What Factors Affect a Brain Tumor Prognosis?

Intracranial tumors, also known as brain tumors and craniocerebral tumors, refer to tumors of the nervous system that occur in the cranial cavity, including tumors originating from neuroepithelium, peripheral nerves, meninges and germ cells, lymphoid and hematopoietic tissue tumors, and skulls in the sphenoidal region Pharyngeal tumors and granulosa cell tumors, as well as metastatic tumors.

Basic Information

nickname: Brain tumor
English name: intracranialtumors
English alias: cerebroma

Visiting department: Oncology
Multiple groups: 20 to 50 men
Common locations: Intracranial
Contagious: no

Classification of intracranial tumors

1. According to their origin, they can be divided into primary intracranial tumors (tumors originating from intracranial tissues) and secondary intracranial tumors (metastasis metastasized from distant parts of the body or extending from adjacent parts into the skull).

2. According to their biological behavior, they can be divided into benign intracranial tumors and malignant intracranial tumors.

Causes of intracranial tumors

Environmental factor

Includes physical, chemical, and biological factors such as ionizing rays (such as X-rays) and non-ionic rays (such as radio frequency waves and low-frequency electromagnetic fields), pesticides, benzene and other organic solvents, nitrosamine compounds, tumor-causing viruses, and other infections Factors, etc., some of them are inconclusive. The oncogenic viruses that have been basically identified are mainly human papilloma vacuole virus type JC (high-grade astrocytoma, cerebellar medulloblastoma), EB virus (central nervous system lymphoma), and human adenovirus (embryonic tumors). , Such as neuroblastoma, medulloblastoma, myeloid epithelioma, or optic neuroblastoma), SV40 virus (intracranial sarcoma tumor).

Host factor

Including the host's medical history, personal history, family history, etc. For example, the risk of meningiomas in head trauma is increased. Tuberculosis can be associated with glioma. Toxoplasma gondii infection is related to the onset of astrocytomas and meningiomas. 60% to 85% of patients with central nervous system malignant lymphoma Patients with AIDS or organ transplants, female hormones may be related to the occurrence and development of certain tumors (such as meningioma). The occurrence of certain brain tumors has a family background or genetic factors (such as neurofibromatosis type and , and (Arthrosclerosis, Li-Fraumeni syndrome, Cowden syndrome, vonHippel-Lindau disease, Turcot syndrome and Gorlin syndrome).

Intracranial tumor examination

Medical history and neurological examination are still the most important basic evidence for the diagnosis of intracranial disease.

Medical history

If patients have typical headaches, epilepsy, non-specific cognitive or personality changes, or intracranial tumors when typical intracranial pressure increases and localized signs are present, they should be asked if they have a history of otitis media or other infections, a history of tuberculosis, parasitism History of worms, head trauma, and cancer of other organs to distinguish them from inflammation and other intracranial non-tumor diseases.

2. Symptoms and signs

It can be caused by the tumor itself, or it can be caused by tumor-related secondary factors (peritumor edema, hydrocephalus, displacement of important structures in the skull, etc.); the appearance and progression of symptoms and signs are related to the tumor location and pathological properties.

(1) General symptoms and signs : Occupation effect of brain tumor itself and volume of cranial contents exceeds the limit of physiological regulation during cerebral edema, or obstruction of hydrocephalus caused by tumor close to cerebrospinal fluid circulation, or obstruction of venous return caused by compression of sinus To. Mainly can be: headaches are mostly episodic, progressive headaches, heavy in the morning or sleep, often aggravated by exertion, sneezing, coughing, bowing or stool, and can temporarily relieve or disappear after sitting, standing or vomiting. Vomiting often occurs in severe headaches, and it is easy to occur in the morning. Visual impairment is mainly papillary edema and vision loss. Dizziness, dizziness, dizziness (feeling out of balance), and dizziness (rotating around), the most common are tumors in the posterior cranial fossa. Seizures Epilepsy can occur in about 30% of brain tumors. Epilepsy caused by increased intracranial pressure is usually a large seizure, and focal seizures are often localized. Diplopia . Mental and conscious disturbances are manifested as indifferent, unresponsive, slow thinking, indifferent to external things, reduced activity, memory loss, disorientation, etc. A few have obsessive-compulsive disorder, schizophrenia or psychomotor episodes, and late-stage drowsiness and coma And other disorders of consciousness. Head enlargement Infants' anterior palate bulges, head and tail enlargement, and cranial suture separation. Percussion cracks (Macewen sign). Changes in vital signs such as increased blood pressure, slowed pulse, and irregular breathing (Chyne-Stroke breathing).

