Arteriovenous fistulas resulting from gunshot wounds to the head

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Introduction

A characteristic feature of modern warfare is the capability to employ high-precision missile and artillery weapons to strike targets at significant distances, which multiplies the number of casualties with gunshot wounds. At the same time, the widespread use of individual and collective protective equipment significantly influences the nature of wounds and injuries. Providing specialized medical care within the shortest timeframes has increased the survival rate of patients with injuries previously deemed incompatible with life [1]. This primarily concerns penetrating gunshot wounds to the head and neck. Some of these clinical observations are unique, on one hand, due to the nature of the injuries sustained, and on the other, due to the improvement of disabling symptoms and successful restoration of impaired neurological functions despite significant damage to brain structures.

Craniocerebral injuries exhibit high mortality rates and represent the most frequent cause of death both among those who perish on the battlefield and those evacuated to medical facilities. In modern armed conflicts, mortality from various types of gunshot head injuries ranges widely (4.3–76.3%), depending on the type of projectile (mortality is significantly higher with bullet wounds), severity at admission, accessibility of medical care, and treatment methods employed [2]. Survival rates for wounded patients with Glasgow Coma Scale scores of 3–5 at admission reach 35% with rapid aeromedical evacuation and of ultra-early or early (within 5 hours) decompressive craniotomy, while for scores of 6–8, they reach 90% [3, 4]. Among casualties with combined injuries, despite advances in combat trauma management (application of Damage Control Resuscitation principles), an increase in the proportion of deaths from gunshot head wounds from 57% to 73% has been observed [5].

The high incidence of adverse outcomes in gunshot wounds to the head is explained by both the vital function of the brain and the multifactorial damaging effects of high-energy projectiles, comprising four components: shock wave, penetrating projectile, cavitation energy, and vortex flow [6]. In penetrating gunshot wounds to the head, each of these components carries risks of damaging cerebral arteries, veins, and venous sinuses beyond direct brain tissue injury. Passage of the projectile through the Sylvian fissure in cranial gunshot wounds may injure M1 and M2 segments of the middle cerebral artery, branches of the anterior cerebral artery, intracranial segments of the internal carotid artery (ICA), vertebrobasilar arteries, cavernous sinus, or other venous sinuses [7]. In addition to intracranial hemorrhages due to vascular wall rupture, intracranial vascular injury may cause traumatic occlusion leading to secondary ischemic damage resembling stroke (including in-hospital ischemic stroke (IS)), whose clinical significance may exceed the neurological deficit directly caused by the penetrating gunshot wound itself [1]. When delayed neurological symptoms occur in victims with gunshot head injuries, post-traumatic vascular malformations must be ruled out. Traumatic brain injuries account for 0.4–0.7% of aneurysms. Traumatic intracranial arterial aneurysms occur in 5–42% of combat-related skull and brain injuries [8].

Traumatic arteriovenous fistulas (AVFs) are abnormal direct communications between an artery and a vein, leading to direct flow of arterial blood into the venous system, bypassing the capillary network. AVFs (shunts) can be extracranial (resulting from penetrating neck injuries) or intracranial (resulting from penetrating head injuries, skull base fractures), forming either within the first hours after injury or in a delayed period depending on the degree of arterial wall damage. In 90% of cases, traumatic AVFs result from penetrating injuries [9].

According to an analysis of literature sources in the Medline Complete-PubMed database from 1829 to 2019, conducted by J.A. Asensio et al., 291 patients with AVFs resulting from penetrating injuries were registered [10]. Post-traumatic AVFs following neck injuries (69 patients, 23.7%) rank third in incidence after extremity injuries (89, 30.6%) and abdominal injuries (87, 30%); thoracic injuries (46 cases) account for 15.8%. Among the most commonly affected vessels described are the vertebral artery (38, 13%) and the popliteal vein (32, 11.7%). In the context of modern armed conflicts, it is resonable to believe that the number of clinical observations of variously localized post-traumatic AVFs will significantly increase.

