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Tsunamis hiding in plain sight: spreading depression in clinical neurology
Friday March 13^th, 2026 at 4:07 PM

Nature Reviews Neurology

Leão, A. A. P. Spreading depression of activity in cerebral cortex. J. Neurophysiol. 7, 359–390 (1944).

Thomsen, A. V., Sorensen, M. T., Ashina, M. & Hougaard, A. Symptomatic migraine: a systematic review to establish a clinically important diagnostic entity. Headache 61, 1180–1193 (2021).

Article PubMed Google Scholar

Major, S. et al. Direct electrophysiological evidence that spreading depolarization-induced spreading depression is the pathophysiological correlate of the migraine aura and a review of the spreading depolarization continuum of acute neuronal mass injury. Geroscience 42, 57–80 (2020).

Article PubMed Google Scholar

Rogawski, M. A. in Jasper’s Basic Mechanisms of the Epilepsies (eds Noebels, J. L. et al.) 930–944 (Oxford Univ. Press, 2012).

Rogawski, M. A. Common pathophysiologic mechanisms in migraine and epilepsy. Arch. Neurol. 65, 709–714 (2008).

PubMed Google Scholar

Ferrari, M. D. et al. Migraine. Nat. Rev. Dis. Prim. 8, 2 (2022).

Article PubMed Google Scholar

Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia 38, 1–211 (2018).

Dreier, J. P. The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease. Nat. Med. 17, 439–447 (2011).

Article CAS PubMed Google Scholar

Ayata, C. & Lauritzen, M. Spreading depression, spreading depolarizations, and the cerebral vasculature. Physiol. Rev. 95, 953–993 (2015).

Article CAS PubMed PubMed Central Google Scholar

Pietrobon, D. & Moskowitz, M. A. Pathophysiology of migraine. Annu. Rev. Physiol. 75, 365–391 (2012).

Article PubMed Google Scholar

Hartings, J. A. et al. The continuum of spreading depolarizations in acute cortical lesion development: examining Leão’s legacy. J. Cereb. Blood Flow Metab. 37, 1571–1594 (2017).

Article PubMed Google Scholar

Hansen, A. J. & Zeuthen, T. Extracellular ion concentrations during spreading depression and ischemia in the rat brain cortex. Acta Physiol. Scand. 113, 437–445 (1981).

Article CAS PubMed Google Scholar

Ziburkus, J., Cressman, J. R., Barreto, E. & Schiff, S. J. Interneuron and pyramidal cell interplay during in vitro seizure-like events. J. Neurophysiol. 95, 3948–3954 (2006).

Article PubMed PubMed Central Google Scholar

Wei, Y., Ullah, G. & Schiff, S. J. Unification of neuronal spikes, seizures, and spreading depression. J. Neurosci. 34, 11733–11743 (2014).

Article CAS PubMed PubMed Central Google Scholar

Somjen, G. G. Mechanisms of spreading depression and hypoxic spreading depression-like depolarization. Physiol. Rev. 81, 1065–1096 (2001).

Article CAS PubMed Google Scholar

Kager, H., Wadman, W. J. & Somjen, G. G. Conditions for the triggering of spreading depression studied with computer simulations. J. Neurophysiol. 88, 2700–2712 (2002).

Article CAS PubMed Google Scholar

Whalen, A. J. et al. Control of spreading depression with electrical fields. Sci. Rep. 8, 8769 (2018).

Article PubMed PubMed Central Google Scholar

Bailey, P. & von Bonin, G. The Isocortex of Man Vol. 1–2 (Univ. Illinois Press, 1951).

Eikermann-Haerter, K. et al. Enhanced subcortical spreading depression in familial hemiplegic migraine type 1 mutant mice. J. Neurosci. 31, 5755–5763 (2011).

Article CAS PubMed PubMed Central Google Scholar

Eikermann-Haerter, K. et al. Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1. J. Clin. Invest. 119, 99–109 (2009).

CAS PubMed Google Scholar

Santos, E. et al. Radial, spiral and reverberating waves of spreading depolarization occur in the gyrencephalic brain. NeuroImage 99, 244–255 (2014).

Article PubMed Google Scholar

Lindquist, B. E. & Shuttleworth, C. W. Adenosine receptor activation is responsible for prolonged depression of synaptic transmission after spreading depolarization in brain slices. Neuroscience 223, 365–376 (2012).

Article CAS PubMed PubMed Central Google Scholar

Sawant-Pokam, P. M., Suryavanshi, P., Mendez, J. M., Dudek, F. E. & Brennan, K. C. Mechanisms of neuronal silencing after cortical spreading depression. Cereb. Cortex 27, 1311–1325 (2017).

CAS PubMed PubMed Central Google Scholar

Eikermann-Haerter, K. et al. Abnormal synaptic Ca²⁺ homeostasis and morphology in cortical neurons of familial hemiplegic migraine type 1 mutant mice. Ann. Neurol. 78, 193–210 (2015).

Article CAS PubMed PubMed Central Google Scholar

Dreier, J. P. et al. Spreading depolarizations in ischaemia after subarachnoid haemorrhage, a diagnostic phase III study. Brain 145, 1264–1284 (2022).

Article PubMed Google Scholar

Dohmen, C. et al. Spreading depolarizations occur in human ischemic stroke with high incidence. Ann. Neurol. 63, 720–728 (2008).

Article PubMed Google Scholar

Carlson, A. P. et al. Cortical spreading depression occurs during elective neurosurgical procedures. J. Neurosurg. 126, 266–273 (2017).

Article PubMed Google Scholar

Fabricius, M. et al. Association of seizures with cortical spreading depression and peri-infarct depolarisations in the acutely injured human brain. Clin. Neurophysiol. 119, 1973–1984 (2008).

Article PubMed PubMed Central Google Scholar

Dreier, J. P. et al. Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex. Brain 135, 259–275 (2012).

Article PubMed Google Scholar

Corby, J. C., Roth, W. T. & Kopell, B. S. Prevalence and methods of control of the cephalic skin potential EEG artifact. Psychophysiology 11, 350–360 (1974).

Article CAS PubMed Google Scholar

Chamanzar, A., Elmer, J., Shutter, L., Hartings, J. & Grover, P. Noninvasive and reliable automated detection of spreading depolarization in severe traumatic brain injury using scalp EEG. Commun. Med. 3, 113 (2023).

Article PubMed PubMed Central Google Scholar

Bastany, Z. J. R., Askari, S., Gorji, A. & Dumont, G. A. Detection of spreading depression features from the scalp of epileptic patients. In Annual International Conference of the IEEE Engineering, Medicine and Biology Society 2023, 1–4 (IEEE, 2023).

Robinson, D., Hartings, J. & Foreman, B. First report of spreading depolarization correlates on scalp EEG confirmed with a depth electrode. Neurocrit. Care 35, 100–104 (2021).

Article PubMed Google Scholar

Hartings, J. A. et al. Spreading depression in continuous electroencephalography of brain trauma. Ann. Neurol. 76, 681–694 (2014).

Article PubMed Google Scholar

Meinert, F. et al. Less-invasive subdural electrocorticography for investigation of spreading depolarizations in patients with subarachnoid hemorrhage. Front. Neurol. 13, 1091987 (2022).

Article PubMed Google Scholar

Bastany, Z. J. R. et al. Association of cortical spreading depression and seizures in patients with medically intractable epilepsy. Clin. Neurophysiol. 131, 2861–2874 (2020).

Article PubMed Google Scholar

Mitlasoczki, B. et al. Hippocampal spreading depolarization as a driver of postictal ambulation. Sci. Transl. Med. 17, eadv3260 (2025).

Article CAS PubMed Google Scholar

Dreier, J. P. et al. Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: review and recommendations of the COSBID Research Group. J. Cereb. Blood Flow Metab. 37, 1595–1625 (2017).

Article PubMed Google Scholar

James, M. F. et al. Cortical spreading depression in the gyrencephalic feline brain studied by magnetic resonance imaging. J. Physiol. 519, 415–425 (1999).

Article CAS PubMed PubMed Central Google Scholar

Hadjikhani, N. et al. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc. Natl Acad. Sci. USA 98, 4687–4692 (2001).

Article CAS PubMed PubMed Central Google Scholar

Kimberly, W. T. et al. Brain imaging with portable low-field MRI. Nat. Rev. Bioeng. 1, 617–630 (2023).

Article CAS PubMed PubMed Central Google Scholar

Viana, M., Tronvik, E. A., Do, T. P., Zecca, C. & Hougaard, A. Clinical features of visual migraine aura: a systematic review. J. Headache Pain 20, 64 (2019).

Article PubMed PubMed Central Google Scholar

Viana, M. et al. Visual migraine aura iconography: a multicentre, cross-sectional study of individuals with migraine with aura. Cephalalgia 44, 3331024241234809 (2024).

Article PubMed Google Scholar

Lashley, K. S. Patterns of cerebral integration indicated by the scotomas of migraine. Arch. Neurol. Psychiatry 46, 331–339 (1941).

Article Google Scholar

Russell, M. B. & Olesen, J. A nosographic analysis of the migraine aura in a general population. Brain 119, 355–361 (1996).

Article PubMed Google Scholar

Woitzik, J. et al. Propagation of cortical spreading depolarization in the human cortex after malignant stroke. Neurology 80, 1095–1102 (2013).

Article PubMed Google Scholar

van den Maagdenberg, A. M. et al. A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression. Neuron 41, 701–710 (2004).

Article PubMed Google Scholar

Zhang, X. et al. Activation of central trigeminovascular neurons by cortical spreading depression. Ann. Neurol. 69, 855–865 (2011).

Article PubMed PubMed Central Google Scholar

Zhang, X. et al. Activation of meningeal nociceptors by cortical spreading depression: implications for migraine with aura. J. Neurosci. 30, 8807–8814 (2010).

Article CAS PubMed PubMed Central Google Scholar

Harriott, A. M. et al. Optogenetic spreading depression elicits trigeminal pain and anxiety behavior. Ann. Neurol. 89, 99–110 (2021).

Article PubMed Google Scholar

Harriott, A. M. et al. The effect of sex and estrus cycle stage on optogenetic spreading depression induced migraine-like pain phenotypes. J. Headache Pain 24, 85 (2023).

