| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Fiamingo, Giuseppe Canavero, Isabella Gastaldi, Matteo Coloberti, Elisa Buongarzone, Gabriele Ghiotto, Natascia Bacila, Ana Costa, Alfredo Ravaglia, Sabrina |
| Abstract | Background The syndrome of transient Headache and Neurological Deficits with cerebrospinal fluid (CSF) Lymphocytosis (HaNDL) is classified among secondary headaches attributed to “non-infectious, inflammatory intracranial disease”. Despite its classification among secondary headaches, the current definition of HaNDL does not contemplate a causal agent. Thus, the aetiology, as well as the pathogenesis of both the headache and the transient focal deficits, remains unknown. Case presentation We describe a 29-year-old healthy male developing episodes of thunderclap headaches associated with recurrence of hemiparesis/hemi-paraesthesia; CSF showed lymphocytosis 200/mm3 and increased albumin; brain MRI revealed widespread leptomeningeal enhancement and a non-enhancing, circular diffusion restriction in the splenium of corpus callosum. Screening for neurotropic pathogens detected Epstein-Barr (EBV) DNA in serum and CSF, interpreted as a primary EBV infection once the seroconversion of EBV nuclear antigen (EBNA) IgM to IgG was proven on follow-up. Transcranial Doppler detected, during headache, increased flow velocity in middle cerebral arteries, possibly indicating vasospasm. Oral nimodipine was administered, with prompt clinical recovery, resolution of CSF/MRI abnormalities, and normalization of flow velocities in middle cerebral arteries. Case-based review Although the definition of HaNDL does not contemplate a viral trigger or abnormal brain imaging, we found other literature cases of HaNDL associated with direct or indirect signs of CNS infection. Conclusions At least in a proportion of patients, a viral aetiology may have a role in HaNDL. Whatever the aetiology, we suggest that the pathogenic mechanism may rely on the (viral or other) agent ultimately triggering cerebral vasoconstriction, which would explain both focal symptoms and headache. Calcium channel blockers might be a therapeutic option. |
| Related Links | https://eurjmedres.biomedcentral.com/counter/pdf/10.1186/s40001-022-00815-8.pdf |
| Ending Page | 8 |
| Page Count | 8 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| DOI | 10.1186/s40001-022-00815-8 |
| Journal | European Journal of Medical Research |
| Issue Number | 1 |
| Volume Number | 27 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2022-10-08 |
| Access Restriction | Open |
| Subject Keyword | Medicine Public Health Infectious Diseases Internal Medicine Surgery Oncology Biomedicine RCVS reversible cerebral vasoconstriction Nimodipine Headache Corpus callosum EBV HaNDL Medicine/Public Health |
| Content Type | Text |
| Resource Type | Review |
| Subject | Medicine |
| Journal Impact Factor | 2.8/2023 |
| 5-Year Journal Impact Factor | 2.9/2023 |
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