◆ Posttraumatic Atrophy and Encephalomalacia
Survivors of significant head trauma suer a variety of neurologic symptoms includingcognitive impairment, headache, epilepsy,and persistent focal motor or sensory deficits.
Nonenhanced head CT shows general-ized volume loss, which can develop in as little as 4–6 weeks. Focal encephalomala-cia involving the inferior frontal lobe, the anterior and inferior temporal lobe, the posterior cerebellum, and the parasagittal convexity are common sequelae of cortical contusions. Other findings supporting re-
Fig. 2.16a–f a–c Posttraumatic atrophy following head injury in a 24-year-old. (a) Initial CT and (b) FLAIR MRI show mild swelling, cortical contusions, and shear hemorrhages but near-normal ventricular size and volume for a young adult. (c) CT performed one month after injury shows interval global ventricular and sulcal enlargement as well as focal right-sided encephalomalacia.
d–f Posttraumatic encephalomalacia. Left inferior frontal and bilateral anterior temporal lobe low-atten-uation focal parenchymal changes with mild generalized volume loss, indicated by subtle lateral ventricle temporal tip and fourth ventricle enlargement. This distribution is typical of remote traumatic cortical contusions. (f) Healed left zygomatic arch fracture further supports a remote injury.
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hemorrhage often manifests as dizziness, vomiting, truncal ataxia, and gaze palsies.
Noncontrast CT is the most appropri-ate initial imaging study in patients with clinical stroke symptoms. If a parenchymal hemorrhage is the cause, the size of the bleed as well as any ventricular extension or secondary hydrocephalus are easily as-sessed. Acute hemorrhage (within four hours) appears as a well-defined area of high attenuation and may persist for up to a week. As the bleed ages, the margins be-come less distinct and a surrounding low-attenuation rim develops, reflecting brain edema or extruded serum. Subacute hema-tomas may show peripheral enhancement on postcontrast CT or MRI. Very remote hematomas appear as slitlike, CSF-density lesions.
The volume of a parenchymal hematoma(mL) is estimated by multiplying the threedimensions (in cm) and dividing the prod-uct by 2. Hematoma volumes > 50 mL areassociated with a poor prognosis (Fig. 2.17).
◆Hypertensive Hemorrhage
Twice as common as subarachnoid hem-orrhage, spontaneous intracranial hemor-rhage (ICH) comprises 10–20% of strokes, which are clinically indistinguishable from ischemic stroke and subarachnoid hemor-rhage. Patients with ICH often present with headache, nausea, and vomiting before a focal neurologic deficit becomes evident. In adults with nontraumatic intracranial hemorrhage, hypertension is the most common etiology.
In long-standing, poorly controlled hy-pertension, microaneurysmsdevelop in the perforating arterioles, primarily in the lenticulostriate, pontine, and cerebellar distributions. Accelerated atherosclero-sis and hyalinearteriosclerosis also play a part in the pathologic changes predispos-ing to hypertensive ICH. Bleeding usually occurs in the putamen, thalamus, pons, or cerebellum (in order of decreasing fre-quency), and clinical signs correspond to the location of hemorrhage and function of the involved brain. For example, cerebellar
Fig. 2.17a–fa,b Small hemorrhages in two patients. (a) Small focal hemorrhage in the right internal capsule genu and anterior thalamus. (b) Small left thalamic hemorrhage.
c,d Large left external capsule hemorrhage. Large left-sided hematoma with subfalcine shift, modest intraventricular hemorrhage, and trapping of the right lateral ventricle.
e,f Massive hemorrhage with rupture into the ventricular system and severe hydrocephalus. A large pa-renchymal hematoma obliterates the right basal ganglia and extends into the ventricles. Clot lls the third and fourth ventricles and causes marked hydrocephalus.
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rhages may be present but undetectable on CT. Gradient echo MRI detects these with greater sensitivity.
The dierential diagnosis of lobar hem-orrhage includes atypical hypertensive bleed, venous thrombosis with infarct, ruptured arteriovenous malformation, ruptured aneurysm, and hemorrhagic neoplasm. In younger and middle-aged patients, CT angiography, MRI with gado-linium and angiography, and conventional angiography can be considered to exclude an underlying hemorrhagic neoplasm or vascular lesion (Fig. 2.18).
◆Amyloid Angiopathy
Amyloid angiopathy is due to beta amyloid deposition in cerebral vessels and usually aects adults over age 65. It is a primary cause of cortical and subcortical (lobar) hemorrhage, and this is what brings most patients to clinical attention. Symptoms include sudden focal neurologic deficit, transient ischemic attacks, and variably progressive dementia.
Acute lobar cortical or subcortical hemorrhage against a background of sub-cortical/periventricular white matter low-attenuation changes and cerebral volume loss are typical CT findings. Microhemor-
Fig. 2.18a–da,b Lobar hemorrhage. Noncontrast CT shows peripheral, well-dened, acute right frontal lobar hemor-rhages in two elderly patients. While a hemorrhagic venous infarct could have this appearance, it would be unusual for either a hypertensive bleed or hemorrhagic conversion of an arterial-distribution infarct. Associated background low-attenuation white matter changes and sulcal prominence indicate chronic underlying small-vessel ischemic change.
c,d Amyloid angiopathy. Gradient echo MRI in a dierent patient shows multiple punctate low-signal-intensity foci involving the temporal cortices and subcortical white matter. These lesions correspond to local hemosiderin deposition from tiny subclinical hemorrhages.
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