Dural Arteriovenous Fistula Case Review & Treatment Pathway Coordination

• Date and manner of symptom onset.
• Pulsatile tinnitus side, frequency, intensity and relationship to head position or neck compression.
• Headache, seizure, focal neurological or cognitive symptoms.
• Visual change, diplopia, proptosis, chemosis, ocular pain and orbital bruit.
• Gait, balance, speech, swallowing, brainstem or spinal symptoms.
• Previous intracranial haemorrhage or unexplained venous infarction.
• Current neurological and functional baseline.

• Original DICOM files and formal reports.
• Non-contrast CT showing haemorrhage, hydrocephalus or calcification.
• CTA or MRA showing early venous filling, enlarged vessels or sinus abnormalities.
• MRI sequences showing venous oedema, infarction, haemorrhage, dilated veins or brainstem and thalamic congestion.
• Orbital imaging where cavernous sinus involvement is suspected.
• Spine MRI where perimedullary drainage or myelopathy is present.
• Earlier imaging for comparison.

• Full dynamic DSA series from all relevant external and internal carotid and vertebral injections.
• Early arterial, capillary and complete venous phases.
• Three-dimensional rotational angiography where performed.
• Formal angiography report.
• Precise fistula location and number of shunt points.
• Arterial feeders and potentially hazardous anastomoses.
• Sinus, cortical, deep, orbital or perimedullary venous drainage.
• Venous reflux, stenosis, occlusion, ectasia, varix or collateral rerouting.

Selected screenshots are insufficient for full review because the dynamic sequence and venous phase may alter classification and treatment planning.

• Borden classification and the features supporting it.
• Cognard classification and the features supporting it.
• Presence or absence of cortical venous reflux.
• Venous ectasia, varix or outflow restriction.
• Previous haemorrhage or neurological deficit.
• Evidence of venous congestion or intracranial pressure elevation.
• Any change in drainage pattern over time.

Classification helps communicate venous risk but does not replace review of the full angiographic anatomy and patient condition.

• Laterality, timing and pulse synchrony.
• Effect of posture, exercise, head rotation or gentle neck compression.
• Objective bruit documented by a clinician where present.
• Audiogram and ENT or neuro-otology assessment.
• Impact on sleep, concentration and daily function.
• Alternative causes already assessed, including arterial stenosis, venous sinus disease, tumour and middle-ear pathology.

• Visual acuity, colour vision and visual fields.
• Intraocular pressure and optic-nerve findings.
• Chemosis, proptosis, conjunctival arterialization and corneal status.
• Ocular motility and cranial-nerve examination.
• Orbital venous imaging.
• Rate of visual or cranial-nerve deterioration.

• Date, indication and intended treatment goal.
• Target artery and microcatheter position.
• Liquid embolic, particles, coils or other material used.
• Whether the embolic reached the fistula point and proximal venous side.
• Residual feeders and venous drainage after treatment.
• Stroke, cranial neuropathy, haemorrhage or access complications.
• Planned next stage and follow-up angiography.

• Venous access route and target sinus or venous pouch.
• Coils, liquid embolic material, stent or combined technique.
• Whether a sinus segment was preserved or sacrificed.
• Normal cerebral venous drainage before and after treatment.
• Residual shunting or rerouted cortical drainage.
• Venous infarction, haemorrhage, cranial-nerve or access complications.
• Post-treatment antithrombotic plan where applicable.

• Microsurgical approach and exact draining-vein or fistula disconnection.
• Intraoperative angiography or fluorescence imaging.
• Postoperative angiographic confirmation.
• Radiosurgery platform, target, dose and date where used.
• Latency-period imaging and neurological events.
• Residual or recurrent shunt and later treatment plan.

• Antiplatelet and anticoagulant medication.
• Previous venous sinus thrombosis, trauma, infection or cranial surgery.
• Kidney function and contrast allergy.
• Bleeding or clotting disorders.
• Access to local stroke, neurosurgical, ophthalmological and emergency care.
• Ability to complete MRI, ophthalmological review and follow-up DSA.
• Rehabilitation, caregiver and travel needs.

A dAVF is a dural shunt without a brain-parenchymal nidus. A brain AVM contains a nidus within brain tissue. A direct carotid–cavernous fistula is usually a high-flow connection between the internal carotid artery and cavernous sinus, often related to trauma or aneurysm rupture. These lesions differ in arterial supply, venous drainage, urgency and treatment route.

Fistulas draining only into a venous sinus without cortical reflux generally have a more favourable natural history than lesions with retrograde cortical venous drainage. Cortical reflux, venous ectasia, outflow obstruction and venous congestion increase concern for haemorrhage and neurological injury. Symptoms alone do not reliably classify the risk.

