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Tip basilar syndrome (TOBS) is a special type of ischemic cerebrovascular disease
.
TOBS is a group of clinical syndromes caused by various etiologies caused by blood circulation disorders at the intersection of bilateral posterior cerebral arteries, bilateral superior cerebellar arteries and the top of basilar arteries, with the top of the basilar artery as the center within 2 cm in diameter
.
The clinical manifestations of TOBS are complex and diverse, the condition is critical, the prognosis is poor, and the morbidity and mortality rates are high.
Early diagnosis and treatment are very important
.
Let's learn about basilar apex syndrome today
.
Anatomical structure The tip of the basilar artery refers to the intersection of five blood vessels within a diameter of 2 cm with the top of the basilar artery as the center.
.
➤ Posterior cerebral artery: the terminal branch of the basilar artery, originates near the superior border of the pons, goes backward around the cerebral peduncle, and turns along the hook of the equine gyrus to the medial side of the temporal and occipital lobes
.
Cortical branches are distributed in the medial and basal surfaces of the temporal lobe and in the occipital lobe
.
The central branch originates from the root and penetrates the brain parenchyma from the interpeduncular fossa to supply the dorsal thalamus, medial and lateral geniculate body, hypothalamus, subthalamus,
etc.
➤Superior cerebellar artery: It divides near the end of the basilar artery and reaches the upper part of the cerebellum backward around the cerebral peduncle, and divides into two terminal branches
.
The medial branch supplies blood circulation to the superior cerebellar vermis and the anterior medullary vena, and the lateral branch supplies blood circulation to the upper cerebellar hemisphere
.
Branches along the way also supply the pontine tegmentum, midbrain tectum, choroid tissue of the third ventricle, and the fourth subventricular nucleus
.
➤Basilar artery: The top of the basilar artery sends out multiple branches such as labyrinth artery, lateral pontine artery, and perforating artery, which mainly supply blood circulation to the midbrain
.
Clinical manifestations ➤ Clinical manifestations of anterior brainstem infarction ➤ Eye movement disorders: Different ocular complex signs may appear due to different damage sites
.
Common ones are: 1.
Vertical gaze palsy, which has the highest frequency among all ocular signs; 2.
Excessive adduction of both eyes: the patient's eyes are mostly in the lower position, that is, gazing at the tip of the nose, which is sometimes difficult to distinguish from thalamic hemorrhage; 3.
Dissociative Strabismus: also known as midbrain strabismus, which often occurs at the same time as oculomotor nerve palsy and pupil abnormalities, and the damage is mostly located in the midbrain cerebral peduncle and its gray matter; It can be manifested as eyelid retraction; 5.
Parrino syndrome: one of the most characteristic manifestations of nuclear damage; 6.
Internuclear ophthalmoplegia: mainly due to involvement of the medial longitudinal tract
.
Others include fixed centering of the eyes and abduction of the eyes
.
➤Pupillary changes: is another characteristic manifestation of TOBS
.
Mainly: 1.
Mydriasis: it occurs most in pupil changes, and is caused by lesions involving light reflex afferent fibers or EW nucleus; 2.
Mydriasis: caused by bilateral sympathetic nerve dysfunction; 3.
Pupils are not round; 4 .
Ectopic pupil: refers to the pupil can quickly become partial from the central position, is one of the manifestations of midbrain infarction
.
➤ Consciousness disturbance: Patients can have different degrees of disturbance of consciousness, such as lethargy and lethargy, or even coma, akinetic mutism, and decerebral tonicity
.
The duration of disturbance of consciousness is short, and it is considered to be related to the loosening of emboli to distant displacement and recanalization of blood vessels.
This phenomenon is particularly obvious in patients with cerebral embolism
.
➤ Hallucinations: Also known as cerebral foot hallucinations, the incidence is low
.
➤ Motor and sensory disturbances: The deep perforating branches of the basilar artery and the deep perforating branches of the posterior cerebral artery supply the midbrain and cerebral peduncle.
If TOBS occurs, sensory or motor disturbances may be caused, but the degree is mild and the incidence is low, and it mostly occurs with the recovery of consciousness disturbance.
restore
.
➤ Abnormal visceral function: The reticular structure of the brainstem is a switching station between the ascending visceral sensory bundle and the descending bundle that regulates visceral activity
.
