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When a fistula forms, blood from an artery under high pressure and flow goes directly into a vein, which is a low pressure and low flow structure.  Even though the fistula is not directly on or within the brain, it can nevertheless lead to brain dysfunction by congesting the brain venous system, as will be explained below. Finally, many patients who have dural fistulas of all sizes and locations can have a myriad of symptoms such as different kinds of headache, tiredness, loss of concentration, memory problems, even hallucinations, psychosis or other psychiatric problems.  Unfortunately, in these patients the diagnosis of dural fistula can be significantly delayed because dural fistulas are relatively rare, while the above symptoms are very common and usually not due to a fistula.
For an in-depth presentation on treatment of Brain Dural AV Fistulas, primarily geared towards neurointerventional professionals, you can visit Techniques: Brain Dural AV Fistula Embolization page. Below are pictorial diagrams of what a fistula is like and how it can be treated.  The actual anatomy is much more complicated, but the pictures provide a frame of reference. Finally, post-embolization views, showing the coils in the cavernous sinus (white arrows) and no evidence of fistula on injections of the external carotid artery (brown arrows).  This approach, though technically challenging, can be quite successful when other venues prove unfeasible. This patient developed a fistula on the dural covering that separates the back part of the brain, called cerebellum, from the overlying occipital lobe. MRA images (top) and stereo MRA composite (MIP) images on the bottom, demonstrating multiple intracranial and extracranial vessels (red arrows) feeding the fistula. The microcatheter has been positioned into another branch of the middle meningeal artery, showing residual fistula and aneurysm.  More glue is injected from this position. Post-embolization views of the left common carotid artery, showing that the fistula is gone.
How to cite this article Sanchez TG, Murao M, Medeiros HRT, Kii M, Bento RF, Caldas JG, Alvarez CA, et al.
Very few articles have described the treatment of patients with pulsatile tinnitus besides the description of the case itself.
Three pure-tone audiometric examinations were performed within 2 months and showed different results, with a sensorineural hearing loss varying from mild to severe in the left ear.
Owing to the important decrease in the patient's quality of life, we opted for obliteration of the venous diverticulum. The pulsatile tinnitus runs the gamut of differential diagnosis, including vascular tumors (paragangliomas, hemangiomas), vascular malformations (dural arteriovenous fistula), and other congenital or acquired vascular abnormalities [4,9-11].
The transverse-sigmoid sinus can be asymmetrical in 50-80% of the normal population and absent in up to 5% of people, according to retrograde jugular venographic scans [13].
An aberrant sinus or thrombosis of venous anastomosis can lead to a turbulent blood flow responsible for an objective pulsatile tinnitus. The pulsatile tinnitus in our patient was due to an anatomical variation of the transverse-sigmoid sinus, which insinuated itself on mastoid cells by probable thrombosis of an emissary vein (inside the diploe), modifying the regular laminar blood flow and causing its turbulence. Therapeutic embolization is a viable alternative in cases of pulsatile tinnitus caused by flow alteration, vessel abnormality and, even in some cases, paraganglioma [20]. The use of the stent to avoid coil migration had been described previously but only in arterial circulation and for the treatment of pseudoaneurysms [22,23]. The adequate identification of the possible etiology of pulsatile tinnitus is of utmost importance to determine the appropriate treatment for each case.
2 ) Brain Arteriovenous Malformation (AVM) — pretty much all AVMs visualized on MRI or CT are then evaluated by catheter angiography.
