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Meningioma presenting as stroke: report of two cases and estimation of incidence
  1. R J Komotar,
  2. S C Keswani,
  3. R J Wityk
  1. Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  1. Correspondence to:
 Dr R J Wityk, Meyer 5–181b, The Johns Hopkins Hospital. 600 North Wolfe Street, Baltimore, MD 21287, USA;
 rwityk{at}jhmi.edu

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Meningioma is the most common extra-axial brain tumour in adults and frequently originates in the suprasellar, frontobasal, temporobasal, sphenoid wing, or petroclival regions.1,2 Tumours situated in these locations often involve an intracranial portion of the internal carotid artery (ICA) and may compromise cerebral blood flow.1 While transient cerebral ischaemia has been recognised as a complication of skull base meningiomas,3–7 to our knowledge, there are no documented cases of a meningioma causing stroke by ICA occlusion. We report two cases of meningioma presenting with cerebral infarction as a result of carotid artery compression and estimate the incidence of meningioma related cerebral ischaemia by this mechanism at our institution.

Case reports

Patient 1

A 49 year old right handed man experienced two weeks of left upper extremity weakness. Brain magnetic resonance imaging (MRI) reportedly revealed a right sided mass involving the cavernous sinus, and the patient was referred for a neurosurgical consultation. Two days later the patient noted a sudden increase in symptom severity and presented to an outside hospital. Neurological examination showed a left facial droop, left hand weakness of 2/5 (MRC scale), left proximal upper extremity weakness of 4/5, and decreased sensation on the left hand.

Brain MRI demonstrated a subacute right middle cerebral artery (MCA) territory infarct. In addition, there was a mass in the right cavernous sinus, consistent with a meningioma, which encased the ICA (fig 1A). Cerebral angiography demonstrated occlusion of the right cavernous ICA with radiographic blush from the surrounding meningioma (fig 1B). Flow in the supraclinoidal ICA was reconstituted from the external carotid artery via the ophthalmic artery, and there was cross filling to the right hemisphere via the anterior communicating artery. Transoesophogeal echocardiography was normal without evidence of embolic source. Neuro-ophthalmological examination revealed no signs of emboli. A comprehensive serum hypercoagulable panel revealed no abnormalities.

Figure 1

(A) Coronal T1 weighted MRI with gadolinium demonstrating a meningioma encasing the internal carotid artery (ICA) within the right cavernous sinus. (B) Cerebral angiography with right common carotid artery (CCA) injection demonstrating occlusion of the right ICA and radiographic blush from the surrounding meningioma. (C) Coronal T1 weighted MRI with gadolinium demonstrating a meningioma encasing the right ICA at the apex of the right orbit. (D) Cerebral angiography with right CCA injection demonstrating virtual occlusion of the distal right ICA.

The patient underwent focused radiation therapy of the meningioma and his symptoms gradually improved. However, about six months later he experienced worsening left leg weakness. Brain MRI revealed an acute right MCA and right watershed distribution infarct. There appeared to be fresh thrombus in the right cavernous ICA. The patient was given anticoagulation and has had no further neurological events in over 30 months of follow up.

Patient 2

A 31 year old right handed man had acute onset of complete visual loss in his right eye. The event was painless, and as the patient felt that he could compensate sufficiently, he did not seek medical attention. One morning, about two years later, he experienced sudden onset of left sided numbness, collapsed, and was unable to sit up. Brain MRI revealed a right parietal region infarct, as well as a large mass, consistent with a meningioma, originating from the olfactory groove and encasing the right ICA at the apex of the right orbit (fig 1C). The mass also compressed the right optic nerve. Cerebral angiography demonstrated near occlusion of the right distal ICA (fig 1D) with the majority of perfusion to the right hemisphere being supplied by cross filling from the left ICA. Transoesophogeal echocardiography was normal without evidence of embolic source. Neuro-ophthalmological examination revealed no signs of emboli. A comprehensive serum hypercoagulable panel revealed no abnormalities. The patient underwent complete tumour resection. Over the next several weeks he recovered most neurological function but was left with no vision in the right eye and persistent left arm numbness.

Discussion

Meningiomas are prevalent brain tumours commonly located at the skull base.1,2 By virtue of their position, these tumours have the potential to affect portions of the ICA and compromise cerebral blood blow. Previous reports have suggested that meningiomal compression of the carotid artery may produce transient neurological symptoms including loss of consciousness, hemiparaesis, paresthaesias, and global amnesia.3–7 To our knowledge, however, there has never been a documented case of cerebral infarction as a result of meningioma related ICA compression.

We present two patients with cerebral infarction attributable to meningiomal ICA involvement. In case one, imaging after the first ischaemic episode demonstrated a large cavernous sinus meningioma surrounding and occluding the right ICA. MRI after the second ischaemic episode suggested stump thrombosis in the cavernous ICA. The stroke was probably attributable to both haemodynamic hypoperfusion as well as artery to artery embolisation. In case two, imaging demonstrated a large olfactory groove meningioma encasing the right ICA with near occlusion of the vessel. It seems his stroke also occurred because of a combination of hypoperfusion and thromboembolism. Neither of these patients had evidence of vasculopathy or another aetiology for stroke.

Although meningiomas commonly involve the ICA, they rarely present with symptoms of cerebral ischaemia. These tumours typically do not change vascular patency even when completely encasing the ICA and its bifurcation into the MCA and anterior cerebral artery. It may be possible that meningiomas, being slow growing and non-invasive, do not exert sufficient external force to significantly compress the high pressure arterial vasculature. In addition, the ICA vessel wall is thick with a muscular media segment, thereby offering substantial resistance to vascular compromise. By comparison, cortical veins and dural sinuses, being low pressure compartments with thin walls, are frequently compromised by meningiomas.8 The tumour’s slow growth rate, however, allows for development of substantial collateral drainage, and as a result, cortical infarction attributable to venous insufficiency has only been reported postoperatively after injury to these compensatory pathways.9

The rate at which meningiomas present with symptoms of cerebral ischaemia is unknown. In an attempt to estimate the incidence at which meningiomas manifest symptoms of cerebral ischaemia by ICA compression, we reviewed retrospectively the medical records of 1617 patients with meningiomas evaluated by the surgical neuropathology service at our institution from 1985 to 2001. We identified three patients with meningiomal involvement of the ICA as well as neurological symptoms that could be attributed to ICA compression. The first patient had a parasellar/medial sphenoid wing meningioma that narrowed the right ICA within the cavernous sinus and presented with progressive left hemiparaesis. The second patient had a petroclival meningioma that encased the left ICA and presented with right upper extremity paresthaesias. The third patient had a frontobasal meningioma that involved the right ICA and presented with evolving left hemiparaesis. Thus, while meningiomas frequently involve intracranial portions of the ICA, we estimate the incidence of meningioma related cerebral ischaemia by carotid artery compression to be only 3 of 1617 tumours or 0.19%.

In conclusion, we describe two cases of cerebral infarction as a result of carotid artery compression by a meningioma. We hypothesise that meningiomas typically do not compromise the ICA significantly because of the slow growth rate and non-invasive nature of the tumour, as well as the high arterial pressures of the ICA. Consequently, cerebrovascular insufficiency is an exceedingly uncommon presentation for meningioma.

References

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Footnotes

  • Competing interests: none declared.

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