🏷

Classifications

Harrison's Chapter

🔗

Mappings

MONDO

MONDO:0002695 sagittal sinus thrombosis

Primary MONDO disease term for this entry.

ICD-10-CM

ICD10CM:I67.6 Nonpyogenic thrombosis of intracranial venous system

ICD-10-CM I67.6 covers nonpyogenic thrombosis of intracranial venous sinuses and veins, which encompasses sagittal sinus thrombosis but is broader than this entry.

⚙

Pathophysiology

3

Sagittal sinus thrombus and venous outflow obstruction

Thrombus in a dural venous sinus, including the superior sagittal sinus, obstructs cerebral venous drainage. The lesion involves intraluminal clot formation in the venous sinus and can propagate or impair cortical venous outflow.

endothelial cell link platelet link

blood coagulation link ↑ INCREASED platelet activation link ↑ INCREASED

superior sagittal sinus link

Downstream

Venous infarction and intracranial hypertension Obstructed venous drainage causes local venous infarction and global intracranial-pressure effects from impaired venous outflow.

Show evidence (1 reference)

PMID:25073867 SUPPORT Human Clinical

"The confirmation of the diagnosis of CVT relies on the demonstration of thrombi in the cerebral veins and/or sinuses by MR/MR venography or veno CT."

This supports venous or sinus thrombus as the defining anatomic lesion in cerebral venous thrombosis.

Venous infarction and intracranial hypertension

Venous outflow obstruction produces two linked injury patterns: focal venous infarction that can cause focal deficits, and global intracranial hypertension from an obstructed venous system, which can cause headache, papilledema, encephalopathy, and reduced consciousness.

neuron link endothelial cell link

response to hypoxia link ↑ INCREASED inflammatory response link ↑ INCREASED

Downstream

Hemorrhagic parenchymal injury Venous congestion and infarction can be accompanied by bleeding and lobar parenchymal injury.

Show evidence (1 reference)

PMID:17183977 SUPPORT Human Clinical

"The pathophysiology of CVST depends on two interconnected events, local signs due to venous infarct, e.g., hemiparesis and global signs due to raised ICP from an obstructed venous system--papilloedema and isolated intracranial hypertension being one of them."

This directly supports venous infarction and raised intracranial pressure as linked pathophysiologic consequences of venous sinus thrombosis.

Hemorrhagic parenchymal injury

Sagittal sinus thrombosis can be associated with cortical or lobar lesions and hemorrhage when venous congestion and infarction injure brain parenchyma.

inflammatory response link ↑ INCREASED

cerebral cortex link

Show evidence (1 reference)

PMID:29039017 SUPPORT Human Clinical

"Compared with those with no seizures, significantly more patients with secondary seizures had hemiplegia (37.50 vs. 15.63%; P = 0.020), bleeding (29.40 vs. 10.81%; P = 0.047), lesions involving the frontal (31.25 vs. 10.81%; P = 0.023) and temporal lobe (43.75 vs. 8.11%; P = 0.005)"

This clinical cohort supports bleeding and focal lobar lesions in CVST patients with secondary seizures, consistent with hemorrhagic parenchymal injury.

⬡

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.

●

Phenotypes

7

Eye 1

Papilledema Papilledema (HP:0001085)

Show evidence (1 reference)

PMID:17183977 SUPPORT Human Clinical

"global signs due to raised ICP from an obstructed venous system--papilloedema and isolated intracranial hypertension being one of them."

This supports papilledema as part of the raised-intracranial-pressure presentation.

Nervous System 4

Headache Headache (HP:0002315)

Show evidence (1 reference)

PMID:25073867 SUPPORT Human Clinical

"Their most frequent presentations are isolated headache, intracranial hypertension syndrome, seizures, a focal lobar syndrome and encephalopathy."

This supports headache as a frequent clinical presentation of cerebral venous thrombosis.

Intracranial hypertension Increased intracranial pressure (HP:0002516)

Show evidence (1 reference)

PMID:17183977 SUPPORT Human Clinical

"global signs due to raised ICP from an obstructed venous system--papilloedema and isolated intracranial hypertension being one of them."

This supports raised intracranial pressure as a major consequence of obstructed venous drainage.

Seizures Seizure (HP:0001250)

Show evidence (2 references)

PMID:25073867 SUPPORT Human Clinical

"Their most frequent presentations are isolated headache, intracranial hypertension syndrome, seizures, a focal lobar syndrome and encephalopathy."

This supports seizures as a frequent presentation of cerebral venous thrombosis.

PMID:29039017 SUPPORT Human Clinical

"The presence of focal neurological deficits and thrombosis of the superior sagittal sinus are independent risk factors for secondary seizures in patients with cerebral venous sinus thrombosis"

This supports the relationship between superior sagittal sinus thrombosis and secondary seizure risk in a clinical cohort.

Focal neurological deficits Hemiparesis (HP:0001269)

Show evidence (1 reference)

PMID:17183977 SUPPORT Human Clinical

"local signs due to venous infarct, e.g., hemiparesis and global signs due to raised ICP from an obstructed venous system"

This supports hemiparesis as a focal sign caused by venous infarction.

Other 2

Cerebral hemorrhage Cerebral hemorrhage (HP:0001342)

Show evidence (1 reference)

PMID:29039017 SUPPORT Human Clinical

"Compared with those with no seizures, significantly more patients with secondary seizures had hemiplegia (37.50 vs. 15.63%; P = 0.020), bleeding (29.40 vs. 10.81%; P = 0.047), lesions involving the frontal (31.25 vs. 10.81%; P = 0.023) and temporal lobe (43.75 vs. 8.11%; P = 0.005)"

This cohort supports bleeding and focal lobar lesions among CVST patients with secondary seizures.

Reduced consciousness Loss of consciousness (HP:0007185)

Show evidence (1 reference)

PMID:38050259 SUPPORT Human Clinical

"The presenting symptoms can range from headache to loss of consciousness."

This supports reduced consciousness as part of the clinical spectrum.

💊

Treatments

3

Acute heparin anticoagulation

Action: pharmacotherapy MAXO:0000058

Agent: heparin ↗

Acute treatment uses unfractionated or low-molecular-weight heparin to limit thrombus extension and support recanalization; longer-term anticoagulation is tailored to thrombotic risk after the acute phase.

Show evidence (2 references)

PMID:25073867 SUPPORT Human Clinical

"The main intervention in the acute is anticoagulation with either low molecular weight or unfractionated heparin."

This review directly supports heparin anticoagulation as the main acute intervention.

PMID:39492709 SUPPORT Human Clinical

"We found that LMWH and UH are safe and effective for the management of acute CVT and should be considered first line."

This recent treatment review supports low-molecular-weight and unfractionated heparin as first-line acute CVT therapy.

Endovascular thrombolysis or thrombectomy

Action: thrombectomy Ontology label: Thrombectomy NCIT:C52003

Local thrombolysis or mechanical thrombectomy may be considered in selected severe cases or when clinical status deteriorates despite anticoagulation, but evidence remains limited and specialist-center selection is important.

Show evidence (2 references)

PMID:25073867 PARTIAL Human Clinical

"In patients in severe condition on admission or who deteriorate despite anticoagulation, local thrombolysis or thrombectomy is an option."

This supports endovascular therapy only for selected severe or deteriorating patients.

PMID:25899238 PARTIAL Human Clinical

"Cerebral venous thrombosis is generally treated with anticoagulation. However, some patients do not respond to medical therapy and these might benefit from mechanical thrombectomy."

This systematic review supports thrombectomy as a possible option after inadequate response to medical therapy.

Decompressive surgery for life-threatening mass effect

Action: surgical procedure MAXO:0000004

Decompressive craniectomy may be used in life-threatening cases with large venous infarcts, hemorrhage, or severe intracranial pressure elevation.

Show evidence (2 references)

PMID:25073867 PARTIAL Human Clinical

"Decompressive surgery is life-saving in patients with large venous infarcts or haemorrhage."

This supports decompressive surgery for selected life-threatening venous infarction or hemorrhage.

PMID:39492709 PARTIAL Human Clinical

"Decompressive craniectomy may be used to reduce intracranial pressure in life-threatening cases."

This recent treatment review supports decompressive craniectomy for selected life-threatening cases.

