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Thus purchase kamagra soft 100mg visa erectile dysfunction drug mechanism, each gene does not have a single generic kamagra soft 100 mg line impotence at 50, and lactate purchase 100 mg kamagra soft overnight delivery male erectile dysfunction pills review. Ann O’Rexia, who has an eating unique protein that regulates its transcription. Rather, as different proteins are disorder, needs to maintain a certain blood stimulated to bind to their specific response elements and enhancers in a given glucose level to keep her brain functioning gene, they act cooperatively to regulate expression of that gene (Fig. When her blood glucose levels drop, cortisol (a glucocorticoid) and Overall, a relatively small number of response elements and enhancers and a rel- glucagon (a polypeptide hormone) are atively small number of regulatory proteins generate a wide variety of responses released. In the liver, glucagon increases from different genes. Posttranscriptional Processing of RNA CREB binds to its response element in DNA, After the gene is transcribed (i. Both transcrip- processing of the RNA transcript (hnRNA) into the mature mRNA. The use of alter- tion factors enhance transcription of the native splice sites or sites for addition of the poly(A) tail (polyadenylation sites) can PEPCK gene (see Figure 16. Insulin, result in the production of different mRNAs from a single hnRNA and, conse- which is released when blood glucose levels rise after a meal, can inhibit expression of quently, in the production of different proteins from a single gene. In certain instances, the use of alter- IRE TRE CREII TATA native splicing and polyadenylation sites causes different proteins to be produced –400 –300 –200 –100 +1 from the same gene (Fig. For example, genes that code for antibodies are regulated by alterations in the splicing and polyadenylation sites, in addition to Fig. A simplified view of the regula- undergoing gene rearrangement (Fig. At an early stage of maturation, pre-B tory region of the PEPCK gene. Boxes repre- sent various response elements in the 5 -flank- lymphocytes produce IgM antibodies that are bound to the cell membrane. Not all elements are shorter protein (IgD) is produced that no longer binds to the cell membrane, but labeled. Regulatory proteins bind to these rather is secreted from the cell. DNA elements and stimulate or inhibit the transcription of the gene. This gene encodes the enzyme phosphoenolpyruvate carboxyki- 2. RNA EDITING nase (PEPCK), which catalyzes a reaction of In some instances, RNA is “edited” after transcription. Although the sequence of the gluconeogenesis (the pathway for production gene and the primary transcript (hnRNA) are the same, bases are altered or of glucose) in the liver. Synthesis of the nucleotides are added or deleted after the transcript is synthesized so that the mature enzyme is stimulated by glucagon (by a mRNA differs in different tissues (Fig. Regulation at the Level of Translation and the element; TRE thyroid hormone response Stability of mRNA element; GRE glucocorticoid response ele- ment; IRE insulin response element. INITIATION OF TRANSLATION In eukaryotes, regulation of gene transcription at the level of translation usually involves the initiation of protein synthesis by eIFs (eukaryotic initiation factors), which are regulated through mechanisms involving phosphorylation (see Chap- ter 15, section V. For example, heme regulates translation of globin mRNA in reticulocytes by controlling the phosphorylation of eIF2 (Fig. In retic- ulocytes (red blood cell precursors), globin is produced when heme levels in the cell are high but not when they are low. Because reticulocytes lack nuclei, glo- bin synthesis must be regulated at the level of translation rather than transcrip- tion. Heme acts by preventing phosphorylation of eIF2 by a specific kinase (heme kinase) that is inactive when heme is bound. Thus, when heme levels are high, eIF2 is not phosphorylated and is active, resulting in globin synthesis. Alternative splicing of the calcitonin gene produces an mRNA for calcitonin in thyroid cells and an mRNA for CGRP in neurons. In thyroid cells, the pre-mRNA from the calcitonin gene is processed to form an mRNA that codes for calcitonin. Cleavage occurs at poly(A) site 1, and splicing occurs along the blue dashed lines. In the brain, the pre-mRNA of this gene undergoes alternative splicing and polyadenylation to produce calcitonin gene-related protein (CGRP). Cleavage occurs at poly(A) site 2, and splicing occurs along the black dashed lines. Another example is provided by insulin, which stimulates general pro- tein synthesis by activating the phosphorylation