In the neonatal period, the majority of seizures are acute reactive events provoked by injury. Some etiologies require immediate diagnosis and treatment. Many of these acute, symptomatic seizures resolve once the underlying etiology is corrected or the acute neurological disruption of the causal event subsides. The electroencephalogram (EEG), amplitude-integrated EEG (aEEG), or quantitative electroencephalography (QEEG) may aid in rapid diagnosis and treatment of clinical and subclinical seizures. The new ILAE classification for neonatal seizures emphasizes the need for EEG for accurate diagnosis. Most EEG patterns in the neonate are non-specific to the etiology of seizures. However, even while non-specific, certain patterns can help direct the diagnostic evaluation. In many cases neuromonitoring may have specific characteristics that are helpful to direct further workup. This chapter discusses neuromonitoring in neonatal seizures due to acute causes, including vascular injury (stroke or hemorrhage), infection, acute metabolic disturbance, brain injury of prematurity, and neonatal abstinence syndrome.

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Acute non-traumatic intracerebral haemorrhage (ICH) has a poor prognosis and is the least treatable form of acute stroke.Although less common than acute ischaemic stroke, ICH causes greater premature loss of productive life years on a global scale due to its predilection to affect people at younger ages with devastating consequences.Prognosis from ICH is related to location, initial volume and speed of expansion of the haematoma, and associated intraventricular haemorrhage. Care in a specialised stroke or neurointensive care unit improves outcome. Surgical haematoma evacuation should be pursued as for patients with cerebellar haemorrhage with neurologic deterioration, hydrocephalus, orsd brainstem compression. Haematoma evacuation may be considered, as a life-saving measure, in patients with coma or large haematoma with mass effect.Minimally-invasive surgery in stable patients is of uncertain benefit and is being evaluated in RCTs.Clinicians should not routinely use haemostatic therapies where there is no evidence of coagulopathy or anticoagulant use.When coagulopathy is present, early corrective measures should be taken. Early moderate intensity BP lowering to a systolic BP target of 140 mmHg is reasonable.Medical therapies to reduce mass effect and intracranial pressure should not be used routinely, but hyperventilation and hypertonic saline or colloidal osmotic agents are reasonable in patients with imminent herniation as a bridge to definitive neurosurgical intervention. Corticosteroids should be avoided.Novel neuroprotective approaches hold promise.