Article CAS PubMed PubMed Central Google Scholar

Morais, A., Qin, T., Ayata, C. & Harriott, A. M. Inhibition of persistent sodium current reduces spreading depression-evoked allodynia in a mouse model of migraine with aura. Pain 164, 2564–2571 (2023).

Article CAS PubMed Google Scholar

Drenckhahn, C. et al. Correlates of spreading depolarization in human scalp electroencephalography. Brain 135, 853–868 (2012).

Article PubMed PubMed Central Google Scholar

Hertle, D. N. et al. Effect of analgesics and sedatives on the occurrence of spreading depolarizations accompanying acute brain injury. Brain 135, 2390–2398 (2012).

Article PubMed Google Scholar

Nozari, A. et al. Microemboli may link spreading depression, migraine aura, and patent foramen ovale. Ann. Neurol. 67, 221–229 (2010).

Article PubMed PubMed Central Google Scholar

Zandt, B. J., ten Haken, B., van Dijk, J. G. & van Putten, M. J. Neural dynamics during anoxia and the “wave of death”. PLoS ONE 6, e22127 (2011).

Article CAS PubMed PubMed Central Google Scholar

Dreier, J. P. et al. Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations. Brain 129, 3224–3237 (2006).

Article PubMed Google Scholar

Fabricius, M. et al. Cortical spreading depression and peri-infarct depolarization in acutely injured human cerebral cortex. Brain 129, 778–790 (2006).

Article PubMed Google Scholar

Eriksen, N. et al. Early focal brain injury after subarachnoid hemorrhage correlates with spreading depolarizations. Neurology 92, e326–e341 (2019).

Article PubMed Google Scholar

Dreier, J. P. et al. Cortical spreading ischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoid haemorrhage. Brain 132, 1866–1881 (2009).

Article PubMed PubMed Central Google Scholar

Bosche, B. et al. Recurrent spreading depolarizations after subarachnoid hemorrhage decreases oxygen availability in human cerebral cortex. Ann. Neurol. 67, 607–617 (2010).

Article PubMed PubMed Central Google Scholar

Leng, L. Z., Fink, M. E. & Iadecola, C. Spreading depolarization: a possible new culprit in the delayed cerebral ischemia of subarachnoid hemorrhage. Arch. Neurol. 68, 31–36 (2011).

Article PubMed Google Scholar

Dreier, J. P. et al. Migrainous aura starting several minutes after the onset of subarachnoid hemorrhage. Neurology 57, 1344–1345 (2001).

Article CAS PubMed Google Scholar

Hartings, J. A. et al. Prognostic value of spreading depolarizations in patients with severe traumatic brain injury. JAMA Neurol. 77, 489–499 (2020).

Article PubMed PubMed Central Google Scholar

Strong, A. J. et al. Spreading and synchronous depressions of cortical activity in acutely injured human brain. Stroke 33, 2738–2743 (2002).

Article PubMed Google Scholar

Bouley, J., Chung, D. Y., Ayata, C., Brown, R. H. Jr. & Henninger, N. Cortical spreading depression denotes concussion injury. J. Neurotrauma 36, 1008–1017 (2019).

Article PubMed Google Scholar

Kors, E. E. et al. Delayed cerebral edema and fatal coma after minor head trauma: role of the CACNA1A calcium channel subunit gene and relationship with familial hemiplegic migraine. Ann. Neurol. 49, 753–760 (2001).

Article CAS PubMed Google Scholar

Xiang, Y. et al. Two pediatric patients with hemiplegic migraine presenting as acute encephalopathy: case reports and a literature review. Front. Pediatr. 11, 1214837 (2023).

Article PubMed PubMed Central Google Scholar

Helbok, R. et al. Spreading depolarizations in patients with spontaneous intracerebral hemorrhage: association with perihematomal edema progression. J. Cereb. Blood Flow Metab. 37, 1871–1882 (2017).

Article PubMed Google Scholar

Mohammad, L. M. et al. Spreading depolarization may represent a novel mechanism for delayed fluctuating neurological deficit after chronic subdural hematoma evacuation. J. Neurosurg. 134, 1294–1302 (2020).

Article PubMed Google Scholar

Meadows, C. et al. Spreading depolarization after chronic subdural hematoma evacuation: associated clinical risk factors and influence on clinical outcome. Neurocrit. Care 35, 105–111 (2021).

Article PubMed PubMed Central Google Scholar

Cain, S. M. et al. Hyperexcitable superior colliculus and fatal brainstem spreading depolarization in a model of sudden unexpected death in epilepsy. Brain Commun. 4, fcac006 (2022).

Article PubMed PubMed Central Google Scholar

Suryavanshi, P., Sawant-Pokam, P., Clair, S. & Brennan, K. C. Increased presynaptic excitability in a migraine with aura mutation. Brain 147, 680–697 (2024).

Article PubMed PubMed Central Google Scholar

Lemaire, L., Desroches, M., Krupa, M. & Mantegazza, M. Idealized multiple-timescale model of cortical spreading depolarization initiation and pre-epileptic hyperexcitability caused by Na_V1.1/SCN1A mutations. J. Math. Biol. 86, 92 (2023).

Article PubMed Google Scholar

Zerimech, S. et al. Cholinergic modulation inhibits cortical spreading depression in mouse neocortex through activation of muscarinic receptors and decreased excitatory/inhibitory drive. Neuropharmacology 166, 107951 (2020).

Article CAS PubMed Google Scholar

Hunanyan, A. S. et al. Knock-in mouse model of alternating hemiplegia of childhood: behavioral and electrophysiologic characterization. Epilepsia 56, 82–93 (2015).

Article CAS PubMed Google Scholar

Hatcher, A. et al. Pathogenesis of peritumoral hyperexcitability in an immunocompetent CRISPR-based glioblastoma model. J. Clin. Invest. 130, 2286–2300 (2020).

Article CAS PubMed PubMed Central Google Scholar

Eickhoff, M. et al. Spreading depression triggers ictaform activity in partially disinhibited neuronal tissues. Exp. Neurol. 253, 1–15 (2014).

Article PubMed Google Scholar

Lippmann, K. et al. Epileptiform activity and spreading depolarization in the blood-brain barrier-disrupted peri-infarct hippocampus are associated with impaired GABAergic inhibition and synaptic plasticity. J. Cereb. Blood Flow Metab. 37, 1803–1819 (2017).

Article CAS PubMed Google Scholar

Auffenberg, E. et al. Hyperexcitable interneurons trigger cortical spreading depression in an Scn1a migraine model. J. Clin. Invest. 131, e142202 (2021).

Article CAS PubMed PubMed Central Google Scholar

Kohling, R. et al. Differential sensitivity to induction of spreading depression by partial disinhibition in chronically epileptic human and rat as compared to native rat neocortical tissue. Brain Res. 975, 129–134 (2003).

Article CAS PubMed Google Scholar

Aiba, I. & Noebels, J. L. Spreading depolarization in the brainstem mediates sudden cardiorespiratory arrest in mouse SUDEP models. Sci. Transl. Med. 7, 282ra246 (2015).

Article Google Scholar

Loonen, I. C. M. et al. Spontaneous and optogenetically induced cortical spreading depolarization in familial hemiplegic migraine type 1 mutant mice. Neurobiol. Dis. 192, 106405 (2024).

Article CAS PubMed Google Scholar

Aiba, I., Ning, Y. & Noebels, J. L. A hyperthermic seizure unleashes a surge of spreading depolarizations in Scn1a-deficient mice. JCI Insight 8, e170399 (2023).

Article PubMed PubMed Central Google Scholar

Aiba, I. & Noebels, J. L. Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization. Brain 144, 2863–2878 (2021).

Article PubMed PubMed Central Google Scholar

Tamim, I. et al. Spreading depression as an innate antiseizure mechanism. Nat. Commun. 12, 2206 (2021).

Article CAS PubMed PubMed Central Google Scholar

Bahari, F. et al. Seizure-associated spreading depression is a major feature of ictal events in two animal models of chronic epilepsy. Preprint at bioRxiv https://doi.org/10.1101/455519 (2020).

Norby, J. H. et al. Rodent and human seizures demonstrate a dynamic interplay with spreading depolarizations. Neurobiol. Dis. 211, 106937 (2025).

Article CAS PubMed PubMed Central Google Scholar

Aiba, I. in Jasper’s Basic Mechanisms of the Epilepsies (eds Noebels, J. L. et al.) 1285–1320 (Oxford Univ. Press, 2024).

Aiba, I. & Noebels, J. L. Spreading depolarization and seizures: end of the beginning, or beginning of the end? Epilepsy Curr. 25, 335–340 (2025).

Article PubMed PubMed Central Google Scholar

Ullah, G., Wei, Y., Dahlem, M. A., Wechselberger, M. & Schiff, S. J. The role of cell volume in the dynamics of seizure, spreading depression, and anoxic depolarization. PLoS Comput. Biol. 11, e1004414 (2015).

Article PubMed PubMed Central Google Scholar

Aiba, I., Ning, Y. & Noebels, J. L. Persistent Na⁺ current couples spreading depolarization to seizures in Scn8a gain-of-function mice. Brain 148, 3325–3339 (2025).

Article PubMed PubMed Central Google Scholar

Foreman, B. et al. The relationship between seizures and spreading depolarizations in patients with severe traumatic brain injury. Neurocrit. Care 37, 31–48 (2022).

Article PubMed Google Scholar

Vinogradova, L. V. Initiation of spreading depression by synaptic and network hyperactivity: insights into trigger mechanisms of migraine aura. Cephalalgia 38, 1177–1187 (2018).

Article PubMed Google Scholar

Noebels, J. L. in Jasper’s Basic Mechanisms of the Epilepsies (eds Noebels, J. L. et al.) 1321–1346 (Oxford Univ. Press, 2024).

Loonen, I. C. M. et al. Brainstem spreading depolarization and cortical dynamics during fatal seizures in Cacna1a S218L mice. Brain 142, 412–425 (2019).

Article PubMed PubMed Central Google Scholar

Jansen, N. A. et al. Apnea associated with brainstem seizures in Cacna1a(S218L) mice is caused by medullary spreading depolarization. J. Neurosci. 39, 9633–9644 (2019).

Article CAS PubMed PubMed Central Google Scholar

Noebels, J. L. Brainstem spreading depolarization: rapid descent into the shadow of SUDEP. Brain 142, 231–233 (2019).

