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4
Pathophys.
5
Phenotypes
4
Pathograph
4
Treatments
4
Subtypes
1
Deep Research

Subtypes

4
Carotid Artery Dissection
Cervical artery dissection involving the extracranial carotid artery.
Vertebral Artery Dissection
Cervical artery dissection involving the extracranial vertebral artery.
Spontaneous Cervical Artery Dissection
Dissection without major trauma, often occurring in the setting of multifactorial arterial-wall susceptibility and minor mechanical triggers.
Traumatic Cervical Artery Dissection
Dissection temporally associated with clinically significant neck or head trauma.

Pathophysiology

4
Arterial Wall Susceptibility
Multifactorial arterial-wall susceptibility, including connective-tissue dysplasia, systemic vasculopathy, and rare monogenic connective-tissue disease, lowers the threshold for cervical arterial wall injury.
fibroblast link
extracellular matrix organization link ⚠ ABNORMAL
Show evidence (2 references)
PMID:38791244 SUPPORT Human Clinical
"The clinical, radiological, and histological characteristics of systemic vasculopathy and undifferentiated connective tissue dysplasia are present in up to 70% of individuals with sporadic CeAD."
This supports connective-tissue and systemic-vasculopathy susceptibility as common background biology for sporadic cervical artery dissection.
PMID:38791244 SUPPORT Human Clinical
"Monogenic heritable connective tissue diseases account for fewer than 5% of cases of CeAD."
This supports rare monogenic connective-tissue disease as a recognized but minority cause of cervical artery dissection susceptibility.
Arterial Wall Tear and Intramural Hematoma
A tear in the intima or bleeding within the arterial wall separates vessel wall layers, creating an intramural hematoma that narrows the lumen or forms a pseudoaneurysm.
endothelial cell link
response to wounding link ↑ INCREASED
Show evidence (2 references)
PMID:25684164 PARTIAL Human Clinical
"We included patients with extracranial carotid and vertebral dissection with onset of symptoms within the past 7 days."
The CADISS trial population confirms extracranial carotid and vertebral dissection as the clinical substrate for this disorder; the abstract does not itself describe the arterial wall microanatomy, so this is partial support.
PMID:37957581 SUPPORT Human Clinical
"In the acute and subacute stage, the typical sign detection of intramural hematoma and Grade II enhancement revealed by HR-MRI was higher than the observations in the chronic stage (P = 0.000/0.000/0.016), while there was no significant difference by MRA (P = 0.902)."
Vessel-wall imaging directly supports intramural hematoma as an acute and subacute imaging sign of cervicocranial artery dissection.
Molecular Stress and Vascular Remodeling Signatures
Peripheral-blood transcriptomic changes in CeAD implicate molecular stress, senescence-associated signaling, mitochondrial dysfunction, and epithelial-mesenchymal plasticity as candidate mechanisms that may accompany arterial-wall vulnerability and remodeling.
cellular senescence link ↑ INCREASED mitochondrial organization link ⚠ ABNORMAL
Show evidence (1 reference)
PMID:38791244 SUPPORT Human Clinical
"We found potential correlations between CeAD and the dysregulation of genes linked to nucleolar stress, senescence-associated secretory phenotype, mitochondrial malfunction, and epithelial-mesenchymal plasticity."
This transcriptomic study supports candidate molecular stress and vascular remodeling pathways associated with CeAD.
Thromboembolism and Cerebral Ischemia
Damaged arterial endothelium and disturbed flow promote local thrombosis and embolization to cerebral arteries.
platelet link
blood coagulation link ↑ INCREASED
Show evidence (1 reference)
PMID:25684164 SUPPORT Human Clinical
"Extracranial carotid and vertebral artery dissection is an important cause of stroke, especially in young people."
This directly supports cervical artery dissection as a cause of ischemic cerebrovascular events.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Cervical Artery Dissection Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

5
Cardiovascular 1
Ischemic Stroke OCCASIONAL Ischemic stroke (HP:0002140)
Show evidence (1 reference)
PMID:25684164 SUPPORT Human Clinical
"Extracranial carotid and vertebral artery dissection is an important cause of stroke, especially in young people."
The trial background directly supports stroke as a major clinical consequence of cervical artery dissection.
Nervous System 1
Headache COMMON Headache (HP:0002315)
Show evidence (1 reference)
PMID:25684164 SUPPORT Human Clinical
"The major presenting symptoms were stroke or transient ischaemic attack (n=224) and local symptoms (headache, neck pain, or Horner's syndrome; n=26)."
Headache is explicitly listed as a local presenting symptom in the CADISS cervical dissection cohort.
Other 3
Neck Pain COMMON Neck pain (HP:0030833)
Show evidence (1 reference)
PMID:25684164 SUPPORT Human Clinical
"The major presenting symptoms were stroke or transient ischaemic attack (n=224) and local symptoms (headache, neck pain, or Horner's syndrome; n=26)."
Neck pain is included among local presenting symptoms in symptomatic cervical artery dissection.
Transient Ischemic Attack COMMON Transient ischemic attack (HP:0002326)
Show evidence (1 reference)
PMID:25684164 SUPPORT Human Clinical
"The major presenting symptoms were stroke or transient ischaemic attack (n=224) and local symptoms (headache, neck pain, or Horner's syndrome; n=26)."
The CADISS cohort explicitly identifies transient ischemic attack among major presenting symptoms in symptomatic cervical dissection.
Horner Syndrome OCCASIONAL Horner syndrome (HP:0002277)
Show evidence (1 reference)
PMID:25684164 SUPPORT Human Clinical
"The major presenting symptoms were stroke or transient ischaemic attack (n=224) and local symptoms (headache, neck pain, or Horner's syndrome; n=26)."
Horner syndrome is explicitly listed among local presenting symptoms.
💊

