Does difference in stem design affect accuracy of stem alignment in total hip arthroplasty with a CT-based navigation system?

The efficacy of a computed tomography (CT)-based navigation system to accurately position the stem for intended alignment is unclear. In addition, the influence of stem design on the accuracy of insertion is unknown. We therefore retrospectively compared the accuracy and precision for the intended alignment of two different designs of femoral stem which were implanted with or without the navigation system. Forty-nine total hip arthroplasties (THAs) using a tapered wedge stem and 91 THAs using an anatomic stem were evaluated for the navigation group. Thirty-three THAs using the tapered wedge stem and 15 THAs using the anatomic stem were controls for the non-navigation group. Differences between postoperative measurement and preoperative planning were compared among the groups. In the navigation groups, accuracy (mean absolute difference) and precision (95% limits of agreement) of stem anteversion were 4.3° and ± 10.1° in the tapered wedge stem and 3.1° and ± 6.9° in the anatomic stem. In the non-navigation groups, these were 6.0° and ± 15.2° and 4.8° and ± 12.4°, respectively. The accuracy and precision in the navigation groups were significantly superior to those in the non-navigation group, and those in the anatomic stem group were significantly superior to those in the tapered wedge group. Using the CT-based navigation system, the accuracy and precision for intended stem anteversion were improved. When compared under guidance of navigation system, the accuracy and precision for intended stem anteversion in the anatomic stem were superior to those in the tapered wedge stem.

Effect of improved navigation performance on the accuracy of implant placement in total hip arthroplasty with a CT-based navigation system.

A computed tomography (CT)-based navigation system is one of the support tools to place implant with appropriate alignment and position in total hip arthroplasty (THA). To determine whether the higher performance of the navigation would further improve the accuracy of implant placement in the clinical setting, we retrospectively compared the navigation accuracy of two different versions of a navigation system. The newer version of the navigation system had an upgraded optical sensor with superior positional accuracy. Navigation accuracy, defined as differences between postoperative measurements on CT images and intraoperative records on the navigation system, of 49 THAs performed with the newer version of the navigation system was compared with that of 49 THAs performed with the older version. With the newer version, the mean absolute accuracy (95% limits of agreement) of implant alignment was 1.2° (± 3.3°) for cup inclination, 1.0° (± 2.4°) for cup anteversion, 2.0° (± 4.9°) for stem anteversion, and 1.1° (± 2.4°) for stem valgus angle. The accuracy of the implant position was 1.5 mm (± 3.1 mm), 1.3 mm (± 3.0 mm), and 1.5 mm (± 3.1 mm) for cup x-, y-, and z-axes, respectively, 1.6 mm (± 3.2 mm), 1.4 mm (± 2.9 mm), and 1.5 mm (± 2.7 mm) for stem x-, y-, and z-axes, respectively, and 2.4 mm (± 4.5 mm) for leg length discrepancy. The values for the newer version were significantly more accurate with less variation compared to those of the older version. With upgraded navigation performance, more accurate implant placement was demonstrated in the clinical setting.

Feasibility and safety of intracoronary nicorandil infusion as a novel hyperemic agent for fractional flow reserve measurements.

Fractional flow reserve (FFR) is a useful modality to assess the functional significance of coronary stenoses. Although adenosine triphosphate (ATP) is generally used as the hyperemic stimulus, we sometimes encounter adverse events like hypotension during FFR measurement. Nicorandil, an ATP-sensitive potassium channel opener, recognized as an epicardial and resistance vessel dilator, has not been fully evaluated as a possible alternative hyperemic agent. The aim of this study was to evaluate the feasibility and safety of intracoronary nicorandil infusion compared to intravenous ATP for FFR measurement in patients with coronary artery disease. A total of 102 patients with 124 intermediate lesions (diameter stenosis >40 and <70% by visual assessment) were enrolled. All vessels underwent FFR measurements with both ATP (150 µg/kg/min) and nicorandil (2.0 mg) stimulus. FFR, hemodynamic values, and periprocedural adverse events between the two groups were evaluated. A strong correlation was observed between FFR with ATP and FFR with nicorandil (r = 0.954, p < 0.001). The agreement between the two sets of measurements was also high, with a mean difference of 0.01 ± 0.03. The mean aortic pressure drop during pharmacological stimulus was significantly larger with ATP compared to nicorandil (9.6 ± 9.6 vs. 5.5 ± 5.8 mmHg, p < 0.001). During FFR measurement, transient atrioventricular block was frequently observed with ATP compared to nicorandil (4.0 vs. 0%, p = 0.024). This study suggests that intracoronary nicorandil infusion is associated with clinical utility and safety compared to ATP as an alternative hyperemic agent for FFR measurement.

