About me
I am a neurologist and researcher of the pathological effects that exaggerated sympathetic nervous system responses exert on different body systems. In 2012, after years of scientific and clinical training in neuroscience and neurology, I took a recreational freediving course that unexpectedly introduced me to the most powerful neurological reflex I know: the mammalian diving response (MDR). This multi-pronged neurological response to prolonged voluntary and involuntary apnea provides a unique theoretical framework that adequately explains the pathophysiological effects induced by seizures associated with the sudden and unexpected deaths of otherwise healthy persons with epilepsy.
Blood transiently shifted by the MDR could precipitate SUDEP
Pulmonary edema occurs when the fluid inside pulmonary capillaries leaks into, or through, the capillary-alveolar membrane. When this occurs, gas exchange between alveoli and red blood cells is hindered, or blocked altogether, resulting in low blood oxygen levels.
Several studies show that convulsive seizures often cause transient pulmonary edema. Such edema can be precipitated by increased blood flow through the pulmonary capillaries. As the MDR sparks a rapid shift of the body’s blood from the periphery into the pulmonary circulation during periods of voluntary or involuntary apnea, it is possible that seizure-induced pulmonary edema, and subsequent death, are precipitated by the MDR.
Can SUDEP be predicted?
At any given time, over 60% of the body’s circulating polymorphonucleocytes (a type of immune cell that includes neutrophils, basophils, eosinophils and MAST cells) are in transit through the lungs. But when pulmonary blood flow increases, as it happens when people exercise , become anxious , or have a convulsive seizure , these immune cells are propelled back into the peripheral blood and cause a detectable elevation of the white blood cell count (WBCC). Could the blood shift of the MDR, which fuels an increase in pulmonary blood flow during apnea, explain the transient elevations of the WBCC after seizures? If so, could these elevations reflect individual SUDEP risk?
Circulating immune cells and pulmonary blood flow during deadly seizures
Most, if not all , epileptic convulsions result in a detectable elevations of the white blood cell count. Studies show that the magnitude of these elevations relate to patients’ clinical outcomes . These elevations appear to be linked to breathing abnormalities during or after epileptic convulsions. These results along with my own investigations lead me to believe that WBCCs after seizures are a reflection of seizure-induced apnea.
White blood cell counts after seizures may identify patients at risk of SUDEP
The majority of circulating white blood cells (WBCs) are marginated inside the enormous network of pulmonary capillaries . This is why even minor physiological increases in pulmonary blood flow can expel a portion of these cells into the peripheral circulation and drive transient but detectable increases in the WBC count.
As the MDR appears to be triggered during voluntary or involuntary periods of “dry” apnea, and the MDR increases pulmonary blood flow, transient elevations in the WBC count after seizures suggest that involuntary apnea during or immediately after those seizures. This video shows why and how the WBC count measured after seizures could help identify patients whose epileptic seizures place them at risk of SUDEP.
Severe pulmonary edema in a near-SUDEP patient with stereotypical troponin elevations and increased WBCCs.
Patients that go into cardiac arrest after a seizure and are successfully resuscitated for at least one hour are said to have experienced a “near SUDEP” event. I had such a patient in 2023. She had suffered intermittent epileptic seizures most of her life but never pursued medical care. Her case is interesting because her death would have met “probable” SUDEP criteria had she not been resuscitated. The severity of her pulmonary edema and its correlation with transiently increased WBCCs suggest that her seizures triggered a surge of systemic catecholamines that likely precipitated her sudden and unexpected demise.
Can seizures cause a non-SUDEP sudden death by provoking hemorrhages inside the walls of large blood vessels?
Sometimes arterial dissection – the pathological splitting of a blood vessel wall by an expanding intramural hemorrhage – prevents blood flow to the brain, or drives the formation of blood clots that cause cerebral infarctions and subsequent epileptic seizures; these seizures are typically said to be symptoms of the arterial dissection. However, days usually pass before strokes cause acute symptomatic seizures and yet many patients are completely symptom-free when they suffer a seizure after which they wake up with an arterial dissection symptoms. In this article, I advance the novel argument that seizures at the onset of arterial dissections are not symptoms but triggers of the associated dissections.
The father of the mammalian diving response was lost for over 200 years!
The science behind the mammalian diving response originated with the discovery of diving bradycardia, a primordial oxygen-conserving reflex by which the heart rate of air-breathing vertebrates, including humans, slows down in response to prolonged breathing cessation (i.e., apnea). Curiously, luminaries in the field erroneously attributed its discovery to a famous French physician, Paul Bert , even though his experiments were neither intended nor adequate for such a discovery. Instead, diving bradycardia had been described in the doctoral thesis of a little known British medical student (Edmund Goodwyn) almost 100 years before Bert’s work was published. Ironically, this student’s thesis had been appropriately referenced, for all to see, in Bert’s own list of citations .
Blog