Article PubMed PubMed Central Google Scholar

Colpitts, K., Desai, M. J., Kogan, M., Shuttleworth, C. W. & Carlson, A. P. Brain tsunamis in human high-grade glioma: preliminary observations. Brain Sci. 12, 710 (2022).

Article CAS PubMed PubMed Central Google Scholar

Fisher, C. M. Transient paralytic attacks of obscure nature: the question of non-convulsive seizure paralysis. Can. J. Neurol. Sci. 5, 267–273 (1978).

Article CAS PubMed Google Scholar

IJzerman-Korevaar, M., Snijders, T. J., de Graeff, A., Teunissen, S. C. C. M. & de Vos, F. Y. F. Prevalence of symptoms in glioma patients throughout the disease trajectory: a systematic review. J. Neurooncol. 140, 485–496 (2018).

Article PubMed PubMed Central Google Scholar

Olesen, J. et al. Timing and topography of cerebral blood flow, aura, and headache during migraine attacks. Ann. Neurol. 28, 791–798 (1990).

Article CAS PubMed Google Scholar

Olesen, J., Larsen, B. & Lauritzen, M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann. Neurol. 9, 344–352 (1981).

Article CAS PubMed Google Scholar

Lauritzen, M., Skyhoj Olsen, T., Lassen, N. A. & Paulson, O. B. Changes in regional cerebral blood flow during the course of classic migraine attacks. Ann. Neurol. 13, 633–641 (1983).

Article CAS PubMed Google Scholar

McLeod, G. A., Josephson, C. B., Engbers, J. D. T., Cooke, L. J. & Wiebe, S. Mapping the migraine: intracranial recording of cortical spreading depression in migraine with aura. Headache 65, 658–665 (2025).

Article PubMed Google Scholar

Tfelt-Hansen, P. C. History of migraine with aura and cortical spreading depression from 1941 and onwards. Cephalalgia 30, 780–792 (2010).

Article CAS PubMed Google Scholar

Ashina, M. et al. Migraine and the trigeminovascular system-40 years and counting. Lancet Neurol. 18, 795–804 (2019).

Article PubMed PubMed Central Google Scholar

Olesen, J. et al. Ischaemia-induced (symptomatic) migraine attacks may be more frequent than migraine-induced ischaemic insults. Brain 116 (Pt 1), 187–202 (1993).

Article PubMed Google Scholar

Silverman, I. E. & Wityk, R. J. Transient migraine-like symptoms with internal carotid artery dissection. Clin. Neurol. Neurosurg. 100, 116–120 (1998).

Article CAS PubMed Google Scholar

Klingebiel, R., Friedman, A., Shelef, I. & Dreier, J. P. Clearance of a status aurae migraenalis in response to thrombendarterectomy in a patient with high grade internal carotid artery stenosis. J. Neurol. Neurosurg. Psychiatry 79, 89–90 (2008).

Article CAS PubMed Google Scholar

Morelli, N. et al. Vertebral artery dissection onset mimics migraine with aura in a graphic designer. Headache 48, 621–624 (2008).

Article PubMed Google Scholar

Shin, D. H. et al. Posterior circulation embolism as a potential mechanism for migraine with aura. Cephalalgia 32, 497–499 (2012).

Article PubMed Google Scholar

Park-Matsumoto, Y. C., Tazawa, T. & Shimizu, J. Migraine with aura-like headache associated with Moyamoya disease. Acta Neurol. Scand. 100, 119–121 (1999).

Article CAS PubMed Google Scholar

Kung, S. L., Shen, C. Y. & Ling, T. T. Migraine-like visual aura rriggered by a large aneurysm in the left extracranial internal carotid artery with successful prevention of recurrence by the new anticoagulant dabigatran: first case report. Acta Neurol. Taiwan. 24, 19–24 (2015).

PubMed Google Scholar

Terrin, A., Mainardi, F. & Maggioni, F. The pathological spectrum behind migraine aura status: a case series. Neurol. Sci. 40, 861–864 (2019).

Article PubMed Google Scholar

Rist, P. M., Diener, H. C., Kurth, T. & Schurks, M. Migraine, migraine aura, and cervical artery dissection: a systematic review and meta-analysis. Cephalalgia 31, 886–896 (2011).

Article PubMed PubMed Central Google Scholar

Schwedt, T. J., Demaerschalk, B. M. & Dodick, D. W. Patent foramen ovale and migraine: a quantitative systematic review. Cephalalgia 28, 531–540 (2008).

Article CAS PubMed Google Scholar

Martinez-Sanchez, P. et al. Migraine and hypercoagulable states in ischemic stroke. Cephalalgia 31, 1609–1617 (2011).

Article CAS PubMed Google Scholar

Tietjen, G. E. Migraine as a systemic vasculopathy. Cephalalgia 29, 987–996 (2009).

Article CAS PubMed Google Scholar

Turk, W. E. et al. Aspirin prophylaxis for migraine with aura: an observational case series. Eur. Neurol. 78, 287–289 (2017).

Article PubMed Google Scholar

Mawet, J., Kurth, T. & Ayata, C. Migraine and stroke: in search of shared mechanisms. Cephalalgia 35, 165–181 (2015).

Article PubMed Google Scholar

Chapman, K. M. et al. Pseudomigraine with lymphocytic pleocytosis: a calcium channelopathy? Clinical description of 10 cases and genetic analysis of the familial hemiplegic migraine gene CACNA1A. Headache 43, 892–895 (2003).

Article PubMed Google Scholar

Rogan, M. P., Walsh, K. P. & Gaine, S. P. Migraine with aura following atrial septostomy for pulmonary arterial hypertension. Nat. Clin. Pract. Cardiovasc. Med. 4, 55–58 (2007).

Article PubMed Google Scholar

Gillet, J. L. et al. Pathophysiology of visual disturbances occurring after foam sclerotherapy. Phlebology 25, 261–266 (2010).

Article CAS PubMed Google Scholar

Bahtiri, L., Thomsen, A. V., Ashina, M. & Hougaard, A. Migraine aura-like episodes following sclerotherapy for varicose veins of the lower extremities — a systematic review. Headache 63, 40–50 (2023).

Article PubMed PubMed Central Google Scholar

Fisher, C. M. Late-life migraine accompaniments — further experience. Stroke 17, 1033–1042 (1986).

Article CAS PubMed Google Scholar

Fisher, C. M. Late-life migraine accompaniments as a cause of unexplained transient ischemic attacks. Can. J. Neurol. Sci. 7, 9–17 (1980).

CAS PubMed Google Scholar

Galletti, F. et al. Occipital arteriovenous malformations and migraine. Cephalalgia 31, 1320–1324 (2011).

Article PubMed Google Scholar

Kattah, J. C. & Luessenhop, A. J. Resolution of classic migraine after removal of an occipital lobe AVM. Ann. Neurol. 7, 93 (1980).

Article CAS PubMed Google Scholar

Troost, B. T., Mark, L. E. & Maroon, J. C. Resolution of classic migraine after removal of an occipital lobe AVM. Ann. Neurol. 5, 199–201 (1979).

Article CAS PubMed Google Scholar

Kurita, H., Shin, M. & Kirino, T. Resolution of migraine with aura caused by an occipital arteriovenous malformation. Arch. Neurol. 57, 1219–1220 (2000).

Article CAS PubMed Google Scholar

Kupersmith, M. J., Berenstein, A., Nelson, P. K., ApSimon, H. T. & Setton, A. Visual symptoms with dural arteriovenous malformations draining into occipital veins. Neurology 52, 156–162 (1999).

Article CAS PubMed Google Scholar

Shams, P. N. & Plant, G. T. Migraine-like visual aura due to focal cerebral lesions: case series and review. Surv. Ophthalmol. 56, 135–161 (2011).

Article PubMed Google Scholar

Haas, D. C. Arteriovenous malformations and migraine: case reports and an analysis of the relationship. Headache 31, 509–513 (1991).

Article CAS PubMed Google Scholar

Kowacs, P. A. & Werneck, L. C. Atenolol prophylaxis in migraine secondary to an arteriovenous malformation. Headache 36, 625–627 (1996).

Article CAS PubMed Google Scholar

Silvestrini, M., Cupini, L. M., Calabresi, P., Floris, R. & Bernardi, G. Migraine with aura-like syndrome due to arteriovenous malformation. The clinical value of transcranial Doppler in early diagnosis. Cephalalgia 12, 115–119 (1992).

Article CAS PubMed Google Scholar

Snowden, J. A., Forster, D. M. & McKendrick, M. W. Recurrent migraine-like symptoms and hemiplegia precipitated by fever and associated with an underlying cerebral arteriovenous malformation. Clin. Infect. Dis. 19, 547–548 (1994).

Article CAS PubMed Google Scholar

Spierings, E. L. Daily migraine with visual aura associated with an occipital arteriovenous malformation. Headache 41, 193–197 (2001).

Article CAS PubMed Google Scholar

Bruyn, G. W. Intracranial arteriovenous malformation and migraine. Cephalalgia 4, 191–207 (1984).

Article CAS PubMed Google Scholar

Afridi, S. & Goadsby, P. J. New onset migraine with a brain stem cavernous angioma. J. Neurol. Neurosurg. Psychiatry 74, 680–682 (2003).

Article CAS PubMed PubMed Central Google Scholar

Obermann, M., Gizewski, E. R., Limmroth, V., Diener, H. C. & Katsarava, Z. Symptomatic migraine and pontine vascular malformation: evidence for a key role of the brainstem in the pathophysiology of chronic migraine. Cephalalgia 26, 763–766 (2006).

Article CAS PubMed Google Scholar

Planche, V. et al. Sturge-Weber syndrome with late onset hemiplegic migraine-like attacks and progressive unilateral cerebral atrophy. Cephalalgia 34, 73–77 (2014).

Article PubMed Google Scholar

Izenberg, A. et al. Crescendo transient aura attacks: a transient ischemic attack mimic caused by focal subarachnoid hemorrhage. Stroke 40, 3725–3729 (2009).

Article PubMed Google Scholar

Smith, E. E., Charidimou, A., Ayata, C., Werring, D. J. & Greenberg, S. M. Cerebral amyloid angiopathy-related transient focal neurologic episodes. Neurology 95, 231–238 (2021).

