Chronic Inflammatory Demyelinating Polyneuropathy CIDP - caused by AstraZeneca

Jumping legal hurdles for Jab Harm recognition and compensation claims by victims and their loved ones can take years. Lawyers need to keep up with synonyms.

Sad case of a suicide by an AstraZeneca Jab victim, John Cross, has finally been reviewed and eligibility for compensation granted too late.

The story was covered on SkyNews on 16 June 2026.

UK solicitor Peter J Todd appears in the video and has published the family statement as a pdf for you to download.¹

The family statement includes:

John Cross received a single dose of the AstraZeneca COVID-19 vaccine on 26 January 2021. Two weeks later, he developed tingling and numbness in his feet, rapidly progressing to paralysis and requiring ventilation

Initially diagnosed and treated for Guillain–Barré syndrome (GBS), he later suffered relapses and was subsequently diagnosed with Chronic Inflammatory Demyelinating Polyneuropathy (CIDP).

Made aware by his doctors, he applied to the Vaccine Damage Payment Scheme (VDPS) in September 2021.

In July 2023, his claim was refused, with his disability assessed at 45–55%, below the 60% arbitrary threshold. The decision report contained inaccuracies, a lack of empathy and showed a distinct lack of understanding of his condition.

His illness was chronic and relapsing.

Following another relapse and facing further treatment, John took his own life in October 2023.

An inquest in February 2024 concluded he had endured a severe and debilitating illness since 2021.

His family pursued an appeal, but although the VDPS acknowledged errors, inexplicably it withdrew its earlier acceptance of causation.

John’s family sought expert medical evidence and proceeded to Tribunal.

In May 2026, more than five years after his diagnosis and just a few months away from the tribunal trial, the VDPS have conceded that the AstraZeneca vaccine caused John’s condition and that he met the 60% disability threshold.

“The VDPS took every possible step to avoid reversing their initial decisions, including the appointment of an eminent senior neurologist to comment on the condition without being provided with any details of our father’s case.

Public money has been spent in an effort to defend what we believed to be an indefensible position, and to apply pressure into stopping our pursuit of justice in Dad’s memory.

Ultimately, the VDPS conceded their positions only a few months prior to trial.

We did not give up.”

CIDP versus Guillain-Barré Syndrome

The latest version for CIDP on the US Comparative Toxicogenomics Database (CTD) shows a range of synonyms. Please click to enlarge.

The definition

A slowly progressive autoimmune demyelinating disease of peripheral nerves and nerve roots. Clinical manifestations include weakness and sensory loss in the extremities and enlargement of peripheral nerves. The course may be relapsing-remitting or demonstrate a step-wise progression. Protein is usually elevated in the spinal fluid and cranial nerves are typically spared. GUILLAIN-BARRE SYNDROME features a relatively rapid progression of disease which distinguishes it from this condition. (Adams et al., Principles of Neurology, 6th ed, p1337)

Here are the CTD synonyms for CIDP showing CTD needs more Human curation to overcome the AI collected duplicates.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy | Chronic Inflammatory Polyradiculoneuropathies | Chronic Inflammatory Polyradiculoneuropathy | Chronic Inflammatory Polyradiculopathies | Chronic Inflammatory Polyradiculopathy | CIDP | Inflammatory Polyradiculoneuropathies, Chronic | Inflammatory Polyradiculoneuropathy, Chronic | Inflammatory Polyradiculopathies, Chronic | Inflammatory Polyradiculopathy, Chronic | Polyneuropathy, Inflammatory Demyelinating, Chronic | Polyradiculoneuropathies, Chronic Inflammatory | Polyradiculoneuropathy, Chronic Inflammatory | Polyradiculopathies, Chronic Inflammatory | Polyradiculopathy, Chronic Inflammatory

CTD links CIDP to 594 genes.

Here is the CTD GBS landing page, stating clearly that Chronic Inflammatory Demyelinating Polyneuropathy is specifcally included, as well as the Acute, or Sudden Onset GBS.

The definition

An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)

Here are the CTD synonyms for GBS showing CTD needs more Human curation to overcome the AI collected duplicates.

