Top of basilar syndrome: The tip of the basilar artery divides into two pairs of arteries, the posterior cerebral artery and the superior cerebellar artery, and the blood supply area includes the midbrain, thalamus, superior cerebellum, medial temporal lobe and occipital lobe. The clinical manifestations are oculomotor disturbances, pupillary abnormalities, arousal and behavioral disturbances, with memory loss, and contralateral hemianopsia or cortical blindness, and in a few patients, cerebral foot hallucinations.
Chinese name: basilar artery cusp syndrome
Full name: cerebral infarction
Localization: Cerebellum
Etiology: Heart
1.Basic concept
The basilar artery tip syndrome (TOBS) was first proposed by Caplan in 1980 and accounts for about 7.6% of cerebral infarcts.Caplan divided it into two groups according to its clinical manifestations, namely infarcts of the first end of the brainstem with damage to the midbrain and thalamus and infarcts of the posterior cerebral artery region with damage to the medial temporal lobe and occipital lobe. With the development of imaging, especially the clinical application of MRI, the number of confirmed TOBS is increasing. In this article, we review the issues related to them.
Local anatomy
The superior cerebellar artery starts at the tip of the basilar artery and runs ventrally outward along the cerebellar curtain, distributing to the superior cerebellum, the deep cerebellar medulla and central nuclei such as the dentate nucleus, as well as to the first tegmental part of the pons, the middle peduncle of the pons, and the lateral part of the caudal tegmental part of the midbrain. The posterior cerebral artery travels medially and laterally in the interpeduncular pool, turns laterally around the peduncle, crosses the parahippocampal gyrus, goes posteriorly along the hippocampal sulcus, and enters the talar sulcus posteriorly at the beginning of the corpus callosum pressure, dividing into two terminal branches: the parieto-occipital artery and the talar sulcus artery. The cortical branches of the posterior cerebral artery are located on the floor of the temporal lobe and the medial aspect of the occipital lobe, including the parahippocampal gyrus and the parahippocampal gyrus sulcus, the medial aspect of the occipitotemporal gyrus, the lingual gyrus, the cingulate isthmus, the cuneus, the posterior 1/3 of the precuneus, and the posterior part of the superior parietal lobule. The central branch of the posterior cerebral artery originates from its circumflex and trunk, and the thalamus is mainly innervated by the thalamus-piercing artery, which supplies the inferior part of the medial thalamic nucleus and the midline nucleus, as well as the central medial nucleus and the posterior medial nucleus, and the thalamus-knee. TOBS is caused by impaired circulation in the left and right posterior cerebral arteries, the left and right superior cerebellar arteries and the apical part of the basilar artery within a 2 cm diameter area centered on the apical part of the basilar artery. The geniculate artery generally has 1 – 6 branches, supplying the thalamic occipital and lateral thalamic nucleus groups; the posterior choroidal artery is divided into two groups, medial and lateral, supplying the dorsal lateral thalamic nucleus, thalamic occipital and geniculate. The vessels that innervate the midbrain are slightly different from the rest of the brainstem. The paramedian arteries first form an arterial plexus in the interpeduncular fossa from a small branch from the posterior cerebral artery ring or the root of the posterior communicating artery, and then branch off the plexus into a posterior perforating branch that supplies the paramedian region of the midbrain. The short spinous arteries originate from the posterior cerebral artery ring, the proximal segment of the superior cerebellar artery and the posterior choroidal artery, supplying the lateral part of the lateral substantia nigra and periaqueducta of the peduncle, the lateral thalamic tract and its surrounding reticular formation. The long spinous artery is a branch from the superior cerebellar artery and the tegmental artery of the posterior cerebral artery, supplying the superior and inferior colliculi.
2.Main etiology
Cerebral embolism, accounting for about 61.5%, is mainly of cardiac origin, followed by atherosclerotic plaque dislodgement. Some scholars have studied the etiology of 10 patients with simple cerebellar infarction caused by superior cerebellar artery obstruction, 7 cases had a history of atrial fibrillation and 1 case had a history of myocardial infarction, these 8 cases did not see evidence of atherosclerosis by angiography. finocchi et al. reported that a group of TOBS patients all had a history of atrial fibrillation, and no meaningful changes were seen by Doppler examination of the intracranial and extracranial arteries. This was followed by cerebral thrombosis. The etiology is unknown in some patients. Risk factors are similar to stroke, with primary hypertension being the most common, followed by heart disease (atrial fibrillation, myocardial infarction, etc.), diabetes mellitus, arteritis, smoking, alcoholism, and hyperlipidemia.
