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Arteriovenous malformation within an isocitrate dehydrogenase 1 mutated anaplastic oligodendroglioma.

Lai G, Muller KA, Carter BS, Chen CC - Surg Neurol Int (2015)

Bottom Line: The co-occurrence of intracranial arteriovenous malformations (AVMs) and cerebral neoplasms is exceedingly rare but may harbor implications pertaining to the molecular medicine of brain cancer pathogenesis.Here, we present a case of de novo AVM within an isocitrate dehydrogenase 1 mutated anaplastic oligodendroglioma (WHO Grade III) and review the potential contribution of this mutation to aberrant angiogenesis as an interesting case study in molecular medicine.The co-occurrence of an IDH1 mutated neoplasm and AVM supports the hypothesis that IDH1 mutations may contribute to aberrant angiogenesis and vascular malformation.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, University of California, San Diego, CA, USA.

ABSTRACT

Background: The co-occurrence of intracranial arteriovenous malformations (AVMs) and cerebral neoplasms is exceedingly rare but may harbor implications pertaining to the molecular medicine of brain cancer pathogenesis.

Case description: Here, we present a case of de novo AVM within an isocitrate dehydrogenase 1 mutated anaplastic oligodendroglioma (WHO Grade III) and review the potential contribution of this mutation to aberrant angiogenesis as an interesting case study in molecular medicine.

Conclusion: The co-occurrence of an IDH1 mutated neoplasm and AVM supports the hypothesis that IDH1 mutations may contribute to aberrant angiogenesis and vascular malformation.

No MeSH data available.


Related in: MedlinePlus

Pretreatment imaging: Computed tomography (a) T1 magnetic resonance postcontrast (b) and fluid attenuation inversion recovery (c) showing 6 cm × 5 cm × 5 cm bilateral frontal lobe mass with internal coarse calcifications, marked enhancement, and surrounding vasogenic edema with multiple flow voids and large draining veins. There is abnormal tissue interspersed between vascular elements and large areas of cystic changes and necrosis
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Figure 1: Pretreatment imaging: Computed tomography (a) T1 magnetic resonance postcontrast (b) and fluid attenuation inversion recovery (c) showing 6 cm × 5 cm × 5 cm bilateral frontal lobe mass with internal coarse calcifications, marked enhancement, and surrounding vasogenic edema with multiple flow voids and large draining veins. There is abnormal tissue interspersed between vascular elements and large areas of cystic changes and necrosis

Mentions: The patient is a 44-year-old woman who presented with a sub-acute neurocognitive decline over a several months period, such that she was no longer able to perform routine tasks required for daily activities. Past medical history is notable for Graves disease (diagnosed 2005, treated with methimazole) and endometrial adenocarcinoma s/p total abdominal hysterectomy-bilateral salpingo-oophorectomy and chemotherapy (carboplatin and paclitaxel) in 2009, in remission since. Neurological examination was notable for difficulties recalling the events prior to the presentation and disorganized speech. However, the patient re-oriented easily. Physical examination revealed bilateral and symmetric proptosis. Laboratory values were unremarkable. Computed tomography scan of the brain showed 6.1 cm × 4.8 cm × 4.9 cm mass centered over the anterior falx cerebri with moderate surrounding hypodensity and effacement of adjacent sulci [Figure 1a]. Patchy hyper-density was seen within the mass, with Hounsfield units >200 suggestive of calcification. Magnetic resonance imaging (MRI) demonstrated an irregularly shaped, intra-axial mass with heterogeneous contrast enhancement that abut the anterior communicating artery (ACA) [Figure 1b]. Fluid attenuation inversion recovery imaging revealed complex patterns of hypointense tubular outlines within the lesion, suggestive of considerable vascularity within the lesion [Figure 1c]. MR angiogram showed multiple vascular pedicles emerging from both ACA branches penetrating the lesion as well as prominent venous drainages into the anterior and posterior superior sagittal sinus. Diagnostic cerebral angiogram confirmed extensive blood supply from the bilateral ACAs as well as the left middle cerebral artery (MCA) [Figure 2a] with a 2.4 cm × 1.4 cm × 2.3 cm AVM nidus and prominent venous drainages into the superior sagittal sinus [Figure 2b].


