water disturbance may occur in hemorrhagic and ischemic stroke patients because of the major role that the central nervous system plays in water homeostasis [ 13 ] . post - stroke hypernatremia is generally the consequence of central diabetes insipidus , but it can also take place if the patients do not have free water access , usually as the result of neurological sequels which prevents them from drinking water or even asking for it from their relatives and caretakers . hypodipsia secondary to lesions of the thirst center , not accompanied by other serious neurological damage , is a rare cause of post - stroke hypernatremia , but it may cause significant morbidity if not properly diagnosed and managed . a 56-year - old caucasian man was admitted to the cardiology ward of our hospital due to lethargy and muscle weakness , attributed to the presence of bradycardia . routine admission laboratory tests revealed high plasma sodium levels ( na : 157 meq / l ) , which motivated , on the following day , a request for nephrology evaluation . at nephrology consultation his past medical history revealed that 9 years previously he had had a hemorrhagic stroke and needed brain surgery to clamp a ruptured aneurysm of the anterior communicating artery and to drain a cerebral hemorrhage . a representative figure of patient s cranial computed tomography ( ct ) done at that occasion is presented in figure 1 . the stroke resulted in some impairment of the capacity of space location , moderate reduction of the recent and fixation memory and a certain aversion to water . new laboratory tests were ordered and confirmed hypernatremia : plasma sodium of 155 meq / l and plasma chloride of 116 meq / l . urinalysis : urine - specific gravity of 1026 , no blood or protein and a normal sediment . plasma potassium , creatinine and urea were , respectively , 4 meq / l , 1.07 mg / dl and 41 mg / dl . in the 24 h that followed nephrology consultation , the patient passed only 400 ml of urine . the diagnosis of possible hypernatremia secondary to post - stroke hypodipsia was then made and supervised water intake of 2 l a day was initiated . after this simple measure , there was an increase in diuresis and plasma sodium was reduced to 150 meq / l on the third day and to 144 meq / l on the fourth day after admission . two weeks after hospital discharge , he had gained 3 kg and referred marked improvement in lethargy and muscle weakness . the evolution of the patient s laboratory tests , including the ones collected 2 weeks after hospital discharge , are presented in table 1 . evolution of plasma sodium and other laboratory tests after patient s hospital admission cranial ct scan showing diffuse subarachnoid hemorrhage ( inferior white arrow ) , frontal left intraparenchymatous hematoma ( superior white arrow ) , intraventricular hemorrhage ( inferior black arrow ) and nodular slightly hyperdense image with peripheral calcifications on anterior communicating artery topography , suggestive of giant aneurysm ( superior black arrow ) . hypernatremia is relatively frequent in clinical practice , being common in the elderly and in critically ill patients . in patients with free access to water when plasma sodium ( the main determinant of plasma osmolality ) increases , two defense mechanisms are triggered : stimulation of the thirst center and secretion of antidiuretic hormone ( adh ) . this combination results in increased water intake and reduction in urinary water loss , leading , thus , to normalization of plasma osmolality . this mechanism is highly efficient , keeping plasma osmolality in a narrow range , despite the daily variation of water and sodium intake . in the reported case , the patient s mechanism of adh liberation and the urinary concentration were preserved : when faced with significant hypernatremia , the patient s 24-h urine volume was only 400 ml , and the urine had high specific gravity ( 1.026 ) ; normalization of plasma sodium concentration , urine dilution and weight gain occurred when supervised water intake was warranted . this case illustrates the fact that even when the mechanisms of adh liberation and urine concentration are intact , and if the thirst mechanism is damaged , the body is not capable of maintaining normonatremia [ 3 , 6 , 7 ] . post - stroke hypodipsia may be the result of damage to the hypothalamic thirst center , believed to be present in the lamina terminalis of the third ventricle in the presented case , there was extensive intraventricular hemorrhage  but this may occur even in the absence of ct evidence of hypothalamic damage , possibly due to a cortical central nervous system lesion that interferes with cortical perception of thirst . the clinical symptoms that motivated the patient s hospital admission and that were at the first attributed to bradycardia were apparently caused by hypernatremia . in fact , this patient had been presenting muscle weakness and lethargy very frequently in his daily life and his wife reported that these symptoms had begun after the stroke . indeed , the review of his past laboratory test values revealed that in the course of medical evaluations done in the past , high values of plasma sodium were documented ( 170 meq / l in september 2007 and 151 meq / l in february 2009 ) but were misinterpreted as laboratory artifacts since the patient presented no physical sequels of the hemorrhagic stroke and , as hypernatremia was chronic , significant neurological symptoms were absent . sadly , a second measurement of plasma sodium was not ordered on neither of those two occasions . the patient s weight loss was secondary to true dehydration since it was quickly corrected after appropriate water intake . no medical reason was found for the patient s bradycardia , but when discharged from hospital , his heart rate was 72 b.p.m .
disorders in water metabolism may occur in stroke patients . when hypernatremia arises in this setting , it is usually secondary to the development of central diabetes insipidus or it is the result of neurologic lesions that prevent patients from having free access to water . 
 much rarer are the cases of post - stroke hypernatremia caused by hypodipsia secondary to lesions of the thirst center . 
 we report the case of a patient with severe hypernatremia , probably secondary to post - hemorrhagic stroke hypodipsia . 
 the hypernatremia seen in this case was corrected by scheduling the patient s water intake .