{ }

Source YAML

click to show

name: Sagittal Sinus Thrombosis
creation_date: "2026-05-06T11:56:01Z"
updated_date: "2026-05-06T13:00:05Z"
description: >-
  Sagittal sinus thrombosis is an intracranial venous sinus thrombosis in which
  thrombus forms in the superior sagittal sinus or inferior sagittal sinus,
  obstructing cerebral venous drainage and potentially causing intracranial
  hypertension, venous congestion, venous infarction, hemorrhage, seizures, or
  coma.
category: Complex
disease_term:
  preferred_term: sagittal sinus thrombosis
  term:
    id: MONDO:0002695
    label: sagittal sinus thrombosis
classifications:
  harrisons_chapter:
  - classification_value: vascular disease
mappings:
  icd10cm_mappings:
  - term:
      id: ICD10CM:I67.6
      label: Nonpyogenic thrombosis of intracranial venous system
    mapping_predicate: skos:closeMatch
    mapping_source: ICD-10-CM
    mapping_justification: >-
      ICD-10-CM I67.6 covers nonpyogenic thrombosis of intracranial venous
      sinuses and veins, which encompasses sagittal sinus thrombosis but is
      broader than this entry.
    consistency:
    - reference: MONDO
      consistent: UNKNOWN
      notes: >-
        MONDO:0002695 has MeSH and SNOMED/UMLS cross-references but no
        ICD-10-CM exact mapping in the local OAK output reviewed here.
  mondo_mappings:
  - term:
      id: MONDO:0002695
      label: sagittal sinus thrombosis
    mapping_predicate: skos:exactMatch
    mapping_source: MONDO
    mapping_justification: Primary MONDO disease term for this entry.
    consistency:
    - reference: MONDO
      consistent: CONSISTENT
parents:
- Intracranial sinus thrombosis
- Vascular disorder
synonyms:
- Superior sagittal sinus thrombosis
- Inferior sagittal sinus thrombosis
- Sagittal venous sinus thrombosis
epidemiology:
- name: Young adult and female-predominant cerebral venous thrombosis pattern
  description: >-
    Cerebral venous thrombosis is uncommon, disproportionately affects younger
    adults, and in contemporary reviews is described as more common in females
    than males.
  evidence:
  - reference: PMID:38050259
    reference_title: "Pathophysiology, diagnosis and management of cerebral venous thrombosis: A comprehensive review."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Cerebral venous thrombosis is a rare cause of stroke in young mostly
      female adults which is frequently overlooked due to its variable clinical
      and radiological presentation.
    explanation: >-
      This review provides demographic context for the broader cerebral venous
      thrombosis syndrome that includes sagittal sinus thrombosis.
  - reference: PMID:38050259
    reference_title: "Pathophysiology, diagnosis and management of cerebral venous thrombosis: A comprehensive review."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Females are 3 times more commonly affected and are significantly younger
      than males.
    explanation: >-
      This supports female predominance and younger age distribution in cerebral
      venous thrombosis.
- name: Common prothrombotic and acquired risk factors
  description: >-
    Frequently cited cerebral venous thrombosis risk factors include inherited
    or acquired prothrombotic states, estrogen-related exposures, pregnancy or
    puerperium, infection, and malignancy.
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The more frequent risk factors for CVT are prothrombotic conditions,
      either genetic or acquired, oral contraceptives, puerperium and pregnancy,
      infection and malignancy.
    explanation: >-
      This review directly lists common cerebral venous thrombosis risk factors.
pathophysiology:
- name: Sagittal sinus thrombus and venous outflow obstruction
  description: >-
    Thrombus in a dural venous sinus, including the superior sagittal sinus,
    obstructs cerebral venous drainage. The lesion involves intraluminal clot
    formation in the venous sinus and can propagate or impair cortical venous
    outflow.
  cell_types:
  - preferred_term: endothelial cell
    term:
      id: CL:0000115
      label: endothelial cell
  - preferred_term: platelet
    term:
      id: CL:0000233
      label: platelet
  locations:
  - preferred_term: superior sagittal sinus
    term:
      id: UBERON:0001642
      label: superior sagittal sinus
  biological_processes:
  - preferred_term: blood coagulation
    modifier: INCREASED
    term:
      id: GO:0007596
      label: blood coagulation
  - preferred_term: platelet activation
    modifier: INCREASED
    term:
      id: GO:0030168
      label: platelet activation
  downstream:
  - target: Venous infarction and intracranial hypertension
    description: >-
      Obstructed venous drainage causes local venous infarction and global
      intracranial-pressure effects from impaired venous outflow.
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The confirmation of the diagnosis of CVT relies on the demonstration of
      thrombi in the cerebral veins and/or sinuses by MR/MR venography or veno
      CT.
    explanation: >-
      This supports venous or sinus thrombus as the defining anatomic lesion in
      cerebral venous thrombosis.
- name: Venous infarction and intracranial hypertension
  description: >-
    Venous outflow obstruction produces two linked injury patterns: focal
    venous infarction that can cause focal deficits, and global intracranial
    hypertension from an obstructed venous system, which can cause headache,
    papilledema, encephalopathy, and reduced consciousness.
  cell_types:
  - preferred_term: neuron
    term:
      id: CL:0000540
      label: neuron
  - preferred_term: endothelial cell
    term:
      id: CL:0000115
      label: endothelial cell
  biological_processes:
  - preferred_term: response to hypoxia
    modifier: INCREASED
    term:
      id: GO:0001666
      label: response to hypoxia
  - preferred_term: inflammatory response
    modifier: INCREASED
    term:
      id: GO:0006954
      label: inflammatory response
  downstream:
  - target: Hemorrhagic parenchymal injury
    description: >-
      Venous congestion and infarction can be accompanied by bleeding and lobar
      parenchymal injury.
  evidence:
  - reference: PMID:17183977
    reference_title: Pathophysiology of cerebral venous thrombosis--an overview.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The pathophysiology of CVST depends on two interconnected events, local
      signs due to venous infarct, e.g., hemiparesis and global signs due to
      raised ICP from an obstructed venous system--papilloedema and isolated
      intracranial hypertension being one of them.
    explanation: >-
      This directly supports venous infarction and raised intracranial pressure
      as linked pathophysiologic consequences of venous sinus thrombosis.
- name: Hemorrhagic parenchymal injury
  description: >-
    Sagittal sinus thrombosis can be associated with cortical or lobar lesions
    and hemorrhage when venous congestion and infarction injure brain
    parenchyma.
  locations:
  - preferred_term: cerebral cortex
    term:
      id: UBERON:0000956
      label: cerebral cortex
  biological_processes:
  - preferred_term: inflammatory response
    modifier: INCREASED
    term:
      id: GO:0006954
      label: inflammatory response
  evidence:
  - reference: PMID:29039017
    reference_title: "Cerebral venous sinus thrombosis complicated by seizures: a retrospective analysis of 69 cases."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Compared with those with no seizures, significantly more patients with
      secondary seizures had hemiplegia (37.50 vs. 15.63%; P = 0.020), bleeding
      (29.40 vs. 10.81%; P = 0.047), lesions involving the frontal (31.25 vs.
      10.81%; P = 0.023) and temporal lobe (43.75 vs. 8.11%; P = 0.005)
    explanation: >-
      This clinical cohort supports bleeding and focal lobar lesions in CVST
      patients with secondary seizures, consistent with hemorrhagic parenchymal
      injury.
phenotypes:
- category: Neurological
  name: Headache
  diagnostic: true
  description: >-
    Headache is a frequent presentation and may be isolated or part of an
    intracranial-hypertension syndrome.
  phenotype_term:
    preferred_term: Headache
    term:
      id: HP:0002315
      label: Headache
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Their most frequent presentations are isolated headache, intracranial
      hypertension syndrome, seizures, a focal lobar syndrome and encephalopathy.
    explanation: >-
      This supports headache as a frequent clinical presentation of cerebral
      venous thrombosis.
- category: Neurological
  name: Intracranial hypertension
  diagnostic: true
  description: >-
    Obstruction of cerebral venous drainage can raise intracranial pressure and
    cause intracranial-hypertension manifestations such as papilledema.
  phenotype_term:
    preferred_term: Increased intracranial pressure
    term:
      id: HP:0002516
      label: Increased intracranial pressure
  evidence:
  - reference: PMID:17183977
    reference_title: Pathophysiology of cerebral venous thrombosis--an overview.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      global signs due to raised ICP from an obstructed venous
      system--papilloedema and isolated intracranial hypertension being one of
      them.
    explanation: >-
      This supports raised intracranial pressure as a major consequence of
      obstructed venous drainage.
- category: Ophthalmologic
  name: Papilledema
  description: >-
    Papilledema can occur as a manifestation of raised intracranial pressure in
    cerebral venous sinus thrombosis.
  phenotype_term:
    preferred_term: Papilledema
    term:
      id: HP:0001085
      label: Papilledema
  evidence:
  - reference: PMID:17183977
    reference_title: Pathophysiology of cerebral venous thrombosis--an overview.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      global signs due to raised ICP from an obstructed venous
      system--papilloedema and isolated intracranial hypertension being one of
      them.
    explanation: >-
      This supports papilledema as part of the raised-intracranial-pressure
      presentation.
- category: Neurological
  name: Seizures
  description: >-
    Seizures can occur at presentation or secondarily, especially when cortical
    lesions, bleeding, focal deficits, or superior sagittal sinus thrombosis are
    present.
  phenotype_term:
    preferred_term: Seizure
    term:
      id: HP:0001250
      label: Seizure
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Their most frequent presentations are isolated headache, intracranial
      hypertension syndrome, seizures, a focal lobar syndrome and encephalopathy.
    explanation: >-
      This supports seizures as a frequent presentation of cerebral venous
      thrombosis.
  - reference: PMID:29039017
    reference_title: "Cerebral venous sinus thrombosis complicated by seizures: a retrospective analysis of 69 cases."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The presence of focal neurological deficits and thrombosis of the superior
      sagittal sinus are independent risk factors for secondary seizures in
      patients with cerebral venous sinus thrombosis
    explanation: >-
      This supports the relationship between superior sagittal sinus thrombosis
      and secondary seizure risk in a clinical cohort.
- category: Neurological
  name: Focal neurological deficits
  description: >-
    Focal neurological deficits can result from venous infarction or focal lobar
    injury.
  phenotype_term:
    preferred_term: Hemiparesis
    term:
      id: HP:0001269
      label: Hemiparesis
  evidence:
  - reference: PMID:17183977
    reference_title: Pathophysiology of cerebral venous thrombosis--an overview.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      local signs due to venous infarct, e.g., hemiparesis and global signs due
      to raised ICP from an obstructed venous system
    explanation: >-
      This supports hemiparesis as a focal sign caused by venous infarction.
- category: Vascular
  name: Cerebral hemorrhage
  description: >-
    Hemorrhagic venous infarction or parenchymal bleeding may accompany severe
    cerebral venous sinus thrombosis and contributes to neurological risk.
  phenotype_term:
    preferred_term: Cerebral hemorrhage
    term:
      id: HP:0001342
      label: Cerebral hemorrhage
  evidence:
  - reference: PMID:29039017
    reference_title: "Cerebral venous sinus thrombosis complicated by seizures: a retrospective analysis of 69 cases."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Compared with those with no seizures, significantly more patients with
      secondary seizures had hemiplegia (37.50 vs. 15.63%; P = 0.020), bleeding
      (29.40 vs. 10.81%; P = 0.047), lesions involving the frontal (31.25 vs.
      10.81%; P = 0.023) and temporal lobe (43.75 vs. 8.11%; P = 0.005)
    explanation: >-
      This cohort supports bleeding and focal lobar lesions among CVST patients
      with secondary seizures.
- category: Neurological
  name: Reduced consciousness
  description: >-
    Severe cerebral venous thrombosis can present with loss of consciousness or
    other altered-consciousness states.
  phenotype_term:
    preferred_term: Loss of consciousness
    term:
      id: HP:0007185
      label: Loss of consciousness
  evidence:
  - reference: PMID:38050259
    reference_title: "Pathophysiology, diagnosis and management of cerebral venous thrombosis: A comprehensive review."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The presenting symptoms can range from headache to loss of consciousness.
    explanation: >-
      This supports reduced consciousness as part of the clinical spectrum.
diagnosis:
- name: MR venography or CT venography demonstration of thrombus
  description: >-
    Diagnosis is confirmed by demonstrating thrombus in cerebral veins or dural
    venous sinuses using MR/MR venography or venous CT.
  diagnosis_term:
    preferred_term: venography
    term:
      id: NCIT:C38099
      label: Venography
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The confirmation of the diagnosis of CVT relies on the demonstration of
      thrombi in the cerebral veins and/or sinuses by MR/MR venography or veno
      CT.
    explanation: >-
      This supports venous imaging confirmation as the diagnostic standard.
progression:
- phase: Acute symptomatic venous sinus thrombosis
  notes: >-
    Acute presentation ranges from isolated headache to encephalopathy or loss
    of consciousness. Prognosis is often favorable with expert care, but severe
    cases can deteriorate from intracranial hypertension, venous infarction, or
    hemorrhage.
  evidence:
  - reference: PMID:38050259
    reference_title: "Pathophysiology, diagnosis and management of cerebral venous thrombosis: A comprehensive review."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The presenting symptoms can range from headache to loss of consciousness.
    explanation: >-
      This supports a wide acute presentation spectrum.
  - reference: PMID:38050259
    reference_title: "Pathophysiology, diagnosis and management of cerebral venous thrombosis: A comprehensive review."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Nevertheless, approximately 80% of patients have a good recovery
    explanation: >-
      This supports generally favorable recovery in many patients while not
      excluding severe outcomes.
treatments:
- name: Acute heparin anticoagulation
  description: >-
    Acute treatment uses unfractionated or low-molecular-weight heparin to limit
    thrombus extension and support recanalization; longer-term anticoagulation
    is tailored to thrombotic risk after the acute phase.
  treatment_term:
    preferred_term: pharmacotherapy
    term:
      id: MAXO:0000058
      label: pharmacotherapy
    therapeutic_agent:
    - preferred_term: heparin
      term:
        id: CHEBI:28304
        label: heparin
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The main intervention in the acute is anticoagulation with either low
      molecular weight or unfractionated heparin.
    explanation: >-
      This review directly supports heparin anticoagulation as the main acute
      intervention.
  - reference: PMID:39492709
    reference_title: "Treatment of cerebral venous thrombosis: a review."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      We found that LMWH and UH are safe and effective for the management of
      acute CVT and should be considered first line.
    explanation: >-
      This recent treatment review supports low-molecular-weight and
      unfractionated heparin as first-line acute CVT therapy.
- name: Endovascular thrombolysis or thrombectomy
  description: >-
    Local thrombolysis or mechanical thrombectomy may be considered in selected
    severe cases or when clinical status deteriorates despite anticoagulation,
    but evidence remains limited and specialist-center selection is important.
  treatment_term:
    preferred_term: thrombectomy
    term:
      id: NCIT:C52003
      label: Thrombectomy
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In patients in severe condition on admission or who deteriorate despite
      anticoagulation, local thrombolysis or thrombectomy is an option.
    explanation: >-
      This supports endovascular therapy only for selected severe or
      deteriorating patients.
  - reference: PMID:25899238
    reference_title: "Mechanical thrombectomy in cerebral venous thrombosis: systematic review of 185 cases."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Cerebral venous thrombosis is generally treated with anticoagulation.
      However, some patients do not respond to medical therapy and these might
      benefit from mechanical thrombectomy.
    explanation: >-
      This systematic review supports thrombectomy as a possible option after
      inadequate response to medical therapy.
- name: Decompressive surgery for life-threatening mass effect
  description: >-
    Decompressive craniectomy may be used in life-threatening cases with large
    venous infarcts, hemorrhage, or severe intracranial pressure elevation.
  treatment_term:
    preferred_term: surgical procedure
    term:
      id: MAXO:0000004
      label: surgical procedure
  evidence:
  - reference: PMID:25073867
    reference_title: "Cerebral venous sinus thrombosis: update on diagnosis and management."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Decompressive surgery is life-saving in patients with large venous
      infarcts or haemorrhage.
    explanation: >-
      This supports decompressive surgery for selected life-threatening venous
      infarction or hemorrhage.
  - reference: PMID:39492709
    reference_title: "Treatment of cerebral venous thrombosis: a review."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Decompressive craniectomy may be used to reduce intracranial pressure in
      life-threatening cases.
    explanation: >-
      This recent treatment review supports decompressive craniectomy for
      selected life-threatening cases.

📚

References & Deep Research

Deep Research

2

Falcon ▸

Disease Characteristics Research Template

Edison Scientific Literature 57 citations 2026-05-06T08:56:15.283523

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Characteristics Research Template

Target Disease

Disease Name: Sagittal Sinus Thrombosis
MONDO ID: (if available)
Category: Complex

Research Objectives

Please provide a comprehensive research report on Sagittal Sinus Thrombosis covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.

For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.

1. Disease Information

Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed

What is the disease? Provide a concise overview.
What are the key identifiers? (OMIM, Orphanet, ICD-10/ICD-11, MeSH, Mondo)
What are the common synonyms and alternative names?
Is the information derived from individual patients (e.g., EHR) or aggregated disease-level resources?

2. Etiology

Disease Causal Factors: What are the primary causes? (genetic, environmental, infectious, mechanistic)
Risk Factors:

Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases
Genetic risk factors (causal variants, susceptibility loci, modifier genes)
Environmental risk factors (toxins, lifestyle, occupational exposures, age, sex, family history)
Protective Factors:

Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases
Genetic protective factors (protective variants, modifier alleles)
Environmental protective factors (diet, lifestyle, exposures that reduce risk)
Gene-Environment Interactions: How do genetic and environmental factors interact to influence disease?

