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Muscle weakness

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: M.Umer Tariq [2]

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]

Overview

Muscle weakness (or “lack of strength”) is a direct term for the inability to exert force with ones muscles to the degree that would be expected given the individual’s general physical fitness. A test of strength is often used during a diagnosis of a muscular disorder before the etiology can be identified. Such etiology depends on the type of muscle weakness, which can be true or perceived as well as variable topically. True weakness is substantial, while perceived rather is a sensation of having to put more effort to do the same task. On the other hand, various topic locations for muscle weakness are central, neural and peripheral. Central muscle weakness is an overall exhaustion of the whole body, while peripheral weakness is an exhaustion of individual muscles. Neural weakness are somewhere between. Muscle weakness can be a result of vigorous exercise but abnormal fatigue may be caused by barriers to or interference with the different stages of muscle contraction. In a broader sense, muscle weakness is the physical part of fatigue (medical).

Treatment

Medical Therapy

Treatment varies with the cause of weakness. Physiotherapy may be advised to strengthen the muscles.

References

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Historical Perspective

Historical Perspective

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References

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]

Classification

True vs. Perceived

The term subsumes two other more specific terms, true weakness and perceived weakness.

  • True weakness (or “objective weakness”) describes a condition where the instantaneous force exerted by the muscles is less than would be expected. For instance, if a patient suffers from amyotrophic lateral sclerosis (ALS), motor neurons are damaged and can no longer stimulate the muscles to exert normal force.
  • Perceived weakness (or “subjective weakness”) describes a condition where it seems to the patient that more effort than normal is required to exert a given amount of force.[1] For instance, in some people with chronic fatigue syndrome (CFS) who may struggle to climb a set of stairs when feeling especially fatigued, their muscle strength when objectively measured (eg, the maximum weight they can press with their legs) is essentially normal, though this is not true for CFS patients who may be disabled through post-exertional weakness/malaise etc. and in severe cases may not be able to climb a flight of stairs.

In some conditions, such as myasthenia gravis muscle strength is normal when resting, but true weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of CFS, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions. [2][3][4][5][6][7]

In addition to true/perceived, muscle weaknes can also be central, neural and peripheral. Central muscle weakness manifests as an overall, bodily or systemic, sense of energy deprivation, and peripheral weakness manifests as a local, muscle-specific incapacity to do work. [8][9] Neural weakness can be both central and peripheral.

References

  1. ↑ Enoka RM, Stuart DG (1992). “Neurobiology of muscle fatigue”. J. Appl. Physiol. 72 (5): 1631–48. PMID 1601767.
  2. ↑ Paul L, Wood L, Behan WM, Maclaren WM; Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome. European Journal of Neurology 1999 Jan;6(1):63-69 PMID: 10209352
  3. ↑ McCully K K, Natelson B H; Impaired oxygen delivery to muscle in chronic fatigue syndrome. Clinical Science 1999:97:603-608
  4. ↑ Pascale De Becker, PhD; Johan Roeykens, PT; Masha Reynders, PT; Neil McGregor, MD, PhD; Exercise Capacity in Chronic Fatigue Syndrome. Archives of Internal Medicine Vol. 160 No. 21, November 27, 2000
  5. ↑ De Becker P, McGregor N, De Meirleir K. A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome. J Intern Med 2001;250:234-240.
  6. ↑ Bruce M Carruthers, Anil Kumar Jain, Kenny L De Meirleir, Daniel L Peterson, Nancy G Klimas et al, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Guidelines, A Consensus Document Journal of Chronic Fatigue Syndrome 11(1):7-115, 2003. ISBN 0-7890-227-9
  7. ↑ Jammes Y, Steinberg JG, Mambrini O, Bregeon F, Delliaux S; Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise. J Intern Med., 2005 Mar;257(3):299-310.
  8. ↑ Gandevia SC, Enoka RM, McComas AJ, Stuart DG, Thomas CK (1995). “Neurobiology of muscle fatigue. Advances and issues”. Adv. Exp. Med. Biol. 384: 515–25. PMID 8585476.
  9. ↑ Kent-Braun JA (1999). “Central and peripheral contributions to muscle fatigue in humans during sustained maximal effort”. European journal of applied physiology and occupational physiology. 80 (1): 57–63. PMID 10367724.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]