Additional procedures coupled with cerebral angiography include Wada activation testing (usually performed for various surgical considerations), venous sinus sampling (pituitary issues), venous sinus stenosis (occasionally associated with pseudotumor cerebri, and possibly requiring treatment), among others. As mentioned above, angiography is a lumen-based method.  What you see is dye inside vessel lumen. Complex terminal ICA aneurysm, status post repeat coiling and multiple recurrences, in a patient presenting wtih visual loss. The 50+ patient presented with momentary right-sided weakness, which quickly resolved, followed several days later by dysarthria, which remained. What is the blood supply to this mass?  The surgeon will need to know, and angiography is the best way to answer this specifically.  Regional supply can be anticipated well based on location, but extent of internal carotid (ACA in particular in this case) contribution can only be guessed, but needs to be known definitively. Stereo pairs of same case 1 week (top) and two weeks (bottom) following hemorrhage, demonstrating interval aneurysm growth — in fact showing an enlarging pseudoaneurysm in face of resolving hemorrhage. Transvenous coil embolization of the sigmoid sinus.  Notice that coil mass is tightest near the fistula, which is completely occluded.

Dynamic CT angiography has recently become available.  Similar to CT angiography, dye is injected a high rate into the vein and the head scanned.
Our group at the NYU Langone Medical Center is one of the premier neurointerventional centers in the world.
When a fistula forms between an artery and a vein within the dura, it is called Brain Dural Fistula, or Brain Dural Arteriovenous Fistula, or BDAVF, etc. The total amount of radiation delivered to the patient at conclusion of a dynamic CT scan, however, can be VERY high — in some cases resulting in (usually temporary) hair loss.
The bottom picture is venogram obtained by directly injecting the cavernous sinus to demonstrate the basal vein (dark blue) and ophthalmic vein (light blue arrows).  Some coils have already been placed into the sinus. We describe a 54-year-old man with a disabling objective pulsatile tinnitus due to a diverticulum of the sigmoid sinus toward the ipsilateral mastoid. Owing to this rarity, patients seldom are investigated in a correct manner, decreasing the possibility of having an adequate diagnosis and a compatible treatment. The objective of our study is to report a case of disabling objective pulsatile tinnitus, the surgical treatment of which via an endovascular route led to its cure, reestablishing the patient's quality of life.
He was strongly convinced that his tinnitus was responsible for his hearing difficulty because compression of the left part of his neck caused tinnitus to disappear and hearing to improve.
The results were considered inconclusive once the patient reported great difficulty in performing such examinations because he wanted to compress his jugular vein many times to decrease tinnitus and to be able to distinguish the pure-tone signal.
Preoperative computed tomography scan showing enlargement of the left transverse-sigmoid sinus with the diverticular image protruding toward the mastoid. Preoperative arteriography demonstrating the diverticular image projected from the left transverse-sigmoid sinus and a slow and turbulent blood flow. The procedure was performed under general anesthesia, puncturing the left internal jugular vein and introducing a self-expanding 8- ? 60-mm stent covering the transverse sinus and the opening of the diverticulum. Postoperative arteriography showing the venous diverticulum obliterated by the coils and the mesh of the sten! Owing to the proximity between the ear and large vessels, such as the carotid artery, the sigmoid sinus, and the jugular bulb, pulsatile tinnitus was thought to be more common as a complaint of disease in such vessels [12]. Because such anomalies do not cause evident neurological symptoms, they traditionally were treated in a conservative manner. As this condition does not implicate a neurological risk, it is advisable to employ a less aggressive treatment, aimed at normalization of blood flow and venous drainage and at anatomical preservation of the involved sinus.
In our patient, a technical alternative able simultaneously to preserve the flow within the transverse sinus and to allow the occlusion of the diverticular structure was necessary. We did not find any report associated with coils in pulsatile tinnitus, but this technique significantly increased the safety of the procedure, avoiding coil migration and retaining sinus permeability. Surgical intervention via an endovascular route using coils and stents was an effective procedure for our patient. A posterior temporal vein drains into the left transverse sinus and retrograde to the right.
Nevertheless, a well-tuned sequence, evaluated by a highly experienced radiologist, can now serve as a reasonable screening tool for AV shunting in a patient who is unable, or unwilling, to undergo catheter angiography. Notice hyperemia adjacent to congested inferior temporal lobe vein, and clot-related lucency above it. The patient presented with worst headache of life, and this evaluation was done to look for an aneurysm. The details of any treatment are best discussed with the specialist performing the procedure.