3. Clinical characteristics
TOBS is a special type of ischemic cerebrovascular disease. Due to the local anatomical characteristics of the TOB area, this area often has two or more foci of infarction due to blood circulation disorders, and the clinical manifestations are diverse. Most scholars divide the manifestations into two groups: infarcts in the first end of the brainstem and infarcts in the posterior cerebral artery region. Because the vessels supplying the brainstem primaries are mostly deep penetrating branches or terminal branches and emanate directly from the great vessels, they are prone to vascular injury, so infarcts in the brainstem primaries are common.
3.1 Infarction of the head of the brainstem
3.1.1 Oculomotor impairment
This is one of the main features of TOBS. The medial part of the midbrain periglottis converges the downstream fibers of horizontal and vertical eye movements as well as the nucleus accumbens cluster, and different sites of damage can lead to different compound eye signs: 1.
1, vertical gaze paralysis, the patient lost both casual and reflex vertical gaze, this is due to the infarction of the anterior parietal area and posterior commissure causing superior gaze paralysis, and the medial and dorsal infarction of the red nucleus causing inferior gaze paralysis.
Pseudo-Parinaud’s syndrome is the most characteristic manifestation of nuclear damage, with complete actinic nerve palsy on the focal side and contralateral superior visual impairment. The contralateral upper visual limitation is due to destruction of the superior rectus nucleus on the focal side.
3. The ptosis of both upper eyelids with vertical gaze disturbance is nuclear damage, and the lesion involves the superior rectus nucleus, inferior rectus nucleus, and levator nucleus of the motoneural nucleus group; the medial rectus nucleus and inferior oblique nucleus are relatively unaffected; this is because the superior rectus nucleus and inferior rectus nucleus are located superior to the motoneural nucleus and are involved first, and the levator nucleus is single, so partial damage also causes ptosis of both upper eyelids.
Selhorst et al. suggested that the E-W nucleus contains two groups of cells, each innervating the ipsilateral pupillary iris, and that pupillary abnormalities occur when the two groups of cells are unequally damaged. If the entire E-W nucleus is involved, the pupil may be dilated and the response to light may be lost.
Differentiation points.
1.Long duration of impaired consciousness but relatively mild degree;
2. No improvement in consciousness and pupillary changes after dehydration treatment;
3. No lesions in the cerebral hemispheres and no midline dislocation on CT brain examination;
4.Other vital signs were stable; 5 Mild physical impairment.
3.1.3 Disorders of consciousness and hallucinations TOBS mostly cause different degrees and different nature of disorders of consciousness, the incidence of which is documented in the literature as 77% – 100%, generally lasting 6h – 3d. The incidence is documented to be 77% – 100%, generally lasting 6h – 3d. In patients with basilar artery infarction, the most prominent symptoms are prolonged sleep and motor nerve palsy. All three are part of the nonspecific projection system. The nucleus accumbens is the pacemaker of the thalamus and controls the electrical activity of the cerebral cortex; the nucleus reticularis modifies and regulates the intercortical impulses of the thalamus. Patients with TOBS may have visual hallucinations, which Caplan called “foot-in-the-brain hallucinations,” in which the patient describes the hallucination vividly but knows it is not real. If the hallucination occurs only in the evening, it is called a “twilight hallucination”. The pathological anatomy and pathophysiology of these hallucinations are unclear, but it is thought that they may be related to abnormalities in the midbrain reticular formation and blocked conduction in the subthalamic nucleus and occipital nucleus.