Pathophysiology

Central

The central component to muscle fatigue is generally described in terms of a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output.[1][2][3] It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity.[4][5] The exact mechanisms of central fatigue are unknown although there has been a great deal of interest in the role of serotonergic pathways.[6][7][8]

Neural

Nerves are responsible for controlling the contraction of muscles, determining the number, sequence and force of muscular contraction. Most movements require a force far below what a muscle could in potential generate, and barring pathology nervous fatigue is seldom an issue. For extremely powerful contractions that are close to the upper limit of a muscle’s ability to generate force, nervous fatigue can be a limiting factor in untrained individuals. In novice strength trainers, the muscle’s ability to generate force is most strongly limited by nerve’s ability to sustain a high-frequency signal. After a period of maximum contraction, the nerve’s signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply ‘stop listening’ and gradually cease to move, often going backwards. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout. Part of the process of strength training is increasing the nerve’s ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force. It is this neural training that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrilar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force.

Peripheral

Peripheral muscle fatigue during physical work is considered an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigue–affecting a national average of 72% of adults in the work force in 2002. This causes contractile dysfunction that is manifested in the eventual reduction or lack of ability of a single muscle or local group of muscles to do work. The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue.

The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation is therefore dependent on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed.

Though not universally used, ‘metabolic fatigue’ is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the muscle fiber. This can occur through a simple lack of energy to fuel contraction, or interference with the ability of Ca2+ to stimulate actin and myosin to contract.

Substrates

Substrates within the muscle generally serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5-7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct.

Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so.

Metabolites

Metabolites are the substances (generally waste products) produced as a result of muscular contraction. They include ADP, Mg2+, reactive oxygen species and inorganic phosphate. Accumulation of metabolites can directly or indirectly produce metabolic fatigue within muscle fibers through interference with the release of calcium from the sarcoplasmic reticulum or reduction of the sensitivity of contractile molecules actin and myosin to calcium.

Chloride

Intracellular chloride inhibits the contraction of muscles, preventing them from contracting due to “false alarms”, small stimuli which may cause them to contract (akin to myoclonus). This natural brake helps muscles respond solely to the conscious control or spinal reflexes but also has the effect of reducing the force of conscious contractions.

Potassium

High concentrations of potassium also causes the muscle cells to decrease in efficiency, causing cramping and fatigue. Potassium builds up in the t-tubule system and around the muscle fiber in general. This has the effect of depolarizing the muscle fiber, preventing the sodium-potassium pump from moving Na+ out of the cell. This reduces the amplitude of action potentials, or stops them entirely, resulting in neurological fatigue.

Lactic Acid

It was once believed that lactic acid build-up was the cause of muscle fatigue.[9] The assumption was lactic acid had a “pickling” effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.

Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. This can lower the sensitivity of contractile apparatus to Ca2+ but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell. This counters inhibiting effects of K+ on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving potassium ions as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.

Associated Conditions

Muscle weakness may be due to problems with the nerve supply, neuromuscular disease such as myasthenia gravis or problems with muscle itself. The latter category includes polymyositis and other muscle disorders.

