Intracranial vein thrombosis

Introduction to intracranial venous thrombosis Intracranial venous thrombosis is a rare cerebrovascular disease, mainly refers to venous sinus thrombosis, and cerebral venous thrombosis is rare, and mostly caused by venous sinus thrombosis, according to the nature of the lesion is divided into non-inflammatory And inflammatory intracranial venous thrombosis in two major categories. The intracranial venous system includes the sinus and cerebral veins. basic knowledge The proportion of illness: 0.0007% Susceptible people: no special people Mode of infection: non-infectious Complications: sepsis, epilepsy, disturbance of consciousness, optic disc edema, cavernous sinus thrombus, meningitis, brain abscess, hyponatremia, intracranial venous thrombosis

Causes of intracranial venous thrombosis

(1) Causes of the disease

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

(1) Facial and facial lesions, especially purulent lesions such as sputum, sputum, etc. in the dangerous triangle, easy to 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 periton abscess, maxillary osteomyelitis, etc., can involve the transverse sinus, sinus, cavernous sinus along the venous 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, 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 disease, systemic lupus erythematosus (SLE), ulcerative colitis, antiphospholipid antibodies (including lupus anticoagulant antibodies and anti-lipid antibodies).

(6) Surgery.

(7) Heart disease, congenital or acquired.

(8) Long-term oral contraceptives.

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

(two) pathogenesis

In general, venous thrombosis has the following three major factors, but venous thrombosis in different parts of the body is dominated by 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 thrombosis

There are clear risk factors, such as intracranial infections, facial and facial lesions, especially sputum, sputum and other purulent lesions in the risk triangle, ear lesions such as otitis media or mastoiditis, sphenoid sinus or ethmoid sinus inflammation, deep neck or tonsils Abscess, maxillary osteomyelitis, diabetes, atrial fibrillation, blood diseases such as polycythemia, congenital or acquired coagulation disorders, autoimmune diseases, etc., should be treated as soon as possible, preventive treatment available antiplatelet drugs aspirin 50 ~ 100mg / d, ticlopidine 250mg / d has a positive effect on secondary prevention, recommended application; long-term medication should have a discontinuous period, bleeding tendency should be used with caution.

Intracranial venous thrombosis complications Complications sepsis epilepsy consciousness disorder optic disc edema cavernous sinus thrombus meningitis brain abscess hyponatremia intracranial venous thrombosis

Systemic symptoms are irregular high fever, fatigue, fatigue, body muscle aches, apathetic, subcutaneous congestion and other symptoms of sepsis, focal symptoms such as seizures, disturbance of consciousness, optic disc edema.

Inflammatory intracranial venous thrombosis is secondary to infections, most commonly in the cavernous sinus and sigmoid sinus. If inflammatory cavernous sinus thrombosis occurs, the corresponding symptoms and signs may appear. Common complications are: meningitis. Brain abscess, internal carotid arteritis and pituitary infection, necrosis and dysfunction, water retention and hyponatremia.

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.

Symptoms of intracranial venous thrombosis Common symptoms Increased intracranial pressure Venous thrombosis Increased intracranial pressure Chronic venous insufficiency Congestive disorder Mental venous return obstruction Meningitis Cerebral ischemia Eye drooping

1. General performance

The manifestations of inflammatory intracranial venous thrombosis are divided into systemic symptoms, symptoms of local infections and sinus symptoms, systemic symptoms of irregular high fever, chills, fatigue, body muscle aches, wilting, subcutaneous congestion and other symptoms of sepsis Non-inflammatory intracranial venous thrombosis is mainly characterized by symptoms and sinus symptoms of etiology and risk factors.

2. Clinical manifestations of intracranial venous sinus thrombosis

Lack of specificity, symptoms and signs of different manifestations, acute onset, can also occur slowly after several weeks, the most common symptoms include headache, focal neurological deficit, seizures, disturbance of consciousness, optic disc edema.

Some authors have proposed the following types of performance:

(1) Progressive intracranial hypertension.

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

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

(4) focal damage of the nervous system, with or without seizures and increased intracranial pressure, the disease progresses 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

Simple cerebral venous thrombosis is rare, and most of them are expanded by venous sinus thrombosis.

(1) superficial venous thrombosis often suddenly begins, headache, vomiting, optic disc edema, localized seizures, limb paralysis, cortical sensory disturbances, etc., that is, 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, disturbance of consciousness, hemiparesis, pyramidal tract sign and cortical tonic or cortical state, optic disc edema is rare.

The following are some of the clinical manifestations of several common venous sinus thrombosis:

1 transverse sinus - sigmoid sinus thrombosis: transverse sinus - sigmoid sinus is closely connected in anatomy, the latter is a continuation of the former, so the two are often discussed together clinically.

Transverse sinus-sigmoid sinus thrombosis is mostly unilateral. The typical clinical manifestations are headache, nausea, vomiting and other symptoms of increased intracranial pressure. Because under normal circumstances, most people have more blood on the right side than the left side, so the right side is occluded. It is prone to increased intracranial pressure, 50% of patients have optic disc edema, often bilateral, or unilateral, due to high intracranial pressure and bilateral sinus dilatation imbalance, the baby can be separated or swelled. A small number of localized epilepsy may be associated with hemiplegia, which may be due to the spread of inflammation involving the drainage vein on the lateral side of the cerebral hemisphere. This sign suggests an abscess in the hemisphere.

Double vision may occur when the intracranial pressure is increased or the supraspinal sinus causes the nerve palsy. If there is facial pain (trigeminal involvement), it is called Gradenigo syndrome. The transverse sinus-sigmoid sinus thrombus can spread into the jugular vein. The jugular vein becomes rough and tender.