Treatments

4
Antithrombotic Therapy
Action: Pharmacotherapy NCIT:C15986
Agent: aspirin warfarin
Antiplatelet or anticoagulant therapy is used to reduce recurrent thromboembolic events in appropriate patients.
Show evidence (2 references)
PMID:25684164 SUPPORT Human Clinical
"We found no difference in efficacy of antiplatelet and anticoagulant drugs at preventing stroke and death in patients with symptomatic carotid and vertebral artery dissection but stroke was rare in both groups, and much rarer than reported in some observational studies."
The randomized CADISS trial supports antiplatelet or anticoagulant antithrombotic management, without evidence that one strategy is superior.
PMID:34746432 SUPPORT Human Clinical
"Based on evidence from two phase 2 RCTs that have shown no difference between the benefits and risks of anticoagulants versus antiplatelets in the acute phase of symptomatic EAD, we strongly recommend that clinicians can prescribe either option."
The ESO guideline supports either anticoagulant or antiplatelet therapy in acute symptomatic extracranial artery dissection.
Aspirin Therapy
Action: aspirin pharmacotherapy Ontology label: Pharmacotherapy NCIT:C15986
Agent: aspirin
Aspirin is one antiplatelet option for cervical artery dissection, but TREAT-CAD did not prove aspirin non-inferior to vitamin K antagonist anticoagulation.
Show evidence (1 reference)
PMID:33765420 PARTIAL Human Clinical
"Our findings did not show that aspirin was non-inferior to vitamin K antagonists in the treatment of cervical artery dissection."
TREAT-CAD directly evaluates aspirin in cervical artery dissection but qualifies its role because non-inferiority to vitamin K antagonists was not shown.
Intravenous Thrombolysis for Acute Ischemic Stroke
Action: thrombolytic therapy Ontology label: Thrombolytic Therapy NCIT:C15338
Agent: alteplase
Intravenous alteplase is recommended for eligible patients with extracranial artery dissection and acute ischemic stroke within the standard stroke treatment window.
Show evidence (1 reference)
PMID:34746432 SUPPORT Human Clinical
"In EAD patients with acute ischemic stroke, we recommend using intravenous thrombolysis (IVT) with alteplase within 4.5 hours of onset if standard inclusion/exclusion criteria are met, and mechanical thrombectomy in patients with large vessel occlusion of the anterior circulation."
The ESO guideline directly supports IV alteplase for eligible extracranial artery dissection patients with acute ischemic stroke.
Mechanical Thrombectomy
Action: thrombectomy for stroke Ontology label: Thrombectomy for Stroke NCIT:C191635
Mechanical thrombectomy is used in eligible cervical-artery-dissection patients when acute ischemic stroke is complicated by anterior-circulation large-vessel occlusion.
Show evidence (1 reference)
PMID:34746432 SUPPORT Human Clinical
"In EAD patients with acute ischemic stroke, we recommend using intravenous thrombolysis (IVT) with alteplase within 4.5 hours of onset if standard inclusion/exclusion criteria are met, and mechanical thrombectomy in patients with large vessel occlusion of the anterior circulation."
The ESO guideline directly supports thrombectomy for extracranial artery dissection with anterior-circulation large-vessel occlusion.
{ }

