Weakness can affect few or many muscles and suddenly or develop gradually. Depending on the cause other symptoms may be present. Weakness of certain muscle groups can also cause disorders of eye movements, dysarthria, dysphagia or respiratory depression.
Weakness is one of the most common reasons why patients are presented in primary care. Under weakness, loss of muscle strength will be understood; However, many patients speak of weakness, when they generally feel tired or functional limitations have (z. B. due to pain or limited joint mobility), although the muscle strength is normal. Weakness can affect few or many muscles and suddenly or develop gradually. Depending on the cause other symptoms may be present. Weakness of certain muscle groups can also cause disorders of eye movements, dysarthria, dysphagia or respiratory depression. Pathophysiology Voluntary movements are triggered in the motor cortex, which lies at the rear edge of the frontal lobe. The neurons (upper Motoeuronen or neurons of the pyramidal tract) involved form synapses with neurons of the spinal cord (lower motor neurons, or anterior horn cells). The lower motor neurons transmit impulses to the neuromuscular junction and loosen the muscle contraction from. General mechanisms of weakness thus comprise the dysfunction of upper motor neurons (lesions of the corticospinal tract and corticobulbar tract) Lower motoneurons (z. B. due to peripheral polyneuropathies or cell damage in the ventral horn) neuromuscular junction muscle (for. Example, due to myopathies) The localization certain lesions correlates with the physical findings: a dysfunction of the upper motor neurons leads to disinhibition of the lower motor neurons, which means an increased muscle tone (spasticity), and increased muscle stretch reflexes (hyper-reflexia) entails. A Babinski sign is specific to a dysfunction of the pyramidal tract. However, a dysfunction of the upper motor neurons tone and reflexes may decrease when the motor paralysis occurs suddenly and violently (z. B. spinal cord transection, wherein the tone first decreases and then increases gradually over days and weeks) or if the lesion the motor cortex damage in the area of ??the dentate gyrus alone and not benachtbarten motor association areas. A dysfunction of the lower motor neurons interrupts reflex arcs with the result of reduced muscle tone and hyporeflexia (limpness) and can lead to fasciculations; over time the muscles atrophy. Peripheral neuropathies are usually most pronounced in the longest nervous detected (i.e., the weakness is more pronounced than in the proximal and in the legs in the distal extremity stronger than in the arms..); they produce signs of dysfunction of the lower motor neurons (z. B. reflexes and muscle tone attenuated). The most common disease of the neuromuscular junction-myasthenia gravis typically-causing fluctuating weakness that worsens with activity and improves at rest. Diffuse muscle dysfunction (eg. As in myopathies) are usually most noticeable in the largest muscle groups recognizable (proximal muscles). Etiology The many causes of muscle weakness are in accordance with the location of the lesion categorized (see table: causes of muscle weakness). Usually lesions manifest at a certain point in similar clinical findings. However, some diseases Läsionsmerkmale in more than one location have. For example, , patients with amyotrophic lateral sclerosis exhibit (ALS) is a dysfunction of both the upper and lower motor neurons. Spinal cord diseases can affect strands of the upper, the lower motor neurons (ventral horn cells), or both. Common causes of focal weakness stroke (most common cause of unilateral weakness) neuropathies, including by trauma or entrapment (z. B. carpal tunnel syndrome) caused and the immune-mediated (z. B. Bell palsy) clamping the spinal root (eg. B herniated .) compression of the spinal cord (e.g., cervical syndrome, epidural metastasis, trauma) multiple sclerosis Temporary focal weakness can Todd) paralysis occur as part of a post-ictal (which dissolves usually after several hours or resulting from hypoglycemia; with the treatment, hypoglycemia and the resulting weakness fix. The most common causes of generalized weakness are degradation due to inactivity (disuse atrophy) as a result of disease or infirmity, especially in the elderly generalized muscle wasting due to prolonged immobilisation in an ICU (critical illness myopathy) Cricital illness polyneuropathy (critical illness neuropathy ) Common myopathies. (eg alcoholic myopathy, hypokalemia, Kortikosteroidmyopathie) use of paralytic drugs in intensive care patients cared causes of muscle weakness due suspects findings Diagnostic procedure * Lesions of the upper motor neurons in the brain brain tumors multiple sclerosis stroke Increased muscle tone, hyperreflexia, Babinski sign may more stiffness and loss of fine motor skills (dexterity) and weakness (handle) brain imaging with CT or MRI myelopathy (close the dysfunction of the upper and / or a lower motor neurons) compression of the spinal cord (eg. For example, by spondylosis, Epiduraltumor, hematoma or abscess) cauda equina syndrome ischemia or infarction of the spinal cord autoimmune diseases (eg. As multiple sclerosis, neuromyelitis optica, vasculitis), infections (eg., HTLV-1, HIV, syphilis, human herpes simplex virus 6, EBV, varicella zoster) spinocerebellar atrophies Subacute combined degeneration transverse myelitis copper deficiency dysfunction of the upper and / or lower motor neurons Frequently erectile dysfunction, incontinence of bowel and bladder, lack of Sphinkterreflexe (z. B. anal reflex, Bulbocavernosusreflex) progressive weakness of the limbs and fatigue, clumsiness, spasticity (first legs, then arms, with gradual compression of the spinal cord) Classic Dermatomhöhen sensitivity deficit tests to determine the cause may include: vitamin B12 levels, HIV test, ANA, RPR, NMO IgG Autoantikörpe r (anti-aquaporin-4 antibody), HTLV-1 or VDRL, genetic testing, serum copper and ceruloplasmin, MRI and / or CT myelography of the cord blood (eg. B. Protein, VDRL, IgG index, oligoclonal bands, virus titer, PCR) Somatosensory evoked potentials Moto Euro disorders (upper and / or lower) Amyotrophic lateral sclerosis, hereditary motor neuron diseases (for. Example, spinal muscular atrophies or spinocerebellar atrophies, incl. Spinal and bulbar muscular atrophy) myelopathy Postpoliomyelitissyndrom Progressive supranuclear palsy Viral polio-like disease Progressive weakness and fatigue, clumsiness, spasticity (upper motor neuron) hyporeflexia or slack (lower motor neuron) muscular atrophy (lower motor neuron) fasciculations (lower motor neuron) gynecomastia, diabetes, and testicular atrophy (spinal and bulbar muscular atrophy) Electromyography and MRI of the brain and spinal cord and / or CT myelography Further testing: If necessary, Heavy metal screening in 24-hour urine for the exclusion of a lead-neuropathy, anti-GM1 antibody titres (at multifocal motor neuropathy) and genetic testing (eg. As in spinobulbar muscular atrophy type Kennedy) polyneuropathy (most peripheral polyneuropathies) alcohol Associated neuropathy Critical -Illness polyneuropathy Demyelinating neuropathies (z. B. CIDP, Guillain-Barre syndrome) Diabetic neuropathy through drug induced neuropathies (eg., by vincristine, cisplatin or statins) Hereditary neuropathies infectious neuropathies (eg. as diphtheria, hepatitis C , HIV / AIDS, Lyme disease, syphilis) multifocal motor neuropathy sarcoidosis toxic neuropathies (eg. as heavy metals), vitamin deficiencies (z. B. thiamin, vitamin B6 or B12) Hyporeflexia, sometimes Fasciculations If chronic, muscular atrophy In peripheral polyneuropathy: disproportionate weakness of most distal muscles and often sensory disturbances in the same area (stocking-glove distribution); (Common except CIDP, which equally affects proximal and distal nerves and muscles) studies to confirm the presence of neuropathy: electrodiagnostic tests tests to clarify the Cause: plasma glucose, 2-hour oral glucose tolerance test, hemoglobin A1c (HbA1c), RPR, HIV test, folic acid, vitamin B12, serum protein immunofixation, chest CT and serum ACE levels (sarcoidosis), heavy metal screening in 24-hour urine, anti-MAG antibody (in some demyelinating neuropathies), anti- GM1 antibody titers (with multifocal motor neuropathy) and genetic testing disorders of neuromuscular junction botulism Lambert-Eaton syndrome myasthenia gravis organophosphate Zeckenlähmu ng weakness that varies (e.g. in intensity. As often prominent in myasthenia gravis or Lambert-Eaton syndrome) bulbar findings (z. B. in myasthenia gravis, botulism or organophosphate) Sometimes hyporeflexia (z. B. at Lambert-Eaton syndrome, tick paralysis or organophosphate) tests for the confirmation the mechanism: electrodiagnostic tests If necessary, additional tests to determine a specific disorder (such as acetylcholine receptor antibodies, edrophonium test for suspected myasthenia gravis.) alcoholic myopathy myopathy channelopathies corticosteroid myopathy Cushing’s syndrome Hereditary muscle disorders (eg muscular dystrophies. ) hypocalcemia hypokalemia hypomagnesemia hypophosphatemia Hypothyreotische myopathy Metab olische myopathies polymyositis and dermatomyositis rhabdomyolysis statin-induced myopathy myopathy Thyrotoxic Viral myositis Disproportionated weakness of proximal muscles (same both sides) If chronic muscle wasting In some forms muscle tenderness studies that confirm the mechanism: electrodiagnostic tests, muscle enzymes (eg. B. CK, aldolase), sometimes MRI to confirm the muscular hypertrophy or pseudohypertrophy tests to determine the cause: if necessary, muscle biopsy with special staining and genetic testing for certain hereditary diseases Generalized muscle wasting due to illness and inactivity burns cancer Prolonged bed rest sepsis hunger Diffuse muscular atrophy, normal sensory and reflexes, no fasciculations clinically identifiable risk factors Clinical examination * The tests can vary; Additional tests may be indicated depending on the clinical suspected disorder. Multiple mononeuropathy (mononeuritis multiplex), if it is spread far enough, cause deficits similar to those of the diffuse polyneuropathy clinically. ANA = anti-nuclear antibody, anti-ganglioside GM1 = GM1 antibody, anti-MAG = anti-myelin associated glycoprotein; CIDP = chronic inflammatory demyelinating polyneuropathy; EBV = Epstein-Barr virus, HTLV = human T-lymphotropic virus; NMO-IgG = aquaporin-4 antibody; RPR = rapid Rlasma reagin; VDRL = Venereal Disease Research Laboratory. Fatigue Many patients report weakness when their real problem Ermüdbarkeitist. This can prevent the maximum effort and muscle performance in tests of muscle strength. Common causes of fatigue are almost all acute severe diseases, cancers, chronic infections (eg., HIV, hepatitis, endocarditis, mononucleosis), endocrine disorders, kidney failure, liver failure, heart failure and anemia. Patients with chronic fatigue syndrome, depression, fibromyalgia, or may complain of weakness or fatigue, but have no objectively defined anomalies. Assessment The examination should be made to distinguish a true muscle weakness of fatigue, then it should be looked for findings that help to build the mechanism (eg. As if the weakness of a dysfunction of the brain, spinal cord, plexus, the peripheral nerves, the neuromuscular junction or muscle is based), and then – if possible – the cause. History The history taking to the existing disease should begin with open-ended questions that ask patients to describe in detail what they are experiencing as a weakness. Then specific questions can be asked, v. a. whether certain activities, such as brushing teeth, combing hair, speaking, swallowing, rising from a chair, climbing stairs and walking can be performed. It should also be the beginning of (sudden or gradual) and the progression of symptoms (eg. As consistently, is worsening, intermittent) be requested. A detailed survey is necessary to distinguish whether the symptoms are suddenly occurred or were suddenly noticed; Patients can this suddenly perceive when a slowly progressive weakness exceeds a threshold and then stops to routine activities (eg tie. As walking, shoes). Important Accompanying symptoms include sensory changes, double vision, memory loss, difficulty with speech, seizures and headaches. Factors that aggravate the weakness, such as heat (indicating multiple sclerosis) or repetivie contraction of a muscle (reference to myasthenia gravis) are added. In reviewing the organ systems should be looked for symptoms that indicate a possible cause, including the following: rash: dermatomyositis, Lyme disease or syphilis fever: Chronic infection muscle pain: myositis neck pain: cervical