Clinical manifestations of 1 type. Type ⅰ dural arteriovenous malformation is more common in men than in women. The ratio of male to female is 4∶ 1. The average age of patients is 40 ~ 50 years old, and the lesions are mostly in the thoracolumbar segment. There is no obvious family onset tendency. Demographic data show that dural arteriovenous malformation may be an acquired disease, and these lesions may be related to traumatic factors.
Pain is the most common symptom in patients with spinal arteriovenous malformation. Thoracolumbar pain in the back or buttocks may be the main symptom, and sometimes patients may have nerve root pain. Aminoff and Logue reported that 42% patients complained of pain A as the main symptom, 33% patients had sensory disturbance instead of pain, and some patients often felt allergic to the skin and joint distribution area adjacent to acupuncture hypoesthesia area, losing light touch and sense of position.
1/3 patients with dural arteriovenous malformation have motor dysfunction. These patients usually have signs of mixed dysfunction of upper motor neurons and lower motor neurons related to lumbosacral spinal cord. Gluteal and gastrocnemius atrophy is often accompanied by hyperreflexia of lower limbs. Physical labor, standing for a long time, bending, bending, stretching or buckling and other postures aggravate venous congestion, which can aggravate symptoms.
Subarachnoid hemorrhage is rare in patients with dural arteriovenous malformation. When acute necrotizing myelopathy may lead to sudden paralysis (Foix-alajouine syndrome), it may be caused by sudden thrombosis of reflux vein.
One of the typical medical history of patients with dural arteriovenous malformation is progressive mixed paralysis of upper and lower motor neurons in middle-aged and elderly men, accompanied by pain, sensory disturbance, gluteal muscular atrophy and sphincter dysfunction. Although arteriovenous fistula may be located above or below lumbosacral level, the symptoms are usually related to lumbosacral spinal cord. 80% patients can slowly develop myelopathy, and less than 65,438+00% ~ 65,438+05% patients have severe spinal cord dysfunction, leading to acute onset. The diagnosis of dural arteriovenous malformation is often delayed. Only 1 3 patients were diagnosed within1year, and about 2/3 patients were not diagnosed until 3 years after symptoms appeared.
2. The clinical manifestations of type II and type III spinal vascular malformations occurring in dura mater include type II, type III and type IV. Among them, type ⅱ (spherical vascular malformation) and type ⅲ (immature or extensive vascular malformation) are located in the spinal cord.
Intramedullary lesions account for 10% ~ 15% of all spinal vascular malformations. Compared with dural arteriovenous malformation, the sex distribution of intramedullary diseases is similar. Intramedullary lesions may also occur in young patients. Foreign research reports that 75% of patients with intramedullary diseases are under 40 years old. 46% of the lesions occurred in the cervical spinal cord and 44% in the thoracolumbar spinal cord.
The clinical manifestations of patients with intramedullary arteriovenous malformation are obviously different from those of patients with dural arteriovenous malformation. Patients with intramedullary arteriovenous malformation often have intramedullary and subarachnoid hemorrhage. May or may not be accompanied by acute neurological dysfunction. 76% patients had bleeding at some time, and 24% patients had neurological dysfunction due to bleeding. Intramedullary hemorrhage seems to be more common in cervical arteriovenous malformation. Some patients show progressive weakness, sensory disturbance, abnormal sphincter function and impotence, often accompanied by intramedullary bleeding. About 20% patients with intramedullary arteriovenous malformation can develop intramedullary aneurysms. These spinal cord aneurysms are usually located in the main nutrient vessels supplying intramedullary arteriovenous malformations. The prognosis of patients with middle thoracic lesions is worse than that of patients with other lesions, which may be related to the lack of collateral vessels in this area. Patients with cervical lesions have a good prognosis.
3. The clinical manifestations of type Ⅳ lesions are rare. According to Barrow and his colleagues, among the spinal vascular malformations treated in this medical center, type ⅳ lesions account for 17%.
Patients with type ⅳ lesions are usually younger than patients with type ⅰ lesions. Symptoms often appear before the age of 40. In Barrow's research report, half of arteriovenous malformations are ⅳ a lesions. However, Mourier and his colleagues noticed that 63% of patients had type ⅳc malformation. Most patients present with progressive myelopathy, accompanied by pain, weakness, sensory and sphincter dysfunction or subarachnoid hemorrhage. There is no difference in its distribution between men and women.
