A report describes a case of a 61-year-old woman who got referred to the emergency department for sudden aphasia and right hemiparesis. Her family noticed the abnormality approximately 13 hours after the onset, as she lived alone, and called for emergency assistance. She documented a history of alcoholism, untreated hypertension, and chronic obstructive pulmonary disease related to tobacco smoking. 

Examination revealed a blood pressure of 190/70 mmHg, a heart rate of 114 beats/minute, oxygen saturation of 94% on air, breathing at 15 times/minute, a temperature of 38.1°C, and glycemia as 117 mg/dL. A neurological exam revealed limited fluency, a right hemiparesis with a strength loss evaluated at 3/5 (MRC scale), and a gaze deviation to the left. The plantar response was extensor on the right side, Glasgow Coma Score (GCS) was 14 (E4V4M6) due to confusion, and the National Institute of Health Stroke score (NIHSS) was 15.

One day after the admission, the patient showed no improvement in her clinical condition. Her NIHSS score remained unchanged, and the follow-up brain CT scan performed after 12 hours showed no new lesion. On the second day, the patient could answer questions more appropriately than before but still showed a gaze deviation and a motor deficit. Her serum sodium was recorded as 125 mmol/L under saline perfusion. 

She showed complete regression of symptoms on the third day with a natremia of 129 mmol/L. The brain MRI conducted the same day showed no acute ischemic lesion.

Her Computed tomography (CT) angiography and CT perfusion of the brain conducted a few minutes after the admission did not demonstrate any acute lesion but only an old small-vessel disease lesion. The blood test performed on the admission showed a sodium level of 120 mmol/l, a plasma osmolality of 258 mosm/Kg, no inflammatory syndrome, no coagulation disorder, and normal renal function. The electrocardiogram revealed sinus tachycardia. The electroencephalogram on the same day showed moderate encephalopathy with left hemispheric hypovoltage and absence of no epileptic activity. Other complementary investigations were normal.

Since there wasn′t any change in the patient′s clinic, the high probability of acute ischemic stroke sustained a specific treatment with antiplatelet agents and lipid-lowering drugs. From her admission, she stayed no longer in thrombolysis criteria which was therefore not indicated. She also received a perfusion of saline liquid to correct the hyponatremia.

The patient received a discharge against medical advice on day 4, with complete resolution of her neurologic symptoms and a natremia of 130 mmol/L. The diagnosis of stroke mimic caused by hyponatremia was thus retained. 

She underwent a series of additional investigations to find the origin of the hyponatremia. The complementary investigations, including a thoracic CT scan, a whole body Pet-scan and a breast ultrasound followed by a biopsy, revealed an infiltrating breast carcinoma. The cause of hyponatremia was thus more compatible with the presence of a Schwartz-Bartter syndrome associated with breast cancer.

Tiwet PD, Kuigwa IT, Mendeuka RS, Gazagnes MD. Hyponatremia and stroke mimic: a case report. Pan Afr Med J. 2022 Sep 23;43:39. doi: 10.11604/pamj.2022.43.39.36701. PMID: 36505020; PMCID: PMC9716958.