intracranial venous sinus occlusive intracranial hypertension
Introduction
Introduction to intracranial venous sinus occlusive hypertension Idiopathic intracranial hypertension is a group of diseases characterized by high intracranial pressure, normal cerebrospinal fluid test and neuroradiology without intracranial space and hydrocephalus. The main manifestations of patients are no clear cause. Headache and optic disc edema, intracranial venous sinus and venous thrombosis are the main causes of cerebral venous return and cerebrospinal fluid absorption disorder. The result is a cranial hypertension. This particular type of intracranial hypertension is called venous sinus occlusion. basic knowledge Sickness ratio: 0.0001% Susceptible people: no special people Mode of infection: non-infectious Complications: Diabetes insipidus Upper gastrointestinal bleeding
Cause
Etiology of intracranial venous sinus occlusive hypertension
(1) Causes of the disease
Intravenous sinus occlusion is caused by a variety of causes. Chronic otitis media is the most common cause of venous sinus thrombosis. It can also be caused by some systemic diseases, such as extracranial tumors, blood disorders, metabolic disorders, and taking certain drugs. At present, some people think that the disease is related to menstrual disorders, pregnancy, oral contraceptives, hypervitaminosis A and tetracycline, furan drugs, nalidixic acid and corticosteroids. Epidemiological investigation reports that the body is too heavy. The incidence of obese people is higher than that of normal weight. In recent years, with the extensive application of neuroimaging techniques such as CT, MRI and digital subtraction angiography and the accuracy and increase of laboratory examination items, patients with idiopathic intracranial hypertension In addition to careful patient and physical examination, targeted imaging and laboratory tests should be performed to find out the cause.
The sinus occlusive sinus hypertension occurs mostly in the superior sagittal sinus, the straight sinus, the transverse sinus, and the cavernous sinus thrombosis. The symptoms of thrombosis vary from site to site, and can be divided into two major categories, infectious and non-infective. The latter is caused by traumatic brain injury, wasting disease (such as advanced cancer, cachexia), certain blood diseases (leukemia, polycythemia, severe anemia) and severe dehydration. The former is often secondary to the head, facial infection and Suppurative meningitis, brain abscess, sepsis, etc.
(two) pathogenesis
70% to 80% of cerebral blood volume exists in the cerebral venous system. It is important for the maintenance and rapid regulation of normal intracranial pressure. The cerebral venous system is not exactly the same as the veins in other parts of the body. There is no cerebral vein and venous sinus. Venous valve, the direction of blood flow in the vein can be reversed, and there is a rich anastomosis with the extracranial vein. The cavernous sinus communicates with the facial vein through the ocular vein, through the foramen ovale and the jugular vein and the venous venous plexus. The pharyngeal venous plexus communicates and communicates with the spinal vein through the basal venous plexus. The transverse sinus communicates with the occipital vein via the mastoid vein. The superior sagittal sinus communicates with the extracranial anterior vein through the top guiding vein. These venous traffic is extracranial. The potential pathway for the spread of suppurative infection to the brain. The posterior fossa vein is connected to the venous plexus and is then connected to the veins in other parts of the body. These anastomotic branches are an important channel for tumor metastasis to the central nervous system. There is also the possibility of retrograde embolism. Humans have anatomical continuity between the uterus-vaginal vein, the vertebral vein, the intracranial vein and the dural sinus. When the abdominal pressure is increased, Small emboli may enter the intracranial and dural sinus from the pelvic cavity along the above venous access and form larger emboli in the intracranial venous system.
Primary sinus occlusion is more common in post-natal babies, especially in infants with congenital heart disease or gastrointestinal infections that are associated with wasting and debilitation. Adults often develop malnutrition, dehydration, infectious diseases, tuberculosis, cancer, and heart disease. Right heart failure, hypercoagulable state after surgery, head trauma, cerebral artery occlusion, leukemia, severe anemia, etc., also seen in oral contraceptives, women during pregnancy, postpartum or abortion and intrauterine infusion of hypertonic saline for abortion Hypernatremia, the mechanism of primary embolism is not well understood, anemia, hypotension, dehydration, etc. may be the main predisposing factors, increased blood viscosity and circulation, increased plasma fibrinogen, platelet and blood viscosity These factors play an important role in increasing.
