In Reply: Nonepileptic, Stereotypical, and Intermittent Symptoms (NESIS) in Patients With Subdural Hematoma: Proposal for a New Clinical Entity With Therapeutic and Prognostic Implications

To the Editor: Syndromes are usually born out of intuition. From the earliest classification of epilepsy, circa 1050 BC,1 to the recent definition of Stimulus-induced rhythmic, periodic, or ictal discharges,2 the process to initially describe any clinical entity necessarily starts with the careful observation and identification of a pattern. Broca's aphasia (which he actually called “aphemia”) was first detailed in a single-case report.3 Parkinson's disease proposal was based on 6 cases.4 Acknowledging that “the caution with which hypothetical statements are admitted” was critical to the success of medicine, Parkinson stated, in the preface of his landmark monograph, that he felt “a duty to submit his opinions to the examination of others, even in their present state of immaturity and imperfection.” 4 The pathophysiology of both syndromes was unknown at the time of their publication and the author's initial hypotheses were far from current views. Yet their descriptions were useful and empowered others to better understand, predict, and, to some extent, treat both conditions. We thank Dr Marcellino for their critical review of our work.5 Transient neurological symptoms in subdural hematomas are frequent, and it is our intuition that not all of them are epileptic in nature. Seizures lacking typical convulsive symptoms are a well-accepted phenomenon,6 and we are indeed strong proponents of continuous electroencephalogram (EEG) monitoring in neurocritical care patients. The imperfect sensitivity of scalp EEG is also well documented.7 We do argue, however, that patients with epilepsy, whether it be convulsive or not and whether it be scalp EEG-proven or not, should show a similar, standard, response rate to antiepileptic drugs (AED) or, at the very least, have a prognosis that somehow correlates with response to medication. If they do not, then the diagnosis of epilepsy and its relevance should be questioned. In our series of patients with subdural hematomas and transient neurological symptoms, we find that patients with negative scalp EEG do not respond to conventional antiepileptic medication, yet have better discharge disposition and lower mortality.8 These patients present a distinctive semiology, which can be reliably captured by the NESIS (nonepileptic, stereotypical, and intermittent symptoms) score. This unexpected paradox needs to be studied. The problem is that for any phenomenon to be prospectively studied, it must first be defined. Definition implies naming the entity and proposing criteria, which, at this point, can only be retrospectively generated. We named the entity NESIS because it was self-explanatory. We created the criteria using the best available data while excluding outcome variables that would preclude the prospective use of the criteria, such as mortality or response to AED. Although imperfect, this approach is the first step in better documenting the syndrome prospectively. If our criteria are found to select patients with demonstratable epilepsy, we will need to understand whether these epileptic patients are the majority (in which case NESIS does not exist) or rather minor contaminants in the subgroup (in which case the criteria need to be improved). At the moment, our proposed clinical criteria remain somewhat speculative but should prove useful in prospectively screening patients for future research. Until independently validated, the use of the score in clinical practice should be done with caution and, at best, serve as an additional argument in the decision process rather than as a true diagnostic tool. Generating Evidence on NESIS (GENESIS) will be our first prospective trial on this population and will focus on patients with chronic subdural hematoma, in whom we think diagnosing NESIS is most relevant.9 The existence of NESIS and its clinical importance, however, should definitely be challenged by others. We strongly encourage the scientific community to start independent studies to infirm or confirm the validity of our results and further our understanding of this condition. We recognize the limitations inherent to the retrospective nature of our work, the imperfect diagnostic tool that represents the EEG, and the small cohort with which the criteria were generated. We do believe, however, that the distinctive semiology, therapeutic response, and prognostic evolution justify the need to question and raise the possibility of an alternative underlying process. We believe that such patients are frequently encountered in clinical practice and often raise a diagnostic dilemma in neurologists and neurosurgeons alike. Whether our hypothesis that NESIS is the clinical manifestation of cortical spreading depolarizations is true or not remains to be seen. But, our intuition is that there is something there to be discovered, something which could truly impact the care of patients. Disclosures The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.

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