Hostname: page-component-76fb5796d-x4r87 Total loading time: 0 Render date: 2024-04-28T03:10:59.175Z Has data issue: false hasContentIssue false
  • English
  • Français

Addison’s Disease Presenting with Cerebral Edema

Published online by Cambridge University Press:  18 September 2015

Caroline Geenen ,
Ingrid Tein  and
Robert M. Ehrlich
Caroline Geenen*
Affiliation:
Divisions of Neurology (C.G., IT.) and Endocrinology (R.M.E.), The Hospital for Sick Children, Toronto
Ingrid Tein*
Affiliation:
Divisions of Neurology (C.G., IT.) and Endocrinology (R.M.E.), The Hospital for Sick Children, Toronto
Robert M. Ehrlich*
Affiliation:
Divisions of Neurology (C.G., IT.) and Endocrinology (R.M.E.), The Hospital for Sick Children, Toronto
*
Division of Neurology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8
Division of Neurology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8
Division of Neurology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Background: Increased intracranial pressure with encephalopathy has rarely been reported in Addison’s disease. Method: Case Study. Results: A 16-year-old female who presented with cerebral edema of unknown etiology was eventually diagnosed as having Addison’s disease. She had early morning headaches, fatiguability, diarrhea and deterioration in school performance. She was hyponatremic with a serum sodium of 128 mmol/L and hyperkalemic with a serum potassium of 5.9 mmol/L. She had a low serum osmolality (264 mosm), high urine osmolality (533 mosm) and high urine sodium (87 mosm). She had a postural drop in blood pressure and diffuse hyperpigmentation. An ACTH stimulation test revealed a low baseline Cortisol and no response to ACTH. Plasma renin activity was increased. Serum ACTH was elevated. She responded well to intravenous fluids and solu-cortef and was discharged on hydrocortisone and florinef. She remains well 18 months after the acute episode with no neurologic complaints or findings. Conclusion: Addison’s Disease should be considered in the differential diagnosis of symptomatic cerebral edema and idiopathic intracranial hypertension.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 23 , Issue 2 , February 1996 , pp. 141 - 144
Copyright
Copyright © Canadian Neurological Sciences Federation 1996

References

1.Jefferson, A.Clinical correlation between encephalopathy and papilledema in Addison’s disease. J Neurol Neurosurg Psychiatry 1956; 19:21–27.CrossRefGoogle ScholarPubMed
2.Boudin, G, Funck-Brentano, JL, Gayno, M.Maladie d’Addison par aplasie sur rénale et syndrome para-biermérien. Bull et Mém Soc Méd Hop Paris 1950; 66: 1736–1741.Google Scholar
3.Walsh, FB.Papilledema associated with increased intracranial pressure in Addison’s disease. Arch Ophthamol Chicago 1952; 47: 86.Google ScholarPubMed
4.Klippel, M.Encéphalopathie Addisonnienne. Communication III. Rev Neurol (Paris) 1899; 7: 898–899.Google Scholar
5.Lebrun, R.Contribution a l’étude de l’encephalopathie Addisonnienne. These, Paris 1937.Google Scholar
6.Gosset, AEM.L’encephalopathie Addisonnienne. These, Bordeaux 1941.Google Scholar
7.Wells, HG.Addison’s disease with selective destruction of suprarenal cortex (“suprarenal cortex atrophy”). Arch Pathol Chicago 1930; 10:499–523.Google Scholar
8.Duffin, JD.Cortical necrosis of adrenal glands associated with Addison’s disease: report of 8 cases. Arch Pathol Chicago 1943; 35: 649–666.Google Scholar
9.Eisner, M, Dobrohorska, H, Spychalska-Szymanska, T, Stachowski, A.Objawy rzekomego guza mózgu w przelomie nadnerczowym w przebiegu choroby Addisona. (Polish) (“Addison’s disease with manifestations of pseudotumor cerebri during adrenal crisis). Pol TygLek 1976; 31:585–586.Google ScholarPubMed
10.Baethmann, A, Van Harreveld, A.Effect of adrenal insufficiency on water and electrolyte distribution in the brain. J Neuropathol Exp Neurol 1973; 32:394–407.CrossRefGoogle ScholarPubMed
11.Plum, F, Posner, JB. eds. Multifocal, diffuse and metabolic brain disease causing stupor or coma. In: The Diagnosis of Stupor and Coma. Philadelphia: F.A. Davis Co., 1982; 177–303.Google Scholar
12.Arieff, AI.Hyponatremia, convulsions, respiratory arrest and permanent brain damage after elective surgery in healthy women. N Engl J Med 1986; 314: 1529–1535.CrossRefGoogle ScholarPubMed
13.Fraser, CL, Arieff, AI.Fatal central diabetes mellitus and insipidus resulting from untreated hyponatremia; a new syndrome. Ann Intern Med 1990; 112: 113–119.CrossRefGoogle ScholarPubMed
14.Arieff, AI, Ayus, JC, Fraser, CL.Hyponatremia and death or permanent brain damage in healthy children Br Med J 1992; 304: 1218–1222.CrossRefGoogle ScholarPubMed
15.Prados, SM.Lesiones cerebrales en la enfermedad de Addison. (Spanish). (Cerebral lesions in Addison’s disease). Arch Neurobiol (Madr) 1969; 32: 475–488.Google Scholar
16.Moser, HW, Moser, AE, Singh, I, O’Neill, BP.Adrenoleukodystrophy: survey of 303 cases: biochemistry, diagnosis, and therapy. Ann Neurol 1984; 16:628–641.CrossRefGoogle ScholarPubMed
17.Heffungs, W, Hameister, H, Ropers, HH.Addison disease and cerebral sclerosis in an apparently heterozygous girl: evidence for inactivation of the adrenoleukodystrophy locus. Clin Genet 1980; 18: 184–188.CrossRefGoogle Scholar