Autopsy verifies demyelination and lack of vascular damage in partially reversible radiation myelopathy.

STUDY DESIGN: Case report of recovering radiation myelopathy. OBJECTIVE: To present autopsy and functional imaging findings on a unique case of slowly recovering radiation myelopathy with the aim of the clarification of the underlying mechanism. PATIENT: The cervical spinal cord and the distal part of the medulla oblongata of a 36-year-old thyroid cancer patient had been incorrectly irradiated with a total dose of 61 Gy and a fraction size of 3.4 Gy (J Neurol Sci 1999; 163:39-43), resulting in incomplete cervical transection with a 5-month latency period following the termination of radiotherapy. This was followed by a 9.5-year spontaneous improvement until her demise, during which the check-ups were supplemented by positron emission tomography (PET) investigations; these indicated increased [18F]deoxyglucose and [15O]butanol uptakes, but a diminished [11C]methionine accumulation by the irradiated spinal cord segment. RESULTS: Autopsy revealed demyelination (with axonal loss) and neuronal damage in the cervical spinal cord and the distal part of the medulla oblongata. In the same region, only minimal vascular injury (thickening of some of the capillary walls) was detected, but not cell proliferation or chronic inflammation. Bilateral, secondary pyramidal tract degeneration caudal to the irradiated segment was observed. The PET and autopsy findings, although separated by 2 years, are consistent. CONCLUSIONS: The pathological state of the spinal cord revealed by the autopsy is concordant with the incomplete cervical transection, implying that the functional recovery is supported by a process that probably differs from the restoration of the mechanism destroyed by the radiotherapy. For the restoration of the function, we suggest an altered conduction mechanism of the action potential, involving an increased number of sodium channels along the demyelinated segments of the injured axons, which is fully congruent with the PET findings.

[Platelet glycoprotein IIb/IIIa (LeuPro 33) polymorphism in stroke patients]. / Stroke-betegek thrombocyta glikoprotein IIb/IIIa (Leu Pro 33) polimorfizmusának vizsgálata.

This is the first Hungarian paper on the platelet glycoprotein IIb/IIIa (LeuPro 33) polymorphism in stroke patients. There are conflicting data about the role of this polymorphism in the pathogenesis of arterial thrombosis. The aim of our study was to describe the prevalence of PLA1/PLA2 in healthy persons and in stroke patients. From the same study population other polymorphism (prothrombin gene 20210 G/A) also has been determined. Blood sample was investigated by polymerase chain reaction in 173 unrelated healthy donors and 234 stroke patients. Stroke was documented by CT and MRI. We used a rutin questionnaire to study previous vascular events and conventional risk factors of patients. Prevalence of PLA1/PLA2 was 23.5% among healthy persons. That is higher than in other European countries (15%). It was 30.4% in stroke patients (OR: 1.42, 95%; CI: 0.87-2.31; p = 0.15). Heterozigous PLA was found in patients older than 50 by 33.6% (OR: 1.65, 95%; CI: 0.94-2.87; p = 0.09). Previous vascular events and conventional risk profil were not significantly different between PLA1/PLA1 and PLA1/PLA2 groups of patients. In patients under 50 having 20-85% stenosis of internal carotid artery there was a higher prevalence (p = 0.09). Comparing stroke patients to control population there was a slight increase (OR: 7.0; p = 0.06) in the frequency of two polymorphisms (PLA and factor II) together in the stroke cases. Polymorphism of GP IIb/IIIa LeuPro 33 seemed to be increased in stroke patients above 50 years. Carotid stenosis with polymorphism is a risk factor for young patients. PLA variant together with prothrombin gene polymorphism results very high risk for stroke.

High sensitivity to autoxidation in neonatal calf erythrocytes: possible mechanism of accelerated cell aging.