of an inhibitor of eIF4E, called 4E-BP. When 4E-BP is phosphorylated, it dissociates, leaving eIF4E in the active form. A different mechanism for regulation of translation is illustrated by iron reg- ulation of ferritin synthesis (Fig. Ferritin, the protein involved in the stor- age of iron within cells, is synthesized when iron levels increase. The mRNA for ferritin has an iron response element (IRE), consisting of a hairpin loop near its 5 -end, which can bind a regulatory protein called the iron response element binding protein (IRE-BP). When IRE-BP does not contain bound iron, it binds to the IRE and prevents initiation of translation. When iron levels increase and IRE- BP binds iron, it changes to a conformation that can no longer bind to the IRE on the ferritin mRNA. Therefore, the mRNA is translated and ferritin is pro- duced. Transport and stability of mRNA Stability of an mRNA also plays a role in regulating gene expression, because mRNAs with long half-lives can generate a greater amount of protein than can those with shorter half-lives. The mRNA of eukaryotes is relatively stable (with half-lives measured in hours to days), although it can be degraded by nucleases in the nucleus or cytoplasm before it is translated. To prevent degradation during transport from the nucleus to the cytoplasm, mRNA is bound to proteins that help to prevent its degradation. Sequences at the 3 -end of the mRNA appear to be involved in deter- In addition to stimulating degrada- mining its half-life and binding proteins that prevent degradation. One of these is tion of mRNA, interferon also the poly(A) tail, which protects the mRNA from attack by nucleases. As mRNA causes eIF2 to become phosphory- ages, its poly(A) tail becomes shorter. This is a second mecha- An example of the role of mRNA degradation in control of translation is pro- nism by which interferon prevents synthesis vided by the transferrin receptor mRNA (Fig.

Metabolism of CH3 chylomicrons leads to chylomicron remnant formation order kamagra soft 100 mg with amex erectile dysfunction los angeles. The apoproteins 3 7 (“apo” describes the protein within the shell of the particle in its lipid-free form) not HO only add to the hydrophilicity and structural stability of the particle but have other Deoxycholic acid functions as well: (1) they activate certain enzymes required for normal lipoprotein metabolism and (2) they act as ligands on the surface of the lipoprotein that target specific receptors on peripheral tissues that require lipoprotein delivery for their COO– innate cellular function order kamagra soft 100 mg with visa injections for erectile dysfunction that truly work. Their tissue source buy kamagra soft 100mg mastercard impotence 20s, molecu- CH3 12 lar mass, distribution within lipoproteins, and metabolic functions are shown in Table 34. CH3 The lipoproteins themselves are distributed among eight major classes. Some of their characteristics are shown in Table 34. Each class of lipoprotein has a specific 3 7 function determined by its apolipoprotein content, its tissue of origin, and the pro- HO portion of the macromolecule made up of triacylglycerols, cholesterol esters, free Lithocholic acid cholesterol, and phospholipids (see Tables 34. Structures of the primary and sec- ondary bile salts. The Chylomicrons jugates with taurine or glycine in the liver. After secretion into the intestine, they may be Chylomicrons are the largest of the lipoproteins and the least dense because of their deconjugated and dehydroxylated by the bac- rich triacylglycerol content. They are synthesized from dietary lipids (the “exoge- terial flora, forming secondary bile salts. Note nous” lipoprotein pathway) within the epithelial cells of the small intestine and then that dehydroxylation occurs at position 7, secreted into the lymphatic vessels draining the gut (see Fig. They enter the forming the deoxy family of bile salts. The major apoproteins of chylomicrons are apoB-48, apoCII, and apoE (see Table 34. The apoCII activates lipoprotein lipase 632 SECTION SIX / LIPID METABOLISM Table 34. CHARACTERISTICS OF THE MAJOR APOPROTEINS Primary Tissue Molecular Mass Lipoprotein Apoprotein Source (Daltons) Distribution Metabolic Function ApoA-1 Intestine, liver 28,016 HDL (chylomicrons) Activates LCAT; structural component of HDL ApoA-II Liver 17,414 HDL (chylomicrons) Unknown ApoA-IV Intestine 46,465 HDL (chylomicrons) Unknown (may facilitate transport of other apoproteins between HDL and chylomicrons) ApoB-48 Intestine 264,000 Chylomicrons Assembly and secretion of chylomicrons from small bowel ApoB-100 Liver 540,000 VLDL, IDL, LDL VLDL assembly and secretion structured protein of VLDL, IDL, and LDL ligand for LDL receptor