The Exclusion That Wasn't

A landlord's tenant leases warehouse space, promises to name the landlord as an additional insured, and buys a commercial general liability policy to do it. The tenant's own employee is then badly hurt on the premises and sues the landlord. Does the tenant's CGL carrier owe the landlord a defense and indemnity, or do the policy's employee and workers' compensation exclusions wipe out coverage? In SL 10 Park Place, LLC v. Utica National Insurance Group, the Appellate Division answered squarely for the additional insured, and in doing so drew a bright line that every workers' compensation practitioner should understand.

Long COVID's Dopamine Trail

For years, workers disabled by long COVID have described brain fog, memory loss, apathy, and slowed thinking that employers and carriers dismissed as subjective or unrelated to the job. A new study published in eBioMedicine (a Lancet-family journal) supplies something these claims have historically lacked: an objective, measurable brain signature of the injury. For the workers' compensation bar, that shift from symptom description to biological proof is the story.

What the study found

Researchers at the Brain Health Imaging Centre and the University of Toronto used PET imaging to measure vesicular monoamine transporter 2 (VMAT2), an accepted index of dopamine-releasing neuron density, in the striatum — the brain region governing motivation, movement, and memory. Comparing 24 adults who had long COVID with persistent neuropsychiatric symptoms against 24 age-matched healthy controls, the team found VMAT2 binding was 16% to 20% lower across three striatal regions in the long COVID group.

Crucially, the reductions tracked symptom severity. Lower binding in the ventral striatum correlated with apathy; in the dorsal putamen with motor slowing; and in the dorsal caudate with memory decline. Roughly a quarter of the variance in those symptoms was associated with the measured neuron loss. The authors interpret the pattern as reduced dopaminergic terminal integrity — loss of dopamine nerve terminals — comparable in magnitude to mild-to-moderate Parkinson's disease.

The researchers are careful about limits: the sample is small, participants were selected for significant neuropsychiatric symptoms, and an imaging correlation cannot by itself prove causation. An accompanying commentary notes the changes may not be permanent and calls for longitudinal follow-up. Those caveats matter — but they do not erase the significance of a reproducible, objective marker where none existed before.

Why this matters for workers' compensation

Long COVID claims have always turned on two hard questions: Did the job cause it, and how disabling is it? This research speaks directly to both.

●      Objective medical evidence. New Jersey — like most jurisdictions — requires more than a claimant's subjective complaints to establish a psychiatric or neurologic occupational disease. A biomarker of neuronal injury is precisely the kind of objective corroboration adjudicators look for.

●      Causation and permanency. Evidence that long COVID produces a Parkinson's-comparable loss of dopamine neurons strengthens arguments that resulting apathy, cognitive slowing, and memory deficits are organic sequelae of the infection — not pre-existing or purely psychological — and may support findings of lasting, ratable disability.

●      The occupational-disease framework. Under N.J.S.A. 34:15-31, a compensable occupational disease must be due in a material degree to conditions characteristic of or peculiar to the employment. For essential and frontline workers exposed on the job, biological proof of injury bolsters the nexus between workplace exposure and a measurable, disabling condition.

●      Rebutting the “ordinary disease of life” defense. Carriers routinely argue COVID is a common community illness, not an occupational hazard. Documented, lasting neurological injury reframes the dispute — the issue becomes the demonstrable sequelae of a workplace exposure, not merely where a common virus was contracted.

●      A treatment and mitigation angle. The authors suggest dopamine-augmenting therapies as a research direction. If effective treatments emerge, expect disputes over reasonable and necessary medical care, and over whether symptoms are permanent or amenable to mitigation.

None of this converts a difficult claim into an easy one. Imaging shows association, not causation, and defense experts will press the study's small sample and selection criteria. But the terrain has moved: petitioners can now point to a peer-reviewed, objective neurological substrate for symptoms that were long treated as unprovable.

The New Jersey proof standard

New Jersey courts have long demanded objective medical proof for occupational claims involving the mind and nervous system. In Goyden v. State Judiciary, 256 N.J. Super. 438 (App. Div. 1991), aff'd, 128 N.J. 54 (1992), the Appellate Division required objective evidence of workplace conditions sufficient to contribute to a psychiatric disability — not the claimant's say-so alone. In Brunell v. Wildwood Crest Police Dept., 176 N.J. 225 (2003), the Supreme Court elaborated on the “characteristic of or peculiar to” requirement for occupational disease. And in Magaw v. Middletown Bd. of Educ., 323 N.J. Super. 1 (App. Div. 1999), the court accepted a well-founded medical nexus between disease and workplace where supported by sufficient objective evidence. A validated brain-imaging biomarker fits squarely within the kind of proof these decisions contemplate.

The takeaway

This is early science, not settled law — and practitioners should present it with appropriate candor about its limits. Still, it marks a turning point. For the first time, the invisible, dismissed symptoms at the center of long COVID disability claims have a visible, measurable correlate in the brain. Attorneys, carriers, employers, and adjudicators should watch this line of research closely; it may become a recurring feature of medical proofs in the next generation of long COVID compensation litigation.

Sources

Liu YK, Persaud D, Vieira EL, et al. Loss of vesicular monoamine transporter 2 in striatum of long COVID and relationship to neuropsychiatric symptoms. eBioMedicine (2026). https://doi.org/10.1016/j.ebiom.2026.106339

Bergeson L. New study offers clues about long COVID's brain symptoms. CIDRAP, University of Minnesota (2026).

Guedj E, Beckman D. Accompanying commentary. eBioMedicine (2026).

Goyden v. State Judiciary, 256 N.J. Super. 438 (App. Div. 1991), aff'd, 128 N.J. 54 (1992).

Brunell v. Wildwood Crest Police Dept., 176 N.J. 225 (2003).

Magaw v. Middletown Bd. of Educ., 323 N.J. Super. 1 (App. Div. 1999).

N.J.S.A. 34:15-31 (compensable occupational disease); N.J.S.A. 34:15-36 (proof of disability).

About the Author

Jon L. Gelman of Wayne, NJ, is the author of NJ Workers' Compensation Law (West-Thomson-Reuters) and co-author of the national treatise Modern Workers' Compensation Law (West-Thomson-Reuters).

Blog: Workers' Compensation

LinkedIn: JonGelman

LinkedIn Group: Injured Workers Law & Advocacy Group

Author: Workers' Compensation Law West-Thomson-Reuters

Blue Sky: jongelman@bsky.social

Substack: jongelman.substack.com

© 2026 Jon L. Gelman. All rights reserved.

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