Distraction vs remodeling surgery for craniosynostosis

Objects We designed several distraction devices and applied these instruments in 14 patients with varying types of craniosynostosis. The aim of this report is to clarify the advantages and disadvantages of these surgical methods and to discuss current concepts for the surgical strategy in the treatment of craniosynostosis. Methods From January 2000 to July 2005, 28 patients with craniosynostosis were retrospectively analyzed. Surgical treatment was performed on 14 patients using the distraction method with internal distraction devices that we designed, in which 5 patients had plagiocephaly, 3 brachycephaly, and 6 scaphocephaly. All patients underwent preoperative and postoperative evaluations, which included the patient’s neurological state, and three-dimensional CT. Results With distraction devices, the time required for the surgery could be shortened almost 3 1/3 h; the bleeding during the surgery was decreased with reduced requirement of more than 200 ml of blood transfusion as compared with remodeling surgery. Postoperatively achieved distraction distances varied from 30.0 to 47.5 mm (mean, 42.99 mm). The average increased volume percent of cranium in distraction surgery group was 20.9% (range, −11.5 to 58.9%) after full distraction. Conclusion With distraction surgery, satisfactory cranial volume expansion and aesthetically pleasing morphological states were achieved in all cases, and the efficacy was statistically significantly high as compared with remodeling method.     

Akinetic Mutism and Cognitive-Affective Syndrome Caused by Unilateral PICA Infarction

A 42-year-old man with left posterior inferior cerebellar artery (PICA) infarction presented with akinetic mutism and cognitive impairment. Initially he suffered from akinetic mutism and MRI-documented infarction in the distribution of the left PICA. Twelve days later he developed cognitive impairment. Neuropsychological tests were performed, with the results corrected for age and education being compared with published Korean norms. Impaired performances were evident on executive function testing, with difficulties in planning, abstract reasoning, set-shifting, and perseveration. Akinetic mutism and cognitive-affective syndrome may be a manifestation of unilateral PICA infarction.     

TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice.

Tumor necrosis factor-alpha (TNFalpha) and Fas are induced after traumatic brain injury (TBI); however, their functional roles are incompletely understood. Using controlled cortical impact (CCI) and mice deficient in TNFalpha, Fas, or both (TNFalpha/Fas-/-), we hypothesized that TNFalpha and Fas receptor mediate secondary TBI in a redundant manner. Compared with wild type (WT), TNFalpha/Fas-/- mice had improved motor performance from 1 to 4 days (P<0.05), improved spatial memory acquisition at 8 to 14 days (P<0.05), and decreased brain lesion size at 2 and 6 weeks after CCI (P<0.05). Protection in TNFalpha/Fas-/- mice from histopathological and motor deficits was reversed by reconstitution with recombinant TNFalpha before CCI, and TNFalpha-/- mice administered anti-Fas ligand antibodies had improved spatial memory acquisition versus similarly treated WT mice (P<0.05). Tumor necrosis factor-alpha/Fas-/- mice had decreased the numbers of cortical cells with plasmalemma damage at 6 h (P<0.05 versus WT), and reduced matrix metalloproteinase-9 activity in injured brain at 48 and 72 h after CCI. In immature mice subjected to CCI, genetic inhibition of TNFalpha and Fas conferred beneficial effects on histopathology and spatial memory acquisition in adulthood (both P<0.05 versus WT), suggesting that the beneficial effects of TNFalpha/Fas inhibition may be permanent. The data suggest that redundant signaling pathways initiated by TNFalpha and Fas play pivotal roles in the pathogenesis of TBI, and that biochemical mechanisms downstream of TNFalpha/Fas may be novel therapeutic targets to limit neurological sequelae in children and adults with severe TBI.     

Ethical dilemmas in today's nuclear medicine and radiology practice.

Throughout history, societies have developed their own codes of ethics, including those pertaining to the practice of medicine. In the United States, physicians have adopted a set of ethics based on religious values and historical teachings. We, as physicians, have been presented several codes of ethics, including the American Medical Association Code of Ethics and the American College of Radiology Code of Ethics. Over time, we have learned to appropriately apply these codes to our daily practice. With the advent of new technologies in imaging, we may lose sight as to the transfer of these principles to reflect current conditions. Recent history has shown a trend of new technology leading to potential misuse of this technology and further leading to stricter governmental regulations. It is the purpose of this review to give guidelines for dealing with new technologies, such as PET imaging, and we describe a radiologist's ethical responsibility in a doctor-patient relationship. A historical review of medical ethics will lead to discussions about various issues affecting radiologists and nuclear physicians. To be sure, not all ethical situations are black and white, and therefore there are many gray areas. The opinions expressed in this article are those of the authors and are based on extension of already established rules of ethical conduct.     