Distributional impact of brain microbleeds on global cognitive function in adults without neurological disorder.

BACKGROUND AND PURPOSE: Brain microbleeds (MBs) are considered to be associated with cognitive decline and can be pathologically and topographically classified as cerebral amyloid angiopathy-related (located in lobar regions) and hypertensive microangiopathy-related (located in deep regions). We examined whether different effects on global cognitive function might be seen with different distributions of MBs. METHODS: A total of 1279 adults without neurological disorders were studied prospectively. Subjects were divided into 4 groups: without-MBs group; lobar group; deep group; and with in both areas (diffuse group). The Mini-Mental State Examination was administered to determine global cognitive functions, with scores<27 regarded as subnormal. RESULTS: MBs were detected in 98 subjects (8%): 36 subjects (3%) classified as lobar group, 48 subjects (4%) as deep group, and 14 subjects (1%) as diffuse group. Subnormal scores were found in 76 subjects (5.9%), associated with age, education, hypertension, severe white matter hyperintensities, and distribution and number of MBs. In the final model of logistic regression analysis, the deep group (OR, 2.79; 95% CI, 1.14-6.79) was associated with subnormal scores, whereas the lobar group (OR, 0.77; 95% CI, 0.17-3.44) was not. Trend for the diffuse group did not reach the level of significance (OR, 5.01; 95% CI, 0.88-28.41). These trends were also seen in analysis using another cut-off point for subnormal score. Scores for total Mini-Mental State Examination and attention and calculation were significantly lower in the deep group and the diffuse groups compared with the without-MBs group. CONCLUSIONS: This Japanese cross-sectional study demonstrated that MB-related global cognitive dysfunction seems to occur based on hypertensive pathogenesis rather than on cerebral amyloid angiopathy.

Clustering of metabolic syndrome components attenuates coronary plaque regression during intensive statin therapy in patients with acute coronary syndrome: the JAPAN-ACS subanalysis study.

BACKGROUND: The JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome) trial showed that intensive statin therapy could induce significant coronary plaque regression in acute coronary syndrome (ACS). We evaluated the impact of metabolic syndrome (MetS) and its components on coronary plaque regression in the JAPAN-ACS patients. METHODS AND RESULTS: Serial intravascular ultrasound measurements over 8-12 months were performed in 242 ACS patients receiving pitavastatin or atorvastatin. Patients were divided into groups according to the presence of MetS or the number of MetS components. Although the percent change in plaque volume (%PV) was not significantly different between the MetS (n=119) and non-MetS (n=123) groups (P=0.50), it was significantly associated with an increasing number of MetS components (component 0: -24.0%, n=7; components 1: -20.8%, n=31; components 2: -16.1%, n=69; components 3: -18.7%, n=83; components 4: -13.5%, n=52; P=0.037 for trend). The percent change in body mass index (%BMI) significantly correlated with %PV (r=0.15, P=0.021), especially in the MetS components 4 group (r=0.35, P=0.017). In addition, %BMI was an independent predictor of plaque regression after adjustment for the changes of low- and high-density lipoprotein cholesterol, triglycerides and HbA(1c). CONCLUSIONS: The clustering of MetS components, but not the presence of MetS itself, could attenuate coronary plaque regression during intensive statin therapy in ACS patients. Therefore, to achieve a greater degree of plaque regression, it is necessary to treat to each MetS component and use lifestyle modification.

