Intracranial venous sinus thrombosis

Introduction to intracranial venous sinus thrombosis Cerebral venous system thrombosis (CVST) is a group of special types of cerebrovascular diseases characterized by cerebral venous return obstruction and cerebrospinal fluid absorption disorder caused by various etiologies. The incidence is less than 1% of all strokes. It is usually more common in children and young adults, and in children, it is more common in the side sinus and cavernous sinus caused by infection. Patients with suppurative otitis media and mastoiditis are susceptible to thrombosis of the transverse sinus (transverse portion of lateralsinus) and the sigmoid portion of lateralsinus, collectively referred to as lateral sinus thrombosis (lateralsinusthrombosis). According to the nature of the lesion, it is divided into two categories: non-inflammatory and inflammatory intracranial venous thrombosis. Systemic symptoms manifested as irregular hyperthermia, chills, fatigue, body muscle aches, wilting, subcutaneous congestion and other symptoms of sepsis. Focal symptoms include seizure consciousness disorder and optic disc edema. Inflammatory intracranial venous thrombosis is secondary to infection, most commonly in the cavernous sinus and sigmoid sinus if inflammatory cavernous sinus thrombosis occurs, the corresponding symptoms and signs may appear. Non-inflammatory intracranial venous thrombosis can also occur in primary disease manifestations, such as non-specific inflammation, collagen tissue disease, giant cell vasculitis, chronic infectious diseases and other related symptoms and signs. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complication: cavernous sinus thrombosis

Causes of intracranial venous sinus thrombosis

Cause

1. Inflammatory intracranial venous thrombosis is secondary to infections, most commonly in the cavernous sinus and sigmoid sinus. Common lesions are:

(1) Facial lesions, especially purulent lesions such as sputum and sputum in the dangerous triangle, easily enter the cavernous sinus through the ocular vein.

(2) Ear lesions such as otitis media or mastoiditis can cause sigmoid sinus thrombosis.

(3) Inflammation of the sphenoid sinus or ethmoid sinus, through the venous vein or destruction of the sphenoid sinus wall into the cavernous sinus

(4) deep neck or tonsil abscess, maxillary osteomyelitis, etc. may involve the transverse sinus cavernous sinus along the pterygoid plexus or invading the jugular vein.

(5) Meningitis: Brain abscess can involve the superior sagittal sinus through the cortical vein.

(6) Systemic infections such as sepsis caused by various bacterial infections.

2. Among the causes and risk factors of non-inflammatory intracranial venous thrombosis, there are various diseases or syndromes that cause blood to be hypercoagulable:

(1) systemic failure, dehydration, and chronic wasting disease.

(2) Pregnancy and puerperium.

(3) Brain trauma.

(4) Hematological diseases such as polycythemia vera, acute lymphocytic leukemia, thrombocytopenia, paroxysmal hemoglobinuria, congenital or acquired coagulation disorders (anti-thrombin III deficiency protein C, protein S deficiency, coagulation Factor Vleiden mutation and active protein C resistance, etc.).

(5) Autoimmune diseases such as Bechet's disease, systemic lupus erythematosus (SLE), ulcerative colitis, antiphospholipid antibodies (including lupus anticoagulant antibodies and anti-lipid antibodies, etc.) syndrome.

(6) Surgery.

(7) Congenital or acquired heart disease.

(8) Long-term oral contraceptives.

(9) There are still 20% to 25% of patients without cause or risk factors.

Pathogenesis

In general, venous thrombosis has the following three major factors: venous thrombosis in different parts of the body, mainly based on different factors.

1. Venous blood flow is slow.

2. Intravenous wall damage:

(1) Chemical damage.

(2) Mechanical damage.

(3) Infectious injury.

3. Changes in blood composition:

(1) Increased blood viscosity.

(2) Increased blood coagulation activity.

(3) Reduced anticoagulant activity.

Prevention of intracranial venous sinus thrombosis

prevention

For clear risk factors, such as intracranial infections, facial lesions, especially purulent lesions such as sputum and sputum in the dangerous triangle, ear lesions such as otitis media or mastoiditis, sphenoid sinus or ethmoid sinus inflammation, deep neck or tonsils Abscess, maxillary osteomyelitis, atrial fibrillation, blood diseases such as polycythemia vera congenital or acquired coagulation disorders, autoimmune diseases, etc., should be treated as soon as possible.