myelopathy vomiting or diarrhea: botulism breathlessness: heart failure , lung disease or anemia anorexia and weight loss: cancer or other chronic diseases change the color of urine: porphyria or liver or kidney disease heat or cold intolerance: thyroid dysfunction Depressed mood, poor concentration, anxiety and loss of interest in usual activities: affective disorder the mediziniche history should identify known diseases, weakness or fatigue veru can rsachen as: thyroid, liver, kidney or adrenal disease, cancer or risk factors for cancer (paraneoplastic syndromes-z. B. Lambert-Eaton syndrome) as heavy smoking, osteoarthritis (cervical myelopathy) and infections. Risk factors for possible causes should be evaluated, incl. Those for infections (eg. As unprotected sex, blood transfusions, exposure to tuberculosis) and stroke (eg. As hypertension, atrial fibrillation, atherosclerosis). The complete drug history should be obtained. The family history should include known hereditary diseases (eg. As hereditary muscle diseases, Channelopathies, metabolic myopathies, hereditary neuropathies) and the presence of similar symptoms in family members (indication of a possible unrecognized genetic disease). Due to their variable, incomplete phenotypic expression hereditary motor neuropathies in families often remain undetected. Hammer toes, high arches and poor athletic performance may indicate an undiagnosed hereditary motor neuropathy. In derSozialanamnese following should be considered: The use of alcohol: Note on alcoholic myopathy illicit drug use: signs of an increased risk of HIV / AIDS, bacterial infections, tuberculosis or stroke for cocaine use Professional or other contacts with toxins (eg organophosphate. -insecticides, heavy metals, industrial solvents) Current travel: Points to Lyme disease, tick paralysis, diphtheria, or a parasitic infection through Social stressors: Note suggesting depression Physical examination a complete neurological and muscular examination is performed to findings on identify location or diagnosis. Among the most important results normally include cranial nerve motor reflexes Examination of the cranial nerves includes the inspection of the face of gross asymmetries and ptosis; a slight facial asymmetry can be normal. Extraocular movements and facial muscles, the masseter incl. (Force) are tested. A weakness of the palate is suggested by a nasal voice; to test the gag reflex and to consider the taste buds directly, is less helpful. The inability of certain consonants clearly articulate (z. B. “ta-ta-ta”), and slurred speech (dysarthria lingual) indicate a weakness of the tongue. A slight asymmetry in tongue protrusion may be normal. The Karft of M. sternocleidomastoides and trapezius is tested by the patient turns his head and shoulders pulling against resistance. The patient is asked to repeatedly blink, to determine whether the blinking tired. Motor examination includes inspection, assessment of tone and examination of power. The body is examined for kyphoscoliosis (possible indication of chronic weakness of the paraspinal muscles) and surgical and traumatic scars. A dystonic attitude (z. B. torticollis) can interfere with the movement and mimic a weakness. The muscles are tested for fasciculations and atrophy; both can in ALS focal or start asymmetrical. Fasciculations are most visible on the tongue of patients with advanced ALS. A diffuse atrophy is most evident on the hands, the face and shoulder girdle. Muscle tone is determined by using passive movement. Tapping on a muscle (z. B. hypothenar) can induce fasciculations in neuropathies or myotonic contractions in myotonic dystrophy. The test of muscle strength should be both proximal and distal muscles and extensors and flexors. Some tests of large proximal muscles include: getting up from a seated position, squat down and stand up, bend your body and stretch and turn your head against resistance. The force is often rated on a scale of 0-5: 0: No visible muscle contraction 1: Visible muscle contraction without movement of the limbs 2: movement of the limbs, not against the gravity 3: movement against gravity but not against resistance 4: weakness in resistance 5: Full speed development Although these data appear objective is to assess