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A spasmodic muscle contraction may be caused by many medical conditions, including dystonia. Most commonly, it is a muscle cramp which is accompanied by a sudden burst of pain. A muscle cramp is usually harmless and ceases after a few minutes. It is typically caused by ion imbalance or muscle overload.



A spasm may lead to muscle strains or tears in tendons and ligaments if the force of the spasm exceeds the tensile strength of the underlying connective tissue. This can occur with a particularly strong spasm or with weakened connective tissue.

A hypertonic muscle spasm is a condition of chronic, excessive muscle tone (i.e., tension in a resting muscle). This is the amount of contraction that remains when a muscle is not working. A true hypertonic spasm is caused by malfunctioning feedback nerves. This is much more serious and is permanent unless treated. In this case, the hypertonic muscle tone is excessive, and the muscles are unable to relax.

A subtype of spasm is colic. This is an episodic pain caused by spasm of smooth muscle in a particular organ (e.g., the bile duct). A characteristic of colic is the sensation of having to move about, and the pain may induce nausea or vomiting.

Hemifacial spasm is a nervous system disorder in which the muscles on one side of your face twitch involuntarily. Hemifacial spasm is most often caused by a blood vessel touching or pulsating against a facial nerve. It may also be caused by a facial nerve injury or a tumor. Sometimes there is no known cause.

These contractions often start in the eyelid, then may progress and affect the cheek and mouth on the same side of the face. At first, hemifacial spasms come and go. But eventually, usually over the course of several months to a few years, they occur almost constantly.

Muscle spasms range in intensity from mild, uncomfortable twitches to significant discomfort to intense, severe pain. The spastic muscle may feel harder than normal to the touch and/or appear visibly distorted. It may twitch. Spasms typically last from seconds to 15 minutes or longer, and may recur multiple times before going away.

Muscle spasms can occur at any time to anyone. Whether you are old, young, sedentary or active, you may develop a muscle spasm. It can happen when you walk, sit, perform any exercise or sleep. Some individuals are prone to muscle spasms and get them regularly with any physical exertion.

Muscle spasms can feel like a stitch in the side or be agonizingly painful. You may see a twitch under your skin and it may feel hard to the touch. Spasms are involuntary. The muscles contract and it takes treatment and time for them to relax. They are very common, especially in older adults and athletes.

If the muscle spasm is severe, happens frequently, responds poorly to treatment and is not related to obvious causes, make an appointment with your healthcare provider. The spasms could be related to underlying factors.

When a spasm strikes, you might be exercising, simply sitting or even sleeping in the middle of the night. If only there was a magical injection that could instantly relieve your pain! There are, however, five steps you can take to try to get rid of the spasm:

See your healthcare provider if the spasms are unbearably painful, happen frequently or last for a long time. Also, talk to your healthcare provider right away if you have the following symptoms in addition:

Hemifacial spasm (HFS) is a peripherally induced movement disorder characterized by involuntary, unilateral, intermittent, irregular, tonic or clonic contractions of muscles innervated by the ipsilateral facial nerve. We reviewed the clinical features and response to different treatments in 158 patients (61% women) with HFS evaluated at our Movement Disorders Clinic. The mean age at onset was 48.5+/-14.1 years (range: 15-87) and the mean duration of symptoms was 11.4+/-8.5 (range: 0.5-53) years. The left side was affected in 56% instances; 5 patients had bilateral HFS. The lower lid was the most common site of the initial involvement followed by cheek and perioral region. Involuntary eye closure which interfered with vision and social embarrassment were the most common complaints. HFS was associated with trigeminal neuralgia in 5.1% of the cases and 5.7% had prior history of Bell's palsy. Although vascular abnormalities, facial nerve injury, and intracranial tumor were responsible for symptoms in some patients, most patients had no apparent etiology. Botulinum toxin type A (BTX-A) injections, used in 110 patients, provided marked to moderate improvement in 95% of patients. Seven of the 25 (28%) patients who had microvascular decompression reported permanent complications and the HFS recurred in 5 (20%). Although occasionally troublesome, HFS is generally a benign disorder that can be treated effectively with either BTX-A or microvascular decompression.

