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Ataxia in Institutionalized Patients with Epilepsy

Published online by Cambridge University Press:  18 September 2015

G.B. Young ,
S.R. Oppenheimer ,
B.A. Gordon ,
G.A. Wells ,
L.P.A. Assis ,
J.H. Kreeft ,
N.A. Lohuis  and
W.T. Blume
G.B. Young*
Affiliation:
Department of Clinical Neurological Sciences
S.R. Oppenheimer
Affiliation:
Department of Clinical Neurological Sciences
B.A. Gordon
Affiliation:
Department of Biochemistry
G.A. Wells
Affiliation:
Department of Faculty of Medicine, the University of Western Ontario; the Department of Biostatistics and Epidemiology
L.P.A. Assis
Affiliation:
Department of Radiology
J.H. Kreeft
Affiliation:
Department of Medicine
N.A. Lohuis
Affiliation:
Department of Faculty of Medicine, the University of Ottawa and the University of Toronto
W.T. Blume
Affiliation:
Department of Clinical Neurological Sciences
*
Department of Clinical Neurological Sciences, Victoria Hospital, London, Ontario, Canada N6A 4G5
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Abstract:

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Fifty-four per cent of 41 chronically institutionalized adult patients with epilepsy had ataxia of gait (wide mean stride width). None of the following correlated with stride width: serum phenytoin, previous phenytoin toxicity, seizure frequency, or status epilepticus. Seventeen of the 41 patients had computed tomographic head scans. Patients with radiological evidence of cerebellar atrophy had a wider mean stride width, later age of onset of seizures, greater peak serum concentrations of phenytoin than did those without cerebellar atrophy. Ataxia of gait was inconsistently associated with cerebellar atrophy. Elevated serum/plasma concentrations of phenytoin may be a risk factor for cerebellar atrophy, but seizure frequency or status epilepticus are not independently related to this complication.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 21 , Issue 3 , August 1994 , pp. 252 - 258
Copyright
Copyright © Canadian Neurological Sciences Federation 1994

