Cerebral venous thrombosis diagnosis and treatment of the status quo

Cerebral venous thrombosis (cerebral venus thrombosis, CVT) into venous sinus thrombosis and cerebral venous thrombosis was due to infectious or non-infectious causes formation of venous system thrombosis, caused congestion, resulting in venous return obstacles have brain bleeding, edema and intracranial hypertension , which show a series of related clinical symptoms and signs. CVT complexity of the etiology, involving all age groups, from dissatisfaction with 1-year-old infants to seniors. Its clinical and neuroimaging performance also changed greatly. If taken in the early onset of effective treatment measures, good prognosis. Therefore, early diagnosis is very important.
1, the diagnosis of CVT
Whether there is a clear 1.1 CVT Have the following four kinds of clinical syndrome one should doubt the CVT (1) partial nerve defect with or without intracranial hypertension, the most common form. There will be aphasia, hemiplegia and Blind, etc.. If accompanied by headache, seizures or a state of awareness of the changes will be highly suspected CVT. (2) of pure high intracranial pressure, it is a common type, manifested as headache, as papillary edema and six pairs of cranial nerve palsy, and similar benign intracranial hypertension. (3) subacute encephalopathy type, the level of awareness for the performance drop, sometimes accompanied by epilepsy, no clear positioning signs or intracranial hypertension identifiable characteristics, this type of easily misdiagnosed. (4) the cavernous sinus thrombosis, the incidence usually acute and chronic progress was accompanied with moderate pain and 3 or 6 pairs of cranial nerve palsy. The only headache symptoms for the CVT, with lumbar puncture headache, subarachnoid hemorrhage-induced headache or migraine, and other identification. 1.2 diagnosis 1.2.1 neuroimaging: MRI and magnetic resonance angiography (MRA): MRI and MRA Joint Inspection CVT diagnosis and follow-up is the best way. CVT highly suspected as clinical, MRI and MRA should be a first-line inspection tool MRI shows signs of thrombosis direct different changes with time. The acute phase thrombosis (one week) with a performance of the T1; Such signals, T2 low signal. Subacute (2-4 weeks), T1 and T2 are high signal. Phase III (l months later), recanalization, or thrombosis persistent residues, showed sinus wall and sinus change. Subacute thrombosis period of the typical high signal on the larger significance of the disease, other phases signal not typical, the lack of specificity, coupled with the flow-related artifacts impact on conventional MRI images to make the diagnosis more difficult, especially in the acute phase. MRI, the superior sagittal sinus, and the transverse sinus straight sinus thrombosis most easily identify, brain vein thrombosis and cerebral vein identification has been difficult. MRI showed that the indirect signs including diffuse brain swelling (for the normal signal), edema or infarction (T1 signal or low signal, T2 high-signal), and more in periventricular white matter; Hemorrhagic infarction, T1 and T2 are high signal. MRA showed that the direct signs of thrombosis for development or normal cerebral venous sinus blood flow signal loss or reflect the venous sinus recanalization or on the verge of fuzzy rules without the lower blood flow signal. Indirect signs of venous obstruction distal collateral or other form of abnormal venous drainage channel expansion. These are not signs of thrombosis signal changes of the time, a clear indication of straight sinus, the large vein and the brain brain vein. Application of two-dimensional and three-dimensional time leap Act (time of flight, TOF) and phase control (phase contrast), and other methods to increase the diagnosis rate of MRA. Conventional MRI and MRA of the Joint Inspection CVT will greatly improve the diagnosis rate, arterial angiography instead of the tendency. CT: If no contraindications or MRI MRI, CT scan should first trip. 80% of the cases may have abnormal performance, but a typical example of the CVT only 20%. CVT direct signs of thrombosis are two kinds: air sign (enhanced scan, the superior sagittal sinus in the rear, straight Galen venous sinus and more common, conventional scanning performance for the high-density site) and dense 1.30 levy (dense triangle sign conventional scanning, superior sagittal sinus showed high density). Direct signs of a relatively rare, but high specificity. Indirect signs of non-specific three brain abnormalities (edema or infarction suggested that low-density, high-density suggested that hemorrhagic infarction), fracture - like brain ventricle and the sickle and cerebellum screen strengthening. Spiral CT venography CVT is a valuable inspection tool, a common abnormal filling defect, and the strengthening of sinus wall measurement of the increase in venous drainage. Intra-arterial angiography, was once a key diagnostic method, now used only for inspection MRI and MRA with the CVT is still not clear circumstances. Typical signs include some or all of sinus not by the expansion and enhancement of collateral blood vessels surrounded the spiral cortical venous suddenly interrupted. Ridge 1.2.2 brain wave inspection: Inspection of conventional, chemical, biological and intracranial pressure value. For exclude infection, identifying subarachnoid hemorrhage (Hint hemorrhagic infarction), intracranial pressure and set down intracranial pressure drug application is valuable. Diagnosis 1.3 Many factors can cause or causes CVT (Table 1).
