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Editorial |

Recognizing and Preventing Intracerebral Hematoma Expansion

Louis R. Caplan, MD1
[+] Author Affiliations
1Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts
JAMA Neurol. 2016;73(8):914-915. doi:10.1001/jamaneurol.2016.1899.
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One early and dramatic clinical account of hematoma expansion concerns a man who developed a hematoma that evolved under observation in 1937.1 He was sent to the hospital because of “malignant hypertension.” While his medical history was being taken, the patient complained of weakness, dizziness, and numbness of his hands. He then reported an inability to hear, difficulty in swallowing, and dyspnea. The patient was placed on the examining table, and it was determined that his systolic blood pressure and diastolic blood pressure were 245 and 170 mm Hg, respectively. Under the eyes of several examiners, complete bilateral palsy of the sixth nerves developed; both pupils dilated, and the corneal reflexes disappeared. The patient was still able to talk, but with a bulbar speech, and he appeared almost completely deaf. His left leg became paretic, and rapid clonic movements were observed. The Babinski sign was present bilaterally. Within an hour, the patient became comatose and quadriplegic and soon died. His brainstem had been gradually destroyed by a hypertensive pontine hematoma while physicians watched helplessly. Környey1 commented that this rapidly progressive chain of events was most unpleasant to witness and produced a depressing effect on the nurses and physicians.

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