Non-traumatic dural AVFs are most commonly represented by communication between venous sinuses or cortical veins and branches of the external carotid artery (meningeal arteries, maxillary, ascending pharyngeal, and occipital arteries), less frequently with branches of the ICA and vertebral artery [11]; however, particularly as a result of head injuries and trauma, larger cerebral arteries at the proximal level may be involved. In terms of location, spontaneous dural AVFs most commonly form in the walls of the cavernous, transverse, and sigmoid sinuses, with cases of fistulas in other cerebral sinuses being significantly rarer [12]. Both Russian and foreign literature sources extensively document clinical observations of patients with post-traumatic intracranial carotid-cavernous fistulas, resulting from abnormal communication between the cavernous (C4 according to A. Bouthillier’s classification) segment of the ICA and the cavernous sinus [13]. In most cases, carotid-cavernous AVFs formed during the delayed period after trauma [14–17]. The diagnostic and treatment approach for patients with carotid-cavernous fistulas (including traumatic ones) is well-established, including the widely used classification proposed by D.L. Barrow et al. [18]:

• Type A: Direct high-flow shunts between the ICA and cavernous sinus;
• Type B: Dural shunt between meningeal branches of the ICA and cavernous sinus;
• Type C: Dural shunt between meningeal branches of the external carotid artery and cavernous sinus;
• Type D: Dural shunt between meningeal branches of the ICA, external carotid artery, and cavernous sinus.

According to this classification, direct communications between the ICA and the cavernous sinus of traumatic origin are considered Type A fistulas [19]. Over time, blood flow progressively shifts toward the fistula site, with retrograde outflow of arterial blood occurring through the veins draining the sinus, leading to increasing cerebral hypoperfusion [12, 20].

Below is a unique clinical observation: a case of gunshot wound to the head with formation of a traumatic intracranial carotid-jugular AVF, located extradurally at the level of the petrous ICA segment. This case is remarkable because of the extradural location of the intracranial AVF, as well as a favorable clinical outcome despite a potentially fatal basilar skull injury.

Clinical case

Patient N., 32 years old, sustained a shrapnel gunshot wound to the right chest during mortar shelling. Approximately 30 minutes later, following a repeated ammunition explosion in immediate proximity, he experienced a strong impact to the left occipital region, a sensation of “electric current passing throughout the body”, pain in the hard palate area, burning pain in the tongue area, and a taste of blood in the mouth. In saliva mixed with blood, he discovered a small round-shaped metal fragment (reportedly 3–4 mm in diameter). He did not lose consciousness and clearly recalled events preceding the injury and the moment of wounding itself. He independently stopped bleeding from the occipital area by applying a circular pressure bandage. Approximately one hour after injury, he began experiencing nausea, dizziness, developed repeated vomiting, and significant movement coordination impairment (could only move by crawling or on all fours). Subsequent events are remembered fragmentarily. He was evacuated to receive qualified medical care. Examination diagnosed shrapnel gunshot wound to the head, penetrating chest wound with right-sided hemopneumothorax; right pleural drainage tube placement was performed. The patient was then transferred to specialized care (4th stage of medical care), admission Glasgow Coma Scale score 11; based on additional examination including head and chest computed tomography (CT), diagnosis was established:

• Penetrating through-and-through fragmenting gunshot wound to the left occipital region with comminuted fracture of the occipital bone, intracranial displacement of bone fragments, through-and-through comminuted fracture of the petrous part of the left temporal bone, perforating fracture of the left greater wing of the sphenoid bone, and exit wound in the soft palate region. Pneumocephalus. Traumatic subarachnoid hemorrhage. Severe brain contusion with contusion foci along the wound tract and hemorrhagic imbibition foci in the left cerebellar hemisphere and left temporal lobe. Left-sided deafness.
• Penetrating blind fragmenting gunshot wound to the right chest with contusion of the right lung and hemopneumothorax.

Neurosurgical intervention was performed: primary surgical debridement, resection craniotomy in the left occipital region, removal of intracranial bone fragments, duraplasty, and placement of an external ventricular drain. Antibiotic therapy was initiated. The postoperative period was uncomplicated; drains were removed and wounds healed by primary intention.

