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In their description of this coin spasms and cramps buy zanaflex with american express, Moorhead and Cook (2012: 404) provide a tentative terminus post quem of 1245 for the deposition of the remains within the pit of burial 110 spasms 1983 download buy zanaflex 2 mg on line. It is therefore possible that spasms trapezius discount zanaflex 2 mg with mastercard, being located at the top of the deposit muscle relaxant usage 4mg zanaflex with mastercard, the coin may have been deposited subsequent to the deposition of the human remains muscle relaxant pregnancy proven zanaflex 4mg, potentially much later spasms mid back discount zanaflex 2mg without prescription, with its association possibly coincidental. Deriving from context 4147, part of burial 101, the outlying dentine sample is more problematic. These two samples derived from the same side of the same mandible, yet the later developing tooth was indicated to be older than its developmental precedent. Furthermore, the two teeth demonstrate only three years of overlap between their posterior probability distributions (see Table 16 and Figure 89). It is generally accepted that there is a development interval of approximately ten years between the first and third molar teeth (AlQahtani et al. The samples were taken from approximately the same region, the upper root dentine and in theory together they should demonstrate an overlap of at least ten years. If these remains date to the 11th or 12th century, it is highly unlikely they would have retained such an advanced degree of articulation relative to all other remains within the two deposits, which the majority of the samples indicate date to the early to mid-13th century. It seems more likely then that contamination of the sample is the cause of such an early date relative to most of the other samples. Context 4147 also underwent strontium analysis, with both dentine and enamel sampled from the same tooth. The results demonstrated a reduced strontium signal in the dentine that was also observed in the only other tooth that was similarly sampled from both constituent materials (see Figure 85). It is possible therefore the strontium results indicate tooth dentine was susceptible to extrinsic influences on its mineral content. In this case, the ambiguous radiocarbon analyses from context 4147 might best be explained by contaminating influences deriving from the burial environment if not the burial matrix itself. Given the earlier date deriving from the third molar of context 4147, it is suggested the source of contamination, if confirmed, derives from the earlier sediments or deposits included in the burial matrix of burial 101. Again, both samples derive from the same individual (represented by the M1 and M3 teeth from a right mandible derived 202 from grid/layer context 4203 H L6) and despite both producing date ranges overlapping with the 13th century, they demonstrate no overlap between their posterior probability distributions at all. Once more, extrinsic contamination is suggested as it seems unlikely that intrinsic mixing due to secondary dentine deposition and remodelling would account for such large age ranges and for the substantial interval between them. Results of the T-test showed that the samples are significantly different at the 95% level (Test statistic T = 64. In contrast, context 10153, the isolated head from the inner side of the ditch, is clearly distinct and dates somewhere between the mid-11th and the mid-12th century (Figure 92). The association of the articulated cervical vertebrae and mandibular fragment indicate the presence of soft tissues at the time of deposition, suggesting several scenarios for the incorporation of the head in its final location. The head may have been curated in some way prior to deposition, perhaps used as a symbolic decoration upon the town walls or the tower itself; it is also possible it may have been removed or disturbed from another separate burial context (although the presence of the articulating elements would point to the disturbance of a relatively contemporary burial). In all three instances, it is suggested the remains could easily have become covered in sediment rapidly at the edge of the ditch where refuse and debris would also likely have built up rapidly in a colluvial manner. Concerning the dating of the mass grave deposits, the majority of the remains from burials 101 and 110 represented adults, although at least two older adolescents were also present. We might therefore anticipate a lag between the acceptable dentine sample dates. Similarly, the cranial bone sample dates might well represent bone laid down or remodelled some considerable time prior to the time of death. Therefore, we might reasonably place the actual time of death (and deposition) closer to the later, mid-13th century end of the grouped posterior probability distributions (Figure 92). All this points to a high probability that the event which led to the deaths of these individuals, the creation of the pit and the deposition of the remains within and alongside it, was the Mamluk raid in the Summer of 1253. However, the nature of the radiocarbon dating and the lack of a convenient terminus ante quem means that the Mongol assault on the town in 1260 cannot be ruled out. Although the coin provides relatively good dating 204 evidence, its position towards the top of burial 110 potentially undermines its validity as a terminus post quem, thereby leaving open the possibility that these deposits date to sometime in the earlier half of the 13th century. Several lines of evidence clearly indicate the human remains from both mass grave contexts at Sidon are secondary in nature. Most obviously, the significant numbers of disarticulated elements and the presence of incomplete individuals points to disruption of the original depositional context. There was no evidence of truncation by overlying deposits or any other intrusive disturbance of the grave prior to excavation. There was little indication of any substantial settling of the remains in either deposit and no evidence of complete individuals having become dissociated following deposition. It is therefore clear the human remains were deposited into the grave or placed beside it in the state described at the time of excavation. Figure 104) indicates at least some remains had been left unburied for some time prior to inclusion within burial 110. The presence of partially articulated remains and articulated groups of elements clearly representing body parts or sections. The rate of decomposition would have varied depending on ambient temperature, season and other environmental conditions, but the presence of soft tissue at the time of deposition is clear in both burials 101 and 110. Supporting this, amongst the burnt bone there are also indicators for the presence of fleshed remains within the grave. The demographic profile fits well with the context of inter-group violence and is similar to that demonstrated for other mass graves associated with warfare, both during the Medieval period (Boucherie et al. The presence of a minimum of two subadults present, both older adolescents, with the rest of the remains able to be aged indicating individuals ranging from young adulthood to middle age, is again clearly in line with other mass graves resulting from the contexts referenced above. The lack of any clear indication of females, along with the presence of recidivists, is typical of groups associated with conflict-related mass grave sites. The dating and nature of the cultural material directly associated with the remains from burials 101 and 110. The population at this time would therefore have been swollen by an influx of labourers and specialist stone masons brought in for the construction works, and it seems likely that some of these fell victim to the Mamluk assault, especially if we take the casualty numbers reported to be genuine. Concerning the isotopic evidence, despite being a limited sample, the results of the strontium and oxygen isotopes from the crusader human remains indicated the individuals analysed could be separated into three different groups (see Figure 93 and Strontium and oxygen). Two of these groups (groups one and three, representing a total of six individuals) produced strontium signals lower to that of the seawater signal, but were differentiated by their oxygen isotopes. Group one, consisting of two individuals, demonstrated an oxygen signal lower than group three. The interpretation of group three is rather ambiguous, but the reduced strontium isotopic content compared to seawater suggests they are more likely locals, whilst the difference in oxygen could potentially indicate the two groups originated in areas or regions with slightly different climates or, alternatively, the two groups differed in their cultural practices such as cooking. Group two consisted of three individuals with strontium results above the seawater signal. These individuals are currently considered to be non-locals who grew up elsewhere, in a location with geology different to that of Sidon. Group three, consisted of four individuals with markedly lower strontium isotope levels compared to the other two groups. Three of these individuals formed a very tight cluster, with the fourth (context 4147, see Section 5. Group three is considered most likely to represent local residents who had grown up in this region of the Near East. This interpretation is supported by local environmental data reported by Rich et al. This data also supports the interpretation that the group one individuals represent a second group of non-locals, likely from a different locale to that of group two. However, further work is needed to develop detailed and reliable baseline isotopic data