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Basilar artery atherothrombosis

Pathophysiology of ischemic stroke in the basilar artery basin

The basilar artery is formed through the merger of the vertebral arteries at the point of transition of the pons in the medulla oblongata. After passing along the surface of the base of the pons, it ends in the interpeduncular fossa, where the bifurcation and form the posterior cerebral artery. The branches of the basilar artery supply blood to the base of the pons and the upper part of the cerebellum. The branches of the basilar artery are divided into three groups:

  • paramedian branches, whose number varies from 7 to 10 are provided with a wedge-shaped portion of the pons on both sides of the midline
  • short branch envelopes, numbering between 5 and 7 are provided with a lateral two thirds of the pons, middle and upper legs of the cerebellum
  • two bilateral long circumflex artery (superior cerebellar and anterior / inferior cerebellar artery) are around the pons and provide the cerebellar hemispheres
Atherosclerosis affects the lumen and wall of the basilar artery.

Atherosclerotic lesions can be localized in any part of the course of the trunk of the basilar artery, but most of the proximal basilar (base of the brain) and distal vertebral segments. Typically, lesions lead to blockage (occlusion), the proximal region of the basilar artery and one or both vertebral arteries in their distal parts.

The clinical picture in blockage (occlusion) of the main arteries varies depending on the availability of retrograde collateral blood flow from the posterior communicating artery. Atherosclerosis with thrombosis sometimes leads to blockage (occlusion) of the upper part of the basilar artery. More frequently it is caused by blockage of embolus from the heart or downstream segments of the vertebral arteries and basilar artery. Arterioarterialnye emboli can cause blockage of one of the smaller branches of the basilar artery or one of the posterior cerebral artery.

The basilar artery occlusion symptoms

As in the brain stem in close proximity to each other is a lot of different neuronal systems during ischemia it may have many clinical syndromes. The most significant from this point of view of systems are the cortico- spinal and cortico- bulbar path, middle and upper legs of the cerebellum, spinotalamicheskie ways and cranial nerve nuclei. The figure illustrates some of the vascular syndromes, including those who are waiting for clinical pathology definitions.

Unfortunately, the symptoms of stroke or transient ischemia in the basin of the basilar artery is often not possible to establish whether she hit the main artery or its branches, and yet the differences in the localization of the lesion are important for selecting appropriate treatment. However, to recognize the full picture of basilar insufficiency is simple. Confirmation of the diagnosis are a combination of bilateral symptoms of long wires (sensory and motor), symptoms of cranial nerves, cerebellar dysfunction.

The state of "waking coma", accompanied by a tetraplegic (paralysis of the arms and legs) is observed in the bilateral myocardial pons foundation. In this coma is caused by dysfunction of the reticular formation activating system. Tetraplegia with symptoms of cranial nerve lesions lead to the assumption complete with a heavy heart disorders (stroke) of the pons and the midbrain.

Vertebral arteries merge to form the basilar artery.

The purpose of diagnosis is to recognize threatening occlusion of the basilar artery before the development of such devastating in its consequences to cerebral infarction (stroke). Hence serial transient ischemic attack (TIA) or slowly progressive, with an undulating course of a stroke are only meaningful if a marked atherosclerotic thrombosis distal vertebral artery occlusion or proximal basilar artery.

 

Medullary syndrome:

Signs and symptoms
Structures involved
1. Medial medullary syndrome (occlusion of vertebral artery or of branch of vertebral or lower basilar artery)
On side of lesion:
Paralysis with atrophy of half the tongue Ipsilateral twelfth nerve
On side opposite lesion:
Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive sense over half the body Contralateral pyramidal tract and medial lemniscus
2. Lateral medullary syndrome (occlusion of any of five vessels may be responsible — vertebral, posterior inferior cerebellar, superior, middle, or inferior lateral medullary arteries)
On side of lesion:
Pain, numbness, impaired sensation over half the face Descending tract and nucleus fifth nerve
Ataxia of limbs, falling to side of lesion Uncertain — restiform body, cerebellar hemisphere, cerebellar fibers, spinocerebellar tract (?)
Nystagmus, diplopia, oscillopsia, vertigo, nausea, vomiting Vestibular nucleus
Horner’s syndrome (miosis, ptosis, decreased sweating) Descending sympathetic tract
Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord, diminished gag reflex Issuing fibers ninth and tenth nerves
Loss of taste Nucleus and tractus solitarius
Numbness of ipsilateral arm, trunk, or leg Cuneate and gracile nuclei
Weakness of lower face Genuflected upper motor neuron fibers to ipsilateral facial nucleus
On side opposite lesion:
Impaired pain and thermal sense over half the body, sometimes face Spinothalamic tract
3. Total unilateral medullary syndrome (occlusion of vertebral artery)
Combination of medial and lateral syndromes
4. Lateral pontomedullary syndrome (occlusion of vertebral artery)
Combination of lateral medullary and lateral inferior pontine syndrome
5. Basilar artery syndrome (the syndrome of the lone vertebral artery is equivalent)
A combination of the various brainstem syndromes plus those arising in the posterior cerebral artery distribution
Bilateral long tract signs (sensory and motor; cerebellar and peripheral cranial nerve abnormalities) Bilateral long tract; cerebellar and peripheral cranial nerves
Paralysis or weakness of all extremities, plus all bulbar musculature Corticobulbar and corticospinal tracts bilaterally