References

  1. ↑ Gandevia SC (2001). “Spinal and supraspinal factors in human muscle fatigue”. Physiol. Rev. 81 (4): 1725–89. PMID 11581501.
  2. ↑ Kay D, Marino FE, Cannon J, St Clair Gibson A, Lambert MI, Noakes TD (2001). “Evidence for neuromuscular fatigue during high-intensity cycling in warm, humid conditions”. Eur. J. Appl. Physiol. 84 (1–2): 115–21. PMID 11394239.
  3. ↑ Vandewalle H, Maton B, Le Bozec S, Guerenbourg G (1991). “An electromyographic study of an all-out exercise on a cycle ergometer”. Archives internationales de physiologie, de biochimie et de biophysique. 99 (1): 89–93. PMID 1713492.
  4. ↑ Bigland-Ritchie B, Woods JJ (1984). “Changes in muscle contractile properties and neural control during human muscular fatigue”. Muscle Nerve. 7 (9): 691–9. doi:10.1002/mus.880070902. PMID 6100456.
  5. ↑ Noakes TD (2000). “Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance”. Scandinavian journal of medicine & science in sports. 10 (3): 123–45. PMID 10843507.
  6. ↑ Davis JM (1995). “Carbohydrates, branched-chain amino acids, and endurance: the central fatigue hypothesis”. International journal of sport nutrition. 5 Suppl: S29–38. PMID 7550256.
  7. ↑ Newsholme, E. A., Acworth, I. N., & Blomstrand, E. 1987, ‘Amino acids, brain neurotransmitters and a functional link between muscle and brain that is important in sustained exercise’, in G Benzi (ed.), Advances in Myochemistry, Libbey Eurotext, London, pp. 127-133.
  8. ↑ Newsholme EA, Blomstrand E (1995). “Tryptophan, 5-hydroxytryptamine and a possible explanation for central fatigue”. Adv. Exp. Med. Biol. 384: 315–20. PMID 8585461.
  9. ↑ Muscle fatigue and lactic acid accumulation. abstract

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Causes

Causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]

Causes

Causes in Organ System

Cardiovascular

Peripheral Arterial Disease,

Chemical / poisoning

Cadmium poisoning, Dicamba, Fluoride poisoning, Hexane-2,5-dione, Temik

Dermatologic No underlying causes
Drug Side Effect

3-Quinuclidinyl benzilate, Acamprosate (patient information), Acitretin (patient information), Aluminum Hydroxide (patient information), Amiloride and Hydrochlorothiazide (patient information), Amiodarone Oral (patient information), Beclomethasone Oral Inhalation (patient information), Benztropine Mesylate Oral (patient information), Bezafibrate (patient information), Brompheniramine (patient information), Budesonide Inhalation Powder (patient information), Chloroquine Phosphate Oral (patient information), Chlorothiazide (patient information), Chlorpheniramine (patient information), Chlorthalidone (patient information), Ciclesonide Nasal Spray (patient information), Clofibrate (patient information), Colistimethate Injection (patient information), Cyanocobalamin Injection (patient information), Cyproheptadine (patient information), Cytarabine (patient information), Daptomycin, Desipramine (patient information), Dexamethasone Oral (patient information), Dextroamphetamine and Amphetamine (patient information), Dicyclomine (patient information), Diphenhydramine Oral (patient information), Donepezil (patient information), Dorzolamide and Timolol Ophthalmic (patient information), Doxazosin (patient information), Doxylamine (patient information), Eribulin, Ergotamine tartrate, Ezetimibe (patient information), Fexofenadine and Pseudoephedrine (patient information), Fludrocortisone Acetate (patient information), Flunisolide Nasal Inhalation (patient information), Fluticasone and Salmeterol Oral Inhalation (patient information), Fluvastatin (patient information), Galantamine (patient information), Gemeprost, Glucocorticoids, Hydrochlorothiazide (patient information), Hydrocortisone (Injection) Hydrocortisone (Oral) Hydroxychloroquine (patient information), Hydroxyzine (patient information), Imiquimod (patient information), Insulin lispro, Interferon Beta-1b Injection (patient information), Ixabepilone, lamivudine, Leflunomide (patient information), Letrozole (patient information), Levalbuterol Oral Inhalation (patient information), Lisinopril and Hydrochlorothiazide (patient information), Lithium (patient information), Loprazolam, Lormetazepam, Lovastatin (patient information), Mepyramine, Mepenzolate, Methyclothiazide (patient information), Methyldopa and Hydrochlorothiazide (patient information), Methylprednisolone Oral (patient information), Metolazone (patient information), Nitrazepam, Nitrofurantoin (patient information), Oxaprozin, Oxcarbazepine (patient information), Pralidoxime, Pramipexole (patient information), Pravastatin (patient information), Prazosin and polythiazide (patient information), Prednisone, Procyclidine (patient information), Pseudoephedrine and triprolidine (patient information), Pyridostigmine (patient information), Reserpine, hydralazine, and hydrochlorothiazide (patient information), Riluzole (patient information), Rosuvastatin (patient information), Salmeterol oral inhalation (patient information), Selegiline (patient information), Spironolactone (patient information), Tamoxifen (patient information), Telbivudine (patient information), Teriparatide (rDNA origin) Injection (patient information), Tocopherol, Topiramate, Trastuzumab (patient information), Triamcinolone Nasal Inhalation (patient information), Triamterene (patient information), Trimeprazine (patient information), Zoledronic Acid Injection (patient information)

