I. Clinical information:
The diarrhea (dural sinus horombosis, DST) is an easily misdiagnostic cerebrovascular disease, with risk factors such as pregnancy or perinatal period, infection, dehydration, oral contraception, blood disease, tumours, trauma, vascular malformations, etc., occasionally seen in their own immune diseases, drug use, etc. Pathologically, the formation of a veinal sepsis has led to a repulsion of the cerebral cortex, and even the retip of the sepsis extends to the shallow sepsis of the brain, resulting in the disruption of the aneurysm and the increase of internal pressure, brain oedema and spot bleeding and brain infarction. DST has a relatively young disease and common symptoms include nausea, vomiting, convulsions, optic oedema, neurosis, cognitive disorders and even death.
II. Causes:
1. Inflammatory hemorrhages within the inflammation of the cranium are most commonly found in the stoals of the sponges and the ethyls.
(1) Sphinxes, especially in the dangerous triangle, can easily enter the sponge through eye veins.
(2) Earstoves, such as Chinese ear or emulsion, may cause the formation of a sepsis.
(3) Flutterstine or sifting inflammation, entering the sponges by sifting veins or destroying the walls.
(4) Abscesses in the deep neck or in the body of tonsils, osteoporitis, etc., can be drawn along the Wings’ veins or enter the Cervical veins, and the Sponge Gardens of Sponge Sponge from Treadstone.
(5) Meningococcal anesthesia can pass through cortical veins and upper diarrhea.
(6) All-body infections such as sepsis caused by bacterial infections.
2. Diseases or syndromes that lead to high blood condensation, among the causes and risk factors of intra-inflammatory hemorrhages in the non-inflammatory skull
(1) Full body failure, dehydration, chronic expendable disease.
(2) Pregnancy and puerperium.
(3) Brain trauma.
(4) Blood diseases, such as genuine erythrocytes, acute lymphocyte leukemia, haemogloglobinuria, congenital or impaired access to sexual condensation (anticondensation enzymes) The lack of protein C, protein S, coagulant Vleiden mutations, active protein C resistance, etc.) is like a garden.
(5) Self-immuno-immunological diseases such as Bechet disease, systemic ulcer (SLE) ulcer antiphosphate antibodies (including lupus anticondensation and anti-cartiary antibodies) syndrome.
(6) Surgery.
(7) Innate or acquired heart disease.
(8) Long-term oral contraceptives.
(9) There are still 20 to 25 per cent of patients without cause or risk.
(10) Sitting in the same position for a long time, resulting from a lack of blood on the neck. Like long-term in front of a computer.
III. METHODOLOGY
In general, the following three main factors are involved in the formation of ivulatory embolisms, but in different parts of the organism, which are dominated by different factors.
1. Vector blood flow is slow.
2. Diarrhoeal damage
(1) Chemical impairment
(2) Mechanical damage.
(3) Infectious injuries
3. Changes in blood composition.
(1) Increased blood viscosity
(2) Increased coagulation activity.
(3) Reduced anticondensation activity.
IV. Imaging performance
Both CT and MRI are typical. 1 part: the most common is the upper vector beryllium (SSS), followed by the transistor, the beta beryllium, the sponge beryllium, and the Nautilus. 2CT inspection: Direct indicia are increased in the density of the diseaseal musculinium, in a triangle or in a thread, and in a high-density strip. Indirect signs are brain infarction and haemorrhage, with infarction in the lower part of the cortex and often in the form of high dotage density. Increased scanning of impregnated incisors, typically the back of a vectord diarrhea or the “polymeric” triangle. CTV directly displays the impurities of the veins. Chronic DSTs can see small brain curtains, thicker brain sickle and significantly more. DST performance on 3MRI depends on the age of the embolism and the irradiated signal on T2WI has disappeared. The acute period is a T1 or slightly higher signal and the T2WI is a low signal. Subacute periods are high T1 and T2 signals. Chronic periods show low-sequence signals due to fibrosis and the deposition of lysine. The infarction of the vein brain is an uneven abnormal signal, with T2*WI and SWI showing a low internal signal. DWI is limited in only a fraction of the cases due to the major vascular edema in the pathologies, and is clearly high when cytotoxic edema dominates. As shown in figure 2, DWI only sees a slightly higher signal of the right dome and left bean core, a slightly higher signal of the right pillow leaf, a deep vein and no indication of the direct larvae (arrow), a significantly narrow left crossbar (wielding arrows) and a clear high signal of T2WI (unlisted). The MRI was enhanced to show the reinforcement of the local veins wall and the infarction of the veins was reinforced by the placard. The MRV disease is narrow, irregular or closed, enhancing the MRV (CE-MRV) to show DST more reliably. The 4DSA veins can be seen in a narrow, impregnated or closed vein, while showing a cortical vein expansion, which is mainly used to determine the extent of the haemorrhage before intervention.
