Baylor University Medical Center Proceedings April 2017 - 215

Dural arteriovenous fistula as a treatable dementia
Ikponmwosa Enofe, MBBS, MPH, Ike Thacker, MD, and Sadat Shamim, MD

Dementia is a chronic loss of neurocognitive function that is progressive
and irreversible. Although rare, dural arteriovenous fistulas (DAVFs)
could present with a rapid decline in neurocognitive function with or
without Parkinson-like symptoms. DAVFs represent a potentially treatable and reversible cause of dementia. Here, we report the case of
an elderly woman diagnosed with a DAVF after presenting with newonset seizures, deteriorating neurocognitive function, and Parkinsonlike symptoms.

n this case, we highlight how familiarity with symptoms of
dural arteriovenous ﬁstulas (DAVFs) can reduce the incidence of misdiagnosis of dementia syndromes and lead to
early treatment and better outcomes (1).

CASE PRESENTATION
An 82-year-old woman presented with a 1-year history of
reduced limb control and diﬃculty ﬁnding words. She had been
on carbidopa-levodopa without signiﬁcant improvement. One
month prior, she had a cluster of generalized unprovoked seizures with loss of consciousness with initiation of levetiracetam.
Subsequently, she had progressive loss of memory. In the distant
past, she had dural sinus thrombosis, recurrent deep venous
thrombosis, and pulmonary embolism, for which she was on
warfarin. She also complained of a constant loud whooshing
sound. She had a nonfocal neurological exam with the following
exceptions: speech was ﬂuent, appropriate, but slow; her MiniMental State Examination was 21 with poor recall and attention and an inability to draw overlapping pentagons or write
words; and her clock drawing test showed marked visuospatial
abnormalities (Figure 1a).
Magnetic resonance imaging of the brain revealed a chronic
thrombus in the right transverse sinus with enlarged cerebral
veins and multiple right-sided leptomeningeal collaterals. There
were hyperintense signal changes in the periventricular white
matter on the T2-weighted sequence. A ﬂuid-attenuated inversion recovery sequence showed a hyperintense signal over
a portion of the right transverse sinus with the loss of normal ﬂow void. Cerebral angiography revealed a hypervascular
DAVF predominantly at the left skull base midline parietal
calvarium. Vessels from the external carotid, vertebral, and
subclavian arteries supplied the DAVF, which drained into the
Proc (Bayl Univ Med Cent) 2017;30(2):215-217

torcular Herophili, superior sagittal sinus, and left and right
transverse-sigmoid sinuses. Occlusion or near occlusion of the
right transverse sinus was noted. Marked venous hypertension
was present in the right cerebral hemisphere, deep basal ganglia,
and posterior fossa. Cortical veins were enlarged. There was
prolonged drainage bilaterally from the cerebellar hemispheres
(Figure 2a).
The patient underwent a right partial DAVF transarterial
endovascular embolization (Figure 2b) with marked improvement in her clinical symptoms on repeat evaluation 14 weeks
later. Her Mini-Mental State Examination score increased from
21 to 25. On the clock drawing test, she was able to ﬁll in
numbers correctly into a predrawn circle. Her ability to draw
overlapping pentagons improved, and she could write legible
and comprehensible sentences (Figure 1b). Her whooshing
sounds nearly resolved.
DISCUSSION
DAVF is an abnormal connection between arteries and
veins. It is rare, accounting for about 10% to 15% of vessel
malformations in the brain (1). Blood is supplied to DAVFs
mainly through branches arising from the external carotid artery. Vessels from the internal carotid and meningeal arteries
can also be involved (2).
The exact mechanism of DAVF development is unknown.
A percentage of it is believed to develop from acquired causes
that result in increased pressure in the dural sinuses. The presence of a transverse sinus thrombus in our patient corroborates
previous reports identifying thrombosis in the venous sinuses
as a possible trigger for developing DAVF (3-6). DAVF usually presents in the ﬁfth or sixth decades of life (3, 6). It occurs
with a female-to-male ratio of 1:1.65 (1). No family history or
hereditary pattern predisposes or increases the risk of developing a DAVF (3).
Patients with DAVFs present with a wide array of clinical symptoms. Common symptoms range from the less severe
From the Department of Radiology (Thacker) and the Division of Neurology,
Department of Internal Medicine (Shamim), Baylor University Medical Center
at Dallas.
Corresponding author: Sadat Shamim, MD, 3600 Gaston Avenue, Wadley Tower
Suite 1155, Dallas, TX 75246 (e-mail: sadat.shamim@bswhealth.org).
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