for the region, with particular reference to clarification of the strontium signature and its variability along the coastal region of Lebanon and the southern Levant. This is a little higher than the local group (group three), although some variation in the climate is unsurprising given the time interval since the Late Medieval period. Again, all the remaining Sidon individuals from groups one and two appear to be excluded by the extant soil data, producing lower oxygen isotope signatures than the indicated local signature for the Levantine coast. Clearly, then, there is strong evidence to suggest the Sidon dead were a mixed group consisting of individuals representing at least two, if not three communities originating from differing regions, one of which was most likely local to Sidon. These results confirm male sex for all individuals sampled from burials 101 and 110 (n = 8) and demonstrate a mixed group with diverse ancestries that can also be loosely categorised into three communities: one of recent European ancestry, one of local Lebanese ancestry and one group of two individuals with mixed ancestries (Haber et al. The dietary isotope data indicates the Sidon dead demonstrate a relatively similar diet across the group (Figure 94), that is also consistent with the dietary signal reported for the Middle Bronze Age population at Sidon (Schutkowski and Ogden, 2012), albeit with slightly higher nitrogen signals in general, suggesting perhaps slightly more protein in the diet. For the Bronze Age, this appears to contrast with the contemporary archaeological and funerary evidence for fishing practices (Chahoud and Vila, 2012: 274-275; Doumet-Serhal, 2013: 81) and the results are certainly unexpected placed alongside the historical traditions for western medieval diet at least. A single late medieval individual (context 4304) demonstrated a slightly elevated stable carbon signal suggesting fish may have formed at least a small part of their diet. However, this sample consisted of dentine and therefore may have been subjected to post depositional contamination as indicated by the differences between the tooth enamel and tooth dentine sampled for strontium (see sections 5. Worth noting here is the publication of multiple studies suggesting that some dietary components may drown out other component signals. Additional observations and interpretational details concerning identity are included in the following sections. Yet there are clear suggestions deriving from both the historical evidence and interpretation of the trauma patterning with which each align well. This cautious reluctance to engage in full-scale battle might be used to suggest a lack of individuals experienced in close-quarter fighting. Yet there were clearly individuals and groups with professional military expertise. On the Frankish side, evidence of the skills and experience of the members of the Military Orders comes from their treatment as prisoners. Regarding the Muslim troops, military prowess, especially concerning horsemanship, became increasingly socially significant from the end of the early Islamic period onwards at least, as represented by the increasing prominence and variety in the developing 211 furusiyya literature. The horseman should approach it from the right-hand side at full gallop, just like when he is training to shoot from horseback. When he gets close to it he should, with one swift movement, draw his sword and strike the reed from right to left, cutting [off] the equivalent of one [hand] span. The whole exercise should be repeated again and again until it is perfectly mastered. The horseman, at full gallop, should in one run cut the arrows exactly at the same height, one after the other just beneath the fletching using a very sharp-edged sword. When this is perfectly mastered, two parallel but staggered rows of five arrows each should be planted in the ground. The horseman, again at full gallop, should run between the two rows of arrows cutting them under the fletching as in the previous exercise, striking alternatively to the right and to the leftWhen this is also perfectly mastered, the horseman should be trained to deal blows in all other directions. The emphasis on regular military training, particularly with regard to horsemanship, is clear and this tradition became one of the foundations of the Mamluk armies, who eventually drove the western Christians out of the Levant. Little if any information regarding casualties is provided in the historical sources for these specific sieges, and we cannot be certain how much actual fighting took place, although the reports of the use of siege engines during the 1110 siege suggest at least a minimal amount of aggression. There is no written evidence indicating the burial of dead from any physical engagements. The evidence of stone trebuchet projectiles within the ditch at College Site certainly indicates a siege situation at some point. However, their size is possibly too large and heavy for early catapults such as mangonels and traction catapults, and counterweight trebuchets only became widespread from the late 12th century onwards, although Chevedden (2000) argues they must have developed somewhere earlier. It seems most likely then that these objects date from a later period or at least were re-deposited within the cut inside the ditch at a later time period than the initial sieges at the beginning of the 12th century.

In the de ni ologic muscle relaxant 751 buy 4 mg zanaflex free shipping, form of reduced consciousness in which tions that follow spasms gelsemium semper buy zanaflex overnight, we assume that the patient is the responsiveness of brain systems responsible not unresponsive due to sensory or motor im for cognitive function is globally reduced spasms upper left quadrant buy 4 mg zanaflex with mastercard, so that pairment or psychiatric disease muscle relaxant in spanish purchase zanaflex master card. The content of conscious lationships between the brain systems that are ness represents the sum of all functions medi responsible for wakefulness and sleep can im ated at a cerebral cortical level muscle relaxant starting with b discount 2 mg zanaflex with amex, including both pair consciousness spasms video generic 2mg zanaflex otc. These func mal sleep and wakefulness are reviewed later tions are subserved by unique networks of cor in this chapter. A key difference between sleep tical neurons, and it is possible for a lesion that and coma is that sleep is intrinsically reversible: is strategically placed to disrupt one of the net suf cient stimulation will return the individual works, causing a fractional loss of conscious to a normal waking state. Deli and remain behaviorally unresponsive to all rium is de ned by the Diagnostic and Statisti external stimuli are unconscious by any de ni cal Manual of Mental Disorders, 4th edition 8 tion. Disturbance of con result of brain injury rarely lasts more than 2 to sciousness. A change in cog nition (such as memory de cit, disorientation, Acutely Altered States language disturbance) or the development of a of Consciousness perceptual disturbance that is not better ac counted for by a pre-existing, established or Clouding of consciousness is a term applied to evolving dementia. The disturbance devel minimally reduced wakefulness or awareness, ops over a short period of time (usually hours which may include hyperexcitability and irrit to days) and tends to uctuate during the course ability alternating with drowsiness. Rarely are patients unaware of focal de cit of cognitive function versus those who they are, although sometimes married who have more global impairment. Pa ded patient is usually incompletely oriented to tients are often fearful or irritable and may time and sometimes to place. Such patients are overreact or misinterpret normal activities of inattentive and perform poorly on repeating physicians and nurses. Delusions or hallucina numbers backward (the normal range is at least tions may place the patient completely out of four or ve) and remembering details or even contact with the environment and the exam the meaning of stories. Full-blown delirious states tend to come minent during the day, but agitation may pre on rapidly and rarely last more than 4 to 7 days. However, fragments of misperceptions may the pathophysiology of brain function in such persist for several weeks, especially among al patients has rarely been studied, but Posner and coholics and patients with cerebral involvement 3 Plum found that cerebral oxygen consumption from collagen vascular diseases. More recently, Trze such as atropine poisoning, alcohol or seda pacz and colleagues have identi ed decreased tive drug. It the frontotemporal cortex and right basal gan also occurs with systemic infectious processes glia of patients with subclinical hepatic ence or as a component of encephalitis, during 5 phalopathy. They may have an Pathophysiology of Signs and Symptoms of Coma 7 increased number of hours of sleep and may be de-efferented, but there is a history of sub drowsy between sleep bouts. Even when maximally aroused, the so that they may be treated appropriately by level of cognitive function may be impaired. At the bedside, Such patients can be differentiated from those discussion should be with the patient, not, as with psychiatric impairment, such as catato with an unconscious individual, about the pa nia or severe depression, because they can be tient. Patients with large midpontine lesions of aroused by vigorous stimulation to respond to ten are awake most of the time, with greatly simple stimuli. The patient may havioral responsiveness, and there may be some grimace in response to painful stimuli and limbs overlap among them. Therefore, it is generally may demonstrate stereotyped withdrawal re best to