the strength of 3-5 (typical levels at earlier weakness, ie usually at diagnosis) more subjective; in unilateral symptoms of comparison improves discrimination with the healthy side. It is often useful to describe specifically what the patient can or can not do than simply assign a numerical value to the weakness, v. a. if the changes of weakness over time to be assessed. A cognitive deficit can for lack of endurance motor (inability attention be given to the conclusion of a motor task), motor perseveration, apraxia or insufficient effort be responsible. Simulating and other functional weaknesses are often characterized in that the weakness is yielded, wherein said normal tension suddenly decreases. Coordination tests include finger-nose and chopping Shin-test as well as the toe to heel transition for screening cerebellar dysfunction that a stroke in the cerebellum, a vermis atrophy (z. B. due to alcohol abuse), some hereditary spinocerebellar ataxia, multiple may accompany sclerosis and the Miller Fisher variant of Guillain-Barre syndrome. Gait is observed on the following: “ignition failure” (ignition failure – (temporary freezing at a point when starting with walking, followed by festination): Normalerdruckhydrocephalus or other frontal lobe disorders: as if the feet glued to the floor Parkinson’s disease apraxia festination: Parkinson’s disease Asymmetric limbs, as if the patient strutting one leg behind, they have a reduced e arm movement have, or both: Hemispheric stroke ataxia: cerebellar disease of the midline instability in turning: parkinsonism heel and toe gear to be tested; a distal muscle weakness makes this maneuver difficult. heel gear is particularly difficult when lesions of the corticospinal tract are the cause of weakness. spastic gait is seen slightly bent to the cutter position (legs in the hip and knee, Ersch einungsbild a squatting position, knee and thigh hit each other or cross each other in a scissors-like movement) and toe walking. Stepper gear and foot drop can occur in peroneal palsy. The sensor is checked; sensory deficits (localized the lesion in a spinal segment z. B. the sensory level) in the localization of lesions, the weakness cause, assist or specific reasons for the weakness suggest (z. B. distal sensory disturbances confirm the clinical suspicion of a Guillain-Barre syndrome). Manchetten shaped tingling and pressure are a cord signs that occurs in both intrinsic and extrinsic lesions at. DieReflexe be tested. Seem to lack the muscle stretch reflexes, they can facilitation, z. As the leg reflexes are using the Jendrassik maneuver triggered (the mutually interlocked fingers of both hands are vigorously pulled apart). Hyporeflexia may be normal, especially with age, but the findings should be symmetrical and seemingly absent reflexes should be cause by facilitation. The plantar (Babinskizeichen) is checked. The following responses indicate certain disorders or bodies of lesions: The classic Babinski (lifting of the big toe, abduction of the other toes) is specific to a lesion of the pyramidal tract. A normal masseteric Flex and brisk reflexes in the arms and legs indicate a cervical lesion with damage to the Pryamidenbahn, usually a Zervikalstenose. The tone of the Analmuskulatur, the anal reflex, or both weakened as spinal cord injuries or missing, contact the ascending paralysis in Guillain-Barre syndrome, however. Abdominal reflexes are absent below the level of spinal cord injury. With the cremasteric can be tested in men, whether the upper lumbar cord and the corresponding nerve roots are intact. Clarification includes test for tenderness of the back when tapping (exists with vertebral inflammation, some vertebral tumors and epidural abscesses) Lift the extended leg (painful to sciatica) examination for scapular winging (indicating weakness of the shoulder girdle muscles) General investigation when patients objectively have no motor weakness, the general investigation is particularly important; it should be sought in these patients to diseases that are not neuromuscular origin. Signs of respiratory distress (z. B. tachypnea, weak inspiration) may be added. The skin is examined for jaundice, paleness, rash and striae. Other key findings include: moon face at