[Movement technology in the rehabilitation after stroke: hype or hope?] / Bewegingstechnologische therapieën na een beroerte.

Application of movement technology in the rehabilitation of neurological disorders has gained a firm position within a short time span, but the effectiveness of many technological innovations is still poorly supported by evidence. Should this burst of movement technology be considered a hype or is it offering realistic hope? This perspective focuses on motor rehabilitation after unilateral stroke and addresses the value of rehabilitation robots, virtual-reality training, peripheral neurostimulation, and brain stimulation. Current rehabilitation robots offer added value compared to conventional training, but only early after stroke for patients who are not yet able to walk independently. The effects of peripheral neurostimulation or brain stimulation are still hard to prove or relatively small. Virtual-reality training seems to be most promising for regaining motor skills, particularly when adjusted to individual capacities. Overall, functional benefits of movement technology in the rehabilitation of neurological disorders keep the middle between hype and hope.

The behaviour of the periodontal ligament is influencing the use of new treatment tools.

Orthodontic treatment can cause resorptions on teeth. Factors causing resorptions are forces and moments. Other factors that cause resorptions are less influenced by an orthodontic treatment. By carrying out experiments and finite element calculations, it was possible to demonstrate that forces and moments will produce stress in certain parts of the periodontal ligament and the root. This stress reaches or exceeds the blood pressure in some areas. To avoid high pressure in those areas, new treatment devices were constructed consisting of NiTi wires or a combination of NiTi and stainless steel. In the levelling phase, the acting forces remained below 0.5 N using NiTi wire with a diameter of 0.012' (using elastic ligatures). With a NiTi stainless steel spring molars can be uprighted. The orthodontist can easily choose between an intrusive force, a very low intrusive force and an extrusive force. Because of the use of NiTi elements, there was acting an almost constant moment.

Cytochrome P450 2D6 and glutathione S-transferase genotype in sudden infant death syndrome.

OBJECTIVES: The risk of sudden infant death syndrome (SIDS) has been linked with xenobiotic exposures, race and inheritance. Because cytochrome P450 2D6 (CYP2D6) and glutathione S-transferases (GSTM1 and GSTT1) are genetically regulated, polymorphically distributed, and responsible for detoxification of many centrally acting exogenous and endogenous bioactive compounds, our objective was to determine whether the prevalences of deficiencies in CYP2D6, GSTM1, and GSTT1 differ in SIDS victims compared to healthy controls. METHODS: CYP2D6 mutations (deletion, A, B, and T alleles) and GSTM1 and GSTT1 null genotypes were assessed in DNA from 50 SIDS victims. CYP2D6 phenotype, assigned using dextromethorphan urinary ratios, was assessed in 25 unrelated parents of SIDS victims. RESULTS: The CYP2D6B mutation was the only mutant CYP2D6 allele found in SIDS victims, present in 26.2% of patients (11/42) and 13.1% (11/84) of alleles. Adjusting for race, the prevalence of wild-type CYP2D6 alleles and of homozygous wild-type CYP2D6 phenotype was not different in SIDS victims compared to controls (P = 0.585 and 0.224, respectively). Among the 25 parents of SIDS victims, all subjects were extensive metabolizers, a prevalence not different from controls (P = 0.243). The prevalence of the null genotype for GSTM1, GSTT1 and double-null for GSTM1 and GSTT1 was 33.3%, 21.4% and 9.5%, respectively, among SIDS victims, and was not different than controls (P = 0.61, 0.1, 0.28, respectively). The combination of CYP2D6 homozygous wild-type genotype and the null genotype for GSTM1, GSTT1, or both GSTM1 + GSTT1 also did not differ in SIDS victims and controls. CONCLUSIONS: The frequencies of CYP2D6 mutant genotypes and the null genotypes for GSTM1 and GSTT1 were not different among SIDS victims compared to normal controls, and thus these polymorphisms are unlikely to identify families with a high risk of SIDS.

Haemorrhagic endovasculitis of the placenta: a review with clinical correlation.

Haemorrhagic endovasculitis (HEV) is a recently described vasodestructive process within the placenta. Similarities to several forms of thrombotic microangiopathy are evident. Clinical studies have shown strong associations between HEV, still birth and intrauterine growth retardation (IUGR). Liveborn infants, with affected placentae, evaluated at the age of five, exhibit a high incidence of neurological abnormalities. HEV has been recurrent in successive pregnancies in some patients. Clinicopathological processes, which appear to be associated with HEV, include the presence of chronic villitis (VUA) and maternal hypertension. Viral- and/or Mycoplasma-type particles have been identified in a number of affected placentae examined by electron microscopy. Associated pathological events suggest an infectious aetiology possibly acting in concert with an environmental toxin. Biochemical factors and alterations of immune response within the maternal-placental-fetal unit may be involved.

The surgical pathologist examines the placenta.

