title: Pial arteriovenous fistula as a cause of bilateral thalamic hyperintensities--an unusual case report and review of the literature.
abstract: BACKGROUND
  Isolated bilateral thalamic congestion due to an arteriovenous malformation (AVM) is a rare entity. Few case reports of dural arteriovenous fistula associated with it have been reported in the literature. The association of pial arteriovenous fistula (pial AVF) with thalamic hyperintensities has never been described before. The pial AVF is a recently recognized lesion in which the multiple pial arterial feeders drain into a single venous channel without a nidus like in conventional AVM. In spite of being congenital in origin, these lesions may have expression in adulthood due to abrupt change in the venous drainage system. Successful management of pial AVF associated with bilateral thalamic hyperintensities is described here with review of the literature.
  
  
  METHODS
  A 60-year-old man presented with rapidly progressive gait disturbance and cognitive decline. Magnetic resonance imaging (MRI) showed hyperintensities in the thalami on T2-weighted and fluid attenuated inversion recovery image. Digital subtraction angiography revealed a pial AVF near the splenium of corpus callosum. It had feeders from posterior choroidal arteries and drained into the vein of Galen through an abnormal mesencephalic vein. The stagnation and increase of pressure in the deep venous system led to congestion in the thalami. He was treated by partial transarterial embolization of the feeders followed by gamma knife therapy (GKT). The clinical symptoms and MRI improved rapidly after embolization and further reduction in shunt flow was observed after GKT.
  
  
  CONCLUSIONS
  Strong suspicion of vascular malformation as a cause of bilateral thalamic hyperintensities helps in early detection. Such lesions like pial AVF presented here require active intervention by surgery or endovascular therapy. GKT is an important adjuvant in lesions refractory to either of them.
authors.affiliation: Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Rahul
authors.initials: R
authors.lastname: Gupta
authors.affiliation: Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Shigeru
authors.initials: S
authors.lastname: Miyachi
authors.affiliation: Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Noriaki
authors.initials: N
authors.lastname: Matsubara
authors.affiliation: Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Izumi
authors.affiliation: Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Takehiro
authors.initials: T
authors.lastname: Naito
authors.affiliation: Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Haraguchi
authors.affiliation: Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Wakabayashi
mesh_terms: D015901:Angiography, Digital Subtraction; D001164:Arteriovenous Fistula / Q000150:complications* / Q000601:surgery*; D002533:Cerebral Angiography; D002550:Cerebral Veins / Q000601:surgery*; D003337:Corpus Callosum / Q000473:pathology; D004621:Embolization, Therapeutic; D006801:Humans; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000209:etiology; D009460:Neurologic Examination; D011788:Quality of Life; D016634:Radiosurgery; D013786:Thalamic Diseases / Q000209:etiology* / Q000473:pathology; D014711:Vertebral Artery / Q000473:pathology