Title

Bilateral Hippocampal Infarction

Document Type

Article

Publication Date

7-11-2020

Publication Title

Global Radiology CME

Abstract

Introduction Isolated bilateral hippocampi injury is a known complication of opioid abuse that is a rare cause of memory impairment or amnesia. The imaging findings, however, overlap with other disease processes and therefore require good clinical history and clinical care to rule out other temporal lobe pathology. This case report aims at discussing the imaging findings of toxic encephalopathy related to hippocampal ischemia.

Case Report Patient is a 39 year-old male, with a past medical history only significant for intravenous drug abuse and recent incarceration, who presented to the ED after being found down on the ground for an unknown amount of time. At presentation, the patient was ill-appearing, in acute distress, hypotensive, and somnolent with GSC of 15. On initial questioning, he reported a recent use of heroin “yesterday” but was otherwise a poor historian with uncertainty of last day of drug use before then.Laboratory analysis was remarkable for a white blood cell count of 30.6 (3.5-10.1 bil/L), C-reactive protein of 39.1 (0.0-7.9 mg/L), creatine kinase of 302,793 (40-230 U/L), potassium of 9.1 (3.5-5.2 mmol/L), and troponins were elevated to 1.19 (0.00-0.03 ng/mL. Initial imaging (CT scans of the head, chest, abdomen, and pelvis) were negative. On hospital day 6 and 16, MRI exams of the brain were performed, which demonstrated isolated bilateral hippocampal infarcts (Figs. 1-6). No evidence of infection was found on a lumbar puncture and blood cultures were negative over the course of his hospital stay. Discussion The etiologies of hippocampal injury include: ischemia, infection, toxic/metabolic, paraneoplastic syndrome, and seizures. Toxic exposure secondary to heroin resulting in ischemia has been described in the medical literature (1). Interestingly, bilateral hippocampal infarction has also been described with acute cocaine intoxication (3). Ischemia is the most common neurovascular complication from opioid abuse (1). A pathologic study on chronic heroin addicts demonstrated gliosis preferentially within the Sommer sector of the hippocampus (CA1 region) (1). It is important to decipher if restricted diffusion in the hippocampus is in an arterial distribution (vascular etiology) vs non-vascular distribution. The hippocampus is located within an end arterial vascular territory and supplied by the anterior, middle, and posterior hippocampal arteries. These arteries create an anastomotic network but during ischemic conditions may lead to infarction. All the remaining etiologies, when seen with bilateral changes, can cause hippocampal dysfunctions such as anterograde amnesia syndromes, but have distinctly different imaging patterns. Limbic encephalitis may present with hippocampal edema with typically no restricted diffusion.

A case report by Marinkovic et al. discussed that sudden memory loss, with prolonged cognitive impairment beyond 10 days was seen with hippocampal stroke in their patient (4). In a case series performed by Bhattacharyya et al. 16 patients with restricted diffusion or bilateral hippocampal lesions were studied. Of the 8 patients with presumed hypoxia, 5 presented with symptoms including confusion and amnesia. All the patients who survived the study had persistent anterograde amnesia ranging from a few days to 20 months, which suggest that the imaging findings regarding the bilateral hippocampal restricted diffusion are significant (2). An additional case series performed by Small et all. concluded that a common link of toxic exposure/substance abuse was present in their 4 patients with acute hippocampal gyriform ischemia. They also believe that these cases may be underestimated due to the nature of treating those with substance abuse and relating the patient’s neurological symptoms (confusion, memory loss) to general acute intoxication. The authors also note that bilateral symmetrical lesions, such as with this entity, may not be readily identified by radiologists which also leads to fewer accurate diagnoses (1). Conclusion Our case illustrates acute ischemia of the bilateral hippocampi as a complication of opioid abuse and as a rare cause for amnesia. The initial MRI of the brain demonstrated acute bilateral hippocampal ischemia. An additional small lacunar injury was seen in the left basal ganglia, further suggesting parenchymal ischemia. Over the course of his hospital stay, no clinical evidence was found for other differential diagnoses. The patients age and negative CT scans of the head, chest, abdomen, and pelvis made paraneoplastic syndrome (limbic encephalitis) unlikely. Negative blood cultures and lumbar punctures excluded underlying infectious process (like herpes simplex virus). The 10-day follow-up MRI of the brain demonstrated laminar necrosis and interval enhancement, evidence of evolving changes related to infarction.

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