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(ăt`rəfē), diminution in the size of a cell, tissue, or organ from its fully developed normal size. Temporary atrophy may occur in muscles that are not used, as when a limb is encased in a plaster cast. Interference with cellular nutrition, as through starvation; diseases affecting the nerve supply of tissues, e.g., poliomyelitis and muscular dystrophy; and prolonged disuse may cause a permanent wasting away of tissue. Atrophy may also follow hypertrophyhypertrophy
, enlargement of a tissue or organ of the body resulting from an increase in the size of its cells. Such growth accompanies an increase in the functioning of the tissue. In normal physiology the growth in size of muscles (e.g.
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the decrease in the size of an organ or tissue of the living organism of animals and man, accompanied by a disorder or cessation of functions. Atrophy is the result of a predominance of dissimilation over the processes of assimilation.

Atrophy can be physiological and pathological, systemic and local. Physiological atrophy is a function of the growth changes of an organism (atrophy of the thymus during puberty, atrophy of the sex glands, skin, and bones in old people, and so on). General pathological atrophy (emaciation, cachexia) appears in cases of insufficient nutrition, chronic infection or intoxication, or disorders of the endocrine glands or of the central nervous system. Local pathological atrophy arises from various causes—from a disorder in the regulation of the trophic nerves (for example, atrophy of the skeletal muscles during poliomyelitis), from insufficient supply of blood (for example, atrophy of the brain cortex during atherosclerosis of the blood vessels of the brain); dysfunctional atrophy (for example, atrophy of the optic nerve after removal of an eye), as a result of pressure (for example, atrophy of the kidney in cases of embolism of the urether and accumulation of urine in the renal pelvis), from lack of use (for example, atrophy of the muscles in the extremities after long immobilization), or from the effects of physiological and chemical factors (for example, atrophy of the lymphoid tissue from the effects of solar energy, atrophy of the thyroid gland upon application of iodine preparations).

When an organ atrophies it diminishes in size but subsequently sometimes appears larger as a result of the expansion of fat tissue which replaces the atrophied cellular elements. Pathological atrophy is, up to a certain stage, a reversible process. Treatment consists of the elimination of the causes producing atrophy.


Strukov, A. I. Patologicheskaia anatomiia. Moscow, 1967.
Cameron, G. R. Pathology of the Cell. Edinburgh, 1952.



Diminution in the size of a cell, tissue, or organ that was once fully developed and of normal size.


a wasting away of an organ or part, or a failure to grow to normal size as the result of disease, faulty nutrition, etc.
References in periodicals archive ?
Gene dosage is a mechanism for Charcot-Marie-Tooth disease type 1A.
If creatine kinase remains increased and other causes are excluded, a thorough family history, a physical examination, and a neurologic evaluation are essential for establishing a clinical diagnosis of Charcot-Marie-Tooth disease (CMT).
Serial casting is also employed to increase ankle dorsiflexion range in children and young adults with Charcot-Marie-Tooth disease.
Sample profile: An individual over 18 years of age previously diagnosed with Charcot-Marie-Tooth disease and now suffering with mechanical neck and arm pain.
In those with Charcot-Marie-Tooth disease, treatments include ankle-foot orthosis splinting, plantar fasciotomy, tendon transfers, and foot osteotomies.
Key words: Charcot-Marie-Tooth disease, CMT, HMSN, Genetics, Costa Rica.
Hiding behind this apparently banal complaint it is possible in the course of a single clinic to recognize Parkinson's disease, aortic stenosis, partial complex fits and the first presentation in a 77-year-old of Charcot-Marie-Tooth disease.
To the Editor: Charcot-Marie-Tooth disease (CMT) is a clinically and genetically heterogeneous inherited neuropathy, with Type 1A being the most common.
NASDAQ: XLRN) plans to initiate a Phase 2 clinical trial of ACE-083, the company's locally acting muscle agent, for the treatment of patients with Charcot-Marie-Tooth disease, one of the most common inherited neurologic diseases leading to focal muscle weakness, the company said.
The most recent grant recipients include local and national organizations that serve a variety of communities, including children with Charcot-Marie-Tooth disease, and people interested in adaptive sports opportunities:
In another study, Vinci and Gargiulo [9] investigated the compliance with AFO in Charcot-Marie-Tooth disease (CMT).

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