Hemifacial spasm

Last updated August 04, 2024

Hemifacial spasm (HFS) is a rare neuromuscular disease characterized by irregular, involuntary muscle contractions (spasms) on one side (hemi-) of the face (-facial).^[1] The facial muscles are controlled by the facial nerve (seventh cranial nerve), which originates at the brainstem and exits the skull below the ear where it separates into five main branches.

This disease takes two forms: typical and atypical. In typical form, the twitching usually starts in the lower eyelid in orbicularis oculi muscle. As time progresses, it spreads to the whole lid, then to the orbicularis oris muscle around the lips, and buccinator muscle in the cheekbone area.^[2] The reverse process of twitching occurs in atypical hemifacial spasm; twitching starts in orbicularis oris muscle around the lips, and buccinator muscle in the cheekbone area in the lower face, then progresses up to the orbicularis oculi muscle in the eyelid as time progresses.^[2] The most common form is the typical form, and atypical form is only seen in about 2–3% of patients with hemifacial spasm.^[3] The incidence of hemifacial spasm is approximately 0.8 per 100,000 persons.^[4]

This disorder occurs in both men and women, although it affects middle-aged or elderly women more frequently.^[5] Hemifacial spasm is much more common in some Asian populations.^[1] It may be caused by a facial nerve injury, compression by a blood vessel, a tumor, or it may have no apparent cause. Individuals with spasm on both sides of the face are very rare.

Signs and symptoms

The first sign of hemifacial spasm is typically muscle movement in the patient's eyelid and around the eye. It can vary in intensity.^[6] The intermittent twitching of the eyelid, which can result in forced closure of the eye which gradually spreads to the muscles of the lower part of the face (Typical form- See Image). In atypical form the spasms start in the cheekbone area and spreads to the eyelid.^[2] Ultimately, all the muscles on that side are affected, nearly all the time. This sometimes causes the mouth to be pulled to the side. Experts have linked hemifacial spasm to facial nerve injury, Bell's palsy and tumors. Although the most frequent cause is a blood vessel pressing on the facial nerve at the spot where it leaves the patient's brain stem, sometimes there is no known cause. When the affected individual is younger than 40, doctors suspect an underlying cause such as multiple sclerosis.^[7]

Causes

Three theories exist to explain the facial nerve dysfunction found in hemifacial spasm. The first proposed theory is ephaptic transmission, which is electrical activity crossing from one demyelinated neuron to another resulting in a false synapse.^[8] The second theory involves abnormal activity of axons at the facial nerve root end zone secondary to compressive damage/demyelination.^[9]

The third theory or "Kindling theory" involves increased excitability of the facial nerve nucleus due to feedback from a damaged facial nerve.^[9]

It is generally accepted as compression of the facial nerve by vessels of the posterior circulation.^[9] In detail compression of the seventh cranial nerve by a dolichoectatic (a distorted, dilated, and elongated) anterior inferior cerebellar artery, or posterior inferior cerebellar artery is accepted to be the general cause of hemifacial spasm. Less than 1% of cases are caused by tumor.^[10]^[11] Hemifacial spasm is much more common in some Asian populations.^[1]

Several families with hemifacial spasm have been reported, suggesting a genetic etiology or predisposition in some cases. There appears to be an autosomal dominant pattern of inheritance in these families with low penetrance, and except for a younger age at onset, the clinical features overlap with the idiopathic cases. Evaluation of single-nucleotide polymorphisms in genes related to vascular change causing compression of blood vessels did not show an association with hemifacial spasm. Clarifying the role of genetic susceptibility in hemifacial spasm may help to better understand the pathogenesis of this disease.^[12]

Diagnosis

There are several tests done to diagnose hemifacial spasm. Diagnosing a case of hemifacial spasm begins with a complete neurological exam, including an electromyography (EMG – a test that measures and records electrical activity generated in muscle at rest and in response to muscle contraction), magnetic resonance imaging (MRI – a test that uses magnetic waves to make pictures of structures inside the head), computed tomography (CT scan – a type of x-ray that uses a computer to make pictures of structures inside the head), and angiography (an x-ray exam of the blood vessels when they are filled with a contrast material).^[13]

Studies have shown that the most effective method of hemifacial spasm screening is MRI. In one study only 25% of the CT scans showed the abnormality in hemifacial spasm patients, whilst more than half of the MRI imaging demonstrated a vascular anomaly. MRI imaging should be the initial screening procedure in the assessment of patients with hemifacial spasm.^[14]

Prevention

There is no known way to prevent hemifacial spasm.^[12]

Treatments

Mild cases of hemifacial spasm may be managed with sedation or carbamazepine (an anticonvulsant drug).^[15] Microsurgical decompression and botulinum toxin injections are the current main treatments used for hemifacial spasm.^[14]