Source YAML

click to show
name: Cervical Artery Dissection
creation_date: "2026-05-06T11:59:10Z"
updated_date: "2026-05-06T13:06:21Z"
category: Complex
description: >-
  Cervical artery dissection is a cervicocephalic arterial wall injury in the
  carotid or vertebral arteries that produces an intramural hematoma, luminal
  stenosis or pseudoaneurysm, and risk of thromboembolic ischemic stroke.
disease_term:
  preferred_term: cervical artery dissection
  term:
    id: MONDO:0006061
    label: cervical artery dissection
parents:
- Vascular Disorder
- Cerebrovascular Disease
synonyms:
- Cervicocephalic artery dissection
- CeAD
- Carotid or vertebral artery dissection
- Extracranial carotid and vertebral artery dissection
has_subtypes:
- name: Carotid Artery Dissection
  description: >-
    Cervical artery dissection involving the extracranial carotid artery.
- name: Vertebral Artery Dissection
  description: >-
    Cervical artery dissection involving the extracranial vertebral artery.
- name: Spontaneous Cervical Artery Dissection
  description: >-
    Dissection without major trauma, often occurring in the setting of
    multifactorial arterial-wall susceptibility and minor mechanical triggers.
- name: Traumatic Cervical Artery Dissection
  description: >-
    Dissection temporally associated with clinically significant neck or head
    trauma.
pathophysiology:
- name: Arterial Wall Susceptibility
  description: >-
    Multifactorial arterial-wall susceptibility, including connective-tissue
    dysplasia, systemic vasculopathy, and rare monogenic connective-tissue
    disease, lowers the threshold for cervical arterial wall injury.
  cell_types:
  - preferred_term: fibroblast
    term:
      id: CL:0000057
      label: fibroblast
  biological_processes:
  - preferred_term: extracellular matrix organization
    term:
      id: GO:0030198
      label: extracellular matrix organization
    modifier: ABNORMAL
  evidence:
  - reference: PMID:38791244
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The clinical, radiological, and histological characteristics of systemic
      vasculopathy and undifferentiated connective tissue dysplasia are present
      in up to 70% of individuals with sporadic CeAD.
    explanation: >-
      This supports connective-tissue and systemic-vasculopathy susceptibility
      as common background biology for sporadic cervical artery dissection.
  - reference: PMID:38791244
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Monogenic heritable connective tissue diseases account for fewer than 5%
      of cases of CeAD.
    explanation: >-
      This supports rare monogenic connective-tissue disease as a recognized but
      minority cause of cervical artery dissection susceptibility.
  downstream:
  - target: Arterial Wall Tear and Intramural Hematoma
    description: >-
      A susceptible cervical arterial wall is more likely to dissect after
      mechanical stress or spontaneous mural injury.
- name: Arterial Wall Tear and Intramural Hematoma
  description: >-
    A tear in the intima or bleeding within the arterial wall separates vessel
    wall layers, creating an intramural hematoma that narrows the lumen or forms
    a pseudoaneurysm.
  cell_types:
  - preferred_term: endothelial cell
    term:
      id: CL:0000115
      label: endothelial cell
  biological_processes:
  - preferred_term: response to wounding
    term:
      id: GO:0009611
      label: response to wounding
    modifier: INCREASED
  evidence:
  - reference: PMID:25684164
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      We included patients with extracranial carotid and vertebral dissection
      with onset of symptoms within the past 7 days.
    explanation: >-
      The CADISS trial population confirms extracranial carotid and vertebral
      dissection as the clinical substrate for this disorder; the abstract does
      not itself describe the arterial wall microanatomy, so this is partial
      support.
  - reference: PMID:37957581
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In the acute and subacute stage, the typical sign detection of intramural
      hematoma and Grade II enhancement revealed by HR-MRI was higher than the
      observations in the chronic stage (P = 0.000/0.000/0.016), while there
      was no significant difference by MRA (P = 0.902).
    explanation: >-
      Vessel-wall imaging directly supports intramural hematoma as an acute and
      subacute imaging sign of cervicocranial artery dissection.
  downstream:
  - target: Thromboembolism and Cerebral Ischemia
    description: >-
      The dissected arterial wall and altered lumen promote local thrombosis,
      stenosis, occlusion, and embolization.
- name: Molecular Stress and Vascular Remodeling Signatures
  description: >-
    Peripheral-blood transcriptomic changes in CeAD implicate molecular stress,
    senescence-associated signaling, mitochondrial dysfunction, and
    epithelial-mesenchymal plasticity as candidate mechanisms that may accompany
    arterial-wall vulnerability and remodeling.
  biological_processes:
  - preferred_term: cellular senescence
    term:
      id: GO:0090398
      label: cellular senescence
    modifier: INCREASED
  - preferred_term: mitochondrial organization
    term:
      id: GO:0007005
      label: mitochondrion organization
    modifier: ABNORMAL
  evidence:
  - reference: PMID:38791244
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      We found potential correlations between CeAD and the dysregulation of
      genes linked to nucleolar stress, senescence-associated secretory
      phenotype, mitochondrial malfunction, and epithelial-mesenchymal
      plasticity.
    explanation: >-
      This transcriptomic study supports candidate molecular stress and vascular
      remodeling pathways associated with CeAD.
  downstream:
  - target: Arterial Wall Tear and Intramural Hematoma
    description: >-
      Molecular stress and remodeling signatures may contribute to arterial-wall
      vulnerability and impaired repair.
- name: Thromboembolism and Cerebral Ischemia
  description: >-
    Damaged arterial endothelium and disturbed flow promote local thrombosis and
    embolization to cerebral arteries.
  cell_types:
  - preferred_term: platelet
    term:
      id: CL:0000233
      label: platelet
  biological_processes:
  - preferred_term: blood coagulation
    term:
      id: GO:0007596
      label: blood coagulation
    modifier: INCREASED
  evidence:
  - reference: PMID:25684164
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Extracranial carotid and vertebral artery dissection is an important cause
      of stroke, especially in young people.
    explanation: >-
      This directly supports cervical artery dissection as a cause of ischemic
      cerebrovascular events.
phenotypes:
- name: Headache
  category: Neurologic
  frequency: COMMON
  phenotype_term:
    preferred_term: Headache
    term:
      id: HP:0002315
      label: Headache
  evidence:
  - reference: PMID:25684164
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The major presenting symptoms were stroke or transient ischaemic attack
      (n=224) and local symptoms (headache, neck pain, or Horner's syndrome;
      n=26).
    explanation: >-
      Headache is explicitly listed as a local presenting symptom in the CADISS
      cervical dissection cohort.
- name: Neck Pain
  category: Neurologic
  frequency: COMMON
  phenotype_term:
    preferred_term: Neck pain
    term:
      id: HP:0030833
      label: Neck pain
  evidence:
  - reference: PMID:25684164
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The major presenting symptoms were stroke or transient ischaemic attack
      (n=224) and local symptoms (headache, neck pain, or Horner's syndrome;
      n=26).
    explanation: >-
      Neck pain is included among local presenting symptoms in symptomatic
      cervical artery dissection.
- name: Ischemic Stroke
  category: Neurologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Ischemic stroke
    term:
      id: HP:0002140
      label: Ischemic stroke
  evidence:
  - reference: PMID:25684164
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Extracranial carotid and vertebral artery dissection is an important cause
      of stroke, especially in young people.
    explanation: >-
      The trial background directly supports stroke as a major clinical
      consequence of cervical artery dissection.
- name: Transient Ischemic Attack
  category: Neurologic
  frequency: COMMON
  phenotype_term:
    preferred_term: Transient ischemic attack
    term:
      id: HP:0002326
      label: Transient ischemic attack
  evidence:
  - reference: PMID:25684164
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The major presenting symptoms were stroke or transient ischaemic attack
      (n=224) and local symptoms (headache, neck pain, or Horner's syndrome;
      n=26).
    explanation: >-
      The CADISS cohort explicitly identifies transient ischemic attack among
      major presenting symptoms in symptomatic cervical dissection.
- name: Horner Syndrome
  category: Neurologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Horner syndrome
    term:
      id: HP:0002277
      label: Horner syndrome
  evidence:
  - reference: PMID:25684164
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The major presenting symptoms were stroke or transient ischaemic attack
      (n=224) and local symptoms (headache, neck pain, or Horner's syndrome;
      n=26).
    explanation: >-
      Horner syndrome is explicitly listed among local presenting symptoms.
treatments:
- name: Antithrombotic Therapy
  description: >-
    Antiplatelet or anticoagulant therapy is used to reduce recurrent
    thromboembolic events in appropriate patients.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: aspirin
      term:
        id: CHEBI:15365
        label: acetylsalicylic acid
    - preferred_term: warfarin
      term:
        id: CHEBI:10033
        label: warfarin
  evidence:
  - reference: PMID:25684164
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      We found no difference in efficacy of antiplatelet and anticoagulant drugs
      at preventing stroke and death in patients with symptomatic carotid and
      vertebral artery dissection but stroke was rare in both groups, and much
      rarer than reported in some observational studies.
    explanation: >-
      The randomized CADISS trial supports antiplatelet or anticoagulant
      antithrombotic management, without evidence that one strategy is superior.
  - reference: PMID:34746432
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Based on evidence from two phase 2 RCTs that have shown no difference
      between the benefits and risks of anticoagulants versus antiplatelets in
      the acute phase of symptomatic EAD, we strongly recommend that clinicians
      can prescribe either option.
    explanation: >-
      The ESO guideline supports either anticoagulant or antiplatelet therapy in
      acute symptomatic extracranial artery dissection.
- name: Aspirin Therapy
  description: >-
    Aspirin is one antiplatelet option for cervical artery dissection, but
    TREAT-CAD did not prove aspirin non-inferior to vitamin K antagonist
    anticoagulation.
  treatment_term:
    preferred_term: aspirin pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: aspirin
      term:
        id: CHEBI:15365
        label: acetylsalicylic acid
  evidence:
  - reference: PMID:33765420
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Our findings did not show that aspirin was non-inferior to vitamin K
      antagonists in the treatment of cervical artery dissection.
    explanation: >-
      TREAT-CAD directly evaluates aspirin in cervical artery dissection but
      qualifies its role because non-inferiority to vitamin K antagonists was
      not shown.
- name: Intravenous Thrombolysis for Acute Ischemic Stroke
  description: >-
    Intravenous alteplase is recommended for eligible patients with extracranial
    artery dissection and acute ischemic stroke within the standard stroke
    treatment window.
  treatment_term:
    preferred_term: thrombolytic therapy
    term:
      id: NCIT:C15338
      label: Thrombolytic Therapy
    therapeutic_agent:
    - preferred_term: alteplase
      term:
        id: NCIT:C39607
        label: Alteplase
  evidence:
  - reference: PMID:34746432
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In EAD patients with acute ischemic stroke, we recommend using intravenous
      thrombolysis (IVT) with alteplase within 4.5 hours of onset if standard
      inclusion/exclusion criteria are met, and mechanical thrombectomy in
      patients with large vessel occlusion of the anterior circulation.
    explanation: >-
      The ESO guideline directly supports IV alteplase for eligible
      extracranial artery dissection patients with acute ischemic stroke.
- name: Mechanical Thrombectomy
  description: >-
    Mechanical thrombectomy is used in eligible cervical-artery-dissection
    patients when acute ischemic stroke is complicated by anterior-circulation
    large-vessel occlusion.
  treatment_term:
    preferred_term: thrombectomy for stroke
    term:
      id: NCIT:C191635
      label: Thrombectomy for Stroke
  evidence:
  - reference: PMID:34746432
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In EAD patients with acute ischemic stroke, we recommend using intravenous
      thrombolysis (IVT) with alteplase within 4.5 hours of onset if standard
      inclusion/exclusion criteria are met, and mechanical thrombectomy in
      patients with large vessel occlusion of the anterior circulation.
    explanation: >-
      The ESO guideline directly supports thrombectomy for extracranial artery
      dissection with anterior-circulation large-vessel occlusion.
📚

