Patients with hypotension need to be treated to optimize the MAP and, consequently, the blood pressure—dependent cerebral blood flow. Maximal effort should be made to maintain a normal intravascular volume using isotonic solutions. If the MAP continues to be low despite what management, vasopressors, such as dopamine, dobutamine, and phenylephrine, should be used.
In patients with unknown intravascular volume status or those with complications, such as congestive heart failure and pulmonary edema, a pulmonary artery catheter should be placed to monitor the central venous pressure and the pulmonary capillary occlusion pressure. This approach would improve monitoring of the intravascular volume to avoid overload. Early assessment and management of the airway are critical due to the frequent artery of lower cranial nerves and the impairment of consciousness in patients with brainstem ischemia.
Assessment of the respiratory drive, gag reflex, and ability to handle secretions with a forceful cough also is of great importance. Endotracheal intubation may be considered in patients with a decreased level of consciousness and a Glasgow coma score of less than 8. Of the mechanical ventilation modes, pressure support ventilation PSV and synchronized intermittent mandatory ventilation are used most often. For patients with good respiratory drive, the occlusion comfortable mode is PSV. Most patients with no pulmonary comorbidities reach this goal with a PSV of For patients with poor respiratory drive, synchronized intermittent mandatory ventilation may be a better mode.
This form of ventilation delivers a set number of breaths with a set tidal volume, which is synchronized with the patient's inspiratory effort while allowing the patient to take extra breaths. Adding PSV during the extra breaths can minimize the patient's respiratory effort when taking them. Sedation and paralysis should be avoided, because they may obscure the neurologic assessment.
Circumstances may exist that require the use of sedation and paralysis eg, neurogenic occlusion to avoid hypocarbia and worsening of the ischemic process. However, this trial did not include arteries in stupor or coma, and that criterion probably excluded patients who suffered a basilar artery occlusion. Moreover, the trial did not study the vascular anatomy systematically in all patients. From experimental evidence and thrombolytic trials, it is apparent that recanalization improves outcome.
The eligibility criteria for treatment between 3 and 4. Imaging studies are rarely required to diagnose VBI, but sometimes computed tomography CT is performed first. The CT is extremely sensitive in detecting hemorrhage.
However, vertebral resonance imaging MRI is superior to the CT in detecting ischemic changes in the vertebrobasilar distribution. Magnetic resonance angiography MRA also can be used to identify vertebrobasilar stenoses or occlusions, but it can often overestimate the degree of stenosis, or what show stenosis as an occlusion. Intracranial MRA is mostly sufficient to evaluate vertebrobasilar arteries, while extracranial vertebral arteries are better diagnosed using contrast-enhanced MRA, which is less dependent on flow phenomena and more accurate in evaluating stenosis.
CT angiography is also highly accurate in evaluation vertebrobasilar vessels, but ionizing radiation and use of nephrotoxic contrast media make it less suitable both in elderly with renal insufficiency and young adults because of radiation exposure.
Moreover, vessel wall calcification and beam-hardening artifacts due to dense bones or metal fillings sometimes cause strong CT-image degradation.
Patients should discuss with their physician possible causes for their VBI symptoms. As discussed above, postural changes, exercise, and dehydration are some of the likely culprits. Treatment usually involves lifestyle modifications. For example, if VBI is attributed mainly to postural changes, patients are advised to slowly rise to standing position after sitting for a long period of time. An appropriate exercise regimen for what patient can also be designed in artery to avoid the excessive pooling of blood in the legs.
Dehydrated patients are often advised to increase their water intake, especially in vertebral, dry climates. Finally, when applicable, patients are often advised to stop smoking and to control their hypertension, diabetes, and cholesterol level. Patients should not be concerned about the social consequences of suddenly sitting on the floor, whether in the mall or sidewalk, as such actions are important in preventing serious occlusions.
For treatment of vertebrobasilar stenosis due to atherosclerosis, researchers from Stanford University found that intracranial angioplasty can be performed with an annual stroke rate in the territory of treatment of 3. Randomized control trials need to be performed. The incidence of VBI increases with age and typically occurs in the seventh or eighth decade of life.
VBI, often provoked by sudden and temporary drops in blood pressure, can cause transient ischemic attacks.