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ABSTRACT: The bispectral index (BIS) and the spectral entropy (state entropy, SE, and response entropy, RE) are depth-of-anaesthesia monitors derived from EEG and have been developed to measure the effects of anaesthetics on the cerebral cortex. We studied whether they can differentiate consciousness from unconsciousness during increasing doses of three different anaesthetic agents.
Thirty healthy male volunteers aged 19-30 yr were recruited and divided into three 10-volunteer groups to receive either dexmedetomidine, propofol, or sevoflurane in escalating concentrations at 10 min intervals until loss of consciousness (LOC) was reached. Consciousness was tested at 5 min intervals and after drug discontinuation at 1 min intervals by requesting the subjects to open their eyes. LOC was defined as unresponsiveness to the request and pre-LOC as the last meaningful response. The first meaningful response to the request after drug discontinuation was defined as regaining of consciousness (ROC). For the statistical analysis, pre-LOC and ROC values were pooled to represent the responsive state while LOC values represented the unresponsive state. Prediction probability (P(K)) was estimated with the jack-knife method.
The lowest mean values for BIS, SE, and RE were recorded at LOC with all three drugs. The P(K) values were low for dexmedetomidine (BIS 0.62, SE 0.58, RE 0.59), propofol (BIS 0.73, SE 0.72, RE 0.72), and sevoflurane (BIS 0.70, SE 0.52, RE 0.62).
Because of wide inter-individual variability, BIS and entropy were not able to reliably differentiate consciousness from unconsciousness during and after stepwise increasing concentrations of dexmedetomidine, propofol, and sevoflurane.
BJA British Journal of Anaesthesia 07/2011; 107(4):573-80. · 4.24 Impact Factor
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ABSTRACT: The purpose of this study was to determine the acoustic effects of lingual nerve impairment on speech. Neurophysiologic examination and thermal quantitative sensory testing (QST) were carried out to determine if the profile, type or severity of sensory nerve impairment had effects on the degree of speech changes. The study group consisted of 5 women and 5 men with lingual nerve damage following an oral and maxillofacial surgery procedure. Time interval between the examination and the nerve damage ranged from 1 month to 20 years. Formants and fundamental frequency and duration of vowel sounds were analyzed. The patients underwent sensory tests, blink reflex and thermal QST of the lingual nerve area. The lingual nerve impairment had effects on the central acoustic features of vowel sounds. A relationship was observed between warm detection threshold values and the magnitude of second formant changes in men. It is concluded that lingual nerve impairment has gender-specific effects on speech. The variability in the acoustic changes of vowel sounds between different patients indicates individual compensatory manners of speech production following lingual nerve impairment.
International Journal of Oral and Maxillofacial Surgery 05/2009; 38(7):758-65. · 1.51 Impact Factor
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E Huupponen,
A Maksimow,
P Lapinlampi,
M Särkelä,
A Saastamoinen,
A Snapir,
H Scheinin,
M Scheinin,
P Meriläinen,
S-L Himanen, S Jääskeläinen
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ABSTRACT: Dexmedetomidine, a selective alpha(2)-adrenoceptor agonist, induces a unique, sleep-like state of sedation. The objective of the present work was to study human electroencephalogram (EEG) sleep spindles during dexmedetomidine sedation and compare them with spindles during normal physiological sleep, to test the hypothesis that dexmedetomidine exerts its effects via normal sleep-promoting pathways.
EEG was continuously recorded from a bipolar frontopolar-laterofrontal derivation with Entropy Module (GE Healthcare) during light and deep dexmedetomidine sedation (target-controlled infusions set at 0.5 and 3.2 ng/ml) in 11 healthy subjects, and during physiological sleep in 10 healthy control subjects. Sleep spindles were visually scored and quantitatively analyzed for density, duration, amplitude (band-pass filtering) and frequency content (matching pursuit approach), and compared between the two groups.