(2) Localized signs It is generally considered that the first signs that appear are particularly significant. The temporal lobe and anterior part of the frontal lobe in the non-dominant hemisphere are "silent zones" or "quiet zones", without obvious signs.

1) Frontal tumors often have mental symptoms, manifested by changes in thinking, emotion, intelligence, consciousness, personality, and memory, often euphoria, indifference to the condition, indifference, loneliness, poor orientation, memory loss, unrestricted appearance, Do not like cleanliness, decreased behavior, etc .; hemiparalysis, central facial paralysis, and pyramidal tract signs of contralateral limbs with varying degrees of involvement in the central anterior gyrus; motor aphasia in the Broca area; Inability to fix laterally, with strong grip and groping reflex on the opposite side; tumors near the central anterior gyrus can produce localized epilepsy; frontal-pontine tract involvement can present frontal ataxia, manifested as erect and walking disorders; frontal Compression of the olfactory nerve on the underside of the lobe can cause unilateral or bilateral olfactory disturbances. Compression of the optic nerve can cause ipsilateral optic nerve atrophy and contralateral optic papillary edema (Foster-Kennedy syndrome); damage to the lateral central lobules can cause spastic paralysis of the lower limbs, size Discomfort.

2) Parietal tumors can develop contralateral deep and shallow sensory and cortical sensory disturbances, or limited sensory epilepsy; involvement of the left angular gyrus and superior marginal gyrus can cause aphasia, miscalculation, misuse, indistinguishable left and right, and finger misrecognition ( Gerstmann syndrome); deep parietal tumors involving visual radiation can be blinded in the contralateral (same) quadrant.

3) Tumors in the posterior temporal lobe can cause contralateral hemianopia or upper 1/4 quadrant blindness, central visual field involvement, hallucinations in the two eyes; tumors in the medial temporal lobe can cause temporal lobe epilepsy, often with mental symptoms such as irritability, Funny and aggressive; affected island leaves can cause chest, upper abdomen, and visceral pain, which can be a precursor to epilepsy, and can also be accompanied by autonomic symptoms such as drooling, sweating and dyspnea, and heartbeat changes; involvement of the left superior temporal gyrus can Produce sensory aphasia.

4) The occipital tumor is isotropically blind, but the central visual field is preserved (macular avoidance), and there may be flashes, colors and other hallucinations.

5) Hemi oval center, basal ganglia, thalamus and corpus callosum tumors involved in the front part of the semi-oval center cause spasm paralysis of the contralateral limbs; hemiplegia in the inner capsule affected; muscle rigidity and slow movement of the contralateral limbs involved in extrapyramidal involvement , Tremor, or various forms of hyperkinesia; corpus callosum tumors can manifest as apathy, drowsiness, memory loss, and left-hand apraxia (right-handed); thalamus tumors exhibit contralateral sensory disturbances, persistent severe pain (thalamic pain) .

6) Sphenoid saddle tumors are mainly manifested as endocrine disorders and optic nerve and optic cross compression; secretory pituitary tumors are clinical syndromes caused by excessive secretion of the corresponding hormones (amenorrhea-galactorrhea-infertility, giant disease or Acromegaly, Cushing's disease); non-secretory pituitary adenomas or other sphenoidal tumors cause hypopituitarism, with sexual dysfunction and stunting being the most prominent; larger tumors may have vision loss and primary optic nerve atrophy And different types of visual field defects, especially double temporal hemianopia.

