Идиопатическая интракраниальная гипертензия в 10% случаев может быть обусловлена железодефицитной анемией, коррекция анемии в большинстве случаев приводит к излечению:
Eur Neurol. 2009 Jun 12;62(2):105-108.
Idiopathic Intracranial Hypertension Associated with Iron Deficiency Anaemia: A Lesson for Management.
Mollan SP, Ball AK, Sinclair AJ, Madill SA, Clarke CE, Jacks AS, Burdon MA, Matthews TD.
The Birmingham Neuro-Ophthalmology Unit, Birmingham and Midland Eye Centre, City Hospital, Birmingham, UK.
Aim: To document the causal association of iron deficiency anaemia (IDA) and intracranial hypertension (IH). Methods: A consecutive case note review of patients with a clinical diagnosis of idiopathic intracranial hypertension (IIH) and anaemia presenting to a tertiary referral unit over a 2.5-year period. Demographics, aetiology and clinical details were recorded and analysed. Results: Eight cases were identified from 77 new cases presenting with IIH. All 8 had documented microcytic anaemia with clinical evidence of raised intracranial pressure. There was no evidence of venous sinus thrombosis on MRI and MR venography in 7 subjects and on repeated CT venography in 1. On correction of anaemia alone, 7 cases resolved. One patient with severe progressive visual loss underwent ventriculoperitoneal shunt in addition to treatment of anaemia, with good outcome. The incidence of this association is 10.3%. Conclusion: These cases present an association between IDA and IH, in the absence of cerebral sinus thrombosis. As a clinically significant proportion of cases presenting with signs of IIH have IDA, we recommend all patients presenting with IIH have full blood counts and if they are found to be anaemic, they should be treated appropriately.
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Еще более ранний эвиденс по теме с обзором всех опубликованных случаев:
We found 30 well-documented cases with isolated anemia and papilledema in the English and French literature. Among those, 13 were excluded from our analyses (11 had confounding disorders and 2 had cerebral venous thrombosis). In the remaining 17 cases isolated raised ICP associated with anemia was the most likely diagnosis, although in none of these cases was cerebral venous thrombosis excluded. A lumbar puncture confirmed raised ICP in only 10 cases. The remaining 7 cases did not have a lumbar puncture, therefore raised ICP could not be confirmed; however, the clinical presentations were highly suggestive of raised ICP associated with anemia. There were 14 women and 3 men, with a mean age of 24 years, range 4 to 56; 6 were obese; all had bilateral papilledema, associated with cotton–wool spots (CWS) in 8, peripapillary hemorrhages in 9, and retinal or preretinal hemorrhages in 4; 11 had chronic headaches, 1 had tinnitus, 5 had VIth nerve palsies, and 4 complained of dizziness. The ICP was elevated in all 10 patients in whom a lumbar puncture was performed (mean opening pressure of 385 mm; range, 220–600). All 17 cases had severe anemia, with a mean hemoglobin of 5.4 g/dl, range, 17 to 25 secondary to iron deficiency in 11, B12 deficiency in 1, combined B12 and folate deficiencies in 1, aplastic anemia in 3, and transient erythroblastopenia in 1. Treatment included successful reversal of the anemia in all 17, and lumbar puncture in 10 patients. Visual prognosis was good in 15 patients and unknown in 2.
Anemia and papilledema.
Biousse V, Rucker JC, Vignal C, Crassard I, Katz BJ, Newman NJ.
Am J Ophthalmol. 2003 Apr;135(4):437-46.
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