References

1.Minogue, SJ, Latham, O.Cerebellar degeneration with epilepsy. Med J Australia 1945; 1: 430–433.CrossRefGoogle Scholar
2.Haberland, C.Cerebellar degeneration with clinical manifestations in chronic epileptic patients. Psychiatr Neurol (Basel.) 1962; 143: 29–44.CrossRefGoogle ScholarPubMed
3.Victor, M, Adams, RD, Mancall, EL.A restricted form of cerebellar cortical degeneration occurring alcoholic patients. Arch Neurol 1959; 1:577–688.CrossRefGoogle Scholar
4.Landis, DM, Rosenberg, RN, Landis, SC, Schut, L, Nyhan, WL.Olivopontocerebellar degeration. Clinical and ultrastructural abnormalities. Arch Neurol 1974; 31: 295–307.CrossRefGoogle Scholar
5.Nichols, PJR.Rehabilitation of the severely disabled. 2 – Management. London: Butterworths, 1971: 1–18.Google Scholar
6.Spielmeyer, W.Über einige Beziehungen zwischen Ganglienzellveránderungen und gliösen Erscheinungen, besonders im Kleinhirn. Ztscr f d ges Neurol u Psychiat 1920; 54: 1–38.CrossRefGoogle Scholar
7.Margerison, JH, Corsellis, JAN.Epilepsy and the temporal lobes: a clinical, electroencephalographic and neuropathological study of the brain in epilepsy, with particular reference to the temporal lobes. Brain 1966; 89: 499–530.CrossRefGoogle Scholar
8.Norman, RN.The neuropathology of status epilepticus. Med Sci Law 1964; 4:46–51.CrossRefGoogle ScholarPubMed
9.Zimmerman, HM.The histopathology of convulsive disorders in children. J Pediatr 1938; 13: 859–880.CrossRefGoogle Scholar
10.Salcman, M, Defendini, R, Correll, J, Gilman, S.Neuropathological changes in cerebellar biopsies of epileptic patients. Ann Neurol 1978; 3: 10–19.CrossRefGoogle ScholarPubMed
11.Dam, M.The density and ultrastructure of the Purkinje cells following diphenylhydantoin treatment in animals and man. Acta Neurol Scand 1972; 48 (Suppl 49): 12–63.Google Scholar
12.Meldrum, BS, Horton, RW, Brierley, JB.Epileptic brain damage in adolescent baboons following seizures induced by allylglycine. Brain 1974; 97:407–418.CrossRefGoogle Scholar
13.Meldrum, BS, Vigouroux, RA, Brierley, JB.Systemic factors and epileptic brain damage. Prolonged seizures in paralyzed, artificially ventilated baboons. Arch Neurol 1973; 29: 82–87.CrossRefGoogle ScholarPubMed
14.Rapport, RL, Shaw, CM.Phenytoin-related cerebellar degeneration without seizures. Ann Neurol 1977; 2: 437–439.CrossRefGoogle ScholarPubMed
15.Muñoz-Garcia, D, Ser, TD, Bermejo, F, Portera, A.Truncal ataxia in chronic anticonvulsant treatment. J Neurol Sci 1982; 55: 305–311.CrossRefGoogle ScholarPubMed
16.Julien, RM, Laxer, KD.Cerebellar responses to penicillin-induced cerebral cortical epileptiform discharge. Electroencephalogr Clin Neurophysiol 1974; 37: 123–132.CrossRefGoogle ScholarPubMed
17.Lucas, DR, Newhouse, JP.The toxic effect of sodium L-glutamate on the inner layers of the retina. AMA Arch Ophthalmol 1957; 58: 193–201.CrossRefGoogle ScholarPubMed
18.Olney, JW.Neurotoxicity of excitatory amino acids. In: McGeer, EG, Olney, JW, McGeer, PL, eds. Kainic Acid as a Tool in Neurobiology. New York: Raven, 1978.Google Scholar
19.Rothman, SM, Olney, JW.Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann Neurol 1986; 19: 105–111.CrossRefGoogle ScholarPubMed
20.McGeer, PL, McGeer, EG.Amino acid neurotransmitters. In: Siegel, GL, Albers, RW, Agranoff, BW, Katzman, R, eds. Basic Neurochemistry, 3rd edition. Boston: Little, Brown and Co., 1981: 249.Google Scholar
21.Ottersen, OP, Zhang, N, Walberg, F.Metabolic compartmentation of glutamate and glutamine: morphological evidence obtained by quantitative immunocytochemistry in rat cerebellum. Neuroscience 1992; 46: 519–534.CrossRefGoogle ScholarPubMed
22.Zhongqi, JI, AAs, J-E, Lakke, J, Walberg, F, Ottersen, OP.An electron microscopic, immunogold analysis of glutamate and glutamine in terminals of rat spinocerebellar fibres. J Comp Neurol 1991; 307:296–310.Google Scholar
23.Olney, JW, Collins, RC, Sloviter, RS.Excitotoxic mechanisms of epileptic brain damage. Adv Neurol 1986; 44: 857–877.Google ScholarPubMed
24.Watkins, JC, Evans, RH.Excitatory amino acid transmitters. Ann Rev Pharmacol Toxicol 1981; 21: 165–204.CrossRefGoogle ScholarPubMed
25.Zhang, N, Ottersen, OP.In search of the identity of the cerebellar climbing fiber transmitter: immunocytochemical studies in rats. Can J Neurol Sci 1993; 20 (Suppl 3): S36-S42.Google ScholarPubMed
