Ischemic stroke is characterized by a complex cascade of events starting from vessel occlusion. The term “penumbra” denotes the area of severely hypo-perfused brain tissue surrounding the ischemic core that can be potentially recovered if blood flow is reestablished. From the neurophysiological perspective, there are local alterations—reflecting the loss of function of the core and the penumbra—and widespread changes in neural networks functioning, since structural and functional connectivity is disrupted. These dynamic changes are closely related to blood flow in the affected area. However, the pathological process of stroke does not end after the acute phase, but it determines a long-term cascade of events, including changes of cortical excitability, that are quite precocious and might precede clinical evolution. Neurophysiological tools—such as Transcranial Magnetic Stimulation (TMS) or Electroencephalography (EEG)—have enough time resolution to efficiently reflect the pathological changes occurring after stroke. Even if they do not have a role in acute stroke management, EEG and TMS might be helpful for monitoring ischemia evolution—also in the sub-acute and chronic stages. The present review aims to describe the changes occurring in the infarcted area after stroke from the neurophysiological perspective, starting from the acute to the chronic phase.

Metronidazole-induced encephalopathy (MIE) is a rare and often under-recognized iatrogenic condition. The diagnosis should be considered in metronidazole-treated patients presenting with acute encephalopathy, unprovoked seizures and cerebellar signs. While typical magnetic resonance imaging (MRI) findings strongly support the diagnosis, electroencephalography (EEG) features have been rarely reported and poorly described. We present a longitudinal EEG assessment in one patient with encephalopathy due to metronidazole toxicity who presented a peculiar EEG pattern presentation and evolution. During the acute phase of encephalopathy, the EEG showed a monomorphic, sharply contoured theta activity symmetrically represented over frontal regions with an anterior–posterior progression which evolved in parallel with clinical worsening. Together with a systematic review of the literature, we discuss whether this EEG activity may represent a distinct neurophysiological correlate of ‘cerebellar encephalopathy’.