By H. Fraser. Haverford College. 2018.
Fibers from area 4 occupy the genu of ticonuclear ﬁbers to the nucleus ambiguus may result in weakness of the internal capsule buy generic zenegra 100mg erectile dysfunction options, but those from the frontal eye ﬁelds (areas 8 generic zenegra 100 mg free shipping erectile dysfunction home remedies,6) may palatal muscles contralateral to the lesion; the uvula will deviate to- traverse caudal portions of the anterior limb, and some (from areas wards the ipsilateral (lesioned) side on attempted phonation. In addi- 3,1,2), may occupy the most rostral portions of the posterior limb. In contrast to from area 4 terminate in, or adjacent to, cranial nerve motor nuclei ex- the alternating hemiplegia seen in some brainstem lesions, hemisphere cluding those of III, IV, and VI. In addition, it is important to note the following: 1) vertical gaze palsies (midbrain), 2) the Parinaud syn- that descending cortical ﬁbers (many arising in areas 3, 1, 2) project to drome—paralysis of upward gaze (tumors in area of pineal), 3) internu- sensory relay nuclei of some cranial nerves and to other sensory relay clear ophthalmoplegia (lesion in MLF between motor nuclei of III and nuclei in the brainstem, such as those of the posterior column system. VI), 4) horizontal gaze palsies (lesion in PPRF), or 5) the one-and-a-half Neurotransmitters: Glutamate ( ) is found in many corticofu- syndrome. In the latter case, the lesion is adjacent to the midline and in- gal axons that directly innervate cranial nerve motor nuclei and in volves the abducens nucleus and adjacent PPRF, internuclear ﬁbers those ﬁbers that terminate near (indirect), but not in, the various mo- from the ipsilateral abducens that are crossing to enter the contralat- tor nuclei. The cerebral artery occlusion) or the internal capsule (as in lacunar strokes result is a loss of ipsilateral abduction (lateral rectus) and adduction or occlusion of lenticulostriate branches of M1) give rise to a con- (medial rectus, the “one”) and a contralateral loss of adduction (medial tralateral hemiplegia of the arm and leg (corticospinal ﬁber involve- rectus, the “half ”); the only remaining horizontal movement is con- ment) coupled with certain cranial nerve signs. Strictly cortical lesions tralateral abduction via the intact abducens motor neurons. Abbreviations AbdNu Abducens nucleus OcNu Oculomotor nucleus AccNu Accessory nucleus (spinal accessory nu. Many of brainstem and spinal cord, and the general distribution of tectospinal reticulospinal ﬁbers inﬂuence the activity of lower motor neurons. Tectospinal ﬁbers originate from deeper lay- Clinical Correlations: Isolated lesions of only tectospinal and ers of the superior colliculus, cross in the posterior (dorsal) tegmental reticulospinal ﬁbers are essentially never seen. Tectospinal ﬁbers pro- decussation, and distribute to cervical cord levels. Several regions of ject to upper cervical levels where they inﬂuence reﬂex movement of cerebral cortex (e. Such movements may be diminished or slowed in tum, but the most highly organized corticotectal projections arise from patients with damage to these ﬁbers. Pontoreticulospinal ﬁbers (medial reticulospinal) ulospinal) ﬁbers are excitatory to extensor motor neurons and to neu- tend to be uncrossed, while those from the medulla (bulboreticu- rons innervating axial musculature; some of these ﬁbers may also in- lospinal or lateral reticulospinal) are bilateral but with a pronounced hibit ﬂexor motor neurons. Corticoreticular ﬁbers are bilateral with a (lateral reticulospinal) ﬁbers are primarily inhibitory to extensor mo- slight contralateral preponderance and originate from several cortical tor neurons and to neurons innervating muscles of the neck and back; areas. Neurotransmitters: Corticotectal projections, especially those Reticulospinal (and vestibulospinal) ﬁbers contribute to the spasticity from the visual cortex, utilize glutamate ( ). This substance is also that develops in patients having lesions of corticospinal ﬁbers. Some neurons of the giganto- reticulospinal and vestibulospinal ﬁbers (see Figure 7-13 on page 196) cellular reticular nucleus that send their axons to the spinal cord, as also contribute to the tonic extension of the arms and legs seen in de- reticulospinal