Subdural hematoma is most commonly caused by acceleration- deceleration shearing stresses that rupture the bridging veins that extend from the movable brain to the fixed dural venous sinuses. The blood accumulates in a pre-existing but essentially volumeless subdural space. Normally, the pressure of the CSF holds the arachnoid in contact with the dura, thereby creating a real interval that is without significant volume. Because the subdural space is a real space surrounding all external surfaces of the brain, subdural hemorrhage tends to spread extensively over many aspects of the brain surface.

On CT examination, the typical acute subdural hematoma appears as a diffuse crescent-shaped radiodensity that may extend onto many surfaces of the brain, including the cerebral convexity, skull base, interhemispheric fissure, upper or lower surface of the tentorium, and area around the brain stem (Fig. 6-89). One way to differentiate subdural from epidural hematomas is that subdural hematomas cross sutures lines yet do not cross midline, whereas epidural hematomas do not cross suture lines yet can cross midline. There are two ways of classifying subdural hematomas based on their changing radiographic appearance over time (83). One scheme divides them into acute (i.e., more radiodense than adjacent gray matter), subacute (i.e., isodense to gray matter), and chronic (i.e., hypodense to gray matter). Another scheme simply lumps the subacute and chronic into the chronic category. The subdural hematoma typically effaces the adjacent gyri, produces inward displacement of the gray-white matter junction, and may compress the ventricle or cause brain herniation under the falx or through the tentorium.

FIGURE 6-89. Bilateral panhemispheric chronic subdural hematomas with superimposed acute bleed and hematocrit levels (arrows).

As the subdural hematoma ages, the hemoglobin protein producing its radiodensity is broken down and removed, and a vascular granulation tissue develops along its inner surface. Over a few weeks, the subdural hematoma usually becomes isodense or hypodense to gray matter (84). Because of volume loss, the chronic subdural hematoma may lose its concave inner border and become more focal, even occasionally assuming a biconvex outline. Isodense subdural hematomas are more difficult to discriminate. Their presence can be implied indirectly by their mass effects on the underlying brain. An injection of contrast material will enhance both the vascular membrane and the displaced cortical vessels, allowing discrimination of the hematoma from the adjacent cortex.

Patients who present first with a chronic subdural hematoma may have no recollection of any antecedent trauma because the traumatic episode may have been so slight that it was forgotten. Chronic hematomas commonly involve the elderly, where loss of cerebral volume puts the bridging veins under increased stress and makes them more susceptible to rupture by minor trauma.

MRI has valuable unique imaging properties that make it very sensitive to the detection of some extracerebral hemorrhages. First, the high signal intensity that subacute hematomas display on T1- and T2-weighted images makes MRI more sensitive than CT for detecting hematomas that are isodense by CT (73). Even chronic subdural hematomas remain hyperintense to CSF and gray matter for several months, which is long after they have become isodense or hypodense on CT. Also, the ability of MRI to discern the displaced signal voids of cortical or dural vessels facilitates the identification of small extracerebral hemorrhages. In addition, when the hematoma collects around the obliquely placed tentorium, axial CT images may average it into adjacent tissues. In these cases, the multiplanar imaging properties of MRI can be very valuable. Also, small hematomas next to the calvarium can be better seen by MRI because they are contrasted against the osseous signal void.


Source: Physical Medicine and Rehabilitation - Principles and Practice

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