I. Smoker’s disease.
Smoky disease, also known as anomalous vascular network at the base of the brain, is a group of cerebrovascular diseases characterized by narrowing or occlusion of the siphon segment of the internal carotid artery and the beginning of the anterior and middle cerebral arteries, and the appearance of an abnormal network of small vessels at the base of the brain. It is called smoker’s disease because the cerebral angiogram shows many dense piles of small blood vessel shadows, resembling the smoke exhaled during smoking.
Causes
Some scholars have found that individual families with mothers and sons or siblings can have similar disease, which is considered to be related to congenital factors. However, based on clinical, pathological, immunological and laboratory studies, most scholars believe that this is a group of occlusive cerebrovascular diseases that occur later in life and may be related to allergic cerebral vasculitis.
Clinical manifestations
1. Transient ischemic attack (TIA) type
It is the most common type, and is seen in about 70% of all idiopathic smog. It is characterized by recurrent transient paralysis or weakness, mostly hemiparesis, or alternating right and left hemiparesis or double hemiparesis. There is complete recovery of motor function after an attack. The course of the disease is mostly benign, with a tendency to spontaneous remission or complete cessation of attacks. Very few cases are associated with hemiplegic attacks, headache or migraine. Rarely, there is transient sensory impairment, involuntary movement or mental retardation.
2. Infarct type
Acute stroke resulting in permanent type of paralysis, aphasia, visual impairment and mental retardation.
3.Epileptic type
Frequent seizures, partial seizures, or continuous status epilepticus with EEG epileptiform discharges.
4.Hemorrhagic type
Subarachnoid hemorrhage or brain parenchymal hemorrhage, seen in older children and adult cases.
The last three types of the above clinical typing are called “non-TIA type”, which has a complex and variable course and a poor prognosis, and mostly manifests as a mixed type, such as epileptic type plus infarct type, epileptic type plus TIA type. In case of simple seizures, the prognosis is not necessarily poor. Regardless of the type, the prognosis is worse in those with onset before the age of 4 years. In addition, the clinical symptoms and their severity are determined by the compensatory effect of the collateral circulation. If adequate cerebral perfusion is maintained, there may be no clinical symptoms, or only transient TIA-type seizures, or headaches. If cerebral perfusion cannot be maintained, the symptoms are severe and cause extensive brain damage.
Diagnosis
It is mainly based on imaging, such as CTA, MRA, and DSA for clarity.
Treatment
1.Medical treatment
Patients with infarction are generally treated as thrombosis. Treatment with vasodilators, vasodilators, calcium antagonists, etc. can be used, and hormone therapy can also be used. For ischemia, vasodilators are used, and for hemorrhage, lowering cranial pressure and stopping hemorrhage are the main treatments. If the cause is clear, the cause should be treated actively.
2.Surgical treatment
Smoker’s disease can be treated with intracranial and extracranial vascular anastomosis, cerebral muscle vascular combination and other surgical procedures to reconstruct blood flow and improve prognosis. In case of ischemia, cervical sympathectomy or intracranial and extracranial arterial anastomosis can be considered. If there is intracranial hematoma formation, it should be excluded promptly.
Our department adopts direct vascular anastomosis combined with brain-dural-muscle vascular fusion to provide a reasonable, safe and effective surgical treatment method for smog disease.
II. Cerebral aneurysm.
Intracranial aneurysm refers to a kind of aneurysmal protrusion of the arterial wall caused by the restricted abnormal enlargement of the internal lumen of the cerebral artery. Intracranial aneurysms are mostly caused by local congenital defects of the cerebral arterial wall and cystic bulge on the basis of increased pressure in the lumen, which is the first cause of subarachnoid hemorrhage. In the past, it was called congenital cerebral aneurysm, but in fact, congenital cerebral aneurysms account for 70% to 80% of cerebral aneurysms.
Causes: The causes of aneurysms are not well understood. The causes of aneurysms are not well understood. The causes of aneurysm formation are summarized as follows.
① congenital factors.
②Arteriosclerosis.
(iii) Infection.
