Muscle Pain and Thyroid

Discussion in 'Fibromyalgia Main Forum' started by darude, Jan 19, 2006.

  1. darude

    darude New Member

    Background: Deficiency of thyroid hormone leads to a state called hypothyroidism. Common causes of hypothyroidism include the following:

    Treatment with radioactive iodine I 131 for Graves disease

    Hashimoto disease - An autoimmune process in which lymphocytic infiltration and fibrous tissue accumulation cause replacement of normal thyroid tissue

    Drug-induced hypothyroidism - Known to occur with amiodarone and iodine (ie, Wolff-Chaikoff effect)

    Hereditary disorders of the iodothyronine synthesis pathway (thyroxine [T4] and triiodothyronine [T3])

    Pituitary tumors and related surgical resections
    Hypothyroidism can cause several symptoms, ranging from mild (eg, fatigue, weight gain, cold intolerance, mental slowing, muscle cramping) to severe (eg, heart enlargement, myxedema coma [rare]).

    Without regard to the cause of hypothyroidism, neuromuscular and musculoskeletal manifestations can be observed in many patients with hypothyroidism. These manifestations can occur at any time in the hypothyroidism disease process. These are usually mild and include weakness, pain, stiffness, or ache.

    Hypothyroid myopathy typically manifests as polymyositislike myopathy with proximal muscle weakness and an increased creatine kinase level. But, sometimes, it manifests as muscular enlargement (pseudohypertrophy) and, in adults, is called Hoffmann syndrome. The pattern of proximal weakness with diffuse muscular enlargement in children with hypothyroid disease (cretinism) is referred to as Kocher-Debré-Sémélaigne syndrome.

    Several case reports describe rhabdomyolysis associated with hypothyroidism. In these cases, the hypothyroidism was thought to predispose individuals to rhabdomyolysis.

    Pathophysiology: Hypothyroidism causes a constellation of changes in the body. The lack of thyroid hormone results in slowed or reduced metabolic function, such as decreased protein turnover and impaired carbohydrate metabolism. These metabolic changes occur in many organ systems, including muscle. Pain with muscle exertion is characteristic of defective carbohydrate metabolism.

    Slowed muscle contraction and relaxation, known as hypothyroid myopathy, may be caused by a shift in distribution of muscle fiber type from a fast twitch to a slow twitch. A reduction in muscle mitochondrial oxidative capacity and beta-adrenergic receptors, as well as the induction of an insulin-resistant state, may all cause these changes.

    Recent evidence from a study by Sinclair et al suggests that a decrease in muscle carnitine in both hypothyroidism and hyperthyroidism may contribute to thyroid myopathy in these people.

    The global inhibition of the main oxidative pathways (substrate incorporation, substrate oxidation) and of the respiratory chain within cells also may cause myopathic symptoms. A diminished energetic consumption is related partially to a transition in the myosin isoforms, which express a slower adenosine triphosphatase, and an impairment of the trans-sarcolemmic transports. All these factors may contribute to muscle weakness, fatigue, and exertional pain.

    Exercise intolerance could be due to an abnormal recruitment of several metabolic pathways, such as glycolysis, related to the mitochondrial metabolism impairment. Abnormal accumulation of protons and monovalent phosphate ions, which are involved in the actin-myosin interaction, as well as abnormal Ca++ metabolism, also may be causes of reduced exercise tolerance.

    Hyponatremia often is seen in patients with hypothyroidism. The decreased number of Na+/K+ adenosine triphosphatase–dependent pumps could imply an abnormal intracellular Na+ level and explain frequent disorders of membrane excitability.

    Myoedema is the phenomenon of mounding up of muscle tissue after light percussion. Myoedema occurs in approximately one third of patients with hypothyroidism, but it is not entirely specific for hypothyroidism. Myoedema is thought to be caused by delayed Ca++ reuptake by the sarcoplasmic reticulum, which also prolongs muscle contraction. Although not proven, this type of prolongation of muscle contraction is also thought to cause muscle hypertrophy.


    In the US: Acquired impairment of thyroid function affects about 2% of adult women and about 0.1-0.2% of adult men in North America.
    Neonatal hypothyroidism occurs with a frequency of 0.02% in the white population. Among blacks, the frequency falls to 0.003%.

    Of individuals with hypothyroidism, 30-80% manifest neuromuscular symptoms, depending on the severity of hypothyroidism. Weakness is observed in one third of patients with hypothyroidism. CTS, although not part of the myopathy, is a peripheral nerve dysfunction found in 15-30% of patients with hypothyroidism.

    Internationally: Neonatal screening programs for congenital hypothyroidism in many areas of the world show that hypothyroidism is present in 1 out of every 4000 newborns. In iodine-deficient areas of the world, the incidence of hypothyroidism is 10- to 20-fold higher.
    Mortality/Morbidity: Mortality has not been shown to be increased in patients with hypothyroid myopathy. Morbidity is significantly increased, reflected in performance of activities of daily living (ADL) and quality of life.

