Chapter 2: Cerebrovascular Disease
|Brain perfusion and Cerebrovascular disease|
This chapter is intended as an introduction to the basic concepts of the pathophysiology of ischemic injury of the brain and cerebrovascular disease.
General features of energy metabolism of the brain, selective vulnerability and excitotoxicity
Embolism- A variety of materials within the circulation can travel downstream and lodge in vessels with lumens too narrow to allow passage of the material. Small emboli tend to lodge in distal branches of superficial vessels which results in infarction at the gray-white junction. Multiple small infarcts distributed throughout the cerebral hemispheres at the gray-white junction are characteristic of embolic infarction. The occurrence of a single large wedge-shaped infarct is also another common pattern of cerebral embolism. The most common location of embolic infarction is in the territory of the middle cerebral artery ("the artery of embolization"). Emboli can come from a variety of sources, including: artery-to-artery, the heart, air emboli due to surgical procedures and bone marrow (following long bone fracture).
There are numerous other, less common causes of infarction of the brain.
Evolution of the pathological process -
Intracranial hemorrhage -
Approximately 2% of adults have saccular aneurysms and there is a risk of rupture of 23% per year. The greatest risk of rupture is from 40-60 years of age. 1/3 of patients with catastrophic subarachnoid hemorrhages are dead before treatment, 1/3 die in hospital or have serious sequelae and 1/3 do well. A very high percentage have warning signs which represent minor hemorrhages, most often in the two weeks prior to a catastrophic hemorrhage. It is important to recognize these "sentinel" hemorrhages, because the catastrophic hemorrhage can often be prevented.
Other, less common causes of spontaneous (non-traumatic) brain hemorrhage include amyloid angiopathy, arteriovenous malformation, other vascular malformations, and bleeding disorders. Occasionally, a saccular aneurysm ruptures into the parenchyma resulting in parenchymal hemorrhage, rather than subarachnoid hemorrhage. Amyloid angiopathy can be suspected as the cause of a hemorrhage in an older individual who presents with lobar hemorrhage (a lobe of cerebrum) rather than in the basal ganglia. In the case of coagulopathy, there are often multiple, randomly distributed hemorrhages.
The signs and symptoms of venous thrombosis include: headache (75%), papilledema (54%), focal motor or sensory deficit (34%), seizure (37%) and altered level of consciousness (30%). Neuroimaging reveals thrombosed veins, absence of enhancement of the affected sinus, increased enhancement of congested veins and dura and hemorrhagic infarcts.