Article Google Scholar

Fischer, P. et al. Rapid hematoma growth triggers spreading depolarizations in experimental intracortical hemorrhage. J. Cereb. Blood Flow Metab. 41, 1264–1276 (2021).

Article CAS PubMed Google Scholar

Evcili, G., Ogun, M. N. & Utku, U. Migraine-like visual aura: can it be an early-onset symptom of astrocytoma? Agri 30, 202–205 (2018).

PubMed Google Scholar

Verma, A., Rosenfeld, V., Forteza, A. & Sharma, K. R. Occipital lobe tumor presenting as migraine with typical aura. Headache 36, 49–52 (1996).

Article CAS PubMed Google Scholar

Porta-Etessam, J., Berbel, A., Martinez, A. & Nunez-Lopez, R. Cerebral metastasis presenting as Valsalva-induced migraine with aura. Headache 38, 801 (1998).

Article CAS PubMed Google Scholar

Daly, D. D., Svien, H. J. & Yoss, R. E. Intermittent cerebral symptoms with meningiomas. Arch. Neurol. 5, 287–293 (1961).

Article CAS PubMed Google Scholar

Olesen, J. & Jorgensen, M. B. Leao’s spreading depression in the hippocampus explains transient global amnesia. A hypothesis. Acta Neurol. Scand. 73, 219–220 (1986).

Article CAS PubMed Google Scholar

Evans, J., Wilson, B., Wraight, E. P. & Hodges, J. R. Neuropsychological and SPECT scan findings during and after transient global amnesia: evidence for the differential impairment of remote episodic memory. J. Neurol. Neurosurg. Psychiatry 56, 1227–1230 (1993).

Article CAS PubMed PubMed Central Google Scholar

Tanabe, H. et al. Memory loss due to transient hypoperfusion in the medial temporal lobes including hippocampus. Acta Neurol. Scand. 84, 22–27 (1991).

Article CAS PubMed Google Scholar

Burke, M. J., Lamb, M. J., Hohol, M. & Lay, C. Unique CT perfusion imaging in a case of HaNDL: new insight into HaNDL pathophysiology and vasomotor principles of cortical spreading depression. Headache 57, 129–134 (2017).

Article PubMed Google Scholar

Cifelli, A. & Vaithianathar, L. Syndrome of transient headache and neurological deficits with cerebrospinal fluid lymphocytosis (HaNDL). BMJ Case Rep. https://doi.org/10.1136/bcr.03.2010.2862 (2011).

Article PubMed PubMed Central Google Scholar

Fuentes, B., Diez Tejedor, E., Pascual, J., Coya, J. & Quirce, R. Cerebral blood flow changes in pseudomigraine with pleocytosis analyzed by single photon emission computed tomography. A spreading depression mechanism? Cephalalgia 18, 570–573 (1998).

Article CAS PubMed Google Scholar

Mastria, G. et al. Prevalence and characteristics of Alice in Wonderland syndrome in adult migraineurs: perspectives from a tertiary referral headache unit. Cephalalgia 41, 515–524 (2021).

Article PubMed Google Scholar

Lu, B. et al. Cerebellar spreading depolarization mediates paroxysmal movement disorder. Cell Rep. 36, 109743 (2021).

Article CAS PubMed Google Scholar

Jen, J., Kim, G. W. & Baloh, R. W. Clinical spectrum of episodic ataxia type 2. Neurology 62, 17–22 (2004).

Article CAS PubMed Google Scholar

Pietrobon, D. CaV2.1 channelopathies. Pflug. Arch. 460, 375–393 (2010).

Article CAS Google Scholar

Mikati, M. A., Kramer, U., Zupanc, M. L. & Shanahan, R. J. Alternating hemiplegia of childhood: clinical manifestations and long-term outcome. Pediatr. Neurol. 23, 134–141 (2000).

Article CAS PubMed Google Scholar

Samanci, B., Coban, O. & Baykan, B. Late onset aura may herald cerebral amyloid angiopathy: a case report. Cephalalgia 36, 998–1001 (2016).

Article PubMed Google Scholar

Glossmann, K., Baumgartner, C., Koren, J. P. & Riederer, F. Recurrent migraine aura-like symptoms in an elderly woman: symptomatic cortical spreading depression? BMJ Case Rep. 14, e241479 (2021).

Article PubMed PubMed Central Google Scholar

Brunot, S. et al. Transient ischaemic attack mimics revealing focal subarachnoid haemorrhage. Cerebrovasc. Dis. 30, 597–601 (2010).

Article PubMed Google Scholar

Loeb, J. A. Features of Leao’s spreading depression in patients with lesions near sensory cortex. J. Epilepsy 11, 110–115 (1998).

Article Google Scholar

Russell, M. B., Rasmussen, B. K., Thorvaldsen, P. & Olesen, J. Prevalence and sex-ratio of the subtypes of migraine. Int. J. Epidemiol. 24, 612–618 (1995).

Article CAS PubMed Google Scholar

Alstadhaug, K. B., Hernandez, A., Naess, H. & Stovner, L. J. Migraine among Norwegian neurologists. Headache 52, 1369–1376 (2012).

Article PubMed Google Scholar

Bombardi, L. M., Almeida, A. G., Finsterer, J. & Scorza, F. A. Increased frequency and intensity of complicated migraine sans migraine after third BNT162b2 dose. Clinics 79, 100315 (2024).

Article PubMed PubMed Central Google Scholar

Geller, E. B. & Wen, P. Y. Migraine with aura as the presentation of leukemia. Headache 35, 560–562 (1995).

Article CAS PubMed Google Scholar

Sartor, H. & Thoden, U. [Migraine with aura as early symptom of neurosyphilis]. Schmerz 13, 48–50 (1999).

Article CAS PubMed Google Scholar

Serratrice, J., Disdier, P., de Roux, C., Christides, C. & Weiller, P. J. Migraine and coeliac disease. Headache 38, 627–628 (1998).

Article CAS PubMed Google Scholar

Suwanwela, N. C. et al. Prolonged migraine aura resembling ischemic stroke following CoronaVac vaccination: an extended case series. J. Headache Pain 23, 13 (2022).

Article CAS PubMed PubMed Central Google Scholar

Kirkland, K. E., Kirkland, K., Many, W. J. Jr. & Smitherman, T. A. Headache among patients with HIV disease: prevalence, characteristics, and associations. Headache 52, 455–466 (2012).

Article PubMed Google Scholar

Bowyer, S. M. et al. Analysis of MEG signals of spreading cortical depression with propagation constrained to a rectangular cortical strip. II. Gyrencephalic swine model. Brain Res. 843, 79–86 (1999).

Article CAS PubMed Google Scholar

Eriksen, M. K., Thomsen, L. L. & Olesen, J. Sensitivity and specificity of the new international diagnostic criteria for migraine with aura. J. Neurol. Neurosurg. Psychiatry 76, 212–217 (2005).

Article CAS PubMed PubMed Central Google Scholar

Hansen, J. M. et al. Migraine headache is present in the aura phase: a prospective study. Neurology 79, 2044–2049 (2012).

Article PubMed PubMed Central Google Scholar

Thomsen, A. V. et al. Clinical features of migraine with aura: a REFORM study. J. Headache Pain 25, 22 (2024).

Article PubMed PubMed Central Google Scholar

Moskowitz, M. A., Nozaki, K. & Kraig, R. P. Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms. J. Neurosci. 13, 1167–1177 (1993).

Article CAS PubMed PubMed Central Google Scholar

Melo-Carrillo, A. et al. Selective inhibition of trigeminovascular neurons by fremanezumab: a humanized monoclonal anti-CGRP antibody. J. Neurosci. 37, 7149–7163 (2017).

Article CAS PubMed PubMed Central Google Scholar

Filiz, A. et al. CGRP receptor antagonist MK-8825 attenuates cortical spreading depression induced pain behavior. Cephalalgia 39, 354–365 (2019).

Article PubMed Google Scholar

Cottier, K. E. et al. Loss of blood-brain barrier integrity in a KCl-induced model of episodic headache enhances CNS drug delivery. eNeuro https://doi.org/10.1523/ENEURO.0116-18.2018 (2018).

Article PubMed PubMed Central Google Scholar

Fioravanti, B. et al. Evaluation of cutaneous allodynia following induction of cortical spreading depression in freely moving rats. Cephalalgia 31, 1090–1100 (2011).

Article PubMed PubMed Central Google Scholar

Tang, C. et al. Cortical spreading depolarisation-induced facial hyperalgesia, photophobia and hypomotility are ameliorated by sumatriptan and olcegepant. Sci. Rep. 10, 11408 (2020).

Article CAS PubMed PubMed Central Google Scholar

Langford, D. J. et al. Coding of facial expressions of pain in the laboratory mouse. Nat. Methods 7, 447–449 (2010).

Article CAS PubMed Google Scholar

Kitagawa, S. et al. Sustained effects of CGRP blockade on cortical spreading depolarization-induced alterations in facial heat pain threshold, light aversiveness, and locomotive activity in the light environment. Int. J. Mol. Sci. 23, 13807 (2022).

Article CAS PubMed PubMed Central Google Scholar

Kaur, M. et al. Sex differences in photophobic behaviors following cortical spreading depression in rats. Cephalalgia 45, 3331024241310550 (2025).

Article PubMed PubMed Central Google Scholar

Ayata, C., Jin, H., Kudo, C., Dalkara, T. & Moskowitz, M. A. Suppression of cortical spreading depression in migraine prophylaxis. Ann. Neurol. 59, 652–661 (2006).

Article CAS PubMed Google Scholar

Fischer, P. et al. Spreading depolarizations suppress hematoma growth in hyperacute intracerebral hemorrhage in mice. Stroke 54, 2640–2651 (2023).

Article CAS PubMed PubMed Central Google Scholar

Dell’Orco, M. et al. Repetitive spreading depolarization induces gene expression changes related to synaptic plasticity and neuroprotective pathways. Front. Cell Neurosci. 17, 1292661 (2023).

Article PubMed PubMed Central Google Scholar

Ayata, C. Spreading depression: from serendipity to targeted therapy in migraine prophylaxis. Cephalalgia 29, 1095–1114 (2009).

Article CAS PubMed Google Scholar

Hartings, J. A. et al. Direct current electrocorticography for clinical neuromonitoring of spreading depolarizations. J. Cereb. Blood Flow Metab. 37, 1857–1870 (2017).

