Made on
Tilda
Trigeminal neuralgia causes brief, extremely severe attacks of one-sided facial pain, often described as an electric shock. Accurate diagnosis and medication remain the foundation of treatment. Botulinum toxin may be considered in selected patients when standard treatment does not provide sufficient pain control or causes significant adverse effects.
The trigeminal nerve provides most of the sensation of the face, while its third division also supplies the muscles of mastication. Trigeminal neuralgia causes recurrent, brief attacks of sharp, shooting or electric shock-like pain.
Pain is usually unilateral. Individual attacks may last from a fraction of a second to approximately two minutes and can recur many times during the day.
Classical attacks are very brief, recurrent, electric shock-like and often triggered by otherwise harmless stimuli. Persistent aching or burning facial pain requires a broader diagnostic assessment.
Pain may involve the forehead, upper eyelid or the area around the eye. Isolated V1 involvement is less common.
Pain may be felt in the cheek, upper lip, side of the nose, upper jaw or upper teeth.
Pain may involve the lower lip, lower jaw, chin or lower teeth.
Accurate diagnosis is especially important because very different disorders may be described by patients as “trigeminal nerve pain”.
Associated with neurovascular compression, where a blood vessel contacts the trigeminal nerve root and produces relevant structural changes in the nerve.
The clinical pattern is typical, but no convincing structural cause explaining the neuralgia is identified.
Caused by another neurological disorder, for example demyelination in multiple sclerosis or another structural lesion.
Diagnosis is primarily based on the clinical pattern: duration and character of the attacks, distribution along trigeminal divisions, triggering factors and the neurological examination.
Even when symptoms appear typical, imaging is important because the clinical picture alone cannot reliably exclude a secondary cause. Brain MRI should therefore assess the region of the trigeminal nerve.
Botulinum toxin is not the standard first-line treatment for trigeminal neuralgia. Initial medical treatment usually uses drugs that reduce pathological electrical activity in the nerve.
Carbamazepine and oxcarbazepine are the best established first-choice medications. Effectiveness and tolerability need to be assessed individually.
Depending on the clinical situation, other medicines or combinations may be considered, as well as botulinum toxin and neurosurgical treatment options.
When pain remains inadequately controlled or effective doses produce unacceptable adverse effects, other treatment strategies should be discussed in a timely manner.
Botulinum toxin type A may be considered in selected patients with trigeminal neuralgia, particularly when standard medication provides insufficient pain control or causes significant adverse effects.
It does not remove neurovascular compression and it does not treat the underlying cause of secondary trigeminal neuralgia. It should therefore not be regarded as a universal substitute for other treatments.
In trigeminal neuralgia, the analgesic effect of botulinum toxin is not simply a consequence of weakening muscles. Botulinum toxin can also reduce the release of mediators involved in peripheral pain signalling.
Treatment is therefore not intended to “relax half of the face”. Small amounts are placed locally according to the distribution of pain and trigger zones.
The first step is to determine whether the pain pattern truly fits trigeminal neuralgia.
The distribution of attacks and clinically relevant trigger zones are identified.
Injection sites and depth are individualized according to anatomy and pain distribution.
Follow-up focuses on attack frequency, pain intensity and treatment tolerability.
Trigeminal neuralgia occurs more often in people with multiple sclerosis than in the general population. Demyelinating lesions affecting trigeminal pathways may contribute to the disorder.
In some patients, demyelination and neurovascular contact may coexist, so MRI and the clinical pattern need to be interpreted together.
The general principles of symptomatic treatment remain similar: medications are used first, while additional approaches such as botulinum toxin or surgical treatment may be discussed when pain remains difficult to control.
More information: multiple sclerosis diagnosis and treatment in Israel →
A minimally invasive symptomatic treatment that can reduce pain in some patients, but does not remove vascular compression of the nerve.
In classical trigeminal neuralgia with relevant neurovascular compression, microvascular decompression may be considered to address the conflict between the vessel and the nerve.
Depending on the clinical situation, percutaneous neuroablative procedures or stereotactic radiosurgery may also be considered.
Treatment depends on the type of trigeminal neuralgia, MRI findings, age, comorbidities, medication response and the patient's preferences.
When pain remains poorly controlled or effective medical treatment is poorly tolerated, the full range of appropriate treatment options should be discussed.
Adverse effects are usually local and temporary. Their likelihood depends on the injection area, dose and proximity to facial or masticatory muscles.
Dr Lidiia Prakhova, MD, PhD, is a neurologist in Israel with experience in the diagnosis of complex neurological pain syndromes and in the use of botulinum toxin in neurology.
In patients with facial pain, the first step is to determine whether the clinical pattern truly corresponds to trigeminal neuralgia and whether the diagnostic evaluation is sufficient.
If botulinum toxin treatment is appropriate, injection areas are selected individually according to the distribution of pain and facial anatomy.
If carbamazepine, oxcarbazepine, other medications, injections or surgical procedures have already been tried, information about their effectiveness and adverse effects is useful when planning further treatment.
Typical attacks are very brief, severe and one-sided, often described as electric shock-like pain. They may be triggered by talking, chewing, brushing the teeth, touching the face or cold air.
MRI is generally part of the diagnostic evaluation. It helps exclude secondary causes, assess the trigeminal nerve and evaluate possible neurovascular compression.
Carbamazepine and oxcarbazepine are the principal first-choice medications for typical trigeminal neuralgia. Treatment is individualized according to effectiveness and tolerability.
It may be considered in selected patients when standard medication does not provide sufficient benefit, is poorly tolerated or when an additional method of pain control is needed.
No. It can reduce painful attacks, but it does not remove neurovascular compression or treat a structural cause of secondary trigeminal neuralgia.
Duration of benefit varies. In some patients improvement persists for several months, after which repeat treatment can be considered if the previous response was clinically meaningful.
Surgical options should be discussed when pain remains inadequately controlled with medication or effective medication is poorly tolerated. The choice of procedure depends on the type of neuralgia and MRI findings.
If you have brief attacks of severe one-sided facial pain, medication no longer controls the attacks or treatment causes significant adverse effects, consultation with Dr Lidiia Prakhova can help clarify the diagnosis, review MRI findings and discuss medication, botulinum toxin and other appropriate treatment options.
Book a consultation