A previously healthy 64-year-old Sri Lankan man was admitted to the general medical unit because of progressive impairment of his memory regarding recent events that had occurred during the previous 3 weeks. The memory impairment was associated with irritability and confusion. He had been a smoker for 15 pack-years. Physical examination revealed no fever, and his Glasgow coma scale score was 12/15 with alternating irritability and drowsiness. His pupils were equal in size and reactive to light, and no significant neck stiffness was noted. Focal neurological signs were absent. The patient was not cooperative enough to conduct a proper mini-mental examination. His presentation was suggestive of delirium. Basic hematological investigations and renal and liver profiles were not suggestive of an extracranial cause.
Before performing lumbar puncture, we carried out noncontrast CT of the brain to exclude any pathology causing increased intracranial pressure. CT revealed a hyperdensity in the hypothalamic region surrounded by hypodensities extending toward the temporal lobes bilaterally; these findings were consistent with a possible hypothalamic tumor with perilesional edema (Fig. 1a and b).
Electroencephalography showed generalized slowing that was maximal in the bitemporal regions. On the second day of admission, his serum biochemistry parameters became abnormal with a rising serum sodium level (>160 mEq/L) and normal serum potassium level. We noticed a significant increase in his urine output (average of 5.5 L/day) and lowering of his urine osmolality (190 mOsm/kg). Based on the hypovolemic hypernatremia and low urine osmolality associated with the radiological abnormalities in the hypothalamus, we suspected underlying cranial diabetes insipidus in this patient. He was treated with rehydration and intranasal desmopressin, to which he showed only a partial response. The patient was then transferred to the intensive care unit for close monitoring. Once the patient was stable, gadolinium-enhanced MRI of the brain and brain stem was carried out. The transverse section of the brain showed increased T2-weighted signals in the deep temporal lobes, suggesting the involvement of the limbic system (Fig. 2a). The coronal section of the brain showed increased T2-weighted signals in inner mesial regions (Fig. 2b). Interestingly, the mass lesion had disappeared during the previous 3 days. Therefore, viral or autoimmune encephalitis was considered as a more probable diagnosis than a mass lesion. Lumbar puncture was performed at this point, and samples were sent for screening of viral markers (herpes simplex virus, cytomegalovirus, and Japanese encephalitis virus) and tuberculosis polymerase chain reaction; all results were negative. Cytology of the CSF was negative for any malignant cells; however, lymphocytosis was present, suggesting an underlying inflammatory process. Based on the clinical and radiological picture, PLE with associated predominant hypothalamitis was suspected in this patient. Unfortunately, autoimmune markers were not available, and the patient had financial limitations that prevented further investigation. His condition deteriorated with the development of acute kidney injury caused by severe intravascular hypovolemia due to resistant diuresis. Considering the possibility of an associated malignancy, a chest radiograph was obtained and showed a mass lesion in the right hilum. The patient was not fit enough to undergo contrast-enhanced axial CT of the thorax because of his rising serum creatinine level. However, bronchoscopy was performed, and histological examination of the hilar mass showed a SCLC of the "oat cell" variety. Unfortunately, the patient died before the oncology referral while being treated in the intensive care unit.