CASE REPORTS Subdural Hematoma Mimicking a Transient Ischemic Attack Due to Antihypertensive Medication YEHIA Y. MISHRIKI, MD, Allentown, Pa ABSTRACT: An elderly man had two completely reversible episodes of aphasia, each occurring after taking his antihypertensive medications. He was subsequently found to have a subdural hematoma. The association between subdural hematomas (and other intracranial mass lesions) and reversible neurologic deficits is discussed, as is the pathophysiology of the phenomenon. In addition, the relationship between the effects of the patient’s antihypertensive medications and the neurologic deficits in the setting of a subdural hematoma is explored. SUBDURAL HEMATOMAS and other intracerebral mass lesions can manifest as intermittent, com- pletely reversible neurologic deficits mimicking transient ischemic attacks (TIAs). The impli- cations for treatment are obvious, since re- curring, presumed TIAs are often treated with anticoagulation, a potentially disastrous in- tervention in patients with subdural hemato- mas. Herein, I describe a patient who had re- current transient neurologic deficits induced by the administration of antihypertensive med- ications and who was found to have a subdural hematoma. CASE REPORT An 86-year-old male hypertensive nursing home patient had sudden, nonfluent aphasia accompanied by headache. The episode lasted half an hour before resolving fully. When seen in the hospital, the patient adamantly insisted that it was his new antihypertensive, diltiazem, that had caused his symptoms. It had recently been added to losar- tan to better control his blood pressure. Shortly after admission, the patient once again had profound, nonflu- ent aphasia, which was unaccompanied by motor or sen- sory deficits. The patient indicated that he had a severe headache. On examination, his blood pressure was slightly elevated at 150/86 mm Hg. Auscultation of the lungs dis- closed midinspiratory crackles at the bases, and examina- tion of the heart revealed a regular rhythm and a grade 2/6 midsystolic murmur at the base. There were no gal- lops or clicks. The right carotid artery was of normal From the Department of Medicine/Ambulatory Care, Lehigh Valley Hospital, Allentown, Pa. Reprint requests to Yehia Y, Mishriki, MD, Lehigh Valle Hospital, Department of Medicine, 1210 S Cedar Crest Blvd, Suite 3600, Allentown, PA 18103. i amplitude and contour, whereas the left carotid had a slightly diminished amplitude. There were no carotid - bruits. The patient’s roommate pointed out that the patient had been conversant only half an hour earlier, and a check with the nurse revealed that the patient had received his antihypertensive medications a short time before the most recent neurologic episode. His blood pres- sure had been 188/98 mm Hg at that time. The patient was thought to be having recurrent TIAs, and the headache was attributed to uncontrolled hyper- tension. A heparin drip was to be started, but fortunately it was withheld until the patient had computed tomography (CT) of the brain. The CT scan revealed a moderate sized acute to subacute subdural hematoma overlying the left frontal lobe. A craniotomy with evacuation of the hema- toma was performed, and the patient made a full and uneventful recovery. DISCUSSION This case illustrates the well described but little appreciated phenomenon of the occa- sional intermittence of neurologic symptoms in patients with subdural hematomas. In addi- tion, our patient had the unusual twist of hay- ing his symptoms brought on by his antihyper- tensive medications, presumably by their blood pressure lowering actions. The association between transitory neuro- logic signs or symptoms and subdural hemato- — mas was first described by Schwenke in 1733.' Since then, many reports have described cases of intermittent neurologic deficits occurring in association with subdural hematomas as well as other “mass” lesions and cerebral aneu- rysms.