CTE and ischemic stroke may manifest within minutes or hours, and affected individuals frequently suffer from sensory deficits, limb weakness, ataxia, hemiparesis, speech disturbances, unilateral visual impairment, and reduced consciousness [14]. Headaches, nausea, vomiting and seizures are only observed in some patients.

In contrast, headaches are by far the most common symptom of cerebral vein and sinus thrombosis. They are experienced by almost 90% of affected individuals [8]. More than a third of them sustains seizures, with generalized seizures occurring more frequently than focal seizures. Many patients present with hemiparesis. Other symptoms are observed in a minor share of cases and comprise diplopia and vision loss, aphasia, an altered mental status and reduced consciousness.

Of note, it is rarely possible to deduce the site of lesion from the clinical picture, although the nature of neurological deficits presented by an individual patient reflects the function of the affected brain region. The complexity of the neuronal network doesn't allow for reliable conclusions besides the fact that right-sided paresis indicates an infarction of the left hemisphere and vice versa.

• Weakness

  A 40-year-old female presented as an emergency with a 10-day history of headache and left sided weakness. [ncbi.nlm.nih.gov]

  Common symptoms include weakness on one side of the body or face, but with a BA stroke, the weakness could affect both arms and legs. Other common symptoms include dizziness, nausea, vomiting or speech impairment. Dr. [livestrong.com]

  Sensitive but highly non-specific 25% of patients will have headache alone ( Saposnik 2011 ) Typically is a gradual onset of headache that progresses over days to weeks Rarely, can mimic subarachnoid hemorrhage (acute onset) Neurologic complaints: weakness [coreem.net]

  The triage nurse added, “Weakness, numbness and tingling to the left upper extremity, onset yesterday morning; dropped tea cup from left hand; slight unsteadiness in left leg, onset yesterday.” [acepnow.com]

• Pallor

  She was further evaluated at the higher centre, the physical examination was unremarkable according to them except for the pallor. [hindawi.com]

  In some areas where brain parenchyma was infiltrated by neutrophils there was evidence of necrosis with staining pallor, microvacuolization, and hypereosinophilic neuronal necrosis (Figure 3), raising the possibility of acute infarction rather than early [ncbi.nlm.nih.gov]

• Constitutional Symptom

  symptoms, fever, weight loss, chemotherapy with L Asparaginase or thalidomide, and so forth. [hindawi.com]

  Scalp edema and dilated scalp veins may be seen on examination.68 For lateral sinus thromboses, symptoms related to an underlying condition (middle ear infection) may be noted, including constitutional symptoms, fever, and ear discharge. [ahajournals.org]

  Scalp edema and dilated scalp veins may be seen on examination. 68 For lateral sinus thromboses, symptoms related to an underlying condition (middle ear infection) may be noted, including constitutional symptoms, fever, and ear discharge. [stroke.ahajournals.org]

• Coronary Atherosclerosis

  Coronary thrombosis, arterial thrombosis in a coronary artery, is a complication of coronary atherosclerosis. [medical-dictionary.thefreedictionary.com]

• Diplopia

  Cerebral venous sinus thrombosis presenting with diplopia in pregnancy: a case report. [jmedicalcasereports.biomedcentral.com]

  We report a case of transverse sinus and superior sagittal sinus thrombosis that presented with diplopia in a pregnant woman. [jmedicalcasereports.com]

  A 40-year-old woman with aplastic anemia visited our hospital because of severe headache, nausea, vomiting, blurred vision and diplopia for a period of 1 month. She had taken oxymetholone for 2 years. [ncbi.nlm.nih.gov]

  After five days of admission we discontinued the intravenous heparin. 2 weeks after admission, the headache and diplopia were resolved completely. [jneuro.com]

  Initial symptoms of patients were headache(n=19), epileptic seizures (n=6), blurred vision (n=1), diplopia (n=2) and one of the patient had vertigo. Ten patients had only one sinus thrombosis however 19 patients had more than one sinus thrombosis. [adudspace.adu.edu.tr]

• Blurred Vision

  A 40-year-old woman with aplastic anemia visited our hospital because of severe headache, nausea, vomiting, blurred vision and diplopia for a period of 1 month. She had taken oxymetholone for 2 years. [ncbi.nlm.nih.gov]

  Initial symptoms of patients were headache(n=19), epileptic seizures (n=6), blurred vision (n=1), diplopia (n=2) and one of the patient had vertigo. Ten patients had only one sinus thrombosis however 19 patients had more than one sinus thrombosis. [adudspace.adu.edu.tr]