Clinical characteristics by topographical distribution of brain microbleeds, with a particular emphasis on diffuse microbleeds.

From the perspective of the underlying pathogenesis of primary intracerebral hemorrhage (pICH), the topographical distribution of brain microbleeds (MBs) is divided into the lobar area and the deep brain or infratentorial areas. We investigated clinical features, including ambulatory blood pressure (ABP), of patients with MBs distributed in both areas (diffuse MBs). A total of 124 patients with first-ever acute stroke were enrolled prospectively. Gradient-echo T2∗-weighted magnetic resonance imaging (MRI) was performed using a 1.5-T scanner. Patients were classified into 4 groups: MBs-negative group (n=68), those with MBs in lobar areas (lobar group; n=6), those with MBs in deep or infratentorial areas (deep or infratentorial group; n=31), and those with MBs in both areas (diffuse group; n=19). The admission casual BP (CBP) was recorded in all patients, and ABP was measured in the ischemic stroke patients. There were significant differences in the distribution of MBs (P=.004) among the 6 stroke subtypes. All stroke subtypes except transient ischemic attack had diffuse MBs; pICH had the highest prevalence of it (35%). The severity of white matter hyperintensity (WMH) differed among the 4 groups (P < .0001), with the diffuse group having the highest prevalence of early confluent (47%) and confluent types (21%). ABP and CBP were significantly higher in the deep and diffuse groups compared with the MBs-negative group, but did not differ between the lobar group and the MBs-negative group. Our data suggest that diffuse MBs are associated with hypertensive stroke, elevated BP, and severe WMH. The pathogenesis of diffuse MBs may be related to the more severe microangiopathy involved in hypertensive arteriopathy and cerebral amyloid angiopathy.

Activation of TRPA1 channel facilitates excitatory synaptic transmission in substantia gelatinosa neurons of the adult rat spinal cord.

TRPA1 is expressed in primary sensory neurons and hair cells, and it is proposed to be activated by cold stimuli, mechanical stimuli, or pungent ingredients. However, its role in regulating synaptic transmission has never been documented yet. In the present study, we examined whether activation of the TRPA1 channels affects synaptic transmission in substantia gelatinosa (SG) neurons of adult rat spinal cord slices by using the whole-cell patch-clamp technique. A chief ingredient of mustard oil, allyl isothiocyanate (AITC), superfused for 2 min markedly increased the frequency and amplitude of spontaneous EPSCs (sEPSCs), which was accompanied by an inward current. Similar actions were produced by cinnamaldehyde and allicin. The AITC-induced increases in sEPSC frequency and amplitude were resistant to tetrodotoxin (TTX) and La3+, whereas being significantly reduced in extent in a Ca2+-free bath solution. In the presence of glutamate receptor antagonists CNQX and AP5, AITC did not generate any synaptic activities. The AITC-induced increases in sEPSC frequency and amplitude were reduced by ruthenium red, whereas being unaffected by capsazepine. AITC also increased the frequency and amplitude of spontaneous inhibitory postsynaptic currents; this AITC action was abolished in the presence of TTX or glutamate receptor antagonists. These results indicate that TRPA1 appears to be localized not only at presynaptic terminals on SG neurons to enhance glutamate release, but also in terminals of primary afferents innervating onto spinal inhibitory interneurons, which make synapses with SG neurons. This central modulation of sensory signals may be associated with physiological and pathological pain sensations.

Brain microbleeds and global cognitive function in adults without neurological disorder.

