EEG spectral exponent as a synthetic index for the longitudinal assessment of stroke recovery.

OBJECTIVE: Quantitative Electroencephalography (qEEG) can capture changes in brain activity following stroke. qEEG metrics traditionally focus on oscillatory activity, however recent findings highlight the importance of aperiodic (power-law) structure in characterizing pathological brain states. We assessed neurophysiological alterations and recovery after mono-hemispheric stroke by means of the Spectral Exponent (SE), a metric that reflects EEG slowing and quantifies the power-law decay of the EEG Power Spectral Density (PSD). METHODS: Eighteen patients (n = 18) with mild to moderate mono-hemispheric Middle Cerebral Artery (MCA) ischaemic stroke were retrospectively enrolled for this study. Patients underwent EEG recording in the sub-acute phase (T0) and after 2 months of physical rehabilitation (T1). Sixteen healthy controls (HC; n = 16) matched by age and sex were enrolled as a normative group. SE values and narrow-band PSD were estimated for each recording. We compared SE and band-power between patients and HC, and between the affected (AH) and unaffected hemisphere (UH) at T0 and T1 in patients. RESULTS: At T0, stroke patients showed significantly more negative SE values than HC (p = 0.003), reflecting broad-band EEG slowing. Most important, in patients SE over the AH was consistently more negative compared to the UH and showed a renormalization at T1. This SE renormalization significantly correlated with National Institute of Health Stroke Scale (NIHSS) improvement (R = 0.63, p = 0.005). CONCLUSIONS: SE is a reliable readout of the neurophysiological and clinical alterations occurring after an ischaemic cortical lesion. SIGNIFICANCE: SE promise to be a robust method to monitor and predict patients' functional outcome.

Soluble proteins in the human atherosclerotic plaque. With spectral reference to immunoglobulins, C3-complement component, alpha 1-antitrypsin and alpha 2-macroglobulin.

A number of soluble proteins contained in human aortic intimal tissue was extracted into buffered saline (pH 7.4) and identified and quantitated by immunoelectrophoresis and immunodiffusion. The proteins included IgA, IgG, IgM, B1C (C3), alpha 1-antitrypsin, alpha 2-macroglobulin, fibrinogen, albumin, LDL, HDL, alpha 1-acid glycoprotein, beta 2-glycoprotein, transferrin and ceruloplasmin. The concentration of soluble proteins was significantly higher in the atherosclerotic intima than in the normal intima. The diseased intima also contained a small amount of tissue-bound IgG, IgA and B1C which was extractable with citrate buffer at pH 3.2. The vascular band IgG, and B1C were shown by enzymatic and immunohistochemical studies to be closely associated with the collagenous tissue of the plaque. The Ig contained in the atherosclerotic plaque may be derived in part from the biosynthesis of Ig by the artery, since the incorporation of 14C-labeled leucine into IgG by the atheromatous plaque was demonstrable by radioimmunoelectrophoresis. In contrast to the diseased artery, the normal artery did not synthesize IgG and did not contain vascular bound IgG or complement. However, the normal artery was capable of fixing IgG and B1C eluted from the diseased artery. The present studies suggested that the IgG contained and synthesized by the plaque might represent an immune response to an endogenous or exogenous antigen closely associated with plaque collagen. IgG and B1C either alone or in the form of an immune complex also may play an important role in phagocytosis in the plaque and thereby influence the course of atherosclerosis. The proteolytic inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, found in relatively high concentrations in the plaque, could enhance fibrosis of the lesion because of thier known inhibitory effects on collagenase and elastase.

Arterial uptake and synthesis of low density lipoproteins.

The accumulation of cholesterol in atherosclerotic lesions is associated with an increased uptake of plasma cholesterol and LDL by the arterial wall. During the regression of atherosclerosis, the uptake of these macromolecules returns to or below normal, suggesting that the retention of cholesterol in regressed lesions is due to a defect in the removal of cholesterol from the arterial wall rather than to an abnormality in vascular permeability. Although increased amounts of 125I-LDL were detected in atherosclerotic vessels, the percent distribution and fractional degradation rate of 125I-LDL appeared similar in normal and diseased vessels. The present studies in support of earlier findings in human vessels indicate that LDL in the artery is contained in a number of different cellular and extracellular pools in close association with AMPS. These lipoproteins appeared to be derived not only from the lipoproteins contained in the plasma but also from lipoproteins synthesized by the arterial wall.