الفهرس Only 14 pages are availabe for public view
 |  | from | 202 |  |  |
| | | from | 202 | | |
Abstract
Venous blood from the brain flows via the superficial (cortical) and the deep cerebral veins into the venous dural sinuses. There are numerous connections between the cortical veins and dural sinuses, and also with the venous system of the meninges, scalp and nasal sinuses. This facilitates the spread of thrombus or infection via the emissary veins to the intracranial venous system and adjacent brain parenchyma. The communication between the intracranial and extracranial venous system also may allow the opening of collateral draining vessels in the event of an occlusion.
To understand the symptoms and signs of sinus thrombosis, two different mechanisms should be distinguished: thrombosis of the cerebral veins, with local effects caused by venous obstruction, and thrombosis of the major sinuses, which causes intracranial hypertension and in the majority of patients, these two processes occur simultaneously.
CVT is typically a multifactorial disorder in which more than one risk factor could be identified. Among these factors are inherited and acquired hypercoaguable states. The genetic hypercoaguable factors include: antithrombin deficiency, protein C and protein S deficiency, factor V Leiden mutation, prothrombin mutation, hyperhomocysteinemia and elevated concentrations of factors II, VIII, IX, XI and fibrinogen. However, the acquired hypercoaguable states include: use of oral contraceptives and hormone replacement therapy, pregnancy puerperium and antiphospholipid syndrome. Other risk factors include infection, many organisms are possible and infection can be mixed but Staphylococcus aureus is the commonest pathogen. Trauma and some neurosurgical procedures can also result in cerebral sinus thrombosis. Crohn’s disease and ulcerative colitis increase the risk as does the use of steroids to treat them. Hematological conditions include paroxysmal nocturnal haemoglobinuria, thrombotic thrombocytopenia purpura, sickle cell disease and polycythaemia rubra vera. Some malignancies are associated with risk. Vascular diseases include SLE, Wegener’s granulomatosis and Behçet’s disease. Risk is also increased by nephrotic syndrome, dehydration, cirrhosis and sarcoidosis.
CVT presents with a remarkably wide spectrum of symptoms and clinical presentation can be extremely varied where symptoms can evolve over hours to a few weeks. Headache is the most frequent symptom in patients with CVT. However, headache presenting as the only symptom of CVT is rare and it is usually seen in combination with other neurological signs and symptoms. The most common symptoms and signs are focal seizures with or without secondary generalization, paresis (uni- or bilateral) and papilloedema. Some patients are presented with isolated intracranial hypertension (BIH) type picture (headache, visual disturbance and papilloedema). Other rarer presentations include thunderclap headache mimicking subarachnoid hemorrhage. Cortical vein involvement alone without extension to the dural sinuses is rare and may present with a ‘stroke-like’ episode. Thrombosis of the deep cerebral veins is usually accompanied by impairment of consciousness and occasionally abnormalities of eye movements or pupillary reaction. Involvement of the cavernous sinus produces a localized syndrome of proptosis, cheimosis, painful external ophthalmoplegia, papilloedema and involvement of the ophthalmic and maxillary divisions of the trigeminal nerve. Isolated thrombosis of the lateral sinus present mostly as isolated intracranial hypertension.
Investigations should focus on establishing the diagnosis and searching for underlying causes. Radiological diagnosis is aimed at confirming the presence of the thrombus within the venous system and identifying any secondary effects of the thrombosis upon the brain parenchyma or CSF pathways. Conventional CT will often remain the first imaging modality to be used simply due to availability and also to exclude other conditions such as intracerebral hemorrhage or abscess. Magnetic resonance imaging (MRI) combined with magnetic resonance venography (MRV) have largely replaced invasive cerebral angiography and conventional CT. There are, however, pitfalls of this technique which may, in doubtful cases, make cerebral angiography necessary. More recently, CT venography has been shown to be superior to MRV in visualising sinuses or smaller cerebral veins or cortical veins with low flow, yet this technique is not used routinely at present. Cerebral angiography is an invasive technique and is now considered only if other noninvasive investigations have remained non diagnostic.
Treatment strategies are aimed at treating the underlying pathology, antithrombotic treatment, and symptomatic treatment as controlling intracranial pressure and treatment of seizures or focal deficits caused by cerebral edema or infarction. The aims of antithrombotic treatment in CVT are to recanalise the occluded sinus or vein, to prevent the propagation of the thrombus, and to treat the underlying prothrombotic state. Anticoagulants with subcutaneous or intravenous heparin are widely used as first line therapy. If patients deteriorate despite adequate anticoagulation and other causes of deterioration have been ruled out, thrombolysis or thrombectomy by endovascular and surgical techniques have been employed to remove the clot. Surgical techniques are further used to treat the sequelae of CVST, including hydrocephalus, raised intracranial pressure, visual failure and hemorrhagic stroke.
Cerebral venous thrombosis (CVT) in children is a multifactorial disease that, in the majority of cases, results from a combination of prothrombotic risk factors and/or the underlying clinical condition. It is a serious disease that is being increasingly diagnosed, mainly because of more sensitive diagnostic procedures and increasing clinical awareness of the disease. The clinical presentation shows a wide spectrum of symptoms, eg, seizures, papilloedema, headache, lack of consciousness or lethargy, and focal neurological deficits. However CVT in elderly is of poor prognosis and patients usually presents with disturbed consciousness.