Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum. We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions.

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Psychosis and autism as diametrical disorders of the social brain

This is a very good book and a very important one. The list of authors (107) reads like the ‘Who’s Who’ of spinal cord medicine. The volume is much more than an update of previous volumes of the ‘Handbook’, which also dealt with this topic and were published in 1976 and 1992. New developments have produced important and exciting changes that have altered the subject almost beyond recognition. This statement is true as regards the clinical achievments including diagnosis, prognosis and rehabilitation, but not quite so accurate as regards pre-clinical research. The 38 chapters form five sections. The first section, on development and anatomical perspectives, deals with the growth and maturation of the spinal cord. A good overview of the embryology, both cellular and molecular, is followed by a description of maldevelopment and the implications of molecular and genetic defects. The anatomy and biomechanisms are dealt with in terms of fundamental principles applied to the spinal column and spinal cord, and lead on to spinal cord injury. This is a good base for the following chapters that form the second section and which deal with the diagnosis, prognosis and monitoring of spinal cord trauma. Hopefully, in the future, there will be clinical trials of therapeutic interventions (but more of that later), and this will require accurate and quantitative measurement. The standard and recognized method is the ASIA scale, but this has limitations, and the best potential lies with neurophysiology and with advanced high-resolution neuroimaging techniques.This is dealt with in two excellent and comprehensive chapters. The majority of spinal cord injury outcome measures are understandably related to the younger population. However, the increasingly ageing population in most countries has to be addressed. This is a problem in the entire field of medicine. Specifically, in spinal cord injury, the average age of injury has increased and is still increasing. A short but notable chapter deals with the pathophysiology of the ageing nervous system, the aetiology and clinical presentation, complications and mortality and outcome. The third section deals with acute spinal cord injury: medical and surgical treatment, management and rehabilitation. These are useful straightforward reviews but are also good accounts of exciting developments. It is pointed out, and it cannot be over-emphasized, that spinal cord injury, although interrupting motor and sensory long tracts, still leaves neuronal networks intact below the site of the lesion. This is potentially a much more fruitful area of study than the conventional, and so far fruitless, pursuit of axonal repair. Chapter 20, on the changing field of rehabilitation, gives a brief account of how neural activity has a role in central nervous system (CNS) development and plasticity, but this important subject could have been improved to a great extent. A chapter on spinal cord stimulation (SCS) should have given more prominence to Cook, who, in the early 1970s, was the first to demonstrate improvement in neurological deficit with SCS. He was carrying out this procedure for pain on a young sufferer with multiple sclerosis when to his great surprise he saw a marked improvement in spasticity with consequent improvement in ambulation. The speed of change suggested that this was almost certainly due to an increase in inhibition. Cook took his observations to the neurologists in his hospital and later to the neurological societies in New York. They refused to even investigate this. Subsequent studies (elsewhere) demonstrated recordable and reproducible neurophysiologcal changes at spinal and brain-stem levels and eventually led to the formation of the International Neuromodulation Society. What Cook had observed was no more than that reported by Frohlich and Sherrington in 1902: after decerebration in cat, dog and Macaque, stimulation of the lower thoracic and lumbar region of the spinal cord showed ‘..an effect...constant and regular...evoked marked inhibition of the rigidity..’. Cook deserves much greater recognition. Section 4 is concerned with chronic-stage rehabilitation, and overlaps with the previous section. In fact, it is difficult to see why the two sections were separated. ‘Rehabilitation strategies that optimize spontaneous repair and promote neurological recovery are becoming mainstream’. Is this perhaps rather optimistic? ‘Spontaneous repair’ and ‘neurological recovery’ risks undue raising of hopes. This is based on a single case report about 11 years ago. Nevertheless, this is an interesting section that, in this chapter, deals with the effect of activity including electrical stimulation on synapses. Although the field is not exactly comprehensively covered, a good trenchant point is made: that conventional rehabilitation of spinal cord disease ignores the beneficial effects of afferent feedback and stimulation, which is aninteresting and potentially exciting concept that brings into focus the undamaged, but altered, central nervous system. The final section, section 5, deals with preclinical research ‘bridging the gap between bench and bedside.’ This is the longest section in 15 chapters and approximately one-third of the total volume.The first chapter in this section sets out the goals for therapy, discusses protocols and gives an algorithm for discovery through to clinical use. The authors point out that no clinical trial so far has been shown to be effective (reviewer’s emphasis). An outstanding and thoughtful chapter follows, again emphasizing the improvement in animals and man with appropriate afferent input, and discusses the challenges to be met. However, there is some inconsistency among the contributors, which, though understandable, is somewhat confusing. Chapter 25 states that ‘basic research in spinal cord repair is promising’. A more realistic description might state the opposite. Further chapters point out that there are no satisfactory solutions. Indeed, chapter 33 begins with ‘so far, there is no clinical procedure for inducing severed nerve fibres to regenerate’. Further on, the authors state that ‘the grandfather of the transplantation strategies was espoused by Santiago Ramon y Cajal in the 19th century’. Spinal Cord (2013) 51, 797–799 & 2013 International Spinal Cord Society All rights reserved 1362-4393/13

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Handbook of clinical neurology

Laterality: Functional Asymmetry in the Intact Brain.

