The neurologic hazards ofdiphenylhydantoin in childhood

Patel, Hrishikesh; Crichton, John U.

doi:10.1016/s0022-3476(68)80172-6

Cited by 55 publications

(14 citation statements)

References 44 publications

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“…of the drug (Kutt et al, 1964;Glaser, 1972). Glaser (1972) has summarized and emphasized a less well-known syndrome of subacute or chronic DPH encephalopathy which is frequently overlooked because of the absence of more typical features of toxicity, such as nystagmus or ataxia (Husby, 1963;Frantzen et al, 1967;Pate1 and Crichton, 1968;Perlo and Schwab, 1969;Logan and Freeman, 1969;Reynolds, 1970;Prensky et al, 1971). It is usually associated with high doses and serum levels but can occur with conventional doses and "therapeutic" levels.…”

Section: -mentioning

confidence: 99%

Chronic Antiepileptic Toxicity: A Review

Reynolds

1975

Epilepsia

272

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Section: -mentioning

confidence: 99%

Chronic Antiepileptic Toxicity: A Review

Reynolds

1975

Epilepsia

272

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“…Acute administration of PHT at concentrations >lops M progressively returned Em, elevated at lower PHT concentrations, to control values. This observation provides one explanation for the excitatory effects often observed clinically when plasma PHT concentrations become too high (Schreiner, 1958;Roseman, 1961;Levy and Fenichel, 1965;Patel and Crichton, 1968;Lascelles et al, 1970;Glaser, 1972;Troupin and Ojemann, 1975).…”

Section: Discussionmentioning

confidence: 89%

Effects of Phenytoin on Primary Glial Cell Cultures

et al. 1985

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The activity of enzymes involved in anion and cation transport, the concentration of intracellular potassium (K+i), and the transmembrane potential (Em) were determined following acute and chronic exposure of primary astroglial cultures to micromolar concentrations of phenytoin (PHT). Na+, K+-ATPase activity of homogenates of cultured glial cells was determined in the presence of an increasing K+ concentration (1-20 mM). Acutely, PHT had little effect on the K+ activation pattern of Na+, K+-ATPase. In contrast, the percentage of Na+, K+-ATPase activated by elevating the K+ concentration was dose dependently increased by chronic PHT treatment. This effect was accompanied by a marked increase in K+i and a significant membrane hyperpolarization. The acute effect of PHT on the Em was biphasic, characterized by membrane hyperpolarization at concentrations of 10(-6)-10(-5) M; at concentrations between 10(-5) and 10(-4) M, the Em progressively returned to control values. These results suggest that glial cells acutely and chronically treated with therapeutic concentrations of PHT have an enhanced capacity to control elevated extracellular potassium levels. Return of the Em to control values at PHT concentrations greater than 10(-5) M suggests that these cells are less able to regulate extracellular potassium. These data can partially explain the excitatory effects of PHT at high therapeutic concentrations.

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“…Mild symptoms are relieved by proper dosage adjustment. Continuation of inappropriate dosage may cause permanent neurologic damage (5) or may expose the patient to the hazards of unnecessary diagnostic procedures (6, 7).…”

Section: Discussionmentioning

confidence: 99%