3.1.4 Abnormal visceral behavior Patients with brainstem primordial infarction may present with abnormal visceral sensation and movement. The brainstem reticular formation is a switching station between the superior bundle of visceral sensation and the inferior bundle regulating visceral activity, and the efferent fibers from the lateral hypothalamic region, mainly terminate in the midbrain reticular formation. The dorsomedial thalamic nucleus is richly connected to the prefrontal cortex, hypothalamus, amygdala, substantia nigra, precentral gyrus, and other groups of thalamic nuclei, and is thought to be a center for complex integration of visceral and somatic impulses.Potter et al. previously reported a decrease in ipsilateral olfactory function due to unilateral damage to the dorsomedial thalamic nucleus.Rousseaux et al. reported a case of persistent Rousseaux et al. reported a case of persistent olfactory and gustatory deficits with decreased body mass due to bilateral damage to the dorsal medial thalamic nucleus and intraparietal nucleus.
3.2 Infarcts in the posterior cerebral artery region are mainly characterized by visual impairment and behavioral abnormalities.
Martin et al. reported that infarcts in this region accounted for 35% of TOBS. Visual impairment can be manifested as hypotony, hemianopia or cortical blindness, and in a few cases, flash hallucinations, visual distortion, visual disorientation, etc. Behavioral abnormalities include Balint syndrome, memory loss, personality changes, and agitated delirium, often due to bilateral infarcts.4 The most characteristic feature of brain CT scan is bilateral thalamic symmetry into butterfly-shaped hypodense foci, mostly located in the central part of the thalamus, mainly confined between the central median nucleus and the inner plate nucleus. In addition to thalamic infarcts, infarct foci were also commonly found in the cerebellum, occipital lobe, midbrain and medial temporal lobe, but the detection rate was low, mainly due to the artifact interference and poor resolution of CT scan of the posterior cervical fossa.MRI has high resolution of soft tissue and can image in multiple directions, especially more sensitive to lesions in the posterior cranial fossa, so MRI is more accurate in locating TOBS and can detect very early lesions, sometimes 30 min after onset. The clinical application of DSA can not only clarify the vascular site of the lesion, but also provide evidence for finding the cause of the disease. The recanalization rate of the occluded vessel was 61.5%.5 Treatment and prognosis Previously, it was thought that the prognosis of this disease was poorer than other ischemic cerebrovascular diseases, and few patients were completely cured. However, Gomez et al. reported that early and correct anti-free radical therapy can improve the survival rate of brain cells in the semidark zone, improve microcirculation, and improve the local hypoxic environment of the lesion, thus improving the prognosis of TOBS.
Two pairs of vessels, the superior cerebellar artery and the posterior cerebral artery, branching from the tip of the basilar artery supply the midbrain, thalamus, upper cerebellum, medial temporal lobe and occipital lobe; therefore, the syndrome is mainly manifested by damage to the midbrain, accompanied by ischemic damage to the thalamus, occipital lobe, medial temporal lobe and upper cerebellum; mostly caused by atherosclerotic thrombosis, cardiogenic and arteriogenic causes. The disease may have occipital and temporal lobe symptoms, while cerebellar symptoms are rare; i.e., they manifest as blurred vision, neuro-ocular signs, vertigo, and signs of conscious behavioral, sensory, and motor disturbances of.
(1) Oculomotor and pupillary abnormalities: these include partial or complete paralysis of one or both of the articulatory nerves (mainly due to the involvement of the nucleus or root filaments of the articulatory nerve), manifested by impaired vertical eye movements and inability to look up or up or down, due to the involvement of the horizontal vertical oculomotor center of the superior thalamus.
(2) Disorders of consciousness: may be transient or last for several days, or may be recurrent, due to damage to the reticular activating system of the midbrain or thalamus.
(3) contralateral hemianopia or cortical blindness, due to damage to the occipital visual cortex.
(4) There may be severe memory impairment, due to medial temporal lobe involvement.
(5) A few patients may have brainstem hallucinations, which often occur at dusk.
Diagnosis: signs and/or imaging signs of ischemic infarcts in two or more sites in the supratentorial and infratentorial, brainstem-mesencephalon and posterior cerebral artery innervated hemispheric regions (including infarcts in the midbrain, thalamus, subthalamus, superior pontocerebrum, cerebellum, occipital lobe and medial temporal lobe).
Treatment is mainly directed at the etiological mechanism of ischemic cerebrovascular disease, in addition to strengthening the control and prevention of risk factors, and is still based on a comprehensive approach of early thrombolysis, anticoagulation, volume expansion, and improvement of cerebral blood circulation and brain cell function.