Domain State Model for Exchange Bias

Monte Carlo simulations of a system consisting of a ferromagnetic layer exchange coupled to a diluted antiferromagnetic layer described by a classical spin model show a strong dependence of the exchange bias on the degree of dilution in agreement with recent experimental observations on Co/CoO bilayers. These simulations reveal that diluting the antiferromagnet leads to the formation of domains in the volume of the antiferromagnet carrying a remanent surplus magnetization which causes and controls exchange bias. To further support this domain state model for exchange bias we study in the present paper the dependence of the bias field on the thickness of the antiferromagnetic layer. It is shown that the bias field strongly increases with increasing film thickness and eventually goes over a maximum before it levels out for large thicknesses. These findings are in full agreement with experiments.Comment: 8 pages latex, 3 postscript figure

Modeling exchange bias microscopically

Exchange bias is a horizontal shift of the hysteresis loop observed for a ferromagnetic layer in contact with an antiferromagnetic layer. Since exchange bias is related to the spin structure of the antiferromagnet, for its fundamental understanding a detailed knowledge of the physics of the antiferromagnetic layer is inevitable. A model is investigated where domains are formed in the volume of the AFM stabilized by dilution. These domains become frozen during the initial cooling procedure carrying a remanent net magnetization which causes and controls exchange bias. Varying the anisotropy of the antiferromagnet we find a nontrivial dependence of the exchange bias on the anisotropy of the antiferromagnet.Comment: 7 pages, 5 figure

Metabolite characterization in serum samples from normal healthy human subjects by 1H and 13C NMR spectroscopy

One and two dimensional NMR spectroscopy has been employed to characterize the various metabolites of serum control healthy samples. Two dimensional heteronuclear experiment has been included totake advantage of larger chemical shift spread of 13C resonances allowing a more detailed identification of metabolites not possible in one dimensional spectra. This methodology has successfully allowed the assignment of ninety four resonances of various metabolites. The importance of the work lies in the fact that characteristic fingerprints of various metabolites of serum samples of normal healthy control have been obtained which can identify and distinguish metabolic differences from other diseased specimens or non-diseased/healthy serum samples. This study will help enhance the literature of metabolite identification in serum samples

Neurophysiological studies in acute transverse myelitis

A systematic evaluation of anterior horn cell, motor and sensory pathways is possible by electromyography (EMG), motor (MEPs) and somatosensory (SEPs) evoked potentials, respectively, which may provide valuable information on acute transverse myelitis (ATM). In a prospective hospital-based study, EMG, MEP and SEP studies were carried out on admission and after 3 months in 39 patients with ATM. All the patients also underwent detailed clinical evaluation, and spinal magnetic resonance imaging (MRI) was performed in 28. Outcome was defined at the end of 3 months as poor, partial or complete recovery on the basis of functional status. Spinal MRI revealed hyperintense signal changes in T2 extending for two segments to the entire spinal cord. Central motor conduction time to tibialis anterior (CMCT-TA) was more frequently abnormal (90%), followed by tibial SEP (77%). CMCT to abductor digiti minimi (ADM) was abnormal in 30% and median SEP in 15% of patients. Evidence of denervation on EMG was present in 51% of patients. The CMCT-TA improved in 48% patients and tibial SEP in 32%. Median SEP improved in all patients, and CMCT-ADM remained prolonged in two. At 3 months 2 patients had died, and 18 had poor, 10 partial and 9 complete recovery. CMCT was correlated with miscle power, tone, reflec and MRI changes. Patients' outcome of was correlated with CMCT, SEP and EMG. These results are consistent with pronounced involvement of dorsal region of spinal cord in ATM. MEP is more frequently abnormal than SEP

Can electromyography predict the prognosis of transverse myelitis?

The role of clinical and magnetic resonance imaging (MRI) features on the prognosis of acute transverse myelitis has been studied, but the role of electromyography (EMG) changes, although reported, has not been investigated. Seventeen patients with acute transverse myelitis were subjected to clinical evaluation, MRI scanning and concentric needle EMG. The outcome was defined on the basis of a 3-month Barthel Index (BI) score as good or poor. The EMG changes in these groups were compared. All of the patients had complete paraplegia (power grade 0), except 1 who had grade III power. Mild upper limb weakness was present in 6 patients. Joint position and vibration sense were impaired in the lower limbs, and a horizontal limit to sensory loss to pinprick was present in all of the patients. Spinal MRI was abnormal in 12 of 14 patients. EMG of the lower limb muscles in the acute stage (within 15-30 days of onset) revealed fibrillations or sharp waves or both in 11 patients. At 3-month follow-up, the lower limb power had improved in 8 and upper limbs in all 6 patients. The EMG changes also improved in 6 patients; fibrillations either disappeared or were markedly reduced. The motor unit potentials (MUPs) were of long duration, polyphasic with reduced recruitment. In 5 patients, however, no MUPs could be recorded and fibrillations persisted. Lower limb hypotonia and fibrillations on EMG were significantly related to the 3-month outcome. EMG evidence of denervation in the lower limb muscles in acute transverse myelitis suggests a poor outcome as assessed by 3-month Barthel index score