projections, contain enkephalin ( ) and substance P cerebrate rigidity when spinal motor neurons are released from de- ( ). Enkephalinergic reticulospinal ﬁbers may be part of the descend- scending cortical control. Abbreviations ALS Anterolateral system PO Principal olivary nucleus ATegDec Anterior tegmental decussation PTegDec Posterior tegmental decussation (rubrospinal ﬁbers) (tectospinal ﬁbers) BP Basilar pons Py Pyramid CC Crus cerebri RB Restiform body CRet Corticoreticular ﬁbers RetNu Reticular nuclei CTec Corticotectal ﬁbers RetSp Reticulospinal tract(s) GigRetNu Gigantocellular reticular nucleus RNu Red nucleus LCSp Lateral corticospinal tract RuSp Rubrospinal tract ML Medial lemniscus SC Superior colliculus MLF Medial longitudinal fasciculus SN Substantia nigra MVNu Medial vestibular nucleus SpVNu Spinal (or inferior) vestibular nucleus OcNu Oculomotor nucleus TecSp Tectospinal tract Review of Blood Supply to SC, Reticular Formation of Pons and Medulla, and TecSp and RetSp Tracts in Cord STRUCTURES ARTERIES SC long circumferential branches (quadrigeminal branch) of posterior cerebral plus some from superior cerebellar and posterior choroidal (see Figure 5–27) Pontine Reticular long circumferential branches of basilar plus branches of superior Formation cerebellar in rostral pons (see Figure 5–21) Medullary Recticular branches of vertebral plus paramedian branches of basilar at Formation medulla-pons junction (see Figure 5–14) TecSp and RetSp branches of central artery (TecSp and Medullary RetSp); Tracts penetrating branches of arterial vasocorona (Pontine RetSp) (see Figures 5–14 and 5–6) Motor Pathways 195 Tectospinal and Reticulospinal Tracts CRet CTec Postition of TecSp and RetSp SC CTec SC PTegDec TecSp ML RNu CRet SN PTegDec (TecSp) CRet CC ATegDec (RuSp) MLF Pontine RetNu: oralis TecSp RetNu of Pons caudalis ML ALS BP InfVNu Pontine RetSp MVNu RB MLF TecSp ALS GigRetNu GigRetNu PO ML Pontine RetSp Py TecSp Medullary RetSp LCSp Medullary RetSp to Laminae VII ALS (VI,VII, IX) TecSp Pontine RetSp to Laminae VI, VII (VIII) to Laminae VIII of cervical levels (VII,IX) 196 Synopsis of Functional Components, Tracts, Pathways, and Systems Rubrospinal and Vestibulospinal Tracts 7–13 The origin, course, and position in representative cross-sec- Clinical Correlations: Isolated injury to rubrospinal and vestibu- tions of brainstem and spinal cord, and the general distribution of lospinal ﬁbers is really not seen in humans. Rubrospinal ﬁbers cross in the an- movements seen in monkeys following experimental rubrospinal le- terior (ventral) tegmental decussation and distribute to all spinal levels sions may be present in humans. However, these deﬁcits are over- although projections to cervical levels clearly predominate. Cells in dor- shadowed by the hemiplegia associated with injury to the adjacent cor- somedial regions of the red nucleus receive input from upper extremity ticospinal ﬁbers. The contralateral tremor seen in patients with the areas of the motor cortex and project to cervical cord, but those in ven- Claude syndrome (a lesion of the medial midbrain) is partially related to trolateral areas of the nucleus receive some ﬁbers from lower extremity damage to the red nucleus as well as to the adjacent cerebellothalamic areas of the motor cortex and may project in sparse numbers to lum- ﬁbers. These patients may also have a paucity of most eye movement bosacral levels. The red nucleus also projects, via the central tegmental on the ipsilateral side and a dilated pupil (mydriasis) due to concurrent tract, to the ipsilateral inferior olivary complex (rubroolivary ﬁbers). Medial and lateral vestibular nuclei give rise to the medial and lateral Medial vestibulospinal ﬁbers primarily inhibit motor neurons inner- vestibulospinal tracts, respectively. The former tract is primarily ipsi- vating extensors and neurons serving muscles of the back and neck. Lat- lateral, projects to upper spinal levels, and is considered a component eral vestibulospinal ﬁbers may inhibit some ﬂexor motor neurons, but of the medial longitudinal fasciculus in the spinal cord. The latter tract they mainly facilitate spinal reﬂexes via their excitatory inﬂuence on spinal is ipsilateral and somatotopically organized; ﬁbers to lumbosacral levels motor neurons innervating extensors.
