**7. Acknowledgement**

The authors wish to thanks all physicians from the clinic who participated in the medical care of the patient described in this report. Also, we are grateful to Marta Djordjevic for technical assistance in the computer processing of the images.

**13** 

*Japan* 

Shigeru Miyachi

*Department of Neurosurgery, Nagoya* 

**Hypothetical Mechanism of** 

**of Emissary Vein and Sinuses** 

*University Graduate School of Medicine, Nagoya* 

**the Formation of Dural Arteriovenous** 

**Fistula – The Role and Course of Thrombosis** 

Dural ateriovenous fistula (DAVF) is the acquired and progressive arteriovenous (AV) shunt disease on or between the dura matter, and its etiology is still controversial1-4. This disorder occurs not in the whole dura but at very specific locations. DAVF can be divided into two types based on the intervention of the drainage route and affected sinus; sinus type and non-sinus type. The sinus type has the shunt at the sinus wall or dural vein, and includes DAVF at the cavernous sinus (CS), transverse-sigmoid sinus (TS-SS), anterior condylor confluence (ACC), and superior sagittal sinus (SSS). The non-sinus DAVF has the shunt on the dura and directly drains into the pial veins, and includes tentorial, ethmoidal, craniocervical and spinal DAVF. However, even the sinus type DAVF ultimately changes to the isolated sinus with cortical reflux due to progressive sinus occlusion, similar to the non-sinus type. Such seemingly separated and complex

Previous recognition of the etiology of DAVF has been directed to sinus hypertension1,4 and thrombosis5, 8. It is true that such abnormal situations may create the experimental AV shunt1-4. However, if one considers that the sinus hypertension is the initial trigger, it should be caused secondary to the thrombosis or outlet stenosis. It is unreasonable to adopt this theory into non-sinus type, because this type has no correspondence with the sinus. In other hand AV shunt formation can easily create the condition of sinus hypertension. Thus, the conventional discussion over the etiology of AV shunt formation between sinus occlusion and sinus hypertension is just a chicken-or-egg question. We consider that sinus hypertension concerning sinus wall hypertrophy may not be the cause, but rather one factor in the development of DAVF. Our theory based on inflammatory initiation affecting EV can explain both types of DAVF and subsequent development with pathological changes of the

drainage route is not contradictory to the previous sinus-oriented theory.

**1. Introduction** 

pathogeneses of DAVF remain elusive.

**2. Previous theory about DAVF etiology** 

#### **8. References**

