A 73-year-old independent lady presented with hyponatremia (Serum Na+ - 119mmol/L). She has several weeks of feeling unwell and difficulty concentrating. Her medications included Paroxetine and Irbesartan which were both withheld from admission.
The symptoms were consistent with SIADH. The workup for causes of hyponatraemia showed no underlying problem with thyroid function or hypoadrenalism.
Initial investigations included Xray and CT chest which showed small nonspecific granulomas and an initial MRI brain showed features of small vessel disease.
Her Na+ level slowly corrected with fluid restriction of 135mmol/L over 3 weeks. Afterwards, she complained of visual disturbances followed by non-specific episodes of syncope.
There were no abnormality identified in opthalmic review. Her decreased conscious state did not appear to be consistent with any epileptic phenomenon or cardiac causes. MRI brain and EEG were unremarkable.
The possibility of an underlying psychiatric issue was explored and was Mirtazepine 15mg daily was trialed. Her conscious state deteriorated and a repeat MRI and EEG showed significant changes consistent with hypothalamic encephalitis.
CT Chest and Abdomen showed the same small granulomatous lung lesions and an enlarged paracolic lymph node(1.3 cm).
Lumbar puncture - an elevated protein level and a neuronal western blot revealed a positive PNMA2, suggestive of limbic encephalitis.
A few doses of IVIG were given, however, she continued to deteriorate and passed away in a few days.
Post mortem - Paraneoplastic encephalitis involving hypothalamus, midbrain, pons and part of thalamus.
Discussion
This case was an unusual presentation of euvolaemic hypoosmolar hyponatraemia with the initial presentation not revealing organic pathology on clinical examination or imaging.
A psychiatric or behavioural change in the context of hyponatraemia should alert the clinician to a potential encephalopathic process.
This is one of the only reports in the literature with histopathological confirmation of the targeted hypothalamic structures associated with the CSF protein abnormality.