④ Trauma.
In addition, some rare causes such as tumor can also cause aneurysm, skull base anomalous vascular network, cerebral arteriovenous malformation, intracranial vascular development anomaly and cerebral artery occlusion can also be accompanied by aneurysm.
Clinical manifestations
1.Aneurysm rupture and bleeding symptoms
Once the aneurysm ruptures and bleeds, the clinical manifestation is severe subarachnoid hemorrhage, with rapid onset and severe headache, which is described as “head exploding”. Frequent vomiting, profuse sweating, elevated body temperature, neck stiffness, and positive Creutzfeldt-Jakob sign. There may also be impaired consciousness and even coma. Some patients have triggers such as exertion and emotional excitement before bleeding, while some have no obvious triggers or onset during sleep.
2.Focal symptoms
Depends on the location of the aneurysm, the adjacent anatomy and the size of the aneurysm. Arteriovenous nerve palsy is commonly seen in internal carotid artery-posterior communicating artery aneurysms and aneurysms of the posterior cerebral artery, manifesting as unilateral eyelid ptosis, pupil dilation, inversion, inability to see up or down, and loss of direct and indirect light responses. Sometimes focal symptoms appear before subarachnoid hemorrhage and are considered precursors to aneurysm hemorrhage, such as mild migraine and orbital pain followed by arteriovenous nerve palsy, at which time one should be alert to the ensuing subarachnoid hemorrhage. Patients may develop hemiparesis, motor or sensory aphasia after aneurysm hemorrhage in the middle cerebral artery if a hematoma is formed; or cerebral vasospasm cerebral infarction after aneurysm hemorrhage in other sites. In the case of a giant aneurysm affecting the visual pathway, the patient may have visual field impairment.
Treatment
1.Non-surgical treatment of intracranial aneurysm
The main purpose is to prevent rebleeding and control arterial spasm, etc. It is applicable to the following cases.
①Patients whose condition is not suitable for surgery or whose systemic condition cannot tolerate craniotomy.
②The diagnosis is unclear and further examination is needed.
③Patients refuse surgery or surgery fails.
④As an adjuvant treatment before and after surgery.
2.Surgical treatment of intracranial aneurysm
Patients with subarachnoid hemorrhage should be operated early (clamping of the aneurysm tip or embolization of the aneurysm), intraoperative measures should be taken to protect the brain, and postoperative volume expansion treatment should be provided. The aneurysms of the first part of the basilar artery and posterior cerebral artery should be operated after the neurological symptoms have improved and stabilized.
3. Treatment of special types of aneurysms
(1) Multiple aneurysms The chance of hemorrhage is more than that of single aneurysm, so some people advocate that it is better to treat one aneurysm than none, and all of them than only one, and it is most advantageous to treat all aneurysms in one operation by using one incision. About 96% of hemorrhagic aneurysms can be distinguished based on a comprehensive analysis of imaging and clinical symptoms, and the management of multiple aneurysms is similar to that of single aneurysms, with similar operative mortality.
(2) Giant aneurysm About 1/5 patients can only be treated conservatively due to various reasons, while 4/5 can be treated surgically.
Intracranial aneurysms are equivalent to “time bombs” in the skull, and once they rupture, the death or disability rate is extremely high, causing great danger to patients’ lives. There are two main treatment methods for intracranial aneurysm: one is open aneurysm clamping, and the other is aneurysm lumen embolization (interventional treatment) via femoral artery cannulation. Clamping treatment: microscopic technique to clamp the aneurysm neck; interventional treatment: vascular interventional catheter technique “spring ring” to occlude the aneurysm. Our neurosurgery department is experienced in treating cerebral aneurysms, and we have both microsurgical clamping techniques and interventional endovascular embolization techniques, both of which have strong technical capabilities and can perform individual treatment plans for each patient.