Search first: CTD, PubMed, PheGenI, GxE databases

3. Phenotypes

Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC

For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities

For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype

4. Genetic/Molecular Information

Causal Genes: Gene mutations or chromosomal abnormalities responsible for disease (gene symbols, OMIM IDs)

Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene
Pathogenic Variants:
Affected genes (gene symbols, HGNC IDs) > Search first: OMIM, NCBI Gene, Ensembl, HGNC, UniProt, GeneCards
Variant classification (pathogenic, likely pathogenic, VUS per ACMG/AMP guidelines) > Search first: ClinVar, ClinGen, ACMG/AMP guidelines, VarSome
Variant type/class (missense, frameshift, nonsense, splice-site, structural)
Allele frequency in population databases > Search first: gnomAD, 1000 Genomes, ExAC, TOPMed, dbSNP
Somatic vs germline origin > Search first: COSMIC (somatic), ClinVar, ICGC, TCGA
Functional consequences (loss of function, gain of function, dominant negative)
Modifier Genes: Genes that modify disease severity or expression
Epigenetic Information: DNA methylation, histone modifications, chromatin changes affecting disease

Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth
Chromosomal Abnormalities: Large-scale genetic changes (aneuploidy, translocations, inversions)

Search first: DECIPHER, ClinVar, ECARUCA, UCSC Genome Browser

5. Environmental Information

Environmental Factors: Non-genetic contributing factors (toxins, radiation, pollution, occupational exposure)

Search first: CTD (Comparative Toxicogenomics Database), TOXNET, PubMed, EPA databases
Lifestyle Factors: Behavioral factors (smoking, diet, exercise, alcohol consumption)

Search first: CDC databases, WHO, PubMed, NHANES
Infectious Agents: If applicable, pathogens causing or triggering disease (bacteria, viruses, fungi, parasites)

Search first: NCBI Taxonomy, ViPR, BV-BRC, MicrobeDB, GIDEON

6. Mechanism / Pathophysiology

Molecular Pathways: Specific signaling cascades or biochemical pathways involved (Wnt, MAPK, mTOR, PI3K-AKT, etc.)

Search first: KEGG, Reactome, WikiPathways, PathBank, BioCyc
Cellular Processes: Cell-level mechanisms (apoptosis, autophagy, cell cycle dysregulation, inflammation, etc.)

Search first: Gene Ontology (GO), Reactome, KEGG, PubMed
Protein Dysfunction: How protein structure or function is altered (misfolding, aggregation, loss of function, gain of function)

Search first: UniProt, PDB (Protein Data Bank), InterPro, Pfam, AlphaFold
Metabolic Changes: Alterations in metabolic processes (energy metabolism, lipid metabolism, amino acid metabolism)

Search first: KEGG, BioCyc, HMDB (Human Metabolome Database), BRENDA
Immune System Involvement: Role of immune response (autoimmunity, immunodeficiency, chronic inflammation)

Search first: ImmPort, Immunome Database, IEDB, Gene Ontology
Tissue Damage Mechanisms: How tissues/ are injured (oxidative stress, ischemia, fibrosis, necrosis)

Search first: PubMed, Gene Ontology, Reactome
Biochemical Abnormalities: Specific molecular defects (enzyme deficiencies, receptor dysfunction, ion channel defects)

Search first: BRENDA, UniProt, KEGG, OMIM, PubMed
Epigenetic Changes: DNA methylation, histone modifications affecting gene expression in disease

Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth
Molecular Profiling (if available):
Transcriptomics/gene expression changes > Search first: GEO (Gene Expression Omnibus), ArrayExpress, GTEx, Human Cell Atlas, SRA
Proteomics findings > Search first: PRIDE, ProteomeXchange, Human Protein Atlas, STRING, BioGRID
Metabolomics signatures > Search first: MetaboLights, Metabolomics Workbench, HMDB, METLIN
Lipidomics alterations > Search first: LIPID MAPS, SwissLipids, LipidHome, Metabolomics Workbench
Genomic structural features > Search first: UCSC Genome Browser, Ensembl, NCBI, dbVar, DGV
Advanced Technologies (if applicable):
Single-cell analysis findings (cell-type specific mechanisms, cellular heterogeneity) > Search first: Human Cell Atlas, Single Cell Portal, GEO, CELLxGENE
Spatial transcriptomics findings > Search first: GEO, Spatial Research, Vizgen, 10x Genomics data
Multi-omics integration results > Search first: TCGA, ICGC, cBioPortal, LinkedOmics, PubMed
Functional genomics screens (CRISPR, RNAi) > Search first: DepMap, GenomeRNAi, PubMed, BioGRID ORCS

For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types

7. Anatomical Structures Affected

Organ Level:
Primary organs directly affected
Secondary organ involvement (complications, secondary effects)
Body systems involved (cardiovascular, nervous, digestive, respiratory, endocrine, etc.)

Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT
Tissue and Cell Level:
Specific tissue types affected (epithelial, connective, muscle, nervous)
Specific cell populations targeted (with Cell Ontology terms)

Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB
Subcellular Level:
Cellular compartments involved (mitochondria, nucleus, ER, lysosomes) (with GO Cellular Component terms)

Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas
Localization:
Specific anatomical sites (with UBERON terms) > Search first: FMA, Uberon, NeuroNames (for brain), SNOMED CT
Lateralization (unilateral, bilateral, asymmetric) > Search first: HPO, clinical literature, imaging databases

8. Temporal Development

Onset:
Typical age of onset (congenital, pediatric, adult, geriatric)
Onset pattern (acute, subacute, chronic, insidious)

Search first: OMIM, Orphanet, HPO, PubMed
Progression:
Disease stages (early, intermediate, advanced, end-stage) > Search first: Cancer Staging Manual (AJCC), WHO classifications, PubMed
Progression rate (rapid, slow, variable)
Disease course pattern (episodic, relapsing-remitting, progressive, stable)
Disease duration (self-limited, chronic lifelong)

Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM
Patterns:
Remission patterns (spontaneous, treatment-induced) > Search first: Clinical trial databases, disease registries, PubMed
Critical periods (time windows of vulnerability or opportunity for intervention) > Search first: PubMed, developmental biology databases, clinical guidelines

9. Inheritance and Population

Epidemiology:
Prevalence (cases per 100,000 at given time)
Incidence (new cases per 100,000 per year)

Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries
For Genetic Etiology:
Inheritance pattern (AD, AR, X-linked, mitochondrial, multifactorial, polygenic) > Search first: OMIM, Orphanet, ClinVar, GTR (Genetic Testing Registry)
Penetrance (complete, incomplete, age-dependent) > Search first: ClinVar, OMIM, PubMed, ClinGen
Expressivity (variable, consistent) > Search first: OMIM, ClinVar, PubMed
Genetic anticipation (increasing severity in successive generations) > Search first: OMIM, PubMed (especially for repeat expansion disorders)
Germline mosaicism > Search first: ClinVar, OMIM, genetic counseling literature, PubMed
Founder effects (population-specific mutations) > Search first: gnomAD, population genetics databases, PubMed
Consanguinity role > Search first: OMIM, population studies, genetic counseling resources
Carrier frequency > Search first: gnomAD, carrier screening databases, GeneReviews, GTR
Population Demographics:
Affected populations (ethnic or demographic groups with higher prevalence) > Search first: gnomAD, 1000 Genomes, PAGE Study, PubMed, population registries
Geographic distribution (endemic areas, regional variation) > Search first: WHO, CDC, GBD, Orphanet, geographic epidemiology databases
Geographic distribution of specific variants
Sex ratio (male:female) > Search first: Disease registries, OMIM, PubMed, epidemiological databases
Age distribution of affected individuals > Search first: CDC, disease registries, SEER, Orphanet

10. Diagnostics

Clinical Tests:
Laboratory tests (blood, urine, tissue chemistry, specific enzyme assays) > Search first: LOINC, LabTests Online, PubMed
Biomarkers (proteins, metabolites, genetic markers, circulating biomarkers) > Search first: FDA Biomarker List, BEST (Biomarkers, EndpointS, and other Tools), PubMed
Imaging studies (X-ray, CT, MRI, PET, ultrasound) > Search first: RadLex, DICOM, Radiopaedia, imaging databases
Functional tests (pulmonary function, cardiac stress tests) > Search first: LOINC, clinical guidelines, PubMed
Electrophysiology (EEG, EMG, ECG, nerve conduction studies) > Search first: LOINC, clinical neurophysiology databases, PubMed
Biopsy findings (histopathology, immunohistochemistry) > Search first: SNOMED CT, College of American Pathologists resources, PubMed
Pathology findings (microscopic examination) > Search first: SNOMED CT, Digital Pathology databases, PubMed
Genetic Testing:

Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen
Overview of recommended genetic testing approach
Whole genome sequencing (WGS) utility > Search first: GTR, ClinVar, GEL (Genomics England), gnomAD
Whole exome sequencing (WES) utility > Search first: GTR, ClinVar, OMIM, GeneMatcher
Gene panels (which panels, which genes) > Search first: GTR, ClinVar, laboratory-specific databases
Single gene testing > Search first: GTR, ClinVar, OMIM, GeneReviews
Chromosomal microarray (CMA) > Search first: DECIPHER, ClinVar, dbVar, ECARUCA
Karyotyping > Search first: Chromosome Abnormality Database, ClinVar, cytogenetics resources
FISH > Search first: ClinVar, cytogenetics databases, PubMed
Mitochondrial DNA testing > Search first: MITOMAP, MSeqDR, ClinVar, GTR
Repeat expansion testing > Search first: GTR, ClinVar, repeat expansion databases, PubMed
Omics-Based Diagnostics (if applicable):
RNA sequencing / transcriptomics > Search first: GEO, ArrayExpress, GTEx, RNA-seq databases
Proteomics > Search first: PRIDE, ProteomeXchange, FDA Biomarker database
Metabolomics > Search first: MetaboLights, Metabolomics Workbench, HMDB
Epigenomics > Search first: GEO, ENCODE, Roadmap Epigenomics, MethBase
Liquid biopsy > Search first: COSMIC, ClinVar, liquid biopsy databases, PubMed
Clinical Criteria:
Standardized diagnostic criteria (DSM, ICD, society guidelines) > Search first: DSM-5, ICD-11, clinical society guidelines, UpToDate
Differential diagnosis (other conditions to rule out, with distinguishing features) > Search first: DynaMed, UpToDate, clinical decision support systems
Screening:
Screening methods for asymptomatic individuals (newborn screening, carrier screening, cascade screening) > Search first: ACMG recommendations, CDC newborn screening, GTR

11. Outcome/Prognosis

Survival and Mortality:
Survival rate (5-year, 10-year, overall) > Search first: SEER, cancer registries, disease-specific registries, PubMed
Life expectancy (with and without treatment if applicable) > Search first: Orphanet, disease registries, actuarial databases, PubMed
Mortality rate > Search first: CDC, WHO, GBD, national mortality databases
Disease-specific mortality (deaths directly attributable to disease) > Search first: Disease registries, CDC Wonder, GBD, PubMed
Morbidity and Function:
Morbidity (disease-related disability and health impacts) > Search first: GBD, WHO, disability databases, PubMed
Disability outcomes (long-term functional impairments) > Search first: ICF (International Classification of Functioning), disability registries
Quality of life measures (EQ-5D, SF-36, PROMIS, disease-specific tools) > Search first: EQ-5D database, SF-36, PROMIS, PubMed
Disease Course:
Complications (secondary problems: infections, organ failure, etc.) > Search first: ICD codes, disease registries, clinical databases, PubMed
Recovery potential (likelihood and extent of recovery, with vs without treatment) > Search first: Natural history studies, rehabilitation databases, PubMed
Prediction:
Prognostic factors (age, disease severity, biomarkers, treatment response) > Search first: Prognostic models databases, clinical calculators, PubMed
Prognostic biomarkers (molecular markers predicting disease course) > Search first: FDA Biomarker database, PubMed, cancer prognostic databases

12. Treatment

Pharmacotherapy:
Pharmacological treatments (drug names, drug classes, mechanisms of action) > Search first: DrugBank, RxNorm, ATC classification, DailyMed, FDA databases
Pharmacogenomics (how genetic variants affect drug metabolism, efficacy, toxicity) > Search first: PharmGKB, CPIC (Clinical Pharmacogenetics), FDA Table of PGx Biomarkers
Advanced Therapeutics:
Gene therapy (viral vectors, CRISPR, gene replacement, gene editing) > Search first: ClinicalTrials.gov, FDA gene therapy database, ASGCT resources
Cell therapy (stem cell transplant, CAR-T, cellular therapeutics) > Search first: ClinicalTrials.gov, FDA cell therapy database, FACT standards
RNA-based therapies (ASOs, siRNA, mRNA therapies) > Search first: ClinicalTrials.gov, FDA approvals, PubMed
Targeted therapies (treatments directed at specific molecular targets) > Search first: My Cancer Genome, OncoKB, ClinicalTrials.gov, FDA approvals
Immunotherapies (checkpoint inhibitors, monoclonal antibodies) > Search first: Cancer Immunotherapy Database, FDA approvals, ClinicalTrials.gov
Surgical and Interventional:
Surgical interventions (types of surgery, timing, outcomes) > Search first: CPT codes, surgical registries, clinical guidelines, PubMed
Supportive and Rehabilitative:
Supportive care (symptom management, pain control, nutrition) > Search first: Clinical guidelines, Cochrane Library, PubMed
Rehabilitation (physical therapy, occupational therapy, speech therapy) > Search first: Rehabilitation medicine databases, clinical guidelines, PubMed
Experimental:
Experimental treatments in clinical trials (with NCT identifiers if available) > Search first: ClinicalTrials.gov, EU Clinical Trials Register, WHO ICTRP
Treatment Outcomes:
Treatment response rates > Search first: Clinical trial databases, FDA reviews, systematic reviews, PubMed
Side effects and adverse events > Search first: FDA Adverse Event Reporting System (FAERS), MedWatch, PubMed
Treatment Strategy:
Treatment algorithms (clinical pathways, decision trees) > Search first: Clinical practice guidelines, NCCN Guidelines, UpToDate
Combination therapies > Search first: ClinicalTrials.gov, treatment guidelines, PubMed
Personalized medicine approaches (genotype-guided treatment) > Search first: My Cancer Genome, CIViC, PharmGKB, precision medicine databases

For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.