In visual analysis, EEG activity during dexmedetomidine sedation was similar to physiological stage 2 (S2) sleep with slight to moderate amount of slow-wave activity and abundant sleep spindle activity. In quantitative EEG analyses, sleep spindles were similar during dexmedetomidine sedation and normal sleep. No statistically significant differences were found in spindle density, amplitude or frequency content, but the spindles during dexmedetomidine sedation had longer duration (mean 1.11 s, SD 0.14 s) than spindles in normal sleep (mean 0.88 s, SD 0.14 s; P=0.0014).
Analysis of sleep spindles shows that dexmedetomidine produces a state closely resembling physiological S2 sleep in humans, which gives further support to earlier experimental evidence for activation of normal non-rapid eye movement sleep-promoting pathways by this sedative agent.
Acta Anaesthesiologica Scandinavica 03/2008; 52(2):289-94. · 2.19 Impact Factor
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ABSTRACT: ENTROPY index monitoring, based on spectral entropy of the electroencephalogram, is a promising new method to measure the depth of anaesthesia. We examined the association between spectral entropy and regional cerebral blood flow in healthy subjects anaesthetised with 2%, 3% and 4% end-expiratory concentrations of sevoflurane and 7.6, 12.5 and 19.0 microg.ml(-1) plasma drug concentrations of propofol. Spectral entropy from the frequency band 0.8-32 Hz was calculated and cerebral blood flow assessed using positron emission tomography and [(15)O]-labelled water at baseline and at each anaesthesia level. Both drugs induced significant reductions in spectral entropy and cortical and global cerebral blood flow. Midfrontal-central spectral entropy was associated with individual frontal and whole brain blood flow values across all conditions, suggesting that this novel measure of anaesthetic depth can depict global changes in neuronal activity induced by the drugs. The cortical areas of the most significant associations were remarkably similar for both drugs.
Anaesthesia 10/2005; 60(9):862-9. · 2.96 Impact Factor
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ABSTRACT: The yield of clinical sensory tests and electrophysiologic tests in the diagnostics of inferior alveolar nerve (IAN) damage after bilateral sagittal split osteotomy (BSSO) was studied. The diagnostic value of these tests was evaluated by comparing the test results to the degree of nerve damage at the end of the operation as documented by means of the intraoperative nerve conduction recording of the IAN. Twenty patients undergoing BSSO were analysed preoperatively and 2 weeks postoperatively. The frequency of the IAN disturbance ranged from 10% to 94% depending on the test method and the test site used. Of the clinical sensory tests, the touch detection threshold (TD) test was the most sensitive and clinically useful test. It also correlated best with the electrophysiologically verified intraoperative nerve damage (R = -0.603, P = 0.017 on the right, R = -0.626, P = 0.01 on the left). The blink reflex and quantitative cold detection threshold tests were almost as often abnormal as the TD-test, but nerve conduction study (NCS) was the most sensitive (88%) of all clinical and electrophysiologic tests. The frequency of abnormal findings in the electrophysiologic tests indicating IAN injury, 75% on the right side and 90% on the left side, corresponded exactly with the figures of subjective sensory alteration. Almost all electrophysiologic tests showed obvious associations with the objectively verified IAN damage. All tests, except the NCS, showed only moderate sensitivity. Specificity of the tests was generally high, the only exceptions being the TD test and the NCS. To increase the diagnostic accuracy of the testing and to detect different types of damage in different nerve fibre populations, a combination of different sensory and electrophysiologic tests is recommended.
International Journal of Oral and Maxillofacial Surgery 03/2003; 32(1):15-23. · 1.51 Impact Factor
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ABSTRACT: To evaluate peripheral nervous system involvement in gyrate atrophy of the choroid and retina with hyperornithinemia (GA).
GA is an inborn error of amino acid metabolism caused by mutations in the enzyme ornithine aminotransferase. Patients with GA have hyperornithinemia, progressive centripetal loss of vision, minor CNS abnormalities, and type II muscle fiber atrophy with accumulation of tubular aggregates. The authors previously showed that muscle and brain creatine stores are depleted in the patients with GA.