Article PubMed Google Scholar

Woitzik, J. et al. Delayed cerebral ischemia and spreading depolarization in absence of angiographic vasospasm after subarachnoid hemorrhage. J. Cereb. Blood Flow Metab. 32, 203–212 (2012).

Article PubMed Google Scholar

Hartings, J. A. et al. Spreading depolarisations and outcome after traumatic brain injury: a prospective observational study. Lancet Neurol. 10, 1058–1064 (2011).

Article PubMed Google Scholar

Hartings, J. A. et al. Spreading depolarizations have prolonged direct current shifts and are associated with poor outcome in brain trauma. Brain 134, 1529–1540 (2011).

Article PubMed Google Scholar

Hinzman, J. M., Wilson, J. A., Mazzeo, A. T., Bullock, M. R. & Hartings, J. A. Excitotoxicity and metabolic crisis are associated with spreading depolarizations in severe traumatic brain injury patients. J. Neurotrauma 33, 1775–1783 (2016).

Article PubMed PubMed Central Google Scholar

Magrotti, E., Frascaroli, G. & Mariani, G. Left temporal glioma presenting as migraine with typical aura. Ital. J. Neurol. Sci. 13, 444 (1992).

Article CAS PubMed Google Scholar

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sarcozona

2 hours ago

Epiphyte City

‘It’s surreal’: US sanctions lock International Criminal Court judge out of daily life – The Irish Times
Friday March 13^th, 2026 at 12:49 AM

This summer Kimberly Prost, a Canadian judge at the International Criminal Court (ICC), arrived at her home in The Hague and, as was her habit, called out “Alexa”.

There was silence. The voice-activated assistant did not respond. “Alexa was dead. She wouldn’t talk to me,” Prost recalled in an interview with The Irish Times.

Prost had been added to the United States’ sanctions list, because in 2020 she ruled to authorise an investigation into possible atrocities in Afghanistan, including by US troops. Amazon, obliged to implement the sanctions as a US company, had cancelled her account.

It was just the start of what Prost describes as a “pervasive, negative effect” of the sanctions across all aspects of her life, which has shut her out from much of the international banking system.

The effects of being sanctioned are wide-ranging.

“You immediately lose your credit cards – it doesn’t matter where they were issued or by what bank,” Prost said. Bank transfers can be challenging: a sum of money she tried to send a young couple as a wedding gift has been lost in the system for weeks.

“Online shopping becomes excruciatingly difficult, if not impossible. But there’s other things, everyday things, like ordering an Uber or ordering tickets for something, or booking a hotel.”

“If you have assets in the United States, then they’re frozen,” Prost said. “If you have family or family who works there, visits there, there’s a real danger. One of my colleagues, her daughter’s visa was revoked.”

Sanctioned court staff are from countries including Senegal, Benin, Peru, Fiji and Uganda. Sending money to their home countries has become difficult.

“I can’t buy US dollars, but also I can’t buy some other kinds of currencies, because the transaction would go through the US system,” Prost said. “So for some of my colleagues who are sending money, perhaps to South America or Africa, they have that problem.”

Prost stresses that these relatively minor issues compared with the matters she hears about in cases before the court.

“These are small annoyances, but when they all come together at once in your life, it’s paralysing,” Prost said.

“The purpose is clear. They have said, basically, we’re imposing these sanctions because of decisions you’ve taken in your role as a judge. So effectively, they are interfering directly with the independence of a judge,” Prost said.

“I can’t think of any other way to describe it but an attack on the independence of the judiciary and the International Criminal Court’s independence as an institution, which is why I’m so interested in the public hearing this.”

Prost was added to the sanctions list in August because five years ago she was one of the judges who ruled to authorise an investigation into alleged war crimes by the Taliban, Afghan forces, US forces and the CIA in Afghanistan since 2003.

The US has sanctioned six ICC judges this year, along with the court’s chief prosecutor and two deputy prosecutors.

Israeli prime minister Binyamin Netanyahu. Photograph: Abir Sultan/EPA

The reasons given by the state department relate either to their roles in the Afghanistan investigation or their involvement in the court’s issuing of arrest warrants for Israeli prime minister Binyamin Netanyahu and former defence minister Yoav Gallant in November 2024 for the war crime of starvation as a method of warfare in Gaza, and for crimes against humanity.

[ ICC judges wanted Netanyahu arrested. Now they’re being targeted by TrumpOpens in new window ]

The US and Israel reject the jurisdiction of the court. Neither country is among the 125 signatories of the Rome Statute, which established the ICC in 1998. However, the treaty sets out that nationals of non-member states can be tried for crimes that take place on the territory of states that are signatories.

Afghanistan signed it in 2003 and the state of Palestine in 2014. The court therefore asserts its jurisdiction to prosecute the crimes of genocide, crimes against humanity, war crimes and crimes of aggression that have taken place in Gaza, East Jerusalem or the West Bank, no matter the nationality of the alleged perpetrators.

In an executive order announcing the first round of ICC sanctions this year, US president Donald Trump said the court represented an “unusual and extraordinary threat to the national security and foreign policy of the United States” for its investigations into nationals of the US and Israel. The state department accused the court of conducting “lawfare” and infringing on US sovereignty.

Along with the ICC staff, the US also sanctioned three Palestinian NGOs for engaging with the court in its efforts to “ investigate, arrest, detain or prosecute Israeli nationals”. The court is preparing for the possibility that the ICC itself might be sanctioned as an entity any day.

Originally from Winnepeg, Prost was a public prosecutor in Canada and became specialised in the prosecution of genocide, war crimes and crimes against humanity. She served as a judge on the United Nations’ International Criminal Tribunal for the former Yugoslavia, which led to the conviction of multiple people for carrying out a genocide in Srebrenica.

[ ‘I’m remembering Srebrenica while Srebrenica is happening in Gaza’Opens in new window ]

For five years, she was the ombudsperson for the UN Security Council’s al-Qaeda sanctions, something Prost calls “an odd background twist that makes this very ironic”.

“Basically, my job was to speak to people who wanted to come off the list,” Prost said. “So I know sanctions very well.”

There is a psychological impact on ICC staff, who have spent their lives working within the criminal justice system, when they suddenly find themselves on a sanctions list alongside people implicated in human rights violations, terrorism or organised crime.

Kimberly Prost. Photograph: ICC

“It’s a bit surrealistic,” Prost said. “Now you’re on that same list. So yeah, it’s a bit shocking.”

Prost was part of the Canadian delegation when the Rome Statute was first agreed in 1998. It was the culmination of a century of efforts to establish an international court to try individuals for the worst crimes in the world, a permanent version of the one-off courts established to try the Nazis in Nuremberg and the perpetrators of the Rwandan genocide.

[ When Nazism went on trial: the Irish journalist in the room at NurembergOpens in new window ]

At that time, the negotiating countries had their differences, Prost recalled, but were united in their overall aim.

“[They believed] there should be a system designed to bring accountability for the gravest crimes: crimes against humanity, war crimes, genocide,” she remembered. “There should be an end to impunity. And that’s what infused the entire negotiation.”

Something that sticks with her from her time as a judge is the testimony she heard that led to the conviction of the former head of the Islamic police force that governed Timbuktu in northern Mali when the historic city was overrun by a jihadist takeover in 2012.

Al-Hassan ag Abdoul Aziz was convicted of war crimes and crimes against humanity for overseeing torture, public amputations and floggings.

“I was sitting in a courtroom having witnesses come from Timbuktu, who’d never been outside of Timbuktu, to testify,” she remembered.

“The power of that testimony, and hearing those victims ... standing up and expressing their rights and expressing over and over again: we want justice.”

Court staff are familiar with challenges to their work. Russia retaliated to the court’s issuing of arrest warrants for president Vladimir Putin and military leaders for atrocities in Ukraine by issuing arrest warrants for ICC staff.

Former ICC chief prosecutor Fatou Bensouda. Photograph: Toussaint Kluiters/AFP/Getty Images

Former prosecutor Fatou Bensouda has said she was subject to threats and intimidation after she opened an initial inquiry into atrocities in Afghanistan and by Israeli forces.

However, the US sanctions are unprecedented. Prost has not ruled out litigation in the US, as she believes the legal basis to the sanctions is questionable, though this would be hugely expensive.

She hopes that speaking openly about the effect will galvanise supporters of the court to defend it and limit the effect of the sanctions. Some of the implementation of the measures outside the US is discretionary. The judge believes it is very important that there is no perception that powerful developed countries are exempt from accountability.

“That would damage the court, if we’re unable to do cases equally wherever justice demands,” Prost said. “This is about a basic need, the imperative of justice for all of us.”

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sarcozona

17 hours ago

Epiphyte City

The Curious Case of the Disappearing Data
Thursday March 12^th, 2026 at 5:08 PM

Last night I tried to access a dataset I’ve used many times before.

Over the past year it has suddenly been getting harder and harder to find. At first it quietly disappeared from the CDC and NIH directories. Search the site directly? Nothing. It was like maybe someone didn’t want us looking at the data? Wonder why that would be???

Fine.

Scientists are stubborn little gremlins. Hide something and we immediately want to know why. So I wrote a bit of code to pull the datasets directly.

And access them I did.

Then I compared the numbers with copies of the data I saved earlier in the pandemic.

They didn’t appear MATCH. But mostly a lot was erased. Gone. Poof

That should not happen.

These datasets are historical mortality metadata. Imagine giant spreadsheets full of numbers that only weirdos like me get excited about. But those numbers represent recorded history. Once illness and mortality data is logged, it doesn’t magically change.

You cannot retroactively “update” who died in 2021 or change a billing code for someone with a catastrophic stroke.

At least not unless someone is actively altering or manipulating the data.

So when historical data suddenly shifts, there are really only two explanations.

Either the laws of physics broke overnight.

Or someone doesn’t want those numbers being looked at.

Which raises two extremely obvious questions.

Who is now controlling the data?

And why the hell are they doing it?

These datasets track mortality and disease trends in the United States. Epidemiologists use them to answer the most basic questions in public health.

Are more people dying than expected?

If so, why?

Once we see patterns, researchers investigate the causes and try to fix the problem. That’s literally the job description.

Find the problem.

Study the cause.

Help people.

