Materiały źródłowe

• #1 Intracranial hematoma – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/intracranial-hematoma/symptoms-causes/syc-20356145

  An intracranial hematoma is a collection of blood within the skull. The blood may collect in the brain tissue or underneath the skull, pressing on the brain. It’s usually caused by a blood vessel that bursts in the brain. […] What happens in the brain to cause bleeding varies based on the type of hematoma. There are three categories of hematoma subdural hematoma, epidural hematoma and intracerebral hematoma. An intracerebral hematoma also is known as an intraparenchymal hematoma. […] A subdural hematoma occurs when blood vessels burst between the brain and the outermost of three protective layers that cover the brain. This outermost layer is called the dura mater. The leaking blood forms a hematoma that presses on brain tissue. A hematoma that gets bigger can cause gradual loss of consciousness and possibly death.

• #2 Hematoma | Description, Types, Causes, & Treatment | Britannica

  https://www.britannica.com/science/hematoma

  Hematomas that form within the skull or brain are among the most serious. […] In an epidural hematoma (also called extradural hematoma or epidural hemorrhage), blood pools between the skull and the dura mater (the outermost layer of the meninges, or protective membranes, surrounding the brain and spinal cord). […] In a subdural hematoma, blood pools between the dura mater and the arachnoid mater (the middle layer of the meninges, lying between the dura mater and the pia mater). […] Subarachnoid hemorrhages develop in the space between the pia mater and the arachnoid mater. […] An intracerebral hematoma (also called intraparenchymal hematoma or hemorrhagic stroke) occurs when blood pools within the tissues of the brain; trauma and high blood pressure are common causes.

• #3 Intracranial Hemorrhage: Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/1163977-overview

  Intracerebral hemorrhage most commonly results from hypertensive damage to blood vessel walls (eg, hypertension, eclampsia, drug abuse), but it also may be due to autoregulatory dysfunction with excessive cerebral blood flow (eg, reperfusion injury, hemorrhagic transformation, cold exposure), rupture of an aneurysm or arteriovenous malformation (AVM), arteriopathy (eg, cerebral amyloid angiopathy, moyamoya), altered hemostasis (eg, thrombolysis, anticoagulation, bleeding diathesis), hemorrhagic necrosis (eg, tumor, infection), or venous outflow obstruction (eg, cerebral venous thrombosis). […] Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis, fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating arteries throughout the brain including lenticulostriates, thalamoperforators, paramedian branches of the basilar artery, superior cerebellar arteries, and anterior inferior cerebellar arteries.

• #4

  https://step1.medbullets.com/neurology/113018/intracranial-hemorrhage

  Secondary to uncontrolled hypertension (HTN) […] note that HTN is a common cause of intracerebral hemorrhages […] HTN on the small vessels can result in lipohyalinosis, Charcot-Bouchard microaneurysms. […] Lobar hemorrhage […] Can be secondary to amyloid angiopathy (most common cause) […] Symptoms depend on where the hemorrhage is such as parietal lobe, occipital lobe […] how large the hemorrhage is if large, it can result in symptoms of increased intracranial pressure.

• #5 Intracranial Hemorrhage: Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/1163977-overview

  Predilection sites for intracerebral hemorrhage include the basal ganglia (40-50%), lobar regions (20-50%), thalamus (10-15%), pons (5-12%), cerebellum (5-10%), and other brainstem sites (1-5%). […] Intraventricular hemorrhage occurs in one third of intracerebral hemorrhage cases from extension of thalamic ganglionic bleeding into the ventricular space. Isolated intraventricular hemorrhage frequently arise from subependymal structures including the germinal matrix, AVMs, and cavernous angiomas.