Several days after neurosurgical intervention, the patient complained of pulsating headache and rhythmic noise in the left ear. Subsequently, he was evacuated to the S.M. Kirov Military Medical Academy and admitted to the nervous diseases clinic. On admission, he reported pulsating headache with intensity of 5–6 on the numerical rating scale (predominantly in the left side of the head), rhythmic noise in the left ear (described as similar to the clatter of train wheels), systemic vertigo, pronounced coordination impairment (more pronounced in the left extremities) and gait disturbance (ambulated within the room while holding onto surrounding objects), left-sided deafness, blurred vision, slowed speech, and generalized weakness.

On examination: general condition satisfactory. Post-traumatic round punctate pale pink scars (4 mm) on the soft palate and tongue base. In the left scapulotrapezoid triangle (lateral to the border of the left sternocleidomastoid muscle), pronounced pulsation was visually observed and detected on superficial palpation. Auscultation of this area revealed a harsh systolic murmur.

Neurological status: asthenic. High-amplitude low-frequency horizontal sustained nystagmus on left gaze, medium-amplitude high-frequency horizontal sustained nystagmus on right gaze (Bruns nystagmus); medium-frequency high-amplitude vertical sustained nystagmus on upward gaze. Left-sided deafness. Speech was scanning, slow, with elements of dysarthria. Oral automatism reflex (Marinescu–Radovici sign). Deep reflexes were brisk, (L>R). Superficial abdominal reflexes were moderately brisk, rapidly exhausted, symmetrical. Pathological pyramidal hand reflexes: Rossolimo, Rossolimo–Venderovich, Wartenberg, and Bekhterev reflexes were positive bilaterally. Left-sided hemihypesthesia. Coordination tests with the left limbs showed marked intention tremor and dysmetria. In the Romberg test, the patient was unsteady with a tendency to fall leftward. Walks independently with assistance and support on surrounding objects. Neuropsychological testing: Mini-Mental State Examination score — 23 points; Frontal Assessment Battery score — 15 points; Clock Drawing Test score — 4 points.

Duplex scanning of the brachiocephalic arteries verified signs of arterialization of venous flow in the left internal jugular vein due to arteriovenous shunting, and turbulent flow in the left common carotid artery and left internal jugular vein (Fig. 1).

 

Fig. 1. Duplex ultrasound of the brachiocephalic arteries in patient N. using color Doppler flow mapping.

Ultrasound signs of arteriovenous shunting (A), turbulent flow in the left common carotid artery (B), and arterialization of venous flow in the left internal jugular vein (C).

 

CT angiography revealed occlusion of the left ICA in the petrous segment (C2 per A. Bouthillier) and a carotid-jugular fistula within a bone defect (along the wound tract) in the pyramid of the left temporal bone at the same level (Figs. 2–4).

 

Fig. 2. Head CT of patient N.

1 — post-trepanation defect in the left occipital bone (at the entry site); 2 — intracranial bone fragments in the left cerebellar hemisphere (along the wound tract); 3 — through-and-through defect in the pyramid of the left temporal bone with bone fragments; 4 — wound tract course (exit orifice in the left greater wing of the sphenoid bone).

 

Fig. 3. CT angiography of the neck and head vessels in patient N.

1 — cervical segment (C1 per A. Bouthillier) of the left ICA; 2 — сontrast defect in the petrous segment (C2 per A. Bouthillier) of the left ICA; 3 — carotid-jugular fistula; 4 — left internal jugular vein.

 

Fig. 4. Color 3D reconstruction of CT angiography of the neck and head vessels in patient N., anterior (A) and posterior (B) views.

1 — left common carotid artery; 2 — right common carotid artery; 3 — left internal jugular vein (significant enlargement); 4 — right internal jugular vein; 5 — bifurcation area of the left common carotid artery; 6 — left ICA; 7 — post-trepanation defect in the left occipital bone.

 

Thus, the following were identified in the patient:

• traumatic occlusion of the left ICA in the petrous (C2 per A. Bouthillier) segment;
• intracranial extradural (carotid-jugular) AVF on the left at the level of the petrous (C2 per A. Bouthillier) segment of the left ICA;
• hypodense areas along the wound channel in the left cerebellar hemisphere (25 × 26 mm), left temporal lobe (6 × 13 mm), and right frontal lobe (contusion focus 16 × 20 mm of contrecoup type);
• unrepaired post-trepanation bone defects in the right frontal bone (19 × 20 mm) and left occipital bone (41 × 45 mm).