The dorsomedial nucleus of the thalamus is the center of complex integration of visceral and somatic impulses
.
Such symptoms are often overlooked because of the impaired co-operation caused by the disturbance of consciousness
.
➤Clinical manifestations of infarction in the hemisphere supplying the posterior cerebral artery ➤Visual field defect: Any damage in the path of optic radiation to the optic center can cause different degrees of visual field defect
.
Generally rare, mild and short-lived
.
➤Cortical blindness: The most severe visual deficit occurs when bilateral occipital lobes are involved
.
➤Balint syndrome: This syndrome can occur when bilateral posterior cerebral artery infarction occurs in the blood supply area.
It has the following characteristics: 1.
Global agnosia; 2.
Visual agnosia; 3.
Gaze disturbance; 4.
Others: visual agnosia can occur Distortion, abnormal behavior,
etc.
➤Memory impairment: More often occurs in bilateral middle temporal lobe infarcts, left temporal lobe infarction can lead to Korsakoff syndrome, which can be transient, lasting only a few hours, but can also last up to 6 months
.
In addition, some patients may also have mental disorders, manifested as fictional and emotional disorders
.
Diagnosis Basis ➤ Middle-aged and elderly people with risk factors for cerebrovascular disease, mostly male; ➤ Acute onset and rapid progression, with ischemic lesions in two or more parts of the brainstem, diencephalon and posterior cerebral artery innervation Symptoms and signs; ➤Clinical manifestations include varying degrees of disturbance of consciousness, eye movement disorders and pupil abnormalities, with motor and sensory abnormalities, hemianopia or cortical blindness, behavioral abnormalities and memory impairment, etc.
; ➤CT or MRI examination results are consistent with the basilar artery apex The signs of infarction in the blood supply area of more than 5 blood vessels, especially bilateral thalamic "butterfly" lesions can assist in the diagnosis; ➤DSA can find vascular stenosis and occlusion within 2 cm of the basilar artery tip, which is the gold standard for the diagnosis of this disease; ➤ Pay attention to the identification with poisoning, metabolic encephalopathy, and intracranial infectious encephalopathy
.
Differential diagnosis ➤ Temporal sulcus gyrus hernia: Consciousness disorder and unequal pupil size can also occur, but the patient’s consciousness disorder is severe and lasts for a long time.
After timely and effective dehydration treatment, the pupil can change, and head CT or MRI shows that there are Obvious lesions with midline shift
.
➤Thalamus hemorrhage: Due to the compression of the hematoma, the patient may also have pupillary changes, adjective and downward vision, and in severe cases may also experience disturbance of consciousness, but the patient's limb movement disturbance and sensory disturbance are obvious, and there are predisposing factors and pathogenesis of hemorrhagic diseases.
state, head CT can identify
.
➤ Intracranial deep vein thrombosis: The great cerebral vein is the deep cerebral vein, formed by the confluence of the posterior cerebral vein and the internal cerebral vein, and returns to the internal jugular vein through the straight sinus, transverse sinus and sigmoid sinus
.
When a certain reason (such as infection, contraceptive use, injury, high blood viscosity, etc.
) causes the vein to form thrombosis and block the venous return, it can cause increased intracranial pressure, headache, nausea and vomiting, papilledema, and in severe cases disturbance of consciousness
.
Compared with TOBS, the degree of disturbance of consciousness is more severe, the recovery is slower, and there are fewer ocular signs
.
Line DSA can be clearly identified
.
Treatment principles ➤ Early diagnosis should be made, and thrombolysis within 6 hours should be actively pursued.
If thrombolysis cannot be achieved, anti-fibrillation, anticoagulation, and antiplatelet aggregation therapy can be given
.
Local arterial thrombolysis under catheter intervention has the best effect and fewer sequelae; intravenous thrombolysis is the second most effective, with more sequelae; patients without thrombolysis have a poor prognosis
.
➤ Sufficient use of dehydrating drugs: The midbrain cerebellum and occipital lobe are in the posterior cranial fovea and are close to the medulla oblongata respiratory center and cardiovascular center.
Brain edema at the lesion site can easily induce foramen magnum hernia.
Therefore, sufficient dehydration should be used to reduce intracranial pressure
.
The amount of dehydration drugs cannot be measured by the size of the infarct size of the cerebral hemisphere
.