• #6 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis

  Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis […] The pathogenesis, epidemiology, clinical features, and diagnosis of spontaneous (atraumatic) ICH will be reviewed here. Other aspects of ICH are discussed separately. […] Mechanisms of brain injury — There are several mechanisms of brain injury in ICH. These include: […] Primary mechanical injury to brain parenchyma occurs via hematoma expansion and perilesional edema. Both hematoma volume and edema contribute to the mass effect and increased intracranial pressure (ICP), which in turn can cause reduced cerebral perfusion and ischemic injury, and, in very large ICH, cerebral herniation. […] Secondary brain injury from the breakdown of the blood-brain barrier after the initial hemorrhage includes excitotoxic and inflammatory processes; however, the exact mechanism(s) underlying this remain uncertain.

• #7 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print

  Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis […] Intracerebral hemorrhage (ICH) is the second most common cause of stroke after ischemic stroke and is a substantial cause of morbidity and mortality. […] The pathogenesis, epidemiology, clinical features, and diagnosis of spontaneous (atraumatic) ICH will be reviewed here. Other aspects of ICH are discussed separately. […] Mechanisms of brain injury — There are several mechanisms of brain injury in ICH. These include: […] Primary mechanical injury to brain parenchyma occurs via hematoma expansion and perilesional edema. Both hematoma volume and edema contribute to the mass effect and increased intracranial pressure (ICP), which in turn can cause reduced cerebral perfusion and ischemic injury, and, in very large ICH, cerebral herniation.

• #8 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis

  Enlargement of the hemorrhage is associated with neurologic deterioration, the development of increased intracranial pressure, and worse outcomes. In most cases, the bulk of hemorrhage expansion occurs in the first several hours after onset of ICH. […] Perihematomal edema is frequent in ICH and may be related to mass effect, local neuronal ischemia, or the accumulation of cytotoxic factors. Edema is present on computed tomography (CT) or magnetic resonance imaging (MRI) in at least half of patients when the patient is first imaged and progresses, reaching maximum volume 7 to 12 days after onset; the most rapid expansion occurs in the first 48 hours. Hemorrhage volume, higher admission hematocrit, and a prolonged partial thromboplastin time appear to correlate with peak edema volume. […] The perihematomal region exhibits delayed perfusion and increased diffusivity mixed with areas of reduced diffusion, suggesting the presence of both vasogenic and cytotoxic (ischemic) edema. Acute blood pressure changes with impaired cerebral autoregulation in patients with ICH may contribute to perihematomal ischemia. Underlying hypertensive vasculopathy or cerebral amyloid angiopathy (CAA) may also affect autoregulation in some patients. Increased intracranial pressure and the resulting reduction in cerebral perfusion pressure may play a role; this phenomenon may be exacerbated by blood pressure lowering.

• #9 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print

  Secondary brain injury from the breakdown of the blood-brain barrier after the initial hemorrhage includes excitotoxic and inflammatory processes; however, the exact mechanism(s) underlying this remain uncertain. […] Enlargement of the hemorrhage is associated with neurologic deterioration, the development of increased intracranial pressure, and worse outcomes. In most cases, the bulk of hemorrhage expansion occurs in the first several hours after onset of ICH. […] Perihematomal edema is frequent in ICH and may be related to mass effect, local neuronal ischemia, or the accumulation of cytotoxic factors. Edema is present on computed tomography (CT) or magnetic resonance imaging (MRI) in at least half of patients when the patient is first imaged and progresses, reaching maximum volume 7 to 12 days after onset; the most rapid expansion occurs in the first 48 hours.

• #10 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print

  The perihematomal region exhibits delayed perfusion and increased diffusivity mixed with areas of reduced diffusion, suggesting the presence of both vasogenic and cytotoxic (ischemic) edema. Acute blood pressure changes with impaired cerebral autoregulation in patients with ICH may contribute to perihematomal ischemia. […] Breakdown of the blood-brain barrier due to an inflammatory response to the ICH may be identified by contrast enhancement of brain tissue. In patients with acute and subacute ICH, postcontrast enhancement may be noted in the perihematomal area on CT and MRI. […] Specific etiologies — There are several underlying pathological conditions associated with ICH; hypertension, amyloid angiopathy, and ruptured vascular malformation are most common. […] Hypertensive vasculopathy — Hypertensive hemorrhages occur in the territory of penetrator arteries that branch off major intracerebral arteries, often at 90 degree angles to the parent vessel. These small penetrating arteries may be particularly susceptible to the effects of hypertension, as they are directly exposed to the pressure of the much larger parent vessel, without the protection of a preceding gradual decrease in vessel caliber.

