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Multiple Study Results Demonstrate COVID May Induce a Novel Delayed Brain Disorder Similar to SSPE The reporter advises caution in trusting injectable solutions to avoid contamination of the blood and potential health risks from morning-after effects

Imaging and longitudinal studies show that Long COVID results in similar conditions to Subacute Sclerosing Panencephalitis (SSPE).
WALTER M CHESNUT
JAN 26

记者叮嘱谨慎相信注射液，避免污染血液早晨后遗症健康隐患
多项研究结果表明，新冠肺炎可能会引发一种类似于 SSPE 的新型迟发性脑部疾病
影像学和纵向研究表明，长新冠肺炎会导致与亚急性硬化性全脑炎 (SSPE) 类似的病症。
沃尔特·M·切斯纳特
1月26日

https://open.substack.com/pub/wmcresearch/p/multiple-study-results-demonstrate

From left to right in the first row are cortical atrophy, white matter lesion, and vascular lesions and, in the second row, are lacunar lesion, vascular encephalopathy, and sinusitis.

It was four years ago that I wrote about a mechanism that I saw could be shared between Measles and COVID. With Measles, some individuals experience neuroinvasion which can lead to a form of viral persistence in which its N protein causes a fatal neurological disease, years later.

Subacute sclerosing panencephalitis (SSPE) is thought to be a long-term measles virus infection. The virus sometimes enters the brain during a measles infection. Measles virus may cause immediate symptoms of brain infection (encephalitis), or the virus may remain in the brain for a long time without causing problems.

Subacute Sclerosing Panencephalitis (SSPE)
https://www.merckmanuals.com/home/children-s-health-issues/common-viral-infections-in-infants-and-children/subacute-sclerosing-panencephalitis-sspe

Given that far, far more individuals experience COVID neuroinvasion, the parallel greatly concerned (and still concerns) me.

A DARK STORM GATHERING: DISTURBING PARALLELS BETWEEN THE MEASLES N PROTEIN AND THE SARS-CoV-2 S PROTEIN: SUBACUTE SCLEROSING PANENCEPHALITIS
https://wmcresearch.substack.com/p/a-dark-storm-gathering-disturbing

Now, years later, we have the results of several studies which confirm that long-term damage similar to SSPE is being caused by Long COVID. Let me be clear; I am not stating that it IS SSPE. I am stating that COVID may induce a delayed, persistent viral encephalitis analogous to Subacute Sclerosing Panencephalitis.

First, let’s look at imaging results.

In SSPE, lesions of high signal intensity on T2-weighted images are the most common finding; they frequently involve the periventricular or subcortical white matter.

Thirty-four MRI studies of 26 patients with subacute sclerosing panencephalitis are reported. Lesions of high signal intensity on T2-weighted images are the most common finding; they frequently involve the periventricular or subcortical white matter. Lesions tend to start in the cortex-subcortical white matter and progress with periventricular white matter involvement and diffuse cerebral atrophy. Pial and parenchymal contrast enhancement, local mass effect of parenchymal lesions, and involvement of the splenic portion of the corpus callosum are not infrequent.

MRI findings in subacute sclerosing panencephalitis
https://pubmed.ncbi.nlm.nih.gov/8909443/

Note, again, that they occur in the periventricular and subcortical white matter. This is also the case in Long COVID.

White matter lesions: the Fazekas scale and the Standards for Reporting Vascular Changes on Neuroimaging (STRIVE) criteria are the most commonly used standards. White matter lesions are identified on FLAIR and T2-weighted images as bright (hyperintense) areas located in the periventricular or deep white matter.

Diffuse white matter hyperintensities are observed on FLAIR images. Subcortical infarcts, dilated perivascular spaces, or signs of microvascular disease may also be present. Cortical and subcortical atrophy is frequently associated with ventricular enlargement [17].

Brain Structural Abnormalities in Patients with Post-COVID-19 Headache
https://www.mdpi.com/2035-8377/17/4/50

Another aspect of SSPE is the presence of demyelination and neurofibrillary tangles.

Early stages of CNS infection cause cellular swelling and oxidative damage to genetic material. It is thought that lipid peroxidation causes demyelination in the early course of the disease. This is followed by an acute inflammatory phase where nucleocapsids are evident in oligodendrocytes and neurons, while granulofilamentous inclusions within nuclear bodies are present in astrocytes. Inflammatory cells can be found in perivascular regions along with scattered areas of demyelination and spongiosis.[4][5][8] Neurofibrillary tangles have been found in some cases of SSPE.[9]

Subacute Sclerosing Panencephalitis
https://www.ncbi.nlm.nih.gov/books/NBK560673/

A Swedish study showed that there is, indeed, a marked increase in the occurrence of demyelinating diseases post COVID.

