Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The variation in vasopressin concentrations of ventricular cerebrospinal fluid and plasma throughout a 24-h period was studied in 10 patients with hydrocephalus. In 6 control patients, the diurnal variation in plasma vasopressin concentrations was studied. Vasopressin concentrations were determined by radioimmunoassay in plasma and in extracted and unextracted cerebrospinal fluid. Cortisol and osmolality in plasma were also measured. Vasopressin concentrations measured in extracted cerebrospinal fluid showed only small intra- and interindividual variation, while the corresponding values for unextracted cerebrospinal fluid were 2-5-fold higher and showed more variation. Plasma vasopressin concentrations varied considerably throughout the 24-h period in the individual hydrocephalic patient and between the patients. The pattern of variation was inconstant with no circadian rhythm, and the variation was not related to any changes in plasma osmolality, blood pressure or intracranial pressure. In some of the patients, the normal diurnal pattern of variation in plasma cortisol was broken, however, without a relation to the observed fluctuations in vasopressin concentrations. The abnormal variation of plasma vasopressin and cortisol was considered to reflect stress in connection with the intracranial pressure monitoring procedure. In the control patients, plasma vasopressin showed only small variations and plasma cortisol showed a normal diurnal rhythm. It is concluded that cerebrospinal fluid vasopressin concentration in patients with hydrocephalus is very constant throughout the day, even when plasma vasopressin concentrations show marked episodic increases. Thus, a circadian rhythm in the cerebrospinal fluid vasopressin concentration, as reported in several animal species, could not be confirmed in these patients.
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PMID:24-hour cerebrospinal fluid levels of vasopressin in hydrocephalic patients. 403 58

In 16 patients with primary degenerative dementia mean CSF vasopressin concentration was lower (0.9 +/- 0.1 pg/ml (mean +/- SEM)) than in 28 control patients (1.3 +/- 0.1 (mean +/- SEM)) (p less than 0.01). In 18 patients with normal pressure hydrocephalus and potentially reversible dementia mean CSF vasopressin concentration (1.2 pg/ml +/- 0.1 (mean +/- SEM)) was not different from that found in controls. Several of the demented patients had inappropriate plasma vasopressin concentrations suggesting a defect in osmoregulation. These findings encourage further clinical trials of vasopressin in patients with primary degenerative dementia, but it is emphasised that the low CSF vasopressin concentration in these patients might be only a nonspecific phenomenon due to the diffuse loss of cells within the central nervous system.
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PMID:CSF and plasma vasopressin concentrations in dementia. 664 15

Cerebrospinal fluid and plasma vasopressin were measured in patients with cerebral disorders associated with varying levels of elevated intracranial pressure. The mean cerebrospinal fluid vasopressin concentration was significantly increased in patients with pseudotumor cerebri (2.0 +/- 0.2 [SEM] pg/ml), intracranial tumor (2.3 +/- 0.4 pg/ml), and intracranial hemorrhage (1.9 +/- 0.3 pg/ml) compared with control patients (1.2 +/- 0.1 pg/ml). A significant relationship was found between intracranial pressure and the cerebrospinal fluid vasopressin concentration within all groups of patients and in the whole sample as well (r = 0.79; p less than 0.001). In the groups of patients with intracranial tumor, hydrocephalus, and intracranial hemorrhage, some individuals showed plasma vasopressin concentrations inappropriate to the corresponding plasma osmolality, but no relationship was found between intracranial pressure and plasma vasopressin concentration. It is suggested that increased intracranial pressure is a stimulus to centrally released vasopressin. The clinical importance of increased cerebrospinal fluid vasopressin concentrations is still not known.
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PMID:Cerebrospinal fluid vasopressin and increased intracranial pressure. 673 90

We have studied plasma and cerebrospinal fluid vasopressin (CSF-AVP) and osmolality in 28 patients with cervical or lumbar pain syndromes (control patients), 11 patients with normal pressure hydrocephalus (NPH) and in 5 patients with benign intracranial hypertension (BIH). Vasopressin concentration in lumbar CSF to a high extent reflected the actual ventricular CSF-AVP concentration. In all groups CSF-AVP was lower than plasma AVP. Mean CSF-AVP in the control group was 1.3 pg/ml +/- 0.1 (SEM). In the NPH patients, who all suffered from severe dementia, CSF-AVP level was not different from that found in the control group (1.4 pg/ml +/- 0.2). In contrast to the findings in the two other groups CSF osmolality in BIH patients was higher than plasma osmolality (P less than 0.0). CSF-AVP in the BIH patients, characterized by an elevated intracranial pressure (ICP), was higher than in the control group (2.7 pg/ml +/- 0.4, P less than 0.001).
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PMID:Vasopressin in the cerebrospinal fluid of patients with normal pressure hydrocephalus and benign intracranial hypertension. 711 92

