Tubercle sellar meningioma

Introduction to saddle nodule meningioma Saddle nodule meningiomas were first introduced by Stewart in 1899, and Cushing was equivalent to what it called "saddle meningioma" in 1929. Includes meningiomas originating from saddle nodules, anterior bed processes, saddle septums, and sphenoidal platforms. In the early stage of small tumors, the surgery can be completely removed and cured, and the mortality rate is very low. If the tumor is large, the risk of surgery increases. The literature reports that the operative mortality of this disease varies widely (2.6% to 67.0%). Postoperative visual acuity and visual field improvement were 27.8% to 72.2%, but there were still 5.6% to 38.9% of patients with postoperative visual deterioration. basic knowledge Sickness ratio: 0.0001% Susceptible people: specific people Mode of infection: non-infectious Complications: cerebral infarction subthalamic injury

Saddle nodule meningioma etiology

Cause (20%):

The cause of saddle nodule meningiomas is still unclear. Some people think that it is related to internal environmental changes and genetic variation, but it is not caused by a single factor. Craniocerebral trauma, radiation exposure, viral infection, etc. cause cell chromosomal mutation or cell division speed. It may be related to the occurrence of meningiomas. In recent years, molecular biology studies have confirmed that meningioma is most commonly lacking a gene fragment on 22 pairs of chromosomes.

Pathogenesis (10%):

Saddle nodule meningioma mostly grows spherically, and the boundary with brain tissue is clear. The tumor is cut into dense gray or dark red tissue, sometimes containing sand granules. Intratumoral hemorrhage can be seen in malignant meningioma, saddle nodule and its vicinity. Skeletal bone hyperplasia, sometimes saddle back bone thinning or absorption, pathological types are commonly endothelial cell type, vascular type, fibroblast type, sand type, etc., malignant meningioma and meningeal sarcoma are rare.

Saddle nodule meningioma prevention

There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease. At the same time, avoiding harmful substances (promoting factors) is an important measure to prevent or minimize exposure to harmful substances.

Saddle nodule meningioma complications Complications cerebral infarction hypothalamic injury

1. Optic nerve, optic chiasm

It is the most common complication of saddle nodule meningioma. In addition to direct injury, the vascular injury that supplies visual pathway is also the cause of postoperative vision loss or even blindness. The key to prevention is that the operation should be performed under the microscope, and careful attention should be paid to the optic nerve and the neck. Arteries and oculomotor nerves, etc., and pay attention to protection.

2. Internal carotid artery and its branch injury

When operating under direct vision, suspected cerebral vasospasm and cerebral infarction, early application of papaverine, nimodipine can play a preventive and therapeutic role.

3. Oculomotor injury

If the tumor is adjacent to the oculomotor nerve, separation and pulling of the nerve often causes the patient to have temporary oculomotor paralysis after surgery.

4. Pituitary stalk and hypothalamic injury

Temporary or permanent urinary collapse or other endocrine disorders occur after surgery, as appropriate, to the pituitary vasopressin, long-acting urine collapse and other hormones.

5. Seizures

Anti-epileptic drugs are routinely used after surgery, especially those who have epilepsy before surgery should pay attention to prevention.

Saddle nodule meningioma symptoms common symptoms polyuria libido decreased amenorrhea visual impairment

1. Vision, visual field disorder: the most common symptom of saddle nodule meningioma, almost all patients have vision, visual field changes, more than 80% of patients are the first symptoms, visual impairment is mostly slow, progressive decline, sustainable number Months or years, early side vision loss with temporal side visual field defect, unilateral visual impairment accounted for 55%, followed by contralateral optic nerve and optic chiasm compression showed binocular vision loss or bilateral visual field defect, bilateral visual impairment accounted for 45%, which can lead to blindness, but the changes in bilateral vision or visual field are often asymmetrical, irregular, and even a very small number of patients are blind on one side and normal on the other. These patients are often first diagnosed in ophthalmology. Due to optic nerve and optic chiasm, the primary shrinkage of the optic disc often occurs in the fundus, which can be as high as 80%. In the late stage, secondary fundus edema can occur simultaneously due to increased intracranial pressure.

2. Headache: For the early common symptoms, about half of the patients have a history of headache, mostly with intermittent pain such as forehead, ankle, eyelids, etc., not severe, when the intracranial pressure is increased, the headache is aggravated, accompanied by vomiting, often In the evening and early morning.

3. Pituitary and hypothalamic dysfunction: Pituitary dysfunction and hypothalamic lesions are less common, but when the tumor grows and compresses the pituitary, symptoms of pituitary dysfunction can also occur, such as decreased sexual desire, impotence or amenorrhea. When the lower part of the thalamus is involved, polydipsia, polyuria, obesity and lethargy may also occur.

