bubble_chart Overview

Intracranial space-occupying lesion (intracranial occupying space lesion) is a general term for a group of diseases that occupy a certain space within the cranial cavity. Clinically, it is characterized by increased intracranial pressure (i.e., adult intracranial pressure >1.96 kPa or 200 mmH₂O) and focal neurological damage, with intracranial tumors, brain abscesses, etc., being common.

bubble_chart Etiology

Common disease causes include:

1. Intracranial tumors are divided into primary and metastatic types:
   1. Primary intracranial tumors commonly include gliomas, meningiomas, neurofibromas, and pituitary adenomas.
   2. Metastatic tumors often originate from the lungs, breasts, stomach, prostate, etc., with lung cancer metastases being the most frequent.
2. Brain abscesses mainly result from chronic otitis media or mastoiditis.
3. Intracranial hematomas include spontaneous or traumatic bleeding.
4. Cerebral parasitic diseases refer to conditions like cysticercosis and echinococcosis.
5. Intracranial granulomas can be tuberculous, bacterial, or parasitic.

The cranial cavity is considered a closed structure, primarily containing blood (2–11%), cerebrospinal fluid (10%), and brain tissue (80%). The total volume and proportions of these three components are relatively constant. An increase in one component necessitates a compensatory decrease in the others, but this adjustment has limits. In the initial stage [first stage], the disease has some compensatory capacity, and intracranial pressure elevation is not significant. However, as the lesion expands beyond compensatory limits, intracranial pressure rises rapidly, eventually leading to brain tissue displacement, herniation, and life-threatening conditions. Due to infiltration and compression by the lesion, brain cells are damaged, resulting in focal neurological dysfunction.

bubble_chart Clinical Manifestations

The onset is generally slow and progressively worsens. The main manifestations are symptoms of increased intracranial pressure and focal symptoms.

(1) Symptoms of increased intracranial pressure, namely the three main signs: headache, vomiting, and papilledema.

1. Headache is one of the primary symptoms of increased intracranial pressure, occurring in about 80–90% of cases. It is caused by the traction and distortion of the brain membranes, blood vessels, and nerves due to elevated intracranial pressure. The headache is persistent, progressively worsening with paroxysmal exacerbations, aggravated by factors that increase intracranial pressure (such as coughing, bowel movements, exertion, etc.). It is more severe from midnight to early morning and alleviates in the afternoon. Headaches caused by hemispheric lesions are milder, while those caused by posterior fossa lesions are more severe. When the headache is intense, it is often accompanied by vomiting. In children, due to unfused cranial sutures, headaches are often not obvious.
2. Vomiting is triggered by stimulation of the vagus nerve roots and nuclei. It often occurs in the early morning when the headache is severe, presenting as projectile vomiting unrelated to eating. After vomiting, the headache may lessen. In children, frequent vomiting is often the sole symptom of increased intracranial pressure and can be misdiagnosed as a gastrointestinal disorder.
3. Papilledema is a characteristic sign of increased intracranial pressure. In the late stage [third stage], optic nerve atrophy may occur, leading to visual impairment.
4. False localizing signs, such as bilateral abducens nerve palsy, diplopia, and hemiplegia on the affected side, are caused by the compression and traction of neural structures due to increased intracranial pressure. These signs have no localizing value and are thus termed false localizing signs.

(2) Focal symptoms (localizing signs)

1. Frontal lobe (1) Psychiatric symptoms and progressive cognitive impairment are characteristic features of frontal lobe lesions. Patients exhibit reduced intelligence, apathy, sluggish responses, disheveled clothing, untidiness, and inappropriate urination or defecation. (2) Motor disturbances, manifesting as contralateral focal epilepsy or contralateral monoplegia or mild hemiplegia. (3) Motor aphasia, caused by damage to the left (dominant) hemisphere. (4) Frontal lobe ataxia. (5) Grasping and groping reflexes, as well as conjugate deviation, are also common symptoms of the frontal lobe. Lesions at the base of the frontal lobe may present with ipsilateral optic nerve atrophy and contralateral papilledema, known as Foster-Kennedy syndrome.
2. Parietal lobe (1) Primarily sensory disturbances. If the lesion is irritative, it may cause contralateral focal sensory epilepsy; if destructive, it may lead to contralateral limb cortical complex sensory disturbances. (2) Lesions in the dominant parietal lobe often cause alexia, agraphia, finger agnosia, and left-right disorientation, collectively termed Gerstmann syndrome. Non-dominant lobe lesions may result in hemiplegic unawareness, hemiplegic inattention, and loss of limb sensation, among other body schema disturbances.
3. Temporal lobe (1) Uncinate fits: episodic involuntary chewing, swallowing, olfactory hallucinations, or gustatory hallucinations. (2) Psychomotor epilepsy: manifests as automatisms, memory disturbances, and emotional disturbances. (3) Sensory aphasia and visual field changes (contralateral homonymous hemianopia or quadrantanopia).
4. Occipital lobe Primarily manifests as visual disturbances, which may present as contralateral homonymous hemianopia or epileptic seizures preceded by visual hallucinations.
5. Brainstem Presents with classic crossed sensory disturbances and/or crossed motor disturbances.
6. Cerebellum The main symptom is ataxia. Cerebellar hemisphere lesions cause ipsilateral limb ataxia, while vermis lesions primarily result in truncal ataxia, with the lower limbs more severely affected.
7. Cerebellopontine angle lesions involve cranial nerves V, VII, and VIII, along with cerebellar symptoms. Acoustic neuroma is the most common lesion in this region.
8. Sellar region Causes compression of the optic chiasm and endocrine symptoms, presenting as bitemporal hemianopia, decreased vision, and primary optic nerve atrophy. Endocrine changes may lead to acromegaly or gigantism, adrenal cortical hyperfunction, etc., commonly seen in pituitary adenomas and craniopharyngiomas.

