Calcium & Seizures

Note: The following abstracts are written in extremely technical language and include technical research and case studies. References are provided. For 'user-friendly' informative reading, check out the health topics presented by Dr. Martin and Dr. Davenport. Feel free to contact us for more information or if you have any questions.

Primary care of adults with mental retardation

BACKGROUND: There is a national trend to deinstitutionalize mentally retarded adults, placing them in community residential settings. As a result, community-based primary care physicians will assume responsibility for their medical care. Primary care physicians may have uncertainties regarding the medical care of this population. The purpose of this case series is to describe the medical care of a group of adults with mental retardation during their first year of community residence following deinstitutionalization, and to provide practical advice to family physicians who care for these adults.

METHODS: Medical diagnoses and medications at the time of deinstitutionalization of a series of 21 adults were abstracted from institutional records and transfer forms. Follow-up data were obtained from office medical records.

RESULTS: In the first year following deinstitutionalization, each patient averaged 6.6 office visits to a family physician. Newly identified major health impairments were: chronic persistent hepatitis due to hepatitis B, acid peptic disease, gastroesophageal reflux disease, dysphagia, primary degenerative dementia, absence seizures, bronchiectasis, and idiopathic iridocyclitis. Significant changes in pharmacotherapy included consolidation of multidrug anticonvulsant regimens and discontinuance of psychotropics and laxatives. Health maintenance practices included hepatitis B immunizations, cholesterol determinations, smoking cessation counseling, and calcium supplementation.

CONCLUSIONS: Newly deinstitutionalized patients require careful diagnostic and therapeutic reassessment. Family physicians assuming their care need to look for conditions common in this population, including dysphagia, seizure disorders, chronic hepatitis B, and sensory impairments. Previously neglected health maintenance practices need to be instituted. Pharmacotherapies, particularly anticonvulsants, psychotropics, and laxatives, may be amenable to dosage reduction or discontinuance.

Tyler-CV Jr; Bourguet-C
J-Fam-Pract. 1997 May; 44(5): 487-94

Hypocalcemia and hypomagnesemia after ibuprofen overdose

OBJECTIVE: To report a case of hypocalcemia and hypomagnesemia after ibuprofen overdose.

CASE SUMMARY: A 21-month-old boy developed acute renal failure with severe metabolic acidosis after ingestion of ibuprofen 8 g. The infant developed tonic-clonic seizures 46 hours after ingestion, with significant hypocalcemia and hypomagnesemia that required electrolyte replacement to control the seizures.

DISCUSSION: To our knowledge this is the first case report of hypocalcemia, hypomagnesemia, and seizures in a patient after ibuprofen overdose. The mechanism is unclear, the situation was probably aggravated by the use of sodium polystyrene sulfonate and furosemide.

CONCLUSIONS: In patients with ibuprofen overdose, serum calcium and magnesium concentrations should be evaluated since seizures may be associated with a deficiency of these cations. The management of these patients should include calcium and/or magnesium supplementation when required and furosemide should be avoided.

al-Harbi-NN; Domrongkitchaiporn-S; Lirenman-DS
Ann-Pharmacother. 1997 Apr; 31(4): 432-4

Vitamin D, calcium, and bone status in children with developmental delay in relation to anticonvulsant use and ambulatory status

Reports of abnormalities in vitamin D, calcium, and bone status associated with anticonvulsant use are inconsistent and difficult to interpret because of widely varying study designs, particularly for ambulatory status. We examined the relative effects of anticonvulsant use and ambulatory status on vitamin D, calcium, and bone status in a large group (n = 338) of children who had either normal motor function (ambulatory) or were nonambulatory and either receiving anticonvulsants or not; all had developmental delays. Data included diet records, serum analyses (calcium and calcidiol), and hand-wrist radiographs evaluated for bone maturation and quality. Data were analyzed by using a general linear models (GLM) procedure. Dietary and biochemical data were compared with those of a group of 34 normal children. There were no differences in calcium or vitamin D intakes among the four study groups; however, a high percentage of intakes was below the recommended dietary allowances for calcium (56%) and vitamin D (70%). Vitamin D intakes were positively associated with serum calcium (P < 0.005) and calcidiol (P < 0.01) concentrations. Analysis of covariance indicated that ambulatory status but neither anticonvulsant use nor their interaction contributed significantly to the prediction of serum calcium (P < 0.009) and calcidiol (P < 0.0001), the Z scores for number of ossified centers (P < 0.008), bone age (P < 0.0001), and bone area (P < 0.003). A strong interaction between anticonvulsant use and ambulatory status was seen for percentage cortical area (P < 0.0008), which was entirely due to anticonvulsant use in nonambulatory children (effect size = 0.98). Results suggest that ambulatory status is more important than was recognized previously in relation to abnormalities in vitamin D, calcium, and bone statuses; that all nonambulatory children may be at risk for low serum calcidiol and osteopenia; and that routine monitoring of risk and consideration of prophylactic vitamin D supplementation are warranted.

Baer-MT; Kozlowski-BW; Blyler-EM; Trahms-CM; Taylor-ML; Hogan-MP
Am-J-Clin-Nutr. 1997 Apr; 65(4): 1042-51

Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.

Magnes-Res. 1992 Dec; 5(4): 303-13

Nutritional rickets

Nutritional rickets was diagnosed in 18 infants aged eight to 24 months. Clinical features included progressive leg bowing, poor linear growth, a diet deficient in vitamin D, seizures, and abnormal serum calcium, phosphate and alkaline phosphatase levels. Wrist radiographs and serum alkaline phosphatase levels were the most useful confirmatory tests. Breast milk may not contain enough vitamin D to protect infants, particularly dark-skinned children and those living in cloudy, northern U.S. cities, from rickets after six months of age. As breast feeding becomes more widely practiced, care is required to ensure that infants at high risk for rickets receive appropriate vitamin D supplementation.

Feldman-KW; Marcuse-EK; Springer-DA
Am-Fam-Physician. 1990 Nov; 42(5): 1311-8

Bone complications of anticonvulsants

Anticonculsant drug-induced disorders in mineral and bone metabolism are apparently quite common. Current evidence indicates that these drugs derange bone metabolism, both through induction of increased hepatic catabolism of vitamin D and its biologically active products, as well as by direct effects on membrane cation transport systems. The significant clinical manifestations of the disorder include rickets with defective bone development, decreased bone mass with increased risk of pathological fracture and reductions in serum calcium levels which may predispose to increased seizure frequency. There is a broad range of clinical presentation with a number of factors -- drug dose, duration of therapy, vitamin D intake, amount of sunlight exposure, degree of physical activity and presence of other concurrent diseases -- which appear to determine the severity of the clinical manifestations. Current evidence indicates that appropriate vitamin D and calcium supplementation can significantly reduce the clinical manifestations of this disorder. All patients receiving chronic anticonvulsant drug therapy should be carefully evaluated for the presence of drug-induced osteomalacia and treated appropriately with vitamin D. This is especially important in those patients in whom the presence of multiple risk factors indicates an increased likelihood of deranged mineral metabolism.

Drugs. 1976; 12(3): 201-11

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