  • Blurred Vision, Fainting and loss of consciousness, Seizures • Cases of CSVT are very low, as of 5 in 1 million people in adults, and 3 in 1 million people in children's under age 18. 3. • The major causes of CSVT in the newborns are infection. [slideshare.net]

  But then in a few days things got even worse, with symptoms such as blurred vision, nausea and a sensitivity to light. It was finally a magnetic resonance imaging along with magnetic resonance angiography that identified the problem. [relieve-migraine-headache.com]

• Abnormal Behavior

  Stem Cell Therapy, Stem Cell Treatment > (ITP During Pregnancy, A Look at Newborn Screening, Abdomen, Abdominal Mass, Abdominal Masses in Children, Abdominal Pain, Abdominal Pain During Pregnancy, Abdominal Radiology, Abdominal Trauma, Abdominal X-ray, Abnormalities [nbscience.com]

• Stroke

  The risk of developing atherosclerosis, CTE and ischemic stroke does increase with age, though, and the patients' median age at first-ever stroke is about 70 years. [symptoma.com]

  Plasma tHcy concentrations of stroke patients with normal serum creatinine concentrations were not significantly different to those of controls. Hyperhomocysteinemia in Black patients with stroke may be partially caused by renal insufficiency. [ncbi.nlm.nih.gov]

  This chain of events is part of a stroke that can occur in adults and children. It can occur even in newborns and babies in the womb. A stroke can damage the brain and central nervous system. [hopkinsmedicine.org]

• Seizure

  Symptomatic and prophylactic usage of antiepileptics are recommended in patients with higher risk of seizure (eg, supratentorial lesion involvement) and seizure on presentation. [acepnow.com]

  Seizures, including focal, generalized, and status epilepticus, are seen in 30–40% of patients [7,11]. As seizures are rare in strokes, CVT should be considered in any patient with a focal neurologic deficit and seizure [1,2]. [epmonthly.com]

  In 1884, Bouchut observed cerebral sinovenous thrombosis in infants who had seizures during febrile or debilitating illnesses. The same year, Rilliet and Barthez reported infection as a predisposing factor in young children. [medlink.com]

  Because seizures occur less often in other types of stroke, cerebral venous thrombosis should be considered in patients with seizures and other focal findings consistent with stroke. [webmedcentral.com]

  Seizures Seizures are very common at presentation among patients with CVT. One prospective observational study found seizures in 39.3% of CVT patients and 6.9% of patients had early seizures (within 2 weeks) [112]. [intechopen.com]

• Focal Neurological Deficit

  The diagnosis should be suspected in cases of subacute headache accompanied by other focal neurological deficits, seizures or altered consciousness. [tidsskriftet.no]

  Symptoms headaches decreased/altered conscious state decreased/altered vision nausea/vomiting Signs papilloedema cranial nerve palsies focal neurological deficits seizures coma CVT pathogenesis remains poorly understood 5. [radiopaedia.org]

  Headaches are a typical presenting manifestation of CVT, while focal neurological deficits, seizures, and increased intracranial pressure may develop as the disease progresses. [amboss.com]

  […] brain injury Seizures (35-50%) ( Stam 2005 ) Focal neurologic deficits (25-71%) – hemianopsia, contralateral weakness, aphasia etc Differential Diagnosis Ischemic stroke Intracranial Hemorrhage (ICH) Encephalitis Subarachnoid Hemorrhage Mass Effect [coreem.net]

• Aphasia

  Other symptoms are observed in a minor share of cases and comprise diplopia and vision loss, aphasia, an altered mental status and reduced consciousness. [symptoma.com]

  Papilledema Severe global mental status depression or alteration may signify impending brain herniation Manifestations resulting from focal brain injury Seizures (35-50%) ( Stam 2005 ) Focal neurologic deficits (25-71%) – hemianopsia, contralateral weakness, aphasia [coreem.net]

  This can lead to cerebral edema, infarction, or hemorrhagic infarction, which may manifest with motor and sensory deficits, cranial nerve palsy, aphasia, and seizures.3 Diagnosis American Heart Association/American Stroke Association 2011 guidelines recommend [acepnow.com]

  […] oculomotor palsy) Cortical vein thrombosis: motor deficits, sensory deficits, seizures Sagittal sinus thrombosis: motor deficits, bilateral deficits, seizures Lateral sinus thrombosis: isolated intracranial hypertension Left transverse sinus thrombosis: Aphasia [litfl.com]

• Dizziness

  The person may also be dizzy, nauseous and have a headache in the back of the head. Memory loss can also occur. Eighty percent of strokes can be prevented through positive lifestyle interventions. [livestrong.com]