 

Inferior pontine syndrome:

Signs and symptoms
Structures involved
1. Medial inferior pontine syndrome (occlusion of paramedian branch of basilar artery)
On side of lesion:
Paralysis of conjugate gaze to side of lesion (preservation of convergence) Center for conjugate lateral gaze
Nystagmus Vestibular nucleus
Ataxia of limbs and gait Likely middle cerebellar peduncle
Diplopia on lateral gaze Abducens nerve
On side opposite lesion:
Paralysis of face, arm, and leg Corticobulbar and corticospinal tract in lower pons
Impaired tactile and proprioceptive sense over half of the body Medial lemniscus
2. Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery)
On side of lesion:
Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopia Vestibular nerve or nucleus
Facial paralysis Seventh nerve
Paralysis of conjugate gaze to side of lesion Center for conjugate lateral gaze
Deafness, tinnitus Auditory nerve or cochlear nucleus
Ataxia Middle cerebellar peduncle and cerebellar hemisphere
Impaired sensation over face Descending tract and nucleus fifth nerve
On side opposite lesion:
Impaired pain and thermal sense over half the body (may include face) Spinothalamic tract

 

Midpontine syndrome:

Signs and symptoms
Structures involved
1. Medial midpontine syndrome (paramedian branch of midbasilar artery)
On side of lesion:
Ataxia of limbs and gait (more prominent in bilateral involvement) Pontine nuclei
On side opposite lesion:
Paralysis of face, arm, and leg Corticobulbar and corticospinal tract
Disorders of tactile and proprioceptive sensation in half of the body The medial loop
Variable impaired touch and proprioception when lesion extends posteriorly Medial lemniscus
2. Lateral midpontine syndrome (short circumferential artery)
On side of lesion:
Ataxia of limbs Middle cerebellar peduncle
Paralysis of muscles of mastication Motor fibers or nucleus of fifth nerve
Impaired sensation over side of face Sensory fibers or nucleus of fifth nerve
On side opposite lesion:
Impaired pain and thermal sense on limbs and trunk Spinothalamic tract

 

Midbrain syndrome:

Signs and symptoms
Structures involved
1. Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries)
On side of lesion:
Eye “down and out” secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil Third nerve fibers
On side opposite lesion:
Paralysis of face, arm, and leg Corticobulbar and corticospinal tract descending in crus cerebri
2. Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery)
On side of lesion:
Eye “down and out” secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil Third nerve fibers and/or third nerve nucleus
On side opposite lesion:
Hemiataxia, hyperkinesias, tremor Red nucleus, dentatorubrothalamic pathway

 

Transient ischemic attack (TIA) in the basilar artery basin

Transient ischemic attack (TIA) in the basin of the basilar artery is usually preceded by chronic vertebro- basilar insufficiency (VBN). When transient ischemic attack is a manifestation of blockage (occlusion), the underlying (proximal) part of the basilar artery, in the pathological process may be involved in the medulla oblongata, as well as a pons. Patients often complain of dizziness, and when asked to describe the sensations experienced, they report that "float", "rock", "move", "feeling of instability". They may complain that "the room is turned upside down", "floating floor under your feet" or "close to him".

Dizziness - is the most characteristic symptom of transient ischemia in the basin of the basilar artery, but before thrombosis of the basilar artery leads to heart attacks, vertigo is usually accompanied by other symptoms.

By reducing blood flow in the basin of the vertebral arteries and the main job of the cerebellum is suffering, there is a symptom of dizziness against the vertebro-basilar insufficiency.

Transient dizziness in conjunction with double vision before his eyes (diplopia), speech disorder (dysarthria), facial numbness or perioral area and sensitivity disorders than half of the body indicates a transient cerebrovascular insufficiency (TIA) in the vertebrobasilar system. Typically, half of the weakness of the body (hemiparesis), the patient points to the involvement in the pathological process of the basilar artery regardless of the affected vertebral artery at the same time or not.