The authors searched evidence of peripheral nervous involvement in 40 patients with GA (mean age 31.6 +/- 16.3 years; range 5 to 74 years) by using neurography, quantitative sensory threshold testing, and evoked potential testing.
Neurography revealed abnormalities in 21 (53%) of the patients. The abnormalities associated with the severity of the ophthalmologic changes and the age of the patients. With quantitative sensory threshold testing, abnormal large-fiber function was found in seven (18%) and abnormal small-fiber function was found in four (10%) patients. Somatosensory evoked potential and brainstem auditory evoked potential responses were abolished in five patients.
These findings of peripheral nervous system involvement in GA suggest that GA is a systemic disease affecting not only CNS but also the peripheral nervous system.
Neurology 10/2002; 59(5):735-40. · 8.31 Impact Factor
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ABSTRACT: The relationship between reduced glucose metabolism in positron emission tomography with fludeoxyglucose F 18 ([(18)F]FDG-PET) and hippocampal damage (HD) in patients with temporal lobe epilepsy is still unclear.
To determine whether the presence and severity of HD verified by quantitative magnetic resonance imaging (QMRI) and histopathological analysis affect the degree of hypometabolism.
Sixteen patients with drug-resistant temporal lobe epilepsy underwent [(18)F]FDG-PET and QMRI (hippocampal volumetry and T2 relaxometry) before surgery. Histopathological analysis of the hippocampus included measurements of neuronal loss, proliferation of glial cells, and mossy fiber sprouting. The asymmetry in glucose metabolism described the degree of hypometabolism.
Temporal hypometabolism was not related to severity of HD as measured by QMRI or histopathological analysis. The degree of hypometabolism did not differ in patients with mild, moderate, or severe HD. In addition, [(18)F]FDG-PET revealed significant temporal hypometabolism even though hippocampal QMRI findings were normal or showed only mild HD. Thus, glucose consumption was reduced over and above the histopathological changes.
[(18)F]FDG-PET is sensitive for localizing the epileptogenic region in patients with temporal lobe epilepsy. However, it is insensitive to reflect the severity of HD.
Archives of Neurology 07/2001; 58(6):933-9. · 7.58 Impact Factor
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ABSTRACT: OBJECTIVE/PURPOSE: To investigate clinical variation in a genetically homogenous group of subjects with gyrate atrophy of choroid and retina with hyperornithinemia (GA). The group was made up of homozygotes and compound heterozygotes for mutation L402P in the ornithine aminotransferase (OAT) gene.
Cross-sectional study.
Thirty-five Finnish subjects (18 men) with GA with a mean age of 33 years (range, 5-74 years) carrying the Finnish founder mutation L402P.
All subjects were examined between 1993 and 1995. The analysis was composed of, in addition to careful clinical evaluation, studies of visual fields with Goldmann perimeter, photographing of the eye fundi, and corneal electroretinography (ERG) recordings.
The changes in eye fundi, visual acuity, cataract changes in the lens, visual field constriction, and ERG responses were determined.
Myopia, early cataracts, and highly abnormal ERG were typical for the GA subjects. The changes progressed rather uniformly with age. However, visual acuity, funduscopic findings, and visual fields showed great phenotypic variation. Despite the great interindividual variation, both eyes of each subject were always similarly affected.
This study of 35 subjects with GA carrying a single mutation shows that the ophthalmologic symptoms and findings vary widely. The data also reveal that GA subjects are already affected by severe visual impairment in young adulthood. However, the diagnosis is often made very late.
Ophthalmology 05/2001; 108(4):721-9. · 5.45 Impact Factor
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ABSTRACT: Electrophysiological recording of the electrically elicited blink reflex is the most reliable method of investigating habituation of the startle reflex. The purpose of this study was to compare the habituation and the late R3-component of the blink reflex between control subjects (N=19) and first-episode patients with schizophrenia (N=17), psychotic depression (N=23), and severe non-psychotic depression (N=25).
