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By E. Vigo. College of William and Mary.

Muscle spindles provide information about the muscle Low-threshold motor unit length and the velocity at which the muscle is being Alpha motor stretched buy 25 mg precose with visa. Golgi tendon organs provide information about neurons the force being generated buy generic precose 50mg. Spindles are located in the mass of the muscle purchase 50mg precose, in parallel with the extrafusal muscle fibers. A motor unit consists of Golgi tendon organs are located at the junction of the mus- an alpha motor neuron and the group of extra- fusal muscle fibers it innervates. Functional characteristics, such as cle and its tendons, in series with the muscle fibers (Fig. They occur in CHAPTER 5 The Motor System 93 Secondary Extrafusal Intrafusal endings muscle muscle fibers Afferent fibers Ia II Muscle Efferent spindle Dynamic Primary endings Static Muscle spindle and Golgi ten- FIGURE 5. A, Muscle spindles are located parallel to extrafusal muscle Afferent Nuclear fibers; Golgi tendon organs are in series. B, This en- Golgi Nuclear chain larged spindle shows nuclear bag and nuclear chain tendon bag fiber fiber types of intrafusal fibers; afferent innervation by Ia organ axons, which provide primary endings to both types of fibers; type II axons, which have secondary end- ings mainly on chain fibers; and motor innervation by Bone B the two types of gamma motor axons, static and dy- Tendon namic. The sen- Trail Plate ending sory receptor endings interdigitate with the collagen C A ending fibers of the tendon. The primary endings temporarily such as those of the hand, and in the deep muscles of the cease generating action potentials during the release of a neck. Within the spindle’s expanded middle portion is a fluid- Golgi Tendon Organs. Golgi tendon organs (GTOs) are filled capsule containing 2 to 12 specialized striated muscle 1 mm long, slender receptors encapsulated within the ten- fibers entwined by sensory nerve terminals. The dis- fusal muscle fibers, about 300 m long, have contractile fil- tal pole of a GTO is anchored in collagen fibers of the ten- aments at both ends. The proximal pole is attached to the ends of the tains the cell nuclei (Fig. There are two types of in series with the extrafusal muscle fibers such that con- intrafusal fibers: nuclear bag fibers, named for the large tractions of the muscle stretch the GTO. There are about twice as many nuclear chain eter than the type Ia variety, which innervate the muscle fibers as nuclear bag fibers per spindle. Muscle contraction stretches the GTO and gener- type fibers are further classified as bag1 and bag2, based on ates action potentials in type Ib axons. The GTO output whether they respond best in the dynamic or static phase of provides information to the central nervous system about muscle stretch, respectively. Sensory axons surround both the noncontractile mid- Information entering the spinal cord via type Ia and Ib portion and paracentral region of the contractile ends of axons is directed to many targets, including the spinal in- the intrafusal fiber. The sensory axons are categorized as terneurons that give rise to the spinocerebellar tracts. The axons of These tracts convey information to the cerebellum about both types are myelinated. Type Ia axons are larger in di- the status of muscle length and tension. Alpha motor neurons innervate shaped endings that wrap around the middle of the intra- the extrafusal muscle fibers, and gamma motor neurons in- fusal muscle fiber (see Fig. Cells bodies of both alpha and clear chain fibers are innervated by type Ia axons. Type II gamma motor neurons reside in the ventral horns of the axons innervate mainly nuclear chain fibers and have nerve spinal cord and in nuclei of the cranial motor nerves. This high number reflects the com- ings of both primary and secondary sensory axons of the plex role of the spindles in motor system control. Intrafusal muscle spindles respond to stretch by generating action po- muscle fibers likewise constitute a significant portion of the tentials that convey information to the central nervous sys- total number of muscle cells, yet they contribute little or tem about changes in muscle length and the velocity of nothing to the total force generated when the muscle con- 94 PART II NEUROPHYSIOLOGY A R Ia Response Passive stretch of muscle fibers from resting length Tension Wt. T Passive stretch B Ia response ceases R Stimulate alpha Ia Response motor neuron Tension Wt.

