John Murphy, CEO The COVID-19 Long haul Foundation<\/p>\n\n\n\n
Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), has increasingly revealed itself as a disorder extending well beyond pulmonary injury. Among its most consequential neurological manifestations are dizziness, orthostatic intolerance, autonomic dysfunction, cognitive impairment, altered consciousness, and episodes described by patients as \u201cblackouts.\u201d The word is deceptively simple. A blackout may represent true syncope caused by transient cerebral hypoperfusion; an arrhythmia; orthostatic hypotension or postural tachycardia syndrome (POTS); seizure; impaired cerebral autoregulation; sleep intrusion; or a transient period of profound cognitive disconnection in which the patient remains technically conscious but loses effective awareness of the surrounding world.<\/p>\n\n\n\n
The emerging literature provides biological reasons to take these reports seriously. Studies of Long COVID have identified abnormalities in cerebral blood-flow regulation, autonomic function, brain metabolism, white matter, functional connectivity, and neuroinflammation. A 2025 systematic review encompassing 78 neuroimaging and neurophysiological studies and more than 5,900 participants found abnormalities involving cognition, functional connectivity, electrophysiology and cerebral blood flow, although findings were heterogeneous.<\/p>\n\n\n\n
The most compelling mechanistic possibility is that, in at least a subset of patients, SARS-CoV-2 leaves behind a disorder of the neurovascular-autonomic system<\/strong>: the machinery responsible for maintaining adequate cerebral perfusion when a person stands, exercises, becomes dehydrated, experiences stress, or undergoes changes in blood pressure and carbon dioxide. When that compensatory system fails, the brain can briefly receive inadequate blood flow. The clinical result can be presyncope, visual dimming, cognitive interruption, collapse\u2014and, in extreme circumstances, loss of consciousness.<\/p>\n\n\n\n This phenomenon deserves greater clinical recognition because a blackout occurring while driving, climbing stairs, bathing, working with machinery, or crossing a road can transform an otherwise invisible neurological disorder into a potentially fatal event.<\/p>\n\n\n\n There is a particular vocabulary shared by patients with post-COVID neurological illness.<\/p>\n\n\n\n \u201cI suddenly wasn’t there.\u201d<\/em><\/p>\n\n\n\n \u201cEverything went black.\u201d<\/em><\/p>\n\n\n\n \u201cI was awake, but I couldn’t process anything.\u201d<\/em><\/p>\n\n\n\n \u201cI don’t remember what happened for several seconds.\u201d<\/em><\/p>\n\n\n\n \u201cI stood up and the room disappeared.\u201d<\/em><\/p>\n\n\n\n \u201cI was driving and suddenly I realized I didn’t know where I was.\u201d<\/em><\/p>\n\n\n\n These statements are clinically important precisely because they do not map neatly onto a single neurological diagnosis.<\/p>\n\n\n\n The brain does not possess a single \u201cblackout switch.\u201d<\/p>\n\n\n\n Consciousness is produced through the coordinated operation of the cerebral cortex, thalamus, brainstem arousal systems, cerebral circulation, autonomic nervous system, glucose and oxygen delivery, and innumerable supporting metabolic processes. A temporary disturbance anywhere along this network can produce an alteration of consciousness.<\/p>\n\n\n\n Consequently, the first question when a patient reports a Long-COVID blackout should not be \u201cIs this Long COVID?\u201d<\/strong><\/p>\n\n\n\n It should be:<\/p>\n\n\n\n What physiological system temporarily failed?<\/strong><\/p>\n\n\n\n The brain represents only a small fraction of body mass but consumes approximately one-fifth of resting oxygen and energy.<\/p>\n\n\n\n It therefore cannot tolerate prolonged interruption of blood flow.