The blink reflex was evoked by electrical stimulation of the supraorbital nerve, and the deficient habituation of the R2i-component was measured with a computer-assisted integral area measurement. Prefrontal executive function of the patients was assessed with the Wisconsin Card Sorting Test. Current psychiatric symptoms were assessed with the Brief Psychiatric Rating Scale, the Hamilton Depression Scale, the Positive and Negative Syndrome Scale, and the Calgary Depression Scale.
Deficient habituation of the blink reflex and occurrence of the late R3 component were associated both with a previous diagnosis of psychotic disorder and with the presence of current psychosis. The sensitivity and specificity of the abnormal habituation of the blink reflex in detecting psychotic disorder were 0.50 and 0.80, respectively. The abnormalities of the blink reflex were not associated with psychotropic medication. In schizophrenic patients, defective habituation of the blink reflex was associated with negative and cognitive symptoms, and in depressive patients with the presence of delusions.
The deficient habituation of the blink reflex and occurrence of the late R3 component seem to be both trait and state markers of a psychotic disorder. The results suggest that schizophrenia and psychotic depression share some common neurobiological mechanisms involved in the modulation of the startle reflex.
Schizophrenia Research 08/2000; 44(1):69-79. · 4.75 Impact Factor
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ABSTRACT: To evaluate the degree of possible peripheral nervous system (PNS) involvement in addition to CNS manifestations in Salla disease, a free sialic acid storage disorder leading to severe mental retardation with a wide clinical variation.
Salla disease is a lysosomal storage disorder that affects the white matter of the CNS. MRI findings and recent 1H MRS study results provide evidence for delayed central myelination, but there is no previous evidence for PNS involvement in this disease. The gene coding for a presumptive sialic acid transport protein has recently been identified, and the first disease-causing mutations have been characterized.
Nerve conduction studies; evoked potentials to visual (VEP), brainstem auditory (BAEP), and somatosensory stimuli (SEP); and EEG were carried out on 22 patients (age range 2 months to 57 years) with biochemically and genetically confirmed Salla disease. Brain MRI were available on 14 patients.
Nerve conduction studies revealed abnormalities in nearly half of the patients (10/21). The four severely disabled patients and the oldest patient had greatly reduced nerve conduction velocities and prolonged distal latencies compatible with demyelinating polyneuropathy. In addition, SEP was abnormal in the majority of the patients, but VEP and BAEP in only a few cases. PNS involvement was clearly associated with both the phenotypic severity and MRI findings.
The results indicate that dysmyelination in Salla disease occurs not only in the CNS but also in the peripheral nervous system, contributing to the phenotypic variation, which can now be correlated with the molecular basis of the disease.
Neurology 08/2000; 55(1):99-104. · 8.31 Impact Factor
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ABSTRACT: In gyrate atrophy of the choroid and retina with hyperornithinaemia (GA), a genetically determined deficiency of ornithine delta-aminotransferase activity leads to high ornithine concentrations in body fluids. GA is characterized by centripetally progressing retinal and choroidal destruction and selective atrophy with tubular aggregates in type II skeletal muscle fibres. These findings have been suggested to be mediated by hyperornithinaemia-induced deficiency of high-energy creatine phosphate. As abnormal brain magnetic resonance images and electroencephalograms are found in another disorder of creatine metabolism, guanidinoacetate methyltransferase deficiency, we investigated the central nervous system involvement in GA, which seems to be associated with a milder degree of phosphocreatine deficiency. We compared 23 untreated GA patients with age-matched healthy controls, and with 9 patients who had received creatine or creatine precursor supplementation daily for several years. The mean age of the patients (32 +/- 18 years) was similar to that of the controls (36 +/- 22 years). The MRI or EEG findings of the patients on creatine supplementation did not differ from those of the untreated group. Brain MRI revealed degenerative lesions in the white matter in 50% of the GA patients, and 70% of the patients had premature atrophic changes, with a striking increase in the number of Virchow's spaces. Of the patients whose EEG was recorded, 58% had abnormal slow background activity, focal lesions or high-amplitude beta rhythm (> 50 microV). The EEG findings were not associated with the MRI changes or with the age or the sex of the patients. Early degenerative and atrophic brain changes and abnormal EEG are thus features of GA, in addition to the well-characterized eye and muscle manifestations.