Borden and Cognard systems describe the relationship between the fistula, sinus and cortical venous drainage. They support risk communication and treatment planning but can simplify complex anatomy. Classification should be based on complete angiography, including the venous phase, and should not replace lesion-specific discussion.

A sinus-draining dAVF without cortical reflux may cause severe pulsatile tinnitus, ocular discomfort or headache. Observation can be appropriate in selected cases, but should include symptom review and a plan for reassessment if new neurological, visual or cognitive symptoms develop. Rare changes in venous drainage can alter the risk profile.

Retrograde cortical venous drainage can cause intracerebral, subarachnoid or subdural haemorrhage, venous infarction and seizure. A fistula presenting with haemorrhage or neurological deficit generally requires prompt specialist assessment. The immediate goal is to eliminate the dangerous venous reflux while preserving essential normal venous drainage.

Pulse-synchronous tinnitus is an important clue but is not specific to dAVF. The work-up may include vascular imaging, ENT or neuro-otology assessment and neurological examination. Head-position or neck-compression effects can be documented but should not be used by patients as a diagnostic manoeuvre or treatment. Relief of tinnitus is meaningful, but symptom improvement alone does not prove fistula cure.

Cavernous sinus dAVF may cause chemosis, proptosis, orbital bruit, diplopia, cranial-nerve palsy, ocular pain, elevated intraocular pressure or visual loss. Urgency depends on visual threat, corneal injury, pressure, cranial-nerve progression and intracranial venous drainage. The treatment route is determined by accessible venous pathways and arterial risk anatomy.

Anterior cranial fossa and many tentorial dAVFs drain directly into cortical veins and can behave aggressively despite a small fistula point. Endovascular access may be limited or hazardous because of ophthalmic and cranial-nerve arterial supply. Microsurgical disconnection can be an important option when it offers direct, durable interruption at acceptable risk.

dAVF-related venous hypertension can produce cognitive decline, gait dysfunction, aphasia, parkinsonian features, thalamic or brainstem oedema, papilloedema or myelopathy. These presentations may mimic tumour, inflammation, neurodegeneration or primary venous thrombosis. Reversibility depends on the duration and severity of venous injury and is not guaranteed after treatment.

DSA is commonly required to define all feeders, the shunt point, venous route, reflux, hazardous anastomoses and treatment access. It also supports confirmation of cure. It is invasive and carries stroke, access-site, contrast and other risks. The treating team decides when the information gained justifies the procedure.

Transarterial treatment aims to reach and disconnect the fistula point and its immediate venous side. Closing proximal feeders alone may leave the shunt patent and encourage recruitment of new supply. Safe treatment depends on catheter position, reflux control, external–internal carotid anastomoses and arteries supplying cranial nerves. Risks include stroke, haemorrhage, cranial neuropathy and non-target embolization.

For selected sinus-based fistulas, the venous side may provide the most direct route to the shunt. The team must determine whether a diseased sinus can be occluded without compromising normal cerebral drainage. Coil, liquid-embolic or combined strategies may be used. Sinus sacrifice is not automatically safe simply because the sinus appears stenosed or thrombosed.

Surgery can directly interrupt a dangerous draining vein or fistulous connection, particularly in anterior cranial fossa, tentorial or selected inaccessible lesions. The goal is usually disconnection of pathological arteriovenous flow rather than removal of all dural arteries. Postoperative vascular imaging may be required to confirm complete occlusion.

Radiosurgery may be considered in selected lower-risk fistulas that are unsuitable for direct endovascular or surgical cure. Obliteration is delayed, and the lesion remains patent during the latency period. It is generally not a stand-alone strategy when haemorrhage, cortical venous reflux or progressive neurological injury requires rapid protection.

Reduced bruit, improved tinnitus, lower shunt flow or closure of several feeders may represent progress but does not establish complete disconnection. Residual shunting can continue to expose cortical veins to risk or recruit new arterial supply. Follow-up vascular imaging, often DSA, should confirm the intended result.

Residual or recurrent fistula requires review of previous treatment intent, inaccessible feeders, altered venous routes and current symptoms. A lesion that was previously lower risk may become more concerning if sinus thrombosis or progressive stenosis redirects flow into cortical veins. New symptoms should prompt renewed assessment rather than reliance on an old classification.

dAVFs may be associated with venous sinus thrombosis, trauma, infection or previous cranial surgery, although causation is not always clear. Treating the fistula and managing the underlying venous or systemic condition are separate decisions. Anticoagulation or antiplatelet therapy should not be started, stopped or modified without the treating specialists.

Meaningful outcomes include complete fistula occlusion, elimination of cortical reflux, preservation of normal venous drainage, survival, neurological and visual function, tinnitus burden, cognition and quality of life. Technical catheter success or symptom relief is not enough. Long-term follow-up is individualized according to lesion type, treatment and certainty of angiographic cure.