In this chapter, placental development, morphology, and indications for its examination have been reviewed. Techniques for placental examination with practical suggestions applicable to the surgical pathology laboratory have been pointed out. Several specific examples of clinical conditions in which morphologic alterations within the placenta assist with or establish a diagnosis have been presented. It is hoped that this information will encourage pathologists to use this important organ more fully as a resource in diagnoses and patient care.

Placental hemorrhagic endovasculitis: risk factors and impact on pregnancy outcome.

Two hundred and eighteen cases of hemorrhagic endovasculitis (HEV), a recently recognized abnormality of human placentas, were identified from placentas submitted to the Michigan Placental Tissue Registry over a 2.5-year period. HEV appears to focus on fetal placental blood vessels with resultant fragmentation and destruction of fetal RBCs, hemorrhage into villous stroma, microthrombi in villous capillaries and non-exudative necrosis of medium sized chorionic vessels. Placentas without HEV submitted for evaluation from the same hospitals were selected for comparison. Women with HEV placentas were of similar age, race and parity as control women. The sex of the fetus of HEV cases was somewhat more often female (57% vs. 48%, P = 0.05). The presence of HEV appeared to have a deleterious effect on the outcome of pregnancy: 52% (112/218) of the HEV placentas were associated with stillborn infants, in contrast to only 22% (89/400) of control placentas. The difference in the proportion of stillbirths was greatest when the gestational age was 25 weeks or greater. Other significant positive associations with HEV included the presence of meconium staining, intrauterine growth retardation, smaller placentas, and maternal hypertension or toxemia. Pathologic findings associated with HEV were chronic villitis, erythroblastosis, thrombosis and cord abnormalities. No association was found with infant Apgar score or fetal anomalies. The association of HEV with a high proportion of stillbirths in the registry suggests that further understanding of this lesion might shed light on the problem of unexplained stillbirth.

Hemorrhagic endovasculitis of the placenta: an indepth morphologic appraisal with initial clinical and epidemiologic observations.

A vasodestructive process has been identified within the placenta, which focuses on the entire placental vascular tree. Its presence is correlated with significant fetal mortality; liveborn infants are growth retarded and frequently in distress. Characteristic morphologic features have been identified in chorionic vessels of all sizes and these explicit pathologic changes are repetitive from case to case. Associated events suggest that hemorrhagic endovasculitis of the placenta is a clinicopathologic entity having maximal impact on pregnancies of affected patients. A number of accompanying pathologic and clinical features would suggest an infectious association or cause. There are several known categories of disease which manifest similarity to this placental alteration. These include microangiopathic hemolytic anemia, several postinfectious states, several known types of vasculitis, and AIDS. Long-term studies to gain further insight into this pathologic event are currently underway at the Michigan Placental Tissue Registry. These studies include: an epidemiologic field investigation with followup on growth and development of liveborn infants; data collection and analysis with respect to recurrence, geographic distribution, and the clinical course of affected pregnancies. An indepth pathologic analysis is ongoing including ultrastructural and immunopathologic studies on affected and control placentas. Appropriate microbiologic and serologic studies are planned with reference to the infectious aspects of this entity we have described. It is hoped that increasing awareness of this pathologic process within the placenta, particularly by pathologists, will contribute to our understanding of events which are deleterious to intrauterine growth and survival.

Perinatal infection with Torulopsis glabrata: a case associated with maternal sickle cell anemia.

Torulopsis glabrata is a yeast of low virulence and commensal within the female genitourinary tract. The first case of congenital infection with Torulopsis glabrata was reported in 1980. An additional example of perinatal Torulopsis infection which is associated with maternal sickle cell anemia is reported. The most common source of congenital fungus infection is Candida albicans. Differences in morphology between T glabrata and C albicans are apparent, particularly the pathologic response within the placenta. Pathogenicity in this case may be associated with increased susceptibility to infection in patients with sickle cell anemia.

Hemorrhagic endovasculitis and hemorrhagic villitis of the placenta.

A unique vascular lesion has been identified in 32 placentas sent to the Michigan Placental Tissue Registry, East Lansing, Mich. Half of the associated infants are stillborn; 11 of 16 liveborn were in distress or small for gestational age. Placental vessels show thrombosis, endothelial, and medial hyperplasia and narrowing or obliteration of the lumen. A microangiopathic process is suggested by intraluminal fragmentation of erythrocytes with diapedesis of intact and fragmented RBCs through vessel walls. Red blood cell fragments and hemosiderin are present within villous stroma. Nucleated erythrocytes in placental vessels suggest fetal hypoxia. On gross examination, the placentas are meconium stained. The umbilical cords are frequently edematous, redundant, and around a fetal part; gradual narrowing of placental vessels may be related. Chronic villitis is present in 75% of the cases, intranuclear inclusions have been identified in 10%. An infectious agent, possibly viral, is suggested; toxic and chemical substances must be considered.