ApoC-1 Liver 6,630 Chylomicrons, Unknown; may inhibit hepatic uptake of VLDL, IDL, HDL chylomicron and VLDL remnants ApoC-II Liver 8,900 Chylomicrons, Cofactor activator of lipoprotein lipase (LPL) VLDL, IDL, HDL ApoC-III Liver 8,800 Chylomicrons, Inhibitor of LPL; may inhibit hepatic uptake of VLDL, IDL, HDL chylomicrons and VLDL remnants ApoE Liver 34,145 Chylomicron Ligand for binding of several lipoproteins to the remnants, VLDL, LDL receptor, to the LDL receptor-related IDL, HDL protein (LRP) and possibly to a separate apo-E receptor. Apo(a) Liver Lipoprotein Unknown “little” a (Lp(a)) (LPL), an enzyme that projects into the lumen of capillaries in adipose tissue, cardiac muscle, skeletal muscle, and the acinar cells of mammary tissue. This activation allows LPL to hydrolyze the chylomicrons, leading to the release of free fatty acids derived from core triacylglycerides of the lipoprotein into these target cells. The mus- cle cells then oxidize the fatty acids as fuel while the adipocytes and mammary cells store them as triacylglycerols (fat) or, in the case of the lactating breast, use them for milk formation. The partially hydrolyzed chylomicrons remaining in the bloodstream (the chylomicron remnants), now partly depleted of their core triacylglycerols, retain their apoE and apoB48 proteins. Receptors in the plasma membranes of the liver cells bind to apoE on the surface of these remnants, allowing them to be taken up by the liver through a process of receptor-mediated endocytosis (see below). Very-Low-Density Lipoproteins (VLDL) If dietary intake of fatty acids exceeds the immediate fuel requirements of the liver, the excess fatty acids are converted to triacylglycerols, which, along with free and esterified cholesterol, phospholipids, and a variety of apoproteins (see Table 34. CHARACTERISTICS OF THE MAJOR LIPOPROTEINS Density Particle Range Diameter Electrophoretic Lipid (%)* Lipoprotein (g/mL) (MM) range Mobility TG Chol PL Function Chylomicrons 0. Abbreviations: TG, Triacylglycerols; Chol, the sum of free and esterified cholesterol; PL, phospholipid; VLDL very-low-density lipoproteins; IDL, intermediate-density lipoproteins; LDL, low-density lipoproteins; HDL, high-density lipoproteins. CHAPTER 34 / CHOLESTEROL ABSORPTION, SYNTHESIS, METABOLISM, AND FATE 633 including apoB-100, apoCII, and apoE, are packaged to form VLDL. These particles are then secreted from the liver (the “endogenous” pathway of lipoprotein metabo- lism) into the bloodstream (Fig. The density, particle size, and lipid content of VLDL particles are given in Table 34. These particles are then transported from the hepatic veins to capillaries in skeletal and cardiac muscle and adipose tissue, as well as lactating mammary tissues, where lipoprotein lipase is activated by apoCII in the VLDL particles. The activated enzyme facilitates the hydrolysis of the triacyl- glycerol in VLDL, causing the release of fatty acids and glycerol from a portion of core triacylglycerols. These fatty acids are oxidized as fuel by muscle cells, used in the resynthesis of triacylglycerols in fat cells, and used for milk production in the lac- tating breast. The residual particles remaining in the bloodstream are called VLDL remnants. Approximately 50% of these remnants are taken up from the blood by liver cells through the binding of VLDL apoE to the hepatocyte plasma membrane apoE receptor followed by endocytic internalization of the VLDL remnant. Intermediate-Density Lipoprotein (IDL) and Low-Density Lipoproteins (LDL) Approximately half of the VLDL remnants are not taken up by the liver but, instead, have additional core triacylglycerols removed to form IDL, a specialized class of VLDL remnants. With the removal of additional triacylglycerols from IDL through the action of hepatic triglyceride lipase within hepatic sinusoids, LDL is generated from IDL. Approximately 60% of the LDL is transported back to the liver, where its apoB-100 binds to specific apoB-100 receptors in the liver cell plasma membranes, allowing particles to be endocytosed into the hepatocyte. The remain- ing 40% of LDL particles are carried to extrahepatic tissues such as adrenocortical Capillary walls Blood Glucose L VLDL P FA TG VLDL VLDL TG L Cholesterol Lysosomes CII Amino acids Muscle FA FA CO2 + H2O Pi FA Glycerol + Glycerol Adipose tissue FA TG Stores IDL Liver H IDL T TG G L LDL Cholesterol Macrophage Amino acids Oxidized FA LDL receptor LDL Pi Glycerol Lysosomes Foam cell Peripheral cells Intima of blood vessel Fig. VLDL triacylglycerol (TG) is degraded by LPL, forming IDL. IDL can either be endocytosed by the liver through a receptor-mediated process or further digested, mainly by hepatic triacylglycerol lipase (HTGL), to form LDL. LDL may be endocytosed by receptor-mediated processes in the liver or in peripheral cells. LDL also may be oxidized and taken up by “scavenger” receptors on macrophages. The scavenger pathway plays a role in atherosclerosis. Some of the cholesterol of the internalized LDL is used for membrane synthesis and vitamin D synthesis as well. If an excess of LDL particles is present in the blood, this specific receptor-mediated uptake of LDL by hepatic and nonhepatic tissue becomes saturated. The “excess” LDL particles are now more readily available for nonspecific uptake of LDL by macrophages (scavenger cells) present near the endothelial cells of arteries. This exposure of vascular endothelial cells to high lev- els of LDL is believed to induce an inflammatory response by these cells, a process suggested to initiate the complex cascade of atherosclerosis discussed below. High-Density Lipoprotein (HDL) The fourth class of lipoproteins is HDL, which plays several roles in whole body lipid metabolism. SYNTHESIS OF HDL HDL particles can be created by a number of mechanisms. The first is synthesis of nascent HDL by the liver and intestine as a relatively small molecule whose shell, like that of other lipoproteins, contains phospholipids, free cholesterol, and a vari- ety of apoproteins, predominant among which are apoA1, apoAII, apoC ,I and apoCII (see Table 34. Very low levels of triacylglycerols or cholesterol esters are found in the hollow core of this early, or nascent, version of HDL. A second method for HDL generation is the budding of apoproteins from chy- lomicrons and VLDL particles as they are digested by lipoprotein lipase. The apoproteins (particularly AI) and shells can then accumulate more lipid, as described below.

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We do not know how much stretching in the relaxed position is required order kamagra soft 100 mg overnight delivery erectile dysfunction protocol program; however generic 100 mg kamagra soft mastercard erectile dysfunction forum discussion, it is probably in the range of 4 to 8 hours per day purchase kamagra soft 100 mg without a prescription xenadrine erectile dysfunction. Other treatments to make muscles grow are poorly documented. There are reports in the literature that claim that muscle growth occurred based on increased range of motion after Botox injections17; however, others, with careful assessment, have not found this to be the case. In an unpublished study, we tried to stretch ham- string muscles in children with the use of knee immobilizer splints. A splint was used every night on one leg but not the other. There was a measurable improvement in the popliteal angle, suggesting increased length in the muscle. However, the major problem was that only 30% of the children could fol- low through a 12-week wearing time on one leg only, which suggests that nighttime splinting does not have good acceptance with families or children. When the goal is to stretch the gastrocnemius, it is very important to realize that this cannot be done without also keep- ing the knee extended. This means nighttime ankle bracing without bracing the knee into extension is worse than not bracing because it only stretches the soleus, which is usually not contracted, and allows the gastrocnemius to further contract because the child will sleep with severe knee flexion. Many therapists believe children should wear ankle-foot orthotics (AFO) at night to stretch the contracted gastrocnemius. However, if only AFOs are used, children will flex the knee and only the soleus gets stretched, further increasing the length difference many children already have between the gastrocnemius and soleus muscles (Figure 7. Stretching the gastrocnemius requires the use of a knee exten- sion splint and a dorsiflexion splint, a combination that is bulky and adds to the poor acceptance. The use of casting adds other problems, especially mus- cle atrophy. One of the most efficient ways to shrink the size of a muscle is to rigidly immobilize the joint in a cast so the muscle has no motion possible. No documentation is available to show that a muscle grows longer if im- mobilized under tension in a cast; however, based on knowledge of how muscle grows, it probably does grow longer in addition to developing severe atrophy. The severe atrophy and temporary nature of the clinical length gain make the use of casting for chronic management of short muscles in children with CP a poor choice. The major problem in the research of muscle growth is the difficulty of measuring muscle growth separate from tendon growth. The mechanical stimuli for growth of these two different anatomic structures, muscles and tendons, somewhat