Instead, when I tried to access the database again last night, the page refused to load.

Now it displays a message.

“CDC’s website is being modified to comply with President Trump’s Executive Order.”

Why the hell would a sitting president write an executive order to prevent the data from being accessed? The only answer I can come up with? There are things in there they don’t want people to see. Why? Because it shows how BADLY the US and world fumbled Covid and are directly responsible for millions of unnecessary deaths and now rapidly increasing diseases related to repeated COVID infections.

That’s it.

Just a locked fucking door where the data used to be.

And based on the comparisons I ran, the problem isn’t just that the data is hidden.

Some of the most critical pieces appear to have been permanently erased.

Which should scare the absolute shit out of everyone.

Because that data doesn’t belong to politicians.

It belongs to the public.

It’s the closest thing we have to a black box recorder for the health of the country.

For most people this message probably looks like routine government maintenance.

For researchers it feels more like someone just ripped the batteries out of the smoke alarm while the building is actively on fire.

Public health data is the early warning system for society. It tells scientists when something in the population is changing.

When those systems suddenly start disappearing while disease patterns are shifting in ways we have never seen before, scientists notice.

And we start asking questions.

Loud ones.

If you have ever tried to shut me up, you already know that is the fastest way to guarantee I start yelling louder. I am a scientific chaos gremlin who detests cover ups and blatant lying to the public.

COVID was never just a respiratory virus

Early in the pandemic I started writing about what I was seeing in the numbers.

By mid-January 2020 the data strongly suggested the virus was airborne. By the third week of January it was obvious people were transmitting it before symptoms appeared. Based on particle size it behaved far more like measles than the flu, meaning this wasn’t step back six feet and wear a paper mask- this was full sealed NIOSH approved respirator time. Which I recognized and immediately started doing. So far (knock on wood) no COVID- even though I was in the thick of it.

None of that was particularly popular to say.

I was mocked for it.

By scientists. The hospital I worked for. Colleagues I formally had respected. Pretty much everyone that had a voice and didn’t want to look at the truth. But numbers don’t lie, they are the ones lying and obfuscating the truth

Fun times.

By March 2020 something even stranger was appearing in the data.

Patients were not just experiencing lung infections.

Doctors were reporting strokes in young people. Severe clotting disorders. Heart inflammation. Kidney damage. Neurological issues. New autoimmune diseases popping up out of nowhere.

It looked chaotic.

So I did what scientists are supposed to do when something weird appears in the data.

I asked other experts if they were seeing the same thing.

Back when Twitter was still useful, I reached out to researchers across multiple fields.

“Hey… are you seeing this shit too?”

The responses came back quickly.

“OMG YES! I keep being dismissed.”

Ummm so if you sideline the experts in favor of politicians what does that say?

I honestly felt slightly better that those people who were on the top of the field were also being ignored and gaslit. Hey if we were going down, we were going to do it together and while fighting.

A small network of researchers started comparing notes almost immediately. Epidemiologists, physicians, immunologists, public health experts.

Thousands of independent observations later the picture was becoming painfully clear.

COVID was not just killing people through respiratory failure.

It was damaging the body everywhere.

We raised alarms. We shared data. We proposed simple mitigation strategies that could have reduced the damage before vaccines even existed.

And we were ignored when all we wanted was to provide clear simple messaging to help people understand the risk as well as how to prevent the spread. It wasn’t about creating fear. It was giving people actionable information to help keep themselves and their families safe(r). To give folks some control over an overwhelmingly scary situation.

Covid and the cardiovascular risk

Eventually the larger international datasets caught up.

And they confirmed what many of us already had figured out months prior.

Researchers demonstrated that SARS-CoV-2 infects endothelial cells. These are the cells that line blood vessels throughout the body (Varga et al., 2020).

If you want a simple analogy, think of your circulatory system like the plumbing in your house.

Blood vessels are the pipes.

Endothelial cells are the smooth lining inside those pipes that keeps everything flowing properly.

COVID damages that lining.

When the inside of a pipe becomes inflamed and rough, things start sticking to it. Clots form. Flow becomes turbulent.

Now imagine that happening in the pipes supplying your brain, heart, lungs, kidneys, and every other organ.

That is why COVID behaves less like a respiratory infection and more like a disease of the vascular and immune systems.

Subsequent research has continued to show persistent endothelial damage and vascular inflammation long after infection resolves (Aljadah et al., 2024; Stoichita et al., 2026).

The cardiovascular risks following COVID infection are now well documented.

One of the largest studies examining long-term outcomes analyzed health records from the U.S. Veterans Affairs system. Researchers compared more than 150,000 COVID survivors with millions of uninfected individuals.

They found significantly increased risks of stroke, heart attack, arrhythmias, myocarditis, heart failure, and blood clots for at least a year after infection (Xie, Xu & Al-Aly, 2022).

Overall survivors experienced about a 40 percent increase in major cardiovascular events.

Even people whose infections were mild enough that they were never hospitalized showed elevated risk.

Which means this is not just a severe-case problem.

It is an “everyone who got Covid” problem.

Which would normally be exactly the kind of thing researchers would want to track carefully.

Using national health datasets.

You know.

The ones that are now missing.

Each infection adds more damage.

And while scientists are scrambling to understand how bad that damage is across the population, the datasets used to track those trends have been quietly disappearing over the past year.

Now they are simply locked.

Which raises a question that should make anyone uncomfortable.

Why remove the instruments measuring a problem while the problem appears to be getting worse?

What happens when the immune system’s brakes fail

COVID interferes with how the immune system regulates itself.

The immune system has built-in brakes that shut down inflammation once a threat is neutralized.

Without those brakes the immune system can get stuck in a chronic inflammatory state.

Imagine driving a car with the accelerator pressed down and no functioning brakes.

Eventually something catastrophic happens.

Researchers have documented persistent immune dysfunction after infection, including T-cell exhaustion (Chen-Camaño et al., 2025).

T-cells are critical immune cells that coordinate responses against infections and cancer.

When they become exhausted they stop functioning properly. They produce fewer immune signals and lose the ability to identify abnormal cells. Once these cells are exhausted or even erased, you don’t get them back the same. The older you are? Sorry, but they just don’t return.

Numerous studies now show those immune cell populations remain suppressed 20 months or more after infection (Jiang et al., 2025).

This is why we kept getting so sick as a population after each wave of COVID. It’s not because of lock downs. It’s because Covid took a baseball bat to a critical part of our immune system and destroyed it.

This matters beyond those pesky invasive step infections that were suddenly killing kids, or the weird invasive fungal infections, etc etc etc because those were just the canary in the coal mine governments chose to ignore

That portion of your immune system spends every day hunting for cancer.

Let that sink in please. Covid essentially damaged or destroyed the part of our body that fights cancer. The more you get it the worse the damage is to these cells.

Cells make mistakes constantly while dividing. Normally the immune system finds those mistakes and destroys the abnormal cells before they turn into tumors.

If that surveillance weakens, those errors slip through.

The cancer question

Cardiovascular disease is only part of the story.

Researchers are also watching trends in early-onset cancers, meaning cancers appearing in people under 50.

Colorectal cancer gets the most attention because its rise among younger adults has been particularly dramatic (Siegel et al., 2023).

But colorectal cancer is only one piece of a broader pattern.

A 2024 analysis in The Lancet Oncology found early-onset cancers increasing across fourteen different cancer types worldwide, including breast, pancreatic, kidney, and liver cancers (Sung et al., 2024).

Some hospital systems have reported colorectal cancer diagnoses in people under 50 rising by twenty to thirty percent in just a few years (Patel et al., 2024).

Cancer trends normally move slowly.

When diagnoses jump this quickly, epidemiologists start asking questions.

The body’s ability to suppress abnormal cells weakened.

Both processes are heavily influenced by inflammation and immune function.

Which brings us right back to COVID.

Something changed. It started to change right when Covid hit the scene. I do not believe in a “coincidence”, especially one that is now backed by a tsunami of scientifically vetted evidence.

And right back to the disappearing datasets used to track these trends. It is not science it is a cover up.

The US healthcare problem

Now add another layer of insanity.

The United States already operates the most expensive healthcare system on earth.

And one of the least accessible.

We spend more money than any other country in the world and still manage to produce worse outcomes.

Because the system is built around profit.

When people get sick in that system, they are not just patients.

They are billing codes.

Now imagine hiding national health data while simultaneously making healthcare even harder to access.

Which is exactly what the so-called “Big Beautiful Bill” did by cutting federal healthcare spending and Medicaid access for millions of Americans.

Less preventative care.

Fewer screenings.

Fewer diagnoses.

And fewer medical records entering the datasets that scientists rely on.

It is almost a perfect system for making a public health disaster statistically disappear. The US government is essentially telling US citizens to suck it up and please just quietly go die somewhere. We are too busy building ballrooms to fund basic medical care.

If you cannot measure the problem, you can always pretend it isn’t there.

The number that should have triggered alarm bells

A major analysis of U.S. mortality data found that between 2020 and 2022 more than 300,000 excess deaths occurred among Americans aged 18 to 49 beyond what historical patterns would predict (Faust et al., 2023).

Excess mortality simply means more people died than statistically should have.

Three hundred thousand extra deaths in younger adults should have triggered the largest public health investigation in history.

Instead the datasets used to investigate those deaths are being altered, erased, or locked away.

Which raises a very simple question.

If hundreds of thousands of people have died above expected levels, and researchers cannot access the data used to analyze those deaths, how exactly are we supposed to determine what caused them?

Without data, the investigation cannot happen.

And without the investigation, the answers never appear.

Turning off the dashboard lights

Public health surveillance exists so we can detect problems early.

Imagine airline engineers noticing a pattern of engine failures.

Now imagine someone decides the solution is to remove the instruments that measure engine temperature.

Planes would keep crashing.

You would just stop recording why.

Deleting the evidence does not change the biology.

Inflammation still damages blood vessels.

Immune dysfunction still accumulates.

Cancers still grow.

Reality keeps generating new data whether governments acknowledge it or not.

Eventually the numbers return.

They always do.

And when they do, people are going to ask a very uncomfortable question.

Why did the data start disappearing right when we needed it most?