Acute Autoimmune Neuropathies | Acute Autoimmune Neuropathy | Acute Infectious Polyneuritis | Acute Inflammatory Demyelinating Polyneuropathy | Acute Inflammatory Demyelinating Polyradiculoneuropathy | Acute Inflammatory Polyneuropathies | Acute Inflammatory Polyneuropathy | Acute Inflammatory Polyradiculoneuropathies | Acute Inflammatory Polyradiculoneuropathy | Autoimmune Neuropathies, Acute | Autoimmune Neuropathy, Acute | CIDP, INCLUDED | Demyelinating Polyradiculoneuropathy, Acute Inflammatory | Familial Guillain-Barre Syndrome | Familial Guillain-Barre Syndromes | GBS | Guillain Barre Syndrome | Guillain Barré Syndrome | Guillain-Barré Syndrome | Guillain Barre Syndrome, Familial | Guillain-Barre Syndrome, Familial | Guillain-Barré Syndromes | Guillain-Barre Syndromes, Familial | Guillaine Barre Syndrome | Guillaine-Barre Syndrome | Infectious Polyneuritis, Acute | Inflammatory Demyelinating Polyradiculoneuropathy, Acute | Inflammatory Polyneuropathies, Acute | Inflammatory Polyneuropathy Acute | Inflammatory Polyneuropathy, Acute | Inflammatory Polyradiculoneuropathies, Acute | Landry Guillain Barre Syndrome | Landry-Guillain-Barre Syndrome | Neuropathy, Acute Autoimmune | Polyneuritis, Acute Infectious | Polyneuropathy Acute, Inflammatory | Polyneuropathy, Acute Inflammatory | Polyneuropathy, Inflammatory Demyelinating, Acute | POLYNEUROPATHY, INFLAMMATORY DEMYELINATING, ACUTE; AIDP POLYNEUROPATHY, INFLAMMATORY DEMYELINATING, CHRONIC, INCLUDED | Polyradiculoneuropathies, Acute Inflammatory | Polyradiculoneuropathy, Acute Inflammatory | Polyradiculoneuropathy, Acute Inflammatory Demyelinating | Syndrome, Familial Guillain-Barre | Syndrome, Guillain-Barre | Syndrome, Guillain-Barré | Syndrome, Guillaine-Barre | Syndrome, Landry-Guillain-Barre

As mentioned by numerous authors, the causal link between numerous types of Jabs and GBS is clearly established by science, and now another legal admission.²

In the tragic case of John Cross, his symptoms appeared just 2 weeks after his jab, which I call Acute, and relapsed despite unspecified treatments, then defined as Chronic.

CIDP Literature

PubMed finds 4,232 papers when searching Chronic Inflammatory Demyelinating Polyneuropathy.³ You will see 170 papers published in 2026.

More mentions of drugs with Polyneuropathy as a known side effect.⁴⁵⁶⁷

I mentioned a 1983 report of Peripheral Neuropathy was scathing about a patient who kept his use of DMSO secret for 10 months from his examining neurologists who finally linked his condition to DMSO, rather than another suspect drug.⁸

Peripheral Neuropathy is also caused by Methylene Blue.⁹

Mechanism should be the focus

CIDP is one of numerous autoimmune diseases caused by Jabs.¹⁰

Once mechanism is understood, improved approaches to treatment might follow.

In 1996 Japanese researchers led by Nobuhiro Yuki were investigating CIDP and GBS.¹¹

Abstract

Unlike CNS myelin, Human peripheral nerve myelin has the acidic glycosphingolipids Sialosyl ParaGloboside (SPG), Sialosyl Lactosaminyl ParaGloboside (SLPG), and Sulfated Glucuronyl ParaGloboside (SGPG).

To elucidate the pathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating neuropathy (CIDP), we investigated the autoantibodies to peripheral nerve molecules in patients with these diseases and compared the frequency of the autoantibodies with that of autoantibody to GM1 which is present in both the CNS and PNS.

The report of Sheikh et al. (Ann. Neurol. 1995; 38: 350) that Campylobacter jejuni bears the SGPG epitope led us to study whether sera from patients with GBS subsequent to C. jejuni enteritis have anti-SGPG antibody; but, high anti-SGPG antibody titers were not found in the GBS patients from whom C. jejuni was isolated. Although the frequency of the anti-SPG, anti-SLPG and anti-SGPG antibodies were lower than that of the anti-GM1 antibody in GBS, 5 patients with demyelinating GBS had high IgG anti-SPG antibody titers.

IgG anti-SPG antibody may function in the development of demyelinating GBS. We found that 6 CIDP patients had elevated IgM anti-SGPG antibody titers. Immunoelectrophoresis failed to detect IgM M-protein in 3 of the patients.

IgM anti-SGPG antibody could be a diagnostic marker for a subgroup of CIDP with or without paraprotein.

In 1997 Nobuhiro Yuki showed that Endotoxin is implicated via molecular mimicry, as mentioned in my GBS article (reference 2 below).¹²

Abstract

Some patients developed Guillain-Barré syndrome (GBS) after being given Bovine Gangliosides.

Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside.

Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside.

The existence of molecular mimicry between GM1 and Lipopolysaccharide (Endotoxin) of C. jejuni isolated from a GBS patient and that between GQ1b and C. jejuni Lipopolysaccharides from patients with MFS are shown herein.

The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies and the development of GBS and MFS.

Many researchers have verified the finding by Yuki et al.

US Bioweapons developers are very interested in molecular mimicry.¹³

1. Statement by the Family of Mr John Cross

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3. https://pubmed.ncbi.nlm.nih.gov/?term=Chronic+Inflammatory+Demyelinating+Polyneuropathy

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11. N Yuki, Y Tagawa, S Handa. 1996. Autoantibodies to peripheral nerve glycosphingolipids SPG, SLPG, and SGPG in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. J Neuroimmunol. 70(1):1-6. doi: 10.1016/s0165-5728(96)00042-2.

12. N Yuki. 1997. Molecular mimicry between gangliosides and lipopolysaccharides of Campylobacter jejuni isolated from patients with Guillain-Barré syndrome and Miller Fisher syndrome. J Infect Dis. 176 Suppl 2:S150-3. doi: 10.1086/513800.

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