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

Biochemical evidence for hypoparathyroidism and roentgenographic evidence for hyperparathyroidism were present in a 7-year-old girl with seizures and tetany. She was hypocalcemic (4.7 mg/dl), hyperphosphatemic (11 mg/dl), and normomagnesemic, with elevated parathyroid hormone level (2,603 pg/dl and 3,693 pg/dl in immunoassays utilizing two different antisera). Somatic features of pseudohypoparathyroidism were absent. Increased serum alkaline phosphatase activity (335 IU/liter) with evidence of subperiosteal bone resorption suggested parathyroid hormone activity on bone. Intramuscular administration of parathyroid extract caused a rise in serum calcium level (9.6 mg/dl) and a fall in serum phosphorus level (7.9 mg/dl). The serum calcium, phosphorus, and alkaline phosphatase activity became normal during vitamin D therapy. Parathyroid hormone values and bone roentgenograms became normal. With serum calcium and phosphorus levels normal, ethylenediaminetetraacetic acid infusion was followed by an increase in plasma parathyroid hormone level but not in urinary cyclic adenosine monophosphate (AMP) or phosphaturia; in contrast, parathyroid extract induced cyclic AMP excretion and phosphaturia. These results suggest that endogenous parathyroid hormone in this patient affects bone resorption but not renal handling of phosphate. We infer that this represents a defective endogenous parathyroid hormone.
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PMID:Hypo-hyperparathyroidism: evidence for a defective parathyroid hormone. 19 77

Anticonvulsant therapy of seizure disorders in man is associated with the development of complications involving bone and mineral metabolism including hypocalcemia, elevated serum immunoreactive parathyroid hormone levels, and increased amounts of unmineralized bone or osteoid. The latter has been attributed to a reduction in serum-25-hydroxycholecalciferol levels resulting from increased hepatic metabolism of vitamin D. Using an in vitro recycling hepatic perfusion system, we have demonstrated that 5 d of phenobarbital treatment increases the hepatic production of [(3)H]25-hydroxyvitamin D(3) (4.3+/-0.3 vs. 3.3+/-0.2%/h, P <0.025) without affecting the biliary excretion of radioactivity. Furthermore, rachitic livers perfused with blood obtained from animals treated with phenobarbital for 5 d also manifested an increase in [(3)H]25-hydroxyvitamin D(3) production (4.6+/-0.5 vs. 3.3+/-0.2%/h, P < 0.02). Addition of phenobarbital or its major metabolite, p-hydroxyphenobarbital, directly to the perfusion apparatus had no effect on [(3)H]25-hydroxyvitamin D(3) production. Phenobarbital treatment was also attended by a decrease in the intrahepatic content of [(3)H]vitamin D(3) (11.7+/-0.4 vs. 17.5+/-0.7 dpm/mg liver protein, P < 0.001) without alterations in the content of [(3)H]25-hydroxyvitamin D(3). The data collectively suggest that the increased hepatic conversion of [(3)H]vitamin D(3) to [(3)H]25-hydroxyvitamin D(3) attending phenobarbital treatment is secondary to stimulation of the hepatic 25-hydroxylation system(s) by a metabolite of phenobarbital other than p-hydroxyphenobarbital and/or by metabolic alterations resulting from phenobarbital therapy.
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PMID:Phenobarbital-induced alterations in the metabolism of [3H]vitamin D3 by the perfused rachitic rat liver in vitro. 22 52

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.
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PMID:Hypocalcemia. Differential diagnosis and mechanisms. 22 22

We present a case of a one-month-old infant with hypocalcemia and rickets, with symptoms of focal seizures. The ictal EEG showed left occipital spikes spreading over all of the left hemisphere. From the laboratory studies, we concluded that a low maternal circulating level of vitamin D would cause infantile hypocalcemia and rickets, while immature renal response to parathyroid hormone and transient hypoparathyroidism in infancy would induce hyperphosphatemia. Hypocalcemia may be an important factor in the cause of focal seizures which start even after the age of one month. Further, investigation of maternal vitamin D levels should be done in infantile hypocalcemia.
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PMID:Hypocalcemic focal seizures in a one-month-old infant of a mother with a low circulating level of vitamin D. 189 19