• #11 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis

  Breakdown of the blood-brain barrier due to an inflammatory response to the ICH may be identified by contrast enhancement of brain tissue. In patients with acute and subacute ICH, postcontrast enhancement may be noted in the perihematomal area on CT and MRI. Contrast enhancement remote from the hematoma may also be identified on imaging. One MRI study described a pattern of punctate areas of contrast enhancement in the sulcal areas both contiguous and remote from the hemorrhage suggesting that acute ICH may be associated with a more diffuse inflammatory process leading to widespread breakdown of the blood-brain barrier. […] Specific etiologies — There are several underlying pathological conditions associated with ICH; hypertension, amyloid angiopathy, and ruptured vascular malformation are most common.

• #12 Frontiers | Pathophysiological Mechanisms and Potential Therapeutic Targets in Intracerebral Hemorrhage

  https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2019.01079/full

  Intracerebral hemorrhage (ICH) is a subtype of hemorrhagic stroke with high mortality and morbidity. The resulting hematoma within brain parenchyma induces a series of adverse events causing primary and secondary brain injury. The mechanism of injury after ICH is very complicated and has not yet been illuminated. This review discusses some key pathophysiology mechanisms in ICH such as oxidative stress (OS), inflammation, iron toxicity, and thrombin formation. The corresponding therapeutic targets and therapeutic strategies are also reviewed. […] The initial pathological damage of cerebral hemorrhage to brain is the mechanical compression caused by hematoma. The hematoma mass can increase intracranial pressure, compressing brain and thereby potentially affecting blood flow, and subsequently leading to brain hernia.

• #13 Frontiers | Pathophysiological Mechanisms and Potential Therapeutic Targets in Intracerebral Hemorrhage

  https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2019.01079/full

  Substantial evidence indicates that inflammatory mechanisms are associated with ICH-induced brain injury and microglia/macrophages activation, and polarization is thought to play vital pathophysiological roles. […] OS has been increasingly recognized as a contributing factor in secondary brain injury (SBI) following ICH. […] Increasing evidence suggests that hemoglobin and iron release from the hematoma is a major contributor to brain injury induced by ICH. […] Thrombin is an essential component in the clotting cascade, and it is produced in the brain immediately after ICH induction. However, thrombin can also participate in ICH-induced injury. The deleterious or protective effect of thrombin depends on its concentration. […] The pathophysiology mechanism of injury after ICH is very complicated, which contains OS, inflammation, nerve cell toxicity, thrombin formation, and so on. Preclinical and clinical research evidence in ICH has further revealed the progress of pathophysiology in cerebral hemorrhage, and these works have resulted in much new information about injury mechanisms and potential therapeutic targets. However, truly effective clinical treatments are very limited, mainly because the problem of transforming preclinical research into clinical application has not yet been solved. Therefore, a multi-target neuroprotective therapy will make clinically effective treatment strategies possible, but also requires further study.

• #14 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis

  Hypertensive vasculopathy — Hypertensive hemorrhages occur in the territory of penetrator arteries that branch off major intracerebral arteries, often at 90 degree angles to the parent vessel. These small penetrating arteries may be particularly susceptible to the effects of hypertension, as they are directly exposed to the pressure of the much larger parent vessel, without the protection of a preceding gradual decrease in vessel caliber. […] The blood vessels that give rise to hypertensive hemorrhage are generally the same as those affected by hypertensive occlusive disease and diabetic vasculopathy, which cause lacunar strokes. These vessels supply the pons and midbrain, thalamus, putamen, caudate, and globus pallidus, and cerebellar nuclei. Cerebellar hemorrhage is more common than lacunar infarction in the cerebellum. Hypertensive vasculopathy is also believed to play a role in the development of white matter small vessel disease (leukoaraiosis), which may account for the association between white matter disease and risk of ICH.