  Be wary if you experience the following signs: Headache Confusion or dizziness One side of the body becomes weak or paralyzed Some part of the body suddenly becomes severely numb Sudden loss of vision, or some sort of visual disturbance Walking becomes [visiontimes.com]

  They include: Severe headache especially with vomiting, sleepiness, or double vision Trouble seeing clearly in one or both eyes Severe dizziness or unsteadiness that may lead to losing balance or falling Seizure activity In newborns and infants Seizures [chop.edu]

The sudden onset of neurological deficits is highly suggestive of CT and subsequent infarction. However, the disease may also follow a subacute or chronic course, particularly in case of a partial occlusion of vessels or cerebral vein thrombosis. Furthermore, there is a considerable overlap of symptoms triggered by CT and intracranial hemorrhages, both of which may even occur concomitantly. Because "time is brain" in any type of stroke, it is of utmost importance to confirm the diagnosis, to localize the site of thrombosis and to assess the extent of brain damage as soon as possible. Conventional magnetic resonance imaging/angiography as well as computed tomography scans/angiography are most commonly employed to this end. The following may be observed:

• With respect to magnetic resonance imaging, thrombi initially depict as isointense and hypointense foci in T1- and T2 weighted images, respectively. Over the course of time, the aspect of thrombi changes: After several days, they appear as hyperintense areas in both weightings. Ischemic brain tissue is best visualized in diffusion-weighted images.
• In images obtained by means of contrast-enhanced computed tomography, acute CT may merely display as a filling defect in vascular structures. Remodelling processes eventually lead to thrombi appearing as hypodense areas surrounded by a hyperdense border. An intracranial hemorrhage depicts as a region of hyperdense signal intensity. Of note, non-contrast-enhanced computed tomography is preferred in patients presenting with acute stroke within three hours of symptom onset.

Moreover, transcranial Doppler sonography may be used to visualize an occlusion of vessels forming the circle of Willis or to diagnose CT in patients presenting with vertebrobasilar insufficiency [15].

In any case, blood specimens should be obtained to assess the overall condition of the patient (e.g., glucose, electrolytes, metabolic profile) and to carry out coagulation tests. Depending on the patient's medical history and the presence of additional symptoms, further measures may be necessary to diagnose an underlying condition predisposing for CT.

Treatment primarily aims at reestablishing the blood flow through the occluded vessel. Although dependent brain tissue may already be irreversibly damaged, the ongoing disturbance of blood flow in downstream vasculature does predispose for additional thrombus formation and an exacerbation of the disease. Thrombolysis may be achieved by intravenous administration of recombinant tissue-type plasminogen activator (tPA), which is the only drug approved for ischemic stroke to date. The recommended dosage is 0.9 mg/kg, with a maximum dose of 90 mg. 10% of the total dose are given as a bolus within one minute, and the remaining dose is infused over an hour [16]. tPA application has to be initiated within a few hours after the onset of stroke, and the respective time window has been defined as 3 and 4.5 hours in North America and Europe, respectively. For country-specific recommendations, the reader is referred to a recent publication on this topic [17]. Mechanical thrombolysis may constitute an alternative to tPA therapy, particularly in patients who present past the abovedefined time window or in those individuals who fail to respond to intravenous tPA [18]. Angioplasty and stenting may be performed. Patients suffering from malignant middle cerebral artery occlusion may require an emergency decompression by means of craniotomy. This procedure has been shown to improve survival rates.

Additional therapeutic measures may comprise the following [16]:

• Assessment of airways, breathing and circulation; possibly supplementation of oxygen, mechanical ventilation
• Maintenance of physiological body temperature, e.g., by administering antipyretics
• Fluid therapy
• Oral administration of aspirin as an antiplatelet agent
• Administration of antihypertensive medication like labetalol and nicardipine: While indicated in case of severely increased blood pressure, moderate hypertension may favor cerebral perfusion and recanalization. Patients presenting with hypotension may thus be given vasopressors.

• Antiepileptic treatment in case of seizures

In cases of an association of CT with ischemic or hemorrhagic stroke, morbidity and mortality rates are high. In fact, ischemic infarction has been reported to account for 5 deaths per 100,000 inhabitants and year, while hemorrhagic stroke causes twice as many deaths within the same period of time. Considering that incidence rates of ischemic stroke are much higher, these values indicate a worse prognosis for those patients sustaining hemorrhagic infarction. Case fatality rates for ischemic and hemorrhagic stroke were 6 and 20% at ten days, and 21 and 32% at one year, respectively [12].

