doi: 10.1161/01.STR.0000029380.93948.9E
(Stroke. 2002;33:2148.)
© 2002 American Heart Association, Inc.
Letters to the Editor |
Recurrent Cerebral Venous Thrombosis in a 24-Year-Old Puerperal Woman
Neurological Clinic, "Tor Vergata" University of Rome, Fondazione "Santa Lucia" IRCCS, Rome, Italy
Neurological Clinic, "Tor Vergata" University of Rome, Rome, Italy
To the Editor:
We read with interest the recent short communication by John N. Fink and colleagues1 on mastoid changes in patients with lateral venous sinus thrombosis (LST). Their observations are very interesting. Twenty-three LST were identified in 20 patients. Mastoid abnormalities were detected ipsilateral to 9 of the 23 thrombosed lateral sinuses. Only one patient showed signs of infection, but a diagnosis of mastoiditis seemed unlikely.
This study is the first to suggest a new etiopathogenetic hypothesis for mastoid abnormalities in patients with LST.
We support the authors’ view that in absence of clinical evidence of infection, treatment should be directed at the underlying cerebral venous sinus thrombosis.
With reference to the above-mentioned study, we would like to report the case of a 24-year-old puerperal woman hospitalized and diagnosed with epileptic seizure. Prior to hospitalization, she experienced diffuse headache, right earache, nausea, vomiting, and mild left hemiparesis. At least 2 other members in her family were reported to have an antithrombin III deficiency or suffer from deep venous thrombosis.
She underwent cerebral MRI and MR venography, which showed not only a right transverse sinus, an ipsilateral jugular vein, and a partial superior longitudinal sinus thrombosis but also ipsilateral mastoid abnormality. She then received anticoagulants and empiric antibiotic treatment for 3 months. Follow-up MRI 1 month later showed both a partial resolution of the mastoid abnormality and a recanalization of the venous sinuses.
Two months later, the patient was again admitted for headache, vomiting, nausea, and dizziness. Indeed, it was then discovered that the control of anticoagulant treatment had not been adequate (international normalized ratio <1.5). Cerebral MRI and MR venography were performed and this time showed a left transverse sinus, an ipsilateral jugular vein, straight sinus, and a partial superior longitudinal sinus thrombosis, but, again, ipsilateral mastoid abnormality was observed, whereas no mastoid abnormalities were observed on the other side.
The unusual finding of mastoid abnormalities ipsilateral to recurrent venous thrombosis without signs of infection in the same patient supports the hypothesis of Fink and colleagues.1 Mastoid changes are more likely the result, especially in adult life, of altered drainage of mastoid air sinuses rather than of infective mastoiditis, making long-term antibiotic treatment useless. Whereas mastoiditis is the most common risk factor in children,2,3 in adults there are many other risk factors4–7 that must be screened.
Treatment should be directed at underlying etiologic risk factors such as, in our case, the presence of a moderate decrease in the antithrombin III levels as well as a methylenetetrahydrofolate reductase mutation and a G20210A transition of the prothrombin gene, probably aggravated by puerperium.8 In this case, the detection not only of LST but also of jugular vein thrombosis, without clinical evidence of infection, supports the hypothesis of vascular congestion, interstitial edema, and transudation of fluid into the mastoid air spaces. Therefore, we decided to administer to the patient oral anticoagulants without additional antibiotic treatment.
Follow-up MRI 3 months later demonstrated both a reversal of mastoid changes and a complete recanalization of cerebral sinuses and jugular vein thrombosis.
The results reported by John N. Fink and colleagues are exciting, and we agree that other studies are necessary before confirming this interesting new hypothesis.
References
1. Fink JN, McAuley DL. Mastoid air sinus abnormalities associated with lateral venous sinus thrombosis: cause or consequences? Stroke. 2002; 33: 290–292.
2. Carvalho KS, Bodensteiner JB, Connolly PJ, Garg BP. Cerebral venous thrombosis in children. J Child Neurol. 2001; 16: 574–80.
3. Huisman TA, Holzman D, Martin E, Willi UV. Cerebral venous thrombosis in childhood. Eur Radiol. 2001; 11: 1760–1765.[CrossRef][Medline] [Order article via Infotrieve]
4. Reuner KH, Ruf A, Grau A, Rickmann H, Stolz E, Juttler E, Druschky KF, Patscheke H. Prothrombin gene G20210
A transition is a risk factor for cerebral venous thrombosis. Stroke. 1998; 29: 1765–1769.
5. Biousse V, Conard J, Brouzes C, Horellou MH, Ameri A, Bousser MG. Frequency of the 20210GA mutation in the 3' untranslated region of the prothrombin gene in 35 cases of cerebral venous thrombosis. Stroke. 1998; 29: 1398–1400.
6. Ludemann P, Nabavi DG, Junker R, Wolff E, Papke K, Buchner H, Assmann G, Ringelstein EB. Factor V Leiden mutation is a risk factor for cerebral venous thrombosis: a case-control study of 55 patients. Stroke. 1998; 29: 2507-2510.
7. Stolz E, Kemkes-Matthes B, Potzsch B, Hahn M, Kraus J, Wirbartz A, Kaps M. Screening for thrombophilic risk factors among 25 German patient with cerebral venous thrombosis. Acta Neurol Scand. 2000; 102: 31–36.[CrossRef][Medline] [Order article via Infotrieve]
8. Lamy C, Hamon JB, Coste J, Mas JL. Ischemic stroke in young women: risk of recurrence during subsequent pregnancies: French Study Group on Stroke in Pregnancy. Neurology. 2000; 55: 269–274.
Response
Christchurch School of Medicine, Christchurch, New Zealand
Auckland Hospital, Auckland, New Zealand
We are grateful to Dr Rizzato et al for their interest in our study and for Dr. Rizzato’s contribution to this field. They present a patient with recurrent lateral sinus thrombosis and associated mastoid abnormality. The patient was initially treated with a 3-month course of antibiotics in addition to anticoagulants. The subsequent recurrence of thrombosis on the contralateral side occurred while anticoagulation was inadequate and was again associated with ipsilateral mastoid abnormality. The second course of treatment consisted of anticoagulation alone, without antibiotics, and full resolution of both cerebral venous thrombosis and mastoid changes followed.
Our original series included 8 patients with lateral sinus thrombosis associated with ipsilateral mastoid air sinus abnormalities without clinical signs of infection who made uneventful recoveries after treatment with anticoagulation alone. Rizzato and colleagues’ patient adds another to that series, but importantly, also provides follow-up MRI documentation of resolution of both thrombotic and mastoid changes without antibiotic treatment. Follow-up imaging was available for only 1 of our patients and showed the same result.
The case presented by Dr Rizzato et al further strengthens the evidence we presented that mastoid air sinus changes associated with lateral venous sinus thrombosis may be caused by vascular congestion and do not necessitate prolonged treatment with antibiotics in addition to anticoagulation when there are no clinical signs of infection.
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||