Neurovascular conflict is compression and dysfunction of the cranial nerve due to its contact with a nearby vessel. Most often in practice there is damage to the trigeminal, facial nerve, less often there is compression of other pairs of CN, in addition to the olfactory. The clinical picture depends on the affected nerve, the degree of compression and localization of the pathological focus. The basis for the diagnosis of neurovascular pathology is brain MRI with MR angiography. Treatment of the conflict is conservative: antiepileptic and dopaminergic drugs, botulinum toxin injections. If pharmacotherapy is ineffective, neurosurgical correction is indicated.
ICD 10
G50 G51 G52
General information
Neurovascular conflict (NVC) is a multidisciplinary problem occurring in 15-20 cases per 100 thousand population. The term was introduced into the medical vocabulary back in 1936. The greatest achievements in the study and development of methods for correcting this syndrome belong to the American neurologist P. Janetta. The scientist created the author’s method of neurosurgical decompression, which is known as the “Jannetta Procedure”. However, there are still a number of difficulties in the diagnosis and effective treatment of NVC in practical neurology, so the disease does not lose its relevance.
Causes
The triggering factor of the symptoms of neurovascular conflict is prolonged compression of a certain part of the nerve by an arterial, less often a venous vessel. The main reason is mechanical action due to the transmission of vascular pulsation or the formation of paroxysmal activity due to the interaction of a nerve with an artery or vein. Predisposing conditions for neurovascular conflict:
- Atherosclerosis. When lipid plaques and calcium are deposited in the vascular walls, they become more dense and rigid, and increase in diameter. Even minimal changes are enough to have a mechanical effect on the surrounding tissues. The risk of neurovascular disease increases with concomitant hypertension.
- Vascular anomalies. Changes in the normal size, structure and localization of the vessel causes compression inside the limited space of the cranium. NVC develops with arteriovenous malformations, vascular tumors.
- Pathology of the structure of the skull. With a decrease in the volume of the posterior cranial fossa, the probability of compression of nerves and other structures increases. Neurovascular compression is 3 times more common in the group of patients with Arnold-Chiari anomaly. The provoking factor of the conflict is birth trauma of the skull, severe TBI.
Pathogenesis
In the compression zone, demyelination of type A fibers occurs, which transmit signals about mechanical stimuli and conduct initial pain impulses. The lesion area becomes a focus for the generation of spontaneous impulses that propagate to slow C-fibers responsible for sensitivity to pain. As a result, the cerebral cortex receives pain signals that are not inhibited by the antinociceptive system.
Pain paroxysms are provoked by irritation of the skin, which is innervated by the affected sections of A-fibers. At the same time, the intensity of symptoms depends on the volume of demyelination of nerve fibers and the activity of physiological analgesic mechanisms. With simultaneous neurovascular compression by two vessels (the “sandwich” phenomenon), the probability of conflict increases from 2.3-6.25% to 30-50%.
Symptoms
Trigeminal neuralgia
The most common variant of NVC is associated with a lesion of the trigeminal nerve. It occurs with a frequency of 5:100,000 in women and 2 times less often among men. Patients complain of attacks of burning pain in the face, which lasts from a few seconds to a couple of minutes. The pain is accompanied by facial muscle spasms, lacrimation, salivation. The number of seizures ranges from one to several dozen during the day.
With trigeminal neuralgia, patients freeze, waiting out the pain, because the slightest movement aggravates the situation. Paroxysms of neurovascular conflict are provoked by exposure to pain (trigger) points of the trigeminal nerve. Most seizures are associated with mechanical irritation of these areas: careless brushing of teeth, shaving, chewing food and talking with active facial expressions.
Hemifacial spasm
The clinical picture is caused by compression of the facial nerve in the area of exit from the brain stem. In most cases, unilateral lesion occurs, 0.6-5% of patients have bilateral neurovascular conflict. The disease is more common in middle-aged and older women. Men suffer from hemifacial spasm 2 times less often, they do not have a clear pattern between age and the risk of developing NVC.
In most people, the first sign of pathology is a short-term twitching of the eyelids, which gradually turns into tonic muscle spasms, spontaneous closing of the eyes. Further, spastic phenomena spread over the entire half of the face and neck. Paroxysms occur at any time, even in a dream, provoked by active facial expressions, an overabundance of emotions, physical fatigue.
Vestibular paroxysmia
Neurovascular conflict with the vestibular-cochlear nerve is manifested by attacks of dizziness. They last from a few seconds to several minutes, and increase when the head is tilted back. During paroxysm, nausea is observed, a staggering gait with a deviation towards the pathological focus. In 30% of cases, vestibular disorders are accompanied by damage to the auditory fibers, so patients complain of hearing loss, a feeling of ringing in the ears.
