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At least 19 recordsLinked to original sources
PubMedDate not supplied

Psychogenic polydipsia after traumatic brain injury. A case report.

Electrolyte abnormalities are common medical complications of traumatic brain injury (TBI). Hyponatremia is the most common of these disorders. The syndrome of inappropriate antidiuretic hormone and cerebral salt-wasting are the most well known causes of hyponatremia following TBI. In the presence of polydipsia and polyuria, psychogenic polydipsia should be included in the differential diagnosis. It is important to distinguish among these entities because treatment differs to such an extent that improper diagnosis may lead to a worsening of the patient's condition. We present a patient who presented with a new onset of polyuria and polydipsia after sustaining a TBI. Evaluation, including monitoring of fluid intake and output, serum and urine sodium and osmolarity, as well as a fluid deprivation test revealed the cause to be psychogenic polydipsia. The patient's symptoms improved after institution of a behavioral program and fluid restriction. Various models of drinking behavior have been used to identify the site of dysregulation. Dopaminergic, cholinergic, and hippocampal etiologies have been implicated in this abnormality of fluid homeostasis. If disorders of these systems can lead to psychogenic polydipsia, it is reasonable to believe that a person who has sustained a TBI would be at higher risk of developing psychogenic polydipsia.

Adult↗
PubMed2000

[Psychogenic polydipsia leading to water intoxication].

Psychogenic polydipsia and its frequent complication, water intoxication, are well-known to psychologists. There are biochemical and psychiatric theories of psychogenic polydipsia which often correlate with each other. A 48-year-old man with chronic paranoid schizophrenia developed symptoms of psychogenic polydipsia. This provoked disturbances in electrolyte balance, resulting in a rapid decrease in serum sodium concentration and eventual death. There is a paucity of information and little awareness of this problem in the professional literature.

Drinking Behavior↗
PubMed1987

Psychogenic polydipsia with hyponatremia: report of eleven cases.

Psychogenic polydipsia is an uncommon clinical disorder characterized by excessive water-drinking in the absence of a physiologic stimulus to drink. The excessive water-drinking is well tolerated unless hyponatremia supervenes. This report describes 11 patients with psychogenic polydipsia and hyponatremia (ten men and one woman) who were collectively hospitalized a total of 70 times for treatment of complications of this disorder. This group differs from the classical patient with psychogenic polydipsia, ie, a hospitalized schizophrenic, in that none was institutionalized and there was a high incidence of chronic alcoholism (10), intractable hiccups (7), self-induced vomiting (6), and laboratory evidence for rhabdomyolysis (5).

Adult↗
PubMed1976

Drug-induced hyponatraemia in psychogenic polydipsia.

Two patients with psychogenic polydipsia developed hyponatraemia, one in association with administration of hydrochlorothiazide and the other with that of tolbutamide. It is suggested that the increased fluid intake in such patients may make them more susceptible to the development of hyponatraemia from thiazide or sulphonylurea compounds.

Humans↗
PubMed1992

Functional obstructive uropathy: a significant factor in the hyponatremia of psychogenic polydipsia?

A case is presented of psychogenic polydipsia with hyponatremia. Prolonged observation of the patient revealed that episodes of hyponatremia correlated best with bladder failure and were promptly corrected by bladder catheterization. Bladder catheterization for underlying functional obstructive uropathy should be considered early in the treatment of patients with psychogenic polydipsia and hyponatremia.

Adult↗
PubMed2001

Behavioral treatment of chronic psychogenic polydipsia with hyponatremia: a unique case of polydipsia in a primary care patient with intractable hiccups.

Psychogenic polydipsia is recognized as a dangerous and potentially life threatening disorder. Few studies have focused on the treatment of polydipsia presenting in the outpatient setting. A review of the behavioral treatment literature pertaining to psychogenic polydipsia is presented. This review is followed by a case illustration of an outpatient behavioral approach to the treatment of psychogenic polydipsia in a non-psychiatric, primary car, adult, male patient suffering from intractable hiccup. An ABA single-case design was used, with sodium concentration as the dependent variable. This behavioral method appears promising in settings where restriction of fluid intake is not practical.

Adult↗
PubMed1980

Hyponatremia in psychogenic polydipsia.

Twenty psychotic patients with psychogenic polydipsia had hyponatremia (98 to 124 mEq/L) lasting up to 28 months, with headache, hypertension, dementia, seizures, lethargy, and coma. Two deaths also may be attributed to this syndrome. Patients drank 7 to 43 L of water daily. Urine was dilute during this water load (37 to 95 mOsm/kg), and free water clearance ranged from 12 to 36 L/day, while plasma osmolality was 236 to 244 mOsm/kg. During fluid deprivation in seven such patients, urinary osmolality exceeded plasma osmolality when plasma concentration had risen to between 242 and 272 mOsm/kg, thus suggesting a "reset osmostat" or antidiuretic hormone response to nonosmotic stimuli. This tended to sustain hyponatremia. Polydipsia should be recognized as a cause of hyponatremia, perhaps with reset osmostat. This ultimately may cause dementia or death, possibly secondary to recurrent cerebral edema. This sequence of events is potentially preventable or correctable.

Adult↗
PubMed1983

Somatic findings in patients with psychogenic polydipsia.

An epidemiologic investigation found a 17.5% prevalence of psychogenic polydipsia in 241 hospitalized psychiatric patients. A randomly selected sample of 10 polydipsic patients revealed such associated disorders as sporadic convulsive seizures, comatose states, hydronephrosis, enuresis/urinary incontinence, projectile type vomiting, malnutrition and, in one case, cardiomegaly and edema. Psychogenic polydipsia is a frequently overlooked disorder, and the somatic consequences of the excessive fluid intake are usually ascribed to other causes.

Drinking↗
PubMed1999

Urinary excretion of aquaporin-2 water channel differentiates psychogenic polydipsia from central diabetes insipidus.

The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) water channel under ad libitum water intake is of value to differentiate polyuria caused by psychogenic polydipsia from central diabetes insipidus. A 30-min urine collection was made at 0900 h in 3 groups of: 11 patients with central diabetes insipidus (22-68 yr old), 10 patients with psychogenic polydipsia (28-60 yr old), and 15 normal subjects (21-38 yr old). In the patients with central diabetes insipidus, the plasma arginine vasopressin level was low despite hyperosmolality, resulting in hypotonic urine. Urinary excretion of AQP-2 was 37 +/- 15 fmol/mg creatinine, a value one-fifth less than that in the normal subjects. In the patients with psychogenic polydipsia, plasma arginine vasopressin and urinary osmolality were as low as those in the patients with central diabetes insipidus. However, urinary excretion of AQP-2 of 187 +/- 45 fmol/mg creatinine was not decreased, and its excretion was equal to that in the normal subjects. These results indicate that urinary excretion of AQP-2, under ad libitum water drinking, participates in the differentiation of psychogenic polydipsia from central diabetes insipidus.

Adult↗