Secondary thrombosis can be caused by a skull fracture directly affecting the sinus or after a sagittal sinus puncture in the infant. It can also be seen as a complication of suppurative infection in a local or distant site. In the local infection, the frontal sinus is more common. Upper sagittal sinus thrombosis caused by infection; transverse sinus thrombosis caused by papillary sinus or middle ear infection; cavernous sinus thrombosis caused by infection of the face, especially near the upper lip, nose, cheek, maxilla, eye and ethmoid sinus and sphenoid sinus Formation, thrombus can extend into the sinus along the drainage vein. When the suppurative bacterial infection produces sinusitis, the purulent embolus can extend to the vein branch or other sinus. For example, the transverse sinus lesion can extend to the internal jugular vein, purulent When the lesion is close to the sinus, inflammation of the sinus wall can also produce sinus thrombosis. The embolus can be inflammatory or non-inflammatory. The inflammatory thrombus is brittle and brittle. It enters the heart and lungs with blood flow, causing septic blood. Symptoms and multiple abscesses throughout the body, sinus blood can also be accompanied by epidural, subdural, pia mater and intracerebral abscess.
The surface of the cerebral cortex is rich in venous anastomosis into the venous sinus. Therefore, it is limited to a certain part of the venous sinus thrombosis, which may not cause a large reflux disorder of the cerebral vein. The blood can often bypass the venous sinus occlusion through other channels. In the case of extensive venous sinus thrombosis, venous return will be severely impeded. The affected cortex and subcortical white matter may have congestion, swelling and multifocal hemorrhage. In venous infarction, there is a little or massive bleeding in the white matter. And a large amount of blood quickly flows into the subarachnoid space of the infarct surface. This is a characteristic of venous obstructive infarction and arterial occlusive infarction. The naked eye sees the thrombus-forming sinus and veins as hard clots, most of which are coagulated. The block is light blue and contains some white plaques. The necrotic cortex and white matter are rapidly disintegrated and absorbed. Afterwards, the lesions shrink and become cystic, which is yellow. When the venous sinus and veins are rapidly thrombus, After the pass, it is difficult to find obvious abnormalities by visual inspection. At the time of autopsy, the cerebral venous congestion, brain swelling, cerebral gyrus flattening, appearance and cut surface Hemorrhage or infarction, microscopic examination of the cerebral cortex has extensive ischemic damage, nerve cell shrinkage or loss, shrinking cytoplasm is lightly stained, nuclear deep staining is triangular, oligodendrocytes are vacuolated, capillary Vascular endothelial cells also swell.
When the maternal superior sagittal sinus and cortical vein thrombosis, there are many fine hemorrhage areas at the junction of cortical venules and obstructed cortical veins, as well as severe cerebral edema, intracerebral hemorrhage or ischemic cerebral infarction. Ear or paranasal sinus infection can be complicated by dural, subdural, brain and cerebellar abscesses, transverse sinus, upper sagittal sinus and cortical veins contain red blood clots, hemorrhagic and scattered in the cortex and white matter Non-hemorrhagic cerebral infarction, transverse sinus thrombosis often secondary to otitis media and mastoiditis, can be divided into inflammatory or non-infectious, at the same time, if the left and right lateral sinus at the sinus sinus, the left sinus Thrombosis can block the cerebral infarction caused by large cerebral veins and sinus reflux.
Prevention
Prevention of intracranial venous sinus occlusion
For the prevention of venous sinus occlusive hypertension, the treatment of chronic otitis media and some systemic diseases that may cause the disease, such as extracranial tumors, blood disorders, metabolic disorders.
Complication
Intracranial venous sinus occlusion Complications, diabetes insipidus, upper gastrointestinal bleeding
Consciousness disorder, vision loss, diplopia, convulsions, emotional instability, irritability or crying, or apathy, unresponsiveness, slow movements and thinking, etc., are symptoms of increased intracranial pressure, and can also be regarded as complications . Severe intracranial pressure may result in visceral complications due to hypothalamic and brainstem dysfunction. Commonly, there are upper gastrointestinal bleeding, neurogenic pulmonary edema, acute renal failure, diabetes insipidus, cerebral sodium retention and brain consumption. Sodium syndrome. The serious complications are cerebral palsy and central circulatory respiratory failure leading to deterioration of vital signs.
Symptom
Intracranial sinus occlusion, intracranial hypertension symptoms Common symptoms Venous convulsions, venous thrombosis, edema, tension, tympanic membrane, redness, edema, reflux, secondary optic atrophy, retinal hemorrhage, nausea
Superior sagittal sinus occlusion
Mostly non-infectious, often associated with hemodynamic abnormalities, acute onset, early symptoms include headache, vomiting, convulsions and convulsions, scalp and external nasal veins may have anger and congestion, infantile cardia tension and uplift, sometimes Can have optic disc edema and strabismus, can also produce bilateral cortical hemiplegia, or focal epilepsy, chronic onset, due to the establishment of cortical vein collateral circulation and partial compensation results, only headache, optic disc edema or succession Hair optic atrophy.
