Dopamine[ edit ] Dopamine , a neurotransmitter , has been linked with feeding behaviors. In an experiment, scientists measured how much food and water mice consumed when they were born without dopamine in their systems. They found that without dopamine, the mice would starve and be dehydrated to the point of death. The scientists then injected the mice without dopamine with its precursor, L-DOPA , and the mice started eating again. But, even though the mice were born without dopamine in their systems, they still had the capacity to control their feeding and drinking behaviors, suggesting that dopamine does not play a role in developing those neural circuits. Instead, dopamine is more closely related to the drive for hunger and thirst.
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Adipsic hypernatremia is a rare disease presenting as persistent hypernatremia with disturbance of thirst regulation and hypothalamic dysfunction. As a result of congenital disease, tumors, or inflammation, most cases are accompanied by structural abnormalities in the hypothalamic-pituitary area. While cases with no hypothalamic-pituitary structural lesion have been reported, their etiology has not been elucidated.
Recently, we reported three patients with adipsic hypernatremia whose serum-derived immunoglobulin Ig specifically reacted with mouse subfornical organ SFO tissue. As one of the circumventricular organs CVOs that form a sensory interface between the blood and brain, the SFO is a critical site for generating physiological responses to dehydration and hypernatremia.
These results support a new autoimmunity-related mechanism for inducing adipsic hypernatremia without demonstrable hypothalamic-pituitary structural lesions. In this review, we aim to highlight the characteristic clinical features of these patients, in addition to etiological mechanisms related to SFO function. These findings may be useful for diagnosing adipsic hypernatremia caused by an autoimmune response to the SFO, and support development of new strategies for prevention and treatment.
Body fluids are therefore constantly monitored by osmolality or sodium level sensors in the brain, which control thirst sensation, preference for salt, and AVP 1 , 2. Adipsic hypernatremia is clinically characterized by an increase of both the osmotic set point for AVP release, and the threshold for thirst perception, resulting in persistent hypernatremia with a euvolemic state 4 , 5 , 6.
As a result of congenital disease, tumors, or inflammation, most cases are accompanied by structural abnormalities in the hypothalamic-pituitary area; however, cases with no structural lesion have also been reported since the s 7 , 8 , 9 , 10 , 11 , Some of these cases exhibited hypopituitarism including GH deficiency GHD , rapid obesity, and autonomic failure. These patients generally had a poor prognosis, often due to respiratory failure, such as apnea. Although almost 50 years have passed, the underlying mechanisms for this condition have yet to be clearly elucidated.
In , Hiyama et al. These results suggest a new etiology for adipsic hypernatremia caused by autoimmune responses. Additionally, we recently reported that the serum of three patients, exhibiting adipsic hypernatremia without demonstrable hypothalamus-pituitary lesion, reacted with a mouse SFO, though their sera did not contain anti-Nax antibodies Intriguingly, there were similar clinical features among four patients, likely resulting from specific immune responses to the SFO.
In this review, we summarized the clinical characteristics of those patients with adipsic hypernatremia to highlight common findings, which might have resulted from SFO damage. All lack a blood-brain barrier and contain receptors for many substances that circulate in the blood Among the CVOs, the SFO protrudes ventrally from the fornix into the third ventricle, just caudal to the foramen of Monroe at the confluence of the lateral and third ventricles The peripheral portion, however, is positioned to respond to factors in cerebrospinal fluid CSF , such as sodium Activation of Nax stimulates glial cells to release lactate, which functions as a gliotransmitter and activates GABAergic inhibitory neurons in the SFO The SFO is a unique nucleus in that its afferent and efferent projections are well placed to respond to blood-borne signals and integrate them with neuronal signals In addition, neurons in the core portion of the SFO also project to the parvocellular PVN pPVN , which synthesizes corticotropin-releasing hormone, and the basal nucleus of the stria terminalis
Case Report: Severe hypernatremia from psychogenic adipsia
Comprehensive Metabolic Panel Treatment of Hypernatremia It is essential to diagnose this disorder because sometimes, this condition can be caused by the Cancerous situations. The imbalance of Sodium can be treated with the help of methods like Radiation Chemotherapy Surgery etc The treatment of Hyponatremia consists of monitoring fluids flowing through Veins, monitoring and limiting the intake of fluids including Water and intake of medications for the relief of symptoms. When the level of Sodium increases in the body, patients may suffer from symptoms like Occasional Chorea General Twitching Jerky movements of shoulders, hips and face Patients also suffer from condition known as Hyperreflexia. It is identified by the over activity of reflexes. At this stage, Seizures may also occur.
Hypernatremia – Causes, Symptoms, Treatment and Prognosis
Brain Pathol. Epub Aug 2. Adipsic hypernatremia without hypothalamic lesions accompanied by autoantibodies to subfornical organ. Adipsic or essential hypernatremia is a rare hypernatremia caused by a deficiency in thirst regulation and vasopressin release. In , we reported a case in which autoantibodies targeting the sensory circumventricular organs sCVOs caused adipsic hypernatremia without hypothalamic structural lesions demonstrable by magnetic resonance imaging MRI ; sCVOs include the subfornical organ SFO and organum vasculosum of the lamina terminalis OVLT , which are centers for the monitoring of body-fluid conditions and the control of water and salt intakes, and harbor neurons innervating hypothalamic nuclei for vasopressin release. We herein report three newly identified patients 3- to 8-year-old girls on the first visit with similar symptoms.