Stroke (including ischemic cerebrovascular disease and cerebral hemorrhagic disease) is one of the diseases that seriously endanger human life and health today, with an incidence of about 200 people/100,000 population/year, of which ischemic cerebrovascular disease (including cerebrovascular transient ischemic attack and cerebral thrombosis) accounts for 75-85%; cerebral hemorrhage (mainly arteriosclerotic hypertensive cerebral hemorrhage) accounts for 10-15%. The mortality rate within six months after the occurrence of stroke can reach 54%, and survivors are left with varying degrees of disability. For half a century, neurology and surgery have been devoted to the diagnosis and treatment of cerebrovascular disease, and although there are controversies in the indications and methods of treatment, consensus has always been achieved. Especially with the rapid development of diagnostic neuroradiology, nuclear medicine, microsurgical skills and instruments, and basic research, the surgical treatment of cerebral stroke has made newer progress.
Surgical treatment of ischemic cerebrovascular disease
Studies have shown that when the cerebral vessels are locally stenosed or blocked and the cerebral collateral circulation is poor, three cerebral ischemic thresholds will occur: 1. neurological ischemic threshold: cerebral blood flow (CBF) drops from a normal 55-56 ml/100g per minute to less than 23 ml/100g after limb hemiparesis; 2. neuronal electrical activity ischemic threshold: CBF < 20 ml/100g per minute, cerebral electrical activity is diminished, CBF is 10-15 ml/100g per minute and electrical activity is in a resting state; 3. Ischemic threshold for membrane pump function: when CBF ≤ 10 ml/100g, ATP-depleted neurons release K+, causing an increase in extracellular K+ concentration, accompanied by intra-neuronal calcium overload and abnormal increases in Na+, Cl- and HO2 in glial cells. Neurons in the central zone of focal cerebral ischemia (also known as the dark zone) are in membrane pump failure and cannot reverse survival even if cerebral blood flow is restored within a short period of time. In contrast, the peripheral zone of ischemia (semi-dark zone) only has reduced cerebral blood flow and neuronal excitability, which can tolerate ischemia for a certain period of time without neuronal cell death. Therefore, the surgical treatment of ischemic cerebrovascular disease is to use the ischemia tolerance time (treatment window) of neurons in the semidark zone to restore cerebral blood flow by various methods and save the dying nerve cells. The size of the therapeutic window depends on the duration of ischemia and the establishment of effective collateral circulation. The therapeutic window for cerebral ischemia in humans is generally considered to be 3-6 hours after the onset of ischemia.
I. Carotid endarterectomy
In 1951, Fisher demonstrated clinically and pathologically that extracranial carotid artery stenosis or occlusion was associated with ischemic attacks or infarction, and in 1953, Pickering and Rob first performed carotid endarterectomy for the treatment and prevention of transient ischemic attacks (TIAs). Since then, it has been widely adopted and continuously improved and enriched in terms of surgical indications, methods, intraoperative brain protection and monitoring.
(a) Indications for surgery: 1, recurrent unilateral transient ischemic attacks of the carotid system with carotid angiography showing ipsilateral carotid stenosis ≥ 70%; 2, unilateral transient ischemic attacks of the carotid system with carotid angiography showing severe bilateral carotid stenosis, surgery on the symptomatic side can be done first and the contralateral side can be considered after four weeks; 3, transient black clouding attack or mild complete stroke (reversible ischemic neurological dysfunction), carotid angiography shows stenosis, but not ≥ 70%, but with atherosclerotic plaque or ulcer formation, no large infarct foci on CT, and no peripheral edema; 4. TIA episodes in the vertebrobasilar system, cerebral angiography shows carotid stenosis, while the posterior cerebral artery or more arteries in the vertebrobasilar system are co-blooded by the stenotic internal carotid artery; 5. With or without TIA episodes, but usually Presence of sudden disappearance of vascular murmur and carotid angiography showing severe stenosis or thrombosis of the carotid artery should be operated urgently; 6. Asymptomatic severe stenosis of the internal carotid artery is feasible for prophylactic surgery.