We performed a surgical intervention via the endovascular route using coils to obliterate the diverticulum and a stent to avoid coil migration. Objective tinnitus usually arises from muscular or vascular structures and can be pulsatile (when synchronous with the heartbeat) or nonpulsatile [1-6]. Tinnitus thoroughly disrupted his life, prohibiting normal sleep and concentration patterns and leading to suicidal intentions.

The audiologist also reported a significant difficulty in obtaining the pure-tone thresholds because the patient worried too much about compressing his neck to ascertain the given tone. Then, it usually receives drainage of inconstant veins from the scalp and deep cervical region, called emissary and diploic veins. However, our patient's quality of life was so disrupted because of the pulsatile tinnitus that we were obliged to discover an alternative solution. One alternative would be the placement of coils into the diverticular structure [21], but its large opening would increase the possibility of coil herniation, with consequent occlusion of the transverse sinus. The possibility of the diverticular structure emerging as the cause of the pulsatile tinnitus was clearly proved by the disorder's immediate disappearance after such endovascular treatment. Thus, it may be performed in patients with a disabling pulsatile tinnitus with an etiological diagnosis that calls for such treatment. Pseudotumor syndrome associated with cerebral venous sinus occlusion and antiphospholipid antibodies.
Endovascular treatment of fusiform aneurysms with stent and coil: Technical feasibility in a swine model.
Below is a movie of TWIST (Siemens) dynamic MR angiography of a patient with right carotid occlusion. Pulsatile tinnitus may arise in arterial or venous structures, resulting from a turbulent blood flow due to an increase in blood volume or pressure or to changes in the vessel lumen [4, 7].
Benign intracranial hypertension, compression of the internal jugular vein by the atlas lateral process, a high-dehiscent jugular bulb, and the presence of an abnormal mastoid emissary vein are known causes of venous tinnitus [5, 16, 17]. Therefore, we chose instead first to introduce a stent, which originated as a tool for keeping the arteries open after angioplasties, followed by introduction of the coils through its mesh, using the stent as protection. In G McCafferty, W Coman, R Carroll (eds), Proceedings of the Sixteenth World Congress of Otorhinolaryngology Head and Neck Surgery. Its severity is directly related to the subjective annoyance provoked in patients' lives and, in severe cases, can even lead to suicide [1, 4, 8]. The disorder may be related to hemodynamic changes that occur in systemic diseases (anemia, thyrotoxicosis, valvular cardiac disease) and in the presence of predisposing factors (pregnancy, oral contraceptives, collagenous diseases, hypercoagulability states) [18, 19]. Thus, the coils were kept safe inside the diverticular structure, separating the diverticulum from the normal blood circulation and maintaining a low risk of herniation.
However, during auscultation of the ear, we noticed a pulsatile rough bruit coming from the left external canal and from the mastoid, which completely disappeared with a light compression of the ipsilateral jugular vein.
Laboratory examination results were normal and excluded the systemic causes of pulsatile tinnitus, such as anemia and hyperthyroidism. The stent avoided the migration of the coils into the transverse sinus once the opening of the diverticulum was fairly large.
The auditory brainstem response was normal, although the morphology was poorer in the left side. The pulsatile tinnitus immediately disappeared after the patient recovered from anesthesia. Although no recurrence was seen during the procedure, the patient developed a small cerebellar area of ischemia, resulting in an ataxic walk, which progressively disappeared during the next 2 months.
The computed tomography scan showed an extension of the left transverse-sigmoid sinus, forming a diverticular image protruding into the mastoid area (Fig. Postoperative angiography showed absence of the diverticulum with preservation of the blood flow within the transversesigmoid sinus (Fig. Cerebral angiography confirmed the lesion seen in the computed tomography scan, demonstrating a slow and turbulent blood flow within the diverticular image projected from the left transverse-sigmoid sinus (Fig.

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