Cerebrovascular Accidents and Hemorrhages
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Questions and Answers

What happens to the injured brain from days 2 to 10?

  • It becomes more compact and dense
  • It becomes harder and more solid
  • It becomes more rigid and brittle
  • It turns gelatinous and friable (correct)

    • What happens to the tissue from day 10 to week 3?

  • It becomes more rigid and brittle
  • It liquefies and eventually leaves a fluid-filled cavity (correct)
  • It becomes more solid and compact
  • It becomes more compact and dense

    • What is the most common cause of spontaneous intraparenchymal hemorrhages?

  • Trauma
  • Tumors
  • Vascular malformations
  • Hypertension (correct)

    • What is the typical location of hypertensive intraparenchymal hemorrhages?

    <p>Basal ganglia, thalamus, pons, and cerebellum</p> Signup and view all the answers

    What is the most frequent cause of clinically significant nontraumatic subarachnoid hemorrhage?

    <p>Rupture of a saccular (berry) aneurysm</p> Signup and view all the answers

    What is the characteristic of the tissue reaction after the first 12 hours?

    <p>Ischemic neuronal change and vasogenic edema</p> Signup and view all the answers

    What is the outcome of hypertensive intraparenchymal hemorrhages if the individual survives the acute event?

    <p>Gradual resolution of the hematoma with considerable clinical improvement</p> Signup and view all the answers

    What is the characteristic of early lesions on microscopic examination?

    <p>Clotted blood surrounded by edematous brain tissue</p> Signup and view all the answers

    What is the peak incidence age of spontaneous intraparenchymal hemorrhages?

    <p>60 years</p> Signup and view all the answers

    What is the main cause of intracranial hemorrhages?

    <p>Hypertension and other diseases leading to vascular wall injury</p> Signup and view all the answers

    What is the primary mechanism by which the brain is deprived of oxygen in high-altitude environments?

    <p>Functional hypoxia</p> Signup and view all the answers

    What is the typical outcome for patients who survive severe global cerebral ischemia?

    <p>Severe neurological impairment and a persistent vegetative state</p> Signup and view all the answers

    What is the typical clinical designation applied to all cerebrovascular diseases when symptoms begin acutely?

    <p>Stroke</p> Signup and view all the answers

    What is the term for the autoregulation of vascular resistance that maintains stable cerebral blood flow over a wide range of blood pressure and intracranial pressure?

    <p>Autoregulation</p> Signup and view all the answers

    What is the term for the widespread ischemic-hypoxic injury that can occur in the setting of severe systemic hypotension?

    <p>Global cerebral ischemia</p> Signup and view all the answers

    What is the term for the morphological changes that occur in the brain during global ischemia, characterized by swollen brain tissue with wide gyri and narrowed sulci?

    <p>Cerebral edema</p> Signup and view all the answers

    What is the term for the three main pathogenic mechanisms that underlie cerebrovascular diseases?

    <p>Thrombotic occlusion, embolic occlusion, and vascular rupture</p> Signup and view all the answers

    What is the primary effect of hypertension on the cerebral vasculature in intraparenchymal hemorrhage?

    <p>Vascular wall injury</p> Signup and view all the answers

    What is the characteristic of the tissue reaction after the first 12 hours in ischemic stroke?

    <p>Ischemic neuronal change and cytotoxic edema</p> Signup and view all the answers

    What is the primary underlying cause of subarachnoid hemorrhages?

    <p>Rupture of a saccular aneurysm</p> Signup and view all the answers

    What is the typical location of hypertensive intraparenchymal hemorrhages?

    <p>Basal ganglia, thalamus, pons, and cerebellum</p> Signup and view all the answers

    What is the outcome of intracranial hemorrhages if the individual survives the acute event?

    <p>Resolution of the hematoma with considerable clinical improvement</p> Signup and view all the answers

    What is the characteristic of early lesions in intraparenchymal hemorrhage on microscopic examination?

    <p>Clotted blood surrounded by edematous brain tissue</p> Signup and view all the answers

    What is the peak incidence age of spontaneous intraparenchymal hemorrhages?

    <p>60 years</p> Signup and view all the answers

    What is the primary source of emboli in embolic infarctions?

    <p>Cardiac mural thrombi</p> Signup and view all the answers

    What is the characteristic of nonhemorrhagic infarcts after 48 hours?

    <p>The tissue becomes pale, soft, and swollen</p> Signup and view all the answers

    What is the primary cause of thrombotic occlusions in cerebral infarctions?

    <p>Atherosclerotic plaques</p> Signup and view all the answers

    What is the characteristic of hemorrhagic infarcts?

    <p>Multiple, sometimes confluent, petechial hemorrhages</p> Signup and view all the answers

    What is the effect of collateral blood flow on the size and location of cerebral infarcts?