Microvascular decompression

Endoscope-assisted microvascular decompression in hemifacial spasm with a teflon bridge. Source: Rhomberg, T., Eördögh, M., Lehmann, S. et al. Endoscope-assisted microvascular decompression in hemifacial spasm with a teflon bridge. Acta Neurochir 166, 239 (2024). https://doi.org/10.1007/s00701-024-06142-7

Microvascular decompression appears to be the most popular surgical treatment at present. Microvascular decompression relieves pressure on the facial nerve, which is the cause of most hemifacial spasm cases.^[16] Excellent to good results are reported in 80% or more cases with a 10% recurrence rate.^[17] In the present series approximately 10% had previously failed surgery. Serious complications can follow microsurgical decompressive operations, even when performed by experienced surgeons. These include cerebellar haematoma or swelling, brainstem infarction (blood vessel of the brain stem blocked), cerebral infarction (ischemic stroke resulting from a disturbance in the blood vessels supplying blood to the brain), subdural haematoma and intracerebral infarction (blockage of blood flow to the brain). Death or permanent disability (hearing loss) can occur in 2% of patients of hemifacial spasm.^[18]

Botulinum toxin

Observational data from studies (the updated review in 2020 did not find any randomized controlled trials) indicates that botulinum toxin is safe and effective in the treatment of hemifacial spasm with success rates between 76 - 100%.^[19] The injections are administered as an outpatient or office procedure. Whilst side effects occur, these are never permanent. Repeated injections over the years remain highly effective.^[20] Whilst the toxin is expensive, the cost of even prolonged courses of injections compares favourably with the cost of surgery.^[21] Patients with HFS should be offered a number of treatment options. Very mild cases or those who are reluctant to have surgery or botulinum toxin injections can be offered medical treatment, sometimes as a temporary measure. In young and fit patients microsurgical decompression and botulinum injections should be discussed as alternative procedures. In the majority of cases, and especially in the elderly and the unfit, botulinum toxin injection is the treatment of first choice. Imaging procedures should be done in all unusual cases of hemifacial spasm and when surgery is contemplated.^[14] Patients with hemifacial spasm were shown to have decreased sweating after botulinum toxin injections. This was first observed in 1993 by Khalaf Bushara and David Park. This was the first demonstration of nonmuscular use of BTX-A. Bushara further showed the efficacy of botulinum toxin in treating hyperhidrosis (excessive sweating). BTX-A was later approved for the treatment of excessive underarm sweating. This is technically known as severe primary axillary hyperhidrosis – excessive underarm sweating with an unknown cause which cannot be managed by topical agents (see focal hyperhidrosis).^{[ citation needed ]}

Epidemiology

The incidence of hemifacial spasm is approximately 0.8 per 100,000 persons.^[4] Hemifacial spasm is more prevalent among females over 40 years of age.^[22]^[23] The estimated prevalence for women is 14.5 per 100,000 and 7.4 per 100,000 in men.^[24] Prevalence for hemifacial spasm increase with age, reaching 39.7 per 100,000 for those aged 70 years and older.^[25] One study divided 214 hemifacial patients based on the cause of the disease: The patients who had a compression in the facial nerve at the end of the brainstem as the primary hemifacial spasm and patients who had peripheral facial palsy or nerve lesion due to tumors, demyelination, trauma, or infection as secondary hemifacial spasm. The study found that 77% of hemifacial spasm is due to primary hemifacial spasm and 23% is due to secondary hemifacial spasm. The study also found both sets of patients to share similar age at onset, male to female ratios, and similar affected side.^[26] Another study with 2050 patients presented with hemifacial spasm between 1986 and 2009, only 9 cases were caused by a cerebellopontine angle syndrome, an incidence of 0.44%.^[11]

History

The earliest descriptions about hemifacial spasm is by Shultze in 1875 and Gowers in 1899. The etiology of hemifacial spasm and location of the abnormality have been debated for more than a century.^[4] Surgical treatment for hemifacial spasm in the early 20th century included neurolysis (destruction of nerve tissue), stretching the facial nerve (seventh cranial nerve), and high-pressure irrigation of the nerve with lactate ringer's solution. The medical regimens of that time involved injection of the nerve with ethanol, electrical stimulation, application of toxic compounds (nitrate of silver, zinc, arsenic, bromides) as well as medications such as Dilantin or other anticonvulsants.^[4]^[27]^[8]

Additional advances in understanding the etiology and improving treatments for hemifacial spasm did not occur until the mid-seventies. In 1977, 47 cases of hemifacial spasm underwent microvascular decompression of the facial nerve using the operating microscope. The results illustrated nerve-vessel conflicts (or cholesteatoma) to be located at the root exit zone of the facial nerve in all cases.^[28]^[6] The root exit zone is where the central glial axonal insulation of the nerve ends and the peripheral nerve axonal myelination begins, this is known as The Obersteiner-Redlich zone. Biopsies of the root exit zone demonstrated degeneration of axons, denuded axis cylinder and interrupted myelin. The results of the experiment strengthened the theory that vascular compression of the facial nerve was the primary cause of hemifacial spasm, and proposed a specific region of the facial nerve where the effects of longstanding compression results in nerve dysfunction.^[6]