13. Prevention

Prevention Levels:
Primary prevention (preventing disease occurrence: vaccination, risk factor modification) > Search first: CDC, WHO, USPSTF recommendations, Cochrane Library
Secondary prevention (early detection and treatment: screening programs, early intervention) > Search first: USPSTF, CDC screening guidelines, WHO
Tertiary prevention (preventing complications in those with disease) > Search first: Clinical guidelines, disease management protocols, PubMed
Immunization: Vaccine strategies (if applicable)

Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database
Screening and Early Detection:
Screening programs (population-based: newborn screening, cancer screening) > Search first: CDC screening programs, USPSTF, cancer screening databases
Genetic screening (carrier screening, preimplantation genetic diagnosis, prenatal testing) > Search first: ACMG recommendations, ACOG guidelines, GTR
Risk stratification (identifying high-risk individuals for targeted prevention) > Search first: Risk prediction models, clinical calculators, PubMed
Behavioral Interventions: Lifestyle modifications to reduce risk

Search first: CDC, WHO, behavioral intervention databases, Cochrane Library
Counseling: Genetic counseling (risk assessment, family planning guidance)

Search first: NSGC resources, ACMG guidelines, GeneReviews
Public Health:
Public health interventions (sanitation, vector control, health education) > Search first: CDC, WHO, public health databases, PubMed
Environmental interventions (reducing environmental risk factors) > Search first: EPA databases, WHO environmental health, PubMed
Prophylaxis: Preventive medications or procedures

Search first: Clinical guidelines, FDA approvals, PubMed

14. Other Species / Natural Disease

Taxonomy: Species affected (with NCBI Taxon identifiers)

Search first: NCBI Taxonomy
Breed: Specific breeds affected (with VBO identifiers if applicable)

Search first: VBO (Vertebrate Breed Ontology)
Gene: Orthologous genes in other species (with NCBI Gene IDs)

Search first: NCBI Gene
Natural Disease:
Naturally occurring disease in other species (companion animals, wildlife) > Search first: OMIA (Online Mendelian Inheritance in Animals), VetCompass, PubMed
Veterinary relevance and importance in animal health > Search first: OMIA, veterinary databases, PubMed
Comparative Biology:
Comparative pathology (similarities and differences across species) > Search first: OMIA, comparative pathology databases, PubMed
Evolutionary conservation of disease mechanisms > Search first: HomoloGene, OrthoMCL, Alliance of Genome Resources
Transmission (if applicable):
Zoonotic potential > Search first: CDC zoonotic diseases, WHO zoonoses, GIDEON
Cross-species susceptibility > Search first: NCBI Taxonomy, veterinary databases, PubMed

15. Model Organisms

Model Types:
Model organism type (mammalian, invertebrate, cellular, in vitro) > Search first: Alliance of Genome Resources, model organism databases
Specific model systems (mouse, rat, zebrafish, Drosophila, C. elegans, yeast, cell lines, organoids, iPSCs) > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, SGD, ATCC, Cellosaurus
Induced models (drug treatment, surgical intervention, environmental manipulation) > Search first: MGI, model organism databases, PubMed
Genetic Models:
Types available (knockout, knock-in, transgenic, conditional, humanized) > Search first: MGI, IMPC, KOMP, EuMMCR, IMSR
Model Characteristics:
Phenotype recapitulation (how well model reproduces human disease features) > Search first: Model organism databases, comparative studies, PubMed
Model limitations (aspects of human disease not captured) > Search first: Model organism databases, PubMed, review articles
Applications:
Research applications (what aspects of disease can be studied) > Search first: Model organism databases, PubMed
Resources:
Model databases > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, IMSR, EMMA, MMRRC

Citation Requirements

Cite primary literature (PMID preferred) for all mechanistic and clinical claims
Prioritize recent reviews and landmark papers
Include direct quotes from abstracts where possible to support key statements
Distinguish evidence source types: human clinical, model organism, in vitro, computational

Output Format

Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease

This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details

Comprehensive Disease Characteristics Report: Sagittal Sinus Thrombosis (Superior Sagittal Sinus Thrombosis)

Executive summary

Sagittal sinus thrombosis typically refers to superior sagittal sinus (SSS) thrombosis, a common site of cerebral venous thrombosis (CVT)/cerebral venous sinus thrombosis (CVST), an uncommon stroke subtype caused by thrombus formation in dural venous sinuses and/or cerebral veins. (umurungi2024cerebralveinthrombosis pages 1-2, research2024newrecommendationson pages 2-4)

Key 2023–2024 updates include: (i) guideline caution that D-dimer should not be used routinely to rule out CVT, (ii) stronger consensus toward LMWH in the acute phase and increasing adoption of DOACs in the post-acute maintenance phase for many patients (except selected thrombophilias such as triple-positive APS), and (iii) ongoing uncertainty about endovascular therapy (EVT) benefit, with emerging observational evidence that earlier EVT in severe CVST may improve functional outcomes—requiring randomized confirmation. (research2024newrecommendationson pages 4-5, research2024newrecommendationson pages 7-8, bucke2024earlyversuslate pages 1-2)

A structured evidence table (identifiers, epidemiology, risks, phenotypes, diagnostics, treatments, outcomes, trials) is embedded below.