BACKGROUND AND PURPOSE: Increasing attention has been paid to associations between cognitive dysfunction and brain microbleeds (MBs). Because all previous studies have investigated patients with neurological disorders, we examined subjects without neurological disorder in order to clarify pathogenic relationships. METHODS: A total of 518 consecutive adults without neurological disorder who had undergone health-screening tests of the brain were studied prospectively. Gradient-echo T2*-weighted MRI using a 1.5-T system was used to detect MBs. The Mini-Mental State Examination (MMSE) was administered to determine cognitive functions. MMSE scores <27 or >1.5 SDs below the age-related mean were regarded as subnormal. RESULTS: MBs were found in 35 subjects (6.8%). MMSE score <27 was found in 25 subjects (4.8%), with MMSE score >1.5 SDs below the age-related mean in 34 subjects (6.6%). Univariate analysis showed presence and number of MBs, short duration of education, and severe white matter hyperintensities as significantly associated with subnormal scores. In logistic regression analysis, presence of MBs (odds ratio [OR], 5.44; 95% CI, 1.83 to 16.19) and number of MBs (OR, 1.32; 95% CI, 1.04 to 1.68) still displayed significant associations with MMSE score <27. Logistic regression analysis revealed a significant relationship between presence (OR, 3.93; 95% CI, 1.44 to 10.74) and number (OR, 1.26; 95% CI, 1.01 to 1.59) of MBs and MMSE score >1.5 SDs below the age-related mean. Among MMSE subscores, "attention and calculation" was significantly lower in MB-positive subjects (P=0.017). CONCLUSIONS: MBs appear to be primarily associated with global cognitive dysfunction.

Significantly increased antibody response to heterogeneous nuclear ribonucleoproteins in cerebrospinal fluid of multiple sclerosis patients but not in patients with human T-lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis.

It has been reported that antibodies (Abs) against heterogeneous nuclear ribonucleoproteins (hnRNPs) are associated with human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS). However, these studies were done under nonmasked conditions. In order to determine whether Abs against hnRNPs associate with HAM/TSP and MS, the authors assayed Abs against two major hnRNPs, hnRNP A1 and A2/B1, in 105 cerebrospinal fluid (CSF) samples under fully masked conditions. Samples included 40 cases of HAM/TSP, 28 of MS, and 37 of other neurological diseases. Anti-hnRNP A1 Abs, and especially anti-hnRNP A2/B1 Abs, were found significantly more often in the CSF of MS patients than in other groups. However, there was no difference in the incidence of anti-hnRNP A1 Abs between HAM/TSP and other disease groups.

Identification of a new homozygous frameshift insertion mutation in the SIL1 gene in 3 Japanese patients with Marinesco-Sjögren syndrome.

Marinesco-Sjögren syndrome (MSS) is an autosomal recessive multisystem disorder characterized by cerebellar ataxia, cataracts, progressive muscular weakness, and developmental and mental retardation. Recently, mutations in the SIL1 gene on chromosome 5q31 have been shown to be a cause of MSS. We sequenced the entire SIL1-coding region in 3 unrelated Japanese patients with classical MSS and identified a novel homozygous frameshift insertion mutation, 936_937insG, in exon 9 in all 3 patients.

Vasculitic neuropathy in a patient with hereditary C1 inhibitor deficiency.

OBJECTIVE: To report the clinical, pathological, and mutational features of hereditary C1 inhibitor (C1INH) deficiency as a cause of isolated vasculitic neuropathy. PATIENT: A 35-year-old woman with sensorimotor mononeuritis multiplex and facial palsy. RESULTS: The sural nerve biopsy results showed a decrease of myelinated fibers with axonal degeneration and severe hypersensitivity vasculitis, with deposition of C1q on vessel walls. Mutational analysis of the C1INH gene found a new mutation, a heterozygous 2-base pair deletion in exon 8. The patient was treated with plasmapheresis and intravenous methylprednisolone, followed by oral prednisolone, which resulted in marked improvement. CONCLUSION: Hereditary C1INH deficiency should be included in the differential diagnosis of nonsystemic vasculitis neuropathy.

[A case of alcoholic with vitamin B12 deficiency presenting central pontine and extrapontine myelinolysis on MRI].