7) In the front of the third ventricle tumor , there may be changes in vision, visual field, and fundus caused by compression of the optic nerve and optic cross, insipidus insipidus, obesity, sexual dysfunction, and drowsiness caused by hypothalamic insufficiency. Compression of the body causes Parinaud syndrome (hyperopia in both eyes, pupils' dull or disappeared light reflection), hearing loss in both ears; ataxia in cerebellar involvement.

8) When the fourth ventricle tumor changes position, the fourth ventricle is blocked due to tumor drift in the fourth ventricle, causing severe headache, dizziness and vomiting (Bruns sign).

9) Cerebellar tumors can produce forced head position, nystagmus, ataxia on the affected limb (mainly the trunk is the main part, especially the lower extremities) and decreased muscle tone; cerebellar convulsions (ie, tonic seizures) occur in the later stage, It manifests as paroxysmal back-to-back, stiff limbs with a reflexed angled bow.

10) Cerebellar pontine cerebellar horn tumors often have hearing impairment and vestibular dysfunction; tinnitus and dizziness appear early, progressive hearing loss, facial sensory disturbances, peripheral facial paralysis, cerebellar damage, and hoarseness, difficulty swallowing, and Pyramid tract sign and limb sensory disturbance.

11) Brainstem tumors Intramedullary tumors in the brainstem on one side of the brain stem cause paralysis (ipsilateral cranial nerve palsy and contralateral limb sensory and motor long conduction beam damage); midbrain tumors cause binocular dyskinesia, paroxysmal consciousness, etc .; Pedestrian tumors cause unilateral or bilateral abductor nerve palsy, peripheral facial paralysis, facial sensory disturbances, and contralateral or bilateral long bundle signs; medullary tumors exhibit hoarseness, coughing with drinking water, disappearance of pharyngeal reflexes, and bilateral long bundle signs; And midbrain tumors can also cause involuntary laughter, difficulty urinating, and sweating easily.

(3) Pseudo-localized signs refer to signs of damage to brain tissues and nerves in the vicinity and distant parts of the tumor (such as the expansion of the third ventricle to oppress the intersection of the eyes and cause bilateral temporal hemianopia) due to tumor compression, cerebral edema, and cerebral blood circulation disorders .

Intracranial tumor examination

Physical examination

(1) General examinations include subcutaneous nodules, lymphadenopathy, cutaneous nevus, pigmentation, head scars, bulges, tenderness, anger and murmurs of blood vessels in the head and neck.

(2) Special examination of saddle tumors for vision, visual field, fundus, CPA tumors for hearing and vestibular function, pituitary tumors for endocrine examination.

2. Lumbar puncture

Lumbar puncture is forbidden for those with significant increase in intracranial pressure, especially for posterior cranial fossa tumors.

Should also be cautious for a few symptoms that are atypical, and difficult to distinguish from intracranial inflammation or bleeding.

Tumors located in the ventricle or protruding into the subarachnoid space may have high protein and tumor cells.

3. EEG

Cerebral hemisphere tumors are mostly local slow wave, local low voltage or flat wave, and lazy slow wave phase inversion.

Extensive slow waves may be caused by tumors in the deep or midline, or by metabolic causes.

Electroencephalography can be used for intraoperative monitoring to protect functional areas and nerves, and for intraoperative cortical epilepsy.