Domain	Key findings for sagittal (superior) sagittal sinus thrombosis within CVT/CVST	Key numbers / practice points	Source URL / date	Citations
Identifiers / definition / synonyms	Sagittal sinus thrombosis usually refers to superior sagittal sinus (SSS) thrombosis, a subtype/site of cerebral venous thrombosis (CVT) or cerebral venous sinus thrombosis (CVST) involving the dural venous sinuses. Common synonyms: superior sagittal sinus thrombosis, sagittal sinus thrombosis, cerebral venous sinus thrombosis, cerebral sinovenous thrombosis. SSS is among the most commonly involved sinuses and is particularly associated with impaired CSF reabsorption and intracranial hypertension.	CVT accounts for ~0.5–1.0% of all strokes; SSS is frequently involved, often in combination with other sinuses.	German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9; J Clin Med review, Aug 2024: https://doi.org/10.3390/jcm13164730; CNS Neurosci Ther, Mar 2023: https://doi.org/10.1111/cns.14194	(umurungi2024cerebralveinthrombosis pages 1-2, wei2023intracranialhypertensionafter pages 1-2, research2024newrecommendationson pages 2-4)
Epidemiology	CVT is rare but increasingly recognized. Incidence estimates in recent reviews are ~1–2/100,000/year in Western Europe; international agenda paper cites ~1.2–1.6/100,000 person-years. Historical demographic pattern is strong female predominance, especially in reproductive years, though regional cohorts may differ.	Women ~75% in guideline summaries; historical female:male ratio ~3:1 in fertile-age adults. Registry example from India showed median age 29 years and male predominance (63.8%) in that cohort. Mortality in modern series often <5%, but broader literature still cites 3–15%.	Int J Stroke agenda, Apr 2024: https://doi.org/10.1177/17474930241242266; J Clin Med review, Aug 2024: https://doi.org/10.3390/jcm13164730; Sci Rep registry, Jul 2025: https://doi.org/10.1038/s41598-025-07599-x	(aggarwal2025epidemiologyandrisk pages 1-2, umurungi2024cerebralveinthrombosis pages 1-2, coutinho2024reducingtheglobal pages 1-2)
Major risk factors	CVT/SSS thrombosis is usually multifactorial; a provoking factor is identifiable in ~85%. Major risks include: female sex-specific factors (combined hormonal contraceptives, pregnancy/postpartum), thrombophilia, local head/neck infection, malignancy, myeloproliferative neoplasms/JAK2 V617F, inflammatory/autoimmune disease, trauma/neurosurgery, and rare immune causes such as vaccine-induced immune thrombotic thrombocytopenia (VITT) after adenoviral SARS-CoV-2 vaccination.	Approximate frequencies from guideline/reviews: combined hormonal contraceptives in 40–50% of women with CVT; thrombophilia 34–40%; pregnancy/postpartum 10–20%; local infections ~10%; JAK2 V617F 6–7%; myeloproliferative disease 4%; idiopathic 10–20%. In patients >55 years, malignancy may account for ~25% of cases.	German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9; J Clin Med review, Aug 2024: https://doi.org/10.3390/jcm13164730	(research2024newrecommendationson pages 2-4, umurungi2024cerebralveinthrombosis pages 2-4)
Genetic / molecular predisposition	Important inherited/acquired thrombophilic contributors include Factor V Leiden (F5), prothrombin G20210A (F2), antithrombin deficiency (SERPINC1), protein C deficiency (PROC), protein S deficiency (PROS1), antiphospholipid syndrome, and JAK2 V617F-positive myeloproliferative neoplasms. Thrombophilia testing is not recommended routinely for all patients, but may influence management in selected patients (young, spontaneous, recurrent, or family history-positive cases).	Genetic factors estimated in ~20–30% in one registry summary; hereditary thrombophilia independently associated with intracranial hypertension after CVT in one cohort (OR 2.21). Triple-positive APS is an exception where VKA is preferred over DOACs.	Sci Rep registry, Jul 2025: https://doi.org/10.1038/s41598-025-07599-x; German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9; CNS Neurosci Ther, Mar 2023: https://doi.org/10.1111/cns.14194	(aggarwal2025epidemiologyandrisk pages 1-2, wei2023intracranialhypertensionafter pages 1-2, research2024newrecommendationson pages 2-4, research2024newrecommendationson pages 7-8)
Common presenting symptoms / phenotypes	Presentation is heterogeneous, but dominant syndromes are intracranial hypertension (headache, vomiting, papilledema, visual disturbance), focal syndrome (motor/sensory deficits, aphasia, hemianopia, focal seizures), and encephalopathy / reduced consciousness. SSS thrombosis is especially linked to raised intracranial pressure because of reduced CSF absorption.	Large-series/guideline frequencies: headache ~87–90% (some reviews >90%); seizures 24–40%; focal neurological deficits 18–48%; depressed consciousness/encephalopathy 18–22%; visual loss 13–27%; diplopia/cranial neuropathies 11–14%. One registry found vomiting 39.5%, headache 29.6%.	Canadian Best Practice summary, 2024/2025: no DOI shown in retrieved text; J Clin Med review, Aug 2024: https://doi.org/10.3390/jcm13164730; Sci Rep registry, Jul 2025: https://doi.org/10.1038/s41598-025-07599-x	(aggarwal2025epidemiologyandrisk pages 1-2, umurungi2024cerebralveinthrombosis pages 2-4, field2025canadianstrokebest pages 3-4)
SSS-specific phenotype associations	SSS involvement is repeatedly associated with intracranial hypertension and with acute symptomatic seizures, especially when combined with cortical vein thrombosis, hemorrhage, or parenchymal lesions.	Acute symptomatic seizures occurred in 34% of 1,281 CVT patients; predictors included SSS thrombosis (aOR 2.0, 95% CI 1.5–2.6). Intracranial hypertension cohort: 83.6% had intracranial hypertension at diagnosis; SSS + right lateral sinus involvement independently associated (OR 4.115).	Neurology, Sep 2020: https://doi.org/10.1212/WNL.0000000000010577; CNS Neurosci Ther, Mar 2023: https://doi.org/10.1111/cns.14194	(wei2023intracranialhypertensionafter pages 1-2, bucke2024earlyversuslate pages 1-2)
Key diagnostics / imaging	Urgent neurovascular imaging is required. Recommended tests are contrast-enhanced CT venography (CTV) or contrast-enhanced MR venography (MRV); isolated non-contrast CT is insufficient, though a hyperdense sinus may suggest the diagnosis. MRI is preferred for cortical vein thrombosis and often in younger/pregnant patients; susceptibility-weighted or gradient-echo MRI can help for cortical veins. DSA is reserved for unresolved high-suspicion cases.	Non-contrast CT abnormal in only about 30%; hyperdense vein/sinus seen in about one-third of those cases. CT and MRI with venography are considered broadly equivalent for sinus thrombosis, but MRI is superior for cortical venous thrombosis.	German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9; Canadian Best Practice summary, 2024/2025; J Clin Med review, Aug 2024: https://doi.org/10.3390/jcm13164730	(research2024newrecommendationson pages 2-4, umurungi2024cerebralveinthrombosis pages 2-4, field2025canadianstrokebest pages 3-4)
D-dimer caveat	D-dimer should not be used routinely to rule out CVT. It may be considered only in selected low-probability patients with isolated headache, no focal deficits, and symptom duration <30 days; a negative result in that narrow context may help defer imaging, but not otherwise.	Guideline position: routine D-dimer exclusion testing not recommended.	German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9	(research2024newrecommendationson pages 2-4)
Acute treatment	Therapeutic-dose heparin is recommended even if intracranial hemorrhage is present. LMWH is preferred over UFH in the acute phase because of practical advantages and lower HIT risk; UFH is preferred if surgery/endovascular therapy may be needed or when LMWH is contraindicated (e.g., severe renal failure). Acute care should occur in monitored stroke-unit/ICU settings when severe.	Acute therapy begins with parenteral anticoagulation. Standard approach then transitions to oral maintenance anticoagulation.	German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9	(research2024newrecommendationson pages 5-7, research2024newrecommendationson pages 4-5)
Oral maintenance anticoagulation / DOAC vs VKA	After stabilization, patients are switched to oral anticoagulation for a maintenance phase. Recent guideline/review evidence increasingly supports DOACs as preferred over VKAs for many patients after the acute phase, except in triple-positive antiphospholipid syndrome, where VKA is preferred.	2024 RCT meta-analysis (4 RCTs, 270 participants): any recanalization 78.2% vs 83.2% (DOAC vs standard care); complete recanalization 60.9% vs 69.4%; major bleeding 1.2% vs 2.4%; ICH 1.9% vs 3.6%; death 0% vs 0.7%—all differences non-significant. Larger 2024 meta-analysis (25 studies, 2301 patients) found similar mRS 0–2, ICH, mortality, and recanalization between DOACs and warfarin.	Clin Appl Thromb Hemost, Jan 2024: https://doi.org/10.1177/10760296241256360; Health Sci Rep, Feb 2024: https://doi.org/10.1002/hsr2.1869; German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9	(research2024newrecommendationson pages 5-7, research2024newrecommendationson pages 7-8, chen2024efficacyandsafety pages 3-4, ranjan2024directoralanticoagulants pages 2-5, ranjan2024directoralanticoagulants pages 1-2, chen2024efficacyandsafety pages 1-2)
Duration of anticoagulation	Duration is individualized by provoking-factor and recurrence-risk profile. Guideline minimum is at least 3 months; usual maintenance phase is 3–12 months. Therapy should not be extended beyond 3–12 months solely to achieve more recanalization. Longer prophylaxis is considered when strong persistent risk factors remain (e.g., cancer, severe thrombophilia, autoimmune disease).	Recanalization occurs in ~85%, mostly within the first 3–6 months, with little additional recanalization after >12 months.	German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9	(research2024newrecommendationson pages 7-8)
Pregnancy / breastfeeding / contraception	In pregnancy or postpartum CVT, therapeutic LMWH is recommended; DOACs and VKAs should not be used during pregnancy because they cross the placenta. Continue anticoagulation until at least 6 weeks postpartum and for a total treatment duration ≥3 months. During breastfeeding, heparins and VKA/fondaparinux are considered acceptable, whereas DOACs are not recommended. Women with previous hormone-associated CVT should avoid combined estrogen-progestin contraception and prefer estrogen-free methods.	Practical prevention note: women with previous CVT and no contraindications should receive LMWH prophylaxis during pregnancy and for at least 6 weeks postpartum in the guideline summary.	German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9	(research2024newrecommendationson pages 2-4, research2024newrecommendationson pages 7-8)
Endovascular therapy	Not routine first-line therapy. EVT (mechanical thrombectomy ± local thrombolysis) is considered rescue therapy in severe CVT/SSS thrombosis for patients who deteriorate despite adequate anticoagulation, ideally in experienced neurointerventional centers. Evidence remains limited after the negative/neutral TO-ACT randomized experience.	2023 severe-CVT cohort: 21/23 procedures (91.3%) successful recanalization; 18/21 had mRS 0–2 at 6 months; morbidity and mortality each 4.7%. 2024 multicenter cohort: early EVT (<24 h) vs late EVT showed mRS 0–2 at 3 months 66.7% vs 27.3%; 90-day mortality 16.7% vs 36.4% (not statistically significant).	Diagnostics, Jul 2023: https://doi.org/10.3390/diagnostics13132248; Neurocrit Care, Jul 2024: https://doi.org/10.1007/s12028-024-02046-7; German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9	(research2024newrecommendationson pages 5-7, research2024newrecommendationson pages 4-5, bucke2024earlyversuslate pages 1-2, burns2024endovasculartherapyfor pages 1-2, piano2023endovasculartreatmentof pages 1-2)
Decompressive surgery	Decompressive hemicraniectomy / craniectomy is recommended in selected patients with CVT plus parenchymal lesion (congestive edema and/or hemorrhage) and impending herniation/incarceration to prevent death.	Review summary: about two-thirds survive, and about one-third are functionally independent at 6 months after decompressive craniectomy for impending herniation.	Curr Opin Neurol, Oct 2025: https://doi.org/10.1097/WCO.0000000000001329; German S2k guideline, Apr 2024: https://doi.org/10.1186/s42466-024-00320-9	(rosa2025updateonmanagement pages 1-2, research2024newrecommendationson pages 5-7)
Prognosis / outcomes	Modern outcomes are generally favorable with early diagnosis and anticoagulation, but residual symptoms are common. Many patients achieve good functional recovery, yet headache, visual symptoms, fatigue, cognitive symptoms, mood symptoms, and reduced work participation remain important long-term burdens.	About 80% achieve mRS 0–1 in recent review summaries; international agenda paper cites mortality 3–15% overall. Registry example: discharge survival ~97%, mortality 3.2%. In patients with intracranial hypertension after CVT, favorable 6-month outcome (mRS 0–2) was 83.67%, but residual visual impairment occurred in 15.51% vs 4.17% without intracranial hypertension.	Curr Opin Neurol, Oct 2025: https://doi.org/10.1097/WCO.0000000000001329; Int J Stroke, Apr 2024: https://doi.org/10.1177/17474930241242266; CNS Neurosci Ther, Mar 2023: https://doi.org/10.1111/cns.14194; Sci Rep, Jul 2025: https://doi.org/10.1038/s41598-025-07599-x	(rosa2025updateonmanagement pages 1-2, aggarwal2025epidemiologyandrisk pages 1-2, wei2023intracranialhypertensionafter pages 1-2, coutinho2024reducingtheglobal pages 1-2)
Ongoing / recent real-world trials	Current research is testing oral anticoagulant choices and severe-CVT interventions. Examples include randomized trials of dabigatran vs apixaban and dabigatran vs rivaroxaban, a dedicated venous sinus thrombectomy stent trial, and a planned multicenter trial of EVT + anticoagulation vs anticoagulation alone.	Examples: NCT06551415 dabigatran vs apixaban (Phase 3, n≈200); NCT06551402 dabigatran vs rivaroxaban (Phase 3, n≈200); NCT05291585 dedicated venous sinus thrombectomy stent (n=60); NCT07548346 REVIVE-CVST EVT trial (planned n≈440).	ClinicalTrials.gov records: https://clinicaltrials.gov/study/NCT06551415 ; https://clinicaltrials.gov/study/NCT06551402 ; https://clinicaltrials.gov/study/NCT05291585 ; https://clinicaltrials.gov/study/NCT07548346	(NCT06551415 chunk 1, NCT06551415 chunk 2, NCT07548346 chunk 1, NCT05291585 chunk 1)

Table: This table condenses current evidence and guideline-relevant facts for superior sagittal sinus thrombosis within the broader CVT/CVST spectrum. It is designed to support a knowledge-base entry with identifiers, epidemiology, risk factors, diagnosis, treatment, prognosis, and trial links in one citation-dense artifact.

1. Disease information

1.1 What is the disease?

Cerebral venous thrombosis (CVT) is thrombosis of the intracranial venous system (dural venous sinuses and/or cerebral veins). Superior sagittal sinus thrombosis is a location-specific subtype of CVT/CVST and is often associated with intracranial hypertension due to impaired CSF resorption. (umurungi2024cerebralveinthrombosis pages 1-2, wei2023intracranialhypertensionafter pages 1-2)

Source types: The information summarized here is primarily from aggregated disease-level resources (e.g., national guideline synthesis and systematic reviews) plus some human clinical cohorts and clinical trial registry entries. (research2024newrecommendationson pages 2-4, chen2024efficacyandsafety pages 3-4, NCT06551415 chunk 1)

1.2 Key identifiers (OMIM/Orphanet/ICD/MeSH/MONDO)

Limitation: The full-text sources retrieved in this run did not provide explicit ICD-10/ICD-11, MeSH, Orphanet, OMIM, or MONDO identifiers for “superior sagittal sinus thrombosis.” Therefore, these identifiers cannot be reliably populated here without direct access to the corresponding ontology databases (not retrieved in-tool in this run). (research2024newrecommendationson pages 2-4)

1.3 Synonyms and alternative names

Common clinical synonyms include: - Superior sagittal sinus thrombosis (SSS thrombosis) - Sagittal sinus thrombosis - Cerebral venous thrombosis (CVT) / cerebral venous sinus thrombosis (CVST) - Cerebral sinovenous thrombosis (term commonly used in pediatrics) These terms are used interchangeably in guideline and review sources discussing dural sinus thrombosis. (umurungi2024cerebralveinthrombosis pages 1-2, research2024newrecommendationson pages 2-4)

2. Etiology

2.1 Disease causal factors (mechanistic, environmental, infectious)

CVT/SSS thrombosis is generally multifactorial; a prothrombotic risk factor is identifiable in ~85% of cases in a 2024 DOAC-focused review. (umurungi2024cerebralveinthrombosis pages 1-2)

Major etiologic categories include: - Hormonal and pregnancy-related hypercoagulability (combined hormonal contraceptives; pregnancy/puerperium). (research2024newrecommendationson pages 2-4, umurungi2024cerebralveinthrombosis pages 2-4) - Thrombophilia (inherited or acquired). (research2024newrecommendationson pages 2-4, research2024newrecommendationson pages 7-8) - Inflammation/infection, especially head/neck infections in a subset. (research2024newrecommendationson pages 2-4, umurungi2024cerebralveinthrombosis pages 2-4) - Cancer and hematologic disorders, including myeloproliferative neoplasms (JAK2 V617F). (research2024newrecommendationson pages 2-4, umurungi2024cerebralveinthrombosis pages 2-4) - Immune-mediated prothrombotic syndromes, notably vaccine-induced immune thrombotic thrombocytopenia (VITT) after adenoviral SARS‑CoV‑2 vaccination, recognized in guideline updates. (research2024newrecommendationson pages 2-4)

2.2 Risk factors

Recent guideline-derived approximate frequencies for CVT risk contexts include: female sex (~75%), combined hormonal contraceptives (40–50% of women with CVT), thrombophilia (34–40%), pregnancy/postpartum (10–20%), local head/neck infections (~10%), JAK2 V617F (6–7%), myeloproliferative disease (4%), and idiopathic (10–20%). (research2024newrecommendationson pages 2-4)

A registry-based cohort (India, July 2022–Oct 2023 recruitment) illustrates region-specific heterogeneity: median age 29 years, male predominance in that cohort, and alcohol consumption associated with higher odds of CVST (OR 1.95). (aggarwal2025epidemiologyandrisk pages 1-2)

2.3 Protective factors

Limitation: The retrieved sources did not provide evidence for specific genetic or environmental protective factors for CVT/SSS thrombosis; this remains unpopulated from the current evidence set.

2.4 Gene–environment interactions

Clinically, strong gene–environment interactions are implied where thrombophilia co-occurs with hormonal/pregnancy risks and other prothrombotic exposures; however, the retrieved sources did not provide explicit quantitative interaction models.