overlap and the effort to cause muscle growth probably causes tendon growth as well. Connective Tissue Mechanics Short muscles in CP are clinically well recognized; however, the problem of excessive length of the tendons is often not recognized. However, surgeons who operate on the tendons fre- quently see tendons that are much too long, as if these tendons were trying to make some adjustment for the very short muscles (Figure 7. Tendons grow by interstitial growth throughout, but most of the growth seems to occur at the tendon–bone interface. The stimulus for increased tendon growth and tendon cross-sectional area growth is not well defined, but depends heavily on the force environment. The regulation of length growth is heavily influenced by tension, but the 264 Cerebral Palsy Management Figure 7. Tendons have a growth plate-like structure at the tendon–bone interface and at the muscle–tendon interface, this structure is a high concentration of satellite cells that contribute to muscle growth. In addition, the muscles and tendons also have some inter- stitial growth ability. Tendons contain mechanoreceptors called Golgi tendon organs, which give feedback to the brain and also influence the sensitivity of muscle spindles. In the presence of spasticity with continuous low-level tension, this system may be altered to accommodate for chronic stimulation, possibly by the system dropping mechanoreceptors. Another connective tissue effect that has been long recognized and recently better quantified is the increase in connective tissue in the muscle in the presence of spasticity. This process of increasing connective tissue seems to get worse with increasing magnitude of spasticity, increasing exposure time to spasticity, and increas- ing age of the patient. This is another component of what is defined as the contracture, but is the least understood element of this pathology. Growth of the Muscle–Tendon Unit The current understanding of growth regulation of a muscle–tendon unit is that the muscle fibers grow in response to stretching of the sarcomeres while they are not actively firing. This stretch has to occur for some amount of time each day. The tendon grows in length by summation of the total tension over time. The specific pattern of maximum to minimum tension is unknown. Another factor that is important but not well understood is the influence of motion, which both muscles and tendons need to have for healthy growth. Defining the specific stimulus for growth of tendons compared with muscles would be a useful research project. The length of the muscle fiber di- rectly determines the active total joint range of motion; however, the muscle rest length plus tendon length defines where that active range of motion occurs. Therefore, if the active range of the ankle is from −20° of dor- siflexion to 60° of plantar flexion, there is no definitely known mechanism to lengthen the muscle fiber and create an active range of muscle activity from 30° of dorsiflexion to 60° of plantar flexion. However, by length- ening the Achilles tendon, we can move the 40° active range to 10° of dorsiflexion to 30° of plantar flexion, a much more useful position of the muscle’s active range of mo- tion. This is the principal function of tendon lengthening in short spastic muscles. The physical impact of a short muscle is to decrease joint range of motion. The physi- cal impact of tendon length is to determine the anatomic range in which a muscle can apply its reduced range-of-motion activity. For example, a 50% decrease in the muscle fiber length of the gastrocsoleus will reduce the avail- able range of motion from 60° to 30°. The length of the tendon then will de- termine if active range of motion occurs from −15° dorsiflexion to 45° plan- tar flexion or if the active range of motion will occur from 10° dorsiflexion to 20° of plantar flexion. The tendon length is the surgically approachable aspect of this problem (Figure 7. By lengthening the tendon, surgeons can choose where to place the active range of motion; however, there is no way of increasing the active range of motion, which would require increasing muscle fiber growth. Usually, if the tendon is found to be shorter than would be functionally ideal, the opposing tendon will be long. For example, with the short gastrocsoleus, the tibialis anterior almost always has a tendon that is causing its active range of motion to also function in equinus. By length- ening the short tendon of the gastrocnemius, the too-long tibialis anterior tendon will spontaneously decrease its muscle fiber length and tendon length. Shortening tendons is seldom required, and except for a few upper extrem- ity tendons, does not work well.