describe a patient by indicating what sponses, but the patient does not make local stimuli do or do not result in responses and the izingresponsesordiscretedefensivemovements. However, it is dif cult to equate the lackofmotor responses tothe depth ofthe coma, Subacute or Chronic Alterations as the neural structures that regulate motor re of Consciousness sponses differ from those that regulate con sciousness, and they may be differentially im Dementia de nes an enduring and often pro paired by speci c brain disorders. Conventionally, the paralysis of all four limbs and the lower cranial term implies a diffuse or disseminated reduc nerves. This condition has been recognized at tion in cognitive functions rather than the im least as far back as the 19th century, but its dis pairment of a single psychologic activity such tinctive name was applied in the rst edition of as language. The development of multiple cogni tions of this condition for the diagnosis of coma tive defects manifested by both: (1) Memory and for the specialized care such patients re impairment (impaired ability to learn new in quire. Although not unconscious, locked-in pa formation or to recall previously learned infor tients are unable to respond to most stimuli. A mation); (2) One (or more) of the following high level of clinical suspicion is required on cognitive disturbances: aphasia (language dis the part of the examiner to distinguish a locked turbance), apraxia (impaired ability to carry out in patient from one who is comatose. The most motor activities despite intact motor function), common cause is a lesion of the base and teg agnosia (failure to recognize or identify objects mentum of the midpons that interrupts des despite intact sensory function), disturbance in cending cortical control of motor functions. Usually, the term de may be taught to respond to the examiner by mentia is applied to the effects of primary dis using eye blinks as a code. Rare patients with orders of the cerebral hemispheres, such as subacute motor neuropathy, such as Guillain degenerative conditions, traumatic injuries, Barre syndrome, also may become completely and neoplasms. In some patients, however, it may be applies to chronic conditions carrying limited an essentially permanent condition. Many patients with either etative state, like comatosepatients, show no evi acute or chronic alterations of consciousness dence of awareness of self or their environment. However, when awakened, Unlike brain death, in which the cerebral hemi consciousness is clearly clouded. In the truly spheres and the brainstem both undergo over hypersomniac patient, sleep appears normal whelming functional impairment, patients in and cognitive functions are normal when pa vegetative states retain brainstem regulation of tients are awakened. Hypersomnia results from cardiopulmonary function and visceral autono hypothalamic dysfunction, as indicated later in mic regulation. Other terms in the literature designating the usually associated with bilateral frontal lobe dis vegetative state include coma vigil and the apa ease and, when severe, may evolve into akinetic llic state. Brain death is de ned as the irreversible 14 Akinetic mutism describes a condition of loss of all functions of the entire brain, such silent, alert-appearing immobility that charac that the body is unable to maintain respiratory terizes certain subacute or chronic states of and cardiovascular homeostasis. Although vig altered consciousness in which sleep-wake cy orous supportive care may keep the body pro cles have returned, but externally obtainable cesses going for some time, particularly in an evidence for mental activity remains almost en tirely absent and spontaneous motor activity is lacking. Pathophysiology of Signs and Symptoms of Coma 9 otherwise healthy young person, the loss of diagnosis of structural coma depends on the brain function eventually results in failure of the recognition of the signs of injury to structures systemic circulation within a few days or, rarely, that accompany the arousal pathways through after several weeks. Structural processes that impair the dead for some time prior to the cessation of the function of the arousal system fall into two ca heartbeat is attested to by the fact that the or tegories: (1) supratentorial mass lesions, which gan in such cases is usually autolyzed (respirator may compress deep diencephalic structures and 15 brain) when examined postmortem. Because hence impair the function of both hemispheres, function of the cerebral hemispheres depends and (2) infratentorial mass or destructive le on the brainstem (see ascending arousal system sions, which directly damage the arousal system section below), and because cerebral hemi at its source in the upper brainstem. The re sphere function is extremely dif cult to assess mainder of Chapter 1 will systematically exam when the brainstem is nonfunctioning, physi ine the major arousal systems in the brain and cians in the United Kingdom have developed the physiology and pathophysiology of consci 16 the concept of brainstem death, de ned as ousness. Once the exam Acute alterations of consciousness are dis ination is completed, the examiner should be cussed in Chapters 2 through 5. Subacute and able to determine whether the source of the chronic alterations of consciousness are discus impairment of consciousness is caused by a sed in Chapter 9. The neurologic exam whether the cause of the impairment is struc ination of a patient with impaired conscious tural or metabolic, and what treatments must ness, fortunately, is brief, because the patient be instituted to save the life of the patient. Since cannot detect sensory stimuli or provide vol the last edition of this monograph in 1980, untary motor responses. In appropriate and reactivity of the pupils, (4) the eye move clinical circumstances, if the initial examina ments and oculovestibular responses, and (5) tion suggests structural brain damage, a scan the skeletal motor responses. From this infor may identify the cause of the alteration of con mation, the examiner must be able to recon sciousness and dictate the therapy. However, struct the type of the lesion and move swiftly when the scan does not give the cause, there is to lifesaving measures. Before reviewing the no simple solution; usually no single laboratory components of the coma examination in detail, test or screening procedure will sift out the however, it is necessary to understand the ba criticalinitialdiagnosticcategoriesaseffectively sic pathways in the brain that sustain wakeful, as a careful clinical evaluation. Only from this perspective If the cause of coma is structural, it generally is it possible to understand how the compo is due to a focal injury along the course of the nents of the coma examination test pathways neural pathways that generate and maintain a that are intertwined with those that maintain normal waking brain. He was brought up in Austrian Trieste, studied medicine in Vienna, and in 1906 took a post in the Psychiatric Clinic under Professor Julius von Wagner-Jauregg. In 1916 during World War I, he began seeing cases of a new and previously unrecorded type of encephalitis and published his rst report of this illness in 1917. Although subsequent accounts have often confused this illness with the epidemic of in uenza that swept through Europe and then the rest of the world during World War I, von Economo was quite clear that encephalitis le thargica was not associated with respiratory symptoms, and that its appearance preceded the onset of the latter epidemic. Von Economo continued to write and lecture about this experience for the remainder of his life, until his premature death in 1931 from heart disease. Based on his clinical observations, von Economo proposed a dual center the ory for regulation of sleep and wakefulness: a waking in uence arising from the upper brainstem and passing through the gray matter surrounding the cerebral aqueduct and the posterior third ventricle; and a rostral hypothalamic sleep promoting area. These observations became the basis for lesion studies done by 20 21 22 Ranson in 1939, by Nauta in 1946, and by Swett and Hobson in 1968, in which they showed that the posterior lateral hypothalamic lesions in monkeys, rats, and cats could reproduce the prolonged sleepiness that von Economo had observed. The rostral hypothalamic sleep-promoting area was con rmed exper 21 imentally in rats by Nauta in 1946 and in cats by Sterman and Clemente in the 23 1960s. A photograph of Baron Constantin von Economo, and excerpts from the title page of his lecture on the localization of sleep and wake promoting systems in the brain. These indi viduals would develop episodes of sleep attacks during which they had an over whelming need to sleep. He noted that they also had attacks of cataplexy in which they lost all muscle tone, often when excited emotionally. Von Economo noted accurately that these symptoms were similar to the rare condition previously identi ed by Gelinaux as narcolepsy. He also noted that they had developed symptoms of narcolepsy after recovering from encephalitis lethargica with pos terior hypothalamic lesions. Wilson even described examining a patient in his of ce, with the young house of cer McDonald Critchley, and that the patient indeed had atonic paralysis, with loss of tendon re exes and an extensor plantar response during the attack. However, the most convincing found that after a transection between the me body of evidence was assembled by Baron Con dulla and the spinal cord, a preparation that he 19 stantin von Economo, a Viennese neurologist called the encephale isole, orisolatedbrain, ani who recorded his observations during an epide malsshowed a desynchronized(lowvoltage, fast, mic of a unique disorder, encephalitis