Journal of Inherited Metabolic Disease 12/1999; 22(8):855-66. · 3.58 Impact Factor
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H Suhonen-Polvi,
T Varho,
L Metsähonkala,
L Haataja,
U Ruotsalainen,
M Haaparanta,
J Bergman,
O Solin,
T Aärimaa,
I Holopainen,
L Vainionpää,
T Manner, S Jääskeläinen,
M Renlund,
M Sillanpää,
P Aula
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ABSTRACT: Salla disease is an autosomal recessive lysosomal free sialic acid storage disorder characterized by psychomotor retardation and ataxia. MRI studies have revealed evidence of dysmyelination, but the biological mechanism of the brain dysfunction is unknown.
Nine patients with Salla disease (age 2.5 mo-42 y) presenting the disease in varying degrees of severity were studied by PET using 2-fluoro-2-deoxy-D-glucose (FDG) as a tracer. Local cerebral metabolic rates for glucose (LCMRGlc) in individual brain regions were compared with controls.
The FDG PET results showed significantly increased LCMRGlc values in the frontal and sensorimotor cortex and especially in the basal ganglia of the patients. Cerebellar hypometabolism was present in all seven patients with marked ataxia, whereas the less severely affected patients without obvious ataxia had normal or even high glucose uptake in the cerebellum.
The increased cerebral glucose utilization is a constant finding in Salla disease and may reflect the basic defect of the sialic acid metabolism in this disorder. The FDG PET findings in the cerebellum suggest a correlation between glucose uptake and the severity of the clinical symptoms.
Journal of Nuclear Medicine 02/1999; 40(1):12-8. · 6.38 Impact Factor
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ABSTRACT: The purpose of this study was to evaluate 1/T1rho in relation to 1/T1 and 1/T2 in characterizing normal and diseased muscle. We measured the muscle relaxation rates 1/T1 and 1/T2 at 0.1 T and 1/T1rho at on-resonance locking fields B1 between 10 and 160 microT in myositis patients and normal volunteers. 1/T2 and 1/T1rho of muscle were lower in the patients than in the volunteers, whereas there was no difference in the 1/T1 values. The lower relaxation rates 1/T2 and 1/T1rho in the diseased muscle may be due to fat and connective tissue infiltrations and edema. 1/T1rho contrast between muscle and subcutaneous fat was higher than 1/T2 and 1/T1 contrast. This may be explained by the different B1 dispersion behavior of these two tissue types. 1/T1rho of fat is B1 field independent, whereas 1/T1rho of muscle decreases clearly with increasing B1 field. In conclusion, 1/T1rho provides a useful tool in manipulating contrast in magnetic resonance imaging of diseased muscle.
Magnetic Resonance Imaging 06/1998; 16(4):385-91. · 1.99 Impact Factor
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S Lamusuo,
H M Ruottinen,
J Knuuti,
R Härkönen,
U Ruotsalainen,
J Bergman,
M Haaparanta,
O Solin,
E Mervaala,
U Nousiainen, S Jääskeläinen,
A Ylinen,
R Kälviäinen,
J K Rinne,
M Vapalahti,
J O Rinne
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ABSTRACT: Firstly, to compare the findings of interictal 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) and of single photon emission computed tomography (SPECT) using 99mTc-hexamethyl propylene-amine-oxime (HMPAO) and 123I-iomazenil in localising the epileptogenic cortex in patients who were candidates for epilepsy surgery, but in whom clinical findings, video EEG monitoring (V-EEG), MRI, and neuropsychological evaluations did not give any definite localisation of the seizure onset. Secondly, to assess the ability of these functional methods to help in the decision about the epilepsy surgery.