Most often, transient ischemic attack (TIA) on the background of impending occlusion (blockage) of the basilar artery or its branches are short-lived (for 5-30 min ) and repeated, appearing several times a day. It is rather due to a transient decrease in blood flow than recurrent embolism. Typically, neurological symptoms branches of the basilar artery lesions associated with unilateral lesion of the stem, while the symptoms of transient ischemic attack (TIA microstroke) with the involvement of the basilar artery showed bilateral lesions of the brain stem.

 

Ischemic stroke in the basilar artery basin

Stroke in atherosclerosis with thrombosis in the background of blockage (occlusion) of the basilar artery usually gives the bilateral symptoms of brain stem. Sometimes, on a bilateral ischemia of the brain stem showed paresis of eye or nuclear ophthalmoplegia (weakness or paralysis of the muscles driving the eye) in combination with hemiparesis (muscle weakness half of the body), ie, some combination of cranial nerve lesions and the long pathway (sensitive and / or motor). Frequently observed combination of neurological symptoms of bilateral destruction of the pons base with one - or two-sided structures involving tire cord.

When atherosclerosis with thrombosis of the blockage (occlusion), the branches of the basilar artery in a patient begins to manifest clinically, it is accompanied by a unilateral lesion of motor symptoms, sensory tract, and cranial nerves. Occlusion (blockage) of long envelopes of the branches of the basilar artery provide specific clinical syndromes characteristic of the " lacunar disease".

 

Pathophysiology of ischemic stroke in the superior cerebellar artery basin

Occlusion (blockage), superior cerebellar artery leads to gross cerebellar ataxia on the side of the blockage (due to the destruction of medium and / or the upper legs of the cerebellum), nausea and vomiting, dysarthria, contralateral loss of pain and temperature sensitivity in the extremities, trunk and face (involving spin and trigeminotalamicheskogo the way). Sometimes it may be a partial loss of hearing, atactic tremor in the upper extremity on the affected side, Horner's syndrome, and myoclonus of the soft palate. Often with occlusion (blockage), superior cerebellar artery found partial stroke neurological syndromes.

 

Pathophysiology of ischemic stroke in the anterior inferior cerebellar artery basin

Occlusion (blockage) inferior cerebellar artery front leads to the development of cerebral infarction of varying severity, because the size of this artery and its territory is supplied with blood vary in contrast to those for the posterior inferior cerebellar artery. Major neurological symptoms include deafness on the affected side, the weakness of facial muscles, dizziness true (system), nausea and vomiting, nystagmus, tinnitus, and cerebellar ataxia, Horner's syndrome, paresis of horizontal gaze. At the opposite side of the body with the lost pain and temperature chuvstvitelnost.Okklyuziya (obstruction) near the inferior cerebellar artery front may be accompanied by symptoms of defeats the cortico- spinal path.

Blockage of one of the envelopes of 5-7 short branches of the basilar artery ischemia is a particular area in the lateral two thirds of the pons and / or the middle or upper leg of the cerebellum, while occlusion of one of the 7-10 paramedian branches of basilar artery ischemia is accompanied by a wedge-shaped in a special section with the and other parties in the medial part of the brain stem.

We describe the set of syndromes of the brain stem lesions who received eponimicheskie names, including the syndromes of Weber, Claude Benedict, Fovil, Reymond- Sestan, Miyyar-Zhyuble. In the pons is so much neuronal structures that even small differences in the pools of blood supply of each arterial branch and overlap between vascular pools lead to changes in clinical:

  • dysarthria combined with clumsiness in the hands of a small can think of a heart attack at the base of the pons of the brain;
  • the presence of isolated hemiparesis does not allow to differentiate ischemia from the base of the pons cortico- spinal ischemia in the way of supratentorial part of it, ie, in the posterior knee of the internal capsule;
  • hemiparesis in conjunction with the loss of sensitivity on the same side can think of supratentorial localization of the lesion in stroke;
  • dissociated frustration of sensitivity (loss of only pain and temperature sensitivity ) on the face side of the body and evidence of ischemia of the brain stem;
  • loss of sensitivity with the involvement of all modalities, including pain and temperature, as well as tactile and muscular- articular points to the localization of lesions in the ventral posterior part of the thalamus or in the deep white matter of the parietal lobe and surrounding cortical surface.