4. Neuroimaging

(1) Skull plain radiographs Increased intracranial pressure signs include increased cerebral backpressure traces, atrophy and decalcification of the saddle and posterior bed, mild enlargement of the cranial cavity, and separation of bone sutures; calcification of the pineal gland shifts. Tumor calcifications such as meningiomas, craniopharyngiomas, chordomas, oligodendroglioma, and some astrocytomas. Others such as bone damage or bone hyperplasia caused by meningiomas, bone damage caused by metastases, enlargement of the inner auditory canal of vestibular nerve Schwann cell tumor, enlargement of the sphenoidal adenoma of pituitary adenoma, or localized saddle base destruction.

(2) Cerebral angiography Evaluate the relationship between tumor and important blood vessels before surgery. Determine the degree of compression of the sinus and the openness of the sinus by extramedullary tumors (such as meningiomas). Vascular lesions or tumors with abundant blood supply can show and / or embolize the supplying arteries. Excluding vascular malformations and aneurysms in patients with bleeding.

(3) CT Generally, tumors with a diameter of more than 3mm can be found, showing good effects of calcification, bones, fats and fluids. It is helpful to understand the relationship between tumors and the ventricle, cistern, dura and skull. After enhancement, you can understand the tumor's effect on blood -Cerebrospinal fluid barrier disruption and tumor blood supply. Coronal and sagittal reconstruction, three-dimensional imaging, segmental imaging, and CT angiography of spiral CT are more effective. Tumors of the same density, small volume, without peritumoral edema, and without obvious space occupying effects may be missed on CT. direct signs, including tumor density, location, size, shape, number and edges, with or without necrosis, cystic changes, bleeding, calcification and enhancement. Indirect signs, including edema around the tumor, space occupying manifestations (stenosis, deformation, and displacement of the ventricle, cistern, and sulcus), bone changes (bone hyperplasia and destruction of meningiomas, enlargement and destruction of the papillary saddles) , Inner auditory canal enlargement of vestibular nerve Schwannoma) and soft tissue mass.

(4) Magnetic resonance imaging generally requires first scanning and then enhanced scanning. Tumor location : The extra-parenchymal tumor of the brain is close to the inner surface of the skull, the adjacent brain tissue is compressed and the boundary with the tumor is clear. The adjacent subarachnoid space or brain pool is widened, and there may be adjacent bone changes. Tumor signals Most tumors are long T ₁ low signals and long T ₂ high signals. Lipomas, craniopharyngiomas, and gelatinous cysts can be T ₁ WI high signals, and teratoma T ₁ WI high and low mixed signals. ; Uniform signal intensity is mostly benign tumors, and unevenness is mostly malignant tumors. The morphology of the tumor was a convex meningioma with a spherical shape, a skull base meningioma with a disk shape, a Schwann cell tumor with a dumbbell shape, and a lipoma with a strip shape. The edge of the tumor . The structure and structure of the tumor are mostly benign lesions, and the mixed signals are mostly malignant lesions; calcification, bleeding (MRI is sensitive to small bleeding in the sub-acute period, T ₁ WI is high signal), necrosis, cystic change Cystic changes are more common in malignancies) and can make the signal uneven. The number of tumors Multiple meningiomas and bilateral acoustic neuromas are often associated with hereditary neurotumor syndromes. Different locations and different sizes of parenchymal lesions often indicate metastatic tumors. The presence or absence of the enhancement of the tumor indicates whether the blood-brain barrier has been damaged and the extent of the damage, and the blood supply of the tumor; the extent of the enhancement does not necessarily indicate the actual size of the tumor, especially the invasive growth in the brain Tumors; meningiomas and Schwann cell tumors outside the brain parenchyma often increase significantly. MRI The MRI of edema around the tumor shows better edema than CT; T ₁ WI is low signal and T ₂ WI is high signal. Malignant glioma edema is often obvious and can affect the contralateral hemisphere through the corpus callosum; metastatic tumors often cause obvious edema . Placeholder effect . Secondary changes .

(5) Magnetic resonance functional imaging and metabolic imaging Diffusion imaging can distinguish postoperative tumor residue and edema (high signal of glioma, low signal of peritumoral edema). Perfusion imaging was used to measure blood flow in the tumor, and malignant tumor had high blood flow. Magnetic resonance spectroscopy can grade gliomas, and judge their recurrence, residual and postoperative scar.