    <p>It modifies the size, location, and shape of the infarct</p> Signup and view all the answers

    What is the characteristic of acute hypoxic-ischemic injury in the cerebral cortex?

    <p>Shrunken and eosinophilic cell bodies with pyknotic nuclei</p> Signup and view all the answers

    What is the common finding in viral infections in the cerebral cortex?

    <p>A collection of microglial cells forming a poorly defined nodule</p> Signup and view all the answers

    What percentage of cases have multiple aneurysms?

    <p>20% to 30%</p> Signup and view all the answers

    What is the most common manifestation of arteriovenous malformations (AVMs)?

    <p>Seizures or hemorrhage</p> Signup and view all the answers

    What is the ratio of males to females affected by arteriovenous malformations (AVMs)?

    <p>2:1</p> Signup and view all the answers

    What is the consequence of healing and meningeal fibrosis and scarring after subarachnoid hemorrhage?

    <p>Obstruction of CSF flow or disruption of CSF resorption</p> Signup and view all the answers

    What is the most dangerous type of vascular malformation?

    <p>Arteriovenous malformations (AVMs)</p> Signup and view all the answers

    What is the age range when arteriovenous malformations (AVMs) most commonly manifest?

    <p>10-30 years</p> Signup and view all the answers

    What is the classification of vascular malformations based on?

    <p>Nature of the abnormal vessels</p> Signup and view all the answers

    What is the consequence of rupture of an intracerebral hemorrhage into the ventricular system?

    <p>Hemorrhage into the subarachnoid space</p> Signup and view all the answers

    What is the common cause of hemorrhage into the subarachnoid space?

    <p>All of the above</p> Signup and view all the answers

    Study Notes

    Cerebrovascular Diseases

    • Cerebrovascular diseases are brain disorders caused by pathologic processes involving blood vessels.
    • Three main pathogenic mechanisms:
      • Thrombotic occlusion
      • Embolic occlusion
      • Vascular rupture

    Hemorrhage

    • Hemorrhage into the subarachnoid space can result from:
      • Vascular malformation
      • Trauma
      • Rupture of an intracerebral hemorrhage into the ventricular system
      • Coagulopathies
      • Tumors
    • Subarachnoid hemorrhages can obstruct CSF flow or disrupt CSF resorption, leading to hydrocephalus.

    Vascular Malformations

    • Vascular malformations of the brain are classified into four principal types:
      • Arteriovenous malformations (AVMs)
      • Cavernous malformations
      • Capillary telangiectasias
      • Venous angiomas
    • AVMs are the most common and affect males more than females (2:1).
    • AVMs most commonly manifest between 10 and 30 years of age with seizures, intracerebral hemorrhage, or subarachnoid hemorrhage.

    Stroke

    • Stroke is the clinical designation applied to all cerebrovascular diseases when symptoms begin acutely.
    • Hypoxia, ischemia, and infarction can occur due to:
      • Functional hypoxia (e.g., high altitude, severe anemia)
      • Ischemia (e.g., transient or permanent, due to tissue hypoperfusion)

    Global Cerebral Ischemia

    • Widespread ischemic-hypoxic injury can occur in the setting of severe systemic hypotension, usually when systolic pressures fall below 50 mm Hg.
    • Clinical outcome varies with the severity and duration of the insult.
    • Mild global cerebral ischemia may result in transient postischemic confusional state, with eventual complete recovery.
    • Severe global cerebral ischemia can result in widespread neuronal death, with patients often remaining severely impaired neurologically and in a persistent vegetative state.

    Morphology

    • In the setting of global ischemia, the brain is swollen, with wide gyri and narrowed sulci.
    • Early changes include acute neuronal cell change (red neurons).
    • Subacute changes include necrosis of tissue, influx of macrophages, vascular proliferation, and reactive gliosis.
    • Repair is characterized by removal of necrotic tissue and gliosis.

    Focal Cerebral Ischemia

    • Cerebral arterial occlusion leads to focal ischemia and then to infarction in the distribution of the compromised vessel.
    • Infarct size and location can be modified by collateral blood flow.
    • Embolic infarctions are more common than infarctions due to thrombosis.
    • Cardiac mural thrombi are a frequent source of emboli.
    • Thrombotic occlusions usually occur at the carotid bifurcation, the origin of the middle cerebral artery, and either end of the basilar artery.

    Infarcts

    • Infarcts can be divided into two broad groups:
      • Nonhemorrhagic infarcts result from acute vascular occlusions and may evolve into hemorrhagic infarcts.
      • Hemorrhagic infarcts usually manifest as multiple, sometimes confluent, petechial hemorrhages.
    • Macroscopic appearance of a nonhemorrhagic infarct evolves over time:
      • Unchanged in appearance in the first 6 hours
      • Pale, soft, and swollen by 48 hours
      • Gelatinous and friable from days 2 to 10
      • Fluid-filled cavity from day 10 to week 3

    Microscopically

    • Tissue reaction follows a characteristic sequence:
      • Ischemic neuronal change (red neurons) and cytotoxic and vasogenic edema appear after the first 12 hours.