Prophylactic treatment with antiplatelet drug aspirin 50 ~ 100mg / d ticlopidine 250mg / d for secondary prevention has a positive effect recommended; long-term medication should have intermittent bleeding tendency to be used with caution.

Intracranial venous sinus thrombosis complications Complications cavernous sinus thrombosis

1. Cavernous sinus thrombosis: multiple secondary to the eye and nose infection, showing prominent eyeballs, periorbital conjunctival congestion and edema, eyelid blood stasis, limited eye movement, dilated pupils, facial sensory disturbances.

2. Transverse sinus and sigmoid sinus thrombosis: multiple secondary to suppurative otitis media or sinusitis, showing dysphagia, drinking water cough, poor articulation and ipsilateral eye abduction difficulties.

3. Upper sagittal sinus thrombosis: symptoms of intracranial hypertension, prominent dysfunction, may be associated with seizures (convulsions, etc.), contralateral hemiplegia, lateral numbness.

4. Cerebral cortical venous thrombosis: mostly caused by venous sinus thrombosis, showing headache, vomiting, mental disorders, partial seizures (one side of the body convulsions, etc.), limb paralysis, sensory disturbances, disturbance of consciousness and even coma.

Symptoms of intracranial venous sinus thrombosis Common symptoms Increased intracranial pressure, dull expression, lethargy, coma, confusion, convulsions, consciousness disorder, vomiting

1. General performance

The manifestations of inflammatory intracranial venous thrombosis are classified into systemic symptoms, symptoms of localized infections, and sinus symptoms. Systemic symptoms manifested as irregular hyperthermia, fatigue, body muscle aches, apathetic, subcutaneous congestion and other symptoms of sepsis. Non-inflammatory intracranial venous thrombosis is mainly characterized by symptoms of the cause and risk factors and sinus symptoms.

2. The clinical manifestations of intracranial venous sinus thrombosis are lack of specificity, and their symptoms and signs are different. Acute onset can also occur slowly after several weeks. The most common symptoms include headache, focal neurological deficit, and seizure-conscious disturbance optic disc edema.

Some authors have proposed the following types of performance:

(1) Progressive intracranial hypertension.

(2) Sudden onset of focal neurological focal damage, similar to arterial stroke but no seizures.

(3) Focal damage to the nervous system with or without seizures and increased intracranial pressure progressed within a few days.

(4) focal damage of the nervous system, with or without seizures and increased intracranial pressure, progress in weeks or months.

(5) A sudden onset of headache, similar to subarachnoid hemorrhage, or transient ischemic attack.

3. Clinical manifestations of cerebral venous thrombosis The simple majority of cerebral venous thrombosis is mostly caused by venous sinus thrombosis.

(1) superficial vein thrombosis often occurs suddenly, headache, vomiting, optic disc edema, localized seizures, limb paralysis, cortical sensory disturbances, etc., that is, symptoms of increased intracranial pressure and localized cortical lesions.

(2) The clinical characteristics of deep vein thrombosis are also non-characteristic, mainly manifested as headache, mental disorder, and oligodenidal pyramidal tract signs and cortical tonic or devascularized optic disc edema are rare.

Examination of intracranial venous sinus thrombosis

Laboratory inspection

1. Blood routine, blood electrolytes.

2. Blood sugar, immune items, cerebrospinal fluid examination, if abnormal, there is a differential diagnosis.

Film degree exam

1. Head CT and CTA

The characteristic CT changes were abnormal high-density lesions in the sinus or high-density lesions in the cerebral veins, which showed a triangular shadow, ie, the delta sign, after the superior sagittal sinus. CT changes also included images of cerebral edema, hemorrhage, and infarction and changes in the ventricular system, but 20% to 30% of patients showed normal CT scans. Indirect signs of deep venous thrombosis are images of bilateral thalamus, basal ganglia infarction, or hemorrhagic infarction.

CTA showed thrombotic sinus and vein imaging was poor, but collateral vein imaging was good.