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sarcozona

1 day ago

Epiphyte City

Babies with COVID-19 develop more serious disease than those with RSV, US data reveal
Thursday March 12^th, 2026 at 5:07 PM

Children under two years of age hospitalized for COVID-19 are more likely to die or become seriously ill than babies with respiratory syncytial virus (RSV), according to a study published this week in Open Forum Infectious Diseases.

Babies can become sick and die from both respiratory viruses, even if they were healthy before becoming infected, according to the study, which was led by researchers from the US Centers for Disease Control and Prevention.

2.9% death rate for COVID, 0.4% for RSV

In the study, 39% of babies admitted to an intensive care unit (ICU) because of COVID-19 needed to be put on a ventilator to breathe, compared with 16% of babies with RSV. Children hospitalized for COVID-19 also stayed in the hospital longer than those with RSV in the study, which included 33 hospitals in 28 states and was conducted from November 2023 to March 2024.

In addition, babies hospitalized for COVID-19 were more likely than babies with RSV to receive vasoactive infusions—drugs given intravenously to manage blood pressure, heart rate, and cardiac output by widening or constricting blood vessels. They were also more likely to need extracorporeal membrane oxygenation, a temporary mechanical breathing and heart support used when standard treatments for those problems have already been tried.

In the study, 2.9% of children with COVID-19 died, along with 0.4% of those with RSV. The 1,406 babies in the study arrived at the hospital with acute respiratory failure, a medical emergency in which the lungs cannot provide enough oxygen or remove carbon dioxide. All were hospitalized in the ICU for at least 24 hours. More than 89% of the babies had RSV, 7.5% had COVID-19, and 3.4% were infected with both viruses.

Children hospitalized for RSV or both viruses were younger than those hospitalized with COVID-19. Twenty percent of babies with RSV had an underlying medical condition, compared with 44% of those with COVID-19.

Medical societies recommend vaccination

Although RSV immunizations were approved in 2023, they were not yet widely available during the study. Only 5.5% of babies age six to 23 months were vaccinated against COVID-19 in the study.

Research shows that vaccinations for both RSV and COVID-19 are safe and effective. The American College of Obstetricians and Gynecologists recommends women receive a COVID-19 vaccine at any time during pregnancy and an RSV vaccine between the 32nd and 36th week of pregnancy. Both vaccines can protect newborns too young to be vaccinated.

For babies whose mothers weren’t vaccinated against RSV, the American Academy of Pediatrics recommends newborns under 8 months receive an injection of lab-grown antibodies. The pediatric group also recommends babies age six to 23 months be vaccinated against COVID-19.

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Up to 56,000 people died from COVID-19 or RSV last year

RSV was associated with 190,000 to 350,000 hospitalizations from July 1, 2024, to June 30, 2025, as well as 10,000 to 23,000 deaths, according to new CDC data.

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sarcozona

1 day ago

Epiphyte City

The COVID-19 pandemic at 6 years: Mass death, debilitation and media silence
Thursday March 12^th, 2026 at 5:06 PM

World Socialist Web Site (en)

Six years ago this week, on March 11, 2020, the World Health Organization (WHO) officially declared the global outbreak of COVID-19 a pandemic. In the six years since, the pandemic has killed over 30 million people worldwide, left more than 400 million suffering from Long COVID and inflicted incalculable damage on the social fabric of every country on Earth. It is one of the most catastrophic events in modern history—and it is not over.

World Health Organization Director-General Dr Tedros Adhanom Ghebreyesus (center) declaring the coronavirus pandemic a Public Health emergency of International Concern in March 2020. [Photo: Fabrice Coffrini]

Yet not a single major bourgeois publication has so much as acknowledged this anniversary. The pandemic has been deliberately erased from public consciousness by the political establishment, even as the virus continues to spread, disable and kill on a mass scale. In May 2023, under pressure from the Biden administration, the WHO prematurely ended the Public Health Emergency of International Concern, offering political cover for capitalist governments globally to scrap remaining public health measures. Today, the COVID-19 pandemic remains a serious and deadly ongoing threat whose cumulative toll grows with each passing week.

The ongoing toll: Excess deaths and new studies on Long COVID

According to the latest report from the Pandemic Mitigation Collaborative (PMC) for March 9, 2026, the United States is currently experiencing a sustained wave of viral transmission. The PMC estimates that there are approximately 565,000 new daily infections across the country. This elevated level of transmission means that roughly 1 in 87 Americans—or 1.2 percent of the population—is actively infectious on any given day.

SARS-CoV-2 Daily infections March 9, 2026 [Photo by PMC, courtesy of Dr. Mike Hoerger]

Crucially, what is most alarming is not the peaks but the floor—the period between surges. The wastewater-derived data reveals that between-wave baseline transmission has remained persistently elevated since the Omicron surge of early 2022, never returning to pre-2022 lows. This rising floor of endemic infection is arguably more significant than the dramatic wave peaks: it represents the continuous, unrelenting generation of new infections, Long COVID cases and excess deaths, even in the quietest periods of viral circulation, which objectively defines the term “forever COVID.”

The scale of this unchecked spread guarantees a continuous mass generation of post-viral disability. The PMC estimates that 54 million total infections have occurred in the US in the first three months of 2026 alone. And with this transmission comes a massive burden of Long COVID, with estimates that between 205,000 and 820,000 new Long COVID cases are generated every single week from new infections. The PMC model indicates that between 1,200 and 1,900 excess deaths result from these new weekly infections.

Indeed, using actuarial data, they estimated that for 2025 there were between 109,000 and 175,000 excess deaths, up to 73 percent higher than direct COVID-19 deaths. As their figures demonstrate, these excess deaths are on par with the number of people who died of lung cancer (125,000 deaths) in the US, eclipsing deaths from colon, pancreatic, breast and prostate cancer combined.

PMC estimates of excess deaths in 2025 [Photo by PMC, courtesy of Dr. Mike Hoerger]

Their data closely corroborates a recent cross-sectional study published in JAMA Internal Medicine by CDC scientists, which estimated 1.1 million hospitalizations and 101,300 COVID-19 deaths in the US during the 2022–2023 period. For the following period from 2023–2024, they documented nearly 880,000 hospitalizations and 100,800 deaths. The JAMA study highlighted that older adults bear the brunt of this crisis, with those aged 65 and older accounting for 81.2 percent of all COVID-19 deaths in the latest surveillance period while representing less than 20 percent of the US population.

As the report highlights, these preliminary estimates of COVID-19 deaths are higher than the 89,098 and 59,616 COVID-19 deaths reported by the Division of Vital Statistics Mortality Multiple Cause data file in 2022–2023 and 2023–2024, respectively.

The stark discrepancy is mentioned by the authors, but they fail to provide real answers beyond a perfunctory statement that these may be attributable to the decline in documenting COVID on death certificates or the use of preliminary estimates from the National Center for Health Statistics that undercount the real figures. Notably, they highlight the dramatic decline in vaccination coverage in this period, a byproduct of a bipartisan effort that promoted the erroneous benefits of COVID infection and so-called “natural” or “hybrid” immunity. Their analysis, however, lacks a coherent explanation for this discrepancy.

Dr. Mike Hoerger, in response to a query by this reporter on the aforementioned CDC study about the COVID death toll for 2025, wrote, “Two years flat suggests more of the same until a rigorous publication says otherwise. They have some ‘preliminary’ estimates on their website but do not provide enough detail to be useful, and I would suggest they are prone to minimizing to the extent testing continues to decline even in healthcare settings.”

The bipartisan dismantling of public health

These ongoing massive casualties caused by COVID-19 were not inevitable, but the direct consequence of politically motivated decisions to dismantle all public health protection while the virus continued to rage. The Biden administration systematically dissolved the US pandemic response by allowing the national emergency declarations to expire, triggering the unwinding of Medicaid coverage for millions of vulnerable people and privatizing the distribution of life-saving vaccines and treatments. By deliberately codifying a “forever COVID” policy to prioritize corporate profit and economic normalcy over human needs, the political establishment effectively guaranteed the continued, massive death toll documented in recent studies.

Having established this homicidal “forever COVID” baseline—and having utilized the WHO’s premature declaration ending the global health emergency as political cover—the Biden administration did not merely fail to prevent what followed; it made it structurally inevitable. The attacks on public health carried out under the Biden administration paved the way for the elevation of anti-vaccine quack Robert F. Kennedy Jr. to the position of Health Secretary, where he has overseen the steady dismantling of the Department of Health and Human Services and all of its sub-agencies.

Contrary to the anti-vaccine hysteria whipped up by the far-right, there is a growing body of evidence proving that vaccines were highly protective against death and cardiovascular complications associated with COVID-19 infections. A mid-2024 cohort study published in Nature Communications, which analyzed the health records of nearly 46 million adults in England, provides overwhelming evidence of the cardiovascular safety of COVID-19 vaccines. The researchers found that the incidence of common cardiovascular emergencies, such as acute myocardial infarctions (heart attacks) and ischemic strokes, was significantly lower following vaccination compared to periods before or without vaccination.

Specifically, arterial thromboses were up to 10 percent lower 13 to 24 weeks after a first dose and dropped even further—up to 27 percent lower after an AstraZeneca second dose and 20 percent lower after a Pfizer second dose. Similar declines were observed for common venous thrombotic events, such as pulmonary embolisms and deep vein thrombosis. The researchers concluded that the substantial benefits of first, second and booster doses in preventing common and severe cardiovascular events far outweigh the risks of very rare complications associated with vaccines such as myocarditis, which is more prevalent in those who become infected with SARS-CoV-2.

This comprehensive data refutes anti-vaccine misinformation by demonstrating that COVID-19 vaccines actively reduce the broader cardiovascular risks associated with the virus, offering strong evidence of the need to expand vaccination programs under conditions in which vaccine science is under relentless attack.

The cumulative toll of mass reinfection and immune system damage

The damage inflicted by mass reinfection is equally grave and particularly alarming among populations long dismissed as immune to serious COVID harm. A recent pre-print study available in The American Journal of the Medical Sciences highlights the severe, debilitating impact COVID-19 has had among active-duty military personnel—some of the youngest and fittest sections of the population. Analyzing the electronic health records of over 650,000 service members diagnosed with COVID, researchers found that 42.8 percent—or 278,278 individuals—developed Long COVID. The sheer scale of chronic illness in a population subject to strict age and physical readiness requirements completely shatters the official narrative that the virus poses little threat to the young and healthy.