Hospital admission for COVID-19 was associated with raised risk of subsequent non-multiple sclerosis demyelinating disease, but only 12 individuals had this outcome among the exposed, and of those, 7 has an unspecified demyelinating disease diagnosis. Rates per 100 000 person-years (and 95% confidence intervals) were 3.8 (3.6–4.1) among those without a COVID-19 diagnosis and 9.0 (5.1–15.9) among those admitted to hospital for COVID-19, with an adjusted hazard ratio and (and 95% confidence interval) of 2.35 (1.32–4.18, P = 0.004). Equivalent associations with multiple sclerosis (28 individuals had this outcome among the exposed) were rates of 9.5 (9.1–9.9) and 21.0 (14.5–30.5) and an adjusted hazard ratio of 2.48 (1.70–3.61, P < 0.001).

SARS-CoV-2 infection and risk of subsequent demyelinating diseases: national register–based cohort study
https://academic.oup.com/braincomms/article/6/6/fcae406/7909395

A just-published study shows the relation between Long COVID and the potential development (definite presence of amyloid) of neurofibrillary tangles.

Our study found that patients who develop N-PASC after COVID-19 might share certain clinicopathological features with AD. Indeed, while Tau functions adaptively to stabilise neuronal microtubules under normal physiologic conditions23 and can also be dysregulated and spread by reactive glia,41 especially in the context of chronic inflammation.42 However, the prognostic implications of increases in circulating pTau-181 absent concurrent amyloidosis are unknown. Usually, β-amyloid peptide plays a central role in triggering Tau phosphorylation in ADRD,43 a process that leads to subsequent microtubule destabilisation resulting in threads that coalesce into neuronal tangles.44 Intriguingly, in this study we found that evidence of increased pTau-181 was associated with increases in AB40/42 ratios consistent with a pTau-mediated ADRD. Further studies are needed to determine whether the increased levels of plasma pTau-181 correlate with evidence of cerebral Tauopathy and, if results are replicated, pTau-181 might aid in diagnosis and might serve as an important monitoring and therapeutic target.45

We found that individuals who developed N-PASC had higher Aβ40/42 ratios (AUC = 0.63, P = 0.007), NfL (AUC = 0.59, P = 0.002), and IAB values (AUC = 0.74, P < 0.001) before developing COVID-19. Higher values suggest that N-PASC might be more likely in those individuals who have heightened vulnerability to neurological disease. Amyloidosis often requires a secondary neuropathology to elicit the most severe symptomatology. If these findings indicate that cerebral amyloidosis is present, even in its mildest forms, then the post-COVID-19 increase in pTau-181 may correspond to the onset of pathological Alzheimer’s disease.

Increased phosphorylated tau (pTau-181) is associated with neurological post-acute sequelae of coronavirus disease in essential workers: a prospective cohort study before and after COVID-19 onset
https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(25)00556-0/fulltext

So, we have evidence that COVID may be inducing a potentially very harmful long term CNS disorder. Why this concerns me far more than the SSPE complication of Measles is something that has concerned me from Day One: Reinfections. Measles infection almost always results in lifelong immunity. COVID infection can reoccur within weeks – and regularly. I will continue to investigate this phenomenon, seek therapeutics, and continue to report back to you. Please have a blessed week.

