abstract

1. Primary tumor: various tissues and structures originating in the skull and spinal canal, such as skull, meninges, brain tissues, cranial nerves, cerebral vessels, pituitary gland, pineal gland, choroid plexus, intracranial connective tissues, embryonic residual tissues, spinal membranes, spinal nerves, spinal cord, spinal cord blood vessels and adipose tissues; Glioma is the most common, followed by meningioma, pituitary adenoma, neurofibroma and cerebrovascular malformation.

2. Secondary tumors: metastatic tumors or invasive tumors.

incidence rate

10 ~12/100000 population/year, second only to stomach, lung, uterus, breast and esophagus tumors, accounting for about 2.5% of all tumors. Childhood is 7.5%.

1. Age: It can occur at any age and is more common in adults.

2. Gender: There is little difference between the general incidence and gender, but pineal tumor, glioblastoma multiforme, angioreticuloma, craniopharyngioma, metastatic tumor, schwannoma and teratoma are slightly higher in men than in women (male: female = 3.2: 1), while the incidence of meningioma is mainly in women (female: male = 65438+).

3. The age of onset is related to the location and pathological properties of the tumor:

① Children: medulloblastoma, astrocytoma, ependymoma, craniopharyngioma and pineal tumor are common in the midline of cerebellum;

(2) Adults: Most of them happen on the screen, and a few happen under the screen. Astrocytoma, meningioma, pituitary adenoma and acoustic neuroma are common.

③ Old age: mostly located in the cerebral hemisphere, with glioblastoma multiforme, meningioma or metastatic tumor as the majority.

classify

1. Classification by growth site: It depends on the tumor growing in different parts of the intracranial structure, such as forehead, parietal lobe, occipital region, temporal lobe, cerebellum, brain stem, thalamus, sellar region, ventricle and cerebellopontine angle region.

2. According to pathological nature: WHO (1995)

The level of each category

Glioblastoma Astrocytoma (including glioblastoma multiforme), oligodendroglioma, ependymoma, medulloblastoma, choroid plexus papilloma (cancer), pineal cell tumor, mixed glioblastoma.

Meningiomas include endothelial cell type, fibrous type (fibroblast type), mixed type, sandy type, hemangioma type, nipple type and anaplastic (malignant) meningioma.

Pituitary adenoma a. no secretory adenoma; B. Secretory adenoma: cell adenoma of growth hormone, prolactin, adrenocorticotropic hormone, thyrotropin, follicle-stimulating hormone and melanotropin; C. pituitary adenocarcinoma; D. Pituitary cell tumor

Neurofibroma (including neurilemmoma), acoustic neurilemmoma, trigeminal neurofibroma, glossopharyngeal neuroma, accessory neuroma, etc.

Congenital tumor craniopharyngioma, teratoma, dermoid or epidermoid cyst, Lasik cleft cyst, glial cyst, etc.

Vascular tumor hemangioreticuloma

Metastasis and invasion A. Brain metastasis of cancers such as lung, gastrointestinal tract, breast and genitourinary system; Nasopharyngeal carcinoma, giant cell tumor of bone, chordoma and chondroma invade the brain.

Other tumors include plasmacytoma, lymphoma, melanoma, sarcoma or unclassified tumors.

Glioblastoma is still clinically classified according to Kernohan's four grades: Grade ⅰ: tumor cells are uniform in size, shape and staining, well differentiated and benign, but the clinical and pathological development tends to be malignant; Grade ⅱ: some tumor cells are different in size, and occasionally tumor cells divide, which is a low-grade malignant tumor; Grade Ⅲ and Ⅳ: The tumor cells have poor differentiation, different sizes, different shapes, deep staining, many mitotic stages and giant cells, which are highly malignant tumors.

The exact cause of this disease is not completely clear.

1. Congenital factors: During embryonic development, primitive cells or tissues remain heterotopic in the cranial cavity, and have the function of differentiation and proliferation under certain conditions, which can develop into intracranial congenital tumors. This kind of tumor grows slowly and is mostly benign, such as craniopharyngioma, lipoma and glial cyst.

2. Genetic factors: human gene defects or mutations can form intracranial tumors. Multiple neurofibroma is the most typical representative of nervous system tumor, and it is an autosomal dominant genetic tumor. About half of the patients have a family history. Retinoblastoma is autosomal dominant, with single focus accounting for 3/4 and somatic mutation, and about 12% ~ 17% can be passed on to offspring. Multifocal lesions have cell chromosome changes, and other offspring members in the family are likely to be susceptible, and about 50% ~ 65% can be passed on to future generations.

3. Physical factors:

(1) trauma: it is generally believed that trauma can turn the scar tissue of brain and meninges into tumors.

(2) Radiation: It is found that cell mutation in the radiation area is the basis of tumor formation. Most of these tumors are malignant.