References & Deep Research

Deep Research

1
Falcon
Cervical Artery Dissection (CeAD) — Comprehensive Disease Characteristics Report
Edison Scientific Literature 42 citations 2026-05-06T08:24:29.975005

Cervical Artery Dissection (CeAD) — Comprehensive Disease Characteristics Report

Target disease: Cervical Artery Dissection (carotid and/or vertebral artery dissection, typically extracranial).
Category: Complex (multifactorial; small monogenic fraction).
Evidence note: Many retrieved full texts/abstracts did not include PMIDs in-line; therefore, citations are given to the retrieved sources by evidence IDs plus DOI/URL and publication date when available.


Executive quantitative summary

Domain Key finding (with numbers) Study/source (short) Publication year URL
Incidence and age Extracranial artery dissection incidence ~2.6–3.0 per 100,000/year; mean age for EAD ~44 years (debette2021esoguidelinefor pages 2-4) ESO guideline 2021 https://doi.org/10.1177/23969873211046475
Proportion of ischemic presentations EAD complicated by cerebral ischemia in about two thirds to three quarters of series (debette2021esoguidelinefor pages 1-2); in a real-world cohort, ischemic symptoms in 43/62 (69%) with TIA 16%, minor stroke 27%, major stroke 25% (lodato2025tenyearoutcomesof pages 5-9) ESO guideline; Lodato et al. 2021; 2025 https://doi.org/10.1177/23969873211046475; https://doi.org/10.3390/jcm14196836
Recanalization and aneurysm evolution Stenosis recanalizes in 33–90% within 6 months; dissecting aneurysms resolve/decrease in 40–50%; CADISS-related data: 24/264 aneurysms at baseline vs 36/248 at 3 months, with 12 persistent and 24 new (debette2021esoguidelinefor pages 2-4) ESO guideline 2021 https://doi.org/10.1177/23969873211046475
TREAT-CAD outcomes Primary endpoint: 23.1% (21/91) aspirin vs 14.6% (12/82) VKA; ischemic stroke: 7/91 (7.7%) vs 0/82; major extracranial hemorrhage: 0 vs 1/82 (1.2%); no deaths (engelter2021aspirinversusanticoagulation pages 7-11) TREAT-CAD RCT 2021 https://doi.org/10.1016/S1474-4422(21)00044-2
ESO guideline key recommendations Acute symptomatic EAD: IV alteplase within 4.5 h if eligible; mechanical thrombectomy for anterior-circulation LVO; either anticoagulants or antiplatelets may be prescribed in acute symptomatic EAD; expert consensus supports DOACs as possible VKA substitutes and short-term DAPT for TIA/minor stroke (debette2021esoguidelinefor pages 42-43, debette2021esoguidelinefor pages 37-41) ESO guideline 2021 https://doi.org/10.1177/23969873211046475
HRMR-VWI vs MRA findings In 34 patients/38 vessels, HRMR-VWI detected typical signs in all acute/subacute patients; intimal flap/double-lumen detection superior to MRA (P=0.012); IMH and grade II enhancement higher in acute/subacute vs chronic stage (P=0.000/0.000/0.016); MRA stage differences not significant (P=0.902) (ma2023imaginginvestigationof pages 1-2, ma2023imaginginvestigationof pages 6-9) Ma et al. imaging study 2023 https://doi.org/10.1186/s12880-023-01133-z
STOP-CAD TCD survey 29/58 centers (50%) routinely used TCD; European vs North American use 76.4% vs 34.3% (P=0.007); after HITS detection, 32.8% switched from antiplatelet to anticoagulation; 20.7% switched DAPT to anticoagulation; 12.1% switched SAPT to anticoagulation (guo2024applicationoftranscranial pages 1-2, guo2024applicationoftranscranial pages 4-4, guo2024applicationoftranscranial pages 3-3) Guo et al. STOP-CAD survey 2024 https://doi.org/10.1002/neo2.70004
Long-term outcome cohort Median follow-up 78 months: recurrent ischemic stroke in 2 patients (4%), both within 12 months; 10-year overall survival 71%; 10-year stroke/death-free survival 70%; medically treated subgroup stroke/death-free survival 86% with anticoagulation vs 67% with antiplatelets (lodato2025tenyearoutcomesof pages 5-9) Lodato et al. cohort 2025 https://doi.org/10.3390/jcm14196836

Table: This table compiles the main quantitative findings for cervical artery dissection across epidemiology, presentation, imaging, treatment trials, guideline recommendations, implementation surveys, and long-term outcomes. It is useful as a quick-reference evidence summary anchored to the retrieved context IDs.

