The institutional IRB was consulted and waved the need for approval of the publication of this case. The patient is a 12-year-old, right-handed, 52 kg African-American male without any significant medical history other than nocturnal enuresis. His father woke him up at 04:00 on the morning of admission as was customary in their home to prevent bedwetting. While initially he responded appropriately, the child collapsed to the ground after standing and became unresponsive. He was transported to an outlying emergency department where he was noted to have aphasia and left dense hemiplegia. Computed tomography demonstrated signal attenuation and edema in the vascular distribution of the right middle cerebral artery. Right lateral ventricle compression and midline shift were noted. 
The patient was transferred to our institution by helicopter and was briefly examined in the emergency room prior to transfer to the magnetic resonance (MR) imaging suite. He was awake, with stable airway, anxious and frustrated by inability to speak, but was cooperative and able to follow some commands. Heart rate was 50-60 beats per minute and blood pressure was 130-140/80-90 mm Hg. He demonstrated lack of language expression, flaccid paralysis of the left face, upper extremity, and lower extremity. His NIH stroke score was 16. MRI and MRA studies revealed occlusion of the right middle cerebral artery with restricted diffusion in the right basal ganglia and the posterior lateral aspect of the caudate head (Figure 1). There was mass effect on the right lateral ventricle and midline shift. Our information was that 6 h had elapsed since the onset of neurologic symptoms. Taking into account the possibility of a devastating clinical outcome and in conjunction with adult stroke and interventional radiologist specialist, the decision was made to attempt to restore arterial patency. 
The patient was anesthetized, intubated, and cooled to 33-35 C (mild therapeutic hypothermia). A thrombus was located (Figures 2 and 3); endovascular mechanical embolectomy with a Merci retrieval device was attempted without success. Recombinant tissue plasminogen activator (rt-PA) was infused into the MCA in doses of 0.7, 2, and 4 mg with minimal improvement in blood flow. Abciximab and nitroglycerin (25 mug) were then infused with considerable improvement in blood flow (Figures 4 and 5). 
The patient was transferred to the pediatric ICU and remained sedated and mechanically ventilated. Neurosurgical consultation was obtained for an intracranial pressure (ICP) monitoring, but this was not placed due to recent thrombolytic administration and the initiation of systemic anticoagulation. Heparin was administered for 7 days, Abciximab (10 mug/min for the first 12 h), aspirin (325 mg/day), magnesium sulfate (2000 mg/24 hrs), 25% albumin (1 g/kg IV every 6 h for the first 5 days), and memantine HCL (10 mg nasogastric each day for 3 days). Mild therapeutic hypothermia was maintained for 4 days to decrease acute postischemic cerebral edema followed by passive rewarming over a 24-hour period. A CT scan obtained at 24 hrs showed a decrease in the midline shift.
The central venous pressure (CVP) was maintained at 8-10 cm H2O and mean arterial pressure (MAP) at 75-80 mm Hg. A dual channel near infrared spectroscopy (NIRS) probe was applied to the scalp overlying both frontal lobes. Initially, there was a discrepancy between the two sides with the ischemic right side 10%-15% lower than the left side (40%-50% versus 65%-70%). Increasing CVP or MAP served only to augment the discrepancy. Subsequently, the partial pressure of arterial carbon dioxide was allowed to increase from 35-40 to 46-55 mm Hg with resolution of the discrepancy (both sides equal to 60%-65%). 
MR studies on the 7th day revealed appropriate MCA blood flow and partial resolution of the ischemic changes in the basal ganglia. Mass effect and right lateral ventricle compression by the basal ganglia were improved. He was extubated on day 10 and was able to communicate verbally, written, and receptive but had a small degree of residual left hemiparesis. He was transferred to a rehabilitation facility on day 15 where he exhibited an almost complete recovery within the following two weeks and was discharged home. Subsequent followup by our pediatric neurology service over the next year has demonstrated complete recovery to baseline without deficits. One year later he is taking advanced placement classes in school, playing junior high school basketball and baseball, and having no demonstrable neurological deficits.
Cerebral angiography and serologic studies did not find the presence of dissection, vasculitis, or autoimmune disease; transthoracic echocardiography ruled out structural heart disease, intracardiac thrombus, and right to left intracardiac shunt, and hemoglobin electrophoresis, hypercoagulability studies, and lipid panels were all unremarkable. Doppler studies of the veins of the lower extremities and pelvis were all negative for deep venous thrombosis. An etiology for this patient AIS has not been found. An MRI performed 3 months after the events showed resolution of the edema and restricted diffusion with a residual hyperdense signal abnormally in the periventricular region (Figure 6).