<\/p>\n\n\n\n Fortunately, the brain possesses an extraordinarily sophisticated mechanism called cerebral autoregulation<\/strong>. Cerebral arterioles continually adjust their diameter to maintain relatively stable cerebral perfusion despite changes in systemic blood pressure.<\/p>\n\n\n\n When a healthy person stands upright, gravity causes blood to pool in the legs and abdomen.<\/p>\n\n\n\n The autonomic nervous system responds almost immediately:<\/p>\n\n\n\n In some patients after COVID-19, this system appears to malfunction.<\/p>\n\n\n\n Studies of Long-COVID patients undergoing tilt testing have demonstrated abnormal reductions in cerebral blood flow during orthostatic stress. Importantly, abnormalities in cerebral blood flow can persist even when conventional measures of heart rate and blood pressure become less abnormal over time.<\/p>\n\n\n\n This observation may be extraordinarily important.<\/p>\n\n\n\n A patient can therefore have a blood pressure reading that looks acceptable in a conventional office examination while experiencing abnormal cerebral perfusion during standing<\/strong>.<\/p>\n\n\n\n The blood pressure cuff may say:<\/p>\n\n\n\n \u201cNormal.\u201d<\/p>\n<\/blockquote>\n\n\n\n The brain may effectively be saying:<\/p>\n\n\n\n \u201cNot enough.\u201d<\/p>\n<\/blockquote>\n\n\n\n POTS has emerged as one of the most recognizable autonomic phenotypes associated with Long COVID.<\/p>\n\n\n\n The characteristic physiology is excessive tachycardia upon standing, accompanied by symptoms such as:<\/p>\n\n\n\n But the deeper issue may not be the heart rate itself.<\/p>\n\n\n\n It may be where the blood is going<\/strong>.<\/p>\n\n\n\n A patient can develop substantial peripheral pooling while cerebral circulation fails to compensate adequately. The result is a mismatch between cardiovascular compensation and cerebral demand.<\/p>\n\n\n\n The patient may therefore experience:<\/p>\n\n\n\n standing \u2192 autonomic stress \u2192 cerebral hypoperfusion \u2192 visual disturbance \u2192 cognitive interruption \u2192 presyncope \u2192 syncope.<\/strong><\/p>\n\n\n\n A 2025 deep-phenotyping study of Long-COVID POTS reported widespread autonomic abnormalities together with abnormal cerebral blood-flow measures.<\/p>\n\n\n\n This provides a plausible physiological bridge between the patient’s apparently cardiovascular complaint\u2014\u201cI almost faint\u201d\u2014and a neurological complaint\u2014\u201cmy brain stopped working.\u201d<\/p>\n\n\n\n The brainstem deserves particular attention.<\/p>\n\n\n\n It contains critical networks controlling:<\/p>\n\n\n\n Long-COVID neuroimaging studies have identified abnormalities involving the brainstem and cerebellum, while reviews of the neurological literature have proposed brainstem dysfunction as one contributor to persistent autonomic abnormalities.<\/p>\n\n\n\n This does not<\/strong> establish that SARS-CoV-2 has physically destroyed the brainstem in every Long-COVID patient.<\/p>\n\n\n\n That distinction matters.<\/p>\n\n\n\n The more defensible interpretation is that infection may disrupt several interacting systems\u2014vascular, inflammatory, autonomic, metabolic and neural\u2014which can collectively disturb brainstem-mediated regulation.<\/p>\n\n\n\n The result can resemble a malfunctioning control system rather than a conventional focal brain lesion.<\/p>\n\n\n\n The vagus nerve represents one of the principal communication pathways between the brain and the internal organs.<\/p>\n\n\n\n It participates in regulation of:<\/p>\n\n\n\n Post-COVID neurological reviews have described abnormalities involving autonomic regulation and proposed dysfunction of vagal pathways among possible mechanisms.<\/p>\n\n\n\n If autonomic signaling becomes unreliable, the cardiovascular system may fail to make sufficiently rapid adjustments to posture or physiological stress.<\/p>\n\n\n\n That creates an important conceptual model:<\/p>\n\n\n\n Long COVID \u2192 autonomic dysregulation \u2192 impaired cardiovascular compensation \u2192 cerebral hypoperfusion \u2192 transient neurological dysfunction.