A 55-year-old man with chronic alcoholism was first referred to us in 1992 because of spastic quadriparesis. T2-weighted images of MRI showed pontine and extracapsule lesions as central pontine and extrapontine myelinolysis (CPM/EPM). He had macrocytic anemia with normal serum level of vitamin B12 (B12). Gait disturbance was progressively worsened from the end of 2004 and dysuria appeared from June, 2005. Neurological examination on admission in November, 2005, showed mild impairment of recent memory, spastic paraparesis with hyperreflexia in all limbs, loss of deep sensations in lower limbs and urinary disturbance. The low serum level of B12 with marked macrocytic anemia was noted. On MRI. the pontine lesion extended to the midbrain but no abnormality was found in the spinal cord. We intramuscularly administered B12, resulting in marked improvement of both anemia and neurological symptoms. The brainstem lesion on MRI, however, was unchanged. We assume that B12 deficiency was involved in the formation of CPM/EPM and the neurological symptoms in our patient.

[Usefulness of carotid ultrasonography for the early detection of moyamoya disease].

We report carotid ultrasonographic findings in moyamoya disease. A 44-year-old man was admitted to our hospital because of fever, headache and nausea. Neurological examination showed neck stiffness and Kernig's sign but he was otherwise normal. Brain computed tomography showed hemorrhage in the right thalamus and the lateral ventricle. Conventional carotid ultrasonography (CCU) detected marked narrowing of the right internal carotid artery (ICA) at the proximal portion without arteriosclerosis, which fulfilled the criteria of bottle neck sign, namely, the ratio of diameter of proximal portion of ICA to that of the distal portion of common carotid artery (CCA) was less than 0.5. Additionally, CCU as well as transoral carotid ultrasonography (TOCU) showed the diameter of the ICA to be smaller than that of the external carotid artery (ECA) (diameter reversal sign). These signs strongly suggested moyamoya disease. Cerebral angiography confirmed the occlusions of intracranial ICA and moyamoya vessels. Bottle neck sign and diameter reversal sign of the carotid artery on carotid ultrasonography are useful for the early detection of moyamoya disease.

[Clinical characteristics, diagnostic criteria and treatment of progressive multifocal leukoencephalopathy].

The clinical characteristics, diagnostic criteria and treatment of progressive multifocal leukoencephalopathy (PML) are reviewed. PML is characterized by rapid progression and poor outcome, and therefore requires the diagnosis and treatment as early as possible. Diffusion-weighted and diffusion tensor MRI were reported to be useful for the evaluation of disease activity of PML. The detection of JCV-DNA in the cerebrospinal fluid by PCR has replaced the brain biopsy. Highly active antiretroviral therapy has improved both the survival rate and the neurological functions in HIV-associated PML. However, the treatment for immune reconstitution inflammatory syndrome, which often deteriorates neurological functions, has never been solved.

[Case of Graves' disease presenting only with rapid consciousness disturbance].

A 79-year-old woman was admitted to our hospital because of forgetfulness for a month followed with rapid development of consciousness disturbance. After admission, the depressed consciousness level fluctuated but continued for more than a month. Thyroid function tests showed increased free T3 and T4 level, lowered level of TSH, and increased anti-TSH receptor antibody titer. A diagnosis of Graves' disease was made but we could find none of thyrotoxic manifestations such as goiter, exophthalmos, tachycardia, high body temperature, or sweating. Administration of thiamazole rapidly improved her consciousness level. It should be kept in mind that hyperthyroidism in elderly could present solely with psychoneurologic symptoms or consiousness disturbance.

[An autopsied case of limbic encephalitis associated with extremely high titers of anti-SS-A antibodies in serum and anti-neuronal antibodies in CSF].

A 76-year old man was referred to our department because of several episodes of generalized convulsion followed by a loss of consciousness and the right hemiparesis. The disturbed consciousness and hemiparesis disappeared soon but the personal change persisted thereafter. T2 and diffusion weighted images of MRI taken on the admission showed high intensity lesions in the left medial temporal lobe including the hippocampus. Antibodies (Abs) against herpes simplex virus were not elevated, however, serum titers of antinuclear and anti-SS-A/Ro Abs were extremely elevated. CSF IgG level and IgQ index were increased, and the CSF reacted with 78-kd bands on Western blots of rat brain homogenate. He died of bacterial pneumonia on the 28th day of illness and was autopsied. Malignant tumors were not found in any organs. In the left hippocampus, degeneration and loss of neurons, infiltration of macrophages, and microgliosis were observed. Vasculitis, however, was not found in the lesion. The immunohistochemical study showed that the CSF recognized the cytoplasm of neurons in the human hippocampus and also Purkinje cells. Those immunological and pathological findings thus suggest an antibody-mediated autoimmune limbic encephalitis in our case.

