Cerebral metastasis of renal carcinoma mimicking venous haemorrhagic infarction
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《神经病学神经外科学杂志》
1 Department of Neurology, Humboldt University, Berlin, Germany
2 Department of Diagnostic Radiology, University of Leipzig, Germany
Correspondence to:
Dr G C Petzold;
Department of Neurology, Charité Hospital, Humboldt University, Schumannstr. 20/21, 10098 Berlin, Germany; gabor.petzold@charite.de
Keywords: brain metastasis; hypernephroma; cerebral hemorrhage; venous thrombosis; growth rate
Several months after nephrectomy for hypernephroma, a 52 year old woman developed acute demyelinating neuropathy. Paraneoplastic neuropathy was suspected and she was treated with intravenous immunoglobulins (IGs). On the first day of treatment, she had a secondarily generalised tonic-clonic seizure. Contrast enhanced CT revealed right parieto-occipital intracerebral haemorrhage (fig 1A–D). Angiography disclosed persisting cortical veins (fig 1E–F). Although IG therapy was stopped, the patient continued to deteriorate until her condition stabilized after two weeks. The preliminary diagnosis of immunoglobulin induced venous thrombosis with secondary haemorrhagic infarction was made and treatment with phenprocoumon and carbamazepine was initiated. MRI performed six months later showed a residual hyperintense lesion (fig 2A). Four years later, native CT revealed a small hyperdensity with hypodense rim in the same region (fig 2B). Although repetition with contrast enhancement was suggested, the patient was lost to follow up. Two years later, she was re-admitted for homonymous hemianopsia. MRI disclosed a contrast enhancing focal lesion suggestive of cerebral metastasis (fig 2C). Histology of the neurosurgically excised tissue confirmed hypernephroma. She has remained in remission since then.
Figure 1 A–D, axial CT images revealing intracerebral haemorrhage in the right parieto-occipital region. E–F, digital subtraction angiography showing long persisting cortical veins, leading to the initial suspicion of cerebral venous thrombosis.
Figure 2 Axial follow up images at (A) six months (T2w MRI), (B) three years (CT), and (C) five years (contrast enhanced T1w MRI) after initiation of symptoms, disclosing a focal lesion in the right parieto-occipital region (arrows).
Metastases may settle in infarcts in rare occasions.1 However, the initial angiogram shows only subtle changes without clear evidence for venous thrombosis. Moreover, venous thrombosis following intravenous IG administration progresses over the duration of treatment and is reversible after cessation of treatment.2 Therefore, we believe that it is implausible that the putative thrombosis arose on the first day of treatment, that small cortical veins were affected exclusively, and that symptoms worsened rather than improved after treatment was halted. Hence, although the CT scan in 2000 provided the first unequivocal evidence of cerebral metastasis, we propose that the same metastasis may have caused the haemorrhage and seizure three years earlier. Retrospectively, a small hyperintensity suggestive of the metastasis is indeed visible in the right parieto-occipital region six months after the seizure (fig 2A, arrow).
It has been assumed that tumours account for about 5% of patients initially diagnosed with stroke, with about 30% of these cases having metastases and seizures being the leading symptom.1 Several cases have been reported in which patients presenting with intracerebral haemorrhage were later diagnosed with metastases despite unsuggestive imaging.3 Intensely vascularised hypernephroma metastases are especially prone to haemorrhage.4 There are two reports on hypernephroma micro-metastases below the level of detection by imaging methods causing extensive intracerebral haemorrhage.3,5 Our case is remarkable in that diagnosis and treatment were delayed for five years. Furthermore, this case provides the opportunity to calculate the growth rate of an untreated intracerebral renal carcinoma metastasis. Based on the images in fig 2, an average growth rate of 0.9 cm/year can be estimated. A similar growth rate has been estimated for untreated extracerebral hypernephroma metastases.6
We conclude that special diagnostic care is warranted if the primary neoplasm is at high risk for haemorrhagic complications and when cerebral imaging studies are not suggestive of cerebral metastasis because microscopic metastases of these tumours can cause large intracerebral bleedings.
REFERENCES
Morgenstern LB, Frankowski RF. Brain tumor masquerading as stroke. J Neurooncol 1999;44:47–52.
Frame WD, Crawford RJ. Thrombotic events after intravenous immunoglobulin. Lancet 1986;2:468.
Niizuma H, Nakasato N, Yonemitsu T, et al. Intracerebral hemorrhage from a metastatic brain tumor. Importance of differential diagnosis preceding stereotaxic hematoma aspiration. Surg Neurol 1988;29:232–6.
Mandybur TI. Intracranial hemorrhage caused by metastatic tumors. Neurology 1977;27:650–5.
Spetzger U, Mull M, Sure U, et al. Subarachnoid and intraventricular hemorrhage caused by hypernephroma metastasis, accompanied by innocent bilateral posterior communicating artery aneurysms. Surg Neurol 1995;44:275–8.