Related Research Articles

Botulinum toxin, or botulinum neurotoxin, is a highly potent neurotoxic protein produced by the bacterium Clostridium botulinum and related species. It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction, thus causing flaccid paralysis. The toxin causes the disease botulism. The toxin is also used commercially for medical and cosmetic purposes. Botulinum toxin is an acetylcholine release inhibitor and a neuromuscular blocking agent.

<span class="mw-page-title-main">Trigeminal neuralgia</span> Neurological pain disorder

Trigeminal neuralgia, also called Fothergill disease, tic douloureux, trifacial neuralgia, or suicide disease, is a long-term pain disorder that affects the trigeminal nerve, the nerve responsible for sensation in the face and motor functions such as biting and chewing. It is a form of neuropathic pain. There are two main types: typical and atypical trigeminal neuralgia.

Diabetic neuropathy is various types of nerve damage associated with diabetes mellitus. The most common form, diabetic peripheral neuropathy, affects 30% of all diabetic patients. Symptoms depend on the site of nerve damage and can include motor changes such as weakness; sensory symptoms such as numbness, tingling, or pain; or autonomic changes such as urinary symptoms. These changes are thought to result from a microvascular injury involving small blood vessels that supply nerves. Relatively common conditions which may be associated with diabetic neuropathy include distal symmetric polyneuropathy; third, fourth, or sixth cranial nerve palsy; mononeuropathy; mononeuropathy multiplex; diabetic amyotrophy; and autonomic neuropathy.

Piriformis syndrome is a condition which is believed to result from nerve compression at the sciatic nerve by the piriformis muscle. It is a specific case of deep gluteal syndrome. The largest and most bulky nerve in the human body is the sciatic nerve. Starting at its origin it is 2 cm wide and 0.5 cm thick. The sciatic nerve forms the roots of L4-S3 segments of the lumbosacral plexus. The nerve will pass inferiorly to the piriformis muscle, in the direction of the lower limb where it divides into common tibial and fibular nerves. Symptoms may include pain and numbness in the buttocks and down the leg. Often symptoms are worsened with sitting or running.

Neuralgia is pain in the distribution of a nerve or nerves, as in intercostal neuralgia, trigeminal neuralgia, and glossopharyngeal neuralgia.

Occipital neuralgia (ON) is a painful condition affecting the posterior head in the distributions of the greater occipital nerve (GON), lesser occipital nerve (LON), third occipital nerve (TON), or a combination of the three. It is paroxysmal, lasting from seconds to minutes, and often consists of lancinating pain that directly results from the pathology of one of these nerves. It is paramount that physicians understand the differential diagnosis for this condition and specific diagnostic criteria. There are multiple treatment modalities, several of which have well-established efficacy in treating this condition.

Microvascular decompression (MVD), also known as the Jannetta procedure, is a neurosurgical procedure used to treat trigeminal neuralgia, a pain syndrome characterized by severe episodes of intense facial pain, and hemifacial spasm. The procedure is also used experimentally to treat tinnitus and vertigo caused by vascular compression on the vestibulocochlear nerve. As the goal of the Jannetta procedure is to relieve (vascular) pressure on the trigeminal nerve, it is a specific type of a nerve decompression surgery.

Blepharospasm is a neurological disorder characterized by intermittent, involuntary spasms and contractions of the orbicularis oculi (eyelid) muscles around both eyes. These result in abnormal twitching or blinking, and in the extreme, sustained eyelid closure resulting in functional blindness.

Meralgia paresthetica or meralgia paraesthetica is pain or abnormal sensations in the outer thigh not caused by injury to the thigh, but by injury to a nerve which provides sensation to the lateral thigh.

Spasmodic torticollis is an extremely painful chronic neurological movement disorder causing the neck to involuntarily turn to the left, right, upwards, and/or downwards. The condition is also referred to as "cervical dystonia". Both agonist and antagonist muscles contract simultaneously during dystonic movement. Causes of the disorder are predominantly idiopathic. A small number of patients develop the disorder as a result of another disorder or disease. Most patients first experience symptoms midlife. The most common treatment for spasmodic torticollis is the use of botulinum toxin type A.

<span class="mw-page-title-main">Meige's syndrome</span> Medical condition

Meige's syndrome is a type of dystonia. It is also known as Brueghel's syndrome and oral facial dystonia. It is actually a combination of two forms of dystonia, blepharospasm and oromandibular dystonia (OMD).

