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The hypoxic brain damage induced by stroke is followed by an ischemia-reperfusion injury modulated by oxidative stress. Magnetoencephalographic (MEG) recording of rest and evoked cortical activities is a sensitive method to analyse functional changes following the acute ischemic damage. We aimed at investigating whether MEG signals are related to oxidative stress compounds in acute stroke. Eighteen stroke patients and 20 controls were enrolled. All subjects underwent MEG assessment to record background activity and somatosensory evoked responses (M20 and M30) of rolandic regions, neurological examination assessed by National Institute of Health Stroke Scale (NIHSS) and plasmatic measurement of copper, iron, zinc, ceruloplasmin, transferrin, total peroxides and Total Anti-Oxidant Status. Magnetic Resonance was performed to estimate the lesion site and volume. Delta power and M20 equivalent current dipole (ECD) strength in the affected hemisphere (AH) correlated with NIHSS scores (respectively, rho=.692, p=.006 and rho=-.627, p=.012) and taken together explained 67% of NIHSS variability (p=.004). Higher transferrin and lower peroxides levels correlated with better clinical status (respectively, rho=-.600, p=.014 and rho=.599, p=.011). Transferrin also correlated with AH M20 ECD strength (rho=.638 p=.014) and inversely with AH delta power (rho=-.646 p=.023) and the lesion volume, especially in cortico-subcortical stroke (p=.037). Our findings strengthen MEG reliability in honing the evaluation of neuronal damage in acute ischemic stroke also demonstrating an association between the MEG parameters most representing the clinical status and the oxidative stress compounds. Our results meet at a possible protective role of transferrin in limiting the oxidative damage in acute stroke.

The aim of this paper was to deepen understanding about the role played by brain plasticity in obtaining clinical recovery. Eighteen patients, who had recovered partially or totally from dysfunctions due to a monohemispheric infarction within the middle cerebral artery territory, underwent magnetoencephalographic (MEG) recordings of rolandic areas cerebral activity both in rest state (spectral power properties) and in response to the electrical stimulation of the contralateral median nerve (M20 and M30 cortical sources). MEG evaluation was performed in acute (T0: mean 5 days from ischemic attach) and post-acute phase (T1: median 6 months). At T1, all the inter-hemispheric asymmetries were reduced for both spontaneous and evoked activity parameters with respect to T0. In post-acute phase, lower cortical excitability, higher delta and theta power and lower spectral entropy were associated to a worse clinical state. An unusual recruitment-as revealed by an excessive inter-hemispheric asymmetry of M20 cortical source position-correlated with higher level of clinical amelioration in the patients who showed a partial recovery. In addition to confirmative evidence that "normalization" of neural activity in both the affected and unaffected hemispheres subtends best clinical recovery, present data provide support to the positive role of cerebral plasticity phenomena--i.e. unusual neural recruitments--to regain lost functions in those patients unable to achieve total recovery.

An understanding of the functional readjustments that the brain undergoes during the early days after a stroke would give us a major insight into how and how much neurons are capable to react to an insult. Thirty-two patients affected by an acute monohemispheric ischemic stroke were enrolled in the study. Magnetoencephalography was used to record the somatosensory-evoked fields (SEF) generated in response to median nerve stimulation. Latency, strength, and position of the related early cortical components (M20 and M30) were studied both separately within each hemisphere, and in terms of interhemispheric differences. Interhemispheric cross-correlations among SEF waveshapes in the two hemispheres were also investigated. Overall, except for some source displacement possibly induced by the perilesional edema, results did not demonstrate any unusual neural recruitment. The severity of the clinical picture was found related to the sources' strengths (both as absolute values and as interhemispheric differences), to excessive interhemispheric differences in SEF waveshapes and in the M30 latencies. Signs of an enhanced excitability were present in the affected hemisphere (AH) following a cortical lesion, usually in combination with preserved hand functionality. An enhanced excitability of the unaffected hemisphere (UH) was paired with larger lesions with cortical involvement; signs compatible with an abnormal transcallosal transmission and intracortical function of inhibitory GABAergic interneurons in the AH were found subtending UH enhancement. Spared responsiveness from Brodmann's area (BA) 2 and posterior parietal areas despite an altered response from BA 3b was found in six patients, combined to high hand functionality. Present results in acute phase increase the knowledge of the mechanisms governing brain adaptation/reaction capabilities, for future efforts to establish therapeutic and rehabilitative procedures.