Unilateral Reversible Posterior Leukoencephalopathy Syndrome after Coiling of an Aneurysm
A 36-year-old woman was admitted with acute severe headache. She had also experienced an epileptic seizure and had a slightly lowered consciousness at admission. Nonenhanced computed tomography (CT) showed subtle signs of subarachnoid hemorrhage (SAH) with some frontobasal subarachnoid blood (). CT angiography revealed a 4-mm aneurysm of the left anterior cerebral artery (ACA). At admission her blood pressure was 128/55 mm Hg. On the first day of admission her mean arterial pressure (MAP) varied between 81 and 99 mm Hg, with a mean of 88 mm Hg. She had no history of hypertension, was no taking any medication, and exhibited a good neurological condition (Hunt and Hess grade of 1).\nThe aneurysm was coiled on the same day. The procedure took longer than usual (2 hours) because of the smallness of the aneurysm, which made it difficult to enter it safely with the microcatheter. During the procedure, both internal carotid arteries were catheterized to optimize depiction of the local vascular anatomy (). However, a microcatheter was only advanced in the left ACA to reach the aneurysm. According to the local protocol, 5000 IE of heparin was given during the procedure; no other medication was given during the procedure. The aneurysm was successfully packed with two small coils (3 cm long; 2-mm UltraSoft, Boston Scientific, Natick, MA, USA) using a left approach. No complications were noted and the patient experienced no focal neurological symptoms.\nAfter the procedure the patient developed periods of bradycardia with sinus arrest in the intensive care unit (ICU) but without clinical symptoms. There were assumed to be secondary to the SAH, and were treated conservatively. Transcranial Doppler (TCD) performed during the following week showed mildly increased flow velocities in the middle cerebral artery (MCA) that were just within the normal range (111 and 82 cm/s in the left and right MCAs, respectively), suggesting mild vasospasm. Oral nimodipine at 30 mg taken 12 times daily and triple-H therapy were started according to the local protocol. On day 4 of the triple-H therapy the MAP reached 72-108 mm Hg (mean 93 mm Hg). Slight lung edema was treated with furosemide. TCD performed 5 days later showed normal MCA velocities, although the velocities in the MCA and ACA continued to be higher on the left than on the right, albeit still within the normal range. Triple-H therapy was subsequently stopped. During the hospital stay the clinical status of the patient improved and her headaches gradually diminished. The patient was discharged in good clinical condition after 12 days with a prescription for oral nimodipine (60 mg taken six times daily for 20 days). The MAP at discharge was 100 mm Hg.\nThe evening after taking the last prescription of nimodipine, which was 21 days after coiling and 15 days after the cessation of triple-H therapy, the patient presented at the emergency room with progressive headache, right-sided homonymous hemianopsia, right-sided tactile extinction, and a slight paresis of the right arm. Her MAP during the first day of re-admission was 81-120 mm Hg (mean 108 mm Hg). The cerebrospinal fluid pressure measured via a lumbar puncture was elevated at 42 cmH20. Spinal fluid showed residual signs of the recent SAH but no signs of meningitis. Renal function was normal with serum creatinine, sodium, and potassium levels of 47 µmol/L, 140 mmol/L, and 4.4 mmol/L, respectively. Nonenhanced CT performed 21 days after the first onset of the SAH revealed subcortical hypodense areas in the left hemisphere occipitally and around the insula. Magnetic resonance imaging (MRI) showed vasogenic edema mostly subcortically in the entire left hemisphere, with a preference for the watershed areas (). No susceptibility artifacts were seen within the parenchyma. Diffusion-weighted MRI images showed no signs of ischemia. After gadolinium administration there was patchy enhancement in the lesions (). CT angiography did not show vasospasms or vascular occlusions.\nThe combination of headache, confusion, visual disturbances, and vasogenic edema on MRI was suggestive of RPLS. Further clinical analysis revealed no signs of infection, and dural sinus thrombosis was ruled out with CT venography. Because late-onset secondary brain ischemia was initially suspected clinically, oral nimodipine was restarted at a daily dose of 180 mg. This improved the clinical status of the patient, with headache being the most prominent symptom; this was reduced by prescription of dexamethasone at 2 mg twice daily. Slow tapering of dexamethasone led to the return of slight headaches, but they could now be controlled with acetaminophen. Because the initial clinical suspicion of ischemia was ruled out by the imaging workup, a diagnosis of RPLS was eventually suggested on the fifth day of re-admission based on clinical signs and MRI findings. By the sixth day of re-admission the MAP had decreased to 82-100 mm Hg (mean 89 mm Hg), possibly due to the nimodipine treatment, and so no antihypertensive medication was administered in our patient. The patient was discharged and nimodipine was gradually reduced.\nAt three months after SAH the patient had no neurological symptoms apart from slight balance problems. The MRI abnormalities had diminished but were not completely resolved. However, MRI performed 7 months after the first presentation showed further reduction of the lesions, with a single small area of signal enhancement remaining in the left frontal lobe ().