4. Symptoms of adjacent structure involvement: When the olfactory tract is affected, there is one side or both sides of the olfactory sensation diminished or disappeared. When the frontal lobe is involved, it may cause drowsiness, memory loss, anxiety and other mental symptoms. When the cavernous sinus is compressed, it may cause oculomotor nerve palsy and eyeball protrusion. Wait.

5. Symptoms of increased intracranial pressure: Late tumor, due to tumor enlargement or cerebrospinal fluid circulatory disorder caused by tumor intrusion into the interventricular septum in the third ventricle, caused by hydrocephalus, mainly manifested as headache, nausea, vomiting, optic disc edema Wait.

6. Others: A small number of patients complained of epilepsy, and some patients may have pyramidal tract signs.

Saddle nodule meningioma examination

Lumbar puncture pressure measurement can be increased (late), the number of cells in cerebrospinal fluid test is normal, and the protein is slightly increased.

1. Skull X-ray film

About half of the patients' heads may have a positive finding, with saddle nodule and its adjacent sphenoidal plateau hyperosteogeny, showing nodular hyperplasia, sometimes visible saddle back bone resorption, a few local bone destruction, saddle Generally do not expand.

2. CT examination

Saddle nodular meningioma can be seen on the CT slice in the same density or high density area of the saddle. After the contrast agent is injected, the tumor image is obviously enhanced. The bone window can be seen as the bone density of the saddle nodule is increased or loose. The coronary scan can judge the tumor and the saddle. The relationship between the optic chiasm and the internal carotid artery should be pointed out that after the gradual popularization of CT, CT examination is first used for patients with suspicious saddle lesions. However, for high-density lesions on the saddle, attention should be paid to cerebral angiography and aneurysms. Identification to prevent accidents during surgery.

3. MRI examination

Its effect is the same as that of CT, but it shows that the neighboring relationship between tumor and surrounding important structure is clearer, and the level of tumor signal on T2-weighted image will help to understand the texture of meningioma, that is, T2 weighted image high signal indicates higher tumor water content. The texture is soft; low signal or other signals indicate that the tumor has more fibrosis and calcification, and the texture is harder, which is not conducive to resection. MRA can help to understand the tumor blood supply.

4. Cerebral angiography

When the tumor is small, there is no need for vascular translocation. The middle and upper sized tumors may have the first segment of the anterior cerebral artery and the anterior communicating artery, which will be displaced backwards. The arterial lumen will become thinner, and a few may cause arterial occlusion. Thickened and branched to the saddle nodule meningioma, sometimes seen saddle nodules as a starting point to the surrounding radial radial abnormal blood vessels.

Diagnosis and diagnosis of saddle nodule meningioma

Saddle nodule meningioma is difficult to detect early due to the lack of specific symptoms and signs. Therefore, adults with progressive vision loss, single or bilateral hemianopia, headache, primary optic atrophy or Foster -Kennedy syndrome, that is, the possibility of saddle nodule meningioma should be considered. The diagnosis is mainly based on imaging examination. The popularity of CT and MRI provides a simple, safe and reliable diagnostic method for the diagnosis of this disease. The primary hospital, skull X-ray film and cerebral angiography also have certain diagnostic value.

Differential diagnosis

Saddle nodule meningioma should be identified with the following diseases:

1. Pituitary adenoma: usually in the pituitary gland secretion disorder, more than 70% of patients with endocrine disorders, more than 50% of patients with this as the first symptom, optic nerve compression at the beginning of the visual field defect, visual acuity change is not obvious, skull X film about 97% of patients developed saddle enlargement, deformation or bone destruction.

2. Craniopharyngioma: milder age, diabetes insipidus and obesity and other symptoms of hypothalamic involvement, 66% to 74% of patients with saddle and / or saddle calcification, especially eggshell calcification to determine the diagnosis More valuable.

3. Acropititis of the optic chiasm: slow vision loss, often symptomatic remission, visual field changes are irregular, the sella is normal, there is no bone hyperplasia and destruction near the saddle nodule, and there is no mass in the saddle area of CT scan.

4. Posterior optic neuritis: acute onset, often loss of vision in both eyes, rapid progress, mostly concentric vision reduction, non-surgical treatment is obvious, no increase in the sella, no endocrine disorders, CT scan in the bareback area .

5. ectopic pineal tumor: the age of onset is more common in 7 to 20 years old, mostly with diabetes insipidus as the first symptom, accompanied by other endocrine abnormalities (about 70%), optic nerve may have primary atrophy, tumor calcification uncommon.

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