At the S.M. Kirov Military Medical Academy Department of Neurosurgery, multiprojection selective cerebral angiography was performed, confirming a traumatic carotid-jugular AVF on the left at the petrous segment of the left ICA with drainage into the left jugular vein. The right ICA was functional, with blood supply to the left hemisphere maintained via collateral flow; there were no signs of retrograde filling of the carotid-jugular fistula from the right carotid or vertebrobasilar basins. To prevent fistula rupture, embolization with destructive occlusion of the left ICA was performed. An exchange wire was used to advance a guide catheter subcranially into the left ICA. A microcatheter was advanced and secured proximal to the fistula using a guidewire. Detachable microcoils were deployed with microcatheter withdrawal to achieve filling of the ICA lumen at the cervical segment (C1 per A. Bouthillier classification) with microcoils. Additional embolization using an adhesive glue composition was performed to achieve complete fistula occlusion. Control selective cerebral angiography showed no contrast filling of the fistula (Fig. 5).

 

Fig. 5. Selective cerebral angiography (A) and embolization of carotid-jugular AVF (B) in patient N.

1 — guiding catheter in the left ICA; 2 — contrast filling into the left ICA; 3 — contrast filling of carotid-jugular AVF; 4 — left internal jugular vein (significantly enlarged); 5 — minimal retrograde contrast filling of the left sigmoid sinus during systole; 6 — embolization with microcoils of the cervical (C1 per A. Bouthillier) segment of the left ICA; 7 — absence of contrast filling in the internal jugular vein through the disconnected carotid-jugular AVF.

 

Following the surgical intervention, the patient reported improvement of pulsatile tinnitus in the left ear and significant reduction in headache intensity. Subsequent treatment included continued pharmacotherapy, physical and device-assisted rehabilitation, as well as sessions with a speech therapist and psychologist. By the time of discharge, neurological status improved: significant reduction in cerebellar dysarthria, ataxia, and asthenic syndrome; decreased nystagmus amplitude; disappearance of the Marinescu–Radovici oral automatism reflex; and reduced intensity of pathological pyramidal wrist reflexes were noted. Neuropsychological testing: Mini-Mental State Examination score — 26 points; Frontal Assessment Battery score — 17 points; Clock Drawing Test score — 9 points. The patient resumed service in the Armed Forces of the Russian Federation. At 6-month follow-up examination at the S.M. Kirov Military Medical Academy Clinic of Nervous Diseases, no evidence of traumatic AVF recurrence was found.

Discussion

In current clinical practice, military neurologists and neurosurgeons regularly encounter cases of high-energy projectile head wounds lacking classical manifestations of severe traumatic brain injury such as loss of consciousness, amnesia, generalized cerebral symptoms, or focal neurological deficits. Similarly, in neck injuries involving damage to major brachiocephalic arteries with subsequent thrombotic occlusion, the absence of cerebral ischemia and IS are not uncommon. Contemporary management of gunshot wound casualties also frequently presents inverse scenarios where neurological deficits resulting from secondary ischemic changes (due to traumatic occlusion of major brachiocephalic arteries) exceed the severity of neurological consequences from the primary neck or head wound itself [1].

This clinical case is unique due to several features:

• survival despite a potentially fatal penetrating gunshot wound to the skull base with damage to major brachiocephalic vessels;
• topographic localization of the post-traumatic AVF within the wound tract in the bony defect of the petrous part of the temporal bone;
• no IS development (either at the time of injury or as an in-hospital stroke during treatment stages) despite traumatic injury and occlusion of the left internal carotid artery;
• favorable clinical outcome with good recovery of neurological functions despite extensive traumatic cerebral injuries (contusion of the left cerebellar hemisphere, left temporal lobe, and right frontal lobe) and inner ear damage.

The specific location of the aforementioned post-traumatic AVF, considering the bony traumatic changes in the left temporal bone, leaves open the terminological question regarding its topographic description and classification.