    Race: No predilection for any particular race has been established.

    Sex: The incidence of hypothyroidism is much greater in women than in men. Myxedema coma is extremely rare, but its incidence is higher in elderly women, especially those older than 60 years.

    Age: Hypothyroidism is seen more commonly in women aged 40-60 years; however, it can be seen in persons of all ages.

    CLINICAL Section 3 of 10
    Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography


    Neuromuscular symptoms present in 30-80% of patients with hypothyroidism. These symptoms improve or disappear with correction of the hypothyroid state.
    Patients may complain of muscle cramping, proximal symmetrical muscle weakness, muscle stiffness, and exercise intolerance. These manifestations can occur at any time during the presentation of hypothyroidism.
    With hypothyroid myopathy, slowness of muscle relaxation is noted, as is a slowness of muscle contraction.

    Deep tendon reflexes are delayed in approximately 85% of patients with hypothyroidism.
    Mounding of the muscle after light percussion (ie, myoedema) occurs in one third of patients with hypothyroidism, but it is not necessarily specific to hypothyroidism.
    Muscle enlargement, stiffness, and cramping are a constellation of findings seen in individuals with hypothyroidism. In adults, these findings are known as Hoffman syndrome. In children, these findings are called Kocher-Debré-Sémélaigne syndrome.
    Myokymia, which may be related to a low sodium level, may be seen.
    Causes: See Pathophysiology.

    Hypothyroidism can impair mitochondrial metabolism, which results in a decrease in muscle energy production. A low thyroid hormone level is the main causative factor.
    Certain drugs, such as lipid-lowering drugs, may exacerbate myopathy in patients with hypothyroidism. Lipid-lowering drugs include beta-hydroxy-beta-methylglutaryl-CoA reductase inhibitors such as the following:
    Atorvastatin (Lipitor)
    Fluvastatin (Lescol)
    Simvastatin (Zocor)
    Pravastatin (Pravachol)
    Lovastatin (Mevacor)
    Interferon alfa therapy for hepatitis, as well as the infection itself, has been reported to cause a number of immunologic and/or autoimmune adverse effects. Thyroiditis, seen in 10% of patients, may induce hypothyroidism.
    DIFFERENTIALS Section 4 of 10
    Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

    Acid Maltase Deficiency Myopathy
    Acute Poliomyelitis
    Amyotrophic Lateral Sclerosis
    Becker Muscular Dystrophy
    Limb-Girdle Muscular Dystrophy

    Other Problems to be Considered:

    Myasthenia gravis

    Myasthenia gravis has been associated with Graves disease and hypothyroidism. Patients present with proximal muscle weakness that may be fatigable. Eventually, they can have dysphagia and respiratory distress.

    Other metabolic, mitochondrial, and inflammatory myopathies

    Glycogen metabolism deficiencies, which are divided into dynamic and static deficiencies

    Dynamic myopathies are manifestations with exercise intolerance, pain, muscle cramps, and myoglobinuria.

    Type V - Phosphorylase (McArdle disease)

    Type VII - Phosphofructokinase (Tarui disease)

    Type VIII - Phosphorylase B kinase

    Type IX - Phosphoglycerate kinase

    Type X - Phosphoglycerate mutase

    Type XI - Lactate dehydrogenase

    Static deficiencies are associated with fixed weakness without features of exercise intolerance or myoglobinuria.

    Type II - Alpha-1,4 glucosidase (acid maltase)

    Type III - Debranching

    Type IV - Branching

    Lipid metabolism deficiencies can be accompanied by the following dynamic or static manifestations.

    Carnitine palmitoyl transferase

    Primary systemic/muscle carnitine deficiency

    Secondary carnitine deficiency (eg, beta-oxidation defects, medications such as valproic acid)

    Purine metabolism deficiencies (eg, myoadenylate deaminase deficiency)

    Mitochondrial myopathies

    Pyruvate dehydrogenase complex deficiencies (eg, Leigh syndrome)

    Progressive external ophthalmoplegia

    Kearns-Sayre syndrome

    Mitochondrial encephalopathy with lactic acidosis and strokelike episodes

    Myoclonic epilepsy and ragged red fibers

    Mitochondrial neurogastrointestinal encephalomyopathy

    Mitochondrial depletion syndrome

    Leigh syndrome and neuropathy, ataxia, or retinitis pigmentosa

    Succinate dehydrogenase deficiency

    Channelopathies are another differential diagnosis for myopathy.

    Inflammatory myopathies are another important differential and may be difficult to differentiate from pure endocrine causes, including a heterogenous group of acquired nonhereditary disorders characterized by muscle weakness and inflammation indicated by muscle biopsy.

