The site-selective rise in trigger-point activity under a cognitive stressor is a regional sympathetic vasoconstriction written to a skin territory, as in blushing or blanching. (True if a mental stressor produces a localized fall in skin perfusion over the tender point and not over control skin.)

The hypothesis that stress-induced trigger-point activation represents regional sympathetic vasoconstriction written to a specific skin territory is a speculative interpretation from proponent writings (SRC-JHONG-2026A). The ledger provides no laser Doppler, thermographic, or microvascular recordings demonstrating focal cutaneous vasoconstriction during cognitive tasks over trigger points. The strongest opposing argument is the known phenomenon of localized autonomic vascular responses like blushing, but its link to trigger point activation is unproven.

The proposal that stress-induced trigger-point activation represents regional sympathetic vasoconstriction written to a cutaneous territory is a theoretical conjecture without experimental verification. No studies have measured localized cutaneous perfusion drops coinciding with needle-EMG spikes during cognitive stressors. The strongest opposing consideration is that sympathetic activation can directly stimulate extrafusal or intrafusal muscle fibers via adrenergic receptors without requiring an intermediate vascular vasoconstrictive step.

This is the vascular-write interpretation of the McNulty result, and its own specified test — a localized fall in skin perfusion over the tender point and not over control skin under mental stress — has never been performed; the only anchor is the unverified second essay. The EMG data fit equally well with sympathetic drive to spindles or endplates without any vascular storage, a limitation VASO-E002 records explicitly. The strongest opposing consideration is that no vascular endpoint was measured in any stressor study, so the interpretation currently rides on plausibility alone.

No record tests the specific mechanism: no study measured localized skin perfusion over a tender point under a mental stressor. VASO-E002's own limitations note that sympathetic drive to spindles or endplates fits the EMG data without any vascular write, and the case's neural signature was partly qualified by the endplate-zone findings. This is one consistent reading among several, evidenced by none.

The stress-induced EMG change in VASO-E002 did not measure local skin perfusion, vascular caliber, or vasoconstriction, so it cannot identify the event as a regional sympathetic vascular write. A skeletal endplate or spindle response remains an adequate alternative. The strongest consideration for the claim is the site-selective stress response itself and the general prior that sympathetic activity can alter regional vascular tone, but the proposed causal bridge was not observed.

The stress experiment measured needle EMG but did not measure local skin perfusion, vascular caliber, or sympathetic vasoconstriction. It therefore cannot identify the site-selective electrical rise as a vascular event written to a skin territory. The strongest opposing consideration is the viable alternative explicitly noted in the evidence: sympathetic modulation of spindles or motor endplates without regional vascular storage.

The interpretation of the McNulty stressor effect as regional sympathetic vasoconstriction written to a skin territory is an untested mechanistic gloss offered in the second essay; no concurrent skin-perfusion measurement under cognitive stress at tender versus control sites exists in the ledger. Strongest opposing consideration is that sympathetic drive to spindles or endplates already fits the EMG data without any vascular intermediate.

The claim reinterprets C003’s selective EMG rise as regional sympathetic vasoconstriction written to a skin territory. No ledger record measures local skin perfusion over the tender point during a cognitive stressor; the interpretation is free-standing. Strongest opposing consideration: spindle or endplate sympathetic drive fits the EMG data without any vascular write.

No evidence record bears on this claim in either direction; it is an interpretive re-description of VASO-C003's finding, sourced only to the unverified second proponent essay. It is a genuine, cheap, falsifiable prediction — a mental stressor should produce a localized fall in skin perfusion over the tender point and not over control skin — testable tomorrow by laser Doppler or speckle (VASO-R016). The strongest opposing consideration is that the phenomenon it reinterprets was recorded by needle EMG in muscle, whereas this account relocates it to a skin territory; nothing yet connects the two measurements.

No evidence record in the ledger bears on this reinterpretation; it is a mechanistic proposal in an unverified proponent essay that the stress-evoked trigger-point signal is a regional sympathetic vasoconstriction written to a skin territory. Its virtue is that it is sharply falsifiable — a localised fall in skin perfusion over the tender point and not over control skin during mental arithmetic — and cheap to test at the surface (VASO-R016). Against it, the phenomenon it reinterprets is needle EMG in muscle, and cutaneous vasoconstrictor responses to mental stress are ordinarily regional to whole-limb rather than punctate, so the claim needs an addressing specificity that sympathetic skin physiology is not generally known to provide.