lethargica, i. When awakened, they could interact in a showed a synchronized, or high-voltage, slow relatively unimpaired fashion with the examiner, wave pattern indicative of deep sleep and the but soon fell asleep if not continuously stimu animalswerebehaviorallyunresponsive. Many of these patients suffered from concluded that the forebrain fell asleep due to oculomotor abnormalities, and when they died, the lack of somatosensory and auditory sen they were found to have lesions involving the sory inputs. He did not address why the ani paramedian reticular formation of the midbrain mals failed to respond to visual inputs either at the junction with the diencephalon. Von Economo identi ed the causa by Moruzzi and Magoun, who placed more tive lesion in the gray matter surrounding the selective lesions in the lateral part of the mid anterior part of the third ventricle in the hypo brain tegmentum in cats, interrupting the as thalamus and extending laterally into the basal cending somatosensory and auditory lemniscal ganglia at that level. Laterstudiesshowed for assessing activityofthe cerebralhemispheres that electrical stimulation of the midbrain re remained the clinical examination, this problem ticular core could excite forebrain desynchro 31 could not be resolved. The origin of the pathway was patients with various types of functional impair not established in this early work. The waves of postsynaptic potentials in the cerebral cortex are now un derstood to be due to the intrinsic burst ring of neurons in the thalamus, basal forebrain, and the cortex itself, which produce waves of postsynaptic potentials in cortical neurons. When the membrane potential of burst neurons is close to their ring threshold, they re single action potentials that transmit sensory and other information. How ever, when burst neurons have been hyperpolarized to membrane potentials far below their usual threshold for ring sodium action potentials, a low-threshold calcium channel is deinactivated. When the low-threshold calcium channel is trig gered, calcium entry brings the membrane potential to a plateau that is above the threshold for ring sodium action potentials. As a result, a series of sodium spikes are red, until suf cient calcium has entered the cell to activate a calcium-activated potassium current. This potassium current then brings the cell back to a hyperpo larized state, terminating the burst of action potentials. This brings the cell above the threshold for ring sodium action potentials, which are red in a burst, until this is terminated by a calcium-activated potassiumcurrent that hyperpolarizes and silences the cell. Thalamic axons on their way to the cerebral cortex, and cortical projections to the thalamus, give off collaterals to the reticular nucleus as they pass through it. Recent evidence suggests that the basal forebrain may play a critical role in entraining cortical rhyth mic activity. Basal forebrain neurons also re in bursts that are time-locked to cortical rhythms. These neurons project through the was thought to play a synchronizing, or sleep paramedian midbrain reticular formation to 33 promoting, role. Periods of fore and intralaminar nuclei (which innervate the brain arousal returned after several days if the entire cortex more diffusely), and the reticu animals were kept alive. Other neurons in At the time, little was known about the ori the cholinergic pedunculopontine and later gins of ascending projections from the meso odorsal tegmental nuclei send axons into the pontine tegmentum to the forebrain, and the lateral hypothalamus, where they may contact arousal effect was attributed to neurons in the populations of neurons with diffuse cortical pro reticular formation. Mixed in with the serotoninergic not be reduced to as great a degree as back neurons are a smaller number of dopaminer ground ring. In an awake and aroused in gic cells, which are an extension of the ventral dividual, this alteration in ring may result in tegmental dopamine group along the midline an improvement in signal-to-noise ratio, which of the midbrain, into the area under the ce may be critical in sharpening cortical informa 45 rebral aqueduct. These dopaminergic neu tion processing to avoid misperception of stim rons also project through the paramedian uli, such as occurs during a delirious state. Some of them Although the cholinergic and monoaminergic innervate the midline and intralaminar nuclei neurons in the mesopontine tegmentum have of the thalamus, and others pass through the traditionally been thought to play a major role lateral hypothalamus to the basal forebrain in regulating wake-sleep states, lesions of these and prefrontal cortex. During these periods, eye movements are few and muscle tone drops to very low levels. This usually takes about 45 to 60 minutes, and then the subject often will gradually emerge from the rst bout of slow-wave sleep to stage I again. This pattern, which is typical of young adults, changes dramatically across a life time.

Comparing the characteristics of those who did and who did not report having financial problems in the past 12 months due to autism spasms kidney zanaflex 4mg overnight delivery, the researchers found that spasms kidney stones order 4mg zanaflex amex, among those reporting financial problems spasms near tailbone purchase 4 mg zanaflex with mastercard, a significantly higher proportion had autism limit family activities and had unreimbursed out-of-pocket expenses for doctor or therapy services muscle relaxant non drowsy zanaflex 2mg, the Financial Side of Autism: Private and Public Costs 283 prescription and non-prescription drugs spasms kidney stones best 2 mg zanaflex, and medical interventions infantile spasms 6 months old generic zanaflex 2 mg free shipping. A significantly lower proportion in this group had used speech and language therapy or special education. Two results stood out in the multivariate analysis of factors affecting likelihood of financial problems. First, utilizing medical interventions and having unreimbursed out-of-pocket expenditures for medical doctor or therapy or for education expenses were significant factors in increasing the likelihood of financial problems (by 121%, 264%, and 289%, respectively). Second, consistent with previous research and as would be expected, those with annual income under $40, 000 were more likely to have financial problems than those with annual incomes of $60, 000 or more. These results suggest that, while all families with a child with autism may struggle to meet the demands of the disorder, for low income families the demands can quickly outstrip family resources. For that reason, special attention needs to be given to low income families in the design and delivery of programs and public policy. The researchers also used qualitative research methods to identify common themes in parent report of reasons for financial difficulty. One of most salient sources of financial pressures according to the parents was the high cost of therapy, especially Applied Behavioral Analysis, as well as special foods or supplements. Many of the parents expressed anguish or anger at having to leave the labor market or desperation and fear when considering how to meet financial demands with the income loss. Parents reported struggles with insurance providers to obtain or continue coverage for health related services; protracted battles with school administrators to obtain specific education services or starting to home school their children in an attempt to meet their educational needs. Scheduling and transportation to various therapies and medical appointments also took a toll on parent time. Other sources of financial pressure included replacing items broken, damaged, or destroyed by the child and retraction of public program support due to a misunderstanding of program rules. A poignant aspect of parent report was the extent to which parents mortgaged their own future to obtain therapy and services for their children with autism. Parents cashed out their retirement investments, sold stock, drained the equity in their home, and borrowed money to the point that bankruptcy seemed inevitable. There are many important considerations not shared by families with 284 A Comprehensive Book on Autism Spectrum Disorders neurotypical children. As noted, funding autism treatment can devastate the financial resources of some families and leave little hope for rebuilding the spent wealth. Seeking ways to help a child with autism, families have taken out a home equity loan, charged credit cards to the limit, or declared bankruptcy after exhausting their financial resources. In absence of reform of methods to fund autism treatment, families in this situation will continue to struggle to maintain income and may have to seek help from relatives and public assistance programs just to cover basic expenses. High functioning children may require expensive intense therapy while young, but then incur minimal to no additional autism-related expenses in adolescence or adulthood. In this situation, family financial plans could focus on funding post-secondary education and training. Financial plans for a child that is mid-range to low functioning are quite different. Attention must be paid to lifestyle, legal, financial, and government benefit issues. Decisions must be made regarding where the disabled person will live, behavior management, education and employment activities, as well as social and religious activities. Wills and trusts can be used to distribute parental assets to benefit the disabled child. Careful planning is needed to ensure the disabled individual receives what he/she is entitled to receive and assets transferred from financial gifts, bequests, or other sources do not jeopardize other potentially important