Cerebral venous thrombosis after lumbar puncture and treatment with high-dose corticosteroids.

Lumbar puncture (LP) is a technique often used for diagnostic purposes and less frequently for therapeutic ends. The main complications of the procedure are post-lumbar puncture headache (PPH) and transient nerve root irritation. Other less prevalent complications include cranial neuropathy, infections, brain herniation, vasovagal syncope, cardiac arrest, haemorrhage, and cerebral venous thrombosis (CVT). The last complication is exceptional, but it has been described after epidural anaesthesia, myelography, and diagnostic lumbar puncture. We present the case of a 20-year-old man with no known vascular risk factors, 2 prior episodes of retrobulbar optic neuritis over the 3 preceding years, and normal neuroimaging results. He was admitted for a subacute case of paraesthesia from the lower limbs to the waist. The examination found global hyperreflexia, bilateral ankle clonus, and hypoaesthesia at D10. MRI revealed multiple demyelinating lesions in the brain and another in the spinal cord at D8 with no contrast uptake. LP was performed (procedure was non-traumatic) to complete a biochemical and cytological study of CSF and oligoclonal bands due to suspected multiple sclerosis (MS). The patient was then started on IV methylprednisolone (1 g bolus). Forty-eight hours later, the patient reported headache on standing up; by 5 days, the headache was more intense and did not improve on lying down. Neurological examination showed no focal signs, papilloedema, or new focal signs. Cranial MRI showed partial venous thrombosis of the superior sagittal sinus, with bilateral meningeal venous stasis and acute linear parietal ischaemic infarcts (Figs. 1 and 2). In light of these findings, doctors began treatment with therapeutic doses of low molecular-weight heparin. This was subsequently changed to oral acenocoumarol, with which the patient has been treated for the past 6 months. Progress has been satisfactory from a clinical and radiological standpoint; headache resolved a few days after the patient was admitted and the one-month MRI scan found that sinus patency had been restored. The coagulation test revealed a heterozygous prothrombin G20210A mutation. The test for oligoclonal bands in CSF delivered positive results. Some studies suggest that the mechanism responsible for PPH may contribute to CVT. Onset of PPH takes place 24 to 48 hours after LP and generally resolves in a week. It typically intensifies when the patient is standing and diminishes when the patient lies down. The headache is caused by loss of CSF through the meningeal orifice at the puncture