(b) Efficacy: In recent years, multiple prospective, randomized and controlled studies have shown that carotid artery thromboendarterectomy has significant effect on symptomatic or asymptomatic severe carotid stenosis and can reduce TIA episodes or strokes. The US Veterans Administration et al. multicenter study (91) showed that people with asymptomatic carotid stenosis >50-60% diagnosed by cerebral angiography were randomized to medical and surgical groups with 4-5 years of follow-up, with stroke rates of 5.1-8% in the surgical group and 11-20.6% in the medical group. Those diagnosed with symptomatic carotid stenosis >50-90% were randomized to the medical-surgical group with a follow-up of 3-5 years, and the stroke rate was 3.7-9% in the surgical group and 19.4-26% in the medical group.
II. Middle cerebral artery thrombectomy
After Welch et al. first reported a case of successful middle cerebral artery thrombus removal in 1956, there have been several reports in the literature.
(I) Indications: Middle cerebral artery embolism is mainly confirmed by cerebral angiography, and the treatment window (from arterial embolism to surgical recanalization time) should be within 6-8 hours.
(B) Efficacy: The recanalization rate of middle cerebral artery after surgery is 75%, and the complete restoration of function is 10%.
Intracranial revascularization surgery
Intracranial revascularization is the surgical re-establishment of cerebral collateral circulation pathways, which includes intracranial and external arterial anastomosis, intracranial transplantation of the greater omentum, scalp artery, dural artery, temporalis muscle and cerebral cortex vascular dressing, etc.
In 1951, Miller and Fisher first proposed the theory of intracranial and extracranial vascular bypass for the treatment of intracranial vascular obstruction diseases.
In 1967, Yasargil successfully anastomosed the superficial temporal artery to the cortical branch of the middle cerebral artery for the treatment of cerebral ischemic diseases. Since then, a new chapter of applying microsurgical techniques to reconstruct intracranial vessels for the treatment and prevention of cerebral ischemic diseases has been opened.
(A) Indications: 1. TIA, reversible ischemic neurological dysfunction that is not effective by medical treatment; 2. Middle cerebral artery stenosis or occlusion, poor collateral circulation, internal carotid artery stenosis or occlusion confirmed by cerebral angiography, which is not suitable for carotid endarterectomy; 3. Regional cerebral blood flow measurement with local or lateral cerebral hypoperfusion; 4. One side of the internal carotid artery stenosis, the opposite side of the carotid artery occlusion, want to do the stenosis side If the internal carotid artery is denuded, an extracranial revascularization can be performed on one side first; 5. Vertebrobasilar artery stenosis with symptoms of brainstem ischemia; select Moyamoya disease, with TIA as the main clinical manifestation.
(B) Efficacy: As a new method of treating ischemic diseases, intracranial and extracranial revascularization inevitably has an over-indication bias in the early stage of application. 1985 international cooperative study found that this technique did not reduce the occurrence of stroke, but there is still a controversy around the research method and its application, and the research about improvement is still in progress. Therefore, while strictly controlling the indications for the application of intracranial and extracranial revascularization for cerebral ischemic stroke, in-depth clinical basic research should be carried out.
Percutaneous vasodilation and angioplasty
In 1980, Sundt et al. first used a special catheter to dilate three patients with severe stenosis of the vertebral artery. In the last decade, with the development of microcatheterization and interventional techniques, treatments continue to be reported, but because the intracranial cerebral artery is anatomically different from the extracranial artery (e.g., thin cerebral artery wall, no surrounding soft tissue support, etc.), this technique has been carried out to date and must be done with caution.
V. Endovascular stenting of the carotid artery via the femoral artery
In 1996, Roubin et al. first reported that 99% of patients were successfully stented through the carotid artery.
