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D Reimann

Publications and source records attributed to D Reimann.

10 recordsLinked to original sources
PubMed2001

The role of V2 vasopressin antagonists in hyponatremia.

Hyponatremia is a frequent electrolyte disorder. It is often found in congestive cardiac failure, liver cirrhosis, plasma volume contraction and in SiADH. In these disorders hyponatremia is caused by nonosmotic vasopressin and sustained fluid intake. This provides a rationale for V2 vasopressin receptor antagonists in the treatment of hyponatremia. There is now convincing evidence from different animal models of congestive cardiac failure that peptide and non-peptide V2 vasopressin antagonists effectively increase renal water diuresis and plasma sodium concentration. In addition, several of the experimental studies also showed an improvement of hemodynamic changes of cardiac failure in response to V2 antagonists. Data in patients indicated that oral non-peptide V2-antagonists correct hyponatremia and may improve hemodynamic derangements in cardiac failure. In addition, experimental and clinical studies of V2 antagonists have been undertaken in liver cirrhosis and SiADH. In those studies hyponatremia was improved or corrected, too. Taken together, V2 vasopressin antagonists promise to become therapeutic agents in hyponatremic disorders.

Animals↗
PubMed2001

Treatment of severe hyponatremia: conventional and novel aspects.

Hyponatremia is a frequent electrolyte disorder. A hyponatremia is called acute severe (<115 mM) when the duration has been <36 to 48 h. Such patients often have advanced symptoms as a result of brain edema. Acute severe hyponatremia is a medical emergency. It should be corrected rapidly to approximately 130 mM to prevent permanent brain damage. In contrast, in chronic severe hyponatremia (>4 to 6 d), there is no brain edema and symptoms are usually mild. In such patients, a number of authors have recommended a correction rate <0.5 mM/h to approximately 130 mM to minimize the risk of cerebral myelinolysis. Sometimes it is not possible to diagnose whether a severe hyponatremia is acute or chronic. In such cases, an initial imaging procedure is helpful in deciding whether rapid or slow correction should be prescribed. The modalities of treatment of severe hyponatremia have so far consisted of infusions of hypertonic saline plus fluid restriction. In the near future, vasopressin antagonists will become available. Preliminary experience has already demonstrated their efficiency of inducing a sustained water diuresis and a correction of hyponatremia.

Acute Disease↗
PubMed2000

[Hyponatremia--with comments on hypernatremia].

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.

Diagnosis, Differential↗
PubMed1998

The treatment of severe hyponatremia.

Severe hyponatremia may be chronic (days) or acute (hours), symptomatic or asymptomatic. Severe chronic symptomatic hyponatremia (serum sodium concentration < 110 to 115 mM/liter) occurs most commonly in the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The treatment of this hyponatremia is a challenge to practicing physicians, in part because an overly rapid correction of hyponatremia may cause brain damage. The latter sometimes takes the form of central pontine myelinolysis (CPM). On the basis of available clinical and experimental literature, the rate of correction of this symptomatic hyponatremia should be no more than 0.5 mM per liter per hour, and the initial treatment should be halted once a mildly hyponatremic range of the serum sodium concentration has been reached (approximately 125 to 130 mM/liter). In contrast, severe chronic asymptomatic hyponatremia may be treated sufficiently by a fluid restriction. On the other hand, severe symptomatic acute hyponatremia should be treated promptly and rapidly, using hypertonic saline, to initially reach a mildly hyponatremic level.

Adolescent↗
PubMed1997

[Sudden hyponatremia with unconsciousness. Case report and brief overview of the syndrome of inadequate antidiuresis (SIAD or Schwartz-Bartter syndrome].

A sixty-six year old female was admitted to the hospital with an incomplete hemiparesis on the left side combined with a short episode of unconsciousness. According to her husband's account she had a seizure. Relevant laboratory measurements: plasma sodium concentration 113.9 mmol/l, plasma concentration of ADH 10.3 pg/ml, urine sodium concentration 44.4 mmol/l. The plasma concentrations of creatinine and urea were within normal limits. The working hypothesis was SIAD (syndrome of inappropriate antidiuresis) or Schwartz-Bartter-syndrome. The patient was treated immediately with water restriction (500-1000 ml/day), furosemide and i.v. replacement of urinary sodium losses by 3% NaCl. The analysis of cerebrospinal fluid showed pleocytosis and increased concentrations of immunoglobulins G and M. Serological diagnosis was positive for antigen of varicella-zoster virus. These observations were thought to be compatible with a diagnosis of SIAD in the setting of encephalitis. Under water restriction, infusion of 3% saline, treatment with loop diuretics and aciclovir (3 x 750 mg daily) the neurological function returned to normal within 2 days. A standard oral water load on the 14th hospital days showed a return to a normal water metabolism.

Acyclovir↗
PubMed1995

Vergence eye movement control and multivalent perception of autostereograms.

We introduce a dynamical model for automatic vergence eye movement control. In connection with our dynamical system of binocular model neurons that solves the correspondence problem of stereo-vision, we present a complete model for stereo-vision. Our automatic vergence eye movement control adjusts an image segment, which is of momentary interest to the observer. The adjustment is done in such a way that we only need to define a disparity search range of minimal extension. Recently, a new method of encoding (3D) three-dimensional information in 2D pictures was designed in the form of computer-generated patterns of colored dots. At first glimpse, these so-called autostereograms appear as structured but meaningless patterns. After a certain period of observation, a 3D pattern emerges suddenly in an impressive way. Applying our algorithm to autostereograms, we find a fully satisfactory agreement with the multivalent perception experienced by humans. As in nature, in our model the phase transition between the initial state and the 3D perception state takes place in a very short time. Our algorithm is very robust against noise, and there is no need to interpolate a sparse depth map.

Algorithms↗
PubMed1994

Stereo vision by self-organization.

We propose a new algorithm for stereoscopic depth perception, where the depth map is the momentary state of a dynamic process. To each image point we assign a set of possible disparity values. In a dynamic process with competition and cooperation, the correct disparity value is selected for each image point. Therefore, we solve the correspondence problem by a dynamic, self-organizing process, the structure of which shows analogies to the human visual system. The algorithm can be implemented in a massive parallel manner and yields good results for either artificial or natural images.

Algorithms↗
PubMed1994

Giant axonal neuropathy: a generalized disorder of intermediate filaments with longitudinal grooves in the hair.

Giant axonal neuropathy (GAN) is a generalized neurological disorder with accumulation of intermediate filaments in different cell populations. The hallmark are enormous axonal swellings containing densely packed neurofilaments. Clinical symptoms reported so far are mainly limited to the nervous system. We report on a four-year-old girl with clinical and sural nerve biopsy findings typical of GAN. In addition, scanning electron microscopy (SEM) showed longitudinal grooves in the hairs of our patient. This peculiarity so far has only been described in two other patients with GAN. Scanning electron microscopy of hairs therefore may serve as a method of screening in patients suspected of suffering from GAN.

Axons↗