(6) Nuclear nuclear medicine examination Positron emission tomography (PET) can be used to diagnose brain tumors and distinguish between benign (low metabolism) or malignant (high metabolism) tumors, residual tumors (high metabolism) or scars (low metabolism) To determine the tumor boundary. Single photon emission tomography (SPECT) judges whether the tumor is active and malignant, distinguishes the tumor as meningiomas, Schwann cell tumor or brain parenchymal tumor, and distinguishes tumor recurrence and radiation necrosis.

5. Evoked potential

It is used for tumor diagnosis (the brainstem evoked potentials of vestibular nerve Schwann cell tumors show prolonged interwave latency of waves and ) and intraoperative nerve function monitoring.

6. Laboratory inspection

Mainly through the detection of tumor markers (high sensitivity and specificity) such as proteins, enzymes, nucleic acids or metabolites in body fluids for qualitative diagnosis and assessment of treatment (predicting recurrence).

(1) Germ cell tumor The normal value of alpha-fetoprotein (AFP) plasma is <40ng / ml, which can be elevated in intracranial germ cell tumors, endodermal sinus tumors, embryonic cancers, and mixed germ cell tumors. - chorionic gonadotropin (-HCG) normal plasma <2ng / ml, normal cerebrospinal fluid <0.2ng / ml, can increase in chorionic epithelial cancer, liver cancer, lung adenocarcinoma, malignant melanoma and metastases high. Normal cerebrospinal fluid examination can not completely exclude the diagnosis of germ cell tumors due to normal plasma values. Obtaining cerebrospinal fluid through lumbar puncture is the standard method for tumor diagnosis and monitoring.

(2) Metastatic tumors of the brain and meningiomas The ratio of lactate dehydrogenase (LDH) isoenzymes in the cerebrospinal fluid, LDH1 / LDH2 <1, indicates that brain metastases or meningeal metastases from extracranial tumors are particularly low during meningeal metastases. Elevated levels of carcinoembryonic antigen (CEA) in cerebrospinal fluid (normally <4ng / ml) can be seen in meninges planting of digestive tract, breast, liver, ovary, pancreas and other tumors.

(3) Endocrine examination and test of pituitary function.

(4) Glioma Ganglioside (GD3) is significantly increased in highly malignant gliomas, but it cannot yet be used as a conventional marker of gliomas. The level of TGF- in body fluids (such as urine) of patients with TGF - primary glioma is increased and it is related to the degree of malignancy. Neuroectodermal antigen is specific for the diagnosis of neuroectodermal tumors. The ELISA method of monoclonal antibody G22 found that the antigen level of glioma patients was greater than 0.5 at an optical density of 450 nm, but G22 had cross-reactions with melanoma and lung cancer.

7. Biopsy

Obtaining a biopsy specimen by drilling the skull is called closed biopsy. Stereotactic biopsy combined with CT, MRI, PET, SPECT, and fMRI is a standard biopsy technique. It should be noted that multiple specimens should be taken in different parts to try to Avoid diagnostic errors caused by tumor heterogeneity.

Differential diagnosis of intracranial tumors

Intracranial inflammation

Chronic meningitis can cause extensive skull base adhesions that can cause significant intracranial pressure increases and cerebral palsy. Arachnoiditis can be acute or subacute, and localized cysts can form in chronic cases. Purulent encephalitis (history of chronic otitis media) is similar to low-grade astrocytoma in the acute phase (but with flaky or brain-like enhancement, and the lesion is not limited to white matter), and abscess formation is similar to high-grade astrocytoma (but the wall Thin, uniform, with a sense of tension, no wall nodules, generally more regular); both can be SPECTed by 131I or 201TcHMPAO labeled white blood cells (positive persons are abscesses, but lung metastases often with bacterial infections can be positive, negative (Tumor), magnetic resonance spectroscopy (abscess is an inflammation spectrum without choline, lactic acid, and lipid), MRI diffusion-weighted imaging (cyst or tumor is low signal, high diffusion coefficient, pus is high signal, low diffusion coefficient ). In addition, 90% of patients with cerebral abscesses had faster erythrocyte sedimentation and 77% of C-reactive protein increased.