sources of income or health care support such as Supplemental Security Income or Medicaid. Arrangements need to be made to provide professional money management, oversight of use, maintenance of government or other benefits, and protection of assets. Power of attorney to act on behalf of the disabled person may need to be executed along with end of life health directives. Cost sharing: Public and private sector Central to public policy discussion of autism is deliberation regarding who should share the cost of treatments, to what extent, and by what mechanisms. But, because its efficacy has been supported in the scientific literature, it is highly sought after by families with a child with autism as a therapeutic intervention. Although each of these items offer some help for families with a child with autism, program structure and funding limits often curtail the type and amount of help actually received from these programs. Public schools are short more than 12, 000 special education teachers, and the shortage is expected to rise as teachers retire or leave teaching. Although Congress and the federal Centers for Medicare and Medicaid Services have established the general rules for program operation, each state administers its own Medicaid program. Medicaid waivers allow states to provide home and community based services to individuals that do not meet all eligibility criteria but, without the services provided by the waiver, would require long term institutional care. Total cost to Medicaid to provide services under the waiver cannot exceed what Medicaid would have paid for service in an appropriate institutional setting. In 2007, Colorado, Indiana, Maryland and Wisconsin were the only states with Medicaid waivers focused specifically on children with autism. Since that time, Indiana, Kansas, Maryland, Massachusetts, Missouri, Montana, Nebraska, North Dakota, and Pennsylvania have received Medicaid waivers for autism. A few states, however, explicitly exclude autism from the state developmental disability definition unless the person also has mental retardation (Spigel, 2007). Unfortunately, in practice, relatively few individuals with autism can obtain services under a waiver. Since persons must otherwise require long-term institutional care to be eligible, those at the high functioning end of the autism spectrum could not qualify. To 286 A Comprehensive Book on Autism Spectrum Disorders control costs, states can cap waiver enrollment leading to long waiting lists. In states that focus on providing early intervention behavior therapy under the waiver, children on a long waiting list might no longer be eligible for services once an opening occurred (Spigel, 2007). Medicaid represents about one-fifth of total state spending (National Association of State Budget Officers, 2010), making it one of the largest components of state budgets. The severe national recession in the late 2000s squeezed states between substantial declines in revenue and increased demand for public services, including Medicaid. According to the National Association of State Budget Officers, fiscal years 2009 and 2010 were two of the most difficult years for state budgets since the Great Depression. Attempting to meet budget shortfalls, 41 states made mid-year budget cuts during fiscal 2009; 39 states did so in 2010 (National Association of State Budget Officers, 2010). Across all states, Medicaid and education (K-12 and higher education) bore the brunt of these budget cuts. Given a slow economic recovery, tight state budgets are expected to continue into 2012 and beyond, thus restricting resources available to fund services for families that have a child with autism. In recent years, diligent lobbying efforts from autism advocacy groups and families with a child with autism have resulted in passage of insurance mandates for autism in many states. A health insurance mandate is a requirement that state law places on health plans or insurance providers in that state. Mandates typically force health plans or insurance providers to extend coverage to a broader population than they otherwise would. Individuals and employers can accept or reject the coverage, giving the purchaser some control over policy content and cost. Individuals along with small and medium sized employers purchase health insurance in the market. Currently, 55 % of enrollees in a private sector plan are in a self-insured plan (Fernandez, 2010). As of March 2011, all states except Alaska, Delaware, South Dakota, and Wyoming had passed a state insurance mandate related to autism diagnosis and treatment. Eighteen states have a mental health parity law that may include autism spectrum disorder as a covered mental illness: Alabama, Arkansas, California, District of Columbia, Georgia, Hawaii, Michigan, Minnesota, Mississippi, Nebraska, North Carolina, North Dakota, Ohio, Rhode Island, Utah, Virginia, Washington and West Virginia. Insurers cannot deny otherwise available coverage simply because treatment is used to diagnose or treat autism spectrum disorder. Almost half of the states have broad autism m andates that delineate coverage for assessment, diagnosis and treatment of autism spectrum disorders. These states are Arizona, Colorado, Connecticut, Florida, Illinois, Indiana, Iowa, Kansas, Kentucky, Louisiana, Maine, Massachusetts, Missouri, Montana, Nevada, New Hampshire, New Jersey, New Mexico, Oregon, Pennsylvania, South Carolina, Texas, Vermont, and Wisconsin. In South Carolina, for example, an individual must be diagnosed with an autism spectrum disorder at age eight or younger to be covered. Coverage is typically limited to those aged under age 18, although Illinois and Pennsylvania extend coverage to age 21. Kentucky made a distinction between large and individual / small group health benefit plans. Benefits in large group health plans were capped at $50, 000 per year for children age 1 through their 7th birthday and $1, 000 per month for children age 7 through 21. In individual and small group health benefit plans, the cap was set at $1, 000 per month per covered individual. Some portion of individual policy holders will drop coverage because they can no longer afford to pay the premiums. The cost of paying claims would then be spread over a smaller pool of policy holders. If individuals leave the insurance market, a majority of remaining policy holders would be employers. It is argued that higher premiums would pass to workers in the form of lower net wages or loss of employment. Results of empirical studies of these expected effects have been inconclusive, however. Actuaries with the Council on Affordable Health Insurance estimate an autism mandate will increase the cost of health insurance by about 1 percent, but caution that increasing prevalence rates coupled with coverage of more services could drive premiums up 1 to 3 percent (Bunce, 2009). But, autism is only one of many mandates that state legislatures imposed on insurance providers in recent years. Between 2004 and 2010, the number of insurance mandates for all types of issues across the states rose 18% from 1, 823 to 2, 156. Currently, Rhode Island has the largest number of mandates at 69, whereas Idaho has the least at 13 (Bunce & Wieske, 2010). The total cost of meeting all mandates rather than the marginal cost to meet an autism mandate needs to be considered. Some children would be able to engage in regular classroom instruction without support once the intervention ended. Given the range in treatment effectiveness and expected outcome, they estimated that cost savings in constant dollars would range from $187, 000 to $203, 000 ($263, 670 to $286, 230 in 2011$) per child for ages 3 to 22 years and from $656, 000 to $1, 082, 000 ($924, 960 to $1, 525, 620 in 2011$) per child for ages 3 to 55 years. They estimate that by implementing 3 years of early intervention, the state of Texas would save $208, 500 ($223, 095 2011$) per child across 18 years of education. Health care reform In 2008, President Obama made a campaign pledge to support a federal mandate requiring coverage for autism treatments. The law places new requirements on individuals, employers, and health plans regarding possession and coverage of health insurance. The law also restructures the private health insurance market, sets minimum standards for health coverage and provides financial help to certain individuals and small employers to secure health insurance (Fernandez, 2010). The autism community sees the new law as a win as it will reduce or eliminate opportunity for health insurance companies to impose pre-existing condition exclusions, excessively long waiting periods before coverage begins, or rescissions of coverage. The Financial Side of Autism: Private and Public Costs 289 Further, ability of insurers to set annual or lifetime caps on coverage will be limited (Autism Speaks, 2011b). The only plans required in 2014 to cover essential benefits will include plans offered by state-based exchanges where individuals and businesses purchase coverage, and plans offered in the individual and small group market outside the exchange. Existing coverage, plans offered in large group market outside of the exchanges, and self-insured plans will not be required to supply the essential benefit package to the insured. Thus, in many ways, the new law does not move far beyond the state mandates already in place. Those state mandates were due, in large part, to the lobbying efforts of Autism Speaks, a large autism advocacy organization. It is challenging to establish diagnostic criteria that are consistent across countries. Cultures can differ in behavioral social norms such as eye contact or expected timing of speech development, making it difficult to identify autism-related behavior (Daley & Sigman, 2002; Naqvi, 2009).