Such as involving the jugular foramen or inflammation along the bone tissue (osteomyelitis), can cause IX, X, XI damage to the brain, clinical manifestations of dysphagia, drinking water cough and dysphonic and other symptoms and signs.

The neck-necked neck test is not helpful for the diagnosis of this disease.

2 cavernous sinus thrombosis: cavernous sinus thrombosis often secondary to eyelids, sinus and upper facial suppurative infection, clinically more common with acute onset, often with sepsis-like fever, chills with eye pain, eyelid tenderness, eyeballs Eyelids and conjunctival redness and swelling, the first branch of the III, IV, VI and V brain nerves in the cavernous sinus can cause cavernous sinus syndrome, which is characterized by limited movement of the eye in all directions, in a fixed state, drooping of the eyelids, dilated pupils And the regulation of reflex disappeared, when the sympathetic nerve was involved, the pupil was reduced, and the pupil was dilated when the parasympathetic nerve was involved. When both were involved, the pupil was stiff.

If complication of inflammatory cavernous sinus thrombosis occurs, the corresponding symptoms and signs may appear. Common complications include meningitis, brain abscess, internal carotid arteritis and pituitary infection, necrosis and dysfunction, water retention and hyponatremia. .

3 superior sagittal sinus thrombosis: superior sagittal sinus thrombosis is less common than transverse sinus-sigmoid sinus and cavernous sinus, mostly non-infectious, can be characterized by high intracranial pressure and lack of any focal neurological symptoms and signs.

When the thrombus spreads to the cerebral vein to form a cerebral venous thrombosis, and causes white matter or gray matter to bleed, it shows obvious symptoms and signs. Increased intracranial pressure is the most prominent clinical manifestation of superior sagittal sinus thrombosis. Can appear, mainly manifested as headache, nausea, vomiting and optic disc edema, infants with anterior iliac bulging, separation of the suture and venous congestion in the anterior temporal region, forming the so-called "caput medusae", the upper sagittal sinus thrombosis is different The degree of increase in intracranial pressure is also different.

When the anterior sagittal sinus thrombosis occurs, the cerebral hemisphere exchange venous return is not affected, the cerebrospinal fluid absorption disorder is not obvious, so the intracranial pressure is increased lightly; when the posterior sagittal sinus thrombosis, the bilateral cerebral hemisphere The venous return was completely blocked, so the intracranial pressure was significantly increased.

Focal symptoms and signs of superior sagittal sinus thrombosis include various types of limb paralysis, epilepsy, hemianopia, quadrant blindness, aphasia, aversion, loss of reading, ocular paralysis and bladder dysfunction.

4. Imaging features of venous sinus thrombosis CT characteristic changes are abnormal high-density lesions in the sinus or high-density lesions in the cerebral vein, which are the signs of the sinus. After the scanning, the anterior sagittal sinus can be seen as an empty triangle shadow, ie Signs, CT changes also include cerebral edema, hemorrhage and infarction and changes in the ventricular system, but 20% to 30% of patients with CT scans showed normal.

Head MRI changes: acute phase (onset <1 week), T1, T2 weighted phase upper venous sinus or intravenous normal vascular emptying phenomenon, T1 and other signals, T2 low signal, subacute phase (onset 1 to 2 weeks) T1 and T2 all showed high signal. In the chronic phase (2 weeks to 3 months after onset), vascular emptying appeared again, T1 and T2 signals were weakened. In some patients, MRI showed an intra-luminal equal-density signal after 4 months of onset. No normal emptying, indicating continuous occlusion, MRI indirect signs like CT showed cerebral edema, hemorrhage, infarction and changes in ventricular system, MRA can confirm the occlusion of the main venous and sinus, as above, lower sagittal sinus Straight sinus, transverse sinus, Galen vein, etc., the blood flow signal disappears.

Examination of intracranial venous thrombosis

The necessary selective examinations are based on possible causes.

1. Blood routine, blood electrolytes.

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

3. The characteristic changes of CT and CTA CT in the head are abnormal high-density lesions in the sinus or high-density lesions in the cerebral vein, which are the signs of the sinus. After the scanning, the triangular shadow of the upper sagittal sinus is visible, that is, the delta sign, CT Changes also include images of cerebral edema, hemorrhage, and infarction and changes in the ventricular system, but 20% to 30% of patients showed normal CT scans, and indirect signs of deep venous thrombosis were bilateral thalamus, basal ganglia or hemorrhagic infarction. image.

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

4. In the acute phase of head MRI and MRA (onset <1 week), T1, T2 weighted phase venous sinus or intravenous normal vascular emptying phenomenon disappears, T1 and other signals, T2 low signal; subacute phase (onset 1 to 2) Week), T1, T2 showed high signal; chronic phase (2 weeks to 3 months after onset), vascular emptying phenomenon reappeared, T1, T2 signal weakened, some patients had MRI showed intraluminal density after 4 months of onset Signal, no normal emptying, indicating continuous occlusion, MRI indirect signs like CT with cerebral edema, hemorrhage, infarction and ventricular system changes, MRA can confirm the main venous and venous sinus occlusion, as above, lower vector The sinus, the straight sinus, the transverse sinus, the Galen vein, etc., the blood flow signal disappears.

5. 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 costly. It is suitable for patients who cannot be diagnosed by MPI MRA.

Diagnosis and diagnosis of intracranial venous thrombosis

diagnosis

The clinical manifestations of intracranial venous thrombosis are complex, lacking specific signs, often leading to missed diagnosis and misdiagnosis. When patients have the cause or risk factors of infection or non-inflammatory thrombosis, headache, epilepsy, disturbance of consciousness with or without nerves Imaging findings should be performed during systemic signs. MRI MRA is highly sensitive to the diagnosis of intracranial venous thrombosis, non-invasive, rapid, and simple.

Differential diagnosis

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

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