Table 1 cause of cerebral venous thrombosis risk factors or Infection causes Local Post-traumatic infection Intracranial infection: brain abscess, empyema, meningitis Local infection: otitis media, tonsillitis, sinusitis, stomatitis Systemic Bacteria: sepsis, endocarditis, typhoid, tuberculosis Virus: measles, hepatitis, encephalitis (herpes, human immunodeficiency virus), cytomegalovirus Parasites: malaria, Trichinosis Fungi: Aspergillus Non-infectious causes Local Head injury (open or closed, with or without fracture) Neurosurgery Cerebral infarction or cerebral hemorrhage Tumor: Brain (ridge) membrane tumor, metastatic tumors, gliomas Penetrating brain malformation, arachnoid cyst Subdural dynamic - arteriovenous malformation Systemic Surgery: with or without any of deep vein thrombosis surgery Obstetrics and Gynecology: pregnancy and puerperium Oral contraceptives: Estrogen and progesterone hormones Medicine Heart: congenital heart disease, heart failure, pacemaker placement Cancer: Any visceral cancer, lymphoma, leukemia, L Dong-lactamase day treatment Red blood cell disorders: Erythrocytosis, after hemorrhagic anemia, sickle-cell anemia, paroxysmal Night Hemoglobinuria, iron deficiency, anemia Thrombocytopenia disease: primary or secondary coagulation dysfunction: 3 antithrombin, protein C S and the lack of protein, and activated protein C anticoagulant substances circulating in the resistance increase, and the resulting San intravascular coagulation, heparin and heparin-induced red blood cell type material reduction in amino acid has been Treatment, the lack of blood-fiber, for any reason dehydration caused serious Digestive system: cirrhosis, Crohn's disease, ulcerative colitis Connective tissue: systemic lupus disease, temporal arteritis, Wegener's granulomatosis venous thromboembolism STDs Changed, Hughes-Stovin syndrome Other: Behcet's disease, sarcoidosis (meat-like: a), nephrotic syndrome, neonatal asphyxia, intestinal The injection, the male hormone treatment Primary
Although the infection is still a major CVT clear cause, but with the advent of antibiotics, in the developed countries and some developing countries, the infection rate of CVT has been a marked decline. Infectious CVT usually occurs in facial triangle after infection, the other parts such as the ethmoid sinus infection, the sphenoid sinus, and otitis media periodontal abscess caused by less. In developing countries, young women in the postpartum occurred CVT ratio higher than the gestation period, but in the developed countries, oral contraceptives is an important factor. The large number of non-medical causes of infection, congenital thrombophilia disease is the most common cause, particularly with coagulation factor V leiden variation of activated protein C resistance of the patients and increased prothrombin 20210G-A gene mutation patients. Poort, and other recent reports, the choice of a personal and family history of venous thrombosis of the Netherlands (all types) patients, prothrombin 20210A mutation rate was 18%, the first time without a choice in patients with deep venous thrombosis of prothrombin 20210 A gene mutation rate was 6.2%, normal control of 2.3%. Biousse, and so found 35 cases of patients with cerebral venous thrombosis, prothrombin gene mutation 2021 OA incidence of 5.7%. But the study also found that the single coagulation factor V leiden OA 2021 or prothrombin gene mutation led to the occurrence of thrombosis in low rate, when combined with other congenital thrombophilia or induced thrombosis certain factors, such as trauma, post-natal, head trauma, lumbar puncture and oral contraceptives, the thrombosis risk will be greatly enhanced. Therefore, screening coagulation factor Vleiden 20210 A and prothrombin gene mutation on the prevention of venous thrombosis has important significance. China's 97 cases of venous thrombosis patients and 100 normal study found no leiden coagulation factor V and prothrombin 20210 A gene mutation, and whether the race is not yet clear.
