Medical 277

Cerebrovascular Disease

1. Etiology a. Third most frequent cause of death in industrialized countries b. Leading cause of serious disability in the United States c. Risk factors similar to coronary artery disease

2. Clinicopathological forms a. Global cerebral ischemia i. Fall in blood flow to the brain (shock, cardiac arrest, and hypotensive episodes)

ii. Damage to regions of selective vulnerability: Purkinje neurons, hippocampus CA1, and pyramidal neurons of cortex iii. Infarcts in watershed areas iv. Cortical laminar necrosis

■ Diffuse ischemic necrosis of neocortex • May lead to brain death b. Transient ischemic attack (TIA): reversible, symptoms last less than 24 h; due to small platelet thrombi or atheroemboli c. Infarction: 85% of all stroke cases i. Thrombosis of cerebral artery (atherosclerosis-related)

ii. Cardiogenic embolism iii. Small-vessel disease: arteriolosclerosis, amyloid angiopathy, etc.

d. Hemorrhage: 15% of all stroke cases i. Intracerebral ii. Subarachnoid

3. Infarction a. Thrombotic occlusion i. Due to atherosclerosis ii. Leads to anemic (white) infarct b. Embolic occlusion i. Often due to thromboemboli from cardiac chambers ii. Less frequently due to atheroemboli iii. Leads to hemorrhagic infarct c. Small-vessel disease i. Related to hypertension, resulting in hyaline arteriolosclerosis ii. Leads to lacunar infarcts or lacunae d. Pathology (ie, morphological features of brain infarcts)

Table 29-3. Gross and Microscopic Changes Associated with Cerebral Infarction


Gross Changes

Microscopic Changes

0-12 h

No changes

Minimal or no changes

12-24 h

Minimal changes

Red (hypereosinophilic) neurons with pyknotic nuclei

24—48 h

Indistinct gray-white matter junction

Neutrophilic infiltration

2-10 d

Friable tissue with marked edema

Histiocytic infiltration; neurons disappear

2-3 wk

Tissue liquefies

Liquefactive necrosis; histiocytes filled with products of myelin breakdown

3 wk-mo

Fluid-filled cavity demarcated by gliotic scar

Fluid-filled cavity; reactive astrocytes and lip id-la den macrophages (gitter cells)


Old cyst surrounded by gliotic scar

Astrogliosis surrounding a cyst

Note: Hemorrhagic infarct leads to eryihrocyle degradation and hemosiderin deposition.

Note: Hemorrhagic infarct leads to eryihrocyle degradation and hemosiderin deposition.

e. Clinical manifestations depend on affected artery f. Common neurovascular syndromes i. Anterior cerebral artery (ACA)

• Weakness and sensory loss in contralateral leg

• Transient expressive aphasia

• Abulia ii. Middle cerebral artery (MCA)

■ Contralateral hemiplegia (face and arm) and gaze palsy

• Contralateral sensory loss

• Aphasia if dominant hemisphere affected hi. Posterior cerebral artery (PCA)

• Contralateral hemianopia or total cortical blindness if bilateral

• Alexia without agraphia

■ Thalamic syndrome iv. Dementia: due to recurrent infarcts or small vessel disease 4. Hemorrhage a. Causes 15% of strokes b. Intracerebral (intraparenchymal) hemorrhage i. Hypertension: most frequent predisposing condition; involves basal ganglia, cerebellum, pons, and centrum semiovale ii. Other causes: vascular malformations, especially arteriovenous malformations (AVMs), cerebral amyloid angiopathy, neoplasms, vasculitides, abnormal hemostasis, hematological malignancies, and infections iii. Symptoms: severe headache, frequent nausea/vomiting, steady progression of symptoms over 15-20 minutes, and coma