The anatomical boundary between the sigmoid sinus and the internal jugular vein is the jugular foramen, formed by the jugular notches of the temporal and occipital bones. Consequently, the trajectory of a penetrating gunshot craniobasal wound (suboccipital vector with wound tract: left occipital bone [entry] → posterior cranial fossa → left temporal bone pyramid → middle cranial fossa → left greater wing of the sphenoid bone [exit] → soft palate → oral cavity) should indicate injury to the left sigmoid sinus and allows classification of the aforementioned AVF as an intracranial extradural carotid-sigmoid fistula.

On the other hand, the shape and size of the jugular foramen and jugular fossa exhibit high individual variability, depending on the presence (approximately 50% of cases) or absence (approximately 50% of cases) of the superior bulb of the internal jugular vein. Anatomically, jugular fossae are classified as small (up to 0.5 cm), medium (up to 1.0 cm), and large (over 1.0 cm). A very wide jugular fossa may reach the crus of the posterior semicircular canal, contact the vestibular aqueduct and aperture of the cochlear canaliculus, and deform or alter the diameter of these ducts [21]. Therefore, with a high dome of the jugular fossa, isolated injury to the internal jugular vein within it (without involvement of the sigmoid sinus) cannot be ruled out, nor can the formation of an AVF between its superior bulb and the petrous segment of the ICA through the wound defect area in the intrajugular ridge of the temporal bone. In such a case, the AVF would be termed carotid-jugular and classified as extradural.

In this clinical case, we favor the second topographic localization scenario (resulting from marginal injury to the superior bulb of the left internal jugular vein) due to the absence of intracranial hemorrhage signs on prior CT scans during earlier stages of care and minimal retrograde contrast enhancement of the left sigmoid sinus on CT angiography and selective cerebral angiography. Given that traumatic occlusion of the left ICA did not lead to IS, it can be inferred that the carotid-jugular fistula formed not instantaneously but subacutely — over several hours to days.

Searches in major international databases using keyword combinations “intracranial carotid-jugular fistula”, “intracranial extradural fistula”, “intracranial extradural arteriovenous fistula” yielded no positive results; retrieved data primarily concerned extracranial or intracranial dural (most commonly carotid-cavernous) AVFs. A search for “traumatic carotid-sigmoid fistula” returned one relevant case report describing a gunshot-induced penetrating craniofacial wound that created a fistula along the wound tract between a damaged branch of the external carotid artery in the maxillary region and the venous system at the sigmoid sinus–internal jugular vein junction (20-year-old patient; fatal outcome from hemorrhagic shock within hours of hospitalization) [22]. Thus, at the time of article publication, no clinical reports of traumatic intracranial extradural AVFs were found in Russian or international literature sources.

This clinical case differs from the well-known manifestations of carotid-cavernous fistula, which are caused by elevated pressure in the ophthalmic vein (due to the absence of valvular apparatus) against the background of impaired venous outflow, as well as compression of the III, IV, VI, and first branch of the V (trigeminal) cranial nerves by the enlarged cavernous sinus. The classic triad of symptoms of carotid-cavernous AVF is characterized by pulsating exophthalmos, cephalic bruit (synchronous with pulse, blowing, often resembling a steam engine noise, and excruciating for patients), and conjunctival chemosis. Additional symptoms may include orbital and/or retroorbital pain, decreased visual acuity, diplopia, ophthalmoplegia (usually unilateral but sometimes initially unilateral or progressive to bilateral), and subarachnoid hemorrhage (rarely) [14, 23].

Clinical complications of intracranial AVFs are diverse: depending on fistula size, location, and duration, pathological blood shunting may lead to cerebral hemodynamic disorders and neurological deficits resembling IS due to delayed hypoperfusion disturbances, obstruct venous outflow from cerebral sinuses posing a thrombosis risk, cause right ventricular heart failure syndrome, or result in internal jugular vein rupture. The rate of progression and timing of cardiac decompensation depend on the volume of blood shunted into the venous system.

When managing patients with gunshot wounds to the head, it should be considered that heterogeneous mechanisms of brachiocephalic artery injury resulting from trauma (hypoperfusion disorders, artery-to-artery embolism, thrombosis) can lead to IS development both immediately after injury and in a delayed manner, including as in-hospital ischemic stroke at various stages of medical care [1, 24]. The manifestation of secondary ischemic injury depends on several factors: the pathophysiological mechanism, the rate of dissection formation and traumatic occlusion, the activity of the blood coagulation/anticoagulation system, and the collateral circulation reserve. The latter depends, among other factors, on the structural features of the circle of Willis and cerebrovascular reactivity.

