Component

Neurological deficit score

Neurological deficit score. Species, exposure and limitations are retained in each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. No effect was observed when using the ice pad alone or high-dose dihydrocapsaicin at 1.5 mg/kg alone, while low-dose dihydrocapsaicin at 0.5 mg/kg reduced neurological deficits by 26%.

    Dihydrocapsaicin → Neurological deficit score source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/30090648.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c", "start_char": 0, "end_char": 2110, "text_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c"}
    experimental_model
    Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion
    exposure
    Low-dose dihydrocapsaicin at 0.5 mg/kg or high-dose at 1.5 mg/kg, an ice pad at 31 degrees, and the combination, with an external-temperature-control arm
    limitations
    A large randomised design with a dose-response surprise: the high dose alone did nothing while the low dose worked. That non-monotonicity is recorded because it contradicts the simple dose-response in the other records.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    Tripling the dose did not help and in this design the higher dose alone did nothing at all.
    primary_references
    [dhc-p30090648] Synergistically Induced Hypothermia and Enhanced Neuroprotection by Pharmacological and Physical Approaches in Stroke. (2018). https://pubmed.ncbi.nlm.nih.gov/30090648/ DOI: 10.14336/ad.2017.0817
    tissue_or_cell_type
    Brain

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 348–359

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion · source_derived_draft · unverified_draft

    ### dhc-high-dose-alone-failed No effect was observed when using the ice pad alone or high-dose dihydrocapsaicin at 1.5 mg/kg alone, while low-dose dihydrocapsaicin at 0.5 mg/kg reduced neurological deficits by 26%. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Tripling the dose did not help and in this design the higher dose alone did nothing at all. organism: Rat tissue_or_cell_type: Brain experimental_model: Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion limitations: A large randomised design with a dose-response surprise: the high dose alone did nothing while the low dose worked. That non-monotonicity is recorded because it contradicts the simple dose-response in the other records. exposure: Low-dose dihydrocapsaicin at 0.5 mg/kg or high-dose at 1.5 mg/kg, an ice pad at 31 degrees, and the combination, with an external-temperature-control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/30090648.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c", "start_char": 0, "end_char": 2110, "text_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c"} [dhc-p30090648] Synergistically Induced Hypothermia and Enhanced Neuroprotection by Pharmacological and Physical Approaches in Stroke. (2018). https://pubmed.ncbi.nlm.nih.gov/30090648/ DOI: 10.14336/ad.2017.0817
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Combination therapy of low-dose dihydrocapsaicin and an ice pad significantly improved every measured outcome compared with monotherapies, achieving hypothermia faster by 28.6% than the ice pad, 350% than low-dose dihydrocapsaicin and 200% than high-dose dihydrocapsaicin alone, reducing neurological deficits by 63% against 26% with low-dose alone, reducing reactive oxygen species at 6 and 24 hours, increasing ATP by 42.9% against 25%, and decreasing apoptotic cell death by 48.5% against 24.9%.

    Hypothermia induced by a drug rather than by physical cooling → Hypothermia induced by physical means such as an ice pad or cold fluid source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/30090648.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c", "start_char": 0, "end_char": 2110, "text_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c"}
    experimental_model
    Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion
    exposure
    Low-dose dihydrocapsaicin at 0.5 mg/kg or high-dose at 1.5 mg/kg, an ice pad at 31 degrees, and the combination, with an external-temperature-control arm
    limitations
    A large randomised design with a dose-response surprise: the high dose alone did nothing while the low dose worked. That non-monotonicity is recorded because it contradicts the simple dose-response in the other records.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    Drug plus ice pack cooled faster and protected better than either on its own.
    primary_references
    [dhc-p30090648] Synergistically Induced Hypothermia and Enhanced Neuroprotection by Pharmacological and Physical Approaches in Stroke. (2018). https://pubmed.ncbi.nlm.nih.gov/30090648/ DOI: 10.14336/ad.2017.0817
    tissue_or_cell_type
    Brain

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 335–346

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion · source_derived_draft · unverified_draft

    ### dhc-combination-beats-either Combination therapy of low-dose dihydrocapsaicin and an ice pad significantly improved every measured outcome compared with monotherapies, achieving hypothermia faster by 28.6% than the ice pad, 350% than low-dose dihydrocapsaicin and 200% than high-dose dihydrocapsaicin alone, reducing neurological deficits by 63% against 26% with low-dose alone, reducing reactive oxygen species at 6 and 24 hours, increasing ATP by 42.9% against 25%, and decreasing apoptotic cell death by 48.5% against 24.9%. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Drug plus ice pack cooled faster and protected better than either on its own. organism: Rat tissue_or_cell_type: Brain experimental_model: Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion limitations: A large randomised design with a dose-response surprise: the high dose alone did nothing while the low dose worked. That non-monotonicity is recorded because it contradicts the simple dose-response in the other records. exposure: Low-dose dihydrocapsaicin at 0.5 mg/kg or high-dose at 1.5 mg/kg, an ice pad at 31 degrees, and the combination, with an external-temperature-control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/30090648.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c", "start_char": 0, "end_char": 2110, "text_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c"} [dhc-p30090648] Synergistically Induced Hypothermia and Enhanced Neuroprotection by Pharmacological and Physical Approaches in Stroke. (2018). https://pubmed.ncbi.nlm.nih.gov/30090648/ DOI: 10.14336/ad.2017.0817
    Complete structured claim and evidence