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c. Epidural hemorrhage i. Virtually always traumatic ii. Usually associated with skull fracture iii. Tear of dural arteries, most frequendy middle meningeal artery iv. Leads to cerebral herniation (usually subfalcine) if not promptly evacuated v. Lucid interval before loss of consciousness ("talk and die syndrome")

d. Subdural hemorrhage i. Usually traumatic ii. Caused by rupture of bridging veins (from cerebral convexities to sagittal sinus)

iii. Predisposing conditions: brain atrophy and abnormal hemostasis iv. Headache, drowsiness, focal neurological deficits, sometimes dementia v. Recurs frequendy e. Subarachnoid hemorrhage i. Most frequent cause: ruptured berry aneurysms ii. Less frequent causes: extension of an intracerebral or subdural hematoma, vascular malformations, trauma, abnormal hemostasis, and tumors iii. Sudden ("thunderclap") headache, nuchal rigidity, neurological deficits on one side, and stupor

5. Berry aneurysms a. Thin-walled saccular outpouchings, consisting of intima and adventitia only b. Most frequent cause of subarachnoid hemorrhage c. Most frequent sites: anterior circle of Willis at branching points d. Pathogenesis: congenital focal weakness of artery; not identifiable at birth e. Associated disorders: Marfan syndrome, Ehlers-Danlos type 4, and adult polycystic kidney disease f. Hypertension and cigarette smoking predispose to formation g. Rupture is precipitated by sudden increase in blood pressure h. Prognosis after rupture: 1 /3 die, 1/3 recover, and 1/3 rebleed CNS Trauma

1. Cranial cavity and brain a. Concussion i. Change in the momentum of the head (impact against a rigid surface)

ii. Loss of consciousness and reflexes, temporary respiratory arrest, and amnesia for the event iii. Pathogenesis uncertain iv. Parenchymal injuries may or may not be evident at autopsy b. Contusions i. Impact of parts of brain against inner calvarial surfaces ii. Bruising to the brain resulting from tissue and vessel disruption iii. Sites of injury: crests of orbital gyri in frontal and temporal poles iv. Coup (site of injury) and contrecoup (site diametrically opposite)

v. Coup and contrecoup develop when the head is mobile at the time of impact vi. Acute: hemorrhage of brain tissue in a wedge-shaped area vii. Subacute: necrosis and liquefaction of brain viii. Remote: depressed area of cortex with yellow discoloration ("plaque jaune") c. Diffuse axon al injury i. Injury to the white matter due to acceleration/deceleration ii. Damage to axons at nodes of Ranvier with impairment of axoplasmic flow iii. It is diffuse, but predilection for

• Corpus callosum, periventricular white matter, and hippocampus

• Cerebral and cerebellar peduncles iv. Coma after trauma without evidence of direct parenchymal injuries v. Poor prognosis, related to duration of coma vi. Histopathology: axonal swellings appreciable in the white matter

2. Spinal cord a. Injuries are usually traumatic, due to vertebral displacement b. Symptomatology depends on interruption of ascending and descending tracts c. Lesions to thoracic segments or below: paraplegia d. Lesions to cervical segments: tetraplegia e. Lesions above C4: respiratory arrest due to paralysis of diaphragm

3. Cerebral herniations a. Subfalcine (cingulate gyrus)

i. Cingulate gyrus is displaced underneath the falx to the opposite side ii. Compression of anterior cerebral artery b. Transtentorial (uncal)

i. Uncus of the temporal lobe is displaced over the free edge of the tentorium ii. Compression of the third nerve

• Pupillary dilatation on the same side

• Infarct in dependent territory iii. Advanced stages: Duret hemorrhage within the central pons and midbrain c. Cerebellar tonsillar i. Displacement of cerebellar tonsils through the foramen magnum ii. Compression of medulla: cardiorespiratory arrest D. Developmental Abnormalities

1. Neural tube defects a. Most common developmental CNS abnormalities b. Results from defective closure of the neural tube c. Occurs at the two extremities of the neuraxis d. Folate deficiency involved in pathogenesis e. Anencephaly i. Absence of cranial vault ii. Incompatible with life—babies die soon after birth

Open neural tube defects (not f. Neural tube defects of the spinal cord i. Spina bifida occulta: bony defect of the vertebral arch ii. Meningocele: bony defect with outpouching of meninges spina bifida occulta) lead to increased alfa-fetoprotein during pregnancy, which, in conjunction with ultrasound, allows prenatal diagnosis.


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