Under the first option buy zenegra 100mg otc impotence vs sterile, provider organizations that elected to participate in a given state would receive limited immu- nity from tort suits and federal subsidies for excess liability coverage in exchange for establishing systems for detecting and preventing medical errors and promptly paying economic loss and predefined noneconomic damages for identified classes of avoidable injuries discount 100mg zenegra otc erectile dysfunction vitamin e. Under the second option, all health care providers in the state would be subject to a fed- Chapter 17 / New Directions in Liability Reform 273 erally funded, state-run administrative adjudication system for avoid- able injuries based on predetermined schedules of noneconomic dam- ages, which would replace open-ended tort liability. The IOM recommendation draws heavily on prior research—nota- bly “early offers,” ACEs, and enterprise liability—and is sketchy on details. Still, it has five virtues that distinguish it from other reform proposals. First, it explicitly addresses malpractice reform as a compo- nent of overall health care reform (74). Second, it recognizes the need for targeted financial support to help relieve the current malpractice crisis. Third, it seeks to make compensation for avoidable injury faster and more predictable and not simply to reduce the volume of litigation. Fourth, it fosters sound medical relationships by emphasizing apology and explanation (29,75) and involving patients in the process of iden- tifying and preventing medical errors. Finally, it allows for variation and choice in the health care system rather than assuming that all health care providers, however organized, have the same capacity to improve patient safety (76). A MALPRACTICE SYSTEM FOR MEDICARE AND MEDICAID Getting the Medicare program off the sidelines in the malpractice debate is the surest way to connect the liability and health insurance markets and potentially relieve the strain on the health care system created by the current malpractice crisis. The federal Centers for Medi- care and Medicaid Services (CMS) undoubtedly recognize the potential for malpractice liability to destabilize access to care for Medicare ben- eficiaries in the short term and increase program costs in the long term. However, its forays into medical malpractice reform have essentially been limited to supporting the Bush Administration’s overall prefer- ences for restrictions on general tort litigation (44). Instead, CMS should propose a system of error identification, fair compensation, and dispute resolution that would apply specifically to Medicare and Medicaid patients. The framework of such a system could be adopted by administrative rulemaking, although making it fully operational would likely require congressional action. Because of the voting power of the elderly, converting malpractice liability into a Medicare issue is politically perilous. Since its enactment, Medicare has been largely responsible for funding medical progress, promoting industrialization, and (more recently) imposing cost constraints—the forces described earlier as being prima- rily responsible for the current malpractice crisis: Medicaid has become the largest government health program, and pays for roughly half of 274 Sage U. Therefore, Medicare and Medicaid offer the most visible forum for debating the relationship between what America invests in health care and what it expects to receive when health care goes awry. Moreover, a system that provided immediate information and prompt compensation would have substantial advantages over conventional litigation for elderly claimants. EMPLOYER-SPONSORED HEALTH CARE AND THE WORKERS COMPENSATION ANALOGY Employer-sponsored private health insurance covers most Ameri- cans. Therefore, the current malpractice crisis affects the ability of businesses to attract and retain workers. Active involvement in health care purchasing also has made business better attuned to employees’ experiences as users of medical services. Moreover, industry’s contin- ued tolerance of avoidable physical harm in the health care system, especially when it is traceable to faulty systems design, contrasts sharply with general regulatory and self-regulatory changes since the 1960s, which have created a corporate culture exquisitely sensitive to health and safety issues and their relationship to productivity. Finally, health care is an economic engine throughout the country; liability crises reduce present-day prosperity and jeopardize future prospects. To address these issues, the business community could broker a com- promise approach to malpractice mirroring workers’ compensation, that limits liability but retains incentives for safety and assures prompt, reasonable payment in the event of injury. To accomplish this, employ- ers would need to set aside their parochial interests in using the mal- practice crisis as a poster child for general business tort reform to further their workers’ interests in safe, reliable health care. CONCLUSION This chapter analyzes the first medical malpractice insurance crisis of the 21st century in light of significant changes that have occurred in the health care system since previous crises. It concludes that the established debate over traditional tort reform incompletely defines current problems and leads to ineffective solutions. The chapter began by analogizing the malpractice crisis to the legend of Rip van Winkle and concludes with a different literary parallel.
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