(3) Clinical manifestations of brain herniation In the advanced stage of the disease, severe increased intracranial pressure can cause brain tissue displacement, leading to brain herniation, which is life-threatening. Hence, it is also termed an intracranial hypertension crisis.

1. Tentorial herniation caused by hemispheric mass lesions or sexually transmitted disease can displace the uncus of the temporal lobe into the tentorial notch, compressing the midbrain and oculomotor nerve, also known as uncal herniation. Initial manifestations include ipsilateral pupillary constriction followed by dilation, elevated blood pressure, slowed respiration and pulse, and contralateral hemiplegia. Further progression may lead to decerebrate rigidity, respiratory failure, unconsciousness, and cardiac arrest.
2. Occipital bone foramen magnum herniation is often caused by space-occupying lesions in the posterior cranial fossa, which push the cerebellar tonsils into the occipital bone foramen magnum, also known as cerebellar tonsillar herniation. It compresses the medulla oblongata, manifesting as elevated blood pressure, slowed pulse and respiration, unconsciousness, bilateral pupil dilation, cessation of breathing first, and ultimately cardiac arrest.

bubble_chart Auxiliary Examination

1. The principle of cerebrospinal fluid examination is contraindicated to avoid inducing cerebral herniation. If examination is necessary, it should be performed carefully with a small sample taken, and intracranial pressure-lowering drugs should be administered post-procedure.
2. Type A ultrasound examination can detect whether the midline wave has shifted.
3. Electroencephalography or brain topographic mapping can assist in lateralization and localization.
4. Radiological examinations: (1) Skull X-ray plain films may show signs of increased intracranial pressure, such as decalcification of the dorsum sellae and posterior clinoid processes, increased convolutional markings, and separation of cranial sutures. Additionally, characteristic changes of some tumors can be observed, such as internal auditory canal enlargement in acoustic neuroma and sellar enlargement or destruction in pituitary tumors. (2) Cerebral angiography or ventriculography has definitive diagnostic value and is an important examination method. (3) CT and magnetic resonance imaging (MRI) examinations have extremely high diagnostic value. These methods are safe, rapid, and accurate, capable of detecting tumors smaller than 2 cm.
5. Radioisotope examination, generation and transformation, and endocrine tests are all helpful for diagnosis.

bubble_chart Diagnosis

1. The onset is insidious, presenting with progressive intracranial hypertension, with headache, vomiting, and papilledema as the main symptoms.
2. There are focal neurological localization signs.
3. Auxiliary examinations such as angiography, ventriculography, or CT confirm the presence of space-occupying lesions.

bubble_chart Treatment Measures

1. Disease cause Treatment: Primarily surgical treatment, supplemented by various targeted therapies. For example, brain abscesses can be treated with puncture and pus aspiration or surgical excision, along with high-dose broad-spectrum antibiotics. After tumor removal, chemotherapy or radiation therapy may be administered.
2. Symptomatic treatment: Temporary relief of symptoms, such as decompression or ventricular drainage, and treatment of epileptic seizures. To reduce intracranial pressure, 20% mannitol, 10% glycerol, diuretics, etc., can be used.
3. Treatment of brain herniation
   1. Use dehydrating agents (see treatment for cerebral hemorrhage).
   2. Ventricular puncture and drainage is a rapid and effective emergency measure. Draining fluid under intracranial pressure monitoring yields better results.
   3. Methods such as hypothermia, ice caps or ice packs, and hibernation therapy can significantly help reduce intracranial pressure, alleviate cerebral edema, and enhance the tolerance of brain cells to hypoxia.
   4. Maintain airway patency and monitor water and electrolyte balance.
   5. Once brain herniation is alleviated, immediate surgical intervention is required to remove the disease cause.

bubble_chart Prognosis

It is related to the nature of the lesion, its location, and the timing of treatment.

bubble_chart Prevention

1. Regular health check-ups are essential for early detection and early treatment.
2. Prompt treatment of otitis media and mastoiditis is necessary.
3. Ensure safe production to prevent accidents and reduce the occurrence of brain injuries.
4. Pay attention to dietary hygiene to prevent certain brain Chinese Taxillus Herb parasitic diseases.

bubble_chart Differentiation

1. Benign intracranial hypertension: Also known as pseudotumor cerebri. There is significant intracranial pressure elevation but no focal signs, commonly seen in middle-aged women. The cause of the disease is unclear, possibly related to endocrine metabolic disorders or infectious toxicity, leading to excessive cerebrospinal fluid production and slow absorption. Follow-up observation is necessary to exclude other diseases causing intracranial hypertension. The prognosis of this condition is relatively good, with possible remission.
2. Cerebrovascular disease: Sudden onset, with intracranial pressure elevation less prominent than space-occupying lesions. In difficult cases, CT scans can be performed. Brain tumors appear as localized high-density shadows, while cerebral hemorrhage shows irregular high-density shadows that may extend into the ventricles and subarachnoid space, aiding differentiation.
3. Posterior fossa and optic chiasm arachnoiditis: Often leads to increased intracranial pressure. Differentiation can be made through ventriculography, cerebrospinal fluid examination, or, if available, CT or MRI scans.
4. Sporadic encephalitis: A small number of sporadic encephalitis patients may present with intracranial hypertension. However, sporadic encephalitis has a more acute onset, prominent generalized brain symptoms, and diffuse high-amplitude slow waves on EEG. CT scans can aid in differentiation.
5. Neurasthenia: No symptoms or signs of intracranial hypertension, and no papilledema, allowing for differentiation. Guanneng Disorder: No symptoms of intracranial hypertension or signs, and no fundus edema, enabling differentiation.