Neurologic Control of the Musculoskeletal System 127 harder to treat something that is not there than to remove something of which there is too much proven kamagra soft 100 mg erectile dysfunction doctor uk. This fact is well demonstrated by all the options that are available to decrease muscle tone in children with spasticity order kamagra soft 100 mg fast delivery injections for erectile dysfunction side effects, whereas there is not one option available to increase muscle tone in hypotonic children kamagra soft 100mg for sale causes of erectile dysfunction in 20s. Stabilizing hyperlaxed joints is limited to either surgery or external orthotics. The main problem of poor sitting is addressed with well-designed seating to provide a stable, upright posture. Foot and ankle orthotics are used to sta- bilize the ankle and feet for standing in standers. These children often require supine standers because of poor head control. When the joint instabilities be- come severe, stabilization by fusion, such as posterior spinal fusion for sco- liosis and foot fusion for planovalgus collapse, is commonly performed. Movement Disorders Movement disorders are primary problems related to the ability of children to develop and control motor movement as a pattern. The specific descrip- tion of these deformities is somewhat confusing and varies among authors of different texts. Although there is a large body of scientific work evaluat- ing the function and pathologies of the brain that lead to movement dis- orders, the complexities are so great that there is still no easy clear explana- tion of how motor control is managed in the brain. The primary lesion in most movement disorders is in the basal ganglion, as demonstrated by the development of posttraumatic dystonia. It is beyond the scope of this text to review all the biochemical and anatomic bases of movement disorders that are currently understood. Understanding the specific pathology in individual children may provide important treatment options, such as medication or surgery. However, in many children, it is impossible to specifically localize the pathology, or if it can be localized, it does not help in directly treating these children. It is extremely important for the clinician treating these children to un- derstand the difference between movement disorders and disorders of tone, meaning primarily spasticity. The treatments for these disorders are often diametrically opposed, especially the options that the orthopaedist would consider. A helpful approach for the orthopaedic clinician who deals with these children is to approach them through the conceptualization of dynamic control theory. In this approach, their function will tend to be drawn toward a chaotic attractor, which is called the movement disorder. Many of these patterns are not clearly separate from each other, and they may be best vi- sualized as different strength attractors. The three movement patterns that can be used to categorize most children with CP are dystonia, athetosis, and chorea or ballismus. Dystonia Dystonia is a movement disorder that has a torsional component with strong muscle contractions with major recurrent movement patterns. An example of such a pattern is strong shoulder external rotation extension and ab- duction combined with elbow extension, then alternating with the opposite extreme of elbow flexion, shoulder internal rotation, adduction, and flexion. Dystonia may occur in a single limb, in a single joint, or as a whole-body 128 Cerebral Palsy Management disorder. These movements cannot be volitionally controlled, although there is a sensory feedback element that sometimes allows them to be stopped or reversed. For example, a specific pressure point or body position may stop the forceful elbow and shoulder external rotation contraction. Sometimes, moving a finger passively will break up the forceful dystonic wrist flexion. There is no good anatomic understanding of how these sensory inputs func- tion. These attractor positions in individual patients become very well recognized and can be described easily by the patients themselves as the positions to which their limbs seem to want to go. As noted earlier, both dystonia and spasticity can be present in the same limb, although in our experience, this is not a common occurrence in localized limb dystonia. The presence of both is much more common in generalized dystonia. It is especially difficult to separate generalized dystonia from gen- eralized spasticity, especially when it presents as extensor posturing with opisthotonic patterning. The difference exists because opisthotonic pattern- ing originates primarily from brainstem defects as opposed to dystonia, which originates primarily from basal ganglion lesions. Also, the children with opisthotonic patterning are often in this hyperextended position all the time, including during sleep. Children with dystonia tend to be in a more relaxed and normal position during sleep. The secondary effects of dystonia and spasticity are also very different. Secondary Effects of Dystonia It cannot be overemphasized how important it is for the orthopaedist to iden- tify isolated limb dystonia from spasticity because on the initial evaluation, for example, the limb may present in fixed wrist and elbow flexed position, which has an appearance exactly like a hemiplegic, spastic limb. This same position occasionally occurs with the foot in equinovarus or planovalgus, having the same initial appearance whether the child is spastic or dystonic. The major difference between spasticity and dystonia is determined by a good physical examination and patient history. On physical examination, it often becomes clear in the limb with dystonia that there is no fixed contracture and the muscle appears to be hypertrophic, like a child who has been a weight lifter. During the examination, the child’s muscles will often release and have a temporary appearance of normal tone. When the muscle releases, the joint will have a full range of motion with no contracture present. This appear- ance is very different compared with a child with a spastic limb in whom the contracted deformity is stiff in all conditions and the muscle often has a short, thin appearance on physical examination. A child with a severe equinovarus positioning of the foot from spasticity will always have some level of muscle contracture present. The important question to ask in the his- tory taking is if the foot or hand ever goes in any other position except the one that it is in now. If the problem is dystonia, the parents and the child of- ten will say very readily that sometimes instead of the wrist being in a flexed position, it is stuck back with the fingers flexed but the wrist extended. The history of how the child positions when relaxed, the appearance of the mus- cles, and the sense of the child’s underlying tone when relaxed are the im- portant parameters to use in separating spasticity from dystonia. This dis- tinction is especially true for a quadriplegic child, where the child with pure dystonia will often have very large well-formed muscles and no underlying contractures. A child with significant hyperextension posturing spasticity 4. Neurologic Control of the Musculoskeletal System 129 often has significant contractures, sometimes of the extensor muscles of the neck and often of hip extensors and quadriceps of the knee. Objective measurement of degrees of dystonia is an extremely difficult problem.


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