Reversible leukoencephalopathy with seizures: a case of severe high-altitude cerebral edema

Abstract

Background: Acute high-altitude illness (AHAI) refers to a series of syndromes including acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE). Among these, HACE is a severe and potentially life-threatening condition that can occur when individuals ascend to high altitudes. It is often characterized by ataxia, confusion, and altered mental status. Without appropriate treatment, HACE can rapidly progress to coma, but seizures are infrequent in occurrence.

Case presentation: Here, we report a severe HACE patient with coma and status epilepticus. The patient is a 23-year-old male who was visiting Lhasa for the first time. He initially experienced headaches and dizziness on the first day, and then he was found in coma with limb convulsions on the next day. Immediate medical attention was sought, and brain CT and MRI scans showed reversible white matter lesions, especially in the corpus callosum and subcortical white matter. Although the lesions disappeared on T1 and T2 sequences, microbleeds were observed on the SWI sequence. After treatment with tracheal intubation, glucocorticoids and hyperbaric oxygen, the cerebral edema has resolved and the clinical symptoms improved, the patient has no seizures anymore.

Conclusions: HACE typically follows AMS and poses a significant risk to life. Clinical manifestations mainly include ataxia, alterations of behavior, and impaired consciousness, with severe cases progressing to coma. Seizures, though rarely observed, may occur. Imaging shows reversible white matter lesions, with microbleeds being a significant and persistent imaging marker over time. Administration of glucocorticoids plays a crucial role in treatment. Despite experiencing seizures, this patient did not experienced any further episodes once his condition improved.

Keywords: Case report; High-altitude cerebral edema; Microbleeds; Reversible leukoencephalopathy; Seizures.

Fig. 1

The CT scan conducted at the local hospital in Lhasa revealed cerebral edema and pulmonary edema. a The cortical sulci and gyri have disappeared, and the boundary between gray and white matter is indistinct. b Bilateral patchy edema in both lungs, particularly prominent on the right side

Fig. 2

EEG shows a background of bilateral fast waves with an increased presence of slow waves

Fig. 3

The follow-up brain MRI. There were T1W1 low signals (a, white arrow), T2W1 high signals (b, white arrow), and DWI high signals (c, white arrow) in the corpus callosum, knee region, and junction of the cortex and medulla on June 1st. On June 20th, compared to the June 1st scan, the abnormal signals observed in the T1W1 and T2W1 sequences had significantly decreased (d, e). SWI sequence showed diffuse micro-bleedings (f, white arrow)