Ear Nose Throat

Acute viral nasopharyngitis (common cold)

Endocrine

Addison’s disease, Cushing’s syndrome, Graves’ Disease, Hyperaldosteronism, Hyperpituitarism, Hyperthyroidism, Hypothyroidism, Kennedy disease, Thyrotoxicosis

Environmental No underlying causes
Gastroenterologic Cirrhosis
Genetic

Bassen-Kornzweig syndrome, Becker’s muscular dystrophy, Carnitine palmitoyltransferase I deficiency, Dejerine Sottas syndrome, Devic’s disease, Engelmann syndrome, Glutaric aciduria type 1, Glycogen storage disease type II, GM1 gangliosidoses, Hereditary inclusion body myopathy, Hereditary spastic paraplegia, Metachromatic leukodystrophy, Nemaline myopathy, Phosphofructokinase deficiency, Primary carnitine deficiency, Pyruvate carboxylase deficiency, Sandhoff disease, Walker-Warburg syndrome

Hematologic

Acute intermittent porphyria, Variegate porphyria

Iatrogenic No underlying causes
Infectious Disease

Botulism, Group A streptococcal infection, HIV, Influenza, Polymyositis, Pott’s disease, Rhinovirus

Musculoskeletal / Ortho

Arthrogryposis, Congenital muscular dystrophy, Congenital myasthenic syndrome, Congenital myopathy, Dermatomyositis, Diabetic amyotrophy, Duchenne muscular dystrophy, Emery-Dreifuss Muscular Dystrophy, Facioscapulohumeral muscular dystrophy, Inclusion body myositis, Rhabdomyolysis, Spondylosis

Neurologic

Accessory nerve disorder, Acute peripheral neuropathy, Amyotrophic lateral sclerosis, Arnold-Chiari malformation, Chronic inflammatory demyelinating polyneuropathy, Diabetic neuropathy, Epidural hematoma, Friedreich’s ataxia, Guillain-Barre syndrome, Juvenile primary lateral sclerosis, Machado-Joseph disease, Marinesco-Sjogren syndrome, Motor neurone disease, Multiple sclerosis, Myasthenia gravis, Peripheral neuropathy, Sturge-Weber syndrome, Tabes dorsalis

Nutritional / Metabolic

3-Methylglutaconic aciduria, Guanidinoacetate methyltransferase deficiency, Metabolic acidosis, Vitamin D deficiency

Obstetric/Gynecologic No underlying causes
Oncologic

Adrenal carcinoma

Opthalmologic No underlying causes
Overdose / Toxicity

Benztropine Mesylate Oral (patient information), Fexofenadine and Pseudoephedrine (patient information), Galantamine (patient information), Salmeterol oral inhalation (patient information), Topiramate

Psychiatric

Anorexia nervosa, Bulimia nervosa, Tension myositis syndrome

Pulmonary

Hopkins syndrome

Renal / Electrolyte

Hypercalcemia, Hyperkalaemic periodic paralysis, Hypermagnesemia, Hypermethioninemia, Hypokalemic periodic paralysis, Hypomagnesemia, Hypophosphatemia, Uremia

Rheum / Immune / Allergy

Congenital myasthenic syndrome, Graves’ Disease, Krabbe disease, Lambert-Eaton myasthenic syndrome, Rheumatoid Arthritis, Scleroderma, Sjogren’s Syndrome

Sexual No underlying causes
Trauma

Brachial plexus injury

Urologic No underlying causes
Miscellaneous

Alcoholic polyneuropathy, Chronic fatigue syndrome, Mitochondrial trifunctional protein deficiency, Spinal cord injury, Spinal disc herniation, Spinal stenosis