  2. Neurological deficit scores in the dihydrocapsaicin group were significantly higher than in the cardiopulmonary resuscitation and body surface cooling groups, and there were significantly fewer apoptotic cells in the dihydrocapsaicin and body surface cooling groups than in the resuscitation group.

    Dihydrocapsaicin → Apoptotic cell death source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/29035676.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98", "start_char": 0, "end_char": 2035, "text_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98"}
    experimental_model
    Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays
    exposure
    Dihydrocapsaicin against cardiopulmonary resuscitation alone and against body surface cooling
    limitations
    Proposes the central mechanism and measures each step, but with six animals per group and immunohistochemical rather than functional readouts.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    Fewer brain cells died, by about as much as physical cooling achieved.
    primary_references
    [dhc-p29035676] The Molecular Mechanism and Neuroprotective Effect of Dihydrocapsaicin-Induced Mild Hypothermia After Cardiopulmonary Resuscitation in Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29035676/ DOI: 10.1089/ther.2017.0032
    tissue_or_cell_type
    Hypothalamus, ventral septum and cerebral cortex

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 439–450

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays · source_derived_draft · unverified_draft

    ### dhc-fewer-apoptotic-cells Neurological deficit scores in the dihydrocapsaicin group were significantly higher than in the cardiopulmonary resuscitation and body surface cooling groups, and there were significantly fewer apoptotic cells in the dihydrocapsaicin and body surface cooling groups than in the resuscitation group. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Fewer brain cells died, by about as much as physical cooling achieved. organism: Rat tissue_or_cell_type: Hypothalamus, ventral septum and cerebral cortex experimental_model: Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays limitations: Proposes the central mechanism and measures each step, but with six animals per group and immunohistochemical rather than functional readouts. exposure: Dihydrocapsaicin against cardiopulmonary resuscitation alone and against body surface cooling evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/29035676.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98", "start_char": 0, "end_char": 2035, "text_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98"} [dhc-p29035676] The Molecular Mechanism and Neuroprotective Effect of Dihydrocapsaicin-Induced Mild Hypothermia After Cardiopulmonary Resuscitation in Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29035676/ DOI: 10.1089/ther.2017.0032
    Complete structured claim and evidence

  3. In stroke mice, dihydrocapsaicin infusion begun 90 minutes after the start of reperfusion produced hypothermia, decreased infarct volume by 87% and improved neurofunctional score, and the hypothermic and neuroprotective effects were absent in TRPV1 knockout mice or in mice maintained normothermic with heat support.

    Hypothermia induced by a drug rather than by physical cooling → Cerebral infarct volume source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"}
    experimental_model
    Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion
    exposure
    Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm
    limitations
    The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Mouse
    plain_language
    The stroke damage fell by almost nine tenths, and only when the animal was actually allowed to get cold.
    primary_references
    [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
    tissue_or_cell_type
    Brain and cardiovascular system
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 309–320

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion · source_derived_draft · unverified_draft

    ### dhc-infarct-reduction In stroke mice, dihydrocapsaicin infusion begun 90 minutes after the start of reperfusion produced hypothermia, decreased infarct volume by 87% and improved neurofunctional score, and the hypothermic and neuroprotective effects were absent in TRPV1 knockout mice or in mice maintained normothermic with heat support. Condition category: machinery_impairment nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The stroke damage fell by almost nine tenths, and only when the animal was actually allowed to get cold. organism: Mouse tissue_or_cell_type: Brain and cardiovascular system experimental_model: Focal cerebral ischaemia-reperfusion in conscious wild-type and TRPV1 knockout mice with osmotic-pump infusion limitations: The two control arms are what make this the strongest record here: the knockout shows the receptor is required, and the heat-support arm shows the temperature drop rather than receptor activation is what protects. exposure: Dihydrocapsaicin 1.25 mg/kg subcutaneously, begun 90 minutes after the start of reperfusion, with normothermia by external heat support as a control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/24305062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17", "start_char": 0, "end_char": 1711, "text_sha256": "6f48560ff0df2e92e757c483dad96056155b0b629ddf0b5d5b41416201adfe17"} [dhc-p24305062] Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion. (2014). https://pubmed.ncbi.nlm.nih.gov/24305062/ DOI: 10.1152/ajpregu.00329.2013
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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