Oda T, Miyao N, Takahashi A, et al. Growth rates of primary and metastatic lesions of renal cell carcinoma. Int J Urol 2001;8:473–7.(G C Petzold1, J M Valduez)
2 Department of Diagnostic Radiology, University of Leipzig, Germany
Correspondence to:
Dr G C Petzold;
Department of Neurology, Charité Hospital, Humboldt University, Schumannstr. 20/21, 10098 Berlin, Germany; gabor.petzold@charite.de
Keywords: brain metastasis; hypernephroma; cerebral hemorrhage; venous thrombosis; growth rate
Several months after nephrectomy for hypernephroma, a 52 year old woman developed acute demyelinating neuropathy. Paraneoplastic neuropathy was suspected and she was treated with intravenous immunoglobulins (IGs). On the first day of treatment, she had a secondarily generalised tonic-clonic seizure. Contrast enhanced CT revealed right parieto-occipital intracerebral haemorrhage (fig 1A–D). Angiography disclosed persisting cortical veins (fig 1E–F). Although IG therapy was stopped, the patient continued to deteriorate until her condition stabilized after two weeks. The preliminary diagnosis of immunoglobulin induced venous thrombosis with secondary haemorrhagic infarction was made and treatment with phenprocoumon and carbamazepine was initiated. MRI performed six months later showed a residual hyperintense lesion (fig 2A). Four years later, native CT revealed a small hyperdensity with hypodense rim in the same region (fig 2B). Although repetition with contrast enhancement was suggested, the patient was lost to follow up. Two years later, she was re-admitted for homonymous hemianopsia. MRI disclosed a contrast enhancing focal lesion suggestive of cerebral metastasis (fig 2C). Histology of the neurosurgically excised tissue confirmed hypernephroma. She has remained in remission since then.
Figure 1 A–D, axial CT images revealing intracerebral haemorrhage in the right parieto-occipital region. E–F, digital subtraction angiography showing long persisting cortical veins, leading to the initial suspicion of cerebral venous thrombosis.
Figure 2 Axial follow up images at (A) six months (T2w MRI), (B) three years (CT), and (C) five years (contrast enhanced T1w MRI) after initiation of symptoms, disclosing a focal lesion in the right parieto-occipital region (arrows).
Metastases may settle in infarcts in rare occasions.1 However, the initial angiogram shows only subtle changes without clear evidence for venous thrombosis. Moreover, venous thrombosis following intravenous IG administration progresses over the duration of treatment and is reversible after cessation of treatment.2 Therefore, we believe that it is implausible that the putative thrombosis arose on the first day of treatment, that small cortical veins were affected exclusively, and that symptoms worsened rather than improved after treatment was halted. Hence, although the CT scan in 2000 provided the first unequivocal evidence of cerebral metastasis, we propose that the same metastasis may have caused the haemorrhage and seizure three years earlier. Retrospectively, a small hyperintensity suggestive of the metastasis is indeed visible in the right parieto-occipital region six months after the seizure (fig 2A, arrow).
It has been assumed that tumours account for about 5% of patients initially diagnosed with stroke, with about 30% of these cases having metastases and seizures being the leading symptom.1 Several cases have been reported in which patients presenting with intracerebral haemorrhage were later diagnosed with metastases despite unsuggestive imaging.3 Intensely vascularised hypernephroma metastases are especially prone to haemorrhage.4 There are two reports on hypernephroma micro-metastases below the level of detection by imaging methods causing extensive intracerebral haemorrhage.3,5 Our case is remarkable in that diagnosis and treatment were delayed for five years. Furthermore, this case provides the opportunity to calculate the growth rate of an untreated intracerebral renal carcinoma metastasis. Based on the images in fig 2, an average growth rate of 0.9 cm/year can be estimated. A similar growth rate has been estimated for untreated extracerebral hypernephroma metastases.6
We conclude that special diagnostic care is warranted if the primary neoplasm is at high risk for haemorrhagic complications and when cerebral imaging studies are not suggestive of cerebral metastasis because microscopic metastases of these tumours can cause large intracerebral bleedings.
REFERENCES
Morgenstern LB, Frankowski RF. Brain tumor masquerading as stroke. J Neurooncol 1999;44:47–52.
Frame WD, Crawford RJ. Thrombotic events after intravenous immunoglobulin. Lancet 1986;2:468.
Niizuma H, Nakasato N, Yonemitsu T, et al. Intracerebral hemorrhage from a metastatic brain tumor. Importance of differential diagnosis preceding stereotaxic hematoma aspiration. Surg Neurol 1988;29:232–6.
Mandybur TI. Intracranial hemorrhage caused by metastatic tumors. Neurology 1977;27:650–5.
Spetzger U, Mull M, Sure U, et al. Subarachnoid and intraventricular hemorrhage caused by hypernephroma metastasis, accompanied by innocent bilateral posterior communicating artery aneurysms. Surg Neurol 1995;44:275–8.
Oda T, Miyao N, Takahashi A, et al. Growth rates of primary and metastatic lesions of renal cell carcinoma. Int J Urol 2001;8:473–7.(G C Petzold1, J M Valduez)