Hyponatremia has been reported in up to one third of patients with intracranial disease and has frequently been associated with tuberculous meningitis, often complicated by hydrocephalus. The lowered plasma sodium levels were previously attributed to the syndrome of inappropriate secretion of antidiuretic hormone. A controlled prospective study of 24 patients with tuberculous meningitis and hydrocephalus was carried out. Analyses of serum electrolytes and cerebrospinal fluid were performed. Plasma and cerebrospinal fluid levels of atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) were measured by radioimmunoassay. Fifteen patients were found to be hyponatremic (plasma sodium < 130 mmol/L) and ANP levels of 12 to 1,488 pg/ml were present (median, 26 pg/ml). The remaining 9 patients had normal plasma sodium values between 130 and 145 mmol/L, and in these, plasma ANP values varied between 12 and 21.7 pg/ml (median, 12 pg/ml). The difference between these two groups was not statistically significant. (Control values from patients undergoing myelography were established to range between 12 and 40 pg/ml; median, 14.4 pg/ml.) ANP levels were undetectable in the cerebrospinal fluid in all. Plasma ADH levels in the hyponatremic group were between 7 and 159 pg/ml (median, 40 pg/ml). In the normonatremic group, plasma ADH levels of 25 to 250 pg/ml (median, 29 pg/ml) were obtained. (The controls ranged between 3.6 and 35 pg/ml; median, 10.4 pg/ml). In the hyponatremic group, there was a moderate negative correlation (r = -0.683) between plasma ANP and plasma sodium (P = 0.02). No correlation between plasma ADH and plasma sodium was found (r = -0.168; P = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremic natriuretic syndrome in tuberculous meningitis: the probable role of atrial natriuretic peptide. 808 8

Hypernatremia was detected in a dog that was evaluated because of seizures. During hospitalization, the dog was fully conscious and remained hypernatremic when drinking voluntarily and when water was added to the food. Urine volume increased and urine osmolality decreased during an infusion of hypertonic saline (2.5% NaCl) solution, despite development of progressive hyperosmolality. There was no correlation between plasma antidiuretic hormone concentration and osmolality during the infusion study. The dog released antidiuretic hormone normally after nonosmotic stimulation (ie, apomorphine administration). These findings allowed a diagnosis of hypodipsic hypernatremia caused by destruction of hypothalamic osmoreceptors. At necropsy, there was hydrocephalus, atrophy of the septum pellucidum, and neuraxonal dystrophy of the cuneate nuclei. The underlying neurologic disease responsible for the CNS lesions could not be determined, but hydrocephalus may have led to pressure atrophy in the region of the hypothalamus that contains osmoreceptors.
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PMID:Hypodipsic hypernatremia in a dog with defective osmoregulation of antidiuretic hormone. 818 13

Bacterial meningitis has special clinical features in the newborn infant. Major complications and sequelae result from the infectious involvement of the CNS in the majority of these children. We studied 109 newborn infants with bacterial meningitis accompanied from January 1977 to April 1987. The mortality rate was 34.8%. Perinatal risk factors were not found. The majority (80.5%) were term newborn infants. The main signs at admission were convulsion (53.2%), bulging fontanel (37.6%) and apnea (20.2%), and the main symptoms were neurosensorial depression (64.2%), nursing refuse (64.2%), fever (50.5%) and irritability (35.8%). Complications during hospitalization were ventriculitis (34.9%), inappropriate antidiuretic hormone secretion syndrome (27.5%), subdural collection (8.3%), brain abscess (4.6%) and brain infarction (2.8%). Inappropriate antidiuretic hormone secretion syndrome and ventriculitis were closely associated with high mortality. Seventy one children survived: 44 (62%) had gross abnormalities at the neurologic examination, and 29 (40.8%) developed hydrocephalus. Neurological follow-up of these children is important. Prognostic can change along the course of long time follow-up.
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PMID:[Bacterial meningitis in the neonatal period. Clinical evaluation and complications in 109 cases]. 821 34

We describe symptomatic hydrocephalus and secondary syndrome of inappropriate antidiuretic hormone as clinical manifestations of vertical atlantoaxial subluxation in a patient with severe rheumatoid arthritis. We found no reports of this association as a complication of rheumatoid cervical involvement. We discuss the difficulties of differential diagnosis and treatment in this patient.
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PMID:Hydrocephalus and secondary syndrome of inappropriate antidiuretic hormone due to rheumatoid vertical atlantoaxial subluxation. 878 47

One-hundred-and-thirty-six children below 12 years of age hospitalized with a diagnosis of tuberculous meningitis (TBM) have been investigated to identify the underlying cause of convulsions. One-hundred-and-one children (74 per cent) presented with seizures before and/or during hospitalization. Generalized tonic and clonic seizures (GTCS) were the commonest (58 per cent) type of seizures followed by focal seizures (FS) (38 per cent) and tonic spasms (TS) (4 per cent). EEG changes were more frequently observed in cases with FS and in those children with GTCS who presented after first week of hospitalization. EEG findings included generalized dysrythmia with paroxysmal slow activity (38 per cent), interhemispheric asymmetry (23 per cent), multiple spike and wave pattern (10 per cent), and focal spike and wave pattern (15 per cent). CT scan findings were more common in those children with GTCS and TS who presented with recurrent seizures and/or seizures manifesting after first week of hospitalization. FS presenting at any stage of the disease were associated with CT scan abnormalities. Abnormalities detected in CT scan of brain included meningeal enhancement (55 per cent), hydrocephalus (32 per cent), tuberculomas (27 per cent), and cerebral infarctions (13 per cent). Clinical presentation and investigations indicate that the probable cause of convulsions could be attributed to cerebral edema (57 per cent), syndrome of inappropriate secretion of antidiuretic hormone (35 per cent), hydrocephalus (32 per cent), tuberculoma (27 per cent), abnormal electric focus (25 per cent), and cerebral infarction (13 per cent).
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PMID:Convulsions in tuberculous meningitis. 898 21

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
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PMID:The normal and pathological physiology of brain water. 907 71


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