2. Head MRI and MRA

In the acute phase (onset <1 week), T1, T2 weighted phase venous sinus or intravenous normal vascular emptying disappeared, T1 and other signals, T2 low signal; subacute phase (onset 1 to 2 weeks), T1, T2 Show high signal; chronic phase (2 weeks to 3 months after onset), vascular emptying phenomenon reappeared, T1, T2 signal weakened. In some patients, MRI showed an intra-luminal equal-density signal after 4 months of onset, and there was no normal emptying, indicating continuous occlusion. Indirect signs of MRI appear as images of cerebral edema, hemorrhage, infarction, and changes in the ventricular system as well as CT. MRA can confirm the occlusion of the main venous and venous sinus, such as the sagittal sinus, the straight sinus, the transverse sinus, the Galen vein, etc., and the blood flow signal disappears.

3. Angiography can show partial or complete occlusion of the venous sinus and vein. The cortical vein of the drainage area is spirally dilated. It also shows venous reflux, but the disadvantage is that it is traumatic and expensive. It is suitable for MRI, and MRA cannot be diagnosed.

Diagnosis and differentiation of intracranial venous sinus thrombosis

Diagnostic criteria

1. The medical history is mostly acute or subacute, and a few onset are slow. Inflammatory patients have a history of facial, eye, mouth, throat, paranasal sinus, middle ear, mastoid or intracranial infection; non-inflammatory patients have systemic failure, dehydration, puerperium, myocardial infarction, blood disease, high fever before illness Or a history of craniocerebral trauma, brain tumors, etc.

2. Neurological symptoms vary depending on the location and extent of the affected sinus, the degree of thrombosis, the speed, and the establishment of the collateral circulation. Older people have more mild symptoms, which can cause difficulty in diagnosis. Generally have the following performance:

(1) Increased intracranial pressure.

(2) scalp adjacent to the embolized sinus, swelling of the face, varicose veins; cavernous sinus thrombosis is more eyelids, conjunctival swelling and congestion and eye sinus (non-pulsating and no vascular murmur, can be associated with cavernous sinus aneurysm and arteriovenous ), and the same symptoms can be seen in the contralateral cavernous sinus through the sinus.

(3) In addition to the incomplete occlusion of the transverse sinus, sinus and upper sagittal sinus, the brain presents various limitations due to edema, secondary hemorrhagic infarction or hemorrhage and hematoma. 1 superior sagittal sinus thrombosis. Lower limbs or proximal end are severe limb paralysis (double lower limb paralysis, hemiplegia, limbs or quadriplegia), limited epilepsy, binocular deviation, cortical dysfunction, mental symptoms and transient urinary retention. 2 sponge sinus thrombosis. Due to the involvement of the oculomotor nerve and the trigeminal nerves I and II, the eye movement is limited or fixed, and facial pain and corneal reflex disappear. 3 Sigmoid sinus thrombosis. Trigeminal and abductor nerve paralysis when the sinus is involved; when the thrombus expands into the jugular vein, the pharyngeal, vagus, and accessory nerves are involved. 4 straight sinus thrombosis. There is a tendency to go to cerebral rigidity and involuntary movement.

3. Inflammatory patients may be associated with sepsis, severe illness or severe symptoms may be secondary to meningeal-encephalitis and mental confusion, paralysis or coma.

4. Cerebrospinal fluid pressure increased, inflammatory people still have inflammatory changes. When the transverse sinus or sigmoid sinus thrombus, the Tobey-Ayer sign is positive. There may be stale or fresh bleeding.

5. Radiological examination: 1 The head flat film of the person with trauma can be seen with a fracture or a fracture line crossing the sinus. 2 bilateral cerebral angiography can be found that venous sinus is not developed or partially developed, but the time is prolonged, and there may be distortion, dilation and abnormal anastomosis of nearby veins and sinuses. 3 skull CT showed enhanced cerebral gyrus in the sinus distribution area, and hemorrhagic softening on both sides of the diseased sinus.

6. Nuclide scanning shows the concentration of nuclide at the brain softening area, which can last for several months.

Differential diagnosis :

In particular, it should be differentiated from arterial ischemia or hemorrhagic stroke, brain abscess, brain tumor encephalitis and benign intracranial hypertension.

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