A major factor relating to the oversight of neurological dysfunction and seizures caused by magnesium (Mg++) depletion, involves the buffer functions of the skeletal system orchestrated primarily by the parathyroid. A Mg++ depleted subject may appear relatively asymptomatic until a short period after homeostatic responses go into effect. The results can be devastating if not recognized promptly and treated appropriately. This series of events can best be demonstrated in veterinary medicine but we propose that analogous syndromes occur in clinical medicine. Evidence is presented to support the hypothesis that in subjects with parathyroid hyperactivity and Mg++ deficiency, the stimulus of a rise in serum ionic calcium (Ca++), and the resultant inhibition of parathyroid hormone (PTH) secretion, trigger the transfer of Ca++, Mg++ and other ions from the extracellular space into the exchangeable bone compartment. More importantly, there is a transfer of Mg++ ions from the cerebrospinal fluid into the blood and ultimately into the bone compartment. If the gradient is large and the stimulus adequate, neurological signs and symptoms may be induced. The degree of Ca++ and Mg++ depletion of the peripheral bone and the amount and duration of Ca++ ion increase largely determine the duration and severity of symptoms. The symptom complex is facilitated by sympathetic stimulation. An analogous situation may exist with sodium (Na+).
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PMID:Skeletal buffer function and symptomatic magnesium deficiency. 205 30

A 34-year-old women without history of seizures was admitted to our hospital because of the diminished responsiveness and the repeated blinking for two days. Her past history showed neither surgery nor inflammation of the thyroid gland. General physical examination was normal. On neurological examination, the patient was blinking frequently and staring without any responsiveness. However, she occasionally became able to respond correctly to verbal orders, such as "open your eyes", "open your mouth", "stand up" and so on, which occurred abruptly just like the switch-on. She was otherwise normal neurologically. The laboratory data showed hypocalcemia, hyperphosphatemia, decreased level of parathyroid hormone and normal renal function, indicating the presence of idiopathic hypoparathyroidism. EEG showed the continuous generalized 2-4 Hz spike and wave complexes with the maximum intensity on frontal lobes. Skull roentgenograms and MRI CT of the head disclosed hyperostosis frontalis interna (HFI) and the compression of superior medial frontal lobes by the HIF. SPECT also showed the diminished circulation and hypometabolism in the superior frontal lobes. Based on clinical and EEG findings, the diagnosis of spike-wave stupor was made. She was successfully treated with valproic acid and ethosuximide. Spike and wave complexes on EEG completely disappeared after administration of alfacalcidole. It is assumed that both hypoparathyroidism and HFI were deeply involved in the development of spike-wave stupor in this adult case.
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PMID:[A case of adult-onset spike-wave stupor associated with hypoparathyroidism and hyperostosis frontalis interna (HFI)]. 212 30

A 3 years old boy was admitted due to recurrent attacks of tetany and carpopedal spasm since one and a half years of age. The tetany lasting for 1-2 minutes in each episode was often preceded by an upper respiratory tract infection and occurred 2-3 times a month. Both birth and family history were unremarkable. Physical findings showed mild psychomotor retardation with positive Chvostek sign. Laboratory examination revealed hypocalcemia, hyperphosphatemia, and low serum parathyroid hormone level. EEG showed abnormal tracing with increased slow waves. Head CT Scan demonstrated symmetrical calcification in the basal ganglia region. The clinical features and laboratory findings were consistent with hypoparathyroidism. The mechanism of calcium deposit in the basal ganglia still remains unclear. Tetany, muscle cramping and seizures secondary to hypocalcemia are the most common neurologic signs which respond quickly to calcium replacement. Subsequent supplemental therapy resolved movement disorders and mental retardation. If early treatment prior to the tetanic episodes is instituted in a patient with hypoparathyroidism, it may prevent the development of complications such as intracranial calcifications, cataract and permanent retardation.
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PMID:[Primary hypoparathyroidism with basal ganglia calcification: report of a case]. 263 91

