Hemifacial spasm

The hemifacial spasm (or hemifacial spasm ) is a single (hemi ) occurring involuntary spasm ( spasm ) of the facial muscles. Cause is usually a microvascular compression syndrome.

Epidemiology

The disease usually occurs beyond the age of 60. Predisposing factors are female gender ( M: F = 1:2) and long-standing arterial hypertension. The prevalence for men and women at 7 or 14 hundred thousandths people.

Symptoms

It comes to einschießenden cramps ( spasms ) of the controlled from the facial nerve muscles. These can be painful. Often the symptoms begin around the eye ( orbicularis oculi ) and spreads over months to years to the entire half of the face (up to the platysma ) from. A facial paralysis is very rare and indicates another underlying disease.

Pathogenesis

Cause in over 90% of cases, compression of the facial nerve by a blood vessel in the posterior fossa, so close to the origin of the nervous before his entry into the petrous bone. Here are involved in about 20 % of cases, most commonly the posterior inferior cerebellar artery ( PICA ) in about 40% and the anterior inferior cerebellar artery ( AICA ). These extend mostly through long-standing high blood pressure and then extend increasingly tortuous, until they press against the nerves. The pulsation of the vessel then causes local damage to the myelin sheaths. This loss of electrical insulation electrical excitations can jump between the nerve fibers and thereby trigger the spasms of the facial muscles.

Thus the cause of the spasm is hemifacial identical to the trigeminal neuralgia, only that another cranial nerve is affected.

Rare other causes are vascular malformations ( angiomas ) or tumors or multiple sclerosis.

Diagnostics

For clarification include a magnetic resonance imaging ( MRI). Furthermore, there should be a elektrophysioloische study ( electromyography, neurography ).

This need other differential diagnoses are excluded, especially tumors of the posterior cranial fossa (eg acoustic neuroma ) and multiple sclerosis. Therefore may be useful in individual cases lumbar puncture.

Therapy

The treatment of choice is the injection of botulinum toxin into the affected muscles. This is just all required 3-5 months and has an efficacy of> 80 % for a very good success and> 90 % for a relief. Loss of activity may occur, usually on the basis of antibody formation to botulinum toxin.

Antiepileptic drugs are similar to the effect in trigeminal neuralgia also effective. Most experiences are for carbamazepine before ( often loss of effect specified in the course ). But many newer antiepileptic drugs have been used successfully in certain cases ( gabapentin, pregabalin, topiramate, levetiracetam, zonisamide ).

As a causal therapy is microvascular decompression ( Jannetta operation) in question. The success rate is about 80 %. Since this is a complicated surgery in the posterior fossa, remains the last resort. It should be kept in mind if treatment with medication does not work sufficiently or is tolerated.