Eighteen epileptic patients were studied with FDG-PET and iomazenil-SPECT. HMPAO-SPECT was performed in 11 of these 18 patients. Two references for localisation was used--ictal subdural EEG recordings (S-EEG) and the operated region.
Fifteen of 18 patients had localising findings in S-EEG. FDG-PET findings were in accordance with the references in 13 patients and iomazenil-SPECT in nine patients. HMPAO-SPECT visualised the focus less accurately than the two other methods. In three patients S-EEG showed independent bitemporal seizure onset. In these patients FDG-PET showed no lateralisation. However, iomazenil-SPECT showed temporal lobe lateralisation in two of them.
FDG-PET seemed to localise the epileptogenic cortex more accurately than interictal iomazenil-SPECT in patients with complicated focal epilepsy.
Journal of Neurology Neurosurgery & Psychiatry 01/1998; 63(6):743-8. · 4.76 Impact Factor
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ABSTRACT: The periodic calibration and control of electroretinographic (ERG) stimulators is often neglected due to the difficulties in accurate measurements of the stimuli. Comparison of measurements carried out in different laboratories has been very difficult, as the accurate parameters of the stimuli used usually are not known. In some cases it is assumed that if the stimulator type is known, comparisons can be carried out. We have tested the Ganzfeld flash stimulators used in the departments of clinical neurophysiology of 3 major hospitals in Finland, namely Kuopio University Hospital, Turku Central University Hospital, and Tampere University Hospital, Measurements, performed with a new type of photometer, show that the intensities varied by 42% between the highest and lowest intensity stimulators at nominally identical settings. The measurements underline the findings that identical stimulators will not necessarily produce identical stimuli. These observations also indicate that the stability of the stimuli can be improved by the proper choice of stimulator output settings.
Electroencephalography and Clinical Neurophysiology 06/1996; 100(3):273-4.
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ABSTRACT: Systemic sclerosis (scleroderma) is thought to be the least likely of the collagen vascular disorders to cause nervous system damage. We evaluated the peripheral neuromuscular manifestations in 32 patients with scleroderma. A clinically defined peripheral nervous system (PNS) lesion was manifest in 5 of 32 patients (16%), including 2 patients with trigeminal neuropathy and single cases of polyneuropathy, brachial plexopathy, and lumbosacral radiculopathy. Neurophysiological studies suggested subclinical PNS involvement in 6 additional patients (3 with distal axonal polyneuropathy, 1 with probable myopathy and superimposed polyneuropathy, 1 with trigeminal neuropathy, and 1 with focal ulnar neuropathy). Even though subjective muscular complaints were numerous (16 patients, 50%), a defined primary muscular disease could be demonstrated only in 5 patients (16%). Our results indicate that peripheral neuropathy in scleroderma is not as uncommon as previously estimated.
Muscle & Nerve 12/1993; 16(11):1204-12. · 2.37 Impact Factor
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ABSTRACT: We evaluated central nervous system and psychiatric involvement in a clinical sample of 32 patients with systemic sclerosis (SSc) (scleroderma). All patients underwent clinical neurological examination. Electroencephalography (EEG) and visual evoked potentials (VEPs) were also recorded. Prominent central nervous system (CNS) or psychiatric symptoms were present in 5 patients (16%), including encephalopathy, psychosis, anxiety disorder, grand mal seizures and transient ischemic attack. In addition, abnormal VEPs were recorded from 5/32 patients (16%), suggesting optic neuropathy. EEGs were mainly normal or showed only slight, nonspecific changes. Primary CNS involvement in scleroderma, however, could not be shown in any of the 5 cases with neuropsychiatric symptoms. Our results suggest that neuropsychiatric symptoms in SSc are, if not coincidental, indirectly caused by internal organ involvement of SSc or by possible overlapping connective tissue diseases. On the other hand, optic neuropathy might be a primary complication of SSc.
Acta Neurologica Scandinavica 06/1993; 87(5):382-7. · 2.47 Impact Factor
