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Headache in a woman with hypertension


A 71-year-old woman presents to the emergency department accompanied by her daughter. The patient woke up in the morning "feeling fine" and then complained of a headache. She became progressively less oriented over the next 45 minutes.

A 71-year-old woman presents to the emergency department accompanied by her daughter. The patient woke up in the morning "feeling fine" and then complained of a headache. She became progressively less oriented over the next 45 minutes.

The patient has hypertension. Her daughter reports that her mother often refuses to take her medication because she feels well. The medical history is otherwise noncontributory.

In the emergency department, the patient is confused. Her heart rate is 102 beats per minute; respiration rate, 18 breaths per minute; temperature, 37.2°C (99°F); and blood pressure, 178/112 mm Hg.

A CT scan of the head is ordered. What abnormalities on the CT images point to the cause of the patient's headache?

(Answer begins on page 562.)

Another axial image (B) superior to Figure A also demonstrates the dilated lateral ventricles with extensive hemorrhage. The image demonstrates rounded foci of increased density consistent with clot formation inside the ventricles.

Figure C (inferior to Figure A at the level of the third ventricle) demonstrates a dilated third ventricle with rounded foci of increased density, which represents a clot in the posterior portion of the ventricle. A large amount of hemorrhage is identified within the dilated temporal horns of the lateral ventricles.

Figure D (just inferior to Figure C and inferior to the third ventricle) demonstrates a clot within the cerebral aqueduct.

Figure E (inferior to Figure D at the level of the fourth ventricle) demonstrates a normal-size fourth ventricle without evidence of hemorrhage.

The final diagnosis was hypertensive hemorrhage within the basal ganglia with extension into the lateral and third ventricles. Clot formation within the third ventricle and cerebral aqueduct caused noncommunicating hydrocephalus.

In adults who present with intracranial hemorrhage without preceding trauma, the most likely cause is hypertension.

Intracranial hypertensive hemorrhage can occur at any age but is more common in elderly persons. The etiology is related to the chronicity of the hypertension. Chronic elevated pressures are thought to erode the walls of the smaller intracranial vessels and, over time, lead to an area of "breakdown" with subsequent hemorrhage. The small vessels most commonly associated with this process are located in the basal ganglia, pons, cerebellum, and deep white matter; hence, this is where the process is commonly seen.

When the blood vessel breaks down and intracranial hemorrhage occurs, the intracranial blood incites cerebral edema that compounds the mass effect of the hematoma. Depending on the size and location of these 2 processes, symptoms may be minimal or catastrophic. In addition, the hemorrhage may extend into the ventricular system--as in this case--leading to hydrocephalus caused by obstruction of flow of cerebrospinal fluid.

The CT appearance of hemorrhage changes with time. Initially, within the first 4 to 6 hours, most hemorrhage appears hyperdense relative to brain parenchyma. The increased density is primarily related to the hemoglobin content of the extravasated blood; therefore, the hemorrhage may appear isodense to hypodense in patients with anemia. Abundant edema will often surround the lesion, appearing hypodense within the brain parenchyma. The increased density of the hematoma may persist for up to 7 days, at which time the density of the peripheral portions of the lesion begins to decrease. The hematoma will be completely resorbed at approximately 2 to 4 months, and may often leave a cavity.

Outcome of this case. In this patient, the size of the hematoma and the surrounding edema caused brainstem herniation inferiorly. The patient died as a result. *

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