Cortical Spreading Depolarization in Chronic Subdural Hematoma: Bridging the Gap

Abstract

Cortical spreading depolarization (CSD) is recognized as a cause of transient neurological symptoms (TNS) in various clinical entities. Although scientific literature has been flourishing in the field of CSD, it remains an underrecognized pathophysiology in clinical practice. The literature evoking CSD in relation to subdural hematoma (SDH) is particularly scarce. Patients with SDH frequently suffer from TNS, most being attributed to seizures despite an atypical semiology, evolution, and therapeutic response. Recent literature has suggested that a significant proportion of those patients’ TNS represent the clinical manifestations of underlying CSD. Recently, the term Non-Epileptical Stereoytpical Intermittent Symptoms (NESIS) has been proposed to describe a subgroup of patients presenting with TNS in the context of SDH. Indirect evidence and recent research suggest that the pathophysiology of NESIS could represent the clinical manifestation of CSD. This review should provide a concise yet thorough review of the current state of literature behind the pathophysiology of CSD with a particular focus on recent research and knowledge regarding the presence of CSD in the context of subdural hematoma. Although many questions remain in the evolution of knowledge in this field would likely have significant diagnostic, therapeutic, and prognostic implications.

Cognitive Dysfunction After Analgesia and Sedation: Out of the Operating Room and Into the Pediatric Intensive Care Unit

“…Slow wave sleep is also associated with reductions in brain temperature and metabolic demand for oxygen and glucose, as well as replenishment of ATP and glycogen stores (Aalling et al, 2018;Caporale et al, 2021). REM sleep deprivation decreases the threshold for cortical spreading depressions which are found frequently after acquired brain injuries and thought to contribute to secondary brain injury (De Vasconcelos et al, 2004;Levesque et al, 2021). Interestingly, a recent study of analgesia and sedation after a variety of brain injuries found that benzodiazepine treatment increased the incidence of cortical spreading depressions (Hertle et al, 2012).…”

Pathophysiology of transient neurological deficit in patients with chronic subdural hematoma: A systematic review

“…CSD is a slow spreading wave of altered brain activity that includes changes in neuronal, glial, and vascular function, and might be caused by local mechanical stimulation or injury 18,42 . It is described in a variety of neurological conditions such as migraine, traumatic brain injury, and more recently also in CSDH 33,42–44 . Although several articles in our review mentioned this etiology, none of the articles in our literature review substantiated this with valid arguments.…”

“…18,42 It is described in a variety of neurological conditions such as migraine, traumatic brain injury, and more recently also in CSDH. 33,[42][43][44] Although several articles in our review mentioned this etiology, none of the articles in our literature review substantiated this with valid arguments. This may be the direct result of the invasive method of demonstrating the presence of CSD, such as placement of electrodes directly on the exposed cortex.…”

Nonepileptic, Stereotypical, and Intermittent Symptoms After Subdural Hematoma Evacuation

“…Given our patient’s persistent symptoms, lack of correlation between symptoms and EEG, and lack of response to levetiracetam, we suspected that a seizure was not likely the etiology [ 27 ]. Levesque et al postulated that cortical spreading depolarization may be the etiology behind this presentation and coined the term nonepileptic, stereotypical, and intermittent symptoms (NESIS) to define this syndrome [ 11 , 28 ].…”