Effects of coordinate-system construction methods on postoperative computed tomography evaluation of implant orientation after total hip arthroplasty.

OBJECTIVE: In total hip arthroplasty, it is important to assess postoperative implant orientation. The computed tomography-based (CT-based) three-dimensional (3D) templating method using 3D preoperative planning software is generally recommended. In this method, postoperative implant orientation within a bony coordinate system can be measured by overlaying a 3D computerized model of the implant on a real postoperative CT image of the implant. The bony coordinate system consists of several reference points (RPs) marked on a CT image of the bone surface. Therefore, preoperative and postoperative coordinate systems do not always match. We investigated how the difference between coordinate systems constructed from RPs chosen by manual methods (M1 and M2) and those constructed by the computer matching method influences the results of measurement validation. METHODS: In M1, postoperative RPs were chosen without a specific tool in a single planning module. In M2, postoperative RPs were chosen with as little deviation as possible from preoperative RPs, verifying preoperative RPs on another monitor. RESULTS: M1 and M2 produced mean errors in acetabular cup inclination of 0.7° ± 0.5° and 0.5° ± 0.3°, respectively, and mean errors in cup anteversion of 1.3° ± 1.2° and 0.5° ± 0.4°, respectively, which were statistically significant differences. M1 and M2 produced mean errors in femoral stem anteversion of 2.4° ± 2.0° and 2.7° ± 2.1°, respectively, not a significant difference, but these errors were larger than errors in cup orientation. DISCUSSION: We recommend referring to preoperative RPs when choosing postoperative RPs. Surgeons must be aware that for evaluation of postoperative stem anteversion, manual methods may produce considerable error.

Association between interleukin-6 gene polymorphism and human T-cell leukemia virus type I associated myelopathy.

We studied cytokine gene polymorphisms in the promoter region, including interleukin (IL)-6, IL-1beta, and IL-10, in Japanese patients with human T-cell leukemia virus type I (HTLV-I) associated myelopathy (HAM) (n = 65), asymptomatic HTLV-I carriers (n = 143), and HTLV-I seronegative, normal controls (n = 160). There was a significant difference between HAM patients and HTLV-I carriers in the distribution of IL-6 promoter polymorphism at position -634 (chi(2) = 9.90, p = 0.0071). The IL-6 genotype was also significantly different between HAM patients and normal controls (chi(2) = 11.53, p = 0.0033), while a similar distribution was observed in IL-1beta and IL-10 polymorphisms among HAM patients, carriers, and normal controls. The results suggest that IL-6 gene region may contribute to susceptibility to HAM, and that aberrant cytokine productions could be involved in the development of HAM.

EAAT4 mRNA expression is preserved in the cerebellum of prion protein-deficient mice.

To study the mechanism underlying the selective degeneration of Purkinje cells in the cerebellum of the Nagasaki (Ngsk) prion protein-deficient (PrP(-/-)) mice, the mRNA levels of glutamate transporter EAAT4, the marker highly specific for Purkinje cell synapses, were analyzed by semi-quantitative reverse transcription-polymerase chain reaction. EAAT4 mRNA was expressed in the cerebellum of PrP(-/-) mice presenting with cerebellar ataxia, at the levels identical to those in the cerebellum of non-ataxic PrP(+/-) mice. Furthermore, EAAT4 mRNA was identified in the cerebrum of both PrP(-/-) and PrP(+/-) mice, although its levels were much lower than those in the cerebellum. These results indicate that Purkinje cell degeneration found in the cerebellum of PrP(-/-) mice is not primarily caused by glutamate neurotoxicity, although it remains to be investigated whether preserved expression of EAAT4 might represent a compensatory mechanism for protecting against Purkinje cell degeneration in the PrP(-/-) mice cerebellum.