从左右进入第一行，是皮质萎缩，白质病变和血管病变，并且在第二行中，是血管疮病变，血管脑病和鼻窦炎。 这四年前我写了关于我所看到的机制可以在麻疹和科迪德之间分享。 有麻疹，一些人经历神经蛋白，可以导致一种病毒持久性，其中N蛋白导致致命神经疾病。 亚急性硬化脑膜炎（SSPE）被认为是长期麻疹病毒感染。 病毒有时会在麻疹感染期间进入大脑。 麻疹病毒可能导致脑感染的直接症状（脑炎），或者病毒可能在大脑中留在大脑中长时间而不会引起问题。 亚急性硬化脑膜炎（SSPE）https://www.merckmanuals.com/home/children-s-health-issuess/common-viral-infections-in-infants-and -children/ 一个黑暗的风暴聚集：麻疹N蛋白和SARS-COV-2 S蛋白质之间的扰乱平面：亚急性硬化终连脑炎HTTPS://WMCRESEARCH.substack.com/p/a-dark-storm-gathering 让我清楚; 我并没有说它是SSPE。 我陈述Covid可能诱导延迟，持续的病毒性脑炎，类似于亚急性硬化终连脑炎。 首先，让我们看看成像结果。 在SSPE中，T2加权图像上的高信号强度的病变是最常见的发现; 它们经常涉及围手术或皮质下白物质。 报告了26例亚急性硬化脑膜炎患者的34例MRI研究。 T2加权图像上高信号强度的病变是最常见的发现; 它们经常涉及围手术或皮质下白物质。 病变倾向于从皮质 - 皮质片性白质，并具有脑室白质受累和弥漫性脑萎缩的进展。 药物和实质对比增强，实质损伤的局部质量效应，胼callosum的脾脏部分的涉及不常见。 Supacute Serulate脑炎HTTPS://Pubmed.ncbi.nlm.nih.gov/8909443/再次注意，它们在围手术和皮质下的白质中进行了说明。 这也是长Covid的情况。 白质病变：Fazekas规模和报告神经影像血管变化（努力）标准的标准是最常用的标准。 白质病变在Flair和T2加权图像上鉴定为位于围手术或深白物质中的明亮（超固定）区域。 在Flair图像上观察到弥漫性白耐土性明显。 还可以存在细胞梗塞，扩张的血管内空间或微血管疾病的迹象。 皮质和皮质萎缩通常与心室扩大有关[17]。 Covid-19头痛患者的脑结构异常https://www.mdpi.com/2035-8377/17/4/50 SSPE的另一个方面是存在脱髓鞘和神经纤维纤维缠结。 CNS感染的早期阶段导致遗传物质的细胞溶胀和氧化损伤。 据认为，脂质过氧化会导致疾病早期脱髓鞘。 随后是急性炎症阶段，其中核衣壳在少偶突胶质细胞和神经元中是明显的，而核体内的粒状夹杂物存在于星形胶质细胞中。 炎症细胞可以在血管区中发现，以及分散区域的脱髓鞘和水肺症。[4] [5] [8] 在SSPE的某些情况下已发现神经纤维纤维缠结。[9] Subacute Sylerulase脑炎https://www.ncbi.nlm.nih.gov/books/nbk560673/瑞典研究表明，事实上，发生了显着的增加 Covid-19的医院入学与随后的非多发性硬化症脱髓鞘疾病的提高风险有关，但只有12个个人在暴露的情况下具有这种结果，其中7名具有未指明的脱髓鞘疾病诊断。 每10 000人（和95％的置信区间）的费率为3.8（3.6-4.1），其中没有Covid-19诊断和9.0（5.1-15.9），其中包含对Covid-19的医院，具有调整后的危险比 与多发性硬化的等同缔合（28个曝光的结果）是9.5（9.1-9.9）和21.0（14.5-30.5）的速率，调整后的危险比为2.48（1.70-3.61，p SARS-COV-2感染和随后的脱髓苷酸疾病的风险：基于国家寄存器的队列研究HTTPS://academer.oup.com/braincomms/article/6/6/fcae406/7909395 a只是 - 我们的研究发现，在Covid-19之后开发N-PASC的患者可能与广告共享某些临床病理学特征。 实际上，虽然TAU适应性地在正常的生理条件下稳定神经元微管，但也可以通过反应性胶质胶质胶质剂，特别是在慢性炎症的范围内进行过度消退和扩散。然而，预后意义 通常，β-淀粉样肽在触发ADRD中的Tau磷酸化方面发挥着核心作用，43例导致随后的微管稳定化的过程导致导致螺纹的螺纹粘性， 需要进一步的研究来确定增加的血浆ptau-181水平是否与脑介性的证据相关，如果结果复制，则Ptau-181可能有助于诊断，并可作为一个重要的监测和治疗目标.45我们 更高的值表明，在那些对神经疾病脆弱性脆弱的人中，N-PASC可能更有可能。 淀粉样症通常需要次要神经病理学，以引发最严重的症状。 如果这些发现表明存在脑淀粉样蛋白病，即使在其最温和的形式中，PTAU-181的后Covid-19增加也可能对应于病理阿尔茨海默病的发作。 增加磷酸化Tau（Ptau-181）与基本工作者中冠状病毒病的神经系统后急性后遗症有关：在Covid-19发作之前和之后的前瞻性队列研究：/ wwww.thelancet。 为什么这令我担心我的SSPE对麻疹的并发症是从第一天开始关注我的东西：重生。 麻疹感染几乎总是导致终身免疫力。 Covid感染可以在几周内重新加以在几周内和定期的。 我将继续调查这种现象，寻求治疗方法，并继续向您汇报。 请有一个幸福的一周。