4. Chemical factors: The induced tumor can be glioma, meningioma, sarcoma, pituitary adenoma and pineal tumor.

5. Biological factors: Common carcinogenic viruses include adenovirus, sarcoma virus, deoxyribonucleic acid virus, ribonucleic acid virus, polyoma virus and monkey vacuolation virus. These viruses can induce meningioma, pineoma, sarcoma, astrocytoma, glioblastoma, ependymoma, choroid plexus papilloma and medulloblastoma. The tumorigenic mechanism of the virus is that when the virus enters the cell and synthesizes DNA in the nucleus (that is, the S phase of the cell), it quickly attaches to and changes the genetic characteristics of chromosomes, which distorts the cell proliferation and division functions and forms tumors.

clinical picture

It depends on the location, nature and growth rate of brain tumors, and is related to the particularity of brain anatomy and physiology.

How slow the onset is. The first symptom may be increased intracranial pressure or neurolocalization symptoms such as myasthenia, limb numbness and epilepsy. After weeks, months or years, the symptoms get worse and the condition gets worse.

Acute onset can suddenly worsen within a few hours or days, leading to paralysis and coma, which is more common in tumor cystic degeneration, tumor hemorrhage (tumor stroke), highly malignant tumor or metastatic tumor complicated with acute diffuse brain edema, or because the tumor suddenly blocks cerebrospinal fluid circulation, intracranial pressure rises sharply, leading to brain hernia crisis.

1. Increased intracranial pressure: 85%.

(1) Reason:

1. tumor occupying effect: the tumor grows expansively or infiltratively in the skull, which exceeds the compensation limit of the cranial cavity (about 8% ~ 10% of the volume of the cranial cavity), that is, the intracranial pressure increases.

2. Obstruction of cerebrospinal fluid circulation pathway: tumor compression or tumor hinders cerebrospinal fluid absorption.

3. Tumors oppress brain tissues and cerebral vessels, affect blood supply, lead to brain metabolism disorder, or stimulate the reaction and toxicity of tumors, especially malignant gliomas and metastatic foreign bodies (such as vascular endothelial growth factor and vascular permeability factor), causing localized or extensive brain edema around tumors.

4. Intracranial venous reflux disorder: The tumor compresses larger veins or sinuses, which can lead to venous reflux disorder and brain tissue congestion.

5. Tumor stroke and degeneration: Acute bleeding (tumor stroke) and cystic degeneration or necrosis of tumor tissue make tumor volume increase rapidly and brain edema suddenly aggravate.

6. Other factors: excessive water intake, repeated vomiting, severe cough or exertion, improper lumbar puncture, lung infection or brain hypoxia caused by high fever can all cause increased intracranial pressure.

(2) Symptoms:

1. Headache: It is mostly caused by the change of intracranial pressure and the direct influence of tumor, and the stimulation of intracranial sensitive structures such as meninges, cerebral vessels, venous sinuses and nerves. As a common early symptom, 90% patients with brain tumors have headaches.

Most of them are pulsating pain or dull pain, paroxysmal or persistent, sometimes light and sometimes heavy. It usually appears in the early morning or after getting up, and gradually relieves during the day. Severe cases may be accompanied by nausea and vomiting, and headache can be relieved after vomiting. Any factor that causes increased intracranial pressure, such as coughing, sneezing or strenuous exercise, will aggravate the headache.

Some parts of brain tumors can cause headaches with certain regularity. For example, meningiomas often cause headaches in the corresponding parts; Pituitary adenoma is mostly bilateral temporal or frontal headache; The headache of infratentorial tumor is often located in occipital neck and orbital forehead; Intracranial tumors can cause severe increase in intracranial pressure due to tumor position shift and head position change, resulting in paroxysmal severe and unbearable headache. In severe cases, intracranial hypertension crisis may occur.

2. Nausea and vomiting: Early or initial symptoms, mostly accompanied by headache and dizziness. It often occurs on an empty stomach in the morning, and is typically manifested as nausea or jet vomiting unrelated to diet. It often occurs after severe headache and dizziness, which can induce or aggravate head position changes. Vomiting occurs early and frequently in children with posterior cranial fossa tumor, which is easily misdiagnosed as gastrointestinal diseases. Vomiting in adults occurs later. Nausea and vomiting are caused by increased intracranial pressure or tumor directly affecting vagus nerve nucleus (vomiting center).

3. Papillary edema and visual impairment: It is related to the location, nature and course of brain tumor. For example, tumors in the posterior cranial fossa appear early and seriously, and tumors in the cerebral hemisphere appear later and lighter than those in the posterior cranial fossa, while malignant tumors generally appear early, develop quickly and seriously.

It can evolve into secondary optic atrophy, and vision gradually declines. The physiological blind spot is enlarged, the visual field is centripetal narrowed, and the optic papilla is secondary atrophy. Long-term intracranial hypertension often leads to blindness.

Ocular abduction paralysis is usually a sign of increased intracranial pressure, which may lead to strabismus and diplopia.

