Diet and diversity at later medieval Fishergate: The isotopic evidence

We present the results of stable carbon and nitrogen isotope analysis of bone collagen for 155 individuals buried at the Later Medieval (13th to early 16th century AD) Gilbertine priory of St. Andrew, Fishergate in the city of York (UK). The data show significant variation in the consumption of marine foods between males and females as well as between individuals buried in different areas of the priory. Specifically, individuals from the crossing of the church and the cloister garth had consumed significantly less marine protein than those from other locations. Isotope data for four individuals diagnosed with diffuse idiopathic skeletal hyperostosis (DISH) are consistent with a diet rich in animal protein. We also observe that isotopic signals of individuals with perimortem sharp force trauma are unusual in the context of the Fishergate dataset. We discuss possible explanations for these patterns and suggest that there may have been a specialist hospital or a local tradition of burying victims of violent conflict at the priory. The results demonstrate how the integration of archaeological, osteological, and isotopic data can provide novel information about Medieval burial and society.

The aetiology and treatment of developmental stammering in childhood

Developmental stammering (DS, also known as idiopathic stammering or stuttering) is a disorder of speech fluency that affects approximately 0.75% to 1% of the populations of Great Britain, Australia and America,(1-4) although a recent study puts the point prevalence figure at between 1% and 3% in the UK.(5) Prevalence is generally thought to be similar amongst communities worldwide, although there have been occasional suggestions that this figure might be lower in countries where there is less pressure on verbal acuity.(6) DS may be distinguished from neurogenic stammering, which can occur subsequent to neurological damage of various aetiologies (for example, stroke, tumour, degenerative disease) and psychogenic stammering, whose onset can be related to a significant psychological event such as bereavement. While a diagnosis of neurogenic stammering might be made in early childhood and adolescence, both neurogenic and psychogenic types are typically associated with an adult onset. DS is by far the most common form of stammering and usually develops in the pre-school years. The mean age at onset is 4 2, with 75% of cases beginning before the age of 6.(1) However, occasionally, stammering onset may be seen as late as 12 or 13 years of age.

Isotopic examination of links between diet, social differentiation and DISH at the post-medieval Carmelite Friary of Aalst, Belgium

Stable isotope ratios (δ13C and δ15N) were measured in human burials from the post-medieval (16th–18th c. AD) Carmelite friary burial grounds at Aalst, a town in Flanders, Belgium. Dietary patterns of 39 adult individuals were analyzed, from a mixed monastic and lay population buried in three different locations, reflecting groups with differing social status. The data show significant variation in the consumption of perhaps meat, but certainly also marine protein between females and males. This result represents a remarkable continuity with medieval dietary patterns, suggesting that the social and economic changes of the early modern period had a limited effect on everyday life. When both sexes were examined together, individuals buried in the cloister garth consumed significantly less marine protein compared to people buried in the church, likely reflecting social stratification. No statistical differences were observed between isotopic values from the church and the cloister alley, suggesting a similarly diverse diet of the monastic part of the buried population and that of the richer lay population. Finally, the hypothesis that diffuse idiopathic skeletal hyperostosis (DISH) is linked to a diet rich in animal protein was tested. No systematic or statistically significant differences between pathological and non-pathological bones from the same individuals affected with DISH were observed, and no statistical differences were found between individuals with DISH and individuals without DISH

Distinct clinical and neuropathological features of G51D SNCA mutation cases compared with SNCA duplication and H50Q mutation

Background: We and others have described the neurodegenerative disorder caused by G51D SNCA mutation which shares characteristics of Parkinson’s disease (PD) and multiple system atrophy (MSA). The objective of this investigation was to extend the description of the clinical and neuropathological hallmarks of G51D mutant SNCA-associated disease by the study of two additional cases from a further G51D SNCA kindred and to compare the features of this group with a SNCA duplication case and a H50Q SNCA mutation case. Results: All three G51D patients were clinically characterised by parkinsonism, dementia, visual hallucinations, autonomic dysfunction and pyramidal signs with variable age at disease onset and levodopa response. The H50Q SNCA mutation case had a clinical picture that mimicked late-onset idiopathic PD with a good and sustained levodopa response. The SNCA duplication case presented with a clinical phenotype of frontotemporal dementia with marked behavioural changes, pyramidal signs, postural hypotension and transiently levodopa responsive parkinsonism. Detailed post-mortem neuropathological analysis was performed in all cases. All three G51D cases had abundant α-synuclein pathology with characteristics of both PD and MSA. These included widespread cortical and subcortical neuronal α-synuclein inclusions together with small numbers of inclusions resembling glial cytoplasmic inclusions (GCIs) in oligodendrocytes. In contrast the H50Q and SNCA duplication cases, had α-synuclein pathology resembling idiopathic PD without GCIs. Phosphorylated α-synuclein was present in all inclusions types in G51D cases but was more restricted in SNCA duplication and H50Q mutation. Inclusions were also immunoreactive for the 5G4 antibody indicating their highly aggregated and likely fibrillar state. Conclusions: Our characterisation of the clinical and neuropathological features of the present small series of G51D SNCA mutation cases should aid the recognition of this clinico-pathological entity. The neuropathological features of these cases consistently share characteristics of PD and MSA and are distinct from PD patients carrying the H50Q or SNCA duplication.