2. Chronic subdural hematoma

There may be cranial hypertension, mental and conscious disturbances, but the local signs are often not obvious, and the imaging examination can be clear.

3. Cerebral cysticercosis

Combined with medical history, roundworm or subcutaneous nodules, epilepsy, psychiatric symptoms and increased intracranial pressure, blood, cerebrospinal fluid cysticercosis complement test, CT and MRI.

4. Epilepsy

Primary epilepsy usually develops before the age of 20 and has no local signs; local epilepsy in adults with progressively increasing local signs and increased intracranial pressure should be considered in brain tumors.

5. Cerebrovascular disease

Intracranial hemorrhage or necrosis of a small number of intracranial tumors needs to be distinguished from cerebrovascular disease, but cerebrovascular accidents often have hypertension, history of arteriosclerosis, multiple sudden onset, visual papillary edema is rare, and infarcts often have basal direct cortex The triangular low-density area consistent with the distribution of blood vessels, brain gyrus or ring-shaped enhancement can appear at the edge of the infarction after 2 to 3 weeks.

6. Brain contusion

He had a history of trauma, scalp scars, skull fracture lines, CT showed low density of frontal or temporal lobe at 2 to 3 weeks, plaques and enhancement of cerebral gyrus. MRI showed contusion and bleeding in the cerebral cortex.

7. Multiple Sclerosis

It is a common type of demyelination and is characterized by diffuse axonal demyelination and glial hyperplasia. It occurs in the periphery of the ventricle, optic nerve, brain stem, cerebellar white matter, cerebellar horn, spinal cord, and the identification of intracranial tumors. The main points are: more common in young and middle-aged women; remission and recurrence during the course of disease; medical history, physical examination and imaging examination suggest that there are more than two lesions in the white matter of the central nervous system; CT shows a limited low density, new MRI Lesion T ₁ WI is equal or slightly low signal, old lesion T ₁ WI is uniform low signal, T ₂ WI and proton density imaging are uniformly high signal, active lesions can be enhanced, and steroid therapy can reduce the enhanced signal, which is extremely large. Most had no placeholder effect; oligoclonal bands could be separated from IgG by agarose gel electrophoresis after cerebrospinal fluid concentration, and radioimmunoassay was positive for myelin; pseudotumor inflammatory demyelinating gliomas and gliomas were not easy to distinguish, Try methyl Bonitasone experimental treatment or tissue biopsy.

8. mental illness

9. Optic neuritis

There may be visual papillary edema, vision loss and visual field defect, but more eyes are involved, vision loss is obvious and rapidly deteriorated, there may be pain behind the eyes, and it becomes worse when the eyeballs are rotated.

10. Paraneoplastic Syndrome

Non-metastatic distant septum effects of extracranial tumors can cause paraneoplastic syndromes in the central nervous system, which can be seen in breast cancer, ovarian cancer and other tumors. The initial classic manifestation of paraneoplastic cerebellar degeneration is mild ataxia, which may gradually progress to walking inability after weeks or months; early cerebrospinal fluid lymphocytosis, increased protein content, positive IgG and oligoclonal bands, CT and MRI Normal; late stage showed extensive cerebellar atrophy and fourth ventricle enlargement. Plasma containing Yo antibodies was found in patients with breast cancer. Pathological examination revealed that Purkinje cells in the cerebellar granular layer were lost. The anti-Ri syndrome manifests as undulating visual ooclonus, myoclonus, and somatic ataxia, which can be partially resolved spontaneously; early CSF lymphocytes increase, protein increases, CT and MRI are negative, and neurons are present in the plasma Antibodies (Hi antibodies) can react with the nucleus of neurons. Stiff-man syndrome manifests as fluctuating muscle tonics, and most patients have anti-glutamate decarboxylase antibodies.

