Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 36-year-old man with prolonged confusion developed after psychomotor status was reported. He had no past history of epileptic seizures or psychotic disorders. The status continued for 20 hours, and twilight state and a slight fever lasted for about 10 days. Thereafter gross impairment of memory and disorientation became remarkable, and, in addition, strong psychic and autonomic disturbances developed, such as visual and auditory hallucinations, excessive excitement, disturbance of sleep, polyphagia, polydypsia, polyuria and hyperhidrosis. The CT scan, carotide angiography, CSF examination, and complement fixation tests for viruses were all within normal limits. The EEGs showed a slowing of the background activity, 0.6--0.8 Hz periodic high voltage wave discharges and random spikes in each temporal area. The clinical symptoms and EEG findings gradually improved without remarkable damage.
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PMID:A case of prolonged confusion after temporal lobe psychomotor status. 52 Sep 42

A case of cerebral polyuric hyponatremia was reported. A 64-year-old lady had complained of visual disturbance for 4 years. She was operated upon under the diagnosis of tuberculum sellae meningioma. Sever days following operation tremendous polyuria was senn, i. e. polyuria over 40 l/day, massive sodium wasting in the urine, hyponatremia and severe thirst feeling. These situations could not easily controlled by pitressin, and 2 days after the onset of polyuria the level of sodium in the serum decreased up to 112 mEq/l, the amount of excretion of sodium into urine increased up to 186 mEq/l, and the patient had finally a convulsive seizure followed by loss of consciousness. This hyponatremia was easily controlled by infusion of hypertonic NaCl. The pathogenesis of this condition could not be explained by applying the classical concept of "Diabetes Insipidus" nor "SIADH". This hyponatremia might be the result of massive sodium wasting in the urine. And from the results obtained in our patient, these conditions should be classified in the syndrome of "Cerebral Polyuric Hyponatremia" as reported by Oi et al. It should be emphasized that the measurement of osmorality and level of electrolytes in the serum and urine had to be performed frequently when the postoperative polyuric situation was found, so that the clinical diagnosis could be established in the earlier stage. The clinical diagnosis and differentiation of postoperative disorders in water and electrolytes of central origin were discussed.
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PMID:[A case of cerebral polyuric hyponatremia (author's transl)]. 66 77

Two cases of lithium toxicity are reported on in dogs having had lithium hypochlorite chlorinated water as their sole source of drinking water. Clinical signs in one dog included polyuria, polydipsia, loss of body mass; dehydration, diarrhoea and general weakness and in the other case, polyuria, polydipsia, loss of body mass and seizures. Withdrawal of the water resulted in complete recovery.
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PMID:Lithium toxicity in two dogs. 177 Apr 85

Three patients with hyponatremia were found at an residential home of mental developmental delay. Because pimozide had been administered to all of them, it was suggested that pimozide might have induced compulsive water drinking resulting in hyponatremia. To my knowledge, there has been no previous report that pimozide may induce hyponatremia. As children with mental developmental delay and/or autism frequently develop epilepsy, hyponatremia should be included in the differential diagnosis of convulsive seizures. Particularly when antipsychotic drugs such as pimozide have been given, we should pay attention to polydipsia, polyuria and/or general malaise and prevent hyponatremia.
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PMID:[Three cases of hyponatremia during administration of pimozide]. 193 Nov 69

A case of psychogenic polydipsia is presented. A 40 year old female was brought to the emergency room after a sudden seizure at home. The patient had spontaneous eye opening, was making incomprehensible sounds and had abnormal and agitated flexion of the limbs. Severe cerebral edema was seen on the computed tomogram. The patient was found to have hypotonic polyuria and hyponatremia. Two months previously, the patient had stopped taking bromazepam (a benzodiazepine) and on the advice of a neighbour had taken plenty of water to avoid withdrawal symptoms. The diagnosis and therapy are discussed.
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PMID:[Psychogenic polydipsia: pronounced cerebral edema after exaggerated consumption of boiled water]. 200 20

Among patients with psychiatric disorders, especially schizophrenia, a pattern of extreme polydipsia and polyuria sometimes emerges, usually without readily identifiable medical causes. Hyponatremia may develop and progress to water intoxication, with symptoms including restlessness, confusion, seizures, or even death. We review the clinical features and pathophysiology of this syndrome and discuss nursing roles in identifying and managing patients with polydipsia and hyponatremia. While the causes of polydipsia and hyponatremia are unclear, relevant factors seem to include a possible dysfunction in central nervous system (CNS) thirst and osmoregulatory centers, the inappropriate secretion of or sensitivity to antidiuretic hormone (ADH), and psychoactive drugs. Management techniques for affected patients concentrate on careful observation, fluid restriction, and the minimization of possible exacerbating factors such as high neuroleptic dosage and cigarette consumption.
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PMID:Polydipsia and hyponatremia in psychiatric patients: challenge to creative nursing care. 235 13

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications.
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PMID:Polydipsia and hyponatremia in psychiatric patients. 328 1

Parameters of water metabolism were measured serially in nine patients with the syndrome of self-induced water intoxication and psychosis (SIWIP). Clinical and laboratory findings indicated that SIWIP patients are type A of the syndrome of inappropriate antidiuresis. Estimated 24-hour urinary excretion of creatinine and early morning urinary creatinine concentration measurements were used to calculate 24-hour urine volumes. Polyuria was considered present for male patients when excretion was estimated to be greater than 2,600 ml of urine/24 hours or early morning urinary specific gravity was less than or equal to 1.003. Male patients with a specific gravity of less than or equal to 1.003 predictably excreted 28,000 ml of urine/day. Severe hyposthenuria may be a biological marker for a population at risk to develop complications of SIWIP, including seizures, coma, and death.
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PMID:Patterns of urinary excretion among patients with self-induced water intoxication and psychosis. 385 84

Review of 60 consecutive records of patients who died before the age of 53 years in a state mental hospital revealed that 27 of those patients (45%) had a schizophrenic disorder. Of those 27 patients, five (18.5%) died of the complications of self-induced water intoxication and schizophrenic disorders (SIWIS). Clinical, laboratory, and autopsy features of those five SIWIS patients and of an additional five SIWIS cases obtained from the literature include psychosis, polydipsia, polyuria, severe hyposthenuria (specific gravity 1.003 or less), hyponatremia, seizures, coma, and cerebral and visceral edema. SIWIS characteristically develops during Arieti's third or "preterminal" stage (5 to 15 years after onset of psychosis) of schizophrenic disorders and it must be included in the differential diagnosis of unexplained death among psychiatric patients. As there are no pathognomonic SIWIS tissue changes, the pathologist must carefully integrate clinical, laboratory, and autopsy findings to arrive at the proper diagnosis. When premortem findings of polydipsia and hyponatremia are not available, evidence of antecedent severe hyposthenuria and postmortem vitreous humor hyponatremia of less than 120 mEq/1 are strongly supportive of the diagnosis of death due to SIWIS.
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PMID:Death from self-induced water intoxication among patients with schizophrenic disorders. 397 77


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