    Intracranial Hemorrhage

    • Hemorrhages within the brain are caused by:
      • Hypertension and other diseases leading to vascular wall injury
      • Structural lesions such as arteriovenous and cavernous malformations
      • Tumors
    • Subarachnoid hemorrhages most commonly result from ruptured aneurysms.

    Primary Brain Parenchymal Hemorrhage

    • Spontaneous (nontraumatic) intraparenchymal hemorrhages are most common in mid to late adult life, with a peak incidence at about 60 years of age.
    • Most are due to the rupture of a small intraparenchymal vessel.
    • Hypertension is the leading underlying cause, and brain hemorrhage accounts for roughly 15% of deaths among individuals with chronic hypertension.
    • Hypertensive intraparenchymal hemorrhages typically occur in the basal ganglia, thalamus, pons, and cerebellum, with the location and size of the bleed determining its clinical manifestations.

    Cerebrovascular Diseases

    • Cerebrovascular diseases are brain disorders caused by pathologic processes involving blood vessels.
    • The three main pathogenic mechanisms are:
      • Thrombotic occlusion
      • Embolic occlusion
      • Vascular rupture

    Hypoxia, Ischemia, and Infarction

    • Cerebral blood flow normally remains stable over a wide range of blood pressure and intracranial pressure due to autoregulation of vascular resistance.
    • The brain may be deprived of oxygen by two general mechanisms:
      • Functional hypoxia (e.g., high altitude, severe anemia)
      • Ischemia (transient or permanent, due to tissue hypoperfusion)

    Global Cerebral Ischemia

    • Widespread ischemic-hypoxic injury can occur in the setting of severe systemic hypotension, usually when systolic pressures fall below 50 mm Hg.
    • The clinical outcome varies with the severity and duration of the insult.
    • In severe global cerebral ischemia, widespread neuronal death occurs, and patients who survive often remain severely impaired neurologically and in a persistent vegetative state.

    Morphology

    • In the setting of global ischemia, the brain is swollen, with wide gyri and narrowed sulci.
    • Early changes (12-24 hours after the insult) include acute neuronal cell change (red neurons).
    • Subacute changes (24 hours to 2 weeks) include necrosis of tissue, influx of macrophages, vascular proliferation, and reactive gliosis.

    Microscopically

    • The tissue reaction follows a characteristic sequence.
    • After the first 12 hours, ischemic neuronal change (red neurons) and cytotoxic and vasogenic edema appear.

    Intracranial Hemorrhage

    • Hemorrhages within the brain are caused by:
      • Hypertension and other diseases leading to vascular wall injury
      • Structural lesions (e.g., arteriovenous and cavernous malformations)
      • Tumors

    Primary Brain Parenchymal Hemorrhage

    • Spontaneous (nontraumatic) intraparenchymal hemorrhages are most common in mid to late adult life, with a peak incidence at about 60 years of age.
    • Most are due to the rupture of a small intraparenchymal vessel.
    • Hypertension is the leading underlying cause, and brain hemorrhage accounts for roughly 15% of deaths among individuals with chronic hypertension.

    Subarachnoid Hemorrhage and Saccular Aneurysms

    • The most frequent cause of clinically significant nontraumatic subarachnoid hemorrhage is rupture of a saccular (berry) aneurysm.

    Focal Cerebral Ischemia

    • Cerebral arterial occlusion leads to focal ischemia and then to infarction in the distribution of the compromised vessel.
    • The size, location, and shape of the infarct and the extent of tissue damage may be modified by collateral blood flow.

    Embolic Infarctions

    • More common than infarctions due to thrombosis, cardiac mural thrombi are a frequent source of emboli.
    • Myocardial dysfunction, valvular disease, and atrial fibrillation are important predisposing factors.

    Thrombotic Occlusions

    • Thrombotic occlusions usually are superimposed on atherosclerotic plaques.
    • Common sites are the carotid bifurcation, the origin of the middle cerebral artery, and either end of the basilar artery.

    Infarcts

    • Infarcts can be divided into two broad groups:
      • Nonhemorrhagic infarcts result from acute vascular occlusions and may evolve into hemorrhagic infarcts when there is reperfusion of ischemic tissue.
      • Hemorrhagic infarcts manifest as multiple, sometimes confluent, petechial hemorrhages.

    Vascular Malformations

    • Vascular malformations of the brain are classified into four principal types:
      • Arteriovenous malformations (AVMs)
      • Cavernous malformations
      • Capillary telangiectasias
      • Venous angiomas

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    Description

    This quiz covers the causes and effects of hemorrhages in the subarachnoid space, including vascular malformations, trauma, and coagulopathies. It also discusses the resulting complications such as hydrocephalus.

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