Pinhole collimator scintigraphy in differential diagnosis of metastasis, fracture, and infections of the spine

The informational gains obtained by the use of pinhole collimator scintigraphy (PCS) have been well documented. The present study has been undertaken to prospectively investigate its efficacy in diagnosing several commonly occurring spinal diseases. Patient material consisted of metastatic cancer (39 vertebrae), compression fractures (33 vertebrae), tuberculous spondylitis (17 vertebrae), and pyogenic spondylitis (six vertebrae). PCS findings were characterized in terms of localization, appearance, and homogeneity of abnormal radionuclide accumulation. Thus, metastatic cancer manifested as diffusely or focally homogeneous accumulation within the vertebral body or as a typical short-segmental accumulation along the end-plate, whereas compression fracture manifested as characteristic board-like accumulation along the entire length of end-plates. Tuberculous spondylitis, on the other hand, revealed homogeneous accumulation throughout the vertebral body, and pyogenic spondylitis revealed accumulation at the end-zone of opposing vertebral bodies giving sandwich-like appearance. The disk space at the affected level was not narrowed in the former two diseases but it was narrowed in the latter two. It was concluded that PCS may be useful in differentiating metastatic cancer, compression fracture, tuberculous spondylitis, and pyogenic spondylitis.     

Production of uric acid in cerebrospinal fluid after subarachnoid hemorrhage in dogs: investigation of the possible role of xanthine oxidase in chronic vasospasm

Based on accumulating evidence of the role of xanthine oxidase (XO) in generating oxygen free radicals and causing tissue damage during ischemia, we examined the possible role of XO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). After inducing SAH in dogs by two autologous blood injections 2 days apart, chronic vasospasm of the basilar artery was reliably produced. There was a 3.5-fold elevation in uric acid (UA), the product of XO, in the cerebrospinal fluid (CSF) of these animals. Parenteral administration of allopurinol (i.v., 25 mg/kg, every 6 hours), a specific blocker of XO, successfully abolished the elevation in CSF uric acid levels due to SAH. However, angiographic vasospasm measured on Day 7, morphological changes observed by electron microscope, and elevated CSF prostaglandin levels were not altered by the treatment. It can be concluded that the observed activation of the enzyme XO, which is a well-known source of oxygen free radicals in ischemia in various organs, is not playing a major role in the pathogenesis of chronic cerebral vasospasm in this animal.     

High aggregate burden of somatic mtDNA point mutations in aging and Alzheimer's disease brain.

The mitochondrial theory of aging proposes that mitochondrial DNA (mtDNA) accumulates mutations with age, and that these mutations contribute to physiological decline in aging and degenerative diseases. Although a great deal of indirect evidence supports this hypothesis, the aggregate burden of mtDNA mutations, particularly point mutations, has not been systematically quantified in aging or neurodegenerative disorders. Therefore, we directly assessed the aggregate burden of brain mtDNA point mutations in 17 subjects with Alzheimer's disease (AD), 10 elderly control subjects and 14 younger control subjects, using a PCR-cloning-sequencing strategy. We found that brain mtDNA from elderly subjects had a higher aggregate burden of mutations than brain mtDNA from younger subjects. The average aggregate mutational burden in elderly subjects was 2 x 10(-4) mutations/bp. The bulk of these mutations were individually rare point mutations, 60% of which changed an amino acid. Control experiments ensure that these results were not due to artifacts arising from PCR error, mistaken identification of nuclear pseudogenes or ex vivo oxidation. Cytochrome oxidase activity correlated negatively with increasing mutational burden. These findings significantly bolster the mitochondrial theory of aging.     

Urological manifestations of isolated iliac artery aneurysms

Three patients with iliac artery aneurysms were seen at our institution with the chief complaints owing to urological manifestations. Iliac artery aneurysms may present with a transrectally palpable mass, hematuria, bladder outlet obstruction, ureteral obstruction, retroperitoneal fibrosis or renal failure. Any such manifestations may bring the aneurysm to the attention of a urologist before diagnosis.     

Cobalt-dependent potentiation of net inward current density in Helix aspersa neurons.

A low concentration of transition metal ions Co2+ and Ni2+ increases the inward current density in neurons from the land snail Helix aspersa. The currents were measured using a single electrode voltage-clamp/internal perfusion method under conditions in which the external Na+ was replaced by Tris+, the predominant external current carrying cation was Ca2+, and the internal perfusate contained 120 mM Cs+/0 K+; 30 mM tetraethylammonium (TEA) was added externally to block K+ current. In the presence of Co2+ (3 mM) or Ni2+ (0.5 mM) inward Ca2+ currents were stimulated normally by voltage-dependent activation of Ca2+ channels. There was a 5-10% decrease in the rate of rise of the inward current. The principal effect of Co2+ and Ni2+ in increasing the current density seems to be a decrease in the rate at which the inward currents decline during a depolarizing voltage pulse. The results may be due to a decrease in a voltage-dependent or Ca(2+)-dependent outward current and/or an inhibition of Ca2+ channel inactivation. Outward current under these conditions (zero internal K+) was significant and most likely due to Cs+ efflux through the voltage-activated or Ca(2+)-activated nonspecific cation channels. Co2+ is an extremely effective blocker of this outward current. These results are not an artifact of internal perfusion or the special ionic conditions. Intracellular recording of unperfused neurons in normal Helix Ringer's solution showed that the Ca(2+)-dependent action potential duration was increased significantly by low concentrations of Co2+. This result is consistant with the Co(2+)-dependent increase in inward (depolarizing) current seen in voltage-clamp experiments.