Glioblastoma And Stroke: Understanding The Link

can glioblastoma cause a stroke

Glioblastoma is a rapidly growing malignant brain tumour that varies in shape and size and causes various clinical symptoms. Although uncommon, glioblastoma can cause ischaemic strokes due to co-existing deficits from the tumour. This can be clinically challenging to diagnose and treat. The underlying causes of ischaemia are multiple, and several factors may contribute to the occurrence of a stroke in a given patient. Glioblastoma can cause acute ischaemic stroke by mechanical compression, arterial dissection, or tumour infiltration to the vascular wall.

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Glioblastoma can cause acute ischemic stroke by mechanical compression

Glioblastoma is a rapidly growing malignant brain tumour that varies in shape and size and causes various clinical symptoms. Although rare, glioblastoma can cause acute ischemic stroke by mechanical compression, arterial dissection, or tumour infiltration to the vascular wall.

A hypercoagulable state (procoagulant factors secreted by gliomas) is common in glioblastoma patients and partly accounts for the high incidence of deep vein thrombosis in these patients. Structural and/or functional vascular damage, as well as changes in the hemostatic and inflammatory process in glioblastoma, may lead to a local or systemic prothrombotic state, which has yet to be fully elucidated.

In most cases, glioblastomas are associated with seizures, headaches, neurological deficits, aphasia, or bleeding. However, these tumours are rarely associated with cerebral infarction and never so deadly.

The occurrence of postoperative stroke in glioblastoma is known and well-described. These complications may result in interruptions of transcortical or deep arteries during the exeresis surgery.

Glioblastoma should be considered in the aetiology of acute ischemic stroke, where neuroimaging plays an important diagnostic role, enabling a more immediate therapeutic approach, with a consequent impact on survival.

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Tumour embolism can cause stroke

Tumour embolism is a rare cause of acute ischaemic stroke. Tumour emboli can be caused by several factors, including:

  • Tumour cell release of inflammatory cytokines and fibrinolysis inhibitors
  • Heightened neutrophil extracellular trap formation (NETosis)
  • Increased platelet aggregation
  • Circulating tumour and platelet extracellular vesicles
  • Excessive endothelial adhesiveness
  • Increased coagulation factors

Direct tumour embolism is a rare cause of acute ischaemic stroke. Histopathological analysis of the thrombus is required to confirm the diagnosis. Mechanical thrombectomy is a potentially safe and effective treatment.

In patients with systemic cancer, causes of acute ischaemic stroke include hypercoagulability, endocarditis, and metastatic disease. Direct tumour embolism is an extremely rare entity that is not often suspected initially.

In a study of 66 patients with ischaemic stroke in the setting of primary brain tumours, an acute operative complication was the cause in about half of the patients, with a variety of other aetiologies making up the remaining half.

In patients with cancer-related ischaemic stroke, the optimal antithrombotic strategy (anticoagulant versus antiplatelet therapy) is unknown, and clinical trials are needed.

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Glioblastoma can cause stroke via arterial dissection

Glioblastoma is a rapidly growing malignant brain tumour that varies in shape and size and causes various clinical symptoms. Although rare, glioblastoma can cause ischaemic strokes, which are clinically challenging due to co-existing deficits from the tumour.

Glioblastomas can cause acute ischaemic strokes by mechanical compression, arterial dissection, or tumour infiltration to the vascular wall. Arterial dissection occurs when there is a tear in one or more of the three tissue layers of an artery. The vertebral artery, which supplies the brain and spine with oxygen-rich blood, is particularly vulnerable to dissection.

The most common cause of ischaemic strokes in glioblastoma patients is the encasement of the relevant arterial branches by the tumour. In some cases, the tumour may completely surround and compress the affected artery. The middle cerebral artery branches are the most commonly affected.

The risk of arterial dissection is higher in younger patients, with vertebral artery dissection being one of the more common causes of stroke in patients younger than 45 years of age. It is estimated that vertebral artery dissection may be responsible for at least 20% of ischaemic strokes in young people.

The signs and symptoms of vertebral artery dissection can be vague, making diagnosis difficult. They include acute and severe unilateral neck pain and/or a headache, ataxia (trouble with balance or coordination), and slurred speech (dysarthria). Neurological symptoms may be delayed and may not be present at all. However, when they do occur, dizziness, ataxia, dysphagia, disequilibrium, unilateral hearing loss, dysarthria, diplopia, and vertigo are the predominant symptoms.

Imaging studies, such as magnetic resonance imaging (MRI) and computed tomography (CT) scans, are crucial for diagnosing glioblastoma and ischaemic strokes. MRI is particularly useful for diagnosing ischaemia in the setting of a glioblastoma, as the appearances on CT scans may be masked by the tumour itself.

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Glioblastoma can cause stroke via tumour infiltration to the vascular wall

Glioblastoma is a rapidly growing malignant brain tumour that varies in shape and size and causes various clinical symptoms. Although ischaemic strokes are an uncommon occurrence in the setting of glioblastoma, they can be clinically challenging due to co-existing deficits from the tumour.

Tumour infiltration to the vascular wall

Glioblastoma can cause acute ischaemic stroke by tumour infiltration to the vascular wall. This is one of the three mechanisms by which glioblastoma can cause acute ischaemic stroke, the other two being mechanical compression of the artery by the tumour and an embolic phenomenon.

In one case, a 74-year-old woman presented with acute onset of severe left hemiparesis. Imaging showed an acute ischaemic lesion in the territory of the right anterior choroidal artery and a right temporal lobe tumour. The operative findings showed that the anterior choroidal artery was encased in the tumour.

In another case, a 79-year-old woman with a history of atrial fibrillation and coronary heart disease developed glioblastoma multiforme at the site of a previous infarction

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Glioblastoma can cause stroke due to hypercoagulability

Glioblastoma is a rapidly growing malignant brain tumour that varies in shape and size and causes various clinical symptoms. Although glioblastomas are rarely associated with cerebral infarction, they can cause acute ischemic stroke. In fact, in most cases, glioblastomas are associated with seizures, headaches, neurological deficits, aphasia, or bleeding.

Glioblastoma can cause acute ischemic stroke for several reasons. Firstly, a hypercoagulable state (procoagulant factors secreted by gliomas) is common and partly accounts for the high incidence of deep vein thrombosis in these patients. Secondly, structural and/or functional vascular damages and changes in the hemostatic and inflammatory process in glioblastoma may lead to a local or systemic prothrombotic state, which has yet to be fully elucidated. Finally, a systemic inflammatory state mediated by cytokines and acute phase proteins is involved in the increased expression of tissue factor, which can also lead to a hypercoagulable state.

The occurrence of postoperative stroke in glioblastomas is known and well described. These complications may result in interruptions of transcortical or deep arteries during the exeresis surgery. Furthermore, the high proliferation, venous thrombosis, and hypercoagulability of the glioblastoma mass increase the significant risk of thromboembolism, including ischemic stroke.

In summary, glioblastoma can cause stroke due to hypercoagulability, which can be caused by a variety of factors, including procoagulant factor secretion, vascular damage, and systemic inflammation.

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