<\/strong><\/p>\n\n\n\n It is a hypothesis supported by several converging lines of evidence, rather than a single proven mechanism.<\/p>\n\n\n\n Perhaps the most intriguing explanation lies not inside neurons themselves but at the interface between neurons and blood vessels.<\/p>\n\n\n\n The brain depends upon the neurovascular unit<\/strong>, consisting broadly of:<\/p>\n\n\n\n These structures communicate continuously to match local blood flow to neural activity.<\/p>\n\n\n\n Long-COVID research has implicated endothelial dysfunction, altered cerebral perfusion, blood-brain-barrier disturbance and inflammatory processes. Reviews of neurological Long COVID specifically identify vascular dysfunction and hypoperfusion as potentially important mechanisms.<\/p>\n\n\n\n This suggests a provocative possibility:<\/p>\n\n\n\n The Long-COVID blackout may sometimes be less a disease of neurons than a disease of the relationship between neurons and their blood supply.<\/strong><\/p>\n\n\n\n That distinction could eventually change treatment.<\/p>\n\n\n\n Another component is inflammation.<\/p>\n\n\n\n The brain contains resident immune cells called microglia<\/strong>. Under appropriate circumstances they protect neural tissue. When persistently activated, however, they can alter neuronal signaling and contribute to a state of chronic neuroinflammation.<\/p>\n\n\n\n PET studies in Long COVID have identified patterns consistent with altered brain metabolism and microglial activity. Hypometabolic abnormalities have been reported in regions including the olfactory system, thalamus, brainstem and cerebellum.<\/p>\n\n\n\n These findings are important because they suggest that a patient can have profound neurological dysfunction without having a conventional large stroke visible on routine MRI.<\/p>\n\n\n\n This is one of the most misunderstood aspects of Long COVID.<\/p>\n\n\n\n A routine MRI is excellent at identifying many structural abnormalities.<\/p>\n\n\n\n It is not a direct measurement of:<\/p>\n\n\n\n Recent reviews report structural abnormalities in some Long-COVID cohorts, including changes in gray matter and white matter, while functional imaging has demonstrated altered connectivity and metabolism.<\/p>\n\n\n\n A normal conventional MRI therefore cannot be interpreted as:<\/p>\n\n\n\n \u201cNothing is wrong with the brain.\u201d<\/strong><\/p>\n\n\n\n It means something considerably narrower:<\/p>\n\n\n\n \u201cNo detectable structural abnormality was identified by this examination.\u201d<\/strong><\/p>\n\n\n\n That is an important distinction.<\/p>\n\n\n\n The frontal lobes are essential for:<\/p>\n\n\n\n Long-COVID neuroimaging reviews have reported frontal and temporal gray-matter changes and abnormalities in white-matter pathways, with associations between some imaging findings and cognitive deficits.<\/p>\n\n\n\n A transient reduction in effective cerebral perfusion could therefore produce a particularly dangerous phenomenon:<\/p>\n\n\n\n The patient may remain physically awake but lose the cognitive capacity necessary to respond appropriately.<\/p>\n\n\n\n This may be experienced as:<\/p>\n\n\n\n \u201cI was conscious, but my brain disappeared.\u201d<\/strong><\/p>\n\n\n\n That is not necessarily syncope.<\/p>\n\n\n\n It may represent transient impairment of higher-order cortical processing.<\/p>\n\n\n\n The thalamus participates in:<\/p>\n\n\n\n Long-COVID PET studies have identified abnormalities involving the thalamus among other regions.<\/p>\n\n\n\n The thalamus is therefore particularly interesting when patients describe episodes of altered awareness.<\/p>\n\n\n\n The symptom may not be simply \u201cfainting.\u201d<\/p>\n\n\n\n It may be a temporary disruption of the enormous network through which the brain maintains conscious engagement with the environment.<\/p>\n\n\n\n Another characteristic of blackout stories is the missing interval.