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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In idiopathic or generalized epilepsy, serum glucose and cholesterol concentrations tend to be low, especially just before the seizure. Glucose tolerance curves are abnormal and variable. The electrolyte balance is disturbed, and epileptics tend to go readily into alkalosis. Serum [Na+] is usually unaffected, but [K+] is normal to low between attacks and increases during and after the seizure. Serum [Cl-] is usually high just before the seizure. Epileptics are generally mildly hypocalcemic, especially in the period before the seizure. Serum urea and nonprotein nitrogen values are low between paroxysms but increase after the seizure. Serum protein concentration is usually normal. Stress, which releases epinephrine and corticotropin, results in high serum citrate concentration, which probably contributes to decreased serum [Ca2+] just before a seizure. In the healthy individual, any increase in serum citrate is accompanied by increasing [Ca2+]. In the rabbit, convulsions can be induced with corticotropin, a result of increased serum citrate concentration coupled with a decrease in [Ca2+]. The net result is severe hypo-ionic-calcemia. A similar phenomenon has been reported in a few humans. Administration of insulin causes serum citrate concentrations to decrease. Apparently, the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance, through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathormone, is abnormal in the epileptic.
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PMID:Clinical biochemistry of epilepsy. I. Nature of the disease and a review of the chemical findings in epilepsy. 22 Nov 36

We report the case of a term neonate who developed hypocalcemic seizures due to transient hypoparathyroidism on the sixth postnatal day. His brother had had a similar episode after his birth four years earlier. The mother was free of symptoms and had normal calcium and phosphorus levels at the first evaluation. However, repetition of these determinations with a parathormone assay led to the diagnosis of hyperparathyroidism. A parathyroid adenoma was found and removed surgically. This case-report is the opportunity for reviewing presenting manifestations, diagnostic difficulties, potential complications of this infrequent maternofetal condition, and therapeutic aspects.
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PMID:[Hypocalcemic seizures in two newborn siblings revealing hyperparathyroidism in the mother]. 225 40

A 36-year-old with end-stage renal disease secondary to hypertensive nephrosclerosis had a two-day history of epigastric pain and nausea. Soon after admission, multiple grand mal seizures uncontrolled by intravenous phenytoin sodium and diazepam developed. His calcium level was 14 mg/dL and his amylase level was 2,230 mg/dL; lumbar puncture was normal. Hemodialysis lowered his calcium level to 10.7 mg/dL but failed to control his seizures. Secondary hyperparathyroidism was thought to be the cause of his malignant hypercalcemia, and an emergency subtotal parathyroidectomy was performed. Postoperatively, his grand mal seizures resolved. Confusion and aphasia also developed, but they resolved over the ensuing three weeks. Microscopic examination of the parathyroid glands revealed diffuse chief cell hyperplasia. Preoperative parathormone level was 2,196 pg/dL (normal, less than 450 pg/dL). A review of the literature has failed to reveal a similar case.
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PMID:Secondary hyperparathyroidism manifesting as acute pancreatitis and status epilepticus. 728 72

Nutritional secondary hyperparathyroidism (NSH) was diagnosed in six cats during a three-year period, based on clinical, radiographic and laboratory findings. Clinical signs were attributable to severe osteopenia (n = 5) and hypocalcaemia (n = 4), which had resulted in spontaneous fractures of long bones, scapulae, pelvis, nasal bones, or spine, and in excitation, muscle twitching or seizures, respectively. Serum parathormone levels were markedly elevated, and 1,25(OH)2-vitamin D3 mildly elevated, whereas 25(OH)-vitamin D3 was mildly decreased compared to age-matched healthy cats. Treatment was limited to short-term parenteral calcium gluconate injections, as clinically indicated, a balanced diet and cage rest, which resulted in quick clinical recovery in four cases. The remaining two cats had to be euthanased because of progressive neurological deficits secondary to spinal fractures. At the time of writing, a multitude of commercial balanced diets is widely available and diseases secondary to dietary deficiencies have become rare. Nevertheless, NSH is still an important clinical entity, and should be considered in growing cats presenting with spontaneous fractures or seizures.
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PMID:Nutritional secondary hyperparathyroidism in six cats. 1064 98

Rickets usually occurs in the first two years of life and in puberty since metabolic demand is increased due to rapid growth in these two critical periods of life, when peak bone mass is achieved. Rickets remains one of the most prevalent pediatric diseases in developing countries. Although it is considered to have disappeared in developed countries, there is increasing evidence of widespread vitamin D deficiency among immigrants. There are many reports on rickets and osteomalacia in Asian infants, adolescents and pregnant women moving from India, Pakistan and Bangladesh to developed countries with a cooler climate. We describe three teenagers of Pakistani origin. Clinical presentation included limb pains, muscular weakness, knock-knees and seizures. In all three patients, biochemical findings included hypocalcemia, raised serum parathormone and alkaline phosphatase, and reduced 25-hydroxy vitamin D concentrations. After vitamin D treatment and dietary counseling, biochemical findings returned to normal and their symptoms improved. Given the recent increase in the number of immigrants to Spain, this forgotten disease will probably reappear.
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PMID:[Rickets in Asian immigrants during puberty]. 1219 51