Continued monitoring is vital for this population muscle relaxant flexeril order zanaflex cheap online, as some children with cerebral palsy present with normal feeding skills for a number of years before de veloping feeding problems back spasms 35 weeks pregnant zanaflex 4mg with visa. Commonly reported oral and pharyngeal phase impairments in children with cerebral palsy are listed in Table 13 muscle relaxant drug class buy zanaflex discount. Feeding problems are commonly associated with the Moebius sequence as a result of cranial nerve involvement and orofacial malformations (Meyerson and Foushee muscle relaxant parkinsons disease purchase zanaflex, 1978; Cohen and Thompson muscle relaxant headache best order for zanaflex, 1987; Amaya et al knee spasms causes buy zanaflex 2mg mastercard. More speci cally, cleft palate, tongue weakness/palsy, pharyngeal dysfunction, macroglossia, micrognathia and generally poor health of the neonate have been reported as the likely causes for feeding problems (Sjogreen et al. All 25 patients presented with oral phase problems, and only three patients demonstrated pharyn geal phase dif culties. The oral phase was characterized by reduced lip function resulting in poor removal of food from the spoon; anterior spillage of the bolus from the corners of the mouth; neglecting to chew large pieces of food, swallowing them whole; and markedly reduced oral transit time (Sjogreen et al. Impairments of lip and tongue function are the two main de cits of the oral phase in this popula tion. Tongue movement and strength may also be mark edly reduced due to asymmetry, structural de cits causing atrophy, and hypoplasia (Sjogreen et al. Pharyngeal phase problems, most likely due to the bulbar paralysis, included clinical signs of aspiration such as coughing with liquids and choking on food con sistencies. The bulbar paralysis in this population has been linked to aspiration and subsequent pneumonia and respiratory complications (Haslam, 1979). This nding implies that despite persistent feeding impairment, individuals with Moebius sequence are able to compensate for their feeding problems to allow them to achieve a normal oral diet. Relationship between age and feeding impairment Feeding problems may begin from birth in infants with Moebius sequence, and the nature of the impairment typically changes with age. Infants with a facial palsy alone may breast feed successfully and may experience only minor sucking dif culties. The caregiver may simply be required to provide facilitation using their ngers to help the infant achieve adequate lip seal around the nipple (Sjogreen et al. However, children with orofacial anomalies in as sociation with facial palsy often demonstrate more signi cant sucking problems (Sjogreen et al. Overall, impaired tongue function (if glossopharyngeal and hypoglossal nerves are involved) is typically the greatest debilitating factor contributing to sucking problems (Sjogreen et al. Feeding dif culties have been reported to improve with age in individuals with Moebius sequence (Sjorgreen et al. Whilst im paired lingual function is most debilitating for infants and young children, poor lip closure is the greater problem for older children and adults. Excessive drooling, thought to be linked in part to poor lip seal, is very socially limiting for adults and older children. Whilst such strate gies provided good functional outcomes for the individuals with Moebius sequence, management of the underlying impairment may help to reduce the need for such socially limiting compensatory strategies. Prader-Willi syndrome the clinician involved in the dysphagia management of a child with Prader-Willi syndrome from birth to childhood will witness an extraordinary change in the feeding behaviour of the child. Children with Prader-Willi syndrome present with dysmorphic facial features, hypogenitalism, short stature, behav ioural problems, and mental retardation (Bray et al. The clinical presentation of hypotonia, feeding dif culty and dysmorphic appearance is often strong enough to suggest the presence of the disorder in infancy (Dubowitz, 1969). The dysphagia specialist may be heavily involved with the management of chil dren with Prader-Willi syndrome from birth and throughout the rst month when feeding problems are most debilitating, and to a lesser degree throughout the re mainder of infancy when the feeding problems reduce in severity (Airede, 1991). The feeding problems in early infancy are described as poor appetite and an inabil ity to suckle, resulting in the need for supplemental tube feeding (Airede, 1991; Haig and Wharton, 2003). However, around the age of 2 years, tone begins to normalize and the child with Prader-Willi syndrome develops an insatiable appetite and typi cally becomes obese (Airede, 1991; Cassidy, 1992; Haig and Wharton, 2003). No data are reported on the speci c type of feeding dif culties experienced in infancy, nor on the feeding abilities of the children following the development of hyper phagia in early childhood. The Prader-Willi syndrome phenotype also includes symptoms similar to obsessive compulsive disor der, which may also interact to result in food obsession (Dimitropoulos et al. Brachmann de Lange syndrome/Cornelia de Lange syndrome Brachmann de Lange syndrome, or Cornelia de Lange syndrome, is most commonly recognized by forehead hirsuitism, sh-mouth facial appearance, and synophrys (bushy-eyebrows in continuance). In addition, hypoplastic mandible, microcephaly, long curly eyelashes, small nose with anteverted nostrils, delayed dentition, high arched palate, and variable limb reduction de cits are typically present (Hart et al. Children with Brachmann de Lange present with feeding problems related to oral-motor dysfunction, lack of swallow ing coordination, recurrent vomiting, gastroesophageal re ux and poor oesophageal motility, which may result in failure to thrive and life-threatening aspiration pneu monia (Hawley et al. Improved meth ods of diagnosis and management have improved the outcome of children affected with this condition (Bull et al. Aggressive medical and surgical intervention has been advocated for those with gastrointestinal problems or failure to thrive, to prevent complications of dysphagia, oesophagitis, or malnutrition and to ensure an optimal outcome for these children (Bull et al. Medical and surgical treatment includes the use of na sogastric and gastrostomy tubes to supplement feeding, and Nissen fundoplication to prevent re ux and vomiting. However, feeding dif culty is reported to begin at birth with the presence of poor sucking and swallowing (Schinzel, 1979; Qazi et al. Nasogastic and gavage tube feeding are commonly reported in the rst few months (Carey and Hall, 1978; Schinzel, 1979; Qazi et al. Little mention is made in any study regarding the resolution of the feeding and swallowing problems, nor of the type of outcome for oral intake achieved. However data seem to indicate that feeding issues largely resolve after infancy (Carey and Hall, 1978; Schinzel, 1979; Lucaya et al. Severe feeding problems had been reported over her rst month of life only, and were reported to improve gradually. Further potential complications for feeding disorder in this population may in clude: cardiac anomalies, marked respiratory problems, and gastrointestinal disor ders (Cof n and Siris, 1970; Carey and Hall, 1978; Lucaya et al. The impact of heart disease and respiratory issues on feeding skills in the infant is noted elsewhere in this chapter. Recurrent upper and lower respiratory tract infections are also frequent in the rst few years of life in children with Cof n-Siris syndrome (Qazi et al. Despite seminal pa pers stating that aspiration of secretions due to pharyngolaryngeal impairment may represent the major incremental risk factor for mortality, there remain few data spe ci c to feeding or swallowing problems in this population that are not of a purely structural or anatomical nature (Blake et al. Nasopharyngeal deformities may include bilat eral choanal atresia, an abnormally contracted nasopharynx in the lateral and/or vertical dimension, and an abnormally prominent medial pterygoid lamina and thickened posterior nasal septum (Oley et al. Subglottic stenosis may be congenital, or in some cases where children have had a number of minor surgical operations and prolonged periods of intubation, granulation tissue, mucosal ulcera tion and brosis may occur from intubation trauma causing acquired subglottic ste nosis (Hollinger, 1982). Underlying problems found to induce these signs include pharyngo-oesophageal dysmotility and gastroesophageal re ux (Blake et al. Whilst they did not report the cause of these symptoms, they proposed that the com bination of anatomical defects and physiological impairment was likely to lead to a deleterious airway