Key guideline recommendation tables (ESO) were also retrieved as images (debette2021esoguidelinefor media df12240a, debette2021esoguidelinefor media 106e3d8a).


1. Disease Information

1.1 Overview (current understanding)

Cervical artery dissection (CeAD; also “cervical artery dissection/CAD”) is defined by intramural hematoma in the wall of the cervical portion of the internal carotid artery and/or vertebral artery, often producing stenosis/occlusion or a dissecting aneurysm and predisposing to thromboembolism and ischemic stroke. (engelter2021cervicalandintracranial pages 1-2, debette2021esoguidelinefor pages 1-2)

Direct quote (definition hallmark): the Engelter et al. review describes CeAD as having the “hallmark intramural hematoma of the cervical portion of the internal carotid or vertebral arteries.” (engelter2021cervicalandintracranial pages 1-2)

The European Stroke Organisation (ESO) guideline uses the term extracranial artery dissection (EAD) to refer to dissections of the cervical carotid or vertebral arteries and contrasts this with intracranial artery dissection (IAD); EAD/IAD are confirmed by characteristic radiologic signs (mural hematoma, dissecting aneurysm, long tapering stenosis, intimal flap, double lumen, etc.). (debette2021esoguidelinefor pages 2-4)

1.2 Key identifiers (ontology/coding)

  • MONDO / Orphanet / OMIM / MeSH / ICD-10/ICD-11: Not retrievable from the current tool evidence set (no authoritative coding tables were present in the retrieved texts). This should be populated from ontology resources (MONDO, MeSH, ICD) directly.

1.3 Synonyms and alternative names

  • Cervical artery dissection (CeAD) (engelter2021cervicalandintracranial pages 1-2)
  • Cervical artery dissection (CAD) (common abbreviation in multiple sources) (filip2023cervicalarterydissections—a pages 1-2)
  • Extracranial artery dissection (EAD; ESO terminology) (debette2021esoguidelinefor pages 2-4)
  • Carotid artery dissection; vertebral artery dissection (subtypes) (engelter2021cervicalandintracranial pages 1-2, filip2023cervicalarterydissections—a pages 1-2)

1.4 Evidence provenance (patient-level vs aggregated)

The knowledge base content here is derived from aggregated disease-level resources (ESO guideline; systematic reviews) and patient cohorts / pragmatic studies (single-center case series, retrospective cohort, multicenter survey, RCT). (debette2021esoguidelinefor pages 2-4, filip2023cervicalarterydissections—a pages 1-2, ma2023imaginginvestigationof pages 1-2, guo2024applicationoftranscranial pages 1-2, engelter2021aspirinversusanticoagulation pages 7-11, lodato2025tenyearoutcomesof pages 5-9)


2. Etiology

2.1 Disease causal factors (mechanistic framing)

CeAD occurs when a tear in the arterial wall or vasa vasorum results in an intramural hematoma and possibly a false lumen, which can cause luminal stenosis/occlusion and promote local thrombus and artery-to-artery embolism. (filip2023cervicalarterydissections—a pages 1-2, debette2021esoguidelinefor pages 1-2)

2.2 Risk factors

Mechanical / traumatic triggers

CeAD can be spontaneous or traumatic, and minor cervical strain/trauma (including whiplash-type mechanisms) is commonly reported as a trigger. (filip2023cervicalarterydissections—a pages 1-2)

Connective-tissue and arteriopathy associations

Predisposing conditions include fibromuscular dysplasia and heritable connective tissue disorders such as Ehlers–Danlos syndrome and Marfan syndrome. (filip2023cervicalarterydissections—a pages 1-2, blum2015cervicalarterydissection pages 1-3)

Vascular and neurologic comorbidities

Associated factors reported across clinical reviews and cohorts include hypertension and migraine. (filip2023cervicalarterydissections—a pages 1-2, blum2015cervicalarterydissection pages 1-3)

2.3 Protective factors

No specific genetic or environmental protective factors were identified in the retrieved evidence set.

2.4 Gene–environment interactions

The retrieved evidence supports a multifactorial model where an underlying predisposition affecting arterial wall integrity (genetic and/or connective tissue phenotype) may interact with mechanical stressors (minor trauma/exertion) to precipitate dissection, but formal GxE effect-size estimates were not available in the retrieved texts. (filip2023cervicalarterydissections—a pages 1-2, shlapakova2024peripheralbloodgene pages 1-2, nino2024thenaturalhistory pages 84-88)


3. Phenotypes

3.1 Core clinical phenotypes (with HPO suggestions)

CeAD commonly presents with local symptoms (pain, Horner syndrome, cranial nerve palsy) and/or cerebral ischemia (TIA/stroke). In ESO-cited series, ischemia complicates EAD in about two thirds to three quarters of patients. (debette2021esoguidelinefor pages 1-2)

HPO suggestions (non-exhaustive): * Headache — HP:0002315
Neck pain — HP:0000467
Horner syndrome — HP:0000005
Transient ischemic attack — HP:0002326 (approximate)
Ischemic stroke — HP:0002140
Cranial nerve palsy — HP:0001290 (broad)
Vertigo (posterior circulation) — HP:0002321
Ataxia — HP:0001251*

3.2 Phenotype characteristics (age, severity, progression)

  • Age of onset: often young/middle-aged; ESO guideline reports mean age ~44 years for extracranial dissection. (debette2021esoguidelinefor pages 2-4)
  • Onset pattern: typically acute/subacute neurological syndrome. (debette2021esoguidelinefor pages 1-2)
  • Progression: ischemic events often occur early after diagnosis, supporting immediate antithrombotic initiation. (engelter2021cervicalandintracranial pages 1-2)

3.3 Frequency and statistics from cohorts

In a real-world cohort of 62 patients, 69% presented with ischemic manifestations (16% TIA; 27% minor stroke; 25% major stroke). (lodato2025tenyearoutcomesof pages 5-9)

3.4 Quality-of-life impact

Direct QoL instrument data (e.g., EQ-5D, SF-36) were not captured in the retrieved evidence set; however, CeAD is highlighted as a leading cause of stroke in younger adults and thus a major potential driver of disability. (engelter2021cervicalandintracranial pages 1-2, debette2021esoguidelinefor pages 1-2)


4. Genetic/Molecular Information

4.1 Causal genes (monogenic contribution)

A minority of CeAD is attributable to monogenic heritable connective tissue disorders.

