Secondary headaches.

Higgins JN, Cousins C, Owler BK, Sarkies N, Pickard JD. Idiopathic intracranial hypertension: 12 cases treated by venous sinus stenting . J Neurol Neurosurg Psychiatry. 2003;74:1662-1666. Background: The high pressures documented in the intracranial venous sinuses in idiopathic intracranial hypertension (IIH) could be the result of focal stenotic lesions in the lateral sinuses obstructing cranial venous outflow. Objective: To explore the relation between venous sinus disease and IIH. Methods: 12 patients with refractory IIH had dilatation and stenting of the venous sinuses after venography and manometry had shown intracranial venous hypertension proximal to stenoses in the lateral sinuses. Intrasinus pressures were recorded before and after the procedure and correlated with clinical outcome. Results: Intrasinus pressures were variably reduced by stenting. Five patients were rendered asymptomatic, two were improved, and five were unchanged. Conclusions: The importance of venous sinus disease in the aetiology of IIH is probably underestimated. Lateral sinus stenting shows promise as an alternative treatment to neurosurgical intervention in intractable cases. Comment: This is one of the hot topics, that is, whether idiopathic increased intracranial pressure is usually due to a cortical sinus thrombosis, stenosis, or other anomaly. When more advanced techniques in magnetic resonance venography become more widely available and utilized, answers on the frequency of secondary idiopathic intracranial hypertension should become available. SJT Bastin ME, Sinha S, Farrall AJ, Wardlaw JM, Whittle IR. Diffuse brain oedema in idiopathic intracranial hypertension: a quantitative magnetic resonance imaging study. J Neurol Neurosurg Psychiatry. 2003;74:1693-1696. Objectives: To investigate the hypothesis that idiopathic intracranial hypertension is associated with diffuse brain oedema, using quantitative magnetic resonance imaging. Methods: Values for the mean diffusivity of water () and the proton longitudinal relaxation time (T1) were measured for various brain regions in 10 patients with idiopathic intracranial hypertension and 10 age, sex, and weight matched controls. Results: No significant differences in < D> and T1 values were found between patient and control groups in any of the brain regions investigated. Conclusions: The results suggest that idiopathic intracranial hypertension is not associated with abnormalities of convective transependymal water flow leading to diffuse brain oedema. Afridi S, Goadsby PJ. New onset migraine with a brain stem cavernous angioma. J Neurol Neurosurg Psychiatry. 2003;74:680-682. A case of new onset migraine is described following a pontine bleed from a cavernous angioma. Polmear A. Sentinel headaches in aneurysmal subarachnoid haemorrhage: what is the true incidence? A systematic review. Cephalalgia. 2003;23:935-941. The aim of this systematic review was to determine the incidence of sentinel headache reported by patients with aneurysmal subarachnoid haemorrhage, and whether they are likely to be due to recall bias or to misdiagnosis of a previous haemorrhage. Nine studies of good quality, which reported the number of patients with aneurysmal subarachnoid haemorrhage with a history of sentinel headache, gave rates of 10% to 43%. Two case-control studies, in which the frequency of a history of sentinel headache in patients with aneurysmal subarachnoid haemorrhage was compared with that in controls with non-aneurysmal subarachnoid haemorrhage or with stroke, gave an incidence of 5% (95% confidence interval 0.5, 16) in controls, suggesting that only a small number of apparent sentinel headaches are due to recall bias. Sentinel headaches appear to be a real entity. Their true incidence may vary from near zero to about 40% according to the rate of misdiagnosis in the community under consideration. Plus an editorial: Demaerschalk B, Dodick DW. Recognizing sentinel headache as a premonitory symptom in patients with aneurysmal subarachnoid haemorrhage. Cephalalgia. 2003; 23:933-934. Comment: Drs. Demaerschalk and Dodick's editorial notes that Dr. Polmear's study is a systematic review and a meta-analysis, since it is not possible to design a randomized controlled trial (RCT) to answer questions on the nature of sentinel headaches before subarachnoid hemorrhage (SAH). They comment on this article meeting appropriate standards as described in the evidence-based literature of: "1. defining the question, 2. conducting a literature search, 3. identifying relevant studies, 4. applying inclusion and exclusion criteria, 5. appraising the studies, 6. abstracting data and 7. conducting analysis by combining results if appropriate" (Oxman A, Guyatt G, Cook D, Montori V. Summarizing the evidence. In: Guyatt G, Drummond R, eds. Users' Guide to the Medical Literature, A Manual for Evidence-Based Clinical Prctice. Chicago: American Medical Association; 2002:155-173). Finally, they point out that even if the lower number of sentinel headaches precede SAH, "Given the morbidity and mortality of ...[SAH], the finding that sentinel headaches occur in at least 10% of these patients underscores the opportunity... to identify...patients...early." SJT