** When transient neurologic deficits have occurred in patients with subdural hema- Mishriki_ * SUBDURAL HEMATOMA MIMICKING TIA 905 tomas, they have frequently been aphasias with or without hemimotor or hemisensory deficits and have lasted an average of 30 min- utes." In a significant percentage of these patients, a history of head trauma was conspic- uously absent. Various theories have been advanced to explain this counterintuitive phe- nomenon and have included (1) decreased cerebral blood flow (CBF) due to blood vessel compression or to vascular displacement caused by parenchymal edema; (2) seizure activity caused by disruption of normal corti- cal electrical activity; (3) fluctuations in intracranial pressure due to changes in head position or Valsalva’s maneuver; (4) spreading cortical depression as a result of mechanical irritation of brain tissue; and (5) small, repeated hemorrhages into the subdural space and membrane of the hematoma. Any, or several, of these mechanisms might be operative in a given patient.? Several studies have investigated CBF in pa- tients with subdural hematomas. Ikeda and colleagues’ studied regional CBF in 38 patients with unilateral chronic subdural hematoma. They found that preoperative regional CBF was essentially normal in patients without focal neurologic signs but was in the lower limit of age-matched normal val- ues, in general. It was subnormal in some areas in patients who had hemiparesis associ- ated with the hematoma. Nukui and Aiba! also showed a reduction in CBF in older patients with subdural hematomas and focal neuro- logic deficits, in contradistinction to younger patients without focal deficits who had normal values. They theorized that CBF was dimin- ished because of an increase in intracranial pressure. Brodersen and Gjerris’ had similar results in their study, but they found no signifi- cant increase in cerebrospinal fluid pressure at lumbar puncture, which they used as an estimate of intracranial pressure. Further- more, they could not account for the diminu- tion in CBF by alterations in the patients’ Pco. levels. The temporal association between our patient’s two episodes of aphasia and his receiving his antihypertensive medications suggests a cause-and-effect relationship. Given that the patient’s hypertension had been poorly controlled, it was possible that he had diminution or loss of cerebrovascular autoreg- ulation. Therefore, cerebral blood pressure and CBF would have had a more linear rather than sinusoidal relationship. Since cerebral blood pressure is the difference between mean arterial pressure and intracranial pres- sure, a reduction in mean arterial pressure with antihypertensive medications would have resulted in a reduction in cerebral blood pres- sure and, hence, CBF, in turn causing the neu- rologic deficit. This case highlights the fact that subdural hematomas can manifest as intermittent neu- rologic signs and symptoms mimicking TIAs. It also suggests that a subdural hematoma may cause the sudden development of a neuro- logic deficit in a patient with hypertension whose blood pressure is normalized with anti- hypertensive medications. Given that the usual treatment of recurrent TIAs is with anticoagu- lation (a disastrous intervention in a patient with a subdural, hematoma), it is imperative that an imaging study be done in a patient with a transient neurologic deficit to dis- tinguish a true TIA from a subdural hema- toma or other intracranial mass lesion. References 1. Endtz LJ: Post-traumatic hygroma in the eighteenth cen- tury. described by Thomas Schwenke. Surg Neurol 1978; 10:305-307 2. Melamed E, Lavy S, Reches A, et al: Subdural hematoma simulating transient cerebral ischemic attacks: case report. J Neurosurg 1975; 42:101-103 3. Russell NA, Atack DM, Benoit BG: Chronic subdural hematoma, a cause of apparent transient ischemic attacks. Can Med Assoc J 1982; 127:1105-1106 4, Moser ML, Johnston DE, Reinmuth OM: Subdural hema- toma with transient neurological deficits: a review of 15 cases. Ann Neurol 1983; 14:539-542 5. Russell NA, Goumnerova L, Atack EA, et al: Chronic sub- dural hematoma mimicking transient ischemic attacks. J Trauma 1985; 25:1113-1114 6. Traynelis VC: Chronic subdural hematoma in the elderly. Clin Geriatr Med 1991; 7:583-598 7. Ikeda K, Ito H, Yamashita J: Relation of regional cerebral blood flow to hemiparesis in chronic subdural hematoma. Surg Neurol 1990; 33:87-95 8. Nukui H, Aiba T: Regional cerebral blood flow in patients with chronic subdural hematoma. No Shinkei Gaisho 1972; 4:371-382 9. Brodersen P, Gjerris F: Regional cerebral blood flow in patients with chronic subdural hematoma. Acta Neurol Scand 1975; 51:233-239 906 September 1999 * SOUTHERN MEDICAL JOURNAL = Vol. 92, No. 9