No evidence record; anchored only to the unverified second essay. It is the perforator account's reading of VASO-E002 and competes with the guarding and intramuscular readings. Site-specific sympathetic control of skin flow is ordinary physiology, but nothing has measured skin perfusion over a tender point during a stressor.

Held on its anchor (SRC-JHONG-2026A, p. 28), a source the ledger has not read and could not verify; no admitted evidence record. The parent record VASO-E002 on VASO-C003 fits this reading as well as the others but does not select it.

Held on its anchor alone, in a source the ledger has not been able to read; no admitted evidence record bears on it. It is the perforator account's reading of the stressor result recorded on the parent claim (VASO-E002), which measured muscle electrophysiology, not skin perfusion.

Held on its anchor alone, in a source (SRC-JHONG-2026A) the ledger has not read; no admitted evidence record bears on it. Featured as the perforator account's reading of the stress result.

Anchor-only: held on the proponent's second essay (SRC-JHONG-2026A), a source the ledger has not read, with no admitted evidence record. The reading — the stressor's site-selective rise as a regional sympathetic vasoconstriction written to skin — is stated, not observed.

Held on its anchor alone in a source the ledger has not been able to read (SRC-JHONG-2026A); no admitted evidence record bears on it.

Held on its anchor alone, in a source (SRC-JHONG-2026A) the ledger has not read; no admitted evidence record. It is the perforator account's reading of the stressor result on VASO-C003, and it makes a distinct, cheap prediction.

Held on its anchor alone in an unread source (SRC-JHONG-2026A); no admitted evidence record. The needle in McNulty 1994 recorded muscle, not skin, so nothing in the ledger bears on a cutaneous write.

Held on its anchor alone in SRC-JHONG-2026A, a source the ledger has not read; no admitted evidence record bears on it. It is the perforator account's reading of the McNulty result, catalogued as the essay states it.

Held on its anchor alone in SRC-JHONG-2026A, an unread self-published essay; no admitted evidence record. The mechanism it offers for the site-selective stressor result — regional sympathetic vasoconstriction written to a skin territory, as in blushing — is ordinary physiology stated as a reading, not a measurement at any tender point.

Held on its anchor alone, in the proponent's second essay, which the ledger has not been able to read. No admitted evidence record bears on it. It is the perforator account's reading of the McNulty result and is featured as one of three live readings of that one observation.

No evidence records in the ledger measure or evaluate regional cutaneous vasoconstriction over trigger points during cognitive stress. The claim represents a speculative mechanistic hypothesis advanced in proponent essays, but has never been tested experimentally. The strongest opposing consideration is that sympathetic outflow to cutaneous vascular beds displays dermatomal and somatotopic fine structure (as seen in blushing), making regional vasoconstrictive patterning biologically conceivable.

No evidence record bears on this mechanism claim; its only anchor is the unverified second essay's interpretive passage. The observation it interprets (C003) is itself a single weak study, and no perfusion measurement exists at any trigger point in the ledger. The keystone stressor block (R001) would test it, so it is untested rather than untestable.

The stress-induced electrical effect is supported, but no admitted record measured a site-selective skin-perfusion decrease during the stressor. Consequently, identifying the EMG response specifically as regional sympathetic vasoconstriction written to a skin territory is an untested attribution. The strongest opposing consideration is the conventional possibility of direct sympathetic modulation of spindles or motor endplates without a vascular intermediary.

Essay conjecture equating the stressor-induced EMG rise with regional cutaneous vasoconstriction analogous to blushing; no simultaneous skin-perfusion measurement under the stressor appears. Strongest opposing consideration is that a localized perfusion drop would be a strong positive if shown, yet remains untested.

No record measures skin perfusion over a tender point during a mental stressor, which is the claim's own True-if test, and the claim comes from the unverified second essay. Read literally, the identity is strained. The "site-selective rise" is intramuscular needle-EMG activity, the records on that signal place its generator at the motor endplate zone (E031, E032), and the stressor result is already explained by sympathetic drive to spindles or endplates without any vascular event (E002, E016). A localized narrowing of skin vessels could still accompany the EMG rise, so the version that treats it as a correlate remains open. Strongest opposing consideration: if "is" means identity rather than correlation, the endplate-zone evidence already tells against it and the verdict would move toward contradicted. I keep it unresolved, with low confidence, because the claim's own test concerns perfusion, which no one has measured.

Held on the proponent's second essay, which this site has not verified; no evidence record bears on it.