Benign fasciculation syndrome

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Benign fasciculation syndrome
Bfs spasm.gif
Animated image of BFS in the upper eyelid of a 19-year-old male. Symptoms subsided several days later.
Classification and external resources

Benign fasciculation syndrome (BFS) is a neurological disorder characterized by fasciculation (twitching) of various voluntary muscles in the body. The twitching can occur in any voluntary muscle group but is most common in the eyelids, arms, legs, and feet. Even the tongue may be affected. The twitching may be occasional or may go on nearly continuously. Usually intentional movement of the involved muscle causes the fasciculations to cease immediately, but they may return once the muscle is at rest again.

Signs and symptoms[edit]

The main symptom of benign fasciculation syndrome is focal or widespread involuntary muscle activity (twitching), which can occur at random or specific times (or places). Presenting symptoms of benign fasciculation syndrome may include:[1][2][3]

Other symptoms include:

BFS symptoms are typically present when the muscle is at rest and are not accompanied by severe muscle weakness.[citation needed] In some BFS cases, fasciculations can jump from one part of the body to another. For example, it could start in a leg muscle, then in a few seconds jump to the forehead, then the abdomen, etc. While only one part of the body is affected at a time, hardly a beat is missed as it jumps from one area to the next. Because fasciculations can occur on the head, this strongly suggests the brain as the generator due to its exclusive non-dependence on the spinal cord. (Together, the brain and spinal cord comprise the central nervous system.)

Anxiety is often caused as a result of BFS, and a lot of sufferers have hypochondria as BFS mimics symptoms of much more serious diseases such as amyotrophic lateral sclerosis (ALS).

Causes[edit]

The precise cause of BFS is unknown, and it is not known if it is a disease of the motor nerves, the muscles, or the neuromuscular junction. Though twitching is sometimes a symptom of serious diseases such as spinal injury, muscular dystrophy, Lyme disease, Creutzfeldt–Jakob disease (CJD), neurofibromatosis or amyotrophic lateral sclerosis (ALS), causes like BFS and over-exertion are more common. Mitsikostas et al. found that fasciculations "were slightly correlated to the body weight and height and to the anxiety level" in normal subjects.[7]

BFS can also be attributed to long term use of anticholinergics such as diphenhydramine and opiates such as morphine, but the latter case is usually when withdrawal symptoms are present.[citation needed]

Magnesium deficiency can cause both fasciculations and anxiety.[8] A vitamin D deficiency may also cause fasciculations, stemming from reduced ionized calcium in the blood (hypocalcemia).

Recent studies have found an association between widespread fasciculations and/or paresthesias with small fiber neuropathy in up to 82% of cases which have a normal EMG and nerve conduction study.[9][10]

Diagnosis[edit]

Diagnosis of BFS is a diagnosis of exclusion, in other words, other likely causes for the twitching (mostly forms of neuropathy, such as borreliosis Lyme disease neuropathy, motor neuron diseases such as ALS) must be eliminated before BFS can be assumed. An important diagnostic tool here is the electromyography (EMG). Since BFS appears to cause no actual nerve damage (at least as seen on the EMG), patients will likely exhibit a completely normal EMG (or one where the only abnormality seen is fasciculations).

Another important step in diagnosing BFS is checking the patient for clinical weakness. Clinical weakness is often determined through a series of strength tests, such as observing the patient's ability to walk on his or her heels and toes. Resistance strength tests may include raising each leg, pushing forward and backward with the foot and/or toes, squeezing with fingers, spreading fingers apart, and pushing with or extending arms and/or hands. In each such test the test provider will apply resisting force and monitor for significant differences in strength abilities of opposing limbs or digits. If such differences are noted or the patient is unable to apply any resisting force, clinical weakness may be noted.

Lack of clinical weakness along with normal EMG results (or those with only fasciculations) largely eliminates more serious disorders from potential diagnosis.

Especially for younger persons who have only LMN sign fasciculations, "In the absence of weakness or abnormalities of thyroid function or electrolytes, individuals under 40 years can be reassured without resorting to electromyography (EMG) to avoid the small but highly damaging possibility of false-positives". "Equally, however, most subspecialists will recall a small number of cases, typically men in their 50s or 60s, in whom the latency from presentation with apparently benign fasciculations to weakness (and then clear MND) was several years. Our impression is that a clue may be that the fasciculations of MND are often abrupt and widespread at onset in an individual previously unaffected by fasciculations in youth. The site of the fasciculations, for example, those in the calves versus abdomen, has not been shown to be discriminatory for a benign disorder. There is conflicting evidence as to whether the character of fasciculations differs neurophysiologically in MND".[11]

Another abnormality commonly found upon clinical examination is a brisk reflex action known as hyperreflexia. Standard laboratory tests are unremarkable. According to neurologist John C. Kincaid:

In the absence of clinical and electromyographic findings of neurogenic disease, the diagnosis of benign fasciculations is made. I suggest that patients like this be followed for a year or longer with clinical and electromyographic exams at about 6-month intervals before one becomes secure in the diagnosis that the fasciculations are truly benign. My approach to treating fasciculations that appear to be benign is to first reassure the patient that no ominous disease seems to be present.[12]

Treatment[edit]

Some degree of control of the fasciculations may be achieved with the same medication used to treat essential tremor (beta-blockers and anti-seizure drugs). However, often the most effective approach to treatment is to treat any accompanying anxiety. No drugs, supplements, or other treatments have been found that completely control the symptoms. In cases where fasciculations are caused by magnesium deficiency, supplementing magnesium can be effective in reducing symptoms.[13]

In many cases, the severity of BFS symptoms can be significantly reduced through a proactive approach to decrease the overall daily stress. Common ways to reduce stress include: exercising more, sleeping more, working less, meditation, and eliminating all forms of dietary caffeine (e.g. coffee, chocolate, cola, and certain over-the counter medications).