event, or aspiration. Smith-Lemli Opitz syndrome Smith-Lemli Opitz is an autosomal recessive disorder of cholesterol biosynthesis that manifests in multiple congenital anomalies (Cunniff et al. Language, cognitive and motor development are also typically delayed along with attentional issues, and behavioural problems including tantrums, aggressive outbursts and self-injuring be haviours (Tierney et al. Cormier-Daire and colleagues (1996) noted that, although the clinical manifestations of Smith-Lemli Opitz are extremely variable, several features are typically present in children with classical presentations of the disorder, including: micrognathia, severe microcephaly, major ante and postnatal growth retardation, and feeding problems. They also reported that the major ante and postnatal growth retardation seen in children with Smith-Lemli Opitz was due to feeding dif culties (Cormier-Daire et al. Feeding dif culties associated with Smith-Lemli Opitz Often a dysphagia specialist may be one of the rst health professionals involved in the management of a child with Smith-Lemli Opitz. The nature of the feeding dif culties for children with Smith-Lemli Opitz may be diverse and varied, potentially arising from craniofa cial anomalies, tonal issues, gastrointestinal problems, respiratory issues, congenital heart defects, and/or metabolic issues. Impact of craniofacial anomalies on feeding Children with Smith-Lemli Opitz presenting with craniofacial anomalies such as micrognathia or cleft palate will present with feeding issues. Further craniofacial anomalies speci c to this group of children with Smith-Lemli Opitz include: a high arched palate and narrow hard palate, broad and ridged alveolar ridges, and redun dancy of sublingual tissues (Donnai et al. Such physical issues impact mark edly on oral-motor function, and as a result may reduce oral intake. Gastrointestinal abnormalities complicate feeding issues further, whereby pyloric stenosis, vomit ing, gastroesophageal re ux, gastrointestinal irritability, feeding intolerance, and allergies are common (Kelley and Hennekam, 2000). Congenital heart defects may also be present in approximately 50% of children with Smith-Lemli Opitz (Lin et al. Further compounding issues of oral-motor dysfunction, gastrointestinal issues, ef ciency and fatigue for feeding are metabolic/caloric intake considerations, given that a hyper metabolic state has been noted in many patients with Smith-Lemli Opitz (Kelley and Hennekam, 2000). Hypersensitivity and tactile defensiveness has also been reported for the hands, feet, extremities, and the oral region (Tierney et al. Not sur prisingly, given the many factors that may cause feeding dif culty in children with Smith-Lemli Opitz, recurrent episodes of pneumonia are common (Cunniff et al. Enteral feeding is commonly used to offset malnutrition in children with Smith-Lemli Opitz, with gavage feeding needed in newborns, followed by short-term nasogastric feeding, and then longer-term gastrostomy feeding in many children (Cormier-Daire, 1996; Nowaczyk and Waye, 2001; Prasad et al. Down syndrome the presence of feeding dif culties in children with Down syndrome is of signi cant concern, given that a lack of mobility or feeding skills have been more accurate predictors of early death than the medical problems associated with congenital heart disease in the syndrome (Eyman and Call, 1991). Historically the feeding dif culties noted in children with Down syndrome were reported to occur as a result of delayed development. In more recent times however, the pattern of oral-motor dysfunction in children with Down syndrome has been suggested to occur largely as part of an aberrant de velopmental path, rather than due to developmental delay (Spender et al. Speci c feeding dif culties associated with Down syndrome Oral-motor and feeding dysfunction is reported to be most marked in children with Down syndrome from the ages of 9 months to three years (Spender et al. The main feeding issues occur as a result of dysfunction, speci cally hypertonic ity, of the jaw, lips, and tongue (Howard and Herbold, 1982; Limbrock et al. In particular, a pattern of persistent tongue protrusion is the overriding feature, causing anterior spillage or, in more severe presentations, pre venting any food from entering the oral cavity (Gisel et al. Hypoplasia of the mandible and maxilla has been reported to be the main fac tor contributing to the tongue protrusion noted in these children (Fischer-Brandies, 1989). Tongue protrusion may occur on all textures, but some parents report food re fusal and behavioural issues relating to speci c food textures (Spender et al. Adding further to issues of oral containment, children with Down syndrome are frequently mouth breathers due to heavy nasal congestion, and thus typically present with a persistently open-mouth posture during eating (Howard and Herbold, 1982). Texture selectivity has also been noted, with children avoiding solid foods and refusing to chew (Field et al. The aversion to chewable foods has been suggested to be largely due to oral-motor delays whereby children avoid foods due to dif culty chewing, but also due to potential episodes of gagging or choking when foods are not chewed properly (Field et al. Oral-motor delays resulting in chewing dif culty Poor rhythmicity of the jaw, lips and tongue affect mastication for children with Down syndrome. Such problems have implications for the ef ciency of oral intake for children with Down syndrome, with children potentially taking longer to consume adequate amounts of energy. Poor feeding skills occur in children with Down syndrome, but good developmental feeding outcomes have been reported for some in this population de pending upon the factors contributing to the feeding impairment. Rett syndrome Rett syndrome occurs in 1:10, 000 women, arising from a mutation on the X chromo some (Hagberg, 1985; Sugarman-Isaacs et al. Instead the majority of females with Rett syndrome are reported to have normal development during infancy. However a re gression is noted in development around 2 to 3 years, and delays become noticeable, including problems with feeding (Hagberg, 1985; Morton et al. Speci cally, there appears to be regression in oral-motor ability, particularly with decreased lateralization of the anterior tongue and an open-mouth posture, which results in poor chewing skills, and often also results in anterior spillage of food. It is extremely dif cult to determine a reason for dysphagia in Rett syndrome, with the likely aetiologies being complex and multifactorial (Reilly and Cass, 2001). Reilly and Cass (2001) propose that the decreases in growth and oral-motor function with increasing age may be related to declining postural stability, a pattern noted in children with cerebral palsy. When texture tolerance for chewing, crunchy, viscous foods and beverages is high, a larger variety of foods is more likely to be consumed, resulting in higher nutrient intakes. Limited texture tolerance is a poten tial predictor of poor oral ability in managing food and thus the child may demon strate self-restricted eating patterns and a subsequent low nutrient intake (Sugarman et al. Oral and pharyngeal feeding problems Aside from the marked chewing problems identi ed in children with Rett syndrome, other oral-phase dif culties have been reported to include poor tongue lateralization, involuntary dyskinetic tongue writhing, mouth breathing at rest and during feeding, anterior spillage of uids, intermittent drooling, poor bolus formation, poor mid and posterior tongue movement resulting in inef cient oral transit and piecemeal deglu tition, poor glossopharyngeal seal with the palate resulting in premature spillage into the pharynx, oral residue, and a delayed swallow trigger (Budden et al. Whilst feeding problems of the oral phase, including chewing, are most frequently reported, dysphagia in Rett syndrome has also been reported to occur at the pharyn geal level as well. Two subjects aspirated a small amount after the swallow due to signi cant and persistent pharyngeal residue. All three subjects had a history of more than three chest infections in the past year, compared with an average of only 0. Laryngeal penetration was also noted during swallowing, particularly in subjects who were hypertonic or hypotonic (Motil et al. For more information on respiration patterns during feeding, the reader is referred to Chapter 4. Pierre Robin sequence Pierre Robin sequence is characterized by micrognathia and glossoptosis, which leads to respiratory distress due to the large tongue being limited in anterior place ment by the small jaw, causing it to fall back into the pharynx (Marques et al. Pierre Robin sequence can occur in isolation, or in association with other congenital anomalies or syndromes (Shprintzen, 1992).

