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Notes: Comments from the three previous speakers ranged from moderate satisfaction to strong dissatisfaction with the regulatory process. Three different types of research are identified that seem to predict the ease of compliance with the 510(k) process. No one expressed satisfaction with the PMA application. It seems that current evaluation procedures inhibit the developing and marketing of new devices, but foster only enhancements to existing de-vices. The development of new evaluation methods is advocated to provide fast, inexpensive, but rigorous assessment of the clinical safety and treatment value of new devices.

Notes: The accurate and passive fit of dental prostheses supported by endosseous implants is of primary importance in securing long-term restorative success. In the clinical setting, adequate visual and radiographic assessment of joined implant components can be limited. Mechanical engineering principles show a linear relationship between tightening and the degree of rotation of a precision bolted assembly. At a constant torque, with certain variables controlled, a threaded fastener should return to the same rotational end position on repeated tightenings. This study evaluated the terminal screw positions of joined implant components as a potential aid to the clinician in confirming the fit of a fixed and removable prosthesis. There were three areas of experimental inquiry: (1) How reproducible are the various clinical means by which torque is applied to the fastening screws, both in absolute and relative value? (2) How reproducible are the rotational end positions of the gold (attachment) and titanium (center) screws when a controlled torque is applied? (3) Do changes in screw position occur as a function of the magnitude of artifically introduced discrepancies?〈section xml:id="abs1-2"〉〈title type="main"〉Materials and MethodsThree different torque delivery devices were evaluated: a hand-held screwdriver (DIB 048; NobelpharmaUSA, Chicago, IL), a manual torque wrench (DIA 250; NobelpharmaUSA), and an electronic Torque Controller (DEA 020; NobelpharmaUSA), using a calibrated torque measuring dynamometer (Magtrol, Inc, Buffalo, NY). The reproducibility of turning limits were determined for both the titanium and gold screws contained in five Brånemark implant assemblies. Each assembly was subjected to six trials, tightening to recommended torque. The position of each screw head was recorded with a special scribe on acetate sheets and transferred to graph paper. Five implant assemblies were invested in dental stone within a die form mold. A casting was made supported by three implant analogues. Stainless steel shims of 12.7-μm, 25.4-μm, 38.1-μm, and 50.8-μm thickness were used to create impingement and space discrepancies. Controlled trials were conducted, and changes in rotational limits for each screw were recorded.〈section xml:id="abs1-3"〉〈title type="main"〉ResultsThe following values were measured, intending to achieve a torque of 10 Ncm, based on 10 trials for each implement: hand driver, 6.48 (±0.85) Ncm; torque wrench, 7.77 (±0.56) Ncm; and the Torque Controller, 8.54 (±0.19) Ncm. The electronic Torque Controller proved to be the most reproducible instrument and was selected as the delivery vehicle for the remainder of the study. The titanium center screws had a rotational limit that was reproducible to within 0.6° (±0.2°). For the gold screws, it was found that at least two trials had to be conducted for each assembly before the rotational limits conformed to a reproducible position within 1.85° (±1.87°). A linear relationship of approximately 0.9°/μm was observed between the changes in rotational limit and each subsequent shim thickness.〈section xml:id="abs1-4"〉〈title type="main"〉ConclusionsThis study suggests that screw position can be an indicator of fit in dental implant prostheses if the end point of screw rotation is adequately indexed, specific to each assembly and screw.

Notes: Purpose Six impression techniques were evaluated using tapered and square impression copings.Materials and Methods The absolute distortion was measured using a cast metal impression tray with fiduciary reference points external to the impression material. Measurements of the x, y, z coordinates on the master cast and the impressions were directly made with a travelling digitizing microscope. The difference between the coordinates of each of six sites in the impression and the corresponding reference site were compared.Results There was no significant difference between the techniques for the square copings but that there was a significant loss of accuracy in the z-axis with the tapered copings.Conclusions No significant differences were noted.

Notes: Summary Haemodynamic instability is of great importance in clinical management of patients with subarachnoid haemorrhage (SAH). The significance of angiographically demonstrable vasospasm for disturbances of cerebral blood flow (CBF) and cerebral autoregulation has not yet been clarified. The present study was designed to describe disturbances of cerebral autoregulation during the timecourse of experimental SAH (eSAH) in rats. A second aim of the study was to relate the results to a reported timecourse of angiographic vasospasm in the same animal model. Previous studies have shown that the timecourse of angiographically visible vasospasm in eSAH is biphasic with maximal spasm at 10 min and 2 days after induction of eSAH. At 5 days, the vasospasms have resolved. CBF was measured using a133-Xenon intracarotid injection method which allowed serial measurements of mean hemispheric CBF during controlled manipulations of arterial blood pressure. In this way, an autoregulation curve could be constructed. The present study shows that autoregulation is severely disturbed or even totally absent at 2 and 5 days after eSAH. Thus there seems to be no direct correlation between presence of angiographic vasospasm and impairment of autoregulation, or that the impairment of autoregulation is more protracted than the presence of cerebral vasospasm, presuming a correlation exist.