The spinal cord dysfunction in these patients is similar to type ⅰ lesions. Vascular congestion is caused by the increase of epidural venous pressure, and the compression of type ⅳ C lesions significantly affects the function of spinal cord and nerve roots. Barrow speculated that these lesions in some patients may be acquired. Several cases reported that they had undergone intraspinal surgery and/or craniospinal trauma before symptoms appeared, which indicated that in some patients, the onset was acquired, while others were congenital lesions.
4. Clinical manifestations of cavernous vascular malformations These lesions are estimated to account for 5% ~ 12% of all spinal vascular malformations. They may be familial or multiple. The incidence of cavernous vascular malformation in central nervous system is 0.2% ~ 0.4%, and it is estimated that the incidence of cavernous vascular malformation in spinal canal is 3% ~ 5%.
The average age of patients with spinal cavernous vascular malformation is 35 years old. Patients can show acute neurological dysfunction, which is usually related to bleeding. Due to the rapid expansion of blood vessels, bleeding is often complicated. Other patients may show progressive and progressive neurological dysfunction, and there is a tendency to improve neurological function after more serious dysfunction attacks. Repeated bleeding can also occur, and the deterioration of neurological function can last for hours or days after bleeding.
The diagnosis of spinal vascular malformation is mainly based on imaging besides medical history and signs.
Type 1. Abnormal blood vessels can be seen on MRI in grade I diagnosis, but abnormal T2-weighted signal is often the only abnormal manifestation of lumbosacral spinal cord. In CTM, the diagnosis of dural arteriovenous malformation is usually more sensitive and specific. Compared with contrast-enhanced CT, larger and curled blood vessels can be seen in the dorsolateral spinal cord. During radiography, the patient should take the supine position to check the venous reflux in the dura mater. In dural arteriovenous malformation, it is very rare for enhanced CT to show complete occlusion. It can be differentiated from intramedullary tumors on MRI. MRI can show the phenomenon of empty blood flow, which is consistent with the tortuous expansion of veins around the spinal cord. MRI of patients with dural arteriovenous malformation is usually normal. If the patient's MRI results are normal and it is highly suspected that he has dural arteriovenous malformation, myelography should be performed. If the angiography is normal, spinal arteriography is usually not needed.
When enhanced CT or MRI prompts the diagnosis, selective spinal arteriography is the method to determine the diagnosis. Angiography can identify the anterior spinal artery and determine the blood supply related to dural arteriovenous malformation. Identify all the nutrient arteries of the lesion to prevent recurrence of the communicating branch of arteriovenous fistula after operation. Sometimes, the dural arteriovenous fistula near the skull may have spinal venous communication, which can cause spinal venous hypertension and myelopathy. In these patients, in order to diagnose this uncommon disease, it is necessary to selectively inject contrast media into the external carotid artery and internal carotid artery for carotid angiography.
2. The fluid cavity sign on T1weighted images can definitely diagnose the II and III lesions of intramedullary arteriovenous malformation. On T2-weighted images, abnormal signals often appear in the spinal cord, and signs of fluid around the spinal cord suggest that there are lesions around the spinal cord. Spinal arteriography is necessary to determine intramedullary lesions, but it is not always helpful to distinguish type ⅱ and type ⅲ lesions. Selective aortic intubation and angiography of vertebral artery, carotid artery and iliopsoas muscle are necessary to determine the nutrient arteries of intramedullary lesions. The dorsal root and ventral root vessels supply arteriovenous malformation through the branches of anterior spinal artery and posterior spinal artery. The anterior spinal artery may terminate in intramedullary arteriovenous malformation or can still be used as a blood vessel, which can identify spinal cord aneurysms and varicose veins.
3. Type Ⅳ diagnostic magnetic resonance imaging (MRI) sometimes shows large signs of fluid cavity around the spinal cord, mainly manifested as obviously dilated epidural venous reflux. These malformations often appear in the thoracolumbar segment, near the cone and near the ponytail. Selective angiography can show the distribution of anterior spinal artery to arteriovenous fistula and reflux vein.
4. Imaging features of cavernous vascular malformation. The center of mixed signal intensity can be seen on T 1 weighted, T2 weighted and proton density imaging. On the weight of T 1, we can see that this center is surrounded by a low-density iron-containing yellow ring. These lesions are usually not significantly enhanced. Continuous magnetic vibration scanning may change the lesion volume of patients with fluctuating symptoms. There are few abnormalities in myelography and angiography, and it is usually impossible to diagnose cavernous vascular malformation. Sometimes spinal angiography is needed to distinguish cavernous vascular malformations from other types of vascular malformations.