In the presented clinical case, the patient’s circle of Willis was closed (Fig. 6), which, in our opinion, played a key role in preventing IS despite thrombotic occlusion resulting from traumatic injury to the ICA.

 

Fig. 6. Color 3D reconstruction of CT angiography of head vessels.

1 — left posterior communicating artery; 2 — anterior communicating artery; 3 — right posterior communicating artery.

 

The second factor that most likely protected the brain from IS was the low rate of occlusion formation. In traumatic brain injury and gunshot wounds, arteriovenous fistula formation and distal arterial occlusion may occur concurrently and be directly interdependent. The faster the occlusion formation rate, the lower the probability of sufficient collateral cerebral blood flow and the higher the risks of ipsilateral IS.

As combat trauma care practice shows, all patients with head and neck injuries should undergo CT angiography to rule out major arterial and venous injuries, traumatic dissections, aneurysms, and arteriovenous fistulas. CT angiography is superior to ultrasound for its ability to reliably visualize neck vessels regardless of injury level and detect injuries to other neck organs and the spine. Metallic foreign bodies adjacent to vessels significantly increase injury probability but complicate CT angiography assessment due to metal artifacts. Duplex scanning of neck vessels may be used for screening and as an adjunct to CT angiography, given its high sensitivity for detecting intra-arterial floating thrombi, vascular wall dissections, and comprehensive Doppler hemodynamic assessment at extra- and intracranial levels. Magnetic resonance imaging is often limited due to metallic fragments in the bodies of wounded patients [1].

Any major head and neck vascular injuries (dissection, pseudoaneurysm, floating thrombus, etc.) detected by ultrasound or CT, or inability to rule them out, are indications for selective cerebral angiography.

Thus, all patients with gunshot wounds to the head and neck should be considered potentially having occult brachiocephalic vessel injuries and increased risk of in-hospital IS. Early active detection of brachiocephalic vessel injuries enables timely surgical (including endovascular) and pharmacological prevention of potentially disabling acute cerebrovascular events.

About the authors

Igor V. Litvinenko

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0001-8988-3011

Dr. Sci. (Med.), Professor, Head, Department of nervous diseases

Russian Federation, Saint Petersburg

Alexander V. Savello

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0002-1680-6119

Dr. Sci. (Med.), Professor, Deputy Head, Department of neurosurgery

Russian Federation, Saint Petersburg

Sergey V. Kolomentsev

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0002-3756-6214

Cand. Sci. (Med.), lecturer, Department of nervous diseases

Russian Federation, Saint Petersburg

Yulia N. Priporova

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0002-5080-4010

Cand. Sci. (Med.), radiologist, Head, Department of radionuclide diagnostics, Department and clinic of roentgenology and radiology (with a course in ultrasound diagnostics)

Russian Federation, Saint Petersburg

Aleksander V. Ryabtsev

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0002-3832-2780

Cand. Sci. (Med.), lecturer, Department of nervous diseases

Russian Federation, Saint Petersburg

Nataliya V. Kutc

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0001-7865-5400

Cand. Sci. (Med.), Head, Department of functional diagnostics, Clinic of nervous diseases

Russian Federation, Saint Petersburg

Natalia A. Lupina

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0009-0000-3011-5122

Head, Office of ultrasound examinations (central nervous system studies), Department of functional diagnostics, Clinic of nervous diseases

Russian Federation, Saint Petersburg

Daria Z. Malova

S.M. Kirov Military Medical Academy

Email: annaly-nevrologii@neurology.ru
ORCID iD: 0009-0007-4197-7191

clinical resident, Department of nervous diseases

Russian Federation, Saint Petersburg

Nikolay V. Tsygan

S.M. Kirov Military Medical Academy

Author for correspondence.
Email: annaly-nevrologii@neurology.ru
ORCID iD: 0000-0002-5881-2242

Dr. Sci. (Med.), Professor, Deputy Head, Department of nervous diseases

Russian Federation, Saint Petersburg

References

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