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cores run the length of the muscle ber, thus differing from the multiple cores or minicores that are seen in oculopharyngeal and other forms of muscular dystrophy Nemaline (Rod-Body) Myopathy This disorder also expresses itself by hypotonia and impaired motility in infancy and early childhood, but unlike the case in central core disease the muscles of the trunk and limbs (proximal greater than distal), as well as the facial, lingual, and pharyngeal muscles, are strikingly thin and hypoplastic Several forms have been observed One is congenital, with generalized weakness in the neonatal period, making breathing and feeding dif cult The limbs are accid and are exic ( oppy ) Pneumonia and death occur within weeks to months In forms that permit longer survival, the weakness is less severe, involving mainly the proximal muscles Tendon re exes are diminished or absent The young child with this disease usually suffers from inanition and frequent respiratory infections, which may shorten life Strength slowly improves with growth, the latter process evidently counteracting the advance of the disease A slender appearance, narrow face, open mouth, narrow, arched palate, and kyphoscoliosis are regular but not invariable accompaniments of nemaline myopathy These dysmorphic features are not typical of the other congenital polymyopathies Pes cavus or clubfoot may be added Some of the milder cases reach adulthood, at which time a cardiomyopathy may threaten life A G Engel as well as W K Engel and Reznick have observed individuals who rst showed signs of the disease in middle age; the weakness was mainly in proximal muscles and the dysmorphic and skeletal abnormalities of the childhood form were lacking The EMG is myopathic, and serum enzymes are normal or only slightly elevated Cases of nemaline myopathy have come to attention during adulthood in which there is disproportionate involvement of the respiratory muscles (a feature shared with the adult appearance of acid maltase de ciency) Usually, there had been a history of poor physical performance through earlier life Nemaline myopathy appears to be genetically heterogeneous The pattern of inheritance is most often autosomal dominant, with variable penetrance In some families there has been an autosomal recessive or an X-linked pattern of inheritance Studies of the various gene defects have begun to clarify the uncertainties about inheritance and explain the relationships between the different forms of the disease The genes implicated in nemaline myopathy include alpha-tropomyosin, beta-tropomyosin, alpha-actin, nebulin, troponin, and the ryanodine receptor (the last of these is more commonly implicated in central core disease, as mentioned earlier; see Table 52-1) The disease is so named for the rods or coils of thread-like structures in pathology material Frozen muscle tissue stained with Gomori trichrome discloses the characteristic lesion, which can be seen under the light microscope Myriads of bacillus-like rods, singly and in small packets, are seen beneath the plasma membrane of the muscle ber They are composed of material that resembles that of Z bands under the electron microscope, and often actin laments are attached, just as they are to Z bands The type 1 bers, which usually predominate, are smaller than normal, as in central core disease The size of the motor neurons has been reported to be reduced The weakness is probably related to a smallness and reduction in the number of muscle bers and possibly to focal interruption of their cross-striations, particularly the Z bands.

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Centronuclear or Myotubular Myopathy In this familial disease, hypotonia and weakness become manifest soon after birth or in infancy or early childhood Rarely, in the mildest form, the diagnosis does not become evident until adult years All the striated skeletal muscles are involved to some degree, but distinctive features are ptosis and ocular palsies combined with weakness of facial, masticatory, lingual, pharyngeal, laryngeal, and cervical muscles in most of the infants with this disease, but not in adults In the limbs, distal weakness keeps pace with proximal weakness The limbs remain thin and are exic throughout life Motor development is necessarily retarded, though some improvement with maturation can occur; later, however, motor functions that had been acquired may be lost as the disease slowly advances Several patients have shown signs of cerebral abnormality, with seizures and an abnormal electroencephalogram (EEG), but this may not be part of the disease Needle EMG examination shows the usual myopathic pattern, as well as positive sharp waves and brillation potentials in some cases Abundant spontaneous activity should suggest the diagnosis of centronuclear myopathy (Griggs et al) Heckmatt and colleagues have classi ed this disorder into three types, based on severity, mode of presentation, and genetic pattern: (1) a severe neonatal X-linked recessive type; (2) a less severe early-infantile, late-infantile, or childhood autosomal recessive type; and (3) a still milder late childhood adult autosomal dominant type The primary defect in the X-linked form is a mutation in the gene that encodes a protein designated myotubularin; presumably this plays a role in myotube maturation At least one autosomal dominant form has been ascribed to mutations in the protein MYF6, a helix-loop-helix protein that appears to function as a myogenic transcription factor The outstanding pathologic features of the disease are the smallness of muscles and their constituent bers and central nucleation In one group of centronuclear myopathies, there is hypotrophy of type 1 bers (Bethlem et al, Karpati et al) Surrounding most of the centrally placed nuclei is a clear zone, in which there is a lack of organization of contractile elements Because of central nucleation, the disease has incorrectly been referred to as myotubular myopathy, implying an arrest in development of muscle at the myotubular stage Actually, the nature of the pathologic process is obscure The small, centrally nucleated bers do not really resemble typical myotubes Also, there is evidence from electron microscopic studies of changes in the central parts of the bers (lack of enzymatic activity in the clear zones surrounding the nuclei), leading in all probability to ber loss Such changes argue against a purely developmental abnormality Myopathy with Tubular Aggregates The accumulation of tubular aggregates in the subsarcolemmal or more interior regions of muscle bers was rst observed in patients with hypokalemic periodic paralysis and myotonia congenita and later with a number of diverse conditions, such as chronic drug intoxication, hypoxia, and congenital myasthenic syndromes However, tubular aggregates are also the de ning feature of several purely myopathic syndromes: (1) A slowly progressive muscular weakness, in a limbgirdle distribution, with onset in childhood or early adult life; inheritance is either autosomal dominant or recessive in type (2) A childhood onset of proximal weakness, easy fatigability, and myasthenic features; heredity is autosomal recessive This syndrome may respond to pyridostigmine (3) Muscle pain, cramps, and stiffness induced by exercise; the cases to date have been sporadic.

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Salicylic acid is the only beta-hydroxy acid used in cosmeceuticals Salicylic acid is an organic aromatic carboxylic acid with a hydroxyl group in the beta position It is hydrophobic and lipophilic; therefore, it is able to enter the sebaceous unit Salicylic acid acts by solubilizing intercellular corneocyte adhesion, working from the outermost layer downward148 Indications for salicylic acid include comedonal acne (OTC 2%); exfoliation of calluses, corns, and warts; removal of undesquamated corneocytes from the scalp of patients with seborrheic dermatitis and psoriasis; facial peels for patients with photodamage and acne; and patients with sensitive skin (less stinging and burning as the primary ingredient does not readily penetrate to the dermis)149

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