Parry–Romberg syndrome (PRS) is a rare disease presenting in early childhood characterized by progressive shrinkage and degeneration of the tissues beneath the skin, usually on only one side of the face but occasionally extending to other parts of the body. An autoimmune mechanism is suspected, and the syndrome may be a variant of localized scleroderma, but the precise cause and pathogenesis of this acquired disorder remains unknown. It has been reported in the literature as a possible consequence of sympathectomy. The syndrome has a higher prevalence in females and typically appears between 5 and 15 years of age. There has been only one case report of the syndrome appearing in older adults: a 43-year-old woman with symptoms appearing at the age of 33.

Synkinesis is a neurological symptom in which a voluntary muscle movement causes the simultaneous involuntary contraction of other muscles. An example might be smiling inducing an involuntary contraction of the eye muscles, causing a person to squint when smiling. Facial and extraocular muscles are affected most often; in rare cases, a person's hands might perform mirror movements.

In medicine, an avulsion is an injury in which a body structure is torn off by either trauma or surgery. The term most commonly refers to a surface trauma where all layers of the skin have been torn away, exposing the underlying structures. This is similar to an abrasion but more severe, as body parts such as an eyelid or an ear can be partially or fully detached from the body.

Migraine surgery is a surgical operation undertaken with the goal of reducing or preventing migraines. Migraine surgery most often refers to surgical nerve decompression of one or several nerves in the head and neck which have been shown to trigger migraine symptoms in many migraine sufferers. Following the development of nerve decompression techniques for the relief of migraine pain in the year 2000, these procedures have been extensively studied and shown to be effective in appropriate candidates. The nerves that are most often addressed in migraine surgery are found outside of the skull, in the face and neck, and include the supra-orbital and supra-trochlear nerves in the forehead, the zygomaticotemporal nerve and auriculotemporal nerves in the temple region, and the greater occipital, lesser occipital, and third occipital nerves in the back of the neck. Nerve impingement in the nasal cavity has additionally been shown to be a trigger of migraine symptoms.

<span class="mw-page-title-main">Atypical trigeminal neuralgia</span> Medical condition

Atypical trigeminal neuralgia (ATN), or type 2 trigeminal neuralgia, is a form of trigeminal neuralgia, a disorder of the fifth cranial nerve. This form of nerve pain is difficult to diagnose, as it is rare and the symptoms overlap with several other disorders. The symptoms can occur in addition to having migraine headache, or can be mistaken for migraine alone, or dental problems such as temporomandibular joint disorder or musculoskeletal issues. ATN can have a wide range of symptoms and the pain can fluctuate in intensity from mild aching to a crushing or burning sensation, and also to the extreme pain experienced with the more common trigeminal neuralgia.

<span class="mw-page-title-main">Nerve compression syndrome</span> Human medical condition

Nerve compression syndrome, or compression neuropathy, or nerve entrapment syndrome, is a medical condition caused by chronic, direct pressure on a peripheral nerve. It is known colloquially as a trapped nerve, though this may also refer to nerve root compression. Its symptoms include pain, tingling, numbness and muscle weakness. The symptoms affect just one particular part of the body, depending on which nerve is affected. The diagnosis is largely clinical and can be confirmed with diagnostic nerve blocks. Occasionally imaging and electrophysiology studies aid in the diagnosis. Timely diagnosis is important as untreated chronic nerve compression may cause permanent damage. A surgical nerve decompression can relieve pressure on the nerve but cannot always reverse the physiological changes that occurred before treatment. Nerve injury by a single episode of physical trauma is in one sense an acute compression neuropathy but is not usually included under this heading, as chronic compression takes a unique pathophysiological course.

Oromandibular dystonia(OMD) is an uncommon focal neurological condition affecting the jaws, face, and mouth. Oromandibular dystonia is characterized by involuntary spasms of the tongue, jaw, and mouth muscles that result in bruxism, or grinding of the teeth, and jaw closure. These conditions frequently lead to secondary dental wear as well as temporomandibular joint syndrome. In addition, problems with chewing, speaking, and swallowing may result from jaw opening, involuntary tongue movements, or jaw deviation.

Botulinum toxin therapy of strabismus is a medical technique used sometimes in the management of strabismus, in which botulinum toxin is injected into selected extraocular muscles in order to reduce the misalignment of the eyes. The injection of the toxin to treat strabismus, reported upon in 1981, is considered to be the first ever use of botulinum toxin for therapeutic purposes. Today, the injection of botulinum toxin into the muscles that surround the eyes is one of the available options in the management of strabismus. Other options for strabismus management are vision therapy and occlusion therapy, corrective glasses and prism glasses, and strabismus surgery.

Alan Brown Scott was an American ophthalmologist specializing in eye muscles and their disorders, such as strabismus. He is best known for his work in developing and manufacturing the drug that became known as Botox, research described as "groundbreaking" by the ASCRS.

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