• #15 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis

  Pathologic examination of the blood vessels in patients with chronic hypertension and in those with ICH has led to a theory of how hypertensive hemorrhage occurs. The penetrator vessels in patients with chronic hypertension develop intimal hyperplasia with hyalinosis in the vessel wall; this predisposes to focal necrosis, causing injury to the wall of the vessel. These microscopic „pseudoaneurysms” have been associated with small amounts of blood identified in the extravascular space. Pseudoaneurysm formation with subclinical leaks of blood may be relatively common; massive hemorrhage can occur when the clotting system is unable to compensate for these disruptions in the vessel wall. […] Cerebral microbleeds (CMBs) are markers of bleeding-prone microangiopathy that may be found on imaging of patients with ICH due to hypertensive vasculopathy. T2*-weighted gradient echo and susceptibility-weighted MRI sequences can detect CMBs as punctate foci of hemosiderin deposition that represent remnants of clinically silent cerebral microhemorrhage. The anatomic distribution of microbleeds varies with their etiology, with hypertensive microbleeds arising in the basal ganglia, thalamus, pons, and cerebellar nuclei in contrast with CAA-related microbleeds, which are found in more superficial lobar regions of the cerebral hemispheres. This regional distribution is consistent with the usual location of ICH in these conditions.

• #16 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis

  Cerebral amyloid angiopathy — CAA is an important cause of primary lobar ICH in older adults. CAA is characterized by the deposition of congophilic material in small- to medium-sized blood vessels of the brain and leptomeninges. This weakens the structure of the vessel walls and makes them prone to bleeding. CAA usually manifests with spontaneous lobar hemorrhage. The presence of CMBs restricted to the lobar region is associated with CAA. CAA is described in detail separately. […] Other etiologies — Several other less common underlying etiologies of nontraumatic ICH include arteriovenous and other vascular malformations, cerebral venous thrombosis, hemorrhagic infarction, reversible cerebral vasoconstriction syndrome, primary or metastatic tumors, central nervous system infection, mycotic intracranial aneurysm, moyamoya disease, cerebral vasculitis, cerebral hyperperfusion syndrome, sickle cell disease, and bleeding disorders.

• #17 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print

  Pathologic examination of the blood vessels in patients with chronic hypertension and in those with ICH has led to a theory of how hypertensive hemorrhage occurs. The penetrator vessels in patients with chronic hypertension develop intimal hyperplasia with hyalinosis in the vessel wall; this predisposes to focal necrosis, causing injury to the wall of the vessel. […] Cerebral amyloid angiopathy — CAA is an important cause of primary lobar ICH in older adults. CAA is characterized by the deposition of congophilic material in small- to medium-sized blood vessels of the brain and leptomeninges. This weakens the structure of the vessel walls and makes them prone to bleeding. […] Other etiologies — Several other less common underlying etiologies of nontraumatic ICH include arteriovenous and other vascular malformations, cerebral venous thrombosis, hemorrhagic infarction, reversible cerebral vasoconstriction syndrome, primary or metastatic tumor, central nervous system infection, mycotic intracranial aneurysm, moyamoya disease, cerebral vasculitis, cerebral hyperperfusion syndrome, sickle cell disease, and bleeding disorders.