Typical cases
Cerebral arteriovenous malformation
Cerebral arteriovenous malformation is the most common type of cerebrovascular malformation, located in the superficial or deep part of the brain. The arteriovenous malformation is composed of arteries and veins, some of which include aneurysms and venous aneurysms, and the arteriovenous malformation has a variety of sizes and shapes, including blood supplying arteries and draining veins. They occur in the frontal and parietal lobes, but also in the temporal lobe, occipital lobe, ventricles, thalamus, cerebellum and brainstem. According to the size of the lesion: <2.5 cm in diameter is small, 2.5-5 cm is medium, 5-7.5 cm is large, and >7.5 cm is extra large. These arteriovenous malformations can also occur in the dura mater. They often present as epilepsy with spontaneous cerebral hemorrhage, may have incomplete paralysis of the limbs, and in some cases have increased intracranial pressure, similar to a brain tumor. Larger cerebral arteriovenous malformations sometimes cause symptoms of intracranial stasis, and vascular murmurs are sometimes heard on cranio-orbital auscultation.
Etiology
The main cause is cerebrovascular developmental disorder. In the third week of embryonic life, the primitive cerebral vascular network begins to differentiate into arteries and veins and the capillary network between arteries and veins. If the normal development of cerebrovascular vessels is obstructed at this time, direct communication between arteries and veins is formed without capillary network between them, and then arteriovenous malformation is formed. It has been found that the arteries in arteriovenous malformations are already mature, while the endothelial cells of the veins are morphologically at the embryonic level, and it is believed that arteriovenous malformations are caused by venous developmental disorders. Arteriovenous malformations consist of a mass of arteries, veins, and arterialized venous (arteriovenous fistula)-like vessels with direct arterial and venous communication without intervening capillaries. As a result of blood theft from the malformed vessels, the blood supply to the brain tissue around them is reduced and thus the symptoms of blood theft occur. Blood theft is caused by arteriovenous fistulas and is highly visible on cerebral angiography.
Clinical manifestations
The main symptoms are localized cerebral ischemia and recurrent hemorrhage.
1. Hemorrhage
Patients often have no clear cause for the onset of hemorrhage, and the first symptom is the formation of intracerebral hematoma or subarachnoid hemorrhage, accounting for 52% to 70% of patients.
2, ischemia
It is often seen in giant lesions, mostly due to long-term blood theft and causes whole brain atrophy leading to mental retardation, sometimes manifested as progressive mild hemiparesis and other brain dysfunction.
3.Epilepsy
It is the main clinical manifestation of superficial cerebral arteriovenous malformation, second only to hemorrhage, and its incidence is 28%-64%, which is related to the site and size of cerebral arteriovenous malformation.
4.Headache
About 60% of patients usually have vascular headache, which may be caused by vasodilatation.
5.Focal symptoms
Depending on the site of vascular malformation, hematoma compression, cerebral blood circulation disorder and brain atrophy area.
6.Other
Intracranial vascular blowing murmur, psychiatric symptoms, eye protrusion, vascular murmur, secondary intracranial hypertension, diplopia, heart failure and other symptoms.
Diagnosis
Diagnosis of sudden subarachnoid hemorrhage under 40 years of age with history of epilepsy or history of mild hemiparesis, aphasia, and headache before hemorrhage without obvious increase in intracranial pressure should be highly suspected of arteriovenous malformation, but confirming the diagnosis depends on cerebral angiography, and CT and MRI examination can help to confirm the diagnosis.
Treatment
1.Surgical treatment
Microscopic neurosurgery technique is used to remove the diseased vascular mass.
2.Endovascular embolization treatment
For deep lesions, located in important functional areas or high blood flow lesions, embolization therapy is appropriate. Embolization treatment alone can only cure a small part of the lesion, and microsurgical resection can be performed after partial embolization.
3.Stereotactic radiosurgery treatment
That is, X knife or γ knife, non-invasive, but slow effect, suitable for deep lesions less than 3cm in diameter or residual lesions after surgery and embolization.
4.Non-surgical treatment
Measures are.
①Avoid triggering factors, such as violent mood swings, prohibition of smoking and alcohol, etc.
②Prevent and control seizures.
③Prevent rebleeding.
④Symptomatic treatment.
Typical cases