26.Rabe, CS, Tabakoff, B.Glycine site-directed agonists reverse the actions of ethanol at the N-methyl-D-aspartate receptor. Mol Pharmacol 1990; 38: 753–757.Google ScholarPubMed
27.Garthwaite, J.Glutamate, nitric oxide and cell-cell signalling in the nervous system. Trends Neurosci 1991; 14: 60–67.CrossRefGoogle ScholarPubMed
28.Couratier, P, Hugon, J, Sindou, P, Vallat, JM, Dumas, M.Cell culture evidence for neuronal degeneration in amyotrophic lateral solerosis being linked to glutamate AMPA/kainate receptors. Lancet 1993; 341:265–268.CrossRefGoogle ScholarPubMed
29.Smith, SE, Meldrum, BS.Receptor site specificity for the acute effects of B-N-methlamino-alanine in mice. Eur J Pharmacol 1990; 187: 131–134.CrossRefGoogle ScholarPubMed
30.Weiss, JH, Koh, JY, Choi, DW.Neurotoxicity of B-N-methlaminoalanine (BMAA) and B-N-oxalyl-amino-Lalanine (BOAA) on cultured cortical neurons. Brain Res 1989; 497: 64–69.CrossRefGoogle Scholar
31.Botez, MI, Attig, E, Vézina, JL.Cerebellar atrophy in epileptic patients. Can J Neurol Sci 1988; 15: 299–303.CrossRefGoogle ScholarPubMed
32.Kokenge, R.Kutt, H, McDowell, F.Neurological sequelae following Dilantin overdose in a patient and in experimental animals. Neurology 1965; 15: 823–829.CrossRefGoogle Scholar
33.Puro, DG, Woodward, DJ.Effects of diphenylhydantoin on activity of rat cerebellar Purkinje cells. Neuropharmacology 1973; 12: 433–440.CrossRefGoogle ScholarPubMed
34.Alcaca, H, Lertaanangkoon, K, Stenbach, W, Kellaway, P, Horning, MG.The Purkinje cell in phenytoin intoxication: ultrastructural and Golgi studies. Pharmacologist 1978; 20: 240–249.Google Scholar
35.Botez, MI, Gravel, J, Attig, E, Vezina, J-L.Reversible chronic cerebellar ataxia after phenytoin intoxication. Neurology 1985; 35: 1152–1157.CrossRefGoogle ScholarPubMed
36.Kutt, H, Winters, W, Kokenge, R, McDowell, F.Diphenylhydantoin metabolism, blood levels and toxicity. Arch Neurol 1964; 11: 642–648.CrossRefGoogle ScholarPubMed
37.Riley, CG.Chronic hydantoin intoxication: case report. NZ Med J 1972; 76: 425–428.Google ScholarPubMed
38.Selhorst, JB, Kaufman, B, Horwitz, SJ.Diphenyhyldantoin-induced cerebellar degeneration. Arch Neurol 1972; 27: 453–455.CrossRefGoogle ScholarPubMed
39.Ghatak, NR, Santoso, RA, McKinney, WM.Cerebellar degeneration following long-term phenytoin therapy. Neurology 1976; 26: 818–820.CrossRefGoogle ScholarPubMed
40.Iivanainen, M, Viukari, M, Helle, E-RCerebellar atrophy in phenytoin-treated mentally-retarded epileptics. Epilepsia 1977; 18: 375–386.CrossRefGoogle ScholarPubMed
41.Halpern, L, Julien, R.Augmentation of cerebellar Purkinje cell discharge after diphenylhydantoin. Epilepsia 1972; 13: 377–385.CrossRefGoogle ScholarPubMed
42.McLain, LW, Martin, JT, Allen, JH.Cerebellar degeneration due to chronic phenytoin therapy. Ann Neurol 1980; 7: 18–23.CrossRefGoogle ScholarPubMed
43.Van Gelder, NM, Janjua, NA, Metrakos, K, MacGibbin, B, Metrakos, JD.Plasma amino acids in 3/sec spike and wave epilepsy. Neurochem Res 1980; 6: 659–671.CrossRefGoogle Scholar
44.Janjua, NA, Andermann, E, Eeg-Olofsson, O, et al. Plasma glutamic acid elevation in epileptic patients and their relatives. Epilepsia 1986; 27: 615.Google Scholar
45.Berkovic, SF, Andermann, F, Carpenter, S, Wolfe, LS.Progressive myoclonic epilepsies: specific causes and diagnoses. N Eng J Med 1986; 315:296–305.CrossRefGoogle Scholar
46.Wallace, DC.Mitochondrial diseases: genotype versus phenotype. Trends Genet 1993; 9: 128–133.CrossRefGoogle ScholarPubMed
47.Dzimiri, N, Almotrefi, AA.Investigation of class I anti-arrhythmic drug actions on guinea-pig cardiac mitochondrial lactate dehydrogenase activity. Clin Exp Pharmacol Physiol 1993; 20: 201–206.CrossRefGoogle Scholar
48.Reynolds, EH.Chronic antiepileptic toxicity – a review. Epilepsia 1975; 16: 319–352.CrossRefGoogle ScholarPubMed
49.Reizenstein, P, Lund, L.Effects of anticonvulsive drugs on folate absorption and the cerebrospinal folate pump. Scand J Haematol 1973; 11: 158–165.CrossRefGoogle ScholarPubMed
50.Dow, RS, Moruzzi, G.The Physiology and Pathology of the Cerebellum. Minneapolis: University of Minnesota Press, 1958.Google Scholar