• #18 intracerebral hemorrhage | Calgary Guide

  https://calgaryguide.ucalgary.ca/?s=intracerebral%20hemorrhage

  Primary Intracerebral Hemorrhage (~75%) […] Secondary Intracerebral Hemorrhage (~25%) […] Amyloid Angiopathy Amyloid deposits in blood vessels and weakens vessel walls […] Hypertension Lipohyalinosis (lipid and protein aggregation in arterial walls) weakens blood vessels […] Unknown Aneurysm Dilation of a weakened blood vessel […] Drugs (e.g., cocaine, crystal meth, decongestants, anticoagulants) Vascular Malformations […] Note: the pathophysiology and exact mechanism is not well known […] Release of toxic blood plasma components (coagulation factors, immunoglobins) […] Red blood cell lysis […] Cytotoxic hemoglobin (heme, iron) release […] Fenton-type free radical generation (Fe(II) + H2O2 Fe(III) + OH + OH) […] Oxidative damage to carbohydrates, lipids, nucleic acids, and proteins in brain

• #19 Autophagy in Intracerebral Hemorrhage: From Mechanism to Regulation

  https://www.imrpress.com/journal/JIN/22/5/10.31083/j.jin2205134/htm

  This paper focuses on the molecular mechanisms and regulation of autophagy. […] Activation of thrombin and dysfunction of the blood-brain barrier (BBB) cause cytotoxic edema and vasogenic edema, resulting in perihematomal edema (PHE). […] Hematoma formation results in the activation of cytotoxicity and excitotoxicity. Hemoglobin, iron and other blood components also induce injury, while oxidative stress and inflammatory responses induce SBI, leading to neurological dysfunction. […] Autophagy is activated in various brain cells after ICH. […] Excessive autophagy leads to SBI early during the onset of ICH. […] Autophagy is involved in maintaining cellular homeostasis in the latter phases of ICH, thereby protecting against brain injury. […] Autophagy can have both destructive and protective functions in ICH due to regulation by a variety of signaling pathways.

• #20 intracerebral hemorrhage | Calgary Guide

  https://calgaryguide.ucalgary.ca/?s=intracerebral%20hemorrhage

  Necrosis of hypoxic brain tissue […] Rupture of blood vessel(s) […] Accumulation of blood hematoma formation […] Cerebral tissue perfusion ( O2 availability) […] Mitochondrial oxidative phosphorylation (final step in aerobic glucose metabolism) […] Adenosine triphosphate (ATP) production […] Anaerobic glucose metabolism […] Cerebral lactate production […] Cerebral lactic acidosis […] Impaired cellular metabolism […] Death of neurons and glia […] Microglia clear debris and release inflammatory markers (TNF, IF, IL-1) […] Endothelial cell apoptosis and blood-brain barrier permeability […] Cerebral edema […] Increased intracranial pressure: papilledema, sudden headache, non-reactive pupils, level of consciousness (LOC), nausea/vomiting […] Astrocytes release glutamate (main excitatory neurotransmitter)

• #21 Autophagy in Intracerebral Hemorrhage: From Mechanism to Regulation

  https://www.imrpress.com/journal/JIN/22/5/10.31083/j.jin2205134/htm

  The benefit of autophagy after ICH lies in its ability to maintain intracellular homeostasis, thus providing a neuroprotective effect in brain injury. […] Autophagy plays a protective role against thrombin-induced brain injury. […] Autophagy is initiated under specific circumstances, such as nutrient starvation and oxidative stress. […] The initiation mechanism is conserved, and the formation of autophagosomes and autolysosomes is crucial to the process of autophagy. […] The fusion of autophagosome membranes to lysosomes results in the formation of autophagolysosomes. […] The activation of autophagy is crucial for alleviating secondary brain injury after ICH.

• #22 intracerebral hemorrhage | Calgary Guide

  https://calgaryguide.ucalgary.ca/?s=intracerebral%20hemorrhage

  Activation of neuronal metabotropic glutamate receptors […] Ca2+ influx into neurons […] Excitotoxicity (excess stimulation of glutamate receptors leading to neuronal death) […] Dysfunction of Na+/K+ ATPase pump (moves 3 Na+ out of cell and 2 K+ into cell) on neurons […] Na+ efflux and K+ influx […] Neuronal membrane potential becomes less negative (closer to threshold potential) […] Neurons depolarize […] Glutamate release […] General findings: Seizures, lethargy.