We describe a family with autosomal dominant hypoparathyroidism. The 3 affected individuals had no detectable serum parathyroid hormone on radioimmunoassay. The propositus presented with seizures and on CT scan had bilateral basal ganglion calcification and calcification in the frontal lobes. His similarly affected mother had even more intracerebral calcification. The latter manifestation has not been described previously in autosomal dominant hypoparathyroidism.
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PMID:Autosomal dominant hypoparathyroidism with intracranial calcification outside the basal ganglia. 270 81

Striopallidodentate calcinosis (Fahr's disease) is characterized clinically by seizures, rigidity, and dementia and pathologically by mineral deposition in the basal ganglia, dentate nucleus, and cerebral cortex. Disorders of iron and calcium-phosphate metabolism are thought to play a role in its pathogenesis. We present the case of a patient with familial striopallidodentate calcinosis who had porphyria cutanea tarda, refractory anemia, and pseudohypoparathyroidism type 2. The serum level of ferritin was markedly increased, serum iron and iron-binding capacity were below normal, and at autopsy she had deposition of iron in liver, spleen, bone marrow, and brain. She showed intermittent mild hypocalcemia, increased serum values of parathyroid hormone, elevated renal tubular reabsorption of phosphate, and low serum levels of 1,25-dihydroxyvitamin D, suggesting blunted renal responsiveness to endogenous parathyroid hormone. Pseudohypoparathyroidism type 2 was confirmed by infusion of synthetic parathyroid hormone, which gave a normal urinary cyclic adenosine monophosphate response, but a blunted phosphaturic response. After splenectomy for hypersplenism and weekly phlebotomies, she showed progressive improvement in function, mental status, weight, and seizure control. The hypothesis advanced is that the underlying pathophysiology of the separate diseases contributed to the formation of the brain stones through mechanisms of defective iron transport and free radical production.
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PMID:Abnormal systemic metabolism of iron, porphyrin, and calcium in Fahr's syndrome. 281 30

Primary hypomagnesemia with secondary hypocalcemia (PHSH) is a rare type of hypocalcemic disorder which occurs in early infancy and is clinically characterized by recurrent tetany and/or convulsion. In this paper, a male infant with PHSH who had frequent seizures at the age of 9 days is described. Besides PHSH, several illnesses in infancy are manifested by hypomagnesemia and hypocalcemia, i.e. transient neonatal hypomagnesemic hypocalcemia, congenital renal or hepatic insufficiencies, magnesium-losing nephropathy, combined impairments of intestinal absorption and renal reabsorption of magnesium. PHSH is to be differentiated from these illnesses by the demonstration of a combination of the following findings; hypocalcemia refractory to calcium but responsive to magnesium, continuous requirement for magnesium supplementation to maintain normocalcemia, lack of hypermagnesiuria and/or impaired intestinal absorption of magnesium. Twenty cases from the literature were found to exhibit these characteristics. The clinical, biochemical, and endocrine features of PHSH are summarized on the basis of a review of the data of these and the present case. No associated illness was known in the afflicted infants or mothers. Both male and female infants were afflicted at a male to female ratio of 15:6. Some siblings were afflicted but none of the parents or relatives. The onset of tetany and/or convulsion was between the 9th day and 4th month, which is later than that of other neonatal hypocalcemic illnesses. Hypocalcemia was more pronounced than other infantile hypocalcemic illnesses. The role of the parathyroid hormone in the pathogenesis of hypocalcemia has been studied in several studies but no unifying concepts have yet been established.
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PMID:Primary hypomagnesemia with secondary hypocalcemia. Report of a case and review of the world literature. 299 35


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