The Expanding Concept of Just Compensation and the Role of the Appraiser

Compensation for injury to business profits in eminent domain actions has long been the focus of controversy. Historically, the federal and state courts explicitly excluded profits or goodwill from a determination of an award. Under this scheme the measure of compensation quickly settled on the market value of the condemned realty. Where injury to profits was especially evident, the courts sometimes allowed future returns to the business to be included as a factor which would influence the market value. They also developed, in some states, the "specialty" doctrine where the business was unique in any number of ways. Still, the measures of compensation adopted in these cases may have been inadequate to return the business owner to the same financial position as before a taking.In this paper, we review an expanded theory of just compensation currently emerging in the courts and indicate the measure of compensation necessary to effectively return the business owner to the same financial position after a taking as before. We also show that traditional awards have been less than adequate in cases where the cash flows accruing to a business are dependent, in some fashion, on the expropriated realty.Finally, we indicate the nature of awards under a jurisdiction which is unique in the sense that it explicitly requires consideration of all elements of loss resulting from expropriation of business properties. Those awards represent a departure from previous compensation measures and conform to those indicated by the theory developed in this paper. The role of the appraiser is outlined under this expanded system of compensation. Copyright American Real Estate and Urban Economics Association.

Chronic pain : a complex condition with a multi-tangential approach

Chronic pain is known as ongoing pain that lasts longer than three months with increasing healing time. It is approximated that 20% of adults of different sexes, races, and socioeconomic backgrounds fall victim to chronic pain. It is a result of several factors and can have lifelong effects. Pain is a complex matter to measure; therefore, the physician needs to understand the patient’s health state to create a management plan tending to each issue adequately. There are many complications of such pain, and it can interfere terribly with an individual’s quality of life. This article has reviewed the complex pathogenesis of chronic pain and the spectrum of non-pharmacologic modalities and pharmacological treatment options. It has also explored the efficacy of certain drugs and underlined the importance of nonpharmacological options such as physical exercise, cognitive therapy, and physical modalities to treat chronic pain and all the conditions that accompany this disorder

Evidence of a non-progressive course of alternating hemiplegia of childhood: study of a large cohort of children and adults

Alternating hemiplegia of childhood is a neurological disorder characterized by episodes of hemiplegia, various non-epileptic paroxysmal events and global neurological impairment. Characterization of the evolution and outcome into adulthood has not been sufficiently investigated. The goal of this study was to elucidate the natural history of alternating hemiplegia within a large cohort of 157 patients, as part of the European Network for Research on Alternating Hemiplegia project. A questionnaire was formulated to determine the severity of both paroxysmal and global neurological impairment and address progression of the disorder by allocating data to specific age epochs up to and over 24 years of age. Patients in early age groups were consistently present in subsequent later age groups and for each patient, data were collected for each corresponding age epoch. The study was based on predominantly retrospective and, for a period of 2 years, prospective data. At inclusion, patients were aged from 9 months to 52 years. The median age at diagnosis was 20 months. All patients experienced hemiplegic attacks; 86.5% reported episodes of bilateral weakness, 88% dystonic attacks, 53% epileptic seizures, 72% developed chorea and/or dystonia and 92% mental retardation. When data over the course of the illness were examined for the whole cohort, the severity of symptoms did not appear to change, with the exception of abnormal ocular movements and hypotonia that regressed, but did not disappear into adulthood (from 86 to 36% and 76 to 36%, respectively). No statistically significant correlation between a history of severe paroxysmal hemiplegic/dystonic episodes and a worse neurological outcome was identified. Seven patients died, some of whom experienced severe plegic attacks or epileptic seizures at the time of death. History of severe plegic/dystonic attacks was not found to be an aggravating factor for deceased patients. Our results provide evidence that the natural history of alternating hemiplegia is highly variable and unpredictable for individual patients. However, we did not find evidence to support a steadily progressive and degenerative course of the disorder when patients were analysed as a group. For a minority of patients, a risk of sudden death was associated with more severe neurological impairment. The European Network for Research on Alternating Hemiplegia Registry, validated by our study, includes all major neurological signs and symptoms of alternating hemiplegia and may thus be used as a precedent for the progressive inclusion and follow-up of patients as well as a reference for genetic studies and treatment trials.Paroxysmal Cerebral Disorder

De novo mutations in ATP1A3 cause alternating hemiplegia of childhood

Alternating hemiplegia of childhood (AHC) is a rare, severe neurodevelopmental syndrome characterized by recurrent hemiplegic episodes and distinct neurological manifestations. AHC is usually a sporadic disorder and has unknown etiology. We used exome sequencing of seven patients with AHC and their unaffected parents to identify de novo nonsynonymous mutations in ATP1A3 in all seven individuals. In a subsequent sequence analysis of ATP1A3 in 98 other patients with AHC, we found that ATP1A3 mutations were likely to be responsible for at least 74% of the cases; we also identified one inherited mutation in a case of familial AHC. Notably, most AHC cases are caused by one of seven recurrent ATP1A3 mutations, one of which was observed in 36 patients. Unlike ATP1A3 mutations that cause rapid-onset dystonia-parkinsonism, AHC-causing mutations in this gene caused consistent reductions in ATPase activity without affecting the level of protein expression. This work identifies de novo ATP1A3 mutations as the primary cause of AHC and offers insight into disease pathophysiology by expanding the spectrum of phenotypes associated with mutations in ATP1A3