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vical arthritis or gallbladder disease, causing low-grade discomfort by constantly activating their particular segmental neurons, may induce a shift of cardiac pain cephalad or caudad from its usual locale Once it becomes chronic, any pain may spread quite widely in a vertical direction on one side of the body On the other hand, painful stimuli arising from a distant site exert an inhibitory effect on segmental nociceptive exion re exes in the leg, as demonstrated by DeBroucker and colleagues Yet another clinical peculiarity of segmental pain is the reduction in power of muscle contraction that it may cause (re ex paralysis or algesic weakness) Chronic Pain One of the most perplexing issues in the study of pain is the manner in which chronic pain syndromes arise Several theories have been offered, none of which satisfactorily account for all the clinically observed phenomena One hypothesis proposes that in an injured nerve, the unmyelinated sprouts of A- and C bers become capable of spontaneous ectopic excitation and afterdischarge and susceptible to ephaptic activation (see summary by Rasminsky) A second proposal derives from the observation that these injured nerves are also sensitive to locally applied or intravenously administered catecholamines because of an overabundance of adrenergic receptors on the regenerating bers Either this mechanism or ephapsis (nerve-to-nerve cross-activation) is thought to be the basis of causalgia (persistent burning and aching pain in the territory of a partially injured nerve and beyond) and its associated re ex sympathetic dystrophy; either would explain the relief afforded in these conditions by sympathetic block This subject is discussed in greater detail in relation to peripheral nerve injuries (see pages 121 and 189) Central sensory structures, eg, sensory neurons in the dorsal horns of the spinal cord or thalamus, if chronically bombarded with pain impulses, may become autonomously overactive (being maintained in this state perhaps by excitatory amino acids) and may remain so even after the peripheral pathways have been interrupted Peripheral nerve lesions have been shown to induce enduring derangements of central (spinal cord) processing (Fruhstorfer and Lindblom) For example, avulsion of nerves or nerve roots may cause chronic pain even in analgesic zones (anesthesia dolorosa or deafferentation pain ) In experimentally deafferented animals, neurons of lamina V begin to discharge irregularly in the absence of stimulation Later the abnormal discharge subsides in the spinal cord but can still be recorded in the thalamus Hence, painful states such as causalgia, spinal cord pain, and phantom pain are not abolished simply by cutting spinal nerves or spinal tracts Certainly none of these phenomena can adequately explain the entire story of chronic pain One suspects that structural changes in the cord, of the type alluded to above, are able to produce persistent stimulation of pain pathways Newer insights into the molecular changes in the spinal cord that may give rise to persistence of the pain after the cessation of an injurious episode are reviewed by Indo and colleagues It is an open question whether the early treatment of pain may prevent the cascade of biochemical events that allows for both spread and persistence of pain in conditions such as causalgia Pain has several other singular attributes It does not appear to be subject to negative adaptation ie, pain may persist as long as the stimulus is operative whereas other somatic stimuli, if applied continuously, soon cease to be perceived Furthermore, prolonged stimulation of pain receptors sensitizes them, so that they become responsive to even low grades of stimulation, even to touch (allodynia).

9:

Figure 34-13 (Continued)

Signs and symptoms 1 Medial medullary syndrome (occlusion of vertebral artery or branch of vertebral or lower basilar artery) a On side of lesion (1) Paralysis with later hemiatrophy of the tongue b On side opposite lesion (1) Paralysis of arm and leg sparing face (2) Impaired tactile and proprioceptive sense over half the body 2 Lateral medullary syndrome (occlusion of any of ve vessels may be responsible vertebral, posterior inferior cerebellar, or superior, middle, or inferior lateral medullary arteries) a On side of lesion (1) Pain, numbness, impaired sensation over half the face (2) Ataxia of limbs, falling to side of lesion (3) Vertigo, nausea, vomiting (4) Nystagmus, diplopia, oscillopsia (5) Horner syndrome (miosis, ptosis, decreased sweating) (6) Dysphagia, hoarseness, paralysis of vocal cord, diminished gag re ex (7) Loss of taste (rare) (8) Numbness of ipsilateral arm, trunk, or leg (9) Hiccup b On side opposite lesion (1) Impaired pain and thermal sense over half the body, sometimes face 3 Total unilateral medullary syndrome (occlusion of vertebral artery); combination of medial and lateral syndromes 4 Lateral pontomedullary syndrome (occlusion of vertebral artery); combination of medial and lateral syndromes 5 Basilar artery syndrome (the syndrome of the lone vertebral artery is equivalent); a combination of the various brainstem syndromes plus those arising in the posterior cerebral artery distribution The clinical picture comprises bilateral long-tract signs (sensory and motor) with cerebellar and cranial nerve abnormalities a Paralysis or weakness of all extremities, plus all bulbar musculature b Diplopia, paralysis of conjugate lateral and/or vertical gaze, internuclear ophthalmoplegia, horizontal and/or vertical nystagmus c Blindness, impaired vision, various visual eld defects d Bilateral cerebellar ataxia e Coma f Sensation may be strikingly intact in the presence of almost total paralysis Sensory loss may be syringomyelic or the reverse or involve all modalities

Descending tract and nucleus of fth nerve Uncertain restiform body, cerebellar hemisphere, olivocerebellar bers, spinocerebellar tract ( ) Vestibular nuclei and connections Vestibular nuclei and connections Descending sympathetic tract Issuing bers ninth and tenth nerves Nucleus and tractus solitarius Cuneate and gracile nuclei Uncertain Spinothalamic tract

Options quotes seem like cryptic code with no rationale, but once you learn the system, you will be able to quickly work through the options quotes Let s take a look at equities rst because they are a bit more complex then their futures counterparts An equity option symbol is made up of three parts: rst the root symbol, then a month code, and nally a strike price code Equity option symbol Root option symbol strike price code month code

Corticobulbar and corticospinal tracts bilaterally Ocular motor nerves, apparatus for conjugate gaze, medial longitudinal fasciculus, vestibular apparatus Visual cortex Cerebellar peduncles and the cerebellar hemispheres Tegmentum of midbrain, thalami Medial lemniscus, spinothalamic tracts or thalamic nuclei

nod to Crystal Reports When business users talk about Crystal Reports we talk mostly about the formatted reporting coming from this component Several layers of integration make up Crystal Reports, but the other components deal with the user interface, server setup for distribution of reports, and other activities that allow users to share the formatted reports Crystal Reports is designed to work with your database to help you analyze and interpret important information Crystal Reports makes it easy to create simple reports, and it also has the comprehensive tools you need to produce complex or specialized reports Crystal Reports is designed to produce the required reports from both SAP and non-SAP data sources The ability to log on and quickly get up and running with Crystal Reports is enhanced by built-in report wizards to guide you step by step through building reports and completing common reporting tasks Crystal Reports has many of the same functions (such as formulas, cross-tabs, subreports, and conditional formatting) that most other reporting toolsets have, but the primary difference between Crystal Reports and the others is the formatting functionality The following illustration shows the initial worksheet or designer for Crystal Reports

sis, ptosis, decreased sweating); issuing bers of the ninth and tenth nerves (hoarseness, dysphagia, ipsilateral paralysis of the palate and vocal cord, diminished gag re ex); otolithic nucleus (vertical diplopia and illusion of tilting of vision); olivocerebellar and/or spinocerebellar bers and restiform body and inferior cerebellum (ipsilateral ataxia of limbs, falling or toppling to the ipsilateral side, or lateropulsion); descending tract and nucleus of the fth nerve