Data treatment Advice on data interpretation was provided by the study coordinators spasms heat or ice buy generic zanaflex online. In all cases muscle relaxant gel uk cheap zanaflex 2 mg free shipping, the examiner attempted to remain blind to radiological imaging and reports spasms under eye buy line zanaflex, specialist diagnosis and intervention muscle relaxant renal failure order 4mg zanaflex fast delivery, until after the final data were collected muscle relaxant commercial purchase discount zanaflex on line. Cluster analysis in R used Euclidean distance measures and hierarchical clustering to produce dendrograms for interpretation (Blashfield muscle relaxant herniated disc generic zanaflex 2mg free shipping, 1980). In both clinical cases lumbar spine movement restrictions corresponded with self-report scores for pain and disability. Single plane movements are often unrepresentative of the actual movements of the lumbar spine, so have limited value in assessing lumbar function (Pearcy and Hindle, 1989). It is not the intention of this paper to report clinical studies which did not use an objective quantification of lumbar spine movement. Methods A MotionStar 3-D motion tracking system was tested in our laboratory against a custom made triaxial goniometer to test consistency over time (Figure 4. Results demonstrated that the MotionStar is capable of reliably measuring angular movement with an intrinsic precision of 0. Skin marking and sensor mounting over the L1 landmark was performed while the patient maintained a partially flexed lumbar spine position in standing, with their hands on their knees. In a relaxed standing position, all volunteers had their lumbar lordosis (angle between L1 and S1) recorded (Figure 4. Trial data were batch processed using a Butterworth 4th order, low pass (cf 4Hz) filter, to remove high frequency (non-biological) noise. Intra-session reliability studies involving ten normal volunteers indicated there was no warm-up or fatigue effect over five repeated trials. For this reason, after a familiarisation trial, a single data collection was used on each subsequent test session. Data was examined using 10 cases with 5 trials performed for both intra-session and inter session cohorts. Case B was a 62 year old female who presented with chronic, intermittent medial shin pain aggravated by lumbar extension. The core battery of outcome measures were used to assess the patients pre-intervention and at three intervals, post-intervention (Deyo et al. A change of 30% in all measures was considered clinically significant (Ostelo et al. Self-report outcome data for the two cases, for the index assessments are presented in Table 4. Self-report surveys and lumbar kinematics provide insight into the response of low back conditions to management (Deyo et al. Measures should be reliable, valid, practical and, for convenience, brief where possible. However, outcome measures placing emphasis on pain, function and quality of life do not provide the clinician with feedback on the direction and magnitude of movement pattern disturbance (Lyle et al. As spinal movement is not isolated to pure cardinal planes, 3-D information may confer greater insight into the clinical analysis of aberrant spinal mechanics. Interestingly, passive spinal structures make up the majority of the common pathologies in the lumbar spine (Press, 2007). Pearcy and Hindle (1989) discuss the potential diagnostic value of 3-D lumbar movement assessment; however, no studies have substantiated this claim in pathoanatomical terms. In both cases, the self-report results highlight clinically important improvements in pain, disability and health outcomes. Several previous studies have reported planar lumbar motion measures (Pearcy and Hindle, 1989, Madson et al. Furthermore, there seems to be a lack of normative data which can be used to inform outcomes from intervention to manage spinal pain. They also noted the difficulty in attempting a meaningful interpretation of the data due to the varied methodologies, samples and symptoms reported by the different studies. Further studies are currently underway with larger clinical cohorts of cases diagnosed with lumbar stenosis, confirmed facet joint dysfunction or disc herniation. Keywords: Lumbar spine; combined movement examination; facet joint injection; epidural injection; rhizotomy; pain management 5. The lifetime prevalence is as high as 85% and the reported annual incidence in adults is 22-65% (Hoy et al. Improved diagnostic accuracy would confer obvious cost advantages to the health system for enabling treatment to focus on particular sources of pain but more than this would enable pathology-specific interventions to be grouped for clinical research. The literature reports various movement assessments including functional activities of daily living (Bible et al. Of these, 17 individuals received pain management intervention and completed post-intervention examination (Figure 5. Data acquisition and post-processing is described in detail elsewhere (Monie et al. All 17 patients were tested prior to intervention and retested at approximately 14 weeks after intervention. Outcome measures A battery of self-report outcome measures were used to assess cases at each examination visit (Chiarotto et al. Total change scores and z-scores are reported and a significant improvement was considered if the change was of magnitude 1 z-score. A sample of convenience was derived from a tertiary hospital and private practice setting. In each series, post-intervention score minus pre-intervention score was used as the total change, expressed as a percentage. A radial plot and z-scores were derived for each trial in all 17 cases, in order to illustrate inter-session changes. Cases with multi-structure and multi-level pathologies (O, P and Q), who received multi-level interventions, were more difficult to assess and the changes more difficult to interpret. Prior to participating in this study, the patient received a right L4-5 facet injection with minimal benefit. The patient was referred for consideration of an epidural cortisone injection and received almost instant pain relief, attributable to the local anaesthetic. Validated self-report questionnaires were used as additional outcome measures to identify change in pain, stiffness, health and function. This is consistent with facet biomechanics, since flexion causes facet load of less than 1/3 extension loading (Niosi et al. Again, a larger series of cases with these presentations would need to be studied to elaborate on this prediction. This was consistent with our description of the pain pattern of degenerative disc movement, and was noted in their imaging reports. Limitations and future studies these preliminary results must be reviewed within the limitations of the study. Additional sensors would be required to measure intersegmental movement (Alqhtani et al. This cohort investigation was designed to generate hypotheses based upon the possibility of specific movement signatures related to specific pathologies and as such, no formal power calculations were performed. Thirdly, this study was an observational study, which examined routine pain management intervention, therefore was not designed to assess the efficacy of the pain interventions planned for each case. The reasons for no immediate or short-term change may include multi-level pathology, movement adaptations and pain being confounded by dominant psychosocial issues (Deyo, 2015) or comorbidities. Funding sources and potential conflicts of interest There were no sources of funding or conflicts of interest associated with this research. Self-report outcome data showed 11 and seven cases improved by 30% in pain and stiffness, respectively. Three cases experienced clinically significant improvement in health survey and 10 on low back function self report. Bilateral restrictions in extension suggested central or bilateral posterior disc pathology with or without nerve root compression. Keywords: Lumbar spine; combined movement examination; intervertebral disc; radiculopathy; neurosurgery 6. The prevalence of lumbosacral radiculopathy is estimated to be 3-5%, distributed equally in men and women (Tarulli and Raynor, 2007). Improved diagnostic accuracy would confer cost advantages to the health system by enabling treatment to focus on particular sources of pain, and also would enable pathology specific interventions to be grouped for clinical research. The present study used a validated, accurate 3-D motion tracking system MotionStar (Monie et al. Common lumbar pathologies include degenerative disc, disc protrusion (unilateral or centrally) and radiculopathy (Moisa et al. Total change scores and z-scores (standard scores for normally distributed data) are reported. Of these, 18 individuals received neurosurgical intervention and completed post-intervention examination at 14 weeks (Figure 6. A variable can be converted to a z-score if the distribution of normal range for that variable is Gaussian. Total change scores (%) for self-reports and the direction of change in outcomes are depicted in Figure 6. The movement directions showing significant changes in z-scores were compared with specialist diagnosis, intervention and radiological imaging. In each series, post intervention score minus pre-intervention score was used as the total change, expressed as a percentage. The patient had received almost instant relief of pain in the hip and low back, and total change score for decrease in pain in the hip at the final test was 95%. This case stood with a left side lateral shift (Laslett, 2009) and complained of intermittent lower limb pain (R>>L) (Figure 6. The patient was unable to stand due to pain in the lower limbs, and had almost complete pain relief in sitting or flexed lumbar positions. Conservative attempts to control pain and improve function, including over the counter medication, physiotherapy, epidural and nerve root sleeve injections and an exercise program, were refractory. The patient was reviewed by a neurosurgeon and underwent bilateral laminectomy and discectomy with good effect. The patient underwent L5-S1 posterior decompression, discectomy and interbody fusion. Two unilateral discectomies cases (cases A and B), two bilateral discectomy cases (H, J) and two fusion cases (L, M) were used to illustrate this speculation. Removal of the disc material provided reportedly immediate relief of hip symptoms and the ability to stand straight. Modest improvements were observed in the two fusion cases (L and M) and two factors are likely to contribute to this observation. The inclusion criteria for this study did not specify single level, single structure patients. This observational study was designed to test two hypotheses, and more importantly generate additional hypotheses for future research based upon the possibility of specific movement signatures related to specific pathologies. The remaining cases all showed complications which may have mitigated this outcome.

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