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Muscle Pain

Many patients complain of muscle pain, tightness, or spasms.  But what exactly are muscle spasms, how do they develop, and how can we treat them?  Commonly, muscle spasms are normal responses to muscle overexertion, pain, or fatigue.  However, in some circumstances, they imply serious systemic or neurological disease.  It is important to understand the timing, frequency, duration, pattern, and overall setting in which muscles spasms occur.  The following definitions are important to understand: 

A muscle spasm is a sudden, involuntary contraction of one or more muscles.  A spasm results from an abnormally sustained muscle contraction and is often painful.  Various muscles may develop spasms, including the small intrinsic hand muscles of a musician to the larger “charley horse” calf muscles of a runner.  Muscle spasms may involve the skeletal muscles of the limbs and spine, responsible for locomotion and upright posture, or the smooth muscles lining the hollow, tubular internal organs of our body, such as the muscles lining the colon or bladder.  Skeletal and smooth muscles have different embryological origins, functions, innervations, and physiologies.  For the purposes of this discussion, the focus will be on skeletal muscle spasms.

Acute skeletal muscle spasms may be the result of muscle injury or overuse.   They may occur, for instance, when an athlete has not warmed up or stretched prior to vigorous anaerobic exercise, such as sprinting or jumping.  They may also occur during endurance training when, for example, a marathoner has not maintained proper fluid and electrolyte balance, and muscles with increased metabolic demand are depleted of nutrients.  These types of spasms resolve with rest, hydration, and gentle stretching.

Recurrent, widespread, or chronic muscle spasms may signify a more significant underlying medical condition related to toxic-metabolic, nutritional, vascular, or hormonal problems. In peripheral artery disease, for instance, there is a lack of blood supply and oxygen to affected muscles, which cause the spasms of “vascular claudication.” These spasms, or cramps, usually involve the lower extremities and become worse with exertion and better with rest. In kidney or liver disease, there may be volume depletion and/ or rapid body fluid and electrolyte abnormalities responsible for chronic muscle cramps. Similarly, conditions which cause excessive vomiting, diarrhea, or insufficient nutritional intake may result in skeletal muscle cramps.

There may also be accompanying signs and symptoms suggestive of an underlying neurological disease. For instance, a severe muscle spasm can result from irritation or damage to nerves supplying the muscle, such as in spinal stenosis or major disc herniations, which disrupt nerve root signals from the spinal cord. In higher level brain or spinal cord injuries, there is a disruption of normal inhibiting influences from nerve connections from the brain. There are several brain regions responsible for the movement of skeletal muscles, so problems in one or several brain regions or nerve connections can result in abnormal muscle contractions. For example, abnormal, repetitive spasms are seen in conditions such as dystonias (prolonged, repetitive contractions that cause twisting/jerking movements), torticollis syndrome (“wry neck”), blepharism (involuntary blinking), or myoclonus (sudden, irregular, involuntary contractions). These more difficult conditions should be assessed and treated by a neurologist or movement disorder specialist, often with specific medications and therapy.

muscle twitch or fasciculation is the involuntary, uncontrolled fine movement of a small segment of muscle. It can be seen under the skin and involves a few individual muscle fibers. Common muscles prone to benign fasciculations are the eyelid, thumb, calf, and thigh. These tiny muscle twitches may be related to fatigue, stress, or anxiety (i.e, the so-called “benign fasciculation syndrome”), as well as exogenous substances including: caffeine, pseudoephedrine, albuterol, and Adderall. In some cases, fasciculations are attributable to low magnesium or other nutritional deficiencies. Rarer associations are small fiber neuropathy or gluten neuropathy. Generally, the prognosis for benign fasciculation syndrome is very good and can be managed with nutritional supplementation, elimination of the offending related substance, stress management, or in some cases, pharmacotherapy such as anticonvulsants or beta blockers.

On the other end of the spectrum, muscle fasciculations can also be associated with more serious neurological diseases, including: polio, ALS, MS, and myopathy (muscle disease), and are only one sign in a constellation of more serious muscle problems, including weakness and atrophy (muscle wasting). The more serious neurological conditions will often have one or more signs of concurrent central nervous system (brain and spinal cord) dysfunction, which may include: hyperreflexia (overactive tendon reflexes), spasticity (hypertonicity), gait impairment, bulbar palsies (speech and swallow problems), or sensory abnormalities. One can be further evaluated by a specialist if there is concern for neurological compromise with imaging and specialized nerve and muscle tests, including nerve conduction studies and electromyography (EMG).

On the other end of the spectrum, muscle fasciculations can also be associated with more serious neurological diseases, including: polio, ALS, MS, and myopathy (muscle disease), and are only one sign in a constellation of more serious muscle problems, including weakness and atrophy (muscle wasting). The more serious neurological conditions will often have one or more signs of concurrent central nervous system (brain and spinal cord) dysfunction, which may include: hyperreflexia (overactive tendon reflexes), spasticity (hypertonicity), gait impairment, bulbar palsies (speech and swallow problems), or sensory abnormalities. One can be further evaluated by a specialist if there is concern for neurological compromise with imaging and specialized nerve and muscle tests, including nerve conduction studies and electromyography (EMG).

muscle cramp can be considered a type of muscle spasm. Cramps are abrupt, unpleasant, painful sensations caused by sudden muscle contraction or muscle fiber overshortening. Common causes of skeletal muscle cramps are electrolyte imbalances from overexertion, dehydration, or excessive heat/ temperature shifts. The cramped muscle is fatigued, a sign that the individual needs immediate rest and rehydration. Usually the cramp is short-lived, but sometimes muscles soreness can continue up to a week afterwards. Often gentle stretching, heat, and massage are helpful initially.