➤ Active prevention and treatment of complications: damage to the lower part of the brain is prone to autonomic dysfunction, the most common intractable hiccup, upper gastrointestinal bleeding, symptomatic treatment is beneficial to the prognosis of the disease
.
➤ Etiological treatment: The most common cause of TOBS is the shedding of thrombus from the heart or arteriosclerosis, so long-term anticoagulation or antiplatelet therapy is very important
.
Statins can effectively stabilize atherosclerotic plaques and prevent emboli from falling off
.
➤Keep the airway unobstructed and correct respiratory failure: TOBS is prone to bulb paralysis, causing airway obstruction and aggravating brain hypoxia.
Therefore, the patient should be kept in the lateral position to prevent the tongue from falling back.
In severe cases, an oropharyngeal tube or tracheotomy should be placed to maintain Airway patency, improve hypoxia
.
Once the brain is damaged, respiratory rhythm changes
.
Respiratory stimulants or ventilators are required to assist breathing
.
➤ In addition, comprehensive treatment programs such as brain cell protectants, antioxidant free radicals, calcium ion antagonists, blood circulation promoting and stasis removing, awakening, and rehabilitation are also very important
.
References: [1] Yang Xiaohui, Chu Zhaohu.
Research progress on basilar apex syndrome [J].
Jilin Medicine, 2012, 33(34): 7539-7541.
[2] Takashine R, Odaka M, Watanabe Y, et al al.
Case of basilar artery occlusion caused by mucormycotic embolism in the course of myelodysplastic syndrome[J].
Brain Nerve, 2009, 61(9):1079.
[3] Cao Hongmei, Wu Chengbin, Wei Juan.
Basilar apex syndrome[J ].
World Latest Medical Information Digest, 2004(04): 1201-1203.
[4] Lou Zhiyin, Hu Xueqiang.
Research progress of basilar apex syndrome [J].
Anatomical Research, 2005(03): 199-200+ 204.
[5] Caplan LR.
Topofthebasilarsyndrome.
Neurology, 1980, 30: 72.
[6] Wu Jin, Jiang Anjie.
New progress in the treatment of basilar apex syndrome [J].
Chinese Journal of Misdiagnosis, 2007(29):6979-6981 .
.
TOBS is a group of clinical syndromes caused by various etiologies caused by blood circulation disorders at the intersection of bilateral posterior cerebral arteries, bilateral superior cerebellar arteries and the top of basilar arteries, with the top of the basilar artery as the center within 2 cm in diameter
.
The clinical manifestations of TOBS are complex and diverse, the condition is critical, the prognosis is poor, and the morbidity and mortality rates are high.
Early diagnosis and treatment are very important
.
Let's learn about basilar apex syndrome today
.
Anatomical structure The tip of the basilar artery refers to the intersection of five blood vessels within a diameter of 2 cm with the top of the basilar artery as the center.
.
➤ Posterior cerebral artery: the terminal branch of the basilar artery, originates near the superior border of the pons, goes backward around the cerebral peduncle, and turns along the hook of the equine gyrus to the medial side of the temporal and occipital lobes
.
Cortical branches are distributed in the medial and basal surfaces of the temporal lobe and in the occipital lobe
.
The central branch originates from the root and penetrates the brain parenchyma from the interpeduncular fossa to supply the dorsal thalamus, medial and lateral geniculate body, hypothalamus, subthalamus,
etc.
➤Superior cerebellar artery: It divides near the end of the basilar artery and reaches the upper part of the cerebellum backward around the cerebral peduncle, and divides into two terminal branches
.
The medial branch supplies blood circulation to the superior cerebellar vermis and the anterior medullary vena, and the lateral branch supplies blood circulation to the upper cerebellar hemisphere
.
Branches along the way also supply the pontine tegmentum, midbrain tectum, choroid tissue of the third ventricle, and the fourth subventricular nucleus
.
➤Basilar artery: The top of the basilar artery sends out multiple branches such as labyrinth artery, lateral pontine artery, and perforating artery, which mainly supply blood circulation to the midbrain
.
Clinical manifestations ➤ Clinical manifestations of anterior brainstem infarction ➤ Eye movement disorders: Different ocular complex signs may appear due to different damage sites
.
Common ones are: 1.
Vertical gaze palsy, which has the highest frequency among all ocular signs; 2.