Intracranial tumor treatment

1. Basic treatment principles

Comprehensive treatment based on surgery, supplemented by symptomatic treatment according to the condition, such as control of high intracranial pressure, application of corticosteroids and antiepileptic drugs, correction of metabolic abnormalities and supportive treatment.

2. Surgical treatment

(1) The surgical methods are classified into direct surgical resection and palliative surgery (internal decompression, external decompression and cerebrospinal fluid shunt).

(2) The principle of surgery is to remove the tumor as much as possible while protecting the integrity and structure of surrounding brain tissue.

(3) Resection method Surgical resection of benign intracranial tumors is almost the only effective treatment method. Malignant tumors should also be removed intensively, but due to their infiltration or located in important functional areas and other areas difficult to reach by surgery, only partial subtotal resections and partial resections can be performed. Resection or biopsy.

(4) Alternative methods and techniques are helpful to significantly improve the surgical resection level and treatment effect of intracranial tumors: Microneurosurgery with the assistance of bipolar electrocoagulation, ultrasonic suction, laser and neuroendoscopy Stereotactic technology and real-time CT / MRI-based neural navigation system for accurate tumor positioning; Electrophysiology and evoked potential technology of the cerebral cortex make it possible to remove tumors in speech or motor cortex under local anesthesia; Otorhinolaryngology, maxillofacial surgery, orthopedics and other multidisciplinary collaborations to deal with skull base tumors.

3. Radiotherapy

(1) A comprehensive radiotherapy plan must be completed by multidisciplinary cooperation such as neurosurgery, neuroimaging, radiation tumor treatment, and radiophysics.

(2) The application scope of intracranial tumor radiotherapy includes preventing recurrence of tumors or dissemination of tumors in the central nervous system and incompletely resected tumors after tumor resection, but it is contraindicated for children under 3 years of age and not suitable for children aged 3 to 6 years who are not suitable for radiotherapy. Radiotherapy can be postponed through chemotherapy to control the disease; tumors suitable for radiotherapy include anaplastic astrocytoma, glioblastoma, ependymal tumor, embryonic tumor, solid pineal tumor, hemangioblastoma, malignant lymphoma Tumors and sarcomas, as well as incompletely resected benign and sub-malignant tumors (such as pituitary adenoma, meningiomas, chordoma, diffuse astrocytoma and oligodendrocyte tumor); medulloblastoma, anaplastic room Membrane tumors, germ cell tumors, etc. should also be considered for whole-brain spinal cord radiotherapy; tumors deep in the brain or involving important structures such as the thalamus, basal ganglia, and brain stem can be treated with radiation alone; tumors that are highly sensitive to radiotherapy (such as germ cells) Tumors, medulloblastomas, malignant lymphomas, or neuroblastomas) can be considered as separate radiotherapy; optic gliomas can also be treated with radiotherapy alone with longer remission; intracranial Multiple metastatic tumors can be considered whole brain irradiation + local irradiation of the lesion.

(3) Commonly used radiotherapy methods are: conventional segmented radiotherapy. Traditionally, 60Co or linear accelerator is used for whole brain plus local contraction field supplemental irradiation. Unconventional fractionated radiotherapy is only used for rapid radiotherapy of glioblastoma with age> 70 years and poor prognosis. It can be divided into three types: hyperfractionated radiation therapy, accelerated fractionation therapy and less fractionated radiation therapy. Interstitial brachytherapy is generally suitable for primary or metastatic tumors on the screen. CT examination shows that the lesions are more limited, the border is obvious, and the diameter is less than 6cm. Stereotactic radiosurgery is suitable for tumors with intracranial lesions less than 3.0 to 3.5 cm in diameter, which are difficult to achieve with conventional surgery or cannot be controlled with conventional radiotherapy. The dose range is 15 to 20 Gy.