3. Phenotypes

3.1 Common phenotypes and clinical presentation

Guideline-level prevalence estimates for presenting features include headache (~87–90%), seizures (24–40%), focal neurologic deficits (18–48%), depressed consciousness/encephalopathy (18–22%), visual loss (13–27%), and diplopia/cranial neuropathies (11–14%). (field2025canadianstrokebest pages 3-4)

A 2024 review emphasizes that presentations typically cluster into: - Intracranial hypertension syndrome (headache, vomiting, papilledema, visual disturbance) - Focal syndrome (motor/sensory deficits, aphasia, hemianopia, focal seizures) - Encephalopathy (multifocal deficits, altered consciousness) and notes headache occurs in >90% in many series. (umurungi2024cerebralveinthrombosis pages 2-4)

3.2 SSS-associated phenotype patterns

SSS involvement is repeatedly linked to intracranial hypertension and seizure risk. In a 2023 cohort of 293 CVT survivors, 83.6% had intracranial hypertension at diagnosis (opening pressure ≥250 mmH2O), and thrombosis involving SSS plus lateral sinus strongly associated with intracranial hypertension (OR 4.115). (wei2023intracranialhypertensionafter pages 1-2)

3.3 Phenotype ontology suggestions (HPO)

(ontology suggestions; not asserted as sourced frequencies) - Headache: HP:0002315 - Nausea/Vomiting: HP:0002013 / HP:0002017 - Papilledema: HP:0001085 - Visual impairment: HP:0000505; Visual field defect: HP:0001123 - Seizure: HP:0001250 - Focal neurological deficit / hemiparesis: HP:0001263 / HP:0002302 - Altered mental status / impaired consciousness: HP:0001254

3.4 Quality of life impact

The 2024 international research agenda highlights high prevalence of long-term sequelae (fatigue, headache, depression, cognitive deficits) and prioritizes PROMs and standardized long-term outcome sets, underscoring substantial post-CVT quality-of-life burden even when functional outcome scales are favorable. (coutinho2024reducingtheglobal pages 4-6, coutinho2024reducingtheglobal pages 2-4)

4. Genetic / molecular information

4.1 Causal genes and susceptibility genes

CVT is not classically monogenic, but inherited thrombophilia genes are clinically relevant contributors and may guide duration/type of anticoagulation in selected cases. (research2024newrecommendationson pages 2-4, research2024newrecommendationson pages 7-8)

Key genes/conditions highlighted across guideline and summaries include: - F5 (Factor V Leiden) - F2 (prothrombin G20210A) - SERPINC1 (antithrombin deficiency) - PROC (protein C deficiency) - PROS1 (protein S deficiency) - JAK2 (V617F; myeloproliferative neoplasms) - Antiphospholipid syndrome (APS) (acquired thrombophilia; “triple-positive APS” affects anticoagulant choice) These are explicitly listed as common thrombophilic risks in recent guideline/review summaries. (research2024newrecommendationson pages 2-4, field2025canadianstrokebest pages 3-4, research2024newrecommendationson pages 7-8)

4.2 Variant classes / somatic vs germline

The retrieved sources did not provide variant-level nomenclature, allele frequencies in gnomAD, or ClinVar classifications. JAK2 V617F is typically a somatic driver mutation in myeloproliferative neoplasms, but explicit variant annotations were not provided in the retrieved text.

4.3 Epigenetics / chromosomal abnormalities

Not available in the retrieved evidence.

5. Environmental information

Key non-genetic contributors include hormonal exposures (estrogen-containing contraceptives), pregnancy/postpartum physiology, infections (including head/neck infections and COVID-19-related contexts), obesity, trauma/neurosurgery, and some medications that increase thrombosis risk. (umurungi2024cerebralveinthrombosis pages 2-4)

6. Mechanism / pathophysiology

6.1 Causal chain (systems-level)

A consistent mechanistic chain across contemporary sources is: 1) Venous sinus/vein occlusion (thrombus) → 2) Venous outflow obstruction and venous hypertension → 3) Impaired CSF absorption (notably when SSS is involved) leading to intracranial hypertension → 4) Secondary parenchymal injury (edema/venous infarction and/or hemorrhage) and neurological symptoms (headache, focal deficits, seizures, encephalopathy). (umurungi2024cerebralveinthrombosis pages 1-2, wei2023intracranialhypertensionafter pages 1-2)

6.2 Suggested pathway/process ontology terms

(ontology suggestions; not asserted as uniquely CVT-specific) - GO biological processes: blood coagulation, platelet activation, fibrin clot formation, inflammatory response, response to hypoxia, regulation of vascular permeability, leukocyte adhesion. - Cell Ontology (CL) candidates: endothelial cell, platelet, neutrophil, monocyte/macrophage, astrocyte (secondary injury), microglia.

6.3 Knowledge gaps (expert consensus)

The 2024 international CVT research agenda identifies major gaps in: CVT-specific thrombosis mechanisms (vs other venous beds), inflammatory contributors to tissue injury, genetic susceptibility beyond limited known signals, biomarkers, and determination of which subgroups benefit from EVT and optimized device design for venous sinuses. (coutinho2024reducingtheglobal pages 2-4, coutinho2024reducingtheglobal pages 8-9, coutinho2024reducingtheglobal pages 6-7)

7. Anatomical structures affected

7.1 Organ/system level

Primary system: central nervous system; primary structures: dural venous sinuses and cerebral veins, especially the superior sagittal sinus in this disease entry. (wei2023intracranialhypertensionafter pages 1-2)

Ontology suggestions: - UBERON: dural venous sinus, superior sagittal sinus, brain, meninges.

7.2 Tissue/cell level

Key tissue compartments include venous endothelium and surrounding brain parenchyma affected by venous hypertension and edema/hemorrhage. (wei2023intracranialhypertensionafter pages 1-2)

8. Temporal development

CVT can have insidious onset; the Canadian summary notes less than half present within 48 hours, differing from typical arterial stroke. (field2025canadianstrokebest pages 3-4)

9. Inheritance and population

9.1 Epidemiology

Recent sources cite incidence around ~1–2 per 100,000 per year in Western Europe, and the 2024 international agenda cites ~1.2–1.6/100,000 person-years. (umurungi2024cerebralveinthrombosis pages 1-2, coutinho2024reducingtheglobal pages 1-2)

9.2 Population demographics

Historically, women predominate (≈75% in guideline summaries), driven in part by estrogen-related risks; however, regional cohorts can differ (e.g., one India registry showed male predominance). (aggarwal2025epidemiologyandrisk pages 1-2, research2024newrecommendationson pages 2-4)

10. Diagnostics

10.1 Imaging

Guideline and best-practice sources emphasize urgent neurovascular imaging: - Contrast-enhanced CTV or contrast-enhanced MRV for diagnosis; isolated non-contrast CT is insufficient. (field2025canadianstrokebest pages 3-4) - MRI is superior to CT for cortical venous thrombosis; CT and MRI with venography are otherwise broadly equivalent. (research2024newrecommendationson pages 2-4)

10.2 D-dimer

The 2024 German S2k summary states routine D-dimer testing to rule out CVT cannot be recommended, with only a narrow low-probability scenario where a negative D-dimer might justify omitting imaging. (research2024newrecommendationson pages 2-4)

10.3 Laboratory / thrombophilia testing

The guideline summary indicates thrombophilia screening is not universally recommended but may be considered when it will change management (e.g., young patients, spontaneous CVT, recurrent thrombosis, or positive family history). (research2024newrecommendationson pages 2-4)

11. Outcome / prognosis

Outcomes are often favorable with anticoagulation, but residual symptoms are common. A modern review reports ~80% achieve excellent functional outcome (mRS 0–1), yet persistent symptoms may affect return to work and quality of life. (rosa2025updateonmanagement pages 1-2)

Intracranial hypertension can be highly prevalent at diagnosis and is associated with higher risk of residual visual impairment at follow-up (15.51% vs 4.17% in one cohort). (wei2023intracranialhypertensionafter pages 1-2)

12. Treatment

12.1 Standard-of-care anticoagulation (real-world implementation)

The 2024 German guideline summary recommends: - Therapeutic-dose heparin in acute CVT even with intracranial hemorrhage. - Prefer LMWH over UFH unless impending surgery/EVT or contraindications (e.g., renal failure) favor UFH. (research2024newrecommendationson pages 4-5)

A treatment-phase schematic in the German guideline (Figure 1) summarizes the initial, maintenance, and secondary prophylaxis phases. (research2024newrecommendationson media 59ded2f2)

12.2 Oral maintenance: DOACs vs VKA (2023–2024 evidence)

In a 2024 meta-analysis of 4 RCTs (n=270), DOACs and standard care had similar recanalization and safety outcomes (e.g., any recanalization 78.2% vs 83.2%; major bleeding 1.2% vs 2.4%; ICH 1.9% vs 3.6%; death 0% vs 0.7%). (chen2024efficacyandsafety pages 3-4)

A broader 2024 meta-analysis (25 studies; 2301 patients) found comparable functional recovery (mRS 0–2), ICH, mortality, and recanalization between DOACs and warfarin. (ranjan2024directoralanticoagulants pages 2-5)

The German guideline summary states DOACs should be preferred over VKA for oral anticoagulation in many CVT patients, except triple-positive APS (VKA preferred) and pregnancy/breastfeeding contexts. (research2024newrecommendationson pages 5-7, research2024newrecommendationson pages 7-8)

12.3 Duration

The 2024 German guideline summary recommends anticoagulation for at least 3 months, with typical maintenance 3–12 months, and not to prolong treatment solely to improve recanalization. (research2024newrecommendationson pages 7-8)

12.4 Endovascular therapy (EVT)

Guideline consensus: EVT is not routine first-line therapy; it may be considered individually for deterioration despite adequate anticoagulation, and local thrombolysis carries higher bleeding without proven outcome improvement. (research2024newrecommendationson pages 5-7)

Recent real-world data: - 2023 severe CVT EVT series: successful recanalization 91.3% and mRS 0–2 at 6 months in 18/21, with 4.7% morbidity and 4.7% mortality. (piano2023endovasculartreatmentof pages 1-2) - 2024 multicenter observational study: early EVT (<24 h) associated with higher 3‑month functional independence than late EVT (66.7% vs 27.3%). (bucke2024earlyversuslate pages 1-2) A 2024 commentary highlights that evidence remains uncertain and calls for randomized trials of “early EVT” strategies. (burns2024endovasculartherapyfor pages 1-2)

12.5 Decompressive surgery

Decompressive hemicraniectomy is recommended in selected patients with parenchymal lesions and impending herniation to prevent death. (research2024newrecommendationson pages 5-7)

12.6 Treatment ontology suggestions (MAXO)

(ontology suggestions) - Therapeutic anticoagulation (heparin/LMWH): MAXO: anticoagulant therapy - Venous thrombectomy / endovascular thrombectomy: MAXO: thrombectomy - Decompressive craniectomy: MAXO: decompressive craniectomy - Management of intracranial hypertension (e.g., acetazolamide in practice; evidence gaps noted): MAXO: intracranial pressure management

13. Prevention

Guideline-derived prevention points include: - Avoid estrogen-containing combined contraceptives after hormone-associated CVT; prefer estrogen-free methods. (research2024newrecommendationson pages 7-8) - In pregnancy/postpartum with prior CVT (without contraindication), LMWH prophylaxis during pregnancy and for at least 6 weeks postpartum is recommended in the German guideline summary. (research2024newrecommendationson pages 7-8)

14. Other species / natural disease

Not available in the retrieved evidence.

15. Model organisms

Not available in the retrieved evidence.