Direct quote (proportion):Monogenic heritable connective tissue diseases account for fewer than 5% of cases of CeAD.” (Shlapakova et al., 2024) (shlapakova2024peripheralbloodgene pages 1-2)

Examples of single-gene disorders plausibly increasing risk include connective tissue disorder genes such as FBN1 (Marfan) and COL3A1 (vascular Ehlers–Danlos), as well as TGF-β pathway genes in Loeys–Dietz spectrum (e.g., TGFBR1/2, SMAD2/3, TGFB2/3). (maly2025carotidarterydissection pages 2-4, nino2024thenaturalhistory pages 84-88)

4.2 Susceptibility loci / GWAS-implicated genes

GWAS signals in CeAD often map to non-coding variants influencing transcription/RNA processing. Reported CeAD-associated genes/loci include PHACTR1 and LRP1, among others (e.g., PLCE1, IRAG1). (shlapakova2024peripheralbloodgene pages 2-4)

4.3 Variant example with mechanistic follow-through

A mechanistic study of the pleiotropic vascular-risk locus LRP1 rs11172113 supports an allele-specific regulatory mechanism in smooth muscle cells leading to extracellular matrix remodeling and altered signaling:

Direct quote (key abstract statement):Multitrait colocalization analyses pointed at rs11172113 as the most likely causal variant in LRP1 for fibromuscular dysplasia, migraine, pulse pressure, and spontaneous coronary artery dissection.” (Liu et al., Circulation Research, 2024) (liu2024lrp1repressionby pages 1-2)

Mechanistically, the study shows LRP1 perturbation in iPSC-derived smooth muscle cells affects extracellular matrix composition and potentiates canonical TGF-β/SMAD2/3 signaling. (liu2024lrp1repressionby pages 11-12, liu2024lrp1repressionby pages 1-2)

4.4 Transcriptomics and molecular profiling (2024)

Peripheral blood bulk RNA-seq (19 CeAD vs 18 controls) identified differential expression and pathway signals consistent with systemic stress and vascular biology.

Direct quote (key molecular pathways): “We found potential correlations between CeAD and the dysregulation of genes linked to nucleolar stress, senescence-associated secretory phenotype, mitochondrial malfunction, and epithelial–mesenchymal plasticity.” (Shlapakova et al., 2024) (shlapakova2024peripheralbloodgene pages 1-2)

4.5 Suggested ontology terms

GO biological processes (examples): * extracellular matrix organization (GO:0030198) (supported conceptually by ECM remodeling evidence) (liu2024lrp1repressionby pages 11-12, liu2024lrp1repressionby pages 1-2) * transforming growth factor beta receptor signaling pathway (GO:0007179) (liu2024lrp1repressionby pages 11-12, liu2024lrp1repressionby pages 1-2) * smooth muscle cell proliferation/migration (GO:0048660/GO:0016477) (liu2024lrp1repressionby pages 1-2)

Cell Ontology (CL) (examples): * vascular smooth muscle cell — CL:0000192 (liu2024lrp1repressionby pages 11-12, liu2024lrp1repressionby pages 1-2) * endothelial cell — CL:0000115 (implicated in vascular integrity discussions; not directly profiled here)


5. Environmental Information

5.1 Environmental and lifestyle factors

The retrieved evidence emphasizes mechanical neck stress/trauma and vascular risk factors (e.g., hypertension) rather than specific toxins or occupational exposures. (filip2023cervicalarterydissections—a pages 1-2, blum2015cervicalarterydissection pages 1-3)

5.2 Infectious agents

Specific pathogens were not established as causal in the retrieved evidence. However, reviews note infection has been described as a risk factor in broader literature; the retrieved excerpted evidence did not provide quantitative estimates. (shlapakova2024peripheralbloodgene pages 2-4, nino2024thenaturalhistory pages 84-88)


6. Mechanism / Pathophysiology

6.1 Causal chain (trigger → lesion → clinical event)

  1. Trigger/predisposition: underlying arterial wall vulnerability (connective tissue phenotype; genetic susceptibility) ± mechanical stressor (minor trauma/strain). (filip2023cervicalarterydissections—a pages 1-2, shlapakova2024peripheralbloodgene pages 1-2, nino2024thenaturalhistory pages 84-88)
  2. Wall injury: formation of intramural hematoma and potentially an intimal flap/double lumen, producing stenosis/occlusion or dissecting aneurysm. (debette2021esoguidelinefor pages 2-4, ma2023imaginginvestigationof pages 4-6)
  3. Stroke mechanism: local thrombus formation and distal embolization are emphasized as key mechanisms. (guo2024applicationoftranscranial pages 1-2)
  4. Clinical manifestations: local pain/Horner syndrome and/or TIA/stroke depending on embolic burden and hemodynamic compromise. (debette2021esoguidelinefor pages 1-2)

6.2 Upstream vs downstream mechanisms

  • Upstream: genetic regulation of vascular smooth muscle/ECM integrity (e.g., LRP1 regulatory mechanisms; TGF-β pathway), connective tissue dysplasia. (shlapakova2024peripheralbloodgene pages 1-2, liu2024lrp1repressionby pages 11-12, liu2024lrp1repressionby pages 1-2)
  • Downstream: intramural hematoma and luminal stenosis/occlusion; thromboembolism → ischemic lesions. (debette2021esoguidelinefor pages 2-4, guo2024applicationoftranscranial pages 1-2)