2. Transverse sinus thrombosis
Mostly because of otitis media or mastoiditis for several weeks, the patient has a headache, the head is aggravated when rotated, there may be vomiting, venous congestion of the skin after the ear, if the phlebitis has extended to the internal jugular vein, the neck is tender, optic disc edema More limited to the disease side, the degree is not heavy, focal cerebral inflammatory symptoms are convulsions and contralateral hemiparesis, when the left transverse sinus thrombosis can form aphasia, most patients have tympanic membrane perforation, some patients tympanic membrane Redness, redness and swelling behind the ear.
3. Cavernous sinus thrombosis
More secondary to infection around the eyelids, nose, face, etc., clinical manifestations of the eye, facial symptoms are prominent, mainly cranial nerves, sympathetic and venous return disorders, eye movement, trochle, exhibition and trigeminal nerves 1 and 2 Damage, carotid sympathetic plexus damage caused by Horner's sign, retinal hemorrhage, optic disc edema and optic atrophy in the fundus, venous reflux disorder can cause eyeball protrusion and eyelid edema.
4. Intracerebral venous thrombosis
Intracerebral venous thrombosis caused by dural sinus or cortical venous thrombosis is more common in children. The consequence is that hemorrhagic infarction occurs in the vein distribution area. The most prominent parts are transparent septum, striatum, thalamus, and corpus callosum. The ventral side, the lateral side of the occipital lobe, and the inner upper surface of each cerebellum show clinical symptoms.
Examine
Examination of intracranial venous sinus occlusion
When the lumbar puncture is increased, the cerebrospinal fluid is clear or slightly yellow. When hemorrhagic infarction occurs in acute occlusion, the protein quantification and white blood cell count increase.
1. Digital subtraction cerebral angiography is the current accurate method for diagnosing venous sinus occlusion. When the main sinus occlusion is obstructed, the venous phase of angiography can be seen with prolonged circulation time and occlusion of the venous sinus. Some venous sinus occlusion can be seen when venous reflux is observed. phenomenon.
2. CT scan suggested the possibility of venous sinus occlusion, plain CT showed visible follicular hemorrhage in the venous sinus distribution area, and in some patients, the sagittal sinus was enhanced by "" shape and the center of "" shape was filled with thrombus. Contrast agent can not enter, sinus thrombus does not enhance the density after injection, and the sinus wall after thrombus enhancement is obvious, showing high-density triangle shadow, characteristic changes of CT scan, namely "" sign, foreign report 76 The characteristics of venous sinus occlusion CT, 28.6% enhanced scan can be seen "" sign, 20% can see multiple venous sinus bleeding, there are also reports of cortical vein occlusion, the brain surface can have a cord-like change, about 10% of patients can The CT scan is normal.
3. MRI features similar to CT scans, ie, sagittal sinus hemorrhage, sinus infarction, and cerebral palsy after intravenous injection of paramagnetic contrast agent. The occlusion of the venous sinus shows a high signal on the T2 image. The arteries and veins show a flow-out signal. Magnetic resonance angiography has a certain diagnostic value for intracranial venous sinus occlusion, but there are still some artifacts on the vascular imaging, which is not as clear as DSA angiography.
Diagnosis
Diagnosis and diagnosis of intracranial venous sinus occlusive hypertension
diagnosis
The diagnosis of intracranial venous sinus occlusion depends on clinical manifestations such as headache, nausea, vomiting and optic disc edema, as well as localized localized signs and local systemic factors related to local venous sinus thrombosis and CT findings. ", especially in the venous phase of venous venous sinus occlusion can be diagnosed. In recent years, due to the large number of antibiotics, widely used, venous sinus thrombosis caused by local infection tends to subacute and chronic onset, some patients Only chronic cranial hypertension, and other typical manifestations of venous sinus thrombosis, only manifested as high intracranial pressure symptoms.
Differential diagnosis
Venous sinus thrombosis often needs to be associated with eyelid (intraorbital, posterior) cellulitis, cavernous sinus tumor, cavernous sinus arteriovenous fistula, cavernous sinus inflammatory granuloma, upper sagittal sinus thrombosis and sinus The differentiation of meningioma, especially across the midline, can also be similar to the clinical manifestations of superior sagittal sinus infarction, angiography can occur venous sinus occlusion or stenosis, CT scan of the head can help identify.