<\/p>\n\n\n\n A patient may say:<\/p>\n\n\n\n \u201cI remember driving down the road. Then suddenly I was three miles farther along.\u201d<\/p>\n<\/blockquote>\n\n\n\n This is profoundly different from ordinary forgetfulness.<\/p>\n\n\n\n The hippocampus is central to the formation of new episodic memories. Long-COVID research has reported abnormalities in regions involved in memory, including the hippocampal formation, although causality remains uncertain.<\/p>\n\n\n\n A memory gap, however, does not prove a hippocampal lesion.<\/p>\n\n\n\n It may result from:<\/p>\n\n\n\n This is why the word \u201cblackout\u201d must never be treated as a diagnosis.<\/strong><\/p>\n\n\n\n An episode of loss of awareness after COVID should not automatically be attributed to dysautonomia.<\/p>\n\n\n\n Seizures can produce:<\/p>\n\n\n\n Consequently, unexplained episodes may warrant neurological evaluation and, when clinically appropriate, EEG.<\/p>\n\n\n\n The distinction is particularly important because seizure-related impairment can occur without dramatic convulsions.<\/p>\n\n\n\n COVID has also been associated with cardiac complications and arrhythmias.<\/p>\n\n\n\n A published case illustrates the danger particularly well.<\/p>\n\n\n\n A 62-year-old man developed sudden loss of consciousness while driving and subsequently crashed his vehicle. Investigation identified asystole<\/strong>, a prolonged absence of effective cardiac electrical activity. The patient had not experienced warning symptoms such as chest pain, palpitations or lightheadedness before losing consciousness.<\/p>\n\n\n\n This case is not proof that Long COVID caused the accident.<\/p>\n\n\n\n Nor does it establish that every COVID-associated blackout is neurological.<\/p>\n\n\n\n It demonstrates something more fundamental:<\/p>\n\n\n\n Sudden loss of consciousness while driving is a medical emergency regardless of the presumed cause.<\/strong><\/p>\n\n\n\n A particularly illuminating firsthand account was published by UCSF.<\/p>\n\n\n\n Ali Zahir described his experience following COVID. While attempting to sleep after an overnight shift, he developed nausea, dizziness, confusion and a severe headache. He subsequently stumbled out of bed and fell to the ground. When he recovered sufficiently to look outside, he discovered a fire across the street.<\/p>\n\n\n\n This is not a laboratory experiment.<\/p>\n\n\n\n It is one person’s documented account.<\/p>\n\n\n\n Its value lies in demonstrating how neurological symptoms can become dangerous in ordinary life. Confusion, dizziness, impaired balance and altered awareness do not need to produce classic syncope to create a life-threatening situation.<\/p>\n\n\n\n The societal significance of Long-COVID blackouts is potentially much larger than the number of people who actually faint.<\/p>\n\n\n\n Imagine a patient whose symptoms consist of:<\/p>\n\n\n\n Now put that person behind the wheel of an automobile.<\/p>\n\n\n\n The difference between syncope<\/strong> and impaired awareness<\/strong> becomes almost academic.<\/p>\n\n\n\n A car traveling 55 mph covers approximately 80 feet every second.<\/p>\n\n\n\n A five-second episode therefore means approximately 400 feet traveled while the driver’s neurological performance may be severely compromised<\/strong>.<\/p>\n\n\n\n The same principle applies to:<\/p>\n\n\n\n The risk is not simply that the patient might fall.<\/p>\n\n\n\n It is that the patient may continue moving while the brain temporarily fails to perform.<\/p>\n\n\n\n Patients frequently lack the vocabulary to distinguish neurological states.<\/p>\n\n\n\n Consider five possibilities.<\/p>\n\n\n\n Temporary loss of consciousness caused by transient global cerebral hypoperfusion, usually followed by relatively rapid recovery.<\/p>\n\n\n\n The patient remains conscious but experiences:<\/p>\n\n\n\n Abnormal electrical activity produces impaired awareness or loss of consciousness.