7. Anatomical Structures Affected

7.1 Organ/system level

  • Primary: cervical segments of internal carotid arteries and vertebral arteries (cardiovascular system; cerebrovascular interface). (engelter2021cervicalandintracranial pages 1-2, debette2021esoguidelinefor pages 2-4)
  • Secondary: brain ischemia (neurologic system) and rarely intracranial extension/SAH (more relevant to IAD). (debette2021esoguidelinefor pages 1-2)

UBERON suggestions: * internal carotid artery — UBERON:0001645
vertebral artery — UBERON:0001646
cervical region vasculature — (composite; ontology-dependent)

7.2 Tissue/cell level

  • arterial wall layers; vascular smooth muscle and extracellular matrix remodeling are implicated. (shlapakova2024peripheralbloodgene pages 1-2, liu2024lrp1repressionby pages 11-12)

7.3 Lateralization

Unilateral is common; bilateral and multi-vessel dissections occur (ESO: multiple cervical arteries involved in ~15–20% of EAD). (debette2021esoguidelinefor pages 2-4)


8. Temporal Development

8.1 Onset

Often acute/subacute; antithrombotic therapy is recommended to start immediately after diagnosis due to early stroke risk. (engelter2021cervicalandintracranial pages 1-2)

8.2 Progression / natural history

Recanalization is common: ESO guideline reports stenosis recanalization 33–90% within 6 months; dissecting aneurysms resolve/decrease in 40–50% (with dynamic evolution in CADISS follow-up). (debette2021esoguidelinefor pages 2-4)


9. Inheritance and Population

9.1 Epidemiology

  • Incidence estimate for extracranial artery dissection: ~2.6–3.0 per 100,000/year (ESO guideline). (debette2021esoguidelinefor pages 2-4)
  • Mean age reported for EAD: ~44 years. (debette2021esoguidelinefor pages 2-4)

9.2 Inheritance

Most CeAD appears multifactorial/polygenic with rare monogenic CTD contribution (<5%). (shlapakova2024peripheralbloodgene pages 1-2, nino2024thenaturalhistory pages 84-88)


10. Diagnostics

10.1 Imaging-based diagnosis (core)

ESO diagnostic confirmation includes mural hematoma, dissecting aneurysm, long tapering stenosis, intimal flap, double lumen, or characteristic occlusion patterns. (debette2021esoguidelinefor pages 2-4)

10.2 Advanced imaging developments (2023–2024 prioritized)

High-resolution MR vessel wall imaging (HRMR-VWI) provides improved detection of direct wall signs (intimal flap/double lumen/intramural hematoma) and enables staging and quantitative vessel-wall metrics.

In a 2023 BMC Medical Imaging study (34 patients; 38 vessels), intimal flap/double-lumen detection was more common on HRMR-VWI than MRA (P = 0.012), and intramural hematoma and grade II enhancement were more often detected in acute/subacute vs chronic stages. (ma2023imaginginvestigationof pages 1-2, ma2023imaginginvestigationof pages 6-9)

Direct quote: HRMR-VWI “visualizes vessel walls, thereby effectively characterizing the direct signs, such as intimal flap, double lumen, and intramural hematoma (IMH).” (ma2023imaginginvestigationof pages 2-4)

10.3 TCD as an implementation/monitoring tool (STOP-CAD survey, 2024)

A multicenter STOP-CAD survey shows TCD adoption is variable but common.

Direct quotes: * “Half (29 out of 58) of the sites routinely perform TCD on CAD patients…” (guo2024applicationoftranscranial pages 1-2) * “European institutions show a notably higher rate of TCD application… 76.4% compared to… North America… 34.3% (p = 0.007)” (guo2024applicationoftranscranial pages 3-3)

HITS detection often prompts escalation from antiplatelet to anticoagulation in practice. (guo2024applicationoftranscranial pages 4-4, guo2024applicationoftranscranial pages 5-5)

10.4 Differential diagnosis

Not comprehensively addressed in retrieved sources; typical differential in practice includes atherosclerotic stenosis, vasculitis, fibromuscular dysplasia without dissection, and thromboembolic disease without wall hematoma.


11. Outcome/Prognosis

11.1 Short-term outcomes

A review of emergency medicine literature notes generally favorable outcomes with high proportions achieving functional independence (mRS 0–2) at 3–6 months in historical cohorts, and low mortality (reported ~1.9–5%). (robertson2016cervicalarterydissections pages 6-7)

11.2 Long-term outcomes (real-world cohort)

In a 10-year retrospective cohort (n=62), recurrent ischemic stroke was 4% (2 patients), both within the first 12 months, and estimated 10-year overall survival 71% with 10-year stroke/death-free survival 70%. (lodato2025tenyearoutcomesof pages 5-9)


12. Treatment

12.1 Acute reperfusion treatments (guideline + evidence)

ESO guideline suggests: * IV alteplase within 4.5 hours for eligible acute ischemic stroke with EAD (weak recommendation, low-quality evidence). (debette2021esoguidelinefor pages 42-43) * Mechanical thrombectomy for anterior-circulation large-vessel occlusion associated with EAD (weak recommendation, very low-quality evidence). (debette2021esoguidelinefor pages 42-43)

These recommendations are summarized in ESO tables (debette2021esoguidelinefor media df12240a, debette2021esoguidelinefor media 106e3d8a).

12.2 Antithrombotic secondary prevention

ESO guideline: in acute symptomatic EAD, clinicians may prescribe either anticoagulants or antiplatelet therapy (strong recommendation; moderate quality). (debette2021esoguidelinefor pages 42-43, debette2021esoguidelinefor pages 37-41)

RCT evidence (TREAT-CAD)

TREAT-CAD randomized 194 patients to aspirin vs VKA; non-inferiority of aspirin was not demonstrated.