4. Chemotherapy

The current extension of the concept of chemotherapy has been extended to cytotoxic agents, anti-angiogenic drugs, cell differentiation-promoting drugs, anti-invasive drugs and cell signal transduction regulators. Chemotherapy should be started as early as possible after surgery, and chemotherapy or both should be used before postoperative radiotherapy. Drugs with high fat solubility, small molecular weight, non-ionization, short action time, ability to pass the blood-cerebrospinal fluid barrier, and low toxicity to normal brain tissue are suitable for the treatment of intracranial tumors.

Temozolomide (TMZ), a representative new chemotherapeutic drug for brain tumors, is currently being treated for 5 consecutive days, with 28 days as a cycle. It is mainly used to treat glioblastoma (the objective effective rate is 22% to 29%) and Advanced malignant melanoma has the advantages of a broad antitumor spectrum, oral administration, rapid and complete absorption, easy penetration of the blood-brain barrier, no additional toxicity with other drugs, and can be used in patients with resistance to nitrosourea. The common side effects are Malignant, vomiting, bone marrow suppression occurs when the oral dose is greater than 1200 mg / m2.

5. Other adjuvant treatments

(1) Immunotherapy Monoclonal antibody-directed therapy; Application of autologous lymphocyte-activated killer cells (LAK) and interleukin-2 (IL-2), or tumor infiltrating lymphocytes (TIL) to stimulate anti-tumor immunity; application Interferon; Preparation of various tumor vaccines. Use local microwave or radio frequency heating treatment.

(2) Photodynamic therapy uses the photosensitizer Hematoporphyrin Derivative (HPD) to be selectively taken up and retained by tumors. HPD is injected intravenously within 4 to 24 hours before surgery, to keep away from light, and to be removed during craniotomy After the tumor was irradiated with the laser cavity.

(3) Gene therapy Inhibit the malignant proliferation of glial cells; Promote the differentiation of glial cells; Induce tumor cell apoptosis; Promote anti-tumor immunity; Reduce the microinvasiveness of gliomas; Inhibit tumor blood vessels Formation and proliferation; inhibit the expression of resistance genes; increase sensitivity to radiation therapy and tolerance to chemotherapy.

Intracranial tumor follow-up

1. Intensive MRI or CT examination within 48 hours after tumor resection to determine the extent of tumor resection.

2. After receiving adjuvant treatment such as radiotherapy or chemotherapy, intensive MRI or CT examination should be performed for 1 month, and standardized neurological examination and neuroimaging should be performed every 3 months during the follow-up period.

3. The use of imaging methods to determine the efficacy can refer to WHO's recent objective evaluation criteria for solid tumors.

4. Complete remission is the complete disappearance of all visible lesions and maintained for at least 4 weeks.

5. Partial remission is a reduction of the product of the maximum diameter of the tumor lesion and its maximum vertical diameter by more than 50% and maintained for more than 4 weeks.

6. Stability means that the product of the two diameters of the tumor lesion decreases by <50%, or increases by <25%, and no new lesion appears.

7. Progression means that the product of the two diameters of the tumor lesion is reduced by> 50%, or a new lesion appears.

8. The quality of life of patients can be measured by the Karnofsky scoring standard. After the end of the treatment, the increase in the Karnofsky score of 10 points compared with that before treatment is the improvement of the quality of life; the reduction of 10 points is the decrease in the quality of life; the unchanged is stable.

Prognosis of intracranial tumor

Factors that may be related to the prognosis of intracranial tumors include patient age, speed of disease progression, preoperative neurological symptoms and Karnofsky score, tumor location, complete surgical resection, pathological category and histological manifestation of tumor, and tumor proliferation index.