Question explored with the scientific record
Conversation so far
- 1 vaccine induced primary anhidrosis. What would an MRI-PET scan with glucose radio tracer expect to show + a private exchange
- 2 Wouldn't FDG-PET show hypometabolism of eccrine glands rather than hypermetabolism?
- 3 What PET tracer or higher-resolution imaging could target eccrine glands?
- 4 ok, from the formally identified autonomic symptoms described, what would show on PET-MRI, and if not this test, what is the next best line of investigation
Answered on this page ↓
ok, from the formally identified autonomic symptoms described, what would show on PET-MRI, and if not this test, what is the next best line of investigation
FDG-PET/MRI would be expected to show nothing diagnostic in primary anhidrosis; the tests that actually localize the problem are sweat function tests and, if needed, a skin biopsy.
The retrieval is thin for this exact question. It contains no imaging series of anhidrosis and no PET study of eccrine glands. What it does contain is a classification of sweating disorders that separates anhidrosis into congenital and acquired forms [2], and a body of neuroinflammation PET work showing that even dedicated tracers like TSPO ligands struggle with specificity and reproducibility [1]. That second point matters: if research-grade inflammation tracers cannot cleanly resolve a signal, a plain glucose tracer aimed at millimeter-scale sweat coils will show background noise at best.
So the expected PET-MRI finding in vaccine-associated primary anhidrosis is essentially normal, or at most subtle non-specific dermal signal. A normal scan is not a clean bill of health here; it is a limitation of the tool. The mechanism, if it is autoimmune autonomic injury, lives in the nerve fibers and ganglia, not in glucose-hungry tissue PET can see.
The next best line of investigation, outside this retrieval but standard autonomic practice: a thermoregulatory sweat test to map where sweating fails, quantitative sudomotor axon reflex testing (QSART) to separate a central from a peripheral sweat-pathway lesion, and autonomic reflex panels including heart-rate and blood-pressure responses. If those point to a peripheral lesion, a punch skin biopsy with nerve-fiber staining is the confirmatory step. Serology for ganglionic AChR antibodies belongs in the same workup.
My call: skip PET-MRI as a diagnostic step for the anhidrosis itself; go straight to thermoregulatory sweat testing plus QSART, with skin biopsy if the pattern is unclear. Confidence: high on PET-MRI's low yield, moderate on the exact sequencing of the alternative tests.
Sources used 2
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Imaging neuroinflammation in Alzheimer's disease and other dementias: Recent advances and future directions
A comprehensive review of in vivo imaging of neuroinflammation across Alzheimer's disease and other dementias, focusing on TSPO PET ligands (classic and second-generation), alternative imaging targets, limitations, and future directions for multimodal approaches.
DOI: 10.1016/j.jalz.2014.08.105 -
Classification of Systemic and Localized Sweating Disorders
This study classifies hyperhidrosis into generalized and focal types, detailing their causes, symptoms, and implications for diagnosis and treatment.
DOI: 10.1159/000446753