Hemifacial spasm (HFS) is a disorder characterized by paroxysmal, involuntary twitching of facial muscles of one side of the face innervated by the ipsilateral facial nerve (seventh cranial nerve). It is considered a subtype of peripheral (neuromuscular) movement disorder. As the name suggests, the disorder is almost always unilateral except in some rare cases of severe hemifacial spasm (less than 5%), during which one can see the bilateral involvement of facial muscles. This activity reviews the cause of hemifacial spasms and highlights the role of the interprofessional team in their management.

Objectives:Review the etiology of hemifacial spasms.Describe the clinical features of hemifacial spasms.Summarize the treatment of hemifacial spasms.Explain modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by hemifacial spasms.Access free multiple choice questions on this topic.

Hemifacial spasm (HFS) is a disorder characterized by paroxysmal, involuntary twitching of facial muscles of one side of the face innervated by the ipsilateral facial nerve (seventh cranial nerve). It is considered a subtype of peripheral (neuromuscular) movement disorder. As the name suggests, the disorder is almost always unilateral except in some rare cases of severe hemifacial spasm (less than 5%), during which one can see the bilateral involvement of facial muscles.

Hemifacial spasm is a rare condition. The estimated prevalence of hemifacial spasm worldwide is 14.5 per 100,000 women and 7.4 per 100,000 men suggesting females are twice more prone to have hemifacial spasm than males.[1] As reported in some studies, Asians have a slightly higher prevalence as compared to whites, for unknown reasons.[2][3] The onset of disease, especially in primary hemifacial spasm cases, usually begins in adulthood, around the fourth through sixth decades of life. It commonly involves the left side more than the right, as observed in most reported cases. Usually, most cases of hemifacial spasm are sporadic, although there are some rare case reports of familial hemifacial spasm in the scientific literature.

Chronic irritation of the facial nerve nucleus and proximal nerve segment (root) due to several underlying etiological factors is the main pathophysiologic mechanism of hemifacial spasm. Compression of the facial nerve root at the junction of the central (point of exit from brainstem) and peripheral segment (root exit/entry zone) by aberrant/ectatic blood vessels is the most common cause of hemifacial spasm as reported in the literature.[4] The root exit/entry zone is the area of transition of oligodendroglial (central myelination) to Schwann cells (peripheral myelination). Compression of this zone leads to the demyelination of axons in the region. Several theories have been proposed to explain the pathophysiological mechanism by which facial nerve compression leads to hemifacial spasm.

As proposed in this theory, ephaptic transmission of impulses, or the lateral spread of excitation to adjacent nerve fibers, leads to abnormally excessive firing of the facial nerve. This is due to the demyelination of the facial nerve at the site of compression.[5] Myelin is an insulating material and plays an important role during nerve impulse conduction by preventing such abnormal lateral spread resulting in ectopic transmission of impulses that cause hemifacial spasm.

Classically the involuntary tonic/clonic contractions of one side of the face begin with the involvement of orbicularis oculi leading to brief, intermittent, painless, involuntary closure of the ipsilateral eye. This is associated with infrequent elevation of the eyebrow with eye twitching, also known as "other Babinski sign," named after Joseph Babinski, who first described it in 1905. "Other Babinski sign" is pathognomic of hemifacial spasm and helps to differentiate from eye twitching/closure due to blepharospasm, in which it is characteristically absent.

In primary hemifacial spasm, gradually, over several months to years, the irregular tonic/clonic contractions progress to involve lower facial muscles such as perioral muscles (orbicularis oris, mentalis, zygomaticus major, platysma).

In secondary hemifacial spasm, both upper and lower face develop synchronous, intermittent contractions, eventually leading to sustained spasms as the disease progresses. Persistence of contractions during sleep is one of the characteristics of hemifacial spasm distinguishing it from most movement disorders. This may predispose the individual to disturbed sleep and insomnia. In advanced cases, facial deviation/asymmetry and grimacing are evident due to the pull of contracted muscles on one side. There are unusual symptoms such as clicking sound in the ear (due to stapedius involvement), ear pain, and hearing loss reported in some cases of secondary hemifacial spasm. Symptoms are typically worsened by stress, fatigue, eating, and anxiety. Relaxation techniques or simply touching the face subsides the spasm/twitching. Although hemifacial spasm is known for a chronically progressive course, spontaneous resolution can be seen in 10% of cases.[7] 041b061a72


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