<\/p>\n\n\n\n The patient remains technically awake but temporarily loses effective attention, processing or memory.<\/p>\n\n\n\n The brain briefly enters sleep, sometimes for only seconds.<\/p>\n\n\n\n These conditions can feel remarkably similar to the person experiencing them.<\/p>\n\n\n\n The most clinically interesting patients may be those who never completely lose consciousness.<\/p>\n\n\n\n They describe:<\/p>\n\n\n\n \u201cI was there, but I wasn’t there.\u201d<\/p>\n<\/blockquote>\n\n\n\n This could represent transient cerebral hypoperfusion without complete syncope.<\/p>\n\n\n\n A person might continue walking.<\/p>\n\n\n\n Continue driving.<\/p>\n\n\n\n Continue speaking.<\/p>\n\n\n\n Yet subsequently have no memory of several seconds.<\/p>\n\n\n\n This phenomenon deserves systematic study because conventional definitions of syncope may exclude precisely the patients who are experiencing clinically meaningful cerebral dysfunction.<\/p>\n\n\n\n Carbon dioxide is another underappreciated regulator of cerebral circulation.<\/p>\n\n\n\n Hyperventilation lowers arterial CO\u2082.<\/p>\n\n\n\n Lower CO\u2082 causes cerebral vasoconstriction.<\/p>\n\n\n\n Consequently:<\/p>\n\n\n\n hyperventilation \u2192 hypocapnia \u2192 cerebral vasoconstriction \u2192 reduced cerebral blood flow.<\/strong><\/p>\n\n\n\n Some Long-COVID autonomic studies have identified abnormal breathing patterns and hypocapnia during orthostatic testing. One deep-phenotyping study reported abnormal cerebral blood flow alongside autonomic abnormalities.<\/p>\n\n\n\n This creates another possible pathway toward lightheadedness and cognitive dysfunction.<\/p>\n\n\n\n The brain may therefore be receiving less blood because of a combination of:<\/p>\n\n\n\n There is yet another layer.<\/p>\n\n\n\n Neurons require enormous quantities of ATP.<\/p>\n\n\n\n If mitochondrial function is impaired, the neuron may be able to survive but operate inefficiently.<\/p>\n\n\n\n This provides a possible explanation for the paradox of Long COVID:<\/p>\n\n\n\n The brain can appear structurally intact while functioning abnormally.<\/strong><\/p>\n\n\n\n Neuroimaging studies showing altered metabolism provide support for the possibility of persistent cerebral metabolic dysfunction in at least some patients.<\/p>\n\n\n\n The blackout, in this model, would not necessarily represent destruction of brain tissue.<\/p>\n\n\n\n It could represent a temporary failure to meet energetic demand.<\/p>\n\n\n\n Taken together, these observations suggest a broader model.<\/p>\n\n\n\n Rather than viewing Long COVID as a collection of unrelated symptoms, one can conceptualize some neurological phenotypes as a failure of a tightly coupled system:<\/p>\n\n\n\n autonomic nervous system An abnormality anywhere along this chain can theoretically destabilize the system.<\/p>\n\n\n\n An abnormality at several points simultaneously could make the patient dramatically more vulnerable.<\/p>\n\n\n\n The scientific literature does not<\/strong> currently establish that Long COVID routinely causes sudden blackouts.<\/p>\n\n\n\n That claim would go beyond the evidence.<\/p>\n\n\n\n Instead, the evidence establishes several facts:<\/p>\n\n\n\n The unanswered question is how frequently these mechanisms actually produce true syncope or transient loss of consciousness<\/strong> in the Long-COVID population.<\/p>\n\n\n\n That question deserves prospective study.<\/p>\n\n\n\n A serious investigation should not rely solely upon questionnaires.<\/p>\n\n\n\n Patients reporting blackouts should ideally undergo a structured protocol incorporating, where clinically appropriate:<\/p>\n\n\n\n This is especially important because hypoglycemia, anemia, arrhythmia, dehydration, medication effects and metabolic disturbances can mimic Long-COVID neurological phenomena.<\/p>\n\n\n\n A person with diabetes can experience:<\/p>\n\n\n\n Thus a glucose measurement during or immediately after an episode can be extraordinarily informative.