A 59-year-old Caucasian woman presented with severe headache, repeated vomiting, and instability of stance and gait to our Accident and Emergency (A&E) department. She had been experiencing these symptoms for three hours. The patient had long-standing poorly-controlled essential hypertension, for which she took oral atenolol. The family denied head trauma or the ingestion of other medications. She was drowsy and had a blood pressure of 210/130 mmHg and a pulse rate of 110 beats per minute. Her lab tests (which included a coagulation screen) were unremarkable but her emergency non-contrast brain computed tomography (CT) scan revealed right-sided acute deep cerebellar hematoma with mild surrounding edema; no ventricular dilatation developed. She was managed as a case of primary spontaneous hypertensive intra-cerebral hemorrhage. During the following two weeks, she showed a favorable improvement and then she was discharged home on enalapril, metoprolol, hydrochlorothiazide, and simvastatin. Her blood pressure was 125/75 mmHg at that time. She was able to stand and walk with some assistance and her speech was normal. Two weeks later, the patient came in for a scheduled follow-up visit. She was conscious and her speech was normal; she could stand and walk alone, and her blood pressure was 110/85 mmHg. Eight weeks later, the patient presented with drowsiness, slurring of speech, vomiting, and inability to sit and stand unaided for one hour to our A & E. Her blood pressure was 190/100 mmHg. Her routine blood tests were within their normal reference range. An emergency non-contrast brain CT scan showed left-sided acute deep cerebellar hematoma, a contralateral site to the first hematoma. The patient was treated medically and improved gradually over a two week period. On discharge, her speech was scanning and her gait was wide-based and ataxic. She could stand and walk alone with minor assistance. Because of the lack of expertise in our radiology department, conventional cerebral angiography was not ordered; however, a brain magnetic resonance angiogram (MRA) was done two weeks later and the result was unremarkable. We assume that our patient's hemorrhages were hypertensive in etiology.