2 treatment
CVT is a rare disease. Because of its clinical manifestations, imaging, attack forms of diversity, its prognosis still a large degree of unpredictability. At present, this neurological disease physicians still lack experience, the relevant treatment has not yet reached the consistency of views. 21 antithrombotic treatment 2.1.1 low molecular weight heparin (low molecular weight heparin) Nadroparin 90 anti-factor Xa IU / kg subcutaneously 2 times / day, sharing two weeks. After oral anticoagulant applications (such as warfarin) about three months, the international standardization ratio (international normalizedratio, INR) maintained at slips. Meta-analysis of two more influential experimental results show that heparin enable the absolute risk of thrombosis rate dropped 14%, death or disability completely dropped 15%, relative risk rate dropped by their respective 70% and 56%. Currently, advocated heparin as a first-line drug for the treatment of CVT. 2.1.2 thrombolytic therapy: Recently, the 50 cases of patients with thrombolytic results strongly support thrombolytic therapy (urokinase, rt-PA vein thrombosis in the application or direct application). But accurate assessment of the benefit / risk ratio is still very difficult. At present there is no scientific evidence to support the local CVT thrombolytic therapy as the first line of treatment. Only partial thrombolysis for treatment of heparin and symptomatic disease patients is still progress, and the exclusion of other causes of deterioration, such as poor control of epilepsy, secondary pulmonary embolism and physical condition deteriorated. Moderate anticoagulant in the conditions, because thrombosis progress is a result of the deterioration of the rare. This is the indication thrombolysis. 2.2 symptomatic treatment 2.2.1 antiepileptic treatment: According to choose the form of epilepsy corresponding Antiepileptic drugs. 2.2.2 drop intracranial pressure: mannitol, hormones, acetazolamide, lumbar puncture, cerebrospinal fluid (CSF) drainage, the most obvious effect is barbiturate coma (barbiturate coma) and surgical decompression, and so on. Lumbar puncture is necessary, a rapid lowering CSF pressure advantages, especially when vision is threatened. Mannitol and hormone is commonly used method, the other methods use less. 2.2.3 the handling of mental disorders: restlessness obviously can give perphenazine, stability and drugs. 2.2.4 headache treatment: give analgesics such as paracetamol. 2.3 etiology treatment Behcet's disease such as high doses of hormones necessary and sufficient amount of immunosuppressant; Infectious CVT given broad-spectrum antibiotic therapy, sometimes combined surgical treatment required, lesion resection of primary infection.
3 prognosis
CVT's prognosis changed greatly. CVT only in the past when the autopsy to clear diagnosis. Early in the angiography, the mortality rate remains at 30% -50%. In recent years, numerous studies confirm the results, the mortality rate is 10% or less. Factors suggested that the poor prognosis in age too big or too small, coma, cerebellum or deep venous system vein involvement, severe high intracranial pressure, severe infections or malignant reasons, CT showed a hemorrhagic infarction and control bad epilepsy, complications such as pulmonary embolism. Although CVT better prognosis than arterial thrombosis, but there is still a large extent the unpredictability, drowsiness or serious dramatic hemiplegic patients can be left without the restoration of sequelae; On the contrary, only a headache for the patients complained of a sudden deterioration of conditions, such as from the venous sinus thrombosis quickly spread to vein, there will be severe hemiplegia.
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