A multinational study on the outcome of cerebral vein and sinus thrombosis yielded the following results after a median follow-up of 16 months [8]:

• No sequelae in 57% of patients
• Minor, mild, moderate, and severe disability in 22, 8, 3 and 2% of patients, respectively
• Overall mortality of 8%

Unfavorable prognostic factors include increased age, male sex, seizures, hemiparesis, severe neurological deficits, coma, thrombosis of the deep venous system, and intracranial hemorrhage, among others [13].

A plethora of pathologies may lead to CT, either by inducing ICT or by increasing the overall likelihood to develop thrombi and to suffer the consequences of CTE. They may be classified as follows:

• Any inflammatory process affecting the brain - be it encephalitis, meningitis or an inflammation of adjacent tissues - may cause endothelial lesions of brain vessels and trigger the coagulation cascade, leading to ICT. Sinusitis, for instance, is a very common disease that may spread to the brain [1]. Similarly, endothelial damage may be inflicted by trauma sustained during an accident or surgery. Intracranial neoplasms may also interfere with brain vessel function and predispose for local thrombus formation. This applies particularly to hematogenous metastases.
• Some diseases are known to induce cerebral vasculitis and as has been explained above, inflammatory processes facilitate thrombus formation [2]. In detail, cerebral vasculitis and ICT may be observed in patients suffering from these disorders:
• Giant cell arteritis
• Polyarteritis nodosa
• Wegener granulomatosis
• Additionally, any condition leading to generalized hypercoagulability may provoke CT. Since these are systemic disorders, they may be associated with ICT and CTE. The following shall serve as examples:
• Dehydration
• Pregnancy
• Thrombophilia
• Polycythemia
• Antiphospholipid syndrome
• Protein C deficiency
• Protein S deficiency
• Antithrombin III deficiency
• Leiden factor V mutation
• Disseminated intravascular coagulation
• Intake of drugs increasing the risk of thrombosis, particularly of oral contraceptives
• By far the most common cause of ICT and CTE is atherosclerosis. Risk factors for atherosclerosis and thus for the thrombotic occlusion of brain vessels are hypertension, hypercholesterolemia, diabetes mellitus, overweight/obesity and tobacco consumption [3]. Atherosclerotic plaques that develop in cerebral vessels may narrow their lumen and thus render the respective vascular structure more susceptible to thrombotic occlusion, independent of the origin of the thrombus.
• Patients suffering from endocarditis are prone to CTE.
• Further enumeration of pathologies that may lead to peripheral thrombosis and subsequent CTE is beyond the scope of this article, but several extensive works regarding this topic have been published [4] [5].

Cerebral infarction is one of the leading causes of death and long-term disability, especially in developed countries. About 87% of strokes are ischemic, only 10% are hemorrhagic, and 3% result from conditions not discussed in this article [6]. While atherosclerosis with superimposed thrombosis is the most common cause of ischemic infarction, CT only accounts for a minor share of hemorrhagic strokes: Cerebral vein and sinus thrombosis have been estimated to cause less than 1% of strokes [7].

Racial predilection has been reported for ischemic stroke, e.g., first-ever incidence rates in the United States have been calculated to 88, 149, and 191 per 100,000 Caucasians, Hispanics, and Blacks, respectively. The annual incidence of cerebral vein and sinus thrombosis is about 1 per 100,000 inhabitants, with two-thirds of affected individuals being children. The risk of developing atherosclerosis, CTE and ischemic stroke does increase with age, though, and the patients' median age at first-ever stroke is about 70 years.

Gender predilection has been described for cerebral vein and sinus thrombosis, which affects women about three times more often than men [8]. In this context, it has been hypothesized that the wide-spread use of oral contraceptives contributes to women's propensity for CT. Meta-analyses of studies on ischemic stroke did not reveal marked differences between incidence rates in men and women, though [9].

As has been indicated above, CT may affect arteries, veins and vein sinuses: Thrombi rarely form within arteries, but are generally carried here. If thrombi lodge in a cerebral artery, dependent tissues are suddenly deprived of oxygen, glucose and further nutrients, and the affected individual sustains an ischemic stroke. In contrast, thrombi located in veins and vein sinuses hinder the drainage of blood, which may accumulate before the mechanical obstacle and increase the intravascular pressure. This rapidly causes a passage of blood beyond the boundaries of the vascular system, which is the eponym for hemorrhagic infarction or intracranial hemorrhage. Local mass effects largely contribute to the extent of brain damage in these cases.