Metabolic enzymes (C) also show regional variations in their distribution buy precose 50 mg free shipping. Activity of oxidative enzymes is generally higher in gray matter than in white matter purchase precose 25mg otc. Histochemistry of the Brain Stem 149 2 A Iron content of red nucleus and substantia nigra in humans 1 (according to Spatz) 4 5 3 B Distribution of norepine- phrine and dopamine in the human brain stem 1 C Activity of succinate dehydro- genase in the medulla oblongata of a rabbit 9 (according to Friede) 7 10 8 6 Kahle buy precose 50mg line, Color Atlas of Human Anatomy, Vol. Cerebellum Structure 152 Functional Organization 162 Pathways 164 Kahle, Color Atlas of Human Anatomy, Vol. It receives the large develops from the alar plate of the brain corticocerebellar tracts from the cerebral stem and forms the roof of the fourth ven- cortex via the pontine nuclei (pontocerebel- tricle. The superior surface (C) is covered by lum) and represents the apparatus for fine- the cerebrum. There is an unpaired central part, Traditional Nomenclature the vermis of the cerebellum (ACD1, B), and The individual sections of the cerebellum the two cerebellar hemispheres. This triparti- have traditional names unrelated to their tion is only visible at the inferior surface, development or function. According to this where the vermis forms the floor of a fossa, classification, most sections of the vermis the vallecula of the cerebellum (D2). The sur- are associated with a pair of hemispheric face of the cerebellum exhibits numerous lobes: the central lobule (A–C9) with the narrow, almost parallel convolutions, the wing of the central lobule (A14) on each side, folia of the cerebellum. Accordingly, the cerebel- lunar lobule (AD21) and part of the gracile lum is subdivided into two parts, the floc- lobule (AD22), the pyramid (ABD12) with culonodular lobe and the cerebellar body (A3). The cerebellar body is further tonsilla (A24) and the paraflocculus (A25), subdivided by the primary fossa (AC5) into and the nodulus (AB26) with the flocculus anterior lobe and posterior lobe. Flocculonodular Lobe (A6) The pale red arrow A in diagram B refers to Together with the lingula (AB7), this is the the direction of viewing the anterior surface oldest portion (archicerebellum). Anterior Lobe of the Cerebellar Body (A8) This is a relatively old component; together with its central sections, which belong to the vermis (central lobule [A–C9], culmen [A–C10]) and other sections of the vermis (uvula [ABD11], pyramid [ABD12]), it forms the paleocerebellum. It receives the spinocerebellar tracts for proprioceptive sensibility from the muscles (spinocerebel- lum) (p. Subdivision of the Cerebellum 153 7 9 14 8 10 15 5 17 16 3 18 19 20 1 13 21 C 12 22 11 23 24 6 25 10 26 16 18 4 20 A Subdivision of cerebellum 27 9 A 12 7 B Median section 11 through the 26 vermis 15 17 9 5 D 19 10 1 16 18 C View from above 2 21 20 1 12 19 22 11 23 27 D View from below Kahle, Color Atlas of Human Anatomy, Vol. The dentate nucleus (B21) appears as a heavily folded band with the medial Anterior Surface (A) part remaining open (hilum of dentate nu- On both sides, the cerebellum is connected cleus). The cortical fibers of the hemisphere to the brain stem by the cerebellar peduncles terminate in the dentate nucleus, and fibers (A1). All afferent and efferent pathways extend from here as superior cerebellar pass through them. Cerebellar Peduncles (A, C) Between the cerebellar peduncles lies the The efferent and afferent pathways of the roof of the fourth ventricle with the superior cerebellum run through three cerebellar medullary velum (A2) and the inferior peduncles: medullary velum (A3). The inferior cerebellar peduncle (restiform (A4), the central lobule (A5), the nodulus body) (AC22), which ascends from the (A6), the uvula (A7), and also the flocculus lower medulla oblongata; it contains the (A8). The vallecula of the cerebellum (A9) is spinocerebellar tracts and the connec- surrounded on both sides by the tonsillae tions to the vestibular nuclei (A10). The medial cerebellar peduncle (brachium pontis) (AC23) with the fiber masses The following parts are also visible: biven- from the pons, which originate from the tral lobule (A11), superior semilunar lobule pontine nuclei and represent the con- (A12), inferior semilunar lobule (A13), tinuation of the corticopontine tracts simple lobule (A14), quadrangular lobule! The superior cerebellar peduncle (brachium (A15), and wing of the central lobule (A16). It receives fibers from the cortex of the vermis, the vestibular nuclei, and the olive. It sends fibers to the vestibular nuclei and other nuclei of the medulla oblongata. The globose nucleus (B19), too, is thought to receive fibers from the cortex of the vermis and to send fibers to the nuclei of the medulla oblongata. Fibers of the cerebellar cortex from the region between vermis and hemisphere (intermediate part) are thought to terminate at the hilum of the dentate nu- cleus in the emboliform nucleus (B20). The fibers of the latter nucleus run through the Kahle, Color Atlas of Human Anatomy, Vol.