• #23 Subdural Hematoma: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1137207-overview

  The usual mechanism that produces an acute subdural hematoma (SDH) is a high-speed impact to the skull. This causes brain tissue to accelerate or decelerate relative to the fixed dural structures, tearing blood vessels. […] Often, the torn blood vessel is a vein that connects the cortical surface of the brain to a dural sinus (termed a bridging vein). In elderly persons, the bridging veins may already be stretched because of brain atrophy (shrinkage that occurs with age). […] Alternatively, a cortical vessel, either a vein or small artery, can be damaged by direct injury or laceration. An acute SDH due to a ruptured cortical artery may be associated with only minor head injury, possibly without an associated cerebral contusion. […] The head trauma may also cause associated brain hematomas or contusions, subarachnoid hemorrhage, and diffuse axonal injury. Secondary brain injuries may include edema, infarction, secondary hemorrhage, and brain herniation.

• #24 Subdural hematoma | Mechanism, Symptoms, & Management | Britannica

  https://www.britannica.com/science/subdural-hematoma

  subdural hematoma, bleeding into the space between the brain and its outermost protective covering, the dura. It typically results when a traumatic force applied to the head creates significant fast-changing velocities of the contents inside the skull. The expanding hemorrhage can increase the pressure inside the skull and compress the underlying brain tissue. […] A network of veins traverses the space between the surface of the brain and the dura. These veins, the bridging veins, can tear if the contents of the skull experience sudden changes in velocity. Blood leaking from the bridging veins then collects in the subdural space, creating a hematoma. The size of the hematoma and the speed with which it expands depend primarily on the number and size of the tears in the bridging veins. Given that the blood in the bridging veins is coming from the venous side of the circulatory system and is therefore under less pressure, subdural hematomas typically expand at a much lower rate than hematomas that are formed from arterial blood, such as epidural hematomas. The expanding subdural hematoma increases the intracranial pressure and can lead to damage of the underlying brain.

• #25 Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth in: Journal of Neurosurgery Volume 120 Issue 6 (2014) Journals

  https://thejns.org/view/journals/j-neurosurg/120/6/article-p1378.xml

  Most acute subdural hematomas (ASDHs) develop after rupture of a bridging vein or veins. The anatomy of the bridging vein predisposes to its tearing within the border cell layer of the dura mater. Thus, the subdural hematoma actually forms within the dura. The hematoma grows by continued bleeding into the border cell layer. However, the venous pressure would not be expected to cause a large hematoma. Therefore, some type of mechanism must account for the hematoma’s expansion. […] A hypothesis is derived to explain the mechanism of ASDH enlargement. Tearing of one or more bridging veins causes these vessels to bleed into the dural border cell layer. Subsequent ICP elevation from the ASDH, cerebral swelling, or other cause results in elevation of the CVP by increased outflow resistance in the intact bridging veins. The increased ICP causes further bleeding into the hematoma cavity via the torn bridging veins. Thus, the ASDH enlarges via a positive feedback mechanism. […] Enlargement of an ASDH would cease as blood within the hematoma cavity coagulates. This would stop the dissection of the dural border cell layer, and pressure within the hematoma cavity would equalize with that in the torn bridging vein or veins.

• #26 epidural-hematoma-pathogenesis-and-clinical-findings | Calgary Guide

  https://calgaryguide.ucalgary.ca/epidural-hematoma-pathogenesis-and-clinical-findings/epidural-hematoma/

  Epidural Hematoma: Pathogenesis and clinical findings Head trauma (e.g., accidents, falls, assaults) […] General force of trauma transiently disturbs structures involved in consciousness (e.g., axonal injury from shear force) […] EPIDURAL HEMATOMA: Collection of blood in the epidural space between the inner layer of the skull and outer layer of the dura mater […] Fracture lacerates the Middle Meningeal Artery […] Blood accumulates in the epidural space, but not yet to the extent that consciousness is affected […] More blood accumulates intracranial pressure (ICP) […] Intracranial pressure becomes greater than mean arterial pressure […] ICP compresses arterioles in brain cerebral blood flow