Notes: Summary The present study was undertaken in 8 healthy volunteers to examine the effect of a clinically relevant dose of nimodipine (NIM) (15 and 30 microgram/kg/h) on CBF, its CO2 reactivity, and CMRO2. Mean arterial blood pressure (MABP) was measured intra-arterially. Regional CBF was measured by SPECT of inhaled Xenon-133. During the CO2 reactivity tests changes in CBF were estimated by the arterio-venous-oxygen-difference method. Median CBF was 52 ml/ 100 g/min (48–53) with a normal regional distribution, and median baseline MABP was 96 mmHg (92–99). MABP was slightly reduced, by 8 mmHg (7–9), and 9 mmHg (4–11) after infusion of NIM for 2 and 4 hours, respectively. CBF, however, remained constant, although correction for changes in PaCO2, revealed a slight increase after 4 hours (p=0.08). CMRO2 was 3.5 ml/100 g/min (3.2–3.5) and was not changed by the infusion of NIM. At arterial CO2 tensions ranging from 4.0 to 6.5 Kpa the CO2 reactivity was 3.0% CBF/ 0.1 kPa (2.6–3.7) and decreased significantly to 2.6% CBF/0.1 kPa (1.8–3.2) after the infusion of NIM for 3 hours (p=0.02). The median slope of the LnCBFsat/PaCO2 relationship was 1.5 at baseline compared to 1.3 after NIM (p〈0.01). No side effects were observed. The present study shows a decreased CO2 of the cerebral vessels and a maintained coupling of CBF and CMRO2 during the infusion of nimodipine.

Notes: Summary The effect of a clinically relevant dose of ketanserin (10 mg as a bolus followed by an infusion of 6mg/h) on cerebral blood flow (CBF) and CBF autoregulation was examined in 12 healthy volunteers. Changes in CBF were estimated by the cerebral arteriovenous-oxygen saturation difference method, while mean arterial blood pressure (MABP) was increased by norepinephrine and decreased by ganglionic blockade (trimethaphan camphosulphonate) combined with lower body negative pressure one hour after the infusion of ketanserin. During ketanserin infusion, MABP fell insignificantly by 2.5 mmHg (6 to −2), while CBF rose insignificantly by 5 ml/100 g/min. Autoregulation was preserved in all volunteers. CO2-correction factors from 0 to 4.6% CBF/0.1 kPa were used. The lower limit of CBF autoregulation was 82 mmHg (80–86) with an SE of 3 mmHg (1–5) similar to a previous control group of healthy volunteers. Aside from a major decrease in MABP in one subject, no adverse side effects were observed. The present study shows that CBF autoregulation is maintained during ketanserin infusion.

Notes: Summary A possible involvement of perivascular vasodilatory neuropeptides in subarachnoid haemorrhage (SAH) has been evaluated in man by measuring the levels of calcitonin gene related peptide (CGRP)-, substance P (SP)- and vasoactive intestinal peptide (VIP)-like immunoreactivity (LI) in the cranial venous outflow and in CSF in 34 patients admitted to the hospital after an acute SAH. After operation with aneurysm clipping and nimodipine treatment, blood samples were taken from the external jugular vein (EJV) or cerebrospinal fluid (CSF) and analysed for neuropeptide levels with specific radioimmuno assays (RIA) during the postoperative course. The degree of vasoconstriction in the patients was monitored with Doppler ultrasound recordings bilaterally from the middle cerebral (MCA) and internal carotid arteries (ICA) following the EJV blood sampling every second day. The mean value of all CGRP-LI measurements in EJV during the entire course of SAH (n=20) revealed a significantly higher level as compared to controls. The highest CGRP-LI levels were found in patients with the highest velocity index values (vasospasm). The relationship Vmean MCA/Vmean ICA was used as an index of vasoconstriction. In patients with MCA aneurysms (n=10), a significant correlation (r=0.65, p〈0.05) was found between the vasospasm index and CGRP-LI levels. There were no changes observed in the SP- and VIP-LI levels. Alterations in cerebrovascular tone induced by changing arterial CO2 tension or lowering of blood pressure (ketanserin infusion test) did not alter the levels of the perivascular peptides in the EJV. In addition, CGRP-, SP-, VIP- and neuropeptide Y (NPY)-LI were analysed in CSF in the post-operative course after subarachnoid haemorrhage (SAH) in 14 patients. The CSF VIP-LI was lower in SAH than in control (p〈0.05). The CGRP-LI level was measurable in SAH CSF but not in CSF of controls. In individual patients with marked vasoconstriction increased levels of CGRP-LI (up to 14 pmol/L) and NPY-LI (up to 232 pmol/L) were observed. The results of this study are in support of our hypothesis that there is an involvement of the sensory peptide CGRP in a dynamic reflex aimed at counterbalancing vasoconstriction in SAH.

Notes: Summary  Normal Pressure Hydrocephalus (NPH) is a potentially treatable syndrome with abnormal cerebrospinal fluid dynamics. Meningeal fibrosis and/or obliteration of the subarachnoid space have been suggested as one of the patho-anatomical substrates. However, other types of adult onset dementia, predominantly Alzheimer's disease and Vascular Dementia, may mimic the clinical NPH characteristics.  The purpose of the present study was to correlate cerebral parenchymal and leptomeningeal biopsy findings to the clinical outcome after CSF shunting in a prospective group of idiopathic NPH (INPH) patients. The study comprises 27 patients with INPH, diagnosed and shunted according to generally accepted clinical, imaging and hydrodynamic criteria. In all patients a frontal leptomeningeal and brain biopsy was obtained prior to the shunt insertion.  Degenerative cerebral changes, most often Alzheimer (6 cases) or vascular changes (7 cases) were described in 14 out of 27 biopsies. Arachnoid fibrosis was found in 9 of the 18 biopsies containing arachnoid tissue. Overall, nine patients (33%) improved, of whom 6 presented Alzheimer or vascular changes in their biopsies. No correlation was found between clinical outcome and the presence or absence of degenerative cerebral changes and/or arachnoid fibrosis. However, a tendency towards higher improvement rates was noted in the subgroups presenting degenerative cerebral changes or arachnoid fibrosis. The results suggest that no constant morphological element exists in the syndrome of INPH. Various aetiologies may be involved in the pathogenesis and possibly in some cases co-existing: Patients may also improve by shunting despite the presence of degenerative cerebral parenchymal changes.