Muscle weakness is a lack of muscle strength. Its causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Muscle weakness can also be caused by low levels of potassium and other electrolytes within muscle cells. It can be temporary or long-lasting (from seconds or minutes to months or years). The term myasthenia is from my- from Greek μυο meaning "muscle" + -asthenia  ἀσθένεια meaning "weakness". Types
Neuromuscular fatigue can be classified as either "central" or "peripheral" depending on its cause. Central muscle fatigue manifests as an overall sense of energy deprivation, while peripheral muscle fatigue manifests as a local, muscle-specific inability to do work. Neuromuscular fatigue
Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the muscle that it innervates. Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue.For extremely powerful contractions that are close to the upper limit of a muscles ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the muscles ability to generate force is most strongly limited by nerve’s ability to sustain a high-frequency signal.
Results are found through testing a small amount of blood gathered through a heel prick of the infant. As not all states require that this test be done, it is often skipped in those where such testing is not required. Biotinidase deficiency can also be found by sequencing the BTD gene, particularly in those with a family history or known familial gene mutation. Treatment
Treatment is possible but unless continued daily, problems may arise. Currently, this is done through supplementation of 5–10 mg of oral biotin a day. If symptoms have begun to show, standard treatments can take care of them, such as hearing aids for poor hearing. Epidemiology
Based on the results of worldwide screening of biotinidase deficiency in 1991, the incidence of the disorder is:
5 in 137,401 for profound biotinidase deficiency

One in 109,921 for partial biotinidase deficiency
One in 61,067 for the combined incidence of profound and partial biotinidase deficiency
Carrier frequency in the general population is approximately one in 120. See also
Biotin
Biotin deficiency
Multiple carboxylase deficiency
Holocarboxylase synthetase deficiency
3-Methylcrotonyl-CoA carboxylase deficiency

References
Further reading
Dobrowolski, Steven F.; Angeletti, Janine; Banas, Richard A.; Naylor, Edwin W. (2003). "Real time PCR assays to detect common mutations in the biotinidase gene and application of mutational analysis to newborn screening for biotinidase deficiency". Molecular Genetics and Metabolism. 78 (2): 100–7. doi:10.1016/S1096-7192(02)00231-7. PMID 12618081. McMahon, Robert J. (2002). "Biotin in metabolism and molecular biology". Annual Review of Nutrition. 22: 221–39. doi:10.1146/annurev.nutr.22.121101.112819. PMID 12055344. C. Neto, E.; Schulte, J.; Rubim, R.; Lewis, E.; Demari, J.; Castilhos, C.; Brites, A.; Giugliani, R.;  et al. (2004).