Cushing, Parotisvergrößerung, smooth hairless skin, ascites, spider nevi in ??chronic alcohol consumption. Neck, armpits and groin should be keyed to a adenopathy; any thyroid enlargement is noted. Heart and lungs are auscultated on crackling and wheezing, delayed expiration, murmurs and stumbling rhythms. The abdomen is palpated to room requirements, and if a dysfunction of the spinal cord is also conceivable on a greatly enlarged bladder. A rectal examination to Überpüfung of blood in the stool is performed. Range of motion of the joints is determined in case of suspected tick paralysis is the skin, especially the scalp thoroughly for ticks untersucht.Warnhinweise The following findings are of particular importance: weakness, which is heavily in a couple of days dyspnea inability to lift the head against gravity bulbar symptoms (eg. as difficulty chewing, speech and swallowing) loss of ambulation interpretation of the findings using one of history can be distinguished weakness of fatigue, it defines the time course of the disease and is evidence of the anatomical pattern of weakness. Weakness and fatigue usually cause different symptoms: Weakness Patients complain typically about it, that they can not perform certain activities. You can tell in the limbs or stiffness via gravity. Weakness has a certain temporal and / or anatomical pattern in the rule. Fatigue: Ermüdibarkeit, which is reported as a weakness, shows no temporal (eg “all about time tired.”) Or anatomical pattern (eg “everywhere weak.”); The lawsuits are aimed more attention from being too tired to do certain tasks and not to do to the inability of this. A temporal pattern of symptoms is useful. Weakness is within minutes or more violent, is usually based on a severe trauma or stroke; in stroke weakness is usually unilateral, it can be easy or pronounced. Sudden weakness, numbness and pain in an extremity are due more likely to be a local arterial occlusion and ischemia of the limb; this can be clarified by the evaluation of the vessels (z. B. pulse, color, temperature, capillary refill, blood pressure differences in Doppler measurement). A compression of the spinal cord can also lead to paralysis that (but usually over hours or days) are developing within minutes. They are easy to incontinence and clinical spinal cord findings on a particular sensory and motor height detect. Weakness that steadily progresses over hours or days can be caused by acute or subacute disease (eg. B., spinal cord compression, transverse myelitis, spinal cord ischemia or haemorrhage, Guillain-Barre syndrome, sometimes muscle through a critical illness, rhabdomyolysis, botulism , organophosphate poisoning). Weakness that develops over weeks to months, can be caused by subacute or chronic diseases (e. B. cervical myelopathy, most inherited and acquired polyneuropathy, myasthenia gravis, motor neuron disease, acquired muscle diseases, most tumors). From day to day fluctuating weakness can be caused by multiple sclerosis, and sometimes by metabolic myopathies. Weakness that fluctuates throughout the day, Lambert-Eaton syndrome or periodic paralysis can be caused by myasthenia gravis. Das anatomische Muster von Schwäche wird charkatierisiert durch Schwierigkeiten bei der Ausführung bestimmter motorischer Aufgaben. Anatomische Muster deuten auf bestimmte Diagnosen hin: Proximale Muskelschwäche beeinträchtigt Aufwärtsbewegungen (z. B. Haarekämmen, Gegenstände über den Kopf heben), Treppensteigen oder Aufstehen aus einer sitzenden Position; dieses Muster ist typisch für Myopathien. Distale Muskelschwäche beeinträchtigt Aufgaben wie über eine Bordsteinkante steigen, eine Tasse halten, schreiben, knöpfen oder mit einem Schlüssel umgehen; dieses Muster ist typisch für Polyneuropathien und myotone Muskeldystrophie. Viele Erkrankungen (z. B. chronische entzündliche demyelinisierende Polyneuropathie, Guillain-Barré-Syndrom, Myasthenia gravis, Radikulopathien, Lambert-Eaton-Syndrom) verursachen proximale und distale Schwäche, wobei eines der Muster zunächst prominenter erscheinen kann. Bulbäre Schwäche kann eine Gesichtsschwäche, Dysarthrie und Dysphagie verursachen, mit oder ohne Beeinträchtigung der Augenbewegungen; diese Manifestationen sind typisch für bestimmte neuromuskuläre Erkrankungen wie My