<\/p>\n\n\n\n A \u201cLong-COVID blackout\u201d should never be diagnosed without considering ordinary but potentially dangerous causes of transient loss of consciousness.<\/p>\n\n\n\n The most fascinating question is not simply:<\/p>\n\n\n\n Does Long COVID cause blackouts?<\/strong><\/p>\n\n\n\n It is:<\/p>\n\n\n\n Why does SARS-CoV-2 appear capable of disturbing the machinery by which the brain maintains consciousness and cerebral perfusion in some individuals months or years after the initial infection?<\/strong><\/p>\n\n\n\n Several hypotheses converge:<\/p>\n\n\n\n persistent antigen or viral remnants<\/strong><\/p>\n\n\n\n \u2193<\/p>\n\n\n\n immune dysregulation<\/strong><\/p>\n\n\n\n \u2193<\/p>\n\n\n\n endothelial and microvascular dysfunction<\/strong><\/p>\n\n\n\n \u2193<\/p>\n\n\n\n autonomic dysfunction<\/strong><\/p>\n\n\n\n \u2193<\/p>\n\n\n\n abnormal cerebral perfusion<\/strong><\/p>\n\n\n\n \u2193<\/p>\n\n\n\n neuroinflammation and altered metabolism<\/strong><\/p>\n\n\n\n \u2193<\/p>\n\n\n\n impaired neural network function<\/strong><\/p>\n\n\n\n \u2193<\/p>\n\n\n\n cognitive dysfunction \/ presyncope \/ altered awareness<\/strong><\/p>\n\n\n\n The hypothesis remains incomplete.<\/p>\n\n\n\n But it is increasingly biologically coherent.<\/p>\n\n\n\n Perhaps the most important conclusion is also the simplest.<\/p>\n\n\n\n When a patient says:<\/p>\n\n\n\n \u201cSometimes my brain just shuts off.\u201d<\/strong><\/p>\n<\/blockquote>\n\n\n\n the correct response is not automatically:<\/p>\n\n\n\n \u201cYour MRI is normal.\u201d<\/p>\n<\/blockquote>\n\n\n\n Nor is it:<\/p>\n\n\n\n \u201cThat’s anxiety.\u201d<\/p>\n<\/blockquote>\n\n\n\n The correct response is:<\/p>\n\n\n\n \u201cLet’s determine exactly what happens when your consciousness disappears.\u201d<\/strong><\/p>\n\n\n\n Modern medicine possesses the technology to begin answering that question.<\/p>\n\n\n\n Tilt-table testing can interrogate autonomic physiology.<\/p>\n\n\n\n Continuous ECG can reveal arrhythmia.<\/p>\n\n\n\n EEG can investigate seizures.<\/p>\n\n\n\n Transcranial Doppler can measure cerebral blood-flow responses.<\/p>\n\n\n\n MRI can examine structure.<\/p>\n\n\n\n PET can examine metabolism.<\/p>\n\n\n\n Neuropsychological testing can quantify cognitive dysfunction.<\/p>\n\n\n\n Together, these technologies could turn the patient’s vague description of a \u201cblackout\u201d into a measurable physiological event.<\/p>\n\n\n\n Long COVID has forced neurology to confront an uncomfortable possibility: a brain can be profoundly dysfunctional without necessarily being grossly structurally destroyed.<\/strong><\/p>\n\n\n\n The emerging evidence points toward a complex interaction among the autonomic nervous system, cerebral circulation, neurovascular coupling, inflammation, brain metabolism and neural networks. Cerebral hypoperfusion during orthostatic stress has been documented in Long-COVID cohorts; autonomic abnormalities are well described; and neuroimaging studies have demonstrated alterations in brain structure, connectivity and metabolism.<\/p>\n\n\n\n For some patients, the clinical manifestation may be little more than dizziness.<\/p>\n\n\n\n For others, it may be cognitive failure.<\/p>\n\n\n\n For a smaller but critically important group, it may be an episode of transient loss of awareness or consciousness.<\/p>\n\n\n\n And for the patient who experiences such an event while driving, operating machinery, bathing alone, climbing stairs or walking near traffic, a neurological symptom can suddenly become an accident.<\/strong><\/p>\n\n\n\n The darkness itself is therefore not the diagnosis.<\/p>\n\n\n\n It is the final visible moment of a physiological cascade whose origins may lie in the heart, autonomic nervous system, cerebral circulation, brainstem, neurovascular unit, immune system, neuronal metabolism\u2014or several of these systems simultaneously.<\/p>\n\n\n\n The scientific challenge now is to determine which pathway is failing in which patient.