Excessive adduction of both eyes: the patient's eyes are mostly in the lower position, that is, gazing at the tip of the nose, which is sometimes difficult to distinguish from thalamic hemorrhage; 3.
Dissociative Strabismus: also known as midbrain strabismus, which often occurs at the same time as oculomotor nerve palsy and pupil abnormalities, and the damage is mostly located in the midbrain cerebral peduncle and its gray matter; It can be manifested as eyelid retraction; 5.
Parrino syndrome: one of the most characteristic manifestations of nuclear damage; 6.
Internuclear ophthalmoplegia: mainly due to involvement of the medial longitudinal tract
.
Others include fixed centering of the eyes and abduction of the eyes
.
➤Pupillary changes: is another characteristic manifestation of TOBS
.
Mainly: 1.
Mydriasis: it occurs most in pupil changes, and is caused by lesions involving light reflex afferent fibers or EW nucleus; 2.
Mydriasis: caused by bilateral sympathetic nerve dysfunction; 3.
Pupils are not round; 4 .
Ectopic pupil: refers to the pupil can quickly become partial from the central position, is one of the manifestations of midbrain infarction
.
➤ Consciousness disturbance: Patients can have different degrees of disturbance of consciousness, such as lethargy and lethargy, or even coma, akinetic mutism, and decerebral tonicity
.
The duration of disturbance of consciousness is short, and it is considered to be related to the loosening of emboli to distant displacement and recanalization of blood vessels.
This phenomenon is particularly obvious in patients with cerebral embolism
.
➤ Hallucinations: Also known as cerebral foot hallucinations, the incidence is low
.
➤ Motor and sensory disturbances: The deep perforating branches of the basilar artery and the deep perforating branches of the posterior cerebral artery supply the midbrain and cerebral peduncle.
If TOBS occurs, sensory or motor disturbances may be caused, but the degree is mild and the incidence is low, and it mostly occurs with the recovery of consciousness disturbance.
restore
.
➤ Abnormal visceral function: The reticular structure of the brainstem is a switching station between the ascending visceral sensory bundle and the descending bundle that regulates visceral activity
.
The dorsomedial nucleus of the thalamus is the center of complex integration of visceral and somatic impulses
.
Such symptoms are often overlooked because of the impaired co-operation caused by the disturbance of consciousness
.
➤Clinical manifestations of infarction in the hemisphere supplying the posterior cerebral artery ➤Visual field defect: Any damage in the path of optic radiation to the optic center can cause different degrees of visual field defect
.
Generally rare, mild and short-lived
.
➤Cortical blindness: The most severe visual deficit occurs when bilateral occipital lobes are involved
.
➤Balint syndrome: This syndrome can occur when bilateral posterior cerebral artery infarction occurs in the blood supply area.
It has the following characteristics: 1.
Global agnosia; 2.
Visual agnosia; 3.
Gaze disturbance; 4.
Others: visual agnosia can occur Distortion, abnormal behavior,
etc.
➤Memory impairment: More often occurs in bilateral middle temporal lobe infarcts, left temporal lobe infarction can lead to Korsakoff syndrome, which can be transient, lasting only a few hours, but can also last up to 6 months
.
In addition, some patients may also have mental disorders, manifested as fictional and emotional disorders
.
Diagnosis Basis ➤ Middle-aged and elderly people with risk factors for cerebrovascular disease, mostly male; ➤ Acute onset and rapid progression, with ischemic lesions in two or more parts of the brainstem, diencephalon and posterior cerebral artery innervation Symptoms and signs; ➤Clinical manifestations include varying degrees of disturbance of consciousness, eye movement disorders and pupil abnormalities, with motor and sensory abnormalities, hemianopia or cortical blindness, behavioral abnormalities and memory impairment, etc.
; ➤CT or MRI examination results are consistent with the basilar artery apex The signs of infarction in the blood supply area of more than 5 blood vessels, especially bilateral thalamic "butterfly" lesions can assist in the diagnosis; ➤DSA can find vascular stenosis and occlusion within 2 cm of the basilar artery tip, which is the gold standard for the diagnosis of this disease; ➤ Pay attention to the identification with poisoning, metabolic encephalopathy, and intracranial infectious encephalopathy
.
Differential diagnosis ➤ Temporal sulcus gyrus hernia: Consciousness disorder and unequal pupil size can also occur, but the patient’s consciousness disorder is severe and lasts for a long time.