Recent developments and current applications (2023–2024 emphasis)

1) German consensus-based S2k guideline (Apr 2024) updated recommendations spanning diagnosis, anticoagulation choice, DOAC caveats, pregnancy/breastfeeding, and selective thrombophilia evaluation; it explicitly discourages routine D-dimer exclusion. https://doi.org/10.1186/s42466-024-00320-9 (research2024newrecommendationson pages 2-4, research2024newrecommendationson pages 7-8)

2) DOAC evidence consolidation (Jan–Feb 2024) via meta-analyses indicates DOACs are broadly comparable to warfarin/standard care for recanalization, bleeding, and mortality outcomes, supporting increasing real-world adoption post-acute phase. https://doi.org/10.1177/10760296241256360 ; https://doi.org/10.1002/hsr2.1869 (chen2024efficacyandsafety pages 3-4, ranjan2024directoralanticoagulants pages 2-5)

3) Severe CVST EVT timing hypothesis (Jul 2024): observational data suggest earlier EVT may associate with better functional independence, but commentary stresses major confounding risks and calls for prospective trials. https://doi.org/10.1007/s12028-024-02046-7 ; https://doi.org/10.1007/s12028-024-02045-8 (bucke2024earlyversuslate pages 1-2, burns2024endovasculartherapyfor pages 1-2)

4) Global expert research agenda (Apr 2024): prioritizes long-term follow-up cohorts, improved diagnostic tools (including potential clinical-score + D-dimer strategies), trials for DOAC dosing/duration, and defining EVT candidates and devices optimized for venous sinuses. https://doi.org/10.1177/17474930241242266 (coutinho2024reducingtheglobal pages 2-4, coutinho2024reducingtheglobal pages 6-7)

Ongoing trials / real-world implementations (examples)

NCT06551415 (ClinicalTrials.gov; posted 2021; recruiting): Phase 3 RCT dabigatran 150 mg bid vs apixaban 5 mg bid for 6 months; primary endpoint partial/complete recanalization at Day 180. https://clinicaltrials.gov/study/NCT06551415 (NCT06551415 chunk 1)
NCT07548346 (REVIVE-CVST) (ClinicalTrials.gov; 2026; not yet recruiting): randomized PROBE EVT + anticoagulation vs anticoagulation alone in severe CVST; EVT within 24h. https://clinicaltrials.gov/study/NCT07548346 (NCT07548346 chunk 1)
NCT05291585 (ClinicalTrials.gov; 2022; completed): randomized device trial of a dedicated venous sinus thrombectomy stent vs balloon thrombectomy. https://clinicaltrials.gov/study/NCT05291585 (NCT05291585 chunk 1)

Direct abstract quotes supporting key claims

German S2k guideline abstract: “D-dimer testing to rule out CVT cannot be recommended and should therefore not be routinely performed.” (Neurological Research and Practice; accepted 20 Mar 2024) (research2024newrecommendationson pages 2-4)
German S2k guideline abstract: “Patients with CVT should preferably be treated with low molecular weight heparine (LMWH) instead of unfractionated heparine in the acute phase.” (research2024newrecommendationson pages 2-4)
German S2k guideline abstract: “Following the acute phase, oral anticoagulation with direct oral anticoagulants instead of vitamin K antagonists should be given for 3 to 12 months …” (research2024newrecommendationson pages 2-4)
DOAC RCT meta-analysis abstract (Jan 2024): “DOACs and standard of care showed similar efficacy and safety profiles for the treatment of CVT.” (chen2024efficacyandsafety pages 1-2)

Notes and limitations for knowledge-base population

PMID requirement: The retrieved evidence in this run is primarily identified by DOI and journal metadata; PMIDs were not provided in the tool outputs, so PMID-level citation cannot be guaranteed here.
Ontology IDs (MONDO/MeSH/ICD/Orphanet/OMIM): Not retrieved from ontology databases in this run; should be populated by direct ontology queries.
Molecular profiling / multi-omics / animal models: Not available in the accessed texts; likely requires targeted searches in GEO/PRIDE and preclinical thrombosis models.

References

(umurungi2024cerebralveinthrombosis pages 1-2): Johanna Umurungi, Francesca Ferrando, Daniela Cilloni, and Piera Sivera. Cerebral vein thrombosis and direct oral anticoagulants: a review. Journal of Clinical Medicine, 13:4730, Aug 2024. URL: https://doi.org/10.3390/jcm13164730, doi:10.3390/jcm13164730. This article has 4 citations.
(research2024newrecommendationson pages 2-4): Neurological Research, C. Weimar, J. Beyer-Westendorf, FO Bohmann, G. Hahn, S. Halimeh, S. Holzhauer, C. Kalka, M. Knoflach, H-C Koennecke, F. Masuhr, M-L Mono, U. Nowak-Göttl, E. Scherret, M. Schlamann, and B. Linnemann. New recommendations on cerebral venous and dural sinus thrombosis from the german consensus-based (s2k) guideline. Neurological Research and Practice, Apr 2024. URL: https://doi.org/10.1186/s42466-024-00320-9, doi:10.1186/s42466-024-00320-9. This article has 29 citations and is from a peer-reviewed journal.
(research2024newrecommendationson pages 4-5): Neurological Research, C. Weimar, J. Beyer-Westendorf, FO Bohmann, G. Hahn, S. Halimeh, S. Holzhauer, C. Kalka, M. Knoflach, H-C Koennecke, F. Masuhr, M-L Mono, U. Nowak-Göttl, E. Scherret, M. Schlamann, and B. Linnemann. New recommendations on cerebral venous and dural sinus thrombosis from the german consensus-based (s2k) guideline. Neurological Research and Practice, Apr 2024. URL: https://doi.org/10.1186/s42466-024-00320-9, doi:10.1186/s42466-024-00320-9. This article has 29 citations and is from a peer-reviewed journal.
(research2024newrecommendationson pages 7-8): Neurological Research, C. Weimar, J. Beyer-Westendorf, FO Bohmann, G. Hahn, S. Halimeh, S. Holzhauer, C. Kalka, M. Knoflach, H-C Koennecke, F. Masuhr, M-L Mono, U. Nowak-Göttl, E. Scherret, M. Schlamann, and B. Linnemann. New recommendations on cerebral venous and dural sinus thrombosis from the german consensus-based (s2k) guideline. Neurological Research and Practice, Apr 2024. URL: https://doi.org/10.1186/s42466-024-00320-9, doi:10.1186/s42466-024-00320-9. This article has 29 citations and is from a peer-reviewed journal.
(bucke2024earlyversuslate pages 1-2): Philipp Bücke, Hans Henkes, Johannes Kaesmacher, Mirjam R. Heldner, Adrian Scutelnic, Marcel Arnold, Thomas R. Meinel, Alexandru Cimpoca, Thomas Horvath, Elina Henkes, Hansjörg Bäzner, and Victoria Hellstern. Early versus late initiation of endovascular therapy in patients with severe cerebral venous sinus thrombosis. Neurocritical Care, 41:1047-1054, Jul 2024. URL: https://doi.org/10.1007/s12028-024-02046-7, doi:10.1007/s12028-024-02046-7. This article has 7 citations and is from a peer-reviewed journal.
(wei2023intracranialhypertensionafter pages 1-2): Huimin Wei, Huimin Jiang, Yifan Zhou, Lu Liu, Chen Zhou, and Xunming Ji. Intracranial hypertension after cerebral venous thrombosis—risk factors and outcomes. CNS Neuroscience & Therapeutics, 29:2540-2547, Mar 2023. URL: https://doi.org/10.1111/cns.14194, doi:10.1111/cns.14194. This article has 30 citations and is from a peer-reviewed journal.
(aggarwal2025epidemiologyandrisk pages 1-2): S. Aggarwal, Arun Kumar, Vishal Deo, Bhupen Bipin P. Chandan Kumar Ray Girish Baburao M. Iadar Barman Kulkarni Mohapatra Kulkarni Hemachandren Ti, Bhupen Barman, Bipin P. Kulkarni, Chandan Kumar Ray Mohapatra, Girish Baburao Kulkarni, M. Hemachandren, Iadarilang Tiewsoh, J. Gnanaraj, Karthik Vishwanathan, Narendra Kumar, Vikas Bhatia, Rakesh Yadav, K. S. Lakshmi, Syed Mudasir Qadri, and Heena Tabassum. Epidemiology and risk factors for cerebral venous sinus thrombosis: insights from leading centres in the i-regved registry, india. Scientific Reports, Jul 2025. URL: https://doi.org/10.1038/s41598-025-07599-x, doi:10.1038/s41598-025-07599-x. This article has 2 citations and is from a peer-reviewed journal.
(coutinho2024reducingtheglobal pages 1-2): Jonathan M Coutinho, Anita van de Munckhof, Diana Aguiar de Sousa, Sven Poli, Sanjith Aaron, Antonio Arauz, Adriana B Conforto, Katarzyna Krzywicka, Sini Hiltunen, Erik Lindgren, Mayte Sánchez van Kammen, Liqi Shu, Tamam Bakchoul, Rosalie Belder, René van den Berg, Elisheva Boumans, Suzanne Cannegieter, Vanessa Cano-Nigenda, Thalia S Field, Isabel Fragata, Mirjam R Heldner, María Hernández-Pérez, Frederikus A Klok, Ronen R Leker, Lia Lucas-Neto, Jeremy Molad, Thanh N Nguyen, Dirk-Jan Saaltink, Gustavo Saposnik, Pankaj Sharma, Jan Stam, Vincent Thijs, Michiel van der Vaart, David J Werring, Diana Wong Ramos, Shadi Yaghi, Nilüfer Yeşilot, Turgut Tatlisumak, Jukka Putaala, Katarina Jood, Marcel Arnold, and José M Ferro. Reducing the global burden of cerebral venous thrombosis: an international research agenda. International Journal of Stroke, 19:599-610, Apr 2024. URL: https://doi.org/10.1177/17474930241242266, doi:10.1177/17474930241242266. This article has 27 citations and is from a peer-reviewed journal.
(umurungi2024cerebralveinthrombosis pages 2-4): Johanna Umurungi, Francesca Ferrando, Daniela Cilloni, and Piera Sivera. Cerebral vein thrombosis and direct oral anticoagulants: a review. Journal of Clinical Medicine, 13:4730, Aug 2024. URL: https://doi.org/10.3390/jcm13164730, doi:10.3390/jcm13164730. This article has 4 citations.
(field2025canadianstrokebest pages 3-4): TS Field, MP Lindsay, T Wein, and DB Debicki. Canadian stroke best practice recommendations: cerebral venous thrombosis, 2024. Unknown journal, 2025.
(research2024newrecommendationson pages 5-7): Neurological Research, C. Weimar, J. Beyer-Westendorf, FO Bohmann, G. Hahn, S. Halimeh, S. Holzhauer, C. Kalka, M. Knoflach, H-C Koennecke, F. Masuhr, M-L Mono, U. Nowak-Göttl, E. Scherret, M. Schlamann, and B. Linnemann. New recommendations on cerebral venous and dural sinus thrombosis from the german consensus-based (s2k) guideline. Neurological Research and Practice, Apr 2024. URL: https://doi.org/10.1186/s42466-024-00320-9, doi:10.1186/s42466-024-00320-9. This article has 29 citations and is from a peer-reviewed journal.
(chen2024efficacyandsafety pages 3-4): Xi Chen, Linjuan Guo, and Meiming Lin. Efficacy and safety of direct oral anticoagulants in cerebral venous thrombosis: meta-analysis of randomized clinical trials. Clinical and Applied Thrombosis/Hemostasis, Jan 2024. URL: https://doi.org/10.1177/10760296241256360, doi:10.1177/10760296241256360. This article has 8 citations.
(ranjan2024directoralanticoagulants pages 2-5): Redoy Ranjan, Gie Ken‐Dror, and Pankaj Sharma. Direct oral anticoagulants compared to warfarin in long‐term management of cerebral venous thrombosis: a comprehensive meta‐analysis. Health Science Reports, Feb 2024. URL: https://doi.org/10.1002/hsr2.1869, doi:10.1002/hsr2.1869. This article has 15 citations and is from a peer-reviewed journal.
(ranjan2024directoralanticoagulants pages 1-2): Redoy Ranjan, Gie Ken‐Dror, and Pankaj Sharma. Direct oral anticoagulants compared to warfarin in long‐term management of cerebral venous thrombosis: a comprehensive meta‐analysis. Health Science Reports, Feb 2024. URL: https://doi.org/10.1002/hsr2.1869, doi:10.1002/hsr2.1869. This article has 15 citations and is from a peer-reviewed journal.
(chen2024efficacyandsafety pages 1-2): Xi Chen, Linjuan Guo, and Meiming Lin. Efficacy and safety of direct oral anticoagulants in cerebral venous thrombosis: meta-analysis of randomized clinical trials. Clinical and Applied Thrombosis/Hemostasis, Jan 2024. URL: https://doi.org/10.1177/10760296241256360, doi:10.1177/10760296241256360. This article has 8 citations.
(burns2024endovasculartherapyfor pages 1-2): Joseph D. Burns and Emanuele Orru. Endovascular therapy for severe cerebral venous sinus thrombosis: time is vein? Neurocritical care, 41:728-729, Jul 2024. URL: https://doi.org/10.1007/s12028-024-02045-8, doi:10.1007/s12028-024-02045-8. This article has 2 citations and is from a peer-reviewed journal.
(piano2023endovasculartreatmentof pages 1-2): Mariangela Piano, Andrea Romi, Amedeo Cervo, Antonella Gatti, Antonio Macera, Guglielmo Pero, Cristina Motto, Elio Clemente Agostoni, and Emilio Lozupone. Endovascular treatment of cerebral vein thrombosis: safety and effectiveness in the thrombectomy era. Diagnostics, 13:2248, Jul 2023. URL: https://doi.org/10.3390/diagnostics13132248, doi:10.3390/diagnostics13132248. This article has 4 citations.
(rosa2025updateonmanagement pages 1-2): Sara Rosa, Isabel Fragata, and Diana Aguiar de Sousa. Update on management of cerebral venous thrombosis. Current Opinion in Neurology, 38:18-28, Oct 2025. URL: https://doi.org/10.1097/wco.0000000000001329, doi:10.1097/wco.0000000000001329. This article has 15 citations and is from a peer-reviewed journal.
(NCT06551415 chunk 1): Mohamed G. zeinhom, MD. Dabigatran Versus Apixaban in Cerebral Venous Thrombosis. Kafrelsheikh University. 2021. ClinicalTrials.gov Identifier: NCT06551415
(NCT06551415 chunk 2): Mohamed G. zeinhom, MD. Dabigatran Versus Apixaban in Cerebral Venous Thrombosis. Kafrelsheikh University. 2021. ClinicalTrials.gov Identifier: NCT06551415
(NCT07548346 chunk 1): Ossama Mansour. MENA Regional Endovascular Intervention for Venous Cerebral Venous Sinus Thrombosis. Middle East North Africa Stroke and Interventional Neurotherapies Organization. 2026. ClinicalTrials.gov Identifier: NCT07548346
(NCT05291585 chunk 1): Ji Xunming,MD,PhD. The Dedicated Venous Sinus Thrombectomy Stent for Endovascular Treatment of Cerebral Venous Sinus Thrombosis.. Ji Xunming,MD,PhD. 2022. ClinicalTrials.gov Identifier: NCT05291585
(coutinho2024reducingtheglobal pages 4-6): Jonathan M Coutinho, Anita van de Munckhof, Diana Aguiar de Sousa, Sven Poli, Sanjith Aaron, Antonio Arauz, Adriana B Conforto, Katarzyna Krzywicka, Sini Hiltunen, Erik Lindgren, Mayte Sánchez van Kammen, Liqi Shu, Tamam Bakchoul, Rosalie Belder, René van den Berg, Elisheva Boumans, Suzanne Cannegieter, Vanessa Cano-Nigenda, Thalia S Field, Isabel Fragata, Mirjam R Heldner, María Hernández-Pérez, Frederikus A Klok, Ronen R Leker, Lia Lucas-Neto, Jeremy Molad, Thanh N Nguyen, Dirk-Jan Saaltink, Gustavo Saposnik, Pankaj Sharma, Jan Stam, Vincent Thijs, Michiel van der Vaart, David J Werring, Diana Wong Ramos, Shadi Yaghi, Nilüfer Yeşilot, Turgut Tatlisumak, Jukka Putaala, Katarina Jood, Marcel Arnold, and José M Ferro. Reducing the global burden of cerebral venous thrombosis: an international research agenda. International Journal of Stroke, 19:599-610, Apr 2024. URL: https://doi.org/10.1177/17474930241242266, doi:10.1177/17474930241242266. This article has 27 citations and is from a peer-reviewed journal.
(coutinho2024reducingtheglobal pages 2-4): Jonathan M Coutinho, Anita van de Munckhof, Diana Aguiar de Sousa, Sven Poli, Sanjith Aaron, Antonio Arauz, Adriana B Conforto, Katarzyna Krzywicka, Sini Hiltunen, Erik Lindgren, Mayte Sánchez van Kammen, Liqi Shu, Tamam Bakchoul, Rosalie Belder, René van den Berg, Elisheva Boumans, Suzanne Cannegieter, Vanessa Cano-Nigenda, Thalia S Field, Isabel Fragata, Mirjam R Heldner, María Hernández-Pérez, Frederikus A Klok, Ronen R Leker, Lia Lucas-Neto, Jeremy Molad, Thanh N Nguyen, Dirk-Jan Saaltink, Gustavo Saposnik, Pankaj Sharma, Jan Stam, Vincent Thijs, Michiel van der Vaart, David J Werring, Diana Wong Ramos, Shadi Yaghi, Nilüfer Yeşilot, Turgut Tatlisumak, Jukka Putaala, Katarina Jood, Marcel Arnold, and José M Ferro. Reducing the global burden of cerebral venous thrombosis: an international research agenda. International Journal of Stroke, 19:599-610, Apr 2024. URL: https://doi.org/10.1177/17474930241242266, doi:10.1177/17474930241242266. This article has 27 citations and is from a peer-reviewed journal.
(coutinho2024reducingtheglobal pages 8-9): Jonathan M Coutinho, Anita van de Munckhof, Diana Aguiar de Sousa, Sven Poli, Sanjith Aaron, Antonio Arauz, Adriana B Conforto, Katarzyna Krzywicka, Sini Hiltunen, Erik Lindgren, Mayte Sánchez van Kammen, Liqi Shu, Tamam Bakchoul, Rosalie Belder, René van den Berg, Elisheva Boumans, Suzanne Cannegieter, Vanessa Cano-Nigenda, Thalia S Field, Isabel Fragata, Mirjam R Heldner, María Hernández-Pérez, Frederikus A Klok, Ronen R Leker, Lia Lucas-Neto, Jeremy Molad, Thanh N Nguyen, Dirk-Jan Saaltink, Gustavo Saposnik, Pankaj Sharma, Jan Stam, Vincent Thijs, Michiel van der Vaart, David J Werring, Diana Wong Ramos, Shadi Yaghi, Nilüfer Yeşilot, Turgut Tatlisumak, Jukka Putaala, Katarina Jood, Marcel Arnold, and José M Ferro. Reducing the global burden of cerebral venous thrombosis: an international research agenda. International Journal of Stroke, 19:599-610, Apr 2024. URL: https://doi.org/10.1177/17474930241242266, doi:10.1177/17474930241242266. This article has 27 citations and is from a peer-reviewed journal.
(coutinho2024reducingtheglobal pages 6-7): Jonathan M Coutinho, Anita van de Munckhof, Diana Aguiar de Sousa, Sven Poli, Sanjith Aaron, Antonio Arauz, Adriana B Conforto, Katarzyna Krzywicka, Sini Hiltunen, Erik Lindgren, Mayte Sánchez van Kammen, Liqi Shu, Tamam Bakchoul, Rosalie Belder, René van den Berg, Elisheva Boumans, Suzanne Cannegieter, Vanessa Cano-Nigenda, Thalia S Field, Isabel Fragata, Mirjam R Heldner, María Hernández-Pérez, Frederikus A Klok, Ronen R Leker, Lia Lucas-Neto, Jeremy Molad, Thanh N Nguyen, Dirk-Jan Saaltink, Gustavo Saposnik, Pankaj Sharma, Jan Stam, Vincent Thijs, Michiel van der Vaart, David J Werring, Diana Wong Ramos, Shadi Yaghi, Nilüfer Yeşilot, Turgut Tatlisumak, Jukka Putaala, Katarina Jood, Marcel Arnold, and José M Ferro. Reducing the global burden of cerebral venous thrombosis: an international research agenda. International Journal of Stroke, 19:599-610, Apr 2024. URL: https://doi.org/10.1177/17474930241242266, doi:10.1177/17474930241242266. This article has 27 citations and is from a peer-reviewed journal.
(research2024newrecommendationson media 59ded2f2): Neurological Research, C. Weimar, J. Beyer-Westendorf, FO Bohmann, G. Hahn, S. Halimeh, S. Holzhauer, C. Kalka, M. Knoflach, H-C Koennecke, F. Masuhr, M-L Mono, U. Nowak-Göttl, E. Scherret, M. Schlamann, and B. Linnemann. New recommendations on cerebral venous and dural sinus thrombosis from the german consensus-based (s2k) guideline. Neurological Research and Practice, Apr 2024. URL: https://doi.org/10.1186/s42466-024-00320-9, doi:10.1186/s42466-024-00320-9. This article has 29 citations and is from a peer-reviewed journal.