The problem of intracranial calcifications in children has not been widely discussed in the literature yet. The aim of this study is to emphasise different clinical aspects of intracranial calcifications found in subcortical nuclei and cerebellum in children with disturbed calcium metabolism. We report three different cases of hypoparathyroidism in children in whom similar radiological changes on computed tomography (CT) of the brain were found. An 11-year-old boy was referred to us after episode of tetany. We confirmed the diagnosis of idiopatic hypoparathyroidism (presence of Chvostek and Trousseau signs, hypocalcemia, hyperphosphatemia, low parathormone serum concentration). On brain CT small, symmetric calcifications in the subcortical nuclei and frontal lobes were imaged. A diagnosis of pseudohypoparathyroidism type Ib in 10-year-old girl was established on the basis of clinical symptoms (syncope with seizures, recurrent carpopedal spasms in the past) and laboratory investigations (hypocalcemia, hyperphosphatemia, high parathormone serum concentration). In 11-year-old girl autoimmune polyglandular syndrome type I was diagnosed (hypoparathyroidism with chronic mucocutaneous candidiasis and nail dystrophy from the age of 2). CT of the brain showed multiple irregular symmetric calcifications in cerebellar hemispheres, internal capsula and subcortical nuclei on the border of white and grey matter in both frontal lobes.
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PMID:[Association of brain computed tomography images of intracranial calcifications in three different cases of hypoparathyroidism]. 1550 18

(1) Patients who require dialysis for chronic renal failure develop phosphocalcium metabolic disorders that often lead to secondary hyperparathyroidism. Standard treatment consists of a phosphate chelator and vitamin D, along with the use of an appropriate calcium concentration in the dialysis bath, but is difficult to manage. (2) Parathyroid cancer is a rare malignancy frequently associated with hypercalcaemia. (3) Cinacalcet is a calcimimetic agent that reduces the parathormone level. Clinical evaluation includes more than a dozen dose-finding studies and clinical trials. The optimal dose seems to range from 30 to 180 mg/day and varies widely from one patient to another. (4) 3 double-blind placebo-controlled trials, lasting for a maximum of one year and involving a total of 1136 dialysis patients with chronic renal failure, showed no improvement in quality of life with cinacalcet. The target parathormone level was reached by 40% of patients on cinacalcet versus 5% of patients on placebo, while the effects of cinacalcet on calcium levels (-7%) and phosphate levels (-8%) were modest. No impact on bone complications is mentioned in available reports. (5) The assessment of treatment of parathyroid cancer is limited to one ongoing non comparative trial involving 21 patients. (6) During clinical trials, 11% of dialysis patients had low parathormone levels, creating a risk of adynamic bone disease and fractures, but available data are sparse. (7) Two-thirds of patients receiving cinacalcet have episodes of hypocalcaemia, which may in part account for reports of seizures (1.4% of patients), nausea (31%) and vomiting (27%). Many adverse effects seen in animal studies have not been adequately investigated in the clinical setting, such as an increase in the QT interval, thyroid disorders, and sexual dysfunction. Cinacalcet is a powerful CYP 2D6 inhibitor and is also metabolised by isoenzymes CYP 3A4 and CYP 1A2, creating an increased risk of drug interactions. (8) In practice, treatment with cinacalcet seems difficult to manage and to provide only limited benefits. Available assessment reports leave many questions unanswered, and this is a further reason not to use this product outside of clinical trials, either after failure of phosphate chelator and vitamin D therapy (especially as an alternative to surgery) or in parathyroid cancer.
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PMID:Cinacalcet: new drug. Secondary hyperparathyroidism: where are the clinical data? 1676 95

Hypoparathyroidism occurs due to insufficient production of parathyroid hormone to maintain extracellular calcium levels within the normal range. The acute clinical symptoms and signs of hypoparathyroidism are those of hypocalcaemia, ranging from tingling and numbness of limb extremities to intractable seizures. Often seizures are mistaken for epilepsy. Though hypoparathyroidism is not uncommon, the diagnosis is often missed due to its unusual clinical manifestation. This is the first documented report with vitamin D, Parathormone levels and urinary biochemical parameters from India. We present two cases of hypoparathyroidism who presented with seizures along with a short review of literature.
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PMID:Hypoparathyroidism: a rare treatable cause of epilepsy - report of two cases. 1683 12

The value of biochemical tests in treating patients with uncontrolled seizures is unclear. We present the case of an 8-year-old boy with uncontrolled seizures receiving two antiepileptic drugs. He had been diagnosed with recurrent herpes encephalitis and treated with acyclovir 1 year previously. Laboratory blood analyses, performed because of his uncontrolled seizure episodes, revealed hypocalcemia. Hypoparathyroidism was detected with elevated levels of phosphorus and low levels of parathormone. In conclusion, blood tests, especially to measure calcium, in children with uncontrolled seizures are suggested. Hypoparathyroidism causing hypocalcemia, as present here, is not a rare occurrence.
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PMID:Should we routinely perform blood tests in children with uncontrolled seizures? 1700 9

In children, pseudohypoparathyroidism (PHP) is a rare but classical cause of basal ganglia calcifications. It is caused by resistance to parathormone (PTH). Hypocalcemia, which may be symptomatic, is its main feature. We report the case of a 13-year-old boy, affected by type Ib PHP revealed by hypocalcemia and seizures, with basal ganglia calcifications on the CT scan. We describe the characteristics of the 2 main types of PHP and emphasize the search for this disease when basal ganglia calcifications are discovered, even fortuitously, on a cerebral CT scan.
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PMID:[A cause of intracerebral calcifications that should be known: pseudohypoparathyroidism Ib]. 1867 28


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