After timely and effective dehydration treatment, the pupil can change, and head CT or MRI shows that there are Obvious lesions with midline shift
.
➤Thalamus hemorrhage: Due to the compression of the hematoma, the patient may also have pupillary changes, adjective and downward vision, and in severe cases may also experience disturbance of consciousness, but the patient's limb movement disturbance and sensory disturbance are obvious, and there are predisposing factors and pathogenesis of hemorrhagic diseases.
state, head CT can identify
.
➤ Intracranial deep vein thrombosis: The great cerebral vein is the deep cerebral vein, formed by the confluence of the posterior cerebral vein and the internal cerebral vein, and returns to the internal jugular vein through the straight sinus, transverse sinus and sigmoid sinus
.
When a certain reason (such as infection, contraceptive use, injury, high blood viscosity, etc.
) causes the vein to form thrombosis and block the venous return, it can cause increased intracranial pressure, headache, nausea and vomiting, papilledema, and in severe cases disturbance of consciousness
.
Compared with TOBS, the degree of disturbance of consciousness is more severe, the recovery is slower, and there are fewer ocular signs
.
Line DSA can be clearly identified
.
Treatment principles ➤ Early diagnosis should be made, and thrombolysis within 6 hours should be actively pursued.
If thrombolysis cannot be achieved, anti-fibrillation, anticoagulation, and antiplatelet aggregation therapy can be given
.
Local arterial thrombolysis under catheter intervention has the best effect and fewer sequelae; intravenous thrombolysis is the second most effective, with more sequelae; patients without thrombolysis have a poor prognosis
.
➤ Sufficient use of dehydrating drugs: The midbrain cerebellum and occipital lobe are in the posterior cranial fovea and are close to the medulla oblongata respiratory center and cardiovascular center.
Brain edema at the lesion site can easily induce foramen magnum hernia.
Therefore, sufficient dehydration should be used to reduce intracranial pressure
.
The amount of dehydration drugs cannot be measured by the size of the infarct size of the cerebral hemisphere
.
➤ Active prevention and treatment of complications: damage to the lower part of the brain is prone to autonomic dysfunction, the most common intractable hiccup, upper gastrointestinal bleeding, symptomatic treatment is beneficial to the prognosis of the disease
.
➤ Etiological treatment: The most common cause of TOBS is the shedding of thrombus from the heart or arteriosclerosis, so long-term anticoagulation or antiplatelet therapy is very important
.
Statins can effectively stabilize atherosclerotic plaques and prevent emboli from falling off
.
➤Keep the airway unobstructed and correct respiratory failure: TOBS is prone to bulb paralysis, causing airway obstruction and aggravating brain hypoxia.
Therefore, the patient should be kept in the lateral position to prevent the tongue from falling back.
In severe cases, an oropharyngeal tube or tracheotomy should be placed to maintain Airway patency, improve hypoxia
.
Once the brain is damaged, respiratory rhythm changes
.
Respiratory stimulants or ventilators are required to assist breathing
.
➤ In addition, comprehensive treatment programs such as brain cell protectants, antioxidant free radicals, calcium ion antagonists, blood circulation promoting and stasis removing, awakening, and rehabilitation are also very important
.
References: [1] Yang Xiaohui, Chu Zhaohu.
Research progress on basilar apex syndrome [J].
Jilin Medicine, 2012, 33(34): 7539-7541.
[2] Takashine R, Odaka M, Watanabe Y, et al al.
Case of basilar artery occlusion caused by mucormycotic embolism in the course of myelodysplastic syndrome[J].
Brain Nerve, 2009, 61(9):1079.
[3] Cao Hongmei, Wu Chengbin, Wei Juan.
Basilar apex syndrome[J ].
World Latest Medical Information Digest, 2004(04): 1201-1203.
[4] Lou Zhiyin, Hu Xueqiang.
Research progress of basilar apex syndrome [J].
Anatomical Research, 2005(03): 199-200+ 204.
[5] Caplan LR.
Topofthebasilarsyndrome.
Neurology, 1980, 30: 72.
[6] Wu Jin, Jiang Anjie.
New progress in the treatment of basilar apex syndrome [J].
Chinese Journal of Misdiagnosis, 2007(29):6979-6981 .