4. Mental symptoms: caused by cerebral cortex damage, manifested as indifference, dullness, decreased thinking and memory, personality and behavior changes, and then developed into lethargy, obscurity or unconsciousness. In patients with malignant tumors, mental disorders are more obvious. Frontal tumors often cause mental symptoms, or show euphoria, excitement and dementia.

5. Epilepsy: 20% ~ 30%, half of which is the first symptom.

6. Changes of vital signs: If the intracranial pressure rises slowly, most of the vital signs will remain unchanged. A significant or sharp increase in intracranial pressure can indicate bradycardia, usually as slow as 50 beats/min, accompanied by deep breathing and compensatory increase in blood pressure. These are all manifestations of pre-cerebral hernia or existing cerebral hernia. If it continues to deteriorate, there will be rapid pulse, irregular breathing, sobbing or tidal breathing, low blood pressure and systemic circulation failure, and finally breathing will stop. Tumors or malignant tumors in the hypothalamus and ventricles can cause fluctuations in body temperature, which often rises.

Second, the signs of nervous system location: it is the manifestation of brain, nerve and blood vessel damage at the tumor site, reflecting the location of brain tumors.

Third, endocrine and systemic symptoms.

diagnose

1. History and physical examination.

2. Head X-ray examination:

3. Lumbar puncture and cerebrospinal fluid examination: including cerebrospinal fluid pressure, cell count, protein and biochemical determination.

4. Ultrasonic examination of the head.

5. EEG examination: about 90% of brain tumors can have EEG abnormalities.

6. Brainstem auditory evoked potential: The change of cerebral cortical potential recorded from bilateral scalp after cochlear short sound stimulation, which comes from brainstem auditory pathway, so it is called brainstem auditory evoked potential. Clinically, it can be used to objectively evaluate the site of brain stem dysfunction and early diagnose brain stem tumor, acoustic neuroma or cerebellopontine angle meningioma according to the peak condition.

7. Biochemical and immunoassay:

8. Cerebral angiography:

9. Ventriculography: a method of directly puncturing the lateral ventricle by drilling holes in the skull and injecting gas or contrast agent (such as lipiodol and iodobenzene meglumine) into the ventricle to show the ventricular system. Because of the occupying effect of intracranial tumors, the corresponding ventricles and subarachnoid space are often compressed, which makes them deformed, displaced or blocked. According to these changes, it is often possible to make a localized diagnosis of intracranial tumors.

10. CT and MRI scans of the head.

treat cordially

1. surgical treatment: the most basic treatment for intracranial tumors at present. Principle: a. Physiological permission; B. anatomically accessible; C. technically feasible; D. the gains outweigh the losses, and the advantages outweigh the disadvantages.

(1) complete resection

(2) subtotal resection and partial resection

(3) Decompression and cerebrospinal fluid shunt.

2. Radiotherapy: 60 cobalt, linear accelerator or high-energy X-ray.

Principle: When rays pass through tissues, they transfer energy to tissues and cells, and the nucleus is extremely sensitive to radiation. Through the direct or indirect action of free radicals, radiation changes the structure of DNA, leading to the breakage of single-stranded and double-stranded DNA, leading to degeneration and death of irradiated tissues and cells. Cell division and differentiation are important factors affecting the sensitivity of cells to radiation. The lower the degree of differentiation, the more active the division, and the more sensitive the tissue cells are to radiation. Most brain malignant tumor cells have low differentiation and active proliferation, so they are highly sensitive to radiation, which is an important basis for radiotherapy of brain tumors. The damage of tissues and cells after irradiation can be divided into potentially fatal injury, sub-fatal injury and fatal injury, in which potentially fatal injury and sub-fatal injury can be repaired under certain conditions.

3. Chemotherapy: After birth, nerve cells no longer divide, glial cells only regenerate to a low degree, while brain tumor cells continue to divide. The difference between the growth and reproduction of these cells enables antimetabolic or mitotic drugs to inhibit or kill tumor cells without damaging normal nerve cells and glial cells. Chemotherapy for brain tumors requires several conditions:

(1) Tumor blood vessels are relatively abundant and capillary permeability is relatively high;

(2) Chemotherapeutic drugs easily penetrate the blood-cerebrospinal fluid barrier;

(3) Chemotherapy drugs can effectively kill or inhibit tumor cells;

(4) Choose effective methods to make tumor cells in the environment of high concentration of chemotherapy drugs.

4. Hormone therapy:

(1) In order to relieve brain edema, dexamethasone 10 ~ 20 mg/d is usually given intravenously.

(2) Pituitary adenoma or craniopharyngioma as compensatory therapy of endocrine hormones;

(3) Diabetes insipidus occurred after sellar region tumor operation and was treated with pituitrin or long-acting diabetes insipidus injection.

5. Immunotherapy: active or passive immune means. Surgical resection and radiotherapy and chemotherapy should be performed before treatment to reduce the tumor load of the host and maximize the relative immunity of the body.

6. Chinese medicine treatment.