Arteriovenous malformation within an isocitrate dehydrogenase 1 mutated anaplastic oligodendroglioma.

Lai G, Muller KA, Carter BS, Chen CC - Surg Neurol Int (2015)

Pretreatment imaging: Computed tomography (a) T1 magnetic resonance postcontrast (b) and fluid attenuation inversion recovery (c) showing 6 cm × 5 cm × 5 cm bilateral frontal lobe mass with internal coarse calcifications, marked enhancement, and surrounding vasogenic edema with multiple flow voids and large draining veins. There is abnormal tissue interspersed between vascular elements and large areas of cystic changes and necrosis
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4496836&req=5

Figure 1: Pretreatment imaging: Computed tomography (a) T1 magnetic resonance postcontrast (b) and fluid attenuation inversion recovery (c) showing 6 cm × 5 cm × 5 cm bilateral frontal lobe mass with internal coarse calcifications, marked enhancement, and surrounding vasogenic edema with multiple flow voids and large draining veins. There is abnormal tissue interspersed between vascular elements and large areas of cystic changes and necrosis
Mentions: The patient is a 44-year-old woman who presented with a sub-acute neurocognitive decline over a several months period, such that she was no longer able to perform routine tasks required for daily activities. Past medical history is notable for Graves disease (diagnosed 2005, treated with methimazole) and endometrial adenocarcinoma s/p total abdominal hysterectomy-bilateral salpingo-oophorectomy and chemotherapy (carboplatin and paclitaxel) in 2009, in remission since. Neurological examination was notable for difficulties recalling the events prior to the presentation and disorganized speech. However, the patient re-oriented easily. Physical examination revealed bilateral and symmetric proptosis. Laboratory values were unremarkable. Computed tomography scan of the brain showed 6.1 cm × 4.8 cm × 4.9 cm mass centered over the anterior falx cerebri with moderate surrounding hypodensity and effacement of adjacent sulci [Figure 1a]. Patchy hyper-density was seen within the mass, with Hounsfield units >200 suggestive of calcification. Magnetic resonance imaging (MRI) demonstrated an irregularly shaped, intra-axial mass with heterogeneous contrast enhancement that abut the anterior communicating artery (ACA) [Figure 1b]. Fluid attenuation inversion recovery imaging revealed complex patterns of hypointense tubular outlines within the lesion, suggestive of considerable vascularity within the lesion [Figure 1c]. MR angiogram showed multiple vascular pedicles emerging from both ACA branches penetrating the lesion as well as prominent venous drainages into the anterior and posterior superior sagittal sinus. Diagnostic cerebral angiogram confirmed extensive blood supply from the bilateral ACAs as well as the left middle cerebral artery (MCA) [Figure 2a] with a 2.4 cm × 1.4 cm × 2.3 cm AVM nidus and prominent venous drainages into the superior sagittal sinus [Figure 2b].

Bottom Line: The co-occurrence of intracranial arteriovenous malformations (AVMs) and cerebral neoplasms is exceedingly rare but may harbor implications pertaining to the molecular medicine of brain cancer pathogenesis.Here, we present a case of de novo AVM within an isocitrate dehydrogenase 1 mutated anaplastic oligodendroglioma (WHO Grade III) and review the potential contribution of this mutation to aberrant angiogenesis as an interesting case study in molecular medicine.The co-occurrence of an IDH1 mutated neoplasm and AVM supports the hypothesis that IDH1 mutations may contribute to aberrant angiogenesis and vascular malformation.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, University of California, San Diego, CA, USA.

ABSTRACT

Background: The co-occurrence of intracranial arteriovenous malformations (AVMs) and cerebral neoplasms is exceedingly rare but may harbor implications pertaining to the molecular medicine of brain cancer pathogenesis.

Case description: Here, we present a case of de novo AVM within an isocitrate dehydrogenase 1 mutated anaplastic oligodendroglioma (WHO Grade III) and review the potential contribution of this mutation to aberrant angiogenesis as an interesting case study in molecular medicine.

Conclusion: The co-occurrence of an IDH1 mutated neoplasm and AVM supports the hypothesis that IDH1 mutations may contribute to aberrant angiogenesis and vascular malformation.

No MeSH data available.


Related in: MedlinePlus