In any case, a cerebrovascular accident interferes with the function of dependent brain regions. Neurons are highly dependent on aerobic metabolism and upon cessation of blood supply, energy-sparing mechanisms leading to membrane hyperpolarization are initiated. Nevertheless, ATP-dependent processes like the maintenance of membrane potentials by sodium-potassium pumps ceases within minutes [10]. Neurons depolarize and cytotoxic edema develops. A dysregulation of neurotransmitter release ensues and excess glutamate mediates excitotoxicity and an exacerbation of brain damage. Within several hours, vasogenic edema develops. Contrary to cytotoxic edema, vasogenic edema is associated with an overall increased content of water and electrolytes, and this condition leads to an enhanced intracranial pressure.

The primary thrombus (or thromboembolus) does not necessarily occlude the entire lumen of the affect vessel. However, even a small thrombus may induce rheological anomalies that favor the local formation of secondary thrombi. Consequently, the perfusion disorder augments in severity. At the same time, the partial or complete occlusion of a cerebral vessel ensues disturbances of blood flow in downstream vasculature, i.e., CT of a major artery may lead to the formation of secondary thrombi in arterioles, CT of arterioles may be followed by thrombus formation in venules [11].

Atherosclerosis is the single most important risk factor for ICT and CTE and thus, any measure to reduce the formation of atherosclerotic plaques contributes to lower a patient's risk of CT. In detail, such measures may include an adequate control of body weight, blood pressure, glucose and lipid levels. Patients are to be advised to refrain from smoking and to take care of proper hydration, a healthy diet and regular exercise. Furthermore, women at risk of thrombosis should avoid the use of oral contraceptives. Diseases related to hypercoagulability may indicate prophylactic treatment with anticoagulants.

Cerebral thrombosis (CT) refers to the presence of a blood clot in blood vessels of the brain. Thrombi may form within or be carried to cerebral arteries, veins and vein sinuses, and consequently interfere either with oxygen and nutrient supply to brain tissue or with venous drainage. Depending on the type of vessel, the extent of vessel occlusion and vascular wall damage, CT may lead to ischemic infarction or hemorrhagic infarction.

In the narrow sense of the term, CT occurs if a thrombus develops within a cerebral vessel (intrinsic cerebral thrombosis, ICT). On the one hand, this may happen at sites of endothelial lesions that induce activation of the coagulation cascade via the extrinsic pathway. Such lesions, in turn, may be provoked by a local inflammatory process, trauma or neoplasm. Furthermore, systemic coagulopathies may evoke thrombus formation in the whole cardiovascular system, including but not limited to cerebral vessels. Thrombi form more frequently within cerebral veins and vein sinuses than within cerebral arteries.

In contrast, cerebral thromboembolism (CTE) mainly affects cerebral arteries. Here, thrombi develop in any other part of the cardiovascular system and are subsequently dragged away by the bloodstream. Patients sustaining CTE often suffer from atherosclerosis or endocarditis, because both conditions are associated with endothelial lesions. Inside the brain, thrombi may eventually reach an artery whose lumen does not allow the blood clot to pass through. This results in artery occlusion, ischemia and stroke.

Thrombosis refers to the formation of a blood clot within a vessel, and if this process occurs within a cerebral artery, vein or sinus, it is denominated cerebral thrombosis (CT). Additionally, blood clots may form within any other vascular structure, may be dragged away by the bloodstream and lodge in intracranial arteries. Because predisposing factors, clinical symptoms and treatment regimens are largely similar, the latter may also be considered a subtype of CT.

Brain tissue is highly dependent on aerobic metabolism and an occlusion of cerebral vessels is associated with their sudden deprivation of oxygen, glucose and further nutrients, which may result in cerebral infarction or stroke. Common symptoms include visual impairment, ataxia, hemiparesis, and aphasia. On the other hand, CT may be related to subacute or chronic symptoms like recurrent headaches. These may be experienced in case of an incomplete occlusion of cerebral vessels, venous or sinus thrombosis and a reduction of blood drainage. An exacerbation of such apparently mild forms of CT may occur at any time.

Because brain damage is mostly irreversible, CT and stroke should be treated as soon as possible. In this context, the administration of recombinant tissue-type plasminogen activator aims at thrombolysis and recanalization, i.e., at dissolving the blood clot and reestablishing blood flow. Thrombi may also be destroyed mechanically. Additional measures are undertaken to control underlying pathologies that predispose for CT, e.g., hypertension, hypercholesterolemia, diabetes mellitus, and overweight/obesity.

Patients may contribute to lowering their individual risk of CT by preventing the aforementioned conditions, and by undergoing regular check-ups to assure blood pressure, glucose and lipid levels are well controlled. Furthermore, they are advised to refrain from tobacco consumption, to adhere to a healthy diet and to realize physical activity to maintain normal weight.

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