The authors of this text are both plastic surgeons. Dr Dellon has studied sensory nerves extensively, sensibility testing and sensory reeducation in particular. Dr Mackinnon has had a long-term interest in nerve physiology as it relates to surgery on peripheral nerves and, particularly, grafting with autografts and allografts. Both authors are international authorities in their fields, and they also have a large experience with various peripheral nerve problems that are treated surgically. In order to be logical, comprehensive, and nonrepetitious, the authors have chosen to write this text themselves, and this appears to be a very good decision. The focus of this text is the surgery of peripheral nerve disorders, with which the authors have extensive, either clinical or research, experience. They have chosen a strict organization of the contents that starts with a macroscopic, microscopic, and ultrastructural description of the anatomy of peripheral nerves. The physiology of peripheral nerves

Surgery of the Peripheral Nerve

Mammalian spermatogenesis is a complex biological process occurring in the seminiferous tubules in the testis. This process represents a delicate balance between cell proliferation, differentiation, and apoptosis. In most mammals, the testicles are kept in the scrotum 2 to 7°C below body core temperature, and the spermatogenic process proceeds with a blood and oxygen supply that is fairly independent of changes in other vascular beds in the body. Despite this apparently well-controlled local environment, pathologies such as varicocele or testicular torsion and environmental exposure to low oxygen (hypoxia) can result in changes in blood flow, nutrients, and oxygen supply along with an increased local temperature that may induce adverse effects on Leydig cell function and spermatogenesis. These conditions may lead to male subfertility or infertility. Our literature analyses and our own results suggest that conditions such as germ cell apoptosis and DNA damage are common features in hypoxia and varicocele and testicular torsion. Furthermore, oxidative damage seems to be present in these conditions during the initiation stages of germ cell damage and apoptosis. Other mechanisms like membrane-bound metalloproteinases and phospholipase A2 activation could also be part of the pathophysiological consequences of testicular hypoxia.

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The hypoxic testicle: physiology and pathophysiology.

Background: An abscess is a pocket of pus that forms around the root of an infected tooth. In this study, we aimed to investigate the extracellular matrix proteases ADAMTS1, ADAMTS4, osteonectin, and osteopontin expressions in abscess fluid cells in jaws after implantation and prosthesis operation. Materials and methods: In this clinical study, abscess fluids belonging to 17 patients who applied to the Department of Oral and Maxillofacial Surgery were examined histopathologically and immunohistochemically. In the histopathological examination of the abscess fluid, separation of chromatin bridges in the nuclei of neutrophil cells, pyknosis and apoptotic changes in the nucleus, degenerative change in the cytoplasm, and occasional vacuolar structures were observed. Results: The positive reaction of ADAMTS1 was observed in fibroblast cells, plasma cells, and macrophage cells. The positive reaction of ADAMTS4 was observed in fibroblast cells, osteoclast cells, and some apoptotic leukocyte cells. Osteopontin expression in osteoclastic cells and polymorphonuclear cells was defined as positive. Osteonectin expression was positive in polymorphonuclear leukocytes and hypertrophic fibroblast cells. Conclusions: ADAMTS1 and ADAMTS4 may induce bone destruction with its distinctive property in alveolar bone resorption, which promotes the activation of osteoclasts, which can accelerate the destruction of the extracellular matrix in the acute phase. Furthermore, osteoclastic activity increased with the increase of osteonectin and osteopontin protein expression due to inflammation in the abscess cases.

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Histopathologic and immunohistochemical investigations of dental abscess formed in maxillofacial area

Common presentation of atretic parietal cephalocele is mostly seen in infants and young children. It is a palpable midline parietal soft tissue mass which is thought to represent involuted true cephalocele (meningocele or encephalocele) connected to dura mater via a fibrous stalk. Atretic parietal cephalocele is associated with increased incidence of intracranial anomalies.. Parietal cephaloceles comprise about 1% of all cerebrospinal congenital malformations and 10% of cephaloceles. We report here the case of an atretic parietal cephalocele with no associated brain malformations in adult.

