Cerebrovascular diseases

Cerebrovascular diseases

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Cerebrovascular diseases

  • It is the third leading cause of death in the United States
  • It is the most prevalent neurologic disorder in terms of both morbidity and mortality

Brain

  • The brain is a highly aerobic tissue

2% of the body weight

15% of the cardiac output

20% of the oxygen consumed by the body

  • Autoregulation

Interruption of normal blood flow to the brain and spinal cord may cause irreversible parenchymal injury within minutes

it receives 15% of the resting cardiac output and accounts for 20% of the total body oxygen consumption.

Mechanisms of the brain lossing of oxygen:


Functional hypoxia

  • a setting of a low partial pressure of oxygen
  • impaired oxygen-carrying capacity
  • inhibition of oxygen use by tissue

Ischemia ( transient or permanent)

  • interruption of the normal circulatory flow

Global Cerebral Ischemia:

  • It occurs when there is a generalized reduction of cerebral perfusion, such as in cardiac arrest, shock, and severe hypotension.
  • The clinical outcomes dependent on

–the severity of the insult

–variability in the susceptibility of different populations of neurons in different regions of the CNS

It occurs when there is a generalized reduction of cerebral perfusion, usually below systolic pressures of less than 50mmHg, such as in cardiac arrest, shock, and severe hypotension.

Morphology of Global Cerebral Ischemia:

Grossly:

  • The brain is swollen, with wide gyri and narrowed sulci.
  • The cut surface shows poor demarcation between gray and white matter.

Histopathologic changes:

  • Early changes
  • Subacute changes
  • Reparative changes
early histolopathologic change of Cerebral Ischemia
early histolopathologic change of Cerebral Ischemia

Subacute changes:

  • Occurring at 24 hours to 2 weeks
  • Changes include

– necrosis of tissue

–influx of macrophages

–vascular proliferation

– reactive gliosis

reactive gliosis(Subacute change of Cerebral Ischemia )
reactive gliosis(Subacute change of Cerebral Ischemia )

After about 10 days, an area of infarction is characterized by the presence of macrophages and surrounding reactive gliosis

Reparative changes:

  • Approximately 2 weeks later
  • Characterized by

–removal of all necrotic tissue

–loss of normally organized CNS structure

– gliosis

reparative change of Cerebral Ischemia
reparative change of Cerebral Ischemia

Remote small intracortical infarcts are seen as areas of tissue loss with a small amount of residual gliosis.

Focal Cerebral Ischemia/Infarcts:


  • It follows reduction or cessation of blood flow to a localized area of the brain due to embolic or thrombotic arterial occlusion.
  • Infarcts are subdivided into two groups

Hemorrhagic (red) infarction

Nonhemorrhagic (pale, bland, anemic) infarction

thrombus of internal carotic artery
thrombus of internal carotic artery
thromboembolus that originated from mural thrombus in the left atrium
thromboembolus that originated from mural thrombus in the left atrium

A thrombosis of the internal carotid artery is seen here. Arterial thromboses are far more common in the brain than venous thromboses (by a ratio of about 100 to 1).

Acute cerebral infarct
Acute cerebral infarct

An acute cerebral infarct is seen here. Such infarcts are typically the result of arterial thrombosis or embolism.

Hemorrhagic (red) infarction:

large, discolored, focally hemorrhagic region in the left middle cerebral artery distribution

Hemorrhagic (red) infarction
Hemorrhagic (red) infarction

Their morphology is the same as pale infarcts with the addition of blood extravasation and resorption.

Intracranial hemorrhage:


  • Hemorrhage within the skull can occur in a variety of locations, and each location is associated with a set of underlying causes.

– Primary Brain Parenchymal Hemorrhage

– Subarachnoid Hemorrhage and Saccular Aneurysms

–Vascular Malformations

Hemorrhage within the skull can occur in a variety of locations, and each location is associated with a set of underlying causes. Hemorrhages within the brain itself can occur secondary to hypertension or other forms of vascular wall injury. Alternatively, they can arise in a specific lesion like an arteriovenous malformation, a cavernous malformation, or an intraparenchymal tumor. Subarachnoid hemorrhages are most commonly seen with aneurysms but occur also with other vascular malformations. Hemorrhages associated with the dura (in either subdural or epidural spaces) make up a pattern associated with trauma.

Primary Brain Parenchyma Hemorrhage:

  • Middle to late adult life (60 years old)
  • Caused by rupture of a small intraparenchymal vessel.
  • Hypertension is the most common cause (more than 50%).

–Hyline arterioloscerosis of smaller vessles

–Atherosclerosis of the larger arteries

–Minute arterial aneurysm (Charcot –Bouchard microaneurysms

  • Other factors

Brain hemorrhage account for roughly 15% of death among patients with chronic hypertension.

Minute

Other factors cause hemorrhage, such as systemic coagulation disorders, open heart surgery, neoplasms…….

Morphology of Primary Brain Parenchyma Hemorrhage
Morphology of Primary Brain Parenchyma Hemorrhage
basal ganglia thalamus pons cerebellum
basal ganglia thalamus pons cerebellum
Hypertensive hemorrhage in the pons
Hypertensive hemorrhage in the pons

Massive hypertensive hemorrhage rupturing into a lateral ventricle. B, Hypertensive hemorrhage in the pons, with extension to fill the fourth ventricle.

On microscopic examination:

  • Clotted blood surrounded by a rim of brain tissue
  • Anoxic neuronal and glial changes and edema.
  • Pigment- and lipid-laden macrophages
  • Proliferation of reactive astrocytes

Clinical features of Primary Brain Parenchyma Hemorrhage:

  • Evidences of increased intracranial pressure

–Severe headache

–Vomiting

–Loss of consciousness

  • Localizing signs
  • Brain stem compression

–Deep coma, irregular respirations with periods of apnea (Cheyne-Strokes respiration)

–Dilated, nonresponsive pupils

–spasticity

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