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.

/pdf/the-hypoxic-testicle-physiology-and-pathophysiology-3q1awwjo26.pdf

The hypoxic testicle: physiology and pathophysiology.

AIM: To evaluate seven patients with non-traumatic splenic rupture (NSR). NSR is an uncommon dramatic abdominal emergency that requires immediate diagnosis and prompt surgical treatment to ensure the patient’s survival.

METHODS: Within 11 years, seven cases were evaluated for patient characteristics, anamnesis and symptoms, method of diagnosis, findings of laparotomy, and etiology of NSR.

RESULTS: There were six (86%) male and one female (14%) patient, whose mean age was 36 ± 12.8 (17-56) years. We report here four cases of Plasmodium vivax malaria (cases I-IV), one case of hemodialysis (case V), one case of spontaneous splenic rupture (case VI), and one case of hairy cell leukemia (case VII). Splenectomy was performed in all patients. All of them made an uneventful recovery and were discharged in stable condition.

CONCLUSION: NSR is a rare entity that needs a high index of suspicion for diagnosis. Using ultrasonography or computer tomography, and peritoneal aspiration of fresh blood may assist in the diagnosis of NSR. Increased awareness of NSR can enhance early diagnosis and effective treatment.

Non-traumatic splenic rupture: Report of seven cases and review of the literature

The incidence of Bochdalek and Morgagni hernias among adults is very rare The purpose of this study was to determine retrospectively the prevalence and characteristics of adult Bochdalek and Morgagni hernias in a decade Consequently, we demonstrated 12 patients with Bochdalek and 8 patients with Morgagni hernias We presented plain radiography, operation images, and computed tomography findings of an adult patient with symptoms due to Bochdalek and Morgagni hernias In surgical repair, the Morgagni hernia is best approached via laparotomy, and the Bochdalek hernia can be treated through thoracotomy or laparotomy

https://journals.viamedica.pl/folia_morphologica/article/download/19322/15215

A review of Morgagni and Bochdalek hernias in adults.

The corpus callosum (CC) is a major anatomical and functional commissure linking the two cerebral hemispheres. With MR imaging in the sagittal plane, the corpus callosum can be depicted in great detail. Mid-sagittal magnetic resonance images of 80 normal individuals were analyzed to assess whether or not the morphology of the corpus callosum and its parts are related to sex and handedness. The subjects were 40 males (20 right-handers and 20 left-handers) and 40 females (20 right-handers and 20 left-handers). The midsagittal area of the corpus callosum was divided into seven sub-areas using Witelson’s method. The most striking morphological changes concerned left-handers, who had larger areas of the anterior body, posterior body and isthmus than right-handers. In addition, right-handed males had larger rostrums and isthmuses than right-handed females. These significantly increased areas were related to handedness in right-handed males. However, left-handed males had larger anterior and posterior bodies than right-handed males. In contrast, there was no significant difference between left-handers and right-handers in females. The areas of the rostrum and posterior body of the corpus callosum increased significantly with sex in males. Moreover, there were no significant age-related changes in the total corpus callosum and sub-areas of the corpus callosum. In conclusion, these anatomical changes in corpus callosum morphology require taking the sexual definition and dominant handedness into consideration.

Sexual dimorphism and handedness in the human corpus callosum based on magnetic resonance imaging.

This study was designed to determine the effect of molsidomine (MO), a precursor of nitric oxide (NO) donor, on hypoxia inducible factor alpha (HIF-1α) and Sonic hedgehog (Shh) levels considered to be involved in the development of testes ischemia/reperfusion (I-R) injury. Torsions were created by rotating ipsilateral testes 720° in a clockwise direction for 6 h and 1-h detorsion of the testis was performed. A sham operation was performed in group 1 (control, n = 7). In group 2 (I-R/Untreated, n = 7), following 6 h of unilateral testicular torsion, 1-h detorsion of the testis was performed. No drug was given. In group 3 (I-R/MO), after performing the same surgical procedure as in group 2, a NO donor MO was given at the starting time of reperfusion. In group 4 (I-R/L-NAME), after performing the same surgical procedure as in group 2, L-NAME was given at the starting time of reperfusion. Testes malondialdehyde (MDA) levels were determined as well as examining the testes histologically. Treatment of rats with MO produced a significant reduction in the levels of MDA and histopathological score compared to testes I-R groups. The Sonic hedgehog (Shh) expression in the basement membrane of the tubuli seminiferi, and sertoli and germinal cells in testicular tissue, were greatly increased in the I-R/MO group compared to groups 1, 2 and 4. Additionally, the HIF-1α expression in the interstitial spaces in testicular tissue were greatly increased in the I-R/MO group. The results suggest that MO has a protective effect against ischemia/reperfusion injury in rat testes and may affect Shh and HIF-1α signaling pathway.

The effects of molsidomine on hypoxia inducible factor alpha and Sonic hedgehog in testicular ischemia/reperfusion injury in rats.

This study was designed to determine the effect of L-arginine on hypoxia inducible factor alpha (HIF-1 α) and Sonic hedgehog (Shh) levels considered to be involved in the development of ischemia/reperfusion (I/R) injury. Unilaterally nephrectomized Sprague-Dawley rats were subjected to 60 minutes of left renal ischemia followed by 45 minutes of reperfusion. Group 1 were sham-operated animals; group 2, I-R/Untreated animals; and group 3, I-R/L-Arg-treated animals. Serum creatinine, blood urea nitrogen (BUN), and kidney malondialdehyde (MDA) levels were determined as well as examining the kidneys histologically. The treatment of rats with L-Arg produced a significant reduction in the levels of BUN, creatinine, MDA, and histopathological score compared to renal I/R groups. The Shh expression in the tubulus epithelia were intensely increased in the I-R/L-Arg group when compared to that of the Sham-control and the I-R/untreated groups. Additionally, the HIF-1α expression in the tubulus epithelia and the inters...

https://www.tandfonline.com/doi/pdf/10.1080/08860220601166289

Mehmet Cudi Tuncer

Papers

Non-traumatic splenic rupture: Report of seven cases and review of the literature

A review of Morgagni and Bochdalek hernias in adults.

Sexual dimorphism and handedness in the human corpus callosum based on magnetic resonance imaging.

The effects of molsidomine on hypoxia inducible factor alpha and Sonic hedgehog in testicular ischemia/reperfusion injury in rats.

Nitric Oxide Regulates Expression of Sonic Hedgehog and Hypoxia-Inducible Factor-1α in an Experimental Model of Kidney Ischemia-Reperfusion