Lingopharyngeal neuralgia
When the IX pair of CN is squeezed, complaints arise of sharp paroxysmal pains that begin at the root of the tongue or in the area of the tonsils. The pain syndrome quickly spreads to the pharynx and soft palate, gives in the ear, lower jaw and neck. Paroxysms last up to 2 minutes, the strength and nature of the sensations are similar to the symptoms of trigeminal neuralgia.
Lingopharyngeal neuralgia is provoked by movements of the tongue when speaking and swallowing, eating too hot or cold food. Paroxysms develop according to a stereotypical scenario, the symptoms do not change from attack to attack. During the inter-access period, patients do not present neurological or other complaints. In 2-3% of cases, there is a combined lesion of the vagus nerve, so the attacks are accompanied by cardiac arrhythmias.
Spastic torticollis
Symptoms are caused by compression of the accessory nerve, which occurs in 1-3 cases per 100,000 population. Patients complain of painful spasms of the neck muscles on one side. At the same time, there is a violent turn of the head to the side, its inclination to the shoulder. Attacks of spastic torticollis with neurovascular lesion are provoked by careless movements, emotional stress.
Rare variants of NVC
With the conflict of the ocular nerves (oculomotor, block, diverting), there are complaints of double vision, strabismus, difficulties with eye movements. For compression of the hyoid nerve, paroxysmal disorders of swallowing and speech function, weakness of the lingual muscles are typical. Occasionally, during examination, the deviation of the tongue to the side of the lesion is determined.
Complications
In 2.8% of cases, multiple lesions of CN are observed. Simultaneous development of neurovascular conflict involving two nerves and two different vessels or compression of structures by one convoluted artery is possible. Basically, a combined lesion of the trigeminal and facial nerves is diagnosed, which has a more severe clinical course and is difficult to treat.
Pain paroxysms significantly worsen the patient’s quality of life, cause neurosis and anxiety disorder, and cause depression. With frequent and intense attacks, a person loses his ability to work, experiences limitations in everyday life. In the chronic course of neurovascular pathology, facial muscle paralysis, facial asymmetry, hearing and vision impairment are observed.
Complications after neurosurgical treatment of conflict are isolated into a separate group. The most severe consequence of the operation is cerebellar infarction, which occurs in 1-2% of cases. Often there is persistent (3-8%) or transient hearing loss (20%), deterioration of facial sensitivity (5-30%), paresis of facial muscles (5-6%). Complications of radiosurgery include dryness of the sclera, memory impairment, decreased taste and swallowing disorder.
Diagnostics
If a neurovascular conflict is suspected, an extended examination by a neurologist is indicated. To determine the intensity of pain sensations, clinical scales are used: verbal descriptive, facial, visual analog. Next, the neurological status is assessed, the anamnesis of the disease and life is clarified, a full physical examination is performed. To confirm the diagnosis, research results will be required:
- MRI of the brain. In the MR angiography mode, it is possible to visualize the vessel that caused neurovascular disorders. To exclude volumetric neoplasms, the infectious process and other causes of neuralgia, an MRI is prescribed according to the 3D-T2-FSE and FIESTA protocols.
- Electromyography. When analyzing the results of an electrophysiological study, attention is paid to paroxysmal muscle discharges. They consist of rapid and irregular bursts of clonic activity. Often such a picture develops in conditions of controlled nervous stimulation.
Treatment
Conservative therapy
Treatment of neuralgia caused by nerve compression begins with medical methods. Anticonvulsants are used as first-line drugs, which show an effectiveness of about 90%. During the entire period of treatment, the content of antiepileptic drugs in the body is monitored to prevent complications of pharmacotherapy: toxic hepatitis, violation of the cellular composition of the blood.
In case of neurovascular conflict of the facial nerve, botulinum therapy demonstrates the best effectiveness. Controlled administration of botulinum toxin into the facial muscles on the side of the lesion causes their paresis lasting 5-12 months. At the same time, the patient’s clinical manifestations of the disease completely disappear or significantly decrease, and the quality of life improves. Botulinum toxin injections are considered as the method of choice in the early stages of NVC.
Surgical treatment
If conservative therapy is ineffective or impossible, patients are transferred to the department of neurosurgery. To eliminate the cause of symptoms, a microvascular decompression operation is indicated: the differentiation of the CN and the vessel squeezing it, the installation of a special gasket to prevent relapses of neurovascular conflict. The efficiency of the operation is 70-90%.
If there are contraindications to neurosurgical intervention, a minimally invasive method of stereotactic radiosurgery is used: a controlled dose of radiation is applied to the affected area. The effectiveness of the technique is lower compared to microvascular decompression. A year after the manipulation, the effect persists in 60% of patients, in the next 2 years, the effectiveness decreases to 34-40%.
Prognosis and prevention
With timely initiation of therapy, the success rate of treatment is more than 90%. A less optimistic prognosis is associated with a combined lesion of CN, the absence of the effect of surgical intervention, the development of severe postoperative consequences. Prevention of neurovascular conflicts consists in timely detection and therapy of vascular pathology. Methods for preventing congenital brain abnormalities have not been developed.