Key outcomes at 3 months (per protocol): primary endpoint 23.1% aspirin vs 14.6% VKA; ischemic stroke 7.7% aspirin vs 0% VKA; major extracranial hemorrhage 0% vs 1.2%; no deaths. (engelter2021aspirinversusanticoagulation pages 7-11)

Direct quote:non-inferiority of aspirin was not demonstrated.” (engelter2021aspirinversusanticoagulation pages 7-11)

12.3 Expert consensus (ESO) on special situations

ESO expert consensus (when evidence is low) supports: * DOACs as potential substitutes for VKA in symptomatic EAD patients treated with anticoagulation. (debette2021esoguidelinefor pages 37-41) * Short-term dual antiplatelet therapy (aspirin + clopidogrel) for a few weeks in EAD-related TIA/minor stroke. (debette2021esoguidelinefor pages 37-41)

12.4 Real-world practice (TCD-guided escalation)

In the STOP-CAD TCD survey, after HITS detection, some centers switch from SAPT/DAPT to anticoagulation (e.g., 20.7% DAPT→AC; 12.1% SAPT→AC). (guo2024applicationoftranscranial pages 4-4)

12.5 MAXO (Medical Action Ontology) suggestions

  • Antithrombotic therapy — MAXO:0000508 (approximate)
  • Antiplatelet therapy — MAXO:0000515 (approximate)
  • Anticoagulant therapy — MAXO:0000516 (approximate)
  • Intravenous thrombolysis — MAXO:0001025 (approximate)
  • Mechanical thrombectomy — MAXO:0001206 (approximate)
  • Endovascular stenting — MAXO:0001097 (approximate)

(Exact MAXO IDs should be verified against MAXO; provided as best-effort suggestions.)


13. Prevention

13.1 Primary prevention

No evidence-based primary prevention strategy specific to CeAD was captured in the retrieved texts beyond general avoidance of neck trauma in high-risk individuals and control of vascular risk factors.

13.2 Secondary/tertiary prevention

Immediate initiation of antithrombotic therapy after diagnosis is supported by the observation that ischemic events occur early after CeAD diagnosis. (engelter2021cervicalandintracranial pages 1-2)


14. Other Species / Natural Disease

No naturally occurring non-human species evidence was identified in the retrieved texts.


15. Model Organisms

The retrieved evidence includes iPSC-derived human smooth muscle cell models used to test vascular-risk loci mechanisms (LRP1 enhancer/KO) rather than animal models.

Model type: in vitro human iPSC-derived smooth muscle cells + CRISPR editing. (liu2024lrp1repressionby pages 1-2)


Current applications and real-world implementation highlights

  1. Guideline-concordant acute stroke care (IV alteplase, thrombectomy) is recommended for eligible CeAD-related strokes similarly to other causes, with evidence-quality caveats in guidelines. (debette2021esoguidelinefor pages 42-43, engelter2021cervicalandintracranial pages 3-5)
  2. Advanced imaging (HRMR-VWI) is increasingly used to improve early diagnosis and staging, particularly for intramural hematoma and direct dissection signs not reliably seen on lumenography alone. (ma2023imaginginvestigationof pages 1-2, ma2023imaginginvestigationof pages 2-4)
  3. TCD monitoring is used by about half of advanced stroke centers and can change antithrombotic decisions when HITS are detected, although standardized protocols are lacking. (guo2024applicationoftranscranial pages 1-2, guo2024applicationoftranscranial pages 4-4)

Expert opinion & analysis (authoritative sources)

  • ESO guideline authors conclude that, based on two phase-2 RCTs, there is no clear net benefit difference between anticoagulants vs antiplatelets for acute symptomatic EAD; hence either is acceptable, with additional expert consensus for DOACs and short DAPT in selected scenarios. (debette2021esoguidelinefor pages 42-43, debette2021esoguidelinefor pages 37-41)
  • Engelter et al. emphasize that with CADISS and TREAT-CAD, “the evidence to consider aspirin as the standard therapy of CeAD is weak” and advocate immediate antithrombotic initiation. (engelter2021cervicalandintracranial pages 1-2)

Limitations of this report (evidence availability)

  • AHA 2024 scientific statement (“Treatment and outcomes of cervical artery dissection in adults”) was detected in search results but was unobtainable in this run; therefore, its content is not quoted here.
  • PMIDs were not embedded in most retrieved text chunks; thus, PMID-preferred citations could not be consistently provided.
  • Ontology identifiers (MONDO/MeSH/ICD/Orphanet/OMIM) were not available in the retrieved documents and should be filled via dedicated ontology lookups.

References (key retrieved sources with dates/URLs)

  • Debette S, et al. ESO guideline for the management of extracranial and intracranial artery dissection. European Stroke Journal. Sep 2021. https://doi.org/10.1177/23969873211046475 (debette2021esoguidelinefor pages 2-4, debette2021esoguidelinefor pages 42-43, debette2021esoguidelinefor pages 37-41, debette2021esoguidelinefor media df12240a, debette2021esoguidelinefor media 106e3d8a)
  • Ma W, et al. Imaging investigation… using high resolution magnetic resonance VWI and MRA. BMC Medical Imaging. Nov 2023. https://doi.org/10.1186/s12880-023-01133-z (ma2023imaginginvestigationof pages 1-2, ma2023imaginginvestigationof pages 2-4)
  • Guo X, et al. Application of transcranial Doppler… STOP-CAD survey. Clinical Neuroimaging. Mar 2024. https://doi.org/10.1002/neo2.70004 (guo2024applicationoftranscranial pages 1-2, guo2024applicationoftranscranial pages 4-4)
  • Shlapakova PS, et al. Peripheral Blood Gene Expression Profiling… CeAD. Int J Mol Sci. May 2024. https://doi.org/10.3390/ijms25105205 (shlapakova2024peripheralbloodgene pages 1-2, shlapakova2024peripheralbloodgene pages 2-4)
  • Liu L, et al. LRP1 repression by SNAIL results in ECM remodeling… Circulation Research. Nov 2024. https://doi.org/10.1161/CIRCRESAHA.124.325269 (liu2024lrp1repressionby pages 1-2)
  • Engelter ST, et al. Aspirin versus anticoagulation in cervical artery dissection (TREAT-CAD). Lancet Neurology. May 2021. https://doi.org/10.1016/S1474-4422(21)00044-2 (engelter2021aspirinversusanticoagulation pages 7-11)
  • Lodato M, et al. Ten-Year Outcomes of Cervical Artery Dissection. J Clin Med. Sep 2025. https://doi.org/10.3390/jcm14196836 (lodato2025tenyearoutcomesof pages 5-9)

References

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