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Florida Governor’s Select Task Force on Healthcare Professional Liability Insurance precose 25mg visa. Chapter 17 / New Directions in Liability Reform 247 17 New Directions in Medical Liability Reform William M precose 25 mg discount. Sage buy precose 25 mg without a prescription, MD, JD SUMMARY Medical malpractice is the “Rip van Winkle” issue in American health care. However, its periodic awakenings depart from those of its fictional counterpart in an important respect. Neither the participants in the medical malpractice system nor outside observ- ers seem aware that the context for minimizing medical errors, improving legal dispute resolution, and keeping liability insur- ance available and affordable has changed. This chapter explains why the public policy of medical malpractice is so poorly con- nected to overall health policy. It examines three aspects of health system change since the 1970s—medical progress, industrializa- tion, and cost containment—that have exposed serious weaknesses in the medical liability system. It suggests ways to convert liability into a general health policy issue, including having the federal government implement a system of error identification, fair com- pensation, and efficient dispute resolution that would apply to Medicare and Medicaid patients. Key Words: Medical malpractice; tort liability; medical technol- ogy; health insurance; Medicare; managed care; patient safety; medical errors; litigation; liability insurance. In 2002, liability insurance premiums rose suddenly from their stupor after slumbering—sometimes peacefully, sometimes fitfully—for nearly two decades. Much as Washington Irving’s hero found his physi- cal surroundings unlike those he remembered, today’s malpractice sys- tem faces a landscape of health care financing and delivery that has changed much since its last awakening. Rip van Winkle slept through the American revolution, and the intervening years between the last malpractice crisis and the present one have witnessed equally dramatic changes wrought by medical technology, consumer demand, managed care, and Medicare cost containment. Unlike its fictional counterpart, however, the malpractice system does not strike most observers as anachronistic. When Rip van Winkle wandered down from the hills, the townspeople noticed immediately that his musket was antiquated and his clothes were outdated. This is not so for medical liability, although it has been largely out of sight and out of mind (at least for physicians) since the 1980s. With few exceptions, stakeholders and their political allies on both sides of the tort reform debate invoke the same explana- tions and propose the same legislation as they did 20 years ago: mea- sures discouraging lawsuits and limiting damage awards that are at best incomplete and at worst obsolete. To switch metaphors, several commentators have described the current liability insurance crisis as a “perfect storm. These include large jury awards and settlements, harsh eco- nomic conditions that reduce returns on funds invested by liability insurers, a spate of pull-outs and insolvencies among carriers, and a series of catastrophes unrelated to health care that have caused a global contraction in reinsurance capital. However, sailors in the right vessel using proper tactics can ride out even the most severe weather. A properly designed liability system that reduces the incidence of medi- cal error, limits unnecessary monetary and psychic costs associated with redressing injury, and bears residual insurance risk efficiently would have much greater resilience in troughs of the insurance cycle than the structures and processes currently being used. Unfortunately, the storm analogy—which is used to convey the gravity of the current predicament—carries with it a sense of helplessness as well. There- fore, most malpractice reform proposals at most try to steer flimsy craft into (hopefully) calmer waters. Relatively little attention is paid Chapter 17 / New Directions in Liability Reform 249 to re-engineering the system to survive harsh conditions, although forecasts for the future remain rather bleak. In other words, time and tide have changed both the medical mal- practice problem and its range of potential solutions. Yet the evolution of the health care system since the malpractice crisis of the 1980s has gone unrecognized by policymakers and partisans where liability is concerned. Doctors and Lawyers One can identify several possible explanations for the failure of the political process to integrate liability policy with overall health policy. From the perspective of doctors and lawyers—the key stakeholders in the continuing battle over tort reform—the implications of changing the health system muddy the “message” of their campaigns.