The suspension viscosity, formation of methaemoglobin and production of malondialdehyde (MDA) associated with the non-enzymatic oxidation of polyunsaturated fatty acids during auto-oxidation conditions in vitro have been compared in erythrocytes from young calves (2, 4 and 6 weeks of age) and mature cattle. The autoxidation conditions were designed to simulate the oxidative stress to which neonatal erythrocytes are exposed in vivo. Characterisation of lipid peroxidation was also undertaken by a combination of lipid fluorescent measurements and quantification of the superoxide dismutase (SOD) activities of the erythrocytes. The results demonstrated that high SOD activities in the erythrocytes of the neonatal calf was insufficient to afford protection against the increased autoxidation of haemoglobin and subsequent accumulation of lipid peroxidation products. High levels of methaemoglobin formation and lipid peroxidation were able to provide an explanation for an observed reduction in rheological adaptability (increased suspension viscosity) and an accelerated aging of the neonatal cells under in vivo conditions.

Radiation myelopathy with partial functional recovery: PET evidence of long-term increased metabolic activity of the spinal cord.

Postoperative telecobalt irradiation was performed with a biologically effective extrapolated response dose of 165 Gy2 delivered to the spinal cord of a papillary thyroid cancer patient. Incomplete cervical transection developed, followed by a gradual functional improvement, which is still continuing 8 years after radiotherapy. Between the 6th and 8th years of the clinical course, positron emission tomography investigations demonstrated an increased 18F-deoxyglucose accumulation and (15)O-butanol perfusion, but negligible 11C-methionine uptake in the irradiated spinal cord segment. We suggest that the increased metabolism and perfusion, and the lack of detectable protein synthesis may be related to the increased energy demands of action potential conduction, due to the higher than normal density of sodium channels along demyelinated axons displaying restored conduction.

[Successful management of malum perforans resulting from spina bifida]. / Spina bifida occulta következtében kialakuló malum perforans sikeres kezelése.

Authors observed a boy presented a protrusion positioned lumbosacral, existing since his birth. Later, on inner side of both heels ulcers began to take shape, being not curable by local treatment. Neurologic examination verified severe radicular lesion, magnetic resonance investigation showed lumbosacral lipo-meningocele. After its surgical treatment, ulcers on soles healed up. Neurotropic ulcer develops on sites exposed to pressure, being generally painless. Several sickness may lead to its development. In childhood occurrence is relatively rare. At this age mostly various closure troubles of medullary tube may stand in the background. To successful treatment of malum perforans--besides local therapy--that of underlying illness is essential as well.

[Sneddon syndrome (livedo and cerebrovascular lesion)]. / Sneddon-syndroma (livedo és cerebrovascularis laesio).

A typical syndrome going on with skin (livedo racemosa generalisata) and brain (ischemic vascular) involvement is presented. Symptoms of skin and nervous system are made known in detail, as well as possibility of early diagnosis and standpoint of treatment.

Action and interaction of perivascular H+, K+ and Ca++ on pial arteries.

In cats the perivascular space of small pial arteries was perfused with mock CSF by means of micropipettes. Variations of K+, H+ and Ca++ activities in the perfusate cause changes of the diameters of the affected vessels. Increases of H+ and moderate increases of K+ lead to dilatations, Ca++ -increases elicit constrictions. The ions interact in such a way that perivascular Ca++ inhibits the K+ or H+ induced dilator response of the pial arteries. Alkalosis intensifies the constrictor action of Ca++. Perivascular microperfusion with Ca++ -free mock CSF causes dilatation which can be augmented by additional acidosis (pH 6.5). However, an increase of K+ to 10.8-10(-3) mol.1(-1) (4 times normal) does not change the diameters of the vessels already dilated, thus indicating differences in the action of K+ and H+ upon the membranes of the pial vascular smooth muscle cells. Small vessels (less than 80 micron diameter) respond with a significantly stronger dilatation when Ca++ is complexed with EGTA as compared with vessels of more than 80 micron diameter.