If pain or muscle aches are present alongside fasciculations, patients may be advised to take over-the-counter pain medications such as ibuprofen or acetaminophen during times of increased pain. Other forms of pain management may also be employed. Prior to taking any over-the-counter medications, individuals should initiate discussions with their health care provider(s) to avoid adverse effects associated with long-term usage or preexisting conditions.

Prognosis[edit]

The prognosis for those suffering from diagnosed benign fasciculation syndrome is generally regarded as being good to excellent. The syndrome causes no known long-term physical damage. Patients may suffer elevated anxiety even after being diagnosed with the benign condition.[3] Such patients are often directed towards professionals who can assist with reductions and understanding of stress/anxiety, or those who can prescribe medication to help keep anxiety under control.

Spontaneous remission has been known to occur, and in cases where anxiety is thought to be a major contributor, symptoms are typically lessened after the underlying anxiety is treated. In a 1993 study by Mayo Clinic, 121 individuals diagnosed with benign fasciculation syndrome were assessed 2–32 years (~7 years average) after diagnosis.[1][14] Of those patients there were no cases of BFS progressing to a more serious illness, and 50% of the patients reported significant improvement in their symptoms at the time of the follow-up. Only 4% of the patients reported symptoms being worse than those present at the time of their diagnosis.

See also[edit]

References[edit]

  1. ^ a b "AboutBFS.com - Featured Article". Retrieved 4 October 2014. 
  2. ^ a b Blexrud MD, Windebank AJ, Daube JR (October 1993). "Long-term follow-up of 121 patients with benign fasciculations". Ann. Neurol. 34: 622–5. PMID 8215252. doi:10.1002/ana.410340419. Retrieved 4 October 2014. 
  3. ^ a b "BFS Recovery - What is Benign Fasciculation Syndrome?". Retrieved 4 October 2014. 
  4. ^ Hart, I.; Maddison, P.; Newsom-Davis, J.; Vincent, A.; Mills, K. R. (August 2002). "Phenotypic Variants of Autoimmune Peripheral Nerve Hyperexcitability". Brain. 125 (8): 1887–1895. PMID 12135978. doi:10.1093/brain/awf178. 
  5. ^ Allan H. Ropper; Robert H. Brown. "Chapter 55. Disorders of Muscle". Adams and Victor's Principles of Neurology (8th ed.). pp. 1277–1278. 
  6. ^ "Benign Fasciculation Syndrome (BFS) Constant Muscle Twitching". Retrieved 4 October 2014. 
  7. ^ Mitsikostas, D. D.; Karandreas, N.; Coutsopetras, P.; Piperos, P.; Lygidakis, C.; Papageorgiou, C. (April 1998). "Fasciculation Potentials in Healthy People". Muscle & Nerve. 21 (4): 533–535. PMID 9533790. doi:10.1002/(sici)1097-4598(199804)21:4<533::aid-mus14>3.3.co;2-#. 
  8. ^ "The Importance of Magnesium to Human Nutrition". Mbschachter.com. Retrieved 2015-05-06. 
  9. ^ "Benign Fasciculation Syndrome as a Manifestation of Small Fiber Neuropathy (P01.139) -- Tzatha et al. 80 (1001): P01.139 -- Neurology". neurology.org. 
  10. ^ Tzatha E, Chin RL. "Small fiber abnormalities in skin biopsies of patients with benign fasciculations". J Clin Neuromuscul Dis. 16: 12–4. PMID 25137510. doi:10.1097/CND.0000000000000047. 
  11. ^ Turner, MR; Talbot, K (Jun 2013). "Mimics and chameleons in motor neurone disease.". Practical neurology. 13 (3): 153–64. PMC 3664389Freely accessible. PMID 23616620. doi:10.1136/practneurol-2013-000557. 
  12. ^ Kincaid, J. C. (August 1997). "Muscle pain, fatigue, and fasciculations". Neurological Clinic. 15 (3): 697–709. PMID 9227959. doi:10.1016/s0733-8619(05)70340-6. 
  13. ^ "Diet Deficiency & Fasciculations". LIVESTRONG.COM. Retrieved 4 October 2014. 
  14. ^ Blexrud MD, Windebank AJ, Daube JR (October 1993). "Long-term follow-up of 121 patients with benign fasciculations". Ann. Neurol. 34: 622–5. PMID 8215252. doi:10.1002/ana.410340419.