<\/p>\n\n\n\n And the clinical imperative is more immediate:<\/p>\n\n\n\n A person reporting an unexplained blackout should be investigated for its cause rather than having the episode simply attributed to Long COVID.<\/strong><\/p>\n\n\n\n John Murphy, CEO The COVID-19 Long haul Foundation Abstract Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), has increasingly revealed itself as a disorder extending well beyond pulmonary injury. 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\n\n\n\nThe Patient’s Description: \u201cEverything Went Black\u201d<\/h5>\n\n\n\n
\n\n\n\n1. The Cerebral Circulation: The Most Important Piece of the Puzzle<\/h5>\n\n\n\n
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\n\n\n\n2. POTS and the Long-COVID Brain<\/h5>\n\n\n\n
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\n\n\n\n3. The Brainstem: The Possible Autonomic Command Center<\/h5>\n\n\n\n
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\n\n\n\n4. The Vagus Nerve and the Autonomic Highway<\/h5>\n\n\n\n
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\n\n\n\n5. The Neurovascular Unit<\/h5>\n\n\n\n
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\n\n\n\n6. Neuroinflammation and Microglial Activation<\/h5>\n\n\n\n
\n\n\n\n7. MRI Can Be \u201cNormal\u201d While the Brain Is Not<\/h5>\n\n\n\n
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\n\n\n\n8. The Frontal Lobes and Executive Failure<\/h5>\n\n\n\n
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\n\n\n\n9. The Thalamus: The Brain’s Relay Station<\/h5>\n\n\n\n
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\n\n\n\n10. The Hippocampus and Memory Gaps<\/h5>\n\n\n\n
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\n\n\n\n11. Seizure Must Be Considered<\/h5>\n\n\n\n
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\n\n\n\n12. Cardiac Blackouts Are Equally Dangerous<\/h5>\n\n\n\n
\n\n\n\n13. A True Patient Story: The Fire Outside the Window<\/h5>\n\n\n\n
\n\n\n\n14. The Accident Problem<\/h5>\n\n\n\n
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\n\n\n\n15. Why Patients May Call It a \u201cBlackout\u201d<\/h5>\n\n\n\n
Syncope<\/h5>\n\n\n\n
Presyncope<\/h5>\n\n\n\n
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Seizure<\/h5>\n\n\n\n
Cognitive blackout<\/h5>\n\n\n\n
Microsleep<\/h5>\n\n\n\n
\n\n\n\n16. The \u201cGray Zone\u201d May Be the Most Important<\/h5>\n\n\n\n
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\n\n\n\n17. Carbon Dioxide and Cerebral Blood Flow<\/h5>\n\n\n\n
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\n\n\n\n18. The Mitochondrial Dimension<\/h5>\n\n\n\n
\n\n\n\n19. The Emerging Concept: A Neurovascular-Autonomic Syndrome<\/h5>\n\n\n\n
\u2193
cardiovascular regulation
\u2193
cerebral autoregulation
\u2193
neurovascular coupling
\u2193
cerebral blood flow
\u2193
neuronal metabolism
\u2193
consciousness and cognition<\/strong><\/p>\n\n\n\n
\n\n\n\n20. Why the Evidence Must Still Be Interpreted Carefully<\/h5>\n\n\n\n
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\n\n\n\n21. What a Definitive Long-COVID Blackout Study Should Measure<\/h5>\n\n\n\n
Cardiovascular<\/h3>\n\n\n\n
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Autonomic<\/h5>\n\n\n\n
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Cerebrovascular<\/h5>\n\n\n\n
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Neurological<\/h5>\n\n\n\n
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Metabolic<\/h5>\n\n\n\n
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\n\n\n\n22. A Particularly Important Differential Diagnosis: Hypoglycemia<\/h5>\n\n\n\n
\n
\n\n\n\n23. The Central Mystery<\/h5>\n\n\n\n
\n\n\n\n24. The Patient Is Not Imagining the Darkness<\/h5>\n\n\n\n
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\n
\n
\n\n\n\nConclusion<\/h5>\n\n\n\n
\n\n\n\nSelected scientific sources<\/h3>\n\n\n\n
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