Can Assoc Radiol J count the clinical presentation discount precose 25 mg overnight delivery, physical appearance and 4:299-301 the results of appropriate lab tests buy precose 25mg low cost, can lead to prompt 17 precose 25mg on line. Tehranzadeh J, Ter-Organesyan RR, Steinbach LS (2004) recognition of the infection and institution of therapy. In Musculoskeletal disorders associated with HIV infection and selected cases, advanced imaging techniques can be cost- AIDS: Part I: Infectious musculoskeletal conditions. Lazzarini L, Mader JT, Calhoun JH (2004) Osteomyelitis in Radiology of skeletal tuberculosis. Santiago Restrepo C, Gimenez CR, McCarthy K (2003) as multifocal lytic cortical lesions in the femur. Skeletal Radiol Imaging of osteomyelitis and musculoskeletal soft tissue in- 33:244-247 fections: current concepts. Hugosson C, Nyman RS, Brismar J, Lrsson SG, Lindahl S, 109 Lundstedt C (1996) Imaging of tuberculosis. Karchevsky M, Schweitzer ME, Morrison WB, Parellada JA Schepper AM (2003) Imaging features of musculoskeletal tu- (2004) MRI findings of septic arthritis and associated os- berculosis. Horger M, Eschmann SM, Pfannenberg C, Storek D, Magnetic resonance imaging in coccidioidal arthritis. Skeletal Dammann F, Vonthein R, Claussen CD, Bares R (2003) The Radiol 25:661-665 IDKD 2005 Peripheral Arthritis L. Resnik2 1 Department of Radiology, University of Arizona Health Sciences Center, AZ, USA 2 Depatment of Diagnostic Radiology, University of Maryland Medical System, MD, USA Introduction radiographic characteristics at each individual joint, the distribution of joint involvement, and the presence or ab- Radiographs are used in peripheral arthritis to confirm sence of other ancillary radiographic findings. The radiographic findings may be either process is limited to one joint (monoarticular) or involves consistent or inconsistent with the clinical diagnosis. Each joint disease has a inconsistent, alternative diagnosis should be made on the characteristic distribution of joint involvement (Fig. This pattern is based on the or asymmetrically (involvement of a joint on one side Fig. Sites and distribution of com- mon arthritides of the hand (A) and foot (B). The more common sites are encircled with thick lines and the less common sites with thin lines. Note the periosteal reaction or new-bone forma- tion classically identified in Reiter’s disease. Note also the potential for “sausage digit” dis- tribution in psoria- sis. When joints are encircled in isola- tion, the distribution is random and may be isolated to any joint 144 L. Resnik without simultaneous involvement of the corresponding The distribution of joint involvement is characteris- joint on the opposite side). The disease begins in the PIP, MCP, and carpal The specific radiographic characteristics of impor- joints with a more or less symmetrical distribution in tance in establishing or confirming the diagnosis often the right and left extremities. In some cases, the joints are the following: (1) whether the joint space narrowing of the hand and wrist are equally affected, but in others is symmetrical or asymmetrical; (2) whether soft-tissue the destructive process may be much more severe in the swelling is present and whether it is symmetrical (indi- hand than in the carpus. In still others, it may be more cating a joint effusion) or asymmetrical (indicating a pe- severe in the carpus than in the hand. In the foot, the riarticular mass); and the presence or absence of (3) pe- metatarsophalangeal (MTP) joints, particularly the riarticular osteoporosis, (4) periarticular erosions, and (5) fourth and fifth, are often involved in the initial stage spur formation. In fact, characteristic changes of Ancillary radiographic findings include the presence erosion may be present in the heads of the fourth or or absence of periosteal reaction of bones in the vicinity fifth metatarsal when the radiographic changes of the of the involved joint. Therefore, it is im- calcification within the joint cartilage (chondrocalci- portant to examine not only the hands but also the feet nosis) is to be noted. Laboratory values of importance are the erythro- granulation tissue (pannus) at the peripheral margin of cyte sedimentation rate; the presence or absence of serum the joint cartilage.

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