Causes in Alphabetical Order


References

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Differentiating Muscle Weakness from other Diseases

Differentiating Muscle Weakness from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]

Differentiaing Muscle Weakness from other Diseases

Acute/Sub Acute

Chronic Muscle Weakness

The following diseases that cause muscle weakness may be differentiated from one another as follows:

Diseases History and Physical Diagnostic tests Other Findings
Motor Deficit Sensory deficit Cranial nerve Involvement Autonomic dysfunction Proximal/Distal/Generalized Ascending/Descending/Systemic Unilateral (UL)

or Bilateral (BL)

or

No Lateralization (NL)

Onset Lab or Imaging Findings Specific test
Adult Botulism + – + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Diplopia, Hyporeflexia, Hypotonia, possible respiratory paralysis
Infant Botulism + – + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Flaccid paralysis (Floppy baby syndrome), possible respiratory paralysis
Guillian-Barre syndrome[1] + – – – Generalized Ascending BL Insidious CSF: ↑Protein

↓Cells

Clinical & Lumbar Puncture Progressive ascending paralysis following infection, possible respiratory paralysis
Eaton Lambert syndrome[2] + – + + Generalized Systemic BL Intermittent EMG, repetitive nerve stimulation test (RNS) Voltage gated calcium channel (VGCC) antibody Diplopia, ptosis, improves with movement (as the day progresses)
Myasthenia gravis[3] + – + + Generalized Systemic BL Intermittent EMG, Edrophonium test Ach receptor antibody Diplopia, ptosis, worsening with movement (as the day progresses)
Electrolyte disturbance[4] + + – – Generalized Systemic BL Insidious Electrolyte panel ↓Ca++, ↓Mg++, ↓K+ Possible arrhythmia
Organophosphate toxicity[5] + + – + Generalized Ascending BL Sudden Clinical diagnosis: physical exam & history Clinical suspicion confirmed with RBC AchE activity History of exposure to insecticide or living in farming environment. with : Diarrhea, Urination, Miosis, Bradycardia, Lacrimation, Emesis, Salivation, Sweating
Tick paralysis (Dermacentor tick)[6] + – – – Generalized Ascending BL Insidious Clinical diagnosis: physical exam & history – History of outdoor activity in Northeastern United States. The tick is often still latched to the patient at presentation (often in head and neck area)
Tetrodotoxin poisoning[7] + – + + Generalized Systemic BL Sudden Clinical diagnosis: physical exam & dietary history – History of consumption of puffer fish species.
Stroke[8] +/- +/- +/- +/- Generalized Systemic UL Sudden MRI +ve for ischemia or hemorrhage MRI Sudden unilateral motor and sensory deficit in a patient with a history of atherosclerotic risk factors (diabetes, hypertension, smoking) or atrial fibrillation.
Poliomyelitis[9] + + + +/- Proximal > Distal Systemic BL or UL Sudden PCR of CSF Asymmetric paralysis following a flu-like syndrome.
Transverse myelitis[10] + + + + Proximal > Distal Systemic BL or UL Sudden MRI & Lumbar puncture MRI History of chronic viral or autoimmune disease (e.g. HIV)
Neurosyphilis[11][12] + + – +/- Generalized Systemic BL Insidious MRI & Lumbar puncture CSF VDRL-specifc

CSF FTA-Ab -sensitive[13]

History of unprotected sex or multiple sexual partners.

History of genital ulcer (chancre), diffuse maculopapular rash.

Muscular dystrophy[14] + – – – Proximal > Distal Systemic BL Insidious Genetic testing Muscle biopsy Progressive proximal lower limb weakness with calf pseudohypertrophy in early childhood. Gower sign positive.
Multiple sclerosis exacerbation[15] + + + + Generalized Systemic NL Sudden ↑CSF IgG levels

(monoclonal)

Clinical assessment and MRI [16] Blurry vision, urinary incontinence, fatigue
Amyotrophic lateral sclerosis[17] + – – – Generalized Systemic BL Insidious Normal LP (to rule out DDx) MRI & LP Patient initially presents with upper motor neuron deficit (spasticity) followed by lower motor neuron deficit (flaccidity).
Inflammatory myopathy[18] + – – – Proximal > Distal Systemic UL or BL Insidious Elevated CK & Aldolase Muscle biopsy Progressive proximal muscle weakness in 3rd to 5th decade of life. With or without skin manifestations.