The researchers tracked a vast array of persistent symptoms disrupting the lives and physical fitness of service members. Pulmonary issues were the most prevalent, affecting 22.4 percent of those with Long COVID, followed closely by neurological problems (14.6 percent) and chronic fatigue (13.5 percent). Notably, while cognitive symptoms such as “brain fog” and memory impairment were reported by a smaller segment of the sample (3.7 percent), these proved to be the most persistent and long-lasting, raising profound concerns about the potential for enduring cognitive damage. The study also found that preexisting conditions, such as obesity, anxiety, depression and nicotine use, significantly heightened the risk of developing these devastating post-viral complications.

Furthermore, a study by researchers at Shandong University and the University of Toronto, published in the February 2026 issue of the International Journal of Infectious Diseases, revealed that mass SARS-CoV-2 infection causes persistent and chronic immune compromise—with key lymphocyte subsets like CD8+ T cells remaining significantly below baseline up to 20 months post-infection—a condition particularly severe in patients with cardiovascular disease. Analyzing data from over 40,000 patients, researchers found that long after the acute phase of the virus had passed, key immune populations (including CD4+ T cells, CD8+ T cells and natural killer (NK) cells) failed to recover. This chronic immune dysfunction leads to prolonged T-cell exhaustion, leaving individuals highly susceptible to opportunistic pathogens, the reactivation of latent viruses like Epstein-Barr and the onset of Long COVID. This is yet another study confirming the advance warnings made by the most far-sighted scientists as early as 2020, including immunologist Dr. Anthony Leonardi in extensive interviews with the WSWS.

For patients with preexisting cardiovascular disease, this immune collapse was even more profound and highly dangerous. The authors warned that this severe loss of T-cell-mediated immune control fuels chronic vascular inflammation, which can destabilize atherosclerotic plaques and drastically increase the risk of acute thromboembolic events like heart attacks and strokes. These findings provide a concrete immunological mechanism for the long-term cardiac morbidity triggered by the virus, further exposing the criminality of the political establishment’s “forever COVID” policy that subjects the population to endless, damaging reinfections.

The catastrophic implications of Kennedy’s tenure at HHS were recently highlighted in a scathing editorial by The Lancet. Titled “Robert F. Kennedy Jr: 1 year of failure,” the editorial board warned that the destruction Kennedy has wrought in one year might take generations to repair, and that there is little hope for US health and science while he remains at the helm.

Secretary of Health and Human Services Robert F. Kennedy, Jr., speaks in the Oval Office of the White House in Washington, as President Donald Trump, left, and Mehmet Oz, administrator for the Centers for Medicare & Medicaid Services, look on. [AP Photo/Alex Brandon]

The editorial cataloged a relentless assault on evidence-based medicine, including the summary dismissal of agency experts, revisions of guidelines to contradict established science, reductions in cutting-edge scientific research and the promotion of junk science and fringe beliefs. Furthermore, the journal noted that critical federal datasets used to track disease have vanished, leaving the population blind and unprepared for both the ongoing pandemic and emerging threats. This destruction did not arise in a vacuum—it was made possible by the prior bipartisan dismantling of the pandemic response infrastructure that left it hollowed out and vulnerable to precisely this kind of assault.

As the ongoing weekly reports by the PMC demonstrate, the COVID-19 pandemic continues to exact a devastating physiological and social toll, standing as a massive indictment of the entire capitalist political establishment.

Ultimately, the social issues raised by this ongoing collapse of public health have assumed a distinctly political and class character. Kennedy’s ability to act as a disruptive force—promoting anti-science quackery and systematically exposing the population to preventable diseases—is only possible because the ruling class has subordinated human life to corporate profit. The bipartisan acceptance of mass infection demonstrates that the capitalist system is fundamentally incompatible with the basic requirements of human health and well-being.

The normalization of mass death from COVID-19 is of a piece with the broader social barbarism overseen by the same ruling elites. The capitalist governments that have condemned millions to death through “forever COVID” are the same that have enabled and armed the genocide in Gaza and now the criminal US-Israeli war against Iran. The Trump administration’s fascistic assault on public health—accelerated by Kennedy’s demolition of the remaining public health infrastructure—is part of a broader program of social reaction that includes the destruction of all climate change mitigation policies, which in turn fosters the conditions for future pandemics through habitat destruction, zoonotic spillover and the weakening of global health systems. The world is now less prepared for the next pandemic than it was in 2020.

The World Socialist Web Site stands alone in providing continuous, scientifically grounded coverage of the COVID-19 pandemic from the standpoint of the international working class. Since January 2020, the WSWS has published over 5,000 articles on the pandemic—the only publication outside of scientific journals to have covered the science and politics of COVID with this depth and consistency.

One year ago, the WSWS marked the five-year anniversary of the pandemic with a comprehensive series analyzing the origins of the social catastrophe and the unique record of the WSWS in opposing it. The Global Workers’ Inquest into the COVID-19 Pandemic, launched in November 2021, continues to document the testimonies of workers, scientists and public health experts from around the world.

As we have stressed from the very beginning, the defense of science, the restoration of public health infrastructure and the end of the pandemic require the independent political mobilization of the international working class to fight for a socialist reorganization of society.

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sarcozona

1 day ago

Epiphyte City

Screw Covid, I'm going to Sturgis.
Thursday March 12^th, 2026 at 5:05 PM

https://transcendloneliness.substack.com/

Troy Tassier is a professor of economics at Fordham University and the author of The Rich Flee and the Poor Take the Bus: How Our Unequal Society Fails Us during Outbreaks.

A metamorphosis occurs each August in Sturgis, SD. The small 7,000 person town is invaded (peacefully) by a steady stream of Harleys, Indians, and Triumphs among countless other motorcycle brands. The rumbles of their engines bubbling at each intersection can be heard throughout the town. It’s the Sturgis motorcycle rally and Sturgis has grown to a population of around half a million people – It now contains the same population as Kansas City, MO and Raleigh, NC.

In the year 2020 public health authorities warned them not to allow it. Kristi Noem, Governor of South Dakota at the time, ignored them. The mayor threw up his hands and told the NY Times, “do you want me to build a wall around Sturgis or a wall around South Dakota, because that is the only way we could have stopped it.”

He was right, just like every other year, they rolled in. Concerts and crowded bars. Hardly a mask in sight. They even sold t-shirts mocking the pandemic. My kids bought me one off of e-bay as a father’s day joke the next year. “Screw Covid, I’m going to Sturgis.”

What happened next was predictable. Covid spread. It wasn’t like Las Vegas. What happens in Vegas stays in Vegas. What happens in Sturgis doesn’t stay there, it spreads everywhere.

In my book I summarized research estimates from the Center for Health Economics & Policy Studies at San Diego State University. They put the number of cases connected to Sturgis in the range of 115,000-260,000, or 10 to 20 percent of all cases in the US at the time. This was just one month after the rally occurred and it was still spreading. Yesterday a new research study was published that makes the wave of infection that spread out of Sturgis more visible.

In the left column of the graph above you can see the frontline of the Covid wave expanding outward from Sturgis. In the figure below you see the same wave in the top row but it also indicates the intensity of the caseload, with darker colors having more cases.

Sturgis was the epitome of the “you do you, I’ll do me” individual choice mindset at the height of the Covid pandemic. Many people simply wouldn’t accept that their choice had effects on other people. And those people weren’t just their partners and kids or their grandchildren and grandparents. It was also the kids on the school bus and the teachers in the schools. The people you worked with and the people they served. It was the doctors and nurses and other staff at the hospital. It was the barista at Starbucks and the maid at the hotel. The cashiers at CVS and the local grocery. It was all the people connected to them and onward and onward. Individual choices cascaded outward like ripples from a stone tossed in a pond. When you’re sitting in the middle of it, you can’t see the damage spread outward and spiral out of control. Nonetheless, it was there. And now we can see it.

Troy Tassier is a professor of economics at Fordham University and the author of The Rich Flee and the Poor Take the Bus: How Our Unequal Society Fails Us during Outbreaks.

If you would like to see a dynamic visualization of the paper results you can view two short 30 second movies here:

https://doi.org/10.1371/journal.pcbi.1013983.s007

https://doi.org/10.1371/journal.pcbi.1013983.s009

I have found the videos to play most reliably if you copy the address into a web browser and play it from there. In addition, there are other videos and figures of a second wave tracked by the researchers. I encourage you to look at them too. They are available in the “Supporting Information” section of the paper which is available here:

https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1013983#sec014

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sarcozona

1 day ago

Epiphyte City

Tsunamis hiding in plain sight: spreading depression in clinical neurology Friday March 13th, 2026 at 4:07 PM

‘It’s surreal’: US sanctions lock International Criminal Court judge out of daily life – The Irish Times Friday March 13th, 2026 at 12:49 AM

The Curious Case of the Disappearing Data Thursday March 12th, 2026 at 5:08 PM

Babies with COVID-19 develop more serious disease than those with RSV, US data reveal Thursday March 12th, 2026 at 5:07 PM

2.9% death rate for COVID, 0.4% for RSV

Medical societies recommend vaccination

This week's top reads

Up to 56,000 people died from COVID-19 or RSV last year

Our underwriters

Unrestricted financial support provided by

The COVID-19 pandemic at 6 years: Mass death, debilitation and media silence Thursday March 12th, 2026 at 5:06 PM

The ongoing toll: Excess deaths and new studies on Long COVID

The bipartisan dismantling of public health

The cumulative toll of mass reinfection and immune system damage

Screw Covid, I'm going to Sturgis. Thursday March 12th, 2026 at 5:05 PM

Tsunamis hiding in plain sight: spreading depression in clinical neurology
Friday March 13^th, 2026 at 4:07 PM

‘It’s surreal’: US sanctions lock International Criminal Court judge out of daily life – The Irish Times
Friday March 13^th, 2026 at 12:49 AM

The Curious Case of the Disappearing Data
Thursday March 12^th, 2026 at 5:08 PM

Babies with COVID-19 develop more serious disease than those with RSV, US data reveal
Thursday March 12^th, 2026 at 5:07 PM

The COVID-19 pandemic at 6 years: Mass death, debilitation and media silence
Thursday March 12^th, 2026 at 5:06 PM

Screw Covid, I'm going to Sturgis.
Thursday March 12^th, 2026 at 5:05 PM