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Recurrence of atretic parietal cephalocele in adult: a case report and review of literature.

This study has goals of examining whether pre-eclampsia may lead to an increase of elastic tissue fibers in blood vessel walls of placental stem villi or whether there are differences in the thickness of blood vessel walls within these villi when compared to normotensive pregnant women. Non-infarcted placental tissue samples from 28 participants with uncomplicated pregnancies and 26 patients with pre-eclampsia were obtained. After routine histological procedures, the sections were processed either for conventional Verhoeff staining for the demonstration of elastic fiber system. Paraffine sections from placenta biopsies prepared for light microscopic examination were gathered. In uncomplicated pregnancies, terminal villi blood vessels were observed with no stained elastic tissue fibers in most areas. In the pre-eclampsia pregnancy of human placenta, the elastic fibers significiantly increased in terminal villi blood vessel walls which were dark in color, using Verhoeff’s tissue stain, when comparing with the uncomplicated pregnancy group. Our results indicate that an increase of elastic tissue fibers in blood vessels of placental stem villus and terminal villi, and also an increase of wall thickness during pre-eclampsia.

An increase of elastic tissue fibers in blood vessel walls of placental stem villi and differences in the thickness of blood vessel walls in third trimester pre-eclampsia pregnancies

Posterior fossa tumors (PFTs) include medulloblastomas, atypical teratoid/rhabdoid tumors, pilocytic astrocytomas, ependymomas, and brainstem gliomas We evaluated patients with surgery at our clinic, comparing epidemiological, clinical, radiological, and pathological characteristics of medulloblastoma and ependymoma to identify factors that might assist preoperative diagnosis, help to develop treatment algorithms, and have prognostic value after surgery Pediatric patients from 0 to 16 and young adults from 16 to 29 years of age with surgery for pathologically confirmed ependymomas or medulloblastomas between January 2014 and January 2020 were eligible The study included 19 patients, seven with ependymoma (37%) and 12 with medulloblastoma (632%) The ependymoma patients were 529 ± 585 years of age, the medulloblastoma patients were 1158 ± 817 years of age, and 16 patients (84%) were childrenFifteen patients (79%) presented with signs of increased intracranial pressure and four (21%) presented with cerebellar findings MRI found that 74% (14) of the PSTs were located in the midline, including six of the seven ependymomas (86%) and eight of the 12 medulloblastomas (67%) Enhancement was significantly greater in medulloblastomas compared with ependymomas (p = 0022) In according to pathology results; synaptophysin, NSE, chromogranin and 50% GFAP positivity were observed in medulloblastoma Ependymomas were S100 (43%) and vimentin (29%) positive Ependymoma patients were younger than medulloblastoma patients and more were female There were no significant differences in the clinical findings, but ependymomas were larger and had greater rates of enhancement and spinal metastasis compared with medulloblastomas

Comparison of ependymomas and medulloblastomas located in the posterior cranial fossa: An anatomical and histopathological study.

Although fiber-reinforced composites are commonly used in dental practice, whether fiber-reinforced crowns and fixed partial dentures can be used as definitive prostheses remains to be determined. This study used scanning electron microscopy to evaluate the load-bearing capacity of non-reinforced and fiber-reinforced composite (FRC) molar crowns prepared by computer-aided design/computer-aided manufacturing (CAD/CAM). The crowns were fabricated from three empirical FRC blocks, one empirical composite block, and one commercial ceramic block. The FRC resin was prepared by mixing BaO silicate particles, E-glass fiber, and dimethacrylate resin. Specimens were divided into five groups (n = 10), differing in the amounts of filler, resin, and fiber. Crowns were statically loaded until fracture. One-way analysis of variance and Tukey's post hoc multiple comparison tests were used for statistical analyses. The groups showed significant differences in load-bearing capacity; empirical bidirectional FRC resin blocks had the highest capacity, while commercial ceramic blocks had the lowest capacity. Molar crowns formed from FRC resin blocks had higher load-bearing capacity compared to non-reinforced composite resin and ceramic blocks. These results show that fiber reinforcement increased the load-bearing capacity of molar crowns.

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Mehmet Cudi Tuncer

Papers

Histopathologic and immunohistochemical investigations of dental abscess formed in maxillofacial area

Recurrence of atretic parietal cephalocele in adult: a case report and review of literature.

An increase of elastic tissue fibers in blood vessel walls of placental stem villi and differences in the thickness of blood vessel walls in third trimester pre-eclampsia pregnancies

Comparison of ependymomas and medulloblastomas located in the posterior cranial fossa: An anatomical and histopathological study.

Scanning electron microscopy assessment of the load-bearing capacity of cad/cam-fabricated molar crowns.