Movement disorders in Japanese encephalitis

Movement disorders in Japanese encephalitis (JE), although reported, have not been analyzed systematically. In this study, we report an analysis of movement disorders in 14 out of 17 JE patients, correlated with the radiological findings. All patients had at least a four fold rise of IgG antibodies against JE in a haemagglutination inhibition test. The patients' ages ranged between 2 and 54 years and 4 of them were women. Extrapyramidal signs, such as hypokinesia, hypophonia and masking of the face, were present in all patients by the first month as the patients came out of the coma - except for 1 patient. Eight patients had axial and 3 tongue dyskinesia; rigidity was present in 6 and tremor in 2 patients. At 3 months, these symptoms improved considerably in 6 patients. Cranial CT scan revealed thalamic involvement in 10, which was bilateral in 9 patients. Two patients had brain stem and one had cerebellar involvement. Cranial MRI was carried out in 9 patients and revealed additional findings in lentiform nucleus, midbrain and pons in 3 each and cerebellum in 4 patients. Bilateral thalamic involvement on MRI was seen in all the patients, including two patients whose CT scans were normal. SPECT studies using 99mTc-ECD revealed bilateral thalamic hypoperfusion in all (n = 7) and frontal hypoperfusion in 3 patients. In JE, movement disorders are common and may be due to thalamic involvement in isolation or in combination with basal ganglia or midbrain or both

Vitamin B12 deficiency neurological syndromes: correlation of clinical, MRI and cognitive evoked potential

Objective: To evaluate cognitive function in B12 deficiency neurological syndromes and response to B12 therapy. Methods: Patients were diagnosed on the basis of low serum B12 or megaloblastic bone marrow or both. Detailed neurological examination was performed and mental status was evaluated by the Mini Mental State Examination (MMSE).Hemo-globin, RBC indices, blood counts, serum chemistry, HIV, thyroid profile, antiparietal cell antibody and craniospinal MRI were done. Cognitive evoked potential was carried out using the odd ball auditory paradigm and recording was achieved from Fz, Cz and Pz referred to mastoid. P3 latency and amplitude were measured and compared with 33 age and sex matched controls. Three months following B12 therapy, clinical and P3 values were reevaluated and compared with the baseline values. Results: 36 patients, aged 16-80 years were included; 32 patients were above 40 years of age. Their median education level was 14 years. The presenting syndrome was myeloneurocognitive in 9, myeloneuropathy in 10,myelocognitive in 8,myelopathy in 8 and only cognitive in 1 patient.MMSE was abnormal in 17; between 28-19 in 14 and 18-11 in 3 patients. Cranial MRI carried out in 14 patients revealed multiple white matter hyperintensity in T2 in 3 and cortical atrophy in 1. P3 was unrecordable in 7 and latency was prolonged in 8 out of 33 patients. P3 latency was significantly prolonged in patients compared to controls and both MMSE and P3 latency improved significantly at the 3-month followup. Conclusion: MMSE was abnormal in 47 % and P3 in 45.5% of patients with B12 deficiency neurological syndromes which improved following treatment. Significance: There is high incidence of reversible cognitive impairment and P3 abnormalities in B12 deficiency neurological syndromes

Central motor conduction studies in internal capsule and corona radiata infarction

Clinical and evoked-potential studies in internal capsule and corona radiata infarction are lacking. We report the results of a clinical and central motor conduction time (CMCT) study in 16 patients with internal capsule and 17 with computed tomography (CT)-proven corona radiata infarction. Patient's outcome was defined at the end of 3 months on the basis of the Barthel Index score. Four patients with type A capsular infarction (middle third of posterior limb of internal capsule) all had severe weakness, while 2 also had persistently unrecordable CMCT and poor outcome. Twelve patients with type B internal capsular infarction (genu, anterior limb, anterior or posterior third of posterior limb) had a milder degree of weakness, and CMCT was recordable in 9. At 3 months' follow-up, however, CMCT was recordable in all 12 patients. All of these patients had a partial (n = 4) or complete (n = 5) recovery. Thirteen patients with type A corona radiata infarction (middle third of corona radiata) had more pronounced weakness, and CMCT was unrecordable in all of these patients except 1 on initial examination. Follow-up after 3 months was possible in 8 patients, and CMCT became recordable in 3. One of these patients had complete, 3 partial, and 4 poor recovery. In type B corona radiata infarction (anterior or posterior third of corona radiata), the clinical signs and CMCT did not follow a regular pattern. Clinical and CMCT abnormalities in internal capsular infarction followed a more predictable pattern compared with those in corona radiata infarction. A less predictable pattern of weakness and CMCT change in corona radiata infarction may be attributed to a less definite organisation of motor pathways compared with the internal capsule