In chronic subdural hematoma, the traumatic etiology is often less clear. The head injury, especially in elderly persons and in those taking anticoagulant drugs, may have been trivial and forgotten. A period of weeks then follows when headaches (not invariable), light-headedness, slowness in thinking, apathy and drowsiness, unsteady gait, and occasionally a seizure are the main symptoms. The initial impression may be that the patient has a vascular lesion or brain tumor or is suffering from drug intoxication, a depressive illness, or Alzheimer disease. Gradual expansion of the hematoma by one of several mechanisms discussed further on is believed to cause the progression of symptoms. As with acute subdural hematoma, the disturbances of mentation and consciousness (drowsiness, inattentiveness, and confusion) are more prominent than focal or lateralizing signs, and they may fluctuate. Focal signs, when present, consist of mild hemiparesis and, rarely, an aphasic disturbance. Homonymous hemianopia is seldom observed, probably because the geniculocalcarine pathway is deep and not easily compressed; similarly, hemiplegia, that is, complete paralysis of one arm and leg, is usually indicative of a lesion within the cerebral hemisphere rather than a compressive lesion on its surface. Hemiparesis from subdural hematoma may sometimes be ipsilateral to the clot, the result of compression of the contralateral cerebral peduncle against the free edge of the tentorium (Kernohan-Woltman sign; see “Pathoanatomy of Brain Displacement and Herniations” in Chap. 16). If the condition progresses, the patient becomes stuporous or comatose. But this course is often interrupted by striking fluctuations of awareness.
With both large acute and chronic hematomas, dilatation of the ipsilateral pupil is a fairly reliable indicator of the side of the hematoma, although this sign may be misleading, occurring on the opposite side in 10 percent of cases, according to Pevehouse and coworkers. Convulsions are seen occasionally, most often in alcoholics or in patients with cerebral contusions, but they cannot be regarded as a cardinal sign of subdural hematoma. Rare cases of internuclear ophthalmoplegia and of chorea have been reported but have not occurred in our material. Presumably they are a result of distortion of deep structures. Also, brief and self-limited disturbances of neurologic function simulating transient ischemic attacks (TIAs) may occur with chronic hematomas; their mechanism is uncertain, but they do not appear to represent seizures. In infants and children, enlargement of the head, vomiting, and convulsions are prominent manifestations of subdural hematoma.
CT and MRI are the most reliable diagnostic procedures. On CT scans, the acute clot is initially hyperdense but becomes slowly isodense after a period of 1 or more weeks (Fig. 34-10). At that stage it may be difficult to detect except by the tissue shifts it causes. The fluid collection then becomes progressively hypodense (with respect to the adjacent cerebral cortex) over 2 to 6 weeks. The evolution of signal changes in the MRI is similar to the sequential imaging changes found with parenchymal hematomas. The acute clot is hypointense on T2-weighted images, reflecting the presence of deoxyhemoglobin. Over the subsequent weeks, all image sequences show it as hyperintense as a result of methemoglobin formation. Eventually the chronic clot again becomes hypointense on the T1-weighted images. With contrast infusion, both imaging procedures usually reveal the vascular and reactive border surrounding the clot. Usually, by the fourth week, sometimes later, the hematoma becomes very hypodense, giving rise to a chronic subdural hygroma that is indistinguishable from idiopathic ones that are presumably caused by a rent in the arachnoid that allows CSF to escape to the subdural compartment, as discussed further on.