• #27

  https://step1.medbullets.com/neurology/113018/intracranial-hemorrhage

  Intracranial Hemorrhage […] Pathogenesis […] Epidural hematoma […] Typically secondary to rupture of the middle meningeal artery in the setting of fracture of the temporal bone (pterion) […] Initially there may be no symptoms (lucid interval) […] As the hematoma grows, it leads to brain tissue compression which increases intracranial pressure […] This increased intracranial pressure can result in brain herniation such as transtentorial herniation. […] Subdural hematoma […] Secondary to rupture of the bridging veins […] The most common cause is head trauma (e.g., falls, assaults, and motor vehicle accidents) […] Risk factors significant cerebral atrophy, such as in the elderly, chronic alcohol abuse, previous traumatic brain injury. […] Hypertensive hemorrhage

• #28 Epidural hematoma – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/epidural-hematoma/

  Intracranial epidural hematoma (EDH) refers to bleeding between the dura mater and the calvarium. Most cases of EDH are traumatic, resulting from a head injury with an associated skull fracture that ruptures or tears the middle meningeal artery, which lies in close proximity to the skull and dura mater. […] The classic manifestation of EDH is an initial loss of consciousness, followed by a lucid interval in which the patient gains normal or near-normal consciousness, followed by rapid neurological decline. […] Diagnosis is confirmed on a noncontrast CT head, on which EDH appears as a biconvex, hyperdense lesion, typically in the temporal or temporoparietal region. […] Surgical decompression with craniotomy is indicated in patients with large EDH, GCS 8, and evidence of neurological deterioration.

• #29 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis

  Underlying causes — Injury to brain parenchyma occurs via hematoma expansion and perilesional edema as well as secondary excitotoxic and inflammatory injury from the breakdown of the blood-brain barrier. Common conditions associated with intracerebral hemorrhage (ICH) include hypertension, cerebral amyloid angiopathy, and ruptured vascular malformation. Other etiologies include cerebral venous thrombosis, vasculopathies, primary or metastatic tumors, and coagulopathies.

• #30 Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print

  Underlying causes — Injury to brain parenchyma occurs via hematoma expansion and perilesional edema as well as secondary excitotoxic and inflammatory injury from the breakdown of the blood-brain barrier. Common conditions associated with intracerebral hemorrhage (ICH) include hypertension, cerebral amyloid angiopathy, and ruptured vascular malformation. Other etiologies include cerebral venous thrombosis, vasculopathies, primary or metastatic tumors, and coagulopathies.

• #31

  https://journals.lww.com/md-journal/fulltext/2024/10040/the_mechanism_of_quercetin_in_treating.5.aspx

  The prognosis of ICH is generally poor. Current therapeutic approaches for primary injury include conservative treatment, craniotomy, external ventricular drain insertion, and minimally invasive surgery. However, these treatment strategies still face numerous challenges in improving the prognosis of ICH. […] Research findings indicate that quercetin treatment can significantly reduce the neurological deficit scores and brain water content in mice with ICH. […] Quercetin also downregulates the expression of caspase-3 and PARP, reducing neuronal apoptosis, which further confirms its potential in neuroprotection. […] Based on the experimental results and target function analysis, we infer that the interaction between quercetin and these 7 key targets may act through multiple pathways: on one hand, by effectively regulating inflammatory responses, and on the other hand, by promoting cell survival and inhibiting apoptosis. These mechanisms collectively contribute to alleviating neural injury following ICH, thus exerting a positive therapeutic effect in the treatment of ICH. […] In summary, the potential mechanism of quercetin in treating ICH may involve a multi-target-multi-pathway approach. It has the potential to regulate apoptosis, inhibit inflammation, prevent iron death, and modulate angiogenesis, thereby aiding in the reduction of nerve damage resulting from ICH.

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