Abstracts

Rationale: The exact cause and consequence of periodic lateralized discharges (PLDs) on electroencephalogram (EEG) remains somewhat of an enigma. Initially thought to be epileptiform in nature, more recent studies have questioned their association with seizures and the name periodic lateralized epileptiform discharges (PLEDs) was changed to PLDs. While chronic PLDs exist, the acute variant is thought more likely to be associated with an acute or subacute structural injury to the cerebral cortex.  Given PLDs have been associated with a number of different pathologies we felt that a review of the aetiology and outcome of patients with PLDs found on their EEG over a 3 year period at Royal North Shore Hospital in Sydney, a large metropolitan hospital in Australia, may be helpful in determining their significance in our patient population. Methods: 3 years of EEG results were reviewed (May 2014 - May 2017) using the following key words: repetitive discharges, periodic discharges, lateralized discharges, PLEDs, BiPLDs, BiPLEDs and PLDs. We excluded generalized discharges, GPDs and triphasic waves. We excluded repeated EEGs of the same patient and, in each case, analysed only the first EEG to show PLDs. The patients’ files were reviewed and the following data obtained: Age, Sex, Clinical presentation, Presence of clinical seizures, Aetiology, Management used and Outcome.  PLDs were characterized as lateralized or focal, periodic, spike or sharp complexes present throughout most or all of the recording. BiPLDs were defined as bilateral independent periodic lateralized discharges. The patients imaging and pathology results were reviewed to confirm the documented diagnosis. The clinical outcomes were assessed on discharge as independent, dependent or deceased. Results: 6000 EEG results were reviewed and 147 patients were identified using the key words. Once duplicates were excluded 116 patients remained. All of these EEGs were available for morphological analysis to confirm they fulfilled the clinical definitions used.  All patients had clinical data and neuroimaging available for review. The most common cause of PLDs seen was underlying tumour (primary or metastatic) followed by other structural intracranial pathologies such as haemorrhage (both intraparenchymal and subdural), stroke and neurosurgical resection. Less commonly out of hospital cardiac arrest with associated hypoxic brain injury, encephalitis and Creutzfelt-Jakob Disease (CJD) were also seen as were metabolic causes. 66% of patients had clinical seizures during their admission. 55% of the seizures were focal and 45% were generalized. 50% of patients died, either during their admission or shortly after. 35% fully recovered and 15% were left dependent on others for assistance with activities of daily living (ADLs). Conclusions: In the population of patients seen at Royal North Shore Hospital PLDs are commonly associated with focal intracranial pathology. Generalised intracranial pathologies such as hypoxic brain injury and other metabolic causes were much less common. The majority of cases were associated with clinical seizure activity. PLDs appear to be associated with a poor prognosis as 50% of our patients died during their admission and a further 15% were left dependent on others for basic care needs. Most of the patients that recovered have remained on anti-epileptic therapy, usually with more than one drug required. Funding: Nil