Symptoms of cranial nerve dysfunction, including deafness, peripheral paresis of the facial nerve, abducens paresis, paralysis of the oculomotor nerve, are essential for establishing the segmental level of destruction of the pons or the midbrain.

 

Diagnosis and imaging studies of ischemic stroke in the basilar artery basin

Although computed tomography (CT) in most cases allows you to set the location of the lesion in stroke 48 hours after it began, this method gives less reliable results in the detection and localization of acute disorders of cerebral circulation in the posterior fossa. Artifacts from the bones of the skull often lead to "erase" parts of the image. Poor resolution computed tomography (CT) imaging of the brain stem with infarcts (strokes) is due to partial volume artifacts as constraints and cuts.

MRI angiography of cerebral arteries showed narrowing of the basilar artery.

Magnetic resonance imaging (MRI) of the brain is deprived of many of these shortcomings. Magnetic resonance imaging (MRI) brain reveals small (lacunar) infarcts (strokes) at the base of the pons, resulting in occlusion of the paramedian branches of the basilar artery, and heart attacks as a considerable size, with lesions developing directly basilar artery or its larger branches. In addition, magnetic resonance imaging (MRI) of the brain makes it possible to detect ischemic infarction earlier than computed tomography (CT). On the other hand, computed tomography (CT) compared with magnetic resonance imaging (MRI) brain reveals small hematoma better pons, thus enabling them to differentiate from acute ischemic stroke.

Magnetic resonance imaging (MRI) of the brain is more sensitive in determining glioma pons or plaques of multiple sclerosis, which helps to hold the differential diagnosis of a heart attack (stroke) of the brain with these diseases.

Visualize atherosclerosis with thrombosis, which affects the main artery of the brain enables selective cerebral angiography. Because angiography requires the injection of contrast into the artery, this procedure is fraught with potential risk and can lead to stroke, which should be prevented. Such selective angiography with intravascular contrast must be recommended only in cases where the data is derived from it will help in treating a patient.

In rare cases, falling angiographic contrast material in the vertebrobasilar system of the brain can cause impaired consciousness among patients (delirious state), sometimes accompanied by cortical blindness. Such a state after a diagnostic procedure with intravascular administration of contrast can last 24-48 hours, sometimes up to several days. Digital X-ray angiography arterial has enough resolution for diagnosis of atherosclerotic narrowing in the distal parts of the vertebral and basilar artery. Intravenous digital X-ray angiography does not provide adequate resolution.

Performed on cerebral angiography in frontal projection shows atherosclerotic lesion (narrowing) of the main arteries of the brain.

Recently, the replacement of selective cerebral angiography for diagnostic purposes comes multispiral computed tomography (CT angiography) with intravenous contrast. Absolute contraindications for multislice computed tomography (CT) brain vessels does not exist. For relative contraindications for such a diagnosis with intravenous contrast vessels (arteries and veins) of the brain can be attributed:

  • the general plight of the patient (physical, mental), making it impossible to maintain them motionless during the study of cerebral vessels
  • pregnancy
  • overweight patients exceed the maximum permissible load on the table for the model computed tomography

 

Treatment of the ischemic stroke in the basilar artery basin

If you suspect a threatening occlusion of the basilar artery of the brain, manifested transient or fluctuating neurological symptoms, you should assign a short course of treatment with anticoagulants and intravenous heparin after magnetic resonance imaging (MRI) or brain computed tomography (CT) scan of the brain ruled out intracerebral hemorrhage. The question of holding the patient gets up angiography in cases where the diagnosis is uncertain, but research is carried out only after stabilization of the patient.

When stenosis or occlusion of the basilar artery of the brain are accompanied by small or regressing stroke, anticoagulant therapy is recommended long-term (warfarin sodium). If the disease is the cause of the damage of the branches of the basilar artery, warfarin sodium is unlikely to prescribe appropriate. Embolism from the heart or an atherosclerotic plaque, localized in the overlying (distal) section vertebrobasilar system and clog penetrating branch of the basilar artery, an anticoagulant treatment is not indicated.

Therefore, as preventive measures in patients with lesions of the small branches of the basilar artery of the brain should be encouraged:

  • constant monitoring of blood pressure
  • antiplatelet therapy (aspirin, trental)
  • neuroprotective therapy (cerebrolysin, piracetam, instenon)
  • in the rehabilitation period - an active or sedentary life
  • massotherapy
  • reflexology

It should be remembered that long-term anticoagulant treatment is associated with a significant risk to the patient. It is usually performed in atherosclerosis with thrombosis of larger vessels, especially the distal parts of the overlying vertebral and proximal segment of the underlying basilar artery.

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