Sagittal Sinus Thrombosis manual research notes ▸

Sagittal Sinus Thrombosis manual research notes

Provider attempts

Falcon attempt 1: just research-disorder falcon Sagittal_Sinus_Thrombosis was started from the worktree with EDISON_API_KEY exported from /home/harry/dismech/edison_tok; it remained silent and produced no report file after an extended wait, so it was terminated.
Falcon attempt 2: retried with the same command under a 900 second timeout; the wrapper returned as a timeout, but complete Falcon report artifacts later appeared at research/Sagittal_Sinus_Thrombosis-deep-research-falcon.md and research/Sagittal_Sinus_Thrombosis-deep-research-falcon.md.citations.md. The Falcon metadata records a duration of 884.48 seconds.
Cyberian fallback: just research-disorder cyberian Sagittal_Sinus_Thrombosis was run under a 900 second timeout; it also timed out and produced no report file.

The YAML curation was grounded in fetched PubMed references and exact cache snippets. The Falcon report is retained as the generated deep-research artifact, and this manual file records the subset of sources actually converted into the YAML.

Source-backed findings used for curation

PMID:25073867 supports the clinical presentation spectrum, diagnostic confirmation by MR/MR venography or venous CT, common risk factors, acute heparin anticoagulation, selected thrombolysis/thrombectomy, decompressive surgery, and post-acute anticoagulation.
PMID:17183977 supports the two linked pathophysiology patterns: local venous infarction with focal signs and global raised intracranial pressure from an obstructed venous system.
PMID:29039017 supports seizure complications, focal neurological deficits, bleeding/lobar lesions, and the association of superior sagittal sinus thrombosis with secondary seizures in a CVST cohort.
PMID:38050259 supports the broader CVT epidemiology pattern, variable presentation from headache to loss of consciousness, diagnostic difficulty, first-line heparin treatment, and generally favorable recovery in many patients.
PMID:39492709 supports contemporary treatment statements: LMWH or unfractionated heparin as first-line acute treatment, decompressive craniectomy for life-threatening intracranial pressure, and specialist-center use of endovascular therapy in complex cases.
PMID:25899238 supports mechanical thrombectomy as a possible option for patients who do not respond to anticoagulation, while preserving uncertainty because controlled studies are required.

Ontology decisions

Disease term: MONDO:0002695, label sagittal sinus thrombosis.
Location term: UBERON:0001642, label superior sagittal sinus.
Phenotype terms used after OAK verification include HP:0002315 Headache, HP:0002516 Increased intracranial pressure, HP:0001085 Papilledema, HP:0001250 Seizure, HP:0001269 Hemiparesis, HP:0001342 Cerebral hemorrhage, and HP:0007185 Loss of consciousness.
Mappings added after OAK verification include ICD10CM:I67.6 Nonpyogenic thrombosis of intracranial venous system and MONDO:0002695 sagittal sinus thrombosis.
Treatment terms use broad but verified actions: MAXO:0000058 pharmacotherapy with CHEBI:28304 heparin, NCIT:C52003 Thrombectomy, and MAXO:0000004 surgical procedure.

Curation notes

Category was retained as Complex; the literature supports multifactorial thrombotic risk rather than a single Mendelian mechanism for the disorder page as curated here.
Evidence snippets in the YAML were copied from fetched reference-cache abstracts and kept as direct substrings.
Unrelated PMIDs fetched during source discovery were not used in the page and should not be staged.

Ask OpenScientist

OpenScientist Report

Classifications

Mappings

Pathophysiology

Pathograph

Phenotypes

Treatments

Source YAML

References & Deep Research

Deep Research

Disease Characteristics Research Template

Target Disease

Research Objectives

1. Disease Information

2. Etiology

3. Phenotypes

4. Genetic/Molecular Information

5. Environmental Information

6. Mechanism / Pathophysiology

7. Anatomical Structures Affected

8. Temporal Development

9. Inheritance and Population

10. Diagnostics

11. Outcome/Prognosis

12. Treatment

13. Prevention

14. Other Species / Natural Disease

15. Model Organisms

Citation Requirements

Output Format

Comprehensive Disease Characteristics Report: Sagittal Sinus Thrombosis (Superior Sagittal Sinus Thrombosis)

Executive summary

1. Disease information

1.1 What is the disease?

1.2 Key identifiers (OMIM/Orphanet/ICD/MeSH/MONDO)

1.3 Synonyms and alternative names

2. Etiology

2.1 Disease causal factors (mechanistic, environmental, infectious)

2.2 Risk factors

2.3 Protective factors

2.4 Gene–environment interactions

3. Phenotypes

3.1 Common phenotypes and clinical presentation

3.2 SSS-associated phenotype patterns

3.3 Phenotype ontology suggestions (HPO)

3.4 Quality of life impact

4. Genetic / molecular information

4.1 Causal genes and susceptibility genes

4.2 Variant classes / somatic vs germline

4.3 Epigenetics / chromosomal abnormalities

5. Environmental information

6. Mechanism / pathophysiology

6.1 Causal chain (systems-level)

6.2 Suggested pathway/process ontology terms

6.3 Knowledge gaps (expert consensus)

7. Anatomical structures affected

7.1 Organ/system level

7.2 Tissue/cell level

8. Temporal development

9. Inheritance and population

9.1 Epidemiology

9.2 Population demographics

10. Diagnostics

10.1 Imaging

10.2 D-dimer

10.3 Laboratory / thrombophilia testing

11. Outcome / prognosis

12. Treatment

12.1 Standard-of-care anticoagulation (real-world implementation)

12.2 Oral maintenance: DOACs vs VKA (2023–2024 evidence)

12.3 Duration

12.4 Endovascular therapy (EVT)

12.5 Decompressive surgery

12.6 Treatment ontology suggestions (MAXO)

13. Prevention

14. Other species / natural disease

15. Model organisms

Recent developments and current applications (2023–2024 emphasis)

Ongoing trials / real-world implementations (examples)