Baylor University Medical Center Proceedings April 2017 - 216

In our case, increased drainage
was seen in the transverse and
sigmoid dural venous sinus,
which explains the presence of
pulsating tinnitus at the time of
her presentation.
Cortical venous hypertension presents with more severe
symptoms and carries a higher
risk of future neurological
events in comparison to a more
benign clinical course seen in
patients with isolated dural sinus drainage (3). Presentation
of severe cortical venous hypertension includes but is not limited to intracranial hemorrhage
Figure 1. Mini-Mental State Examination (a) 12 days prior to partial embolization of the dural arteriovenous fistula, with
and nonhemorrhagic congestive
a score of 21/30, and (b) about 2.5 months after partial embolization, with a score of 25/30.
neurological deﬁcit such as progressive dementia, parkinsonism, seizures, cerebellar symptoms,
presentations of headache, orbital bruit, pulsatile tinnitus, and
and other focal neurological deﬁcits (3).
ophthalmoplegia to more severe presentations of neurological
The exact pathogenesis for developing dementia in patients
deﬁcits and acute intracranial hemorrhage (1, 3). There are only
with DAVFs remains largely unknown. The occurrence of ischa few reports of DAVFs presenting with dementia syndrome,
emia involving the frontal and temporal lobe is associated with
a decline in neurocognitive function, and parkinsonism (3, 7).
the development of dementia (2, 8). Ischemia occurs from the
The clinical presentation of DAVFs depends on their location
downstream eﬀect of arterialization of cortical venous drainage
and pattern of cerebral venous drainage (1, 3, 6). DAVFs with
from cortical venous hypertension, leading to cerebral venous
isolated dural sinus drainage have a benign clinical course. Most
congestion (3). Some reports have suggested that patients with
cases present with pulsating tinnitus and visual symptoms, deDAVFs involving the superior sagittal sinus have a higher rate
pending on the proximity of the dural venous sinus to adjacent
of presenting clinically with dementia (9).
organs.
The mechanism by which DAVFs cause parkinsonism
DAVFs with isolated dural sinus drainage to the cavernis also unclear (8). Hypoperfusion of the frontal lobe due
ous sinus commonly present with ophthalmoplegia, ptosis,
to venous hypertension is thought to be responsible for
chemosis, retroorbital pain, and decrease in visual acuity. Puldeveloping parkinsonism in patients with DAVFs (2, 8).
sating tinnitus is the most frequent presentation of a DAVF
Another possible explanation is from hypoperfusion of the
with increased drainage to the transverse and sigmoid dural
basal ganglia due to impaired drainage of the deep internal
venous sinuses. Clinical presentation is best explained by the
veins (8).
proximity of the sigmoid sinus to the auditory apparatus (3).
b

Figure 2. (a) Digital subtraction angiogram of the direct left occipital artery injection. An extensive rete of arterial pedicles supplying the fistula is densely radiopaque.
The ipsilateral transverse sinus exhibits early opacification. Note the retrograde drainage via the straight sinus. (b) Unsubtracted completion of the left occipital
angiogram shows hyperdense embolization material throughout feeding vessels, with diminished shunt physiology.
216

Baylor University Medical Center Proceedings

Volume 30, Number 2

Table of Contents for the Digital Edition of Baylor University Medical Center Proceedings April 2017