Electrolyte imbalances, particularly conditions involving low sodium, potassium, and magnesium, are well known causes of cramps and should be corrected. Hypocalcemia (low calcium) may cause a cramping condition known as tetany (characterized by distal muscle spasms of hands and feet, tingling around the mouth, and abnormal reflexes). Tetany is associated with low blood magnesium, hyperventilation (low carbondioxide), or an underfunctioning parathyroid gland.

There is also evidence that hypoxia, lactic acidosis, and hypoglycemic conditions cause cramps. As early as 1965, restless leg syndrome and leg cramps were thought to be a result of excess insulin and hypoglycemia, and avoidance of low blood glucose was used to help cramps.

Nocturnal leg cramps are involuntary muscle contractions that occur typically in the leg muscles at night or during rest. The duration of nocturnal leg cramps is variable, but usually ranges from a few seconds to several minutes. There may be residual muscle soreness, and these cramps are more common in the elderly, who are susceptible to contributing factors. Contributing factors typically involve electrolyte imbalances, ischemia (reduced blood flow) to muscle tissue due to cardiovascular, kidney or liver disease, lumbar stenosis, and particular medications. A few common medications associated with muscle cramps include: potassium-sparing diuretics, raloxifene (Evista), and HMG-CoA inhibitors (statin drugs).

Nocturnal cramps are also common in healthy individuals; for instance in pregnant woman. The precise cause of nocturnal cramps is often unclear.

Muscle spasticity: Traditionally, spasticity is defined as the velocity-dependent resistance to stretch. It should not be confused with the more general term, “muscle tightness,” the latter a descriptor of muscle tension or stress. True muscle spasticity occurs in the setting of central nervous system disorders, and is associated with motor dysfunction and hyperreflexia, including abnormally increased tone of the flexor muscles of the upper extremity, and the extensor muscles of the lower extremity. Muscle spasticity signifies an upper motor neuron problem in the setting of such conditions as stroke, traumatic brain injury, spinal cord injury, MS, and cerebral palsy. Spasticity is a common problem seen by neurologists and physiatrists, and it is managed with custom splints to prevent permanent tendon contractures, botox injections, and antispasmodic medications, including baclofen. Baclofen can be administered both orally and intrathecally, the latter with the use of implantable pumps.

Myalgia: The general medical term for “muscle pain,” can be associated with a large differential of different conditions. Generally, conditions associated with chronic, painful myalgias can be distinguished from spastic neurological or neuromuscular disorders, although the two may coincide.

Trigger point: a term coined by David Simon and Janet Travell in the mid-late 20th century, refers to tender points found within “taut bands” of painful muscle, caused by a shortened group of muscle fibers. Trigger points got their name for their ability to produce pain at more distant sites, defined as their “zones of reference.” They are characterized by a local twitch response, which may be achieved by mechanical stimuli such as cross fiber manual palpation of the taut band or needle penetration.

Myofascial pain: A prevalent, painful muscle condition, which is often underdiagnosed and chronic. It affects almost 15% of the general population and comes at significant cost to the individual and society as a whole in terms of quality of life, disability, and lost productivity. Chronic muscle pain disorders have been misunderstood and studied for centuries, with the earliest attempts made to distinguish joint pain (rheumatism) from muscle pain as far back as the 1700s. Although there remains some ambiguity in terms of the pathophysiology of myofascial pain and its overlap with other chronic pain conditions, including fibromyalgia, it can be agreed that myofascial pain is defined by regional musculoskeletal pain and the presence of associated trigger points. Myofascial pain is often described as a deep gnawing ache or knot, sometimes sharp and very intense, and with clear referral patterns that are well described. Sometimes it is associated with abnormal sensory and even autonomic phenomena, which can mislead the diagnosis. The goal of myofascial providers is to elicit a local twitch response from active trigger points, thereby releasing the affected muscle(s) from an abnormal state of pain. A history of trauma, physical or emotional stress, poor body mechanics/ malalignment, and prolonged postures which force muscles into a state of abnormal, sustained contraction are clearly involved in myofascial pain.

The diagnosis of myofascial pain, according to the 1989 first international symposium on myofascial pain syndrome and fibromyalgia, is made by the presence of: 1. regional pain, 2. referred pain consistent with a trigger point’s pain distribution, 3. palpable taut bands, 4. spot tenderness along the length of a taut band, and 5. some degree of restricted motion.

There remains controversy regarding the diagnosis of myofascial pain, along with trigger points and their origin, as well as a range of treatment options and provider expertise. It takes a fair degree of skill and training to palpate and efficiently release trigger points, whether by deep tissue release, dry needling to elicit a local twitch response, or wet needling (trigger point injections) with local anesthetic. Various theories of interest have been proposed as to the origin of trigger points, including the “energy crisis” theory. This theory involves increased metabolic demand of sarcomeres (muscle cells) that are in a state of sustained contraction, in combination with reduced nutrient supply from the compression of nearby blood vessels, which results in the release of sensitizing substances that activate nociceptive pain and autonomic nerve fibers.

Regardless of their origin, the goal of the myofascial provider is not only to release active trigger points, which directly targets symptoms and is time limited, but also to educate patients about the need for lifestyle modification and self-management. Successful management and optimization of function is achieved through: regular aerobic exercise, balanced muscle stretching and conditioning, proper sleep hygiene and nutrition, and correction of poor postural habits and biomechanics. Mood regulation and psychological therapies, including mind body strategies and stress reduction techniques, are also important to consider.