VI. Craniotomy decompression
Craniotomy is a palliative method for the treatment of significantly increased intracranial pressure due to various intracranial diseases. In the past, it was also used to treat intractable cerebral edema after cerebral infarction, but the development was slow. In recent years, with the in-depth understanding of the pathophysiology of cerebral ischemia, cranial decompression has been emphasized and carried out again.
(I) Indications: Patients with ischemic cerebral infarction (including cerebrum and cerebellum) with impaired consciousness or early manifestations of brain herniation. large ischemic foci with extensive cerebral edema, displacement of midline structures or basal pool compression or brainstem compression or ventricular enlargement as suggested by CT examination, and ineffective internal medical treatment.
(b) Efficacy: According to the literature, 111 cases were treated surgically, 76 of which survived, with a mortality rate of 31.5%, while the mortality rate of medical treatment was more than 70%. Therefore, craniotomy for ischemic stroke with severe cerebral edema to save patients’ lives is an active treatment.
Surgical treatment of arteriosclerotic hypertensive cerebral hemorrhage
The treatment of hypertensive cerebral hemorrhage was first proposed by Cushing in 1903, and the feasibility and indications of surgical operation were first reported by Bagley in 1932 and Penfield in the following year, but the efficacy was not good because there was no diagnostic means. After the 1950s, the application of cerebral angiography in the diagnosis of intracerebral hematoma improved the accuracy of localization and diagnosis, and the surgical treatment of craniotomy to remove cerebral hematoma increased, but the mortality rate of surgery was about 50%, which was comparable to that of medical treatment. With the introduction and widespread use of CT in the 1970s, the diagnosis of hypertensive cerebral hemorrhage is not only accurate, but also provides a series of imaging data for surgical treatment to determine the indications and methods of surgery.
I. Indications for surgery for cerebral hemorrhage: Since 70 years, the principle of surgical treatment for hypertensive cerebral hemorrhage is based on the patient’s state of consciousness, neurological signs, CT imaging diagnosis (including hematoma site, hematoma volume, midline structural displacement, etc.), etc. to determine the indications for surgery.
1. state of consciousness: in drowsiness, somnolence, shallow or moderate coma or wakefulness gradually shifting to a decreasing level of consciousness.
2, pupillary changes: pupils of equal size or bilateral pupils of unequal size, presence or dullness of light reflex.
3. neurological signs: varying degrees of hemiparesis, aphasia (hemorrhage in the dominant hemisphere), unilateral or bilateral pathological reflexes.
4. CT manifestations: (1) Hematoma site: (1) shell nucleus hemorrhage, hematoma extending to the external capsule, or the anterior limb, posterior limb, or anterior and posterior limbs of the internal capsule breaking into the ventricle; (2) thalamic hemorrhage, hematoma confined to the thalamus or breaking into the ventricle or extending into the internal capsule; (3) hemorrhage in the lobes of the brain (subcortical); (4) cerebellar hemorrhage, hematoma confined to the cerebellar hemisphere or breaking into the ventricle; (5) brainstem hemorrhage breaking into the ventricle. (2) Volume of hematoma: supratentorial hematoma > 30 ml, subatentorial hematoma > 10 ml.(3) Midline structural displacement ≥ 0.5-1 cm.
(5) No history of serious heart, lung or kidney disorders, no drug-uncontrollable hypertension ≥26.6/16KPa (200/120mmHg) after onset, no concurrent gastrointestinal bleeding, etc.
In conclusion, the purpose of surgery is to remove the hematoma as soon as possible, lower the intracranial pressure, relieve the pressure on the brain tissue, prevent or alleviate a series of secondary pathological changes after hemorrhage as much as possible, break the life-threatening vicious circle, and thus improve or restore the function of the nerve cells around the hemorrhage.
Bagley advocated surgery after 2 weeks; Mitsuno et al. pointed out that surgery between 24 hours and 48 hours after the onset was the most ideal, because patients were in shock within 24 hours, and after 48 hours, complications such as pulmonary problems were unfavorable to surgery. It is believed that 6-7 hours after hemorrhage, pathological changes such as cerebral edema, cerebral ischemia, and brain tissue necrosis begin to appear around the hematoma and form a vicious circle with time. In order to break the vicious cycle of a series of secondary pathological changes that endanger life soon after hemorrhage, early or ultra-early surgery is advocated for cerebral hemorrhage that is suitable for surgery.
