Validation of non-REM sleep stage decoding from resting state fMRI using linear support vector machines.

A growing body of literature suggests that changes in consciousness are reflected in specific connectivity patterns of the brain as obtained from resting state fMRI (rs-fMRI). As simultaneous electroencephalography (EEG) is often unavailable, decoding of potentially confounding sleep patterns from rs-fMRI itself might be useful and improve data interpretation. Linear support vector machine classifiers were trained on combined rs-fMRI/EEG recordings from 25 subjects to separate wakefulness (S0) from non-rapid eye movement (NREM) sleep stages 1 (S1), 2 (S2), slow wave sleep (SW) and all three sleep stages combined (SX). Classifier performance was quantified by a leave-one-subject-out cross-validation (LOSO-CV) and on an independent validation dataset comprising 19 subjects. Results demonstrated excellent performance with areas under the receiver operating characteristics curve (AUCs) close to 1.0 for the discrimination of sleep from wakefulness (S0|SX), S0|S1, S0|S2 and S0|SW, and good to excellent performance for the classification between sleep stages (S1|S2:~0.9; S1|SW:~1.0; S2|SW:~0.8). Application windows of fMRI data from about 70 s were found as minimum to provide reliable classifications. Discrimination patterns pointed to subcortical-cortical connectivity and within-occipital lobe reorganization of connectivity as strongest carriers of discriminative information. In conclusion, we report that functional connectivity analysis allows valid classification of NREM sleep stages.

Voxel-based morphometry in individual patients: a pilot study in early Huntington disease.

BACKGROUND AND PURPOSE: Voxel-based morphometry (VBM) has proved a powerful method to detect subtle changes of gray matter (GM) at the group level but the role of VBM for the detection of GM changes in single subjects, especially in those with suspected neurodegenerative disorder, remains uncertain. Here, we performed single subject analyses in 22 patients in early stages of Huntington disease (HD), a neurodegenerative disorder with a well-known and characteristic pattern of GM loss. MATERIALS AND METHODS: We applied an ANCOVA with age and gender as covariates and corrected for multiple statistical tests by false discovery rate (P < 0.05). Each patient was compared to 133 healthy controls. The same procedure was applied to 22 of the controls matched for age and gender in a pair-wise manner. RESULTS: Our analyses yielded biologically plausible results in HD patients in which GM decrease within the caudate nucleus could be identified in 15 of the 16 most affected patients while GM decrease was found in only 1 control subject. Lowering the size of the control group yielded comparable results with 99 and 66 control subjects whereas sensitivity decreased with 33 control subjects. CONCLUSIONS: Our pilot study demonstrates a potential role of VBM for the detection of cerebral GM changes in single subjects with suspected neurodegenerative disorder.

[Differential diagnosis of neuralgic amyotrophy and vertebral artery dissection]. / Neuralgische Schulteramyotrophie oder Vertebralisdissektion? : Eine abwegige Differenzialdiagnose?

In most cases the definite diagnosis of neuralgic amyotrophy is not possible, so it is based on the typical course of symptoms after other diagnoses have been excluded. We report an otherwise healthy woman who presented with symptoms typical of neuralgic amyotrophy. However we could diagnose a vertebral artery dissection that probably caused the symptoms by compression of the cervical roots. The differential diagnosis of neuralgic amyotrophy and vertebral artery dissection is discussed.

[Modification of vascular risk factors by intervention on the primary care level. Results of the INVADE project]. / Modifikation vaskulärer Risikofaktoren durch hausärztliche Intervention. Ergebnisse des Projekts INVADE.

BACKGROUND: The so-called INVADE project examines the efficacy of consistent diagnosis and treatment of cerebrovascular risk factors on the incidence of stroke. METHODS: This analysis compares known cardiovascular risk factors (elevated blood pressure, dipositas, hyperlipidemia, diabetes mellitus, and smoking) and respective medication of 2930 patients with respect to cerebrovascular disease, peripheral arterial disease (PAD), and coronary heart disease (CHD) between baseline and follow-up examination after 2 years of intervention. RESULTS: Using the ankle-brachial index (ABI), 381 patients (13%) with asymptomatic PAD were identified. Comparison between baseline and follow-up examination revealed significant reductions in the following risk factors. Cerebrovascular disease: elevated blood pressure -12.8%, dipositas -4.2%, and LDL -8.1%. For PAD the results were: elevated blood pressure -7.2%, smoking -1.2%, elevated cholesterol -6.4%, dipositas -3.2%, and LDL -7.4%. For CHD the results were: elevated blood pressure -11.3%, elevated cholesterol -13.0%, and LDL -14.9%. CONCLUSION: By the use of ABI, previously undiagnosed asymptomatic PAD was identified in 13% of all patients. Two-year intervention on the primary care level yielded significant reduction of known vascular risk factors.

Employment in 1996: jobs up, unemployment down.

Overall job gains were moderated by losses in nondurable goods manufacturing and Federal employment; declining unemployment was tempered by persistent long-term joblessness.

Lymphocytes from SJL/J mice immunized with spinal cord respond selectively to a peptide of proteolipid protein and transfer relapsing demyelinating experimental autoimmune encephalomyelitis.

Relapsing experimental autoimmune encephalomyelitis (R-EAE) can be induced in SJL/J mice by immunization with spinal cord homogenate and adjuvant. The specific Ag(s) responsible for acute disease and subsequent relapses in this model is unknown. Myelin basic protein (BP), an encephalitogenic peptide of BP (BP 87-99), and proteolipid protein (PLP) can each induce R-EAE in SJL/J mice, and a peptide of PLP (PLP 139-151) has been reported to induce acute EAE. To determine the encephalitogens in cord-immunized mice with R-EAE, the in vitro proliferative responses of lymph node cells (LNC) and central nervous system mononuclear cells to BP, BP peptides, and PLP peptides were examined during acute EAE and during relapses. LNC responded only to PLP peptides 139-151 and 141-151 and did not respond to BP or its peptides during acute or chronic disease. Central nervous system mononuclear cells also preferentially responded to PLP 139-151 and 141-151 during acute and relapsing disease. A PLP 139-151 peptide-specific Th cell line was selected from LNC of cord-immunized donors. Five million peptide-specific line cells transferred severe relapsing demyelinating EAE to naive recipients. We conclude that PLP peptide 139-151 is the major encephalitogen for R-EAE in cord-immunized SJL/J mice. We demonstrate for the first time that Th cells specific for this peptide are sufficient to transfer relapsing demyelinating EAE. The predominance of a PLP immune response rather than a BP response in SJL/J mice suggests that genetic background may determine the predominant myelin Ag response in human demyelinating diseases such as multiple sclerosis.