References

  1. ↑ Talukder RK, Sutradhar SR, Rahman KM, Uddin MJ, Akhter H (2011). “Guillian-Barre syndrome”. Mymensingh Med J. 20 (4): 748–56. PMID 22081202.
  2. ↑ Merino-Ramírez MÁ, Bolton CF (2016). “Review of the Diagnostic Challenges of Lambert-Eaton Syndrome Revealed Through Three Case Reports”. Can J Neurol Sci. 43 (5): 635–47. doi:10.1017/cjn.2016.268. PMID 27412406.
  3. ↑ Gilhus NE (2016). “Myasthenia Gravis”. N Engl J Med. 375 (26): 2570–2581. doi:10.1056/NEJMra1602678. PMID 28029925.
  4. ↑ Ozono K (2016). “[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-]”. Clin Calcium. 26 (2): 215–22. doi:CliCa1602215222 Check |doi= value (help). PMID 26813501.
  5. ↑ Kamanyire R, Karalliedde L (2004). “Organophosphate toxicity and occupational exposure”. Occup Med (Lond). 54 (2): 69–75. PMID 15020723.
  6. ↑ Pecina CA (2012). “Tick paralysis”. Semin Neurol. 32 (5): 531–2. doi:10.1055/s-0033-1334474. PMID 23677663.
  7. ↑ Bane V, Lehane M, Dikshit M, O’Riordan A, Furey A (2014). “Tetrodotoxin: chemistry, toxicity, source, distribution and detection”. Toxins (Basel). 6 (2): 693–755. doi:10.3390/toxins6020693. PMC 3942760. PMID 24566728.
  8. ↑ Kuntzer T, Hirt L, Bogousslavsky J (1996). “[Neuromuscular involvement and cerebrovascular accidents]”. Rev Med Suisse Romande. 116 (8): 605–9. PMID 8848683.
  9. ↑ Laffont I, Julia M, Tiffreau V, Yelnik A, Herisson C, Pelissier J (2010). “Aging and sequelae of poliomyelitis”. Ann Phys Rehabil Med. 53 (1): 24–33. doi:10.1016/j.rehab.2009.10.002. PMID 19944665.
  10. ↑ West TW (2013). “Transverse myelitis–a review of the presentation, diagnosis, and initial management”. Discov Med. 16 (88): 167–77. PMID 24099672.
  11. ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). “Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients”. J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
  12. ↑ Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
  13. ↑ Ho EL, Marra CM (2012). “Treponemal tests for neurosyphilis–less accurate than what we thought?”. Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
  14. ↑ Falzarano MS, Scotton C, Passarelli C, Ferlini A (2015). “Duchenne Muscular Dystrophy: From Diagnosis to Therapy”. Molecules. 20 (10): 18168–84. doi:10.3390/molecules201018168. PMID 26457695.
  15. ↑ Filippi M, Preziosa P, Rocca MA (2016). “Multiple sclerosis”. Handb Clin Neurol. 135: 399–423. doi:10.1016/B978-0-444-53485-9.00020-9. PMID 27432676.
  16. ↑ Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). “Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group”. Arch Neurol. 51 (1): 61–6. PMID 8274111.
  17. ↑ Riva N, Agosta F, Lunetta C, Filippi M, Quattrini A (2016). “Recent advances in amyotrophic lateral sclerosis”. J Neurol. 263 (6): 1241–54. doi:10.1007/s00415-016-8091-6. PMC 4893385. PMID 27025851.
  18. ↑ Michelle EH, Mammen AL (2015). “Myositis Mimics”. Curr Rheumatol Rep. 17 (10): 63. doi:10.1007/s11926-015-0541-0. PMID 26290112.

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Epidemiology and Demographics

Epidemiology and Demographics

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References

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Risk Factors

Risk Factors

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References

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Screening

Screening

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References

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]

Complications

Depending on the cause for weakness, following complications may be seen:

References

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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