Third, surgical methods.
1.Craniotomy for hematoma removal: It is a traditional and commonly used surgical method. It is suitable for ① patients in shallow coma, moderate coma or brain herniation; ② shell nucleus hemorrhage expanding to the anterior and posterior limbs of the internal capsule or breaking into the ventricles, thalamus limited hemorrhage or expanding to the internal capsule, subcortical hemorrhage with hematoma volume >50ml, and obvious displacement of midline structures; ③ cerebellar hemorrhage.
2.Borehole or cone hole hematoma removal: It is a simple and minimally invasive surgical method to remove hematoma by using CT-guided or stereotactic techniques to puncture the center of the hematoma and aspirate or repeatedly crush the clot by Archimedes rotation stranding and then aspirate after the introduction of CT, which has been widely used.
Its advantages: (1) it is less invasive and less likely to cause damage to surrounding tissues when aspirating the hematoma; (2) it can generally remove about 70% of the hematoma and relieve intracranial pressure and cerebral compression; (3) it can inject fibrinolytic drugs (such as urokinase) into the residual hematoma cavity through the puncture site and drain the dissolved clot.
Indications: ① senior patients and patients without open cranial conditions; ② small bleeding volume; ③ bleeding in various parts (cerebellar bleeding is used with caution), especially deep bleeding (such as thalamus, brain parenchyma with ventricular bleeding).
3, hematoma fibrinolytic drainage: in the early 80s, Japan Itakura et al. successively reported the fibrinolytic treatment of hypertensive cerebral hemorrhage with urokinase, which was then widely supported and applied.
It is indicated for residual hematoma after craniotomy or borehole hematoma aspiration. 24 hours after surgery, urokinase 6000-10000 U dissolved in 2-5 ml of saline is injected into the hematoma cavity through the drainage tube, and the drainage is released after clamping the drainage tube for 2-4 hours, 1-2 times a day, usually for 3-5 days.
4. Application of endoscopy in hematoma removal: In the past 10 years, endoscopy has been applied in the field of neurosurgery. Aeur et al. used brain endoscopy for removal of intracranial hematoma and compared it with medical treatment, showing that the mortality and disability rate of the endoscopic surgery group was significantly lower than that of the medical group. It is indicated for patients of advanced age or poor general condition within 6 to 48 hours of onset, with hematoma volume <50 ml and no brain herniation.
IV. Factors affecting the efficacy of surgery.
1, the state of consciousness: the more severe the preoperative patient’s consciousness disorder, the worse the efficacy. The postoperative mortality rate was 0, 13%, 32%, 64% and 94% for the preoperative consciousness of wakefulness, drowsiness, shallow coma, moderate coma and deep coma, respectively, as reported by Gong-Hong Minakami in Japan.
2, bleeding site: deep bleeding (such as thalamus) is less effective because it affects important brain structures. Superficial hemorrhage (such as subcortical, lateral shell nucleus) has a more satisfactory outcome.
3, the amount of bleeding: the more bleeding, the worse the prognosis, but still need to be integrated with the site of bleeding analysis.
4, preoperative blood pressure: blood pressure ≥ 26.6/16Kpa and difficult to control, the prognosis is poor.
5, the timing of surgery: the later the surgery, the higher the mortality rate. This refers not only to the preoperative period, but also to the postoperative period due to the vicious circle formed by a series of secondary pathological changes after cerebral hemorrhage and various complications all leading to death.
6. Surgical method: it is difficult to conclude. However, the development of minimally invasive neurosurgery techniques will gradually become the main surgical method
7, age, organic disease: age is not used as a separate factor, but patients with heart, lung, kidney and other organ diseases affect the efficacy.