    Idiopathic inflammatory myopathies



    Inclusion body myositis

    Overlap syndromes with other connective tissue disease

    Sarcoidosis and other granulomatous myositis conditions

    Behcet syndrome

    Inflammatory myopathies and eosinophilia

    Focal myositis

    Myositis ossificans

    Bacterial infections

    Staphylococcus aureus

    Escherichia coli

    Yersinia species


    Gas gangrene (Clostridium welchii)

    Leprous myositis

    Lyme disease

    Viral infections

    Acute influenza or other viral infections

    Retrovirus-related myopathies (human immunodeficiency virus, human T-cell leukemia virus type 1)

    Hepatitis B and C

    Parasitic infections




    Fungal infections

    Candida species

    Cryptococcus species

    Sporotrichosis species

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    Related Articles
    Acid Maltase Deficiency Myopathy

    Acute Poliomyelitis

    Amyotrophic Lateral Sclerosis

    Becker Muscular Dystrophy

    Limb-Girdle Muscular Dystrophy

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    WORKUP Section 5 of 10
    Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

    Lab Studies:

    Nerve conduction studies may show both decremental response to low-rate nerve stimulation and incremental response to high-rate nerve stimulation, suggesting some neuromuscular junction abnormality.
    Needle electromyography is usually normal or may be mildly myopathic.
    Increased thyrotropin is seen in primary hypothyroidism, and decreased thyrotropin is seen in pituitary-hypothalamic disease with secondary hypothyroidism.
    Low free T4 and T3 levels, as well as a low total thyroxine level and a free T4 index, are seen. The degree of myopathy is not necessarily correlated to the degree of hypothyroidism.
    The creatine kinase level can be very high (10-100 times normal) in some patients, but it has no correlation with weakness.
    Histologic Findings: Histologic findings on muscle biopsy are nonspecific. Pale central regions on nicotinamide adenine dinucleotide with accumulation of periodic acid-Schiff–positive material are seen. Decreased numbers of beta-adrenergic receptors are observed, accompanied by glycogenolysis. Some muscle fiber atrophy is noted, and increased numbers of internal nuclei, glycogen aggregates, and, occasionally, deposition of mucopolysaccharides in the connective tissue are characteristic of hypothyroid myopathy. TREATMENT Section 6 of 10
    Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

    Rehabilitation Program:

    Physical Therapy: Skeletal muscle weakness is the ultimate cause of most clinical problems in myopathy. In a study of patients with slowly progressive myopathies, a 12-week moderate-resistance (30% of maximum isometric force) exercise program resulted in strength gains ranging from 4-20% without any notable deleterious effects. In the same population, a 12-week high-resistance (training at the maximum weight a subject could lift 12 times) exercise program showed no further added benefits when compared with the moderate-resistance program, and there was evidence of overwork weakness in some subjects.
    Early intervention with gentle low-impact aerobic exercises may increase muscle efficiency and cardiovascular performance, may fight fatigue and depression, may maintain body weight, and may improve pain tolerance. Activities include walking, swimming, and stationary bicycling.

    Occupational Therapy: Occupational therapy may be needed for training in performance of ADL to enable the patient to compensate for proximal muscle weakness. Occupational therapists are able to provide adaptive equipment to assist the patient when performing ADL.
    Recreational Therapy: Maintaining the ability to do avocational activities that promote physical fitness and mental health is important.
    Medical Issues/Complications: Because there are multiple causes of muscle weakness, patients may not respond well to initial therapy because they have an undiagnosed secondary cause of myopathy. A thorough investigation for all causes is essential.

    Physical medicine and rehabilitation specialist

  2. GBHope

    GBHope New Member

    causes muscle pain too. I just recently went through a bout of this due to a hysterectomy and the pain was awful.

  3. darude

    darude New Member

    I'm thinking because I have pituitary tumour could be affecting the thyroid.
  4. darude

    darude New Member

    How do they diagnose Hasimotos?
  5. Fudge43

    Fudge43 New Member

    my-cat-for-president ... Your symptoms are so like mine .. I have Hashimoto's as well .. the endocrinologist I saw a couple of years ago kept talking about CF as well but I have no idea if I have that no one TOLD me .. too busy trying to handle what I do have .. and that almost daily "window of time" to get things done in the morning is so frustrating ..
    Darude .. with the Hashimoto's you go through periods of almost a flu/virus feeling .. your thyroid swells ..inflames . is sore and tender .. low grade fever .. you are ill .. it can last 24 to 48 hours or longer .. talk about feeling wiped out .. and combine that with the Fibro .. it is horrible.
    Yes .. our levels look almost normal on Synthroid but we don't feel much better .. I'm trying to cut back on my Snythroid .. blood tests coming up soon to see if there is any difference ..
    The whole thing can be overwhelming and so depressing at times .. more so if you still have periods .. mine is lasting 8 days and with so little sleep I'm ready to throw in the towel ..
    It helps to hear other people are in the same position.. so I appreciate reading this !
    Thanks !
    Fudge : )
  6. darude

    darude New Member

    I will ask when I get my Endo appointment. I do have a positive ANA for autoimmune.

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