Article Text
PDF
Statistics from Altmetric.com
Case presentation
A 25-year-old right-handed Scottish man was admitted with a severe bifrontal pulsating headache, without pressure or postural features. This developed on a background 2-month history of a constant dull holocephalic headache, with nausea, vomiting, abrupt onset vertigo, right hemiparesis and incoordination. His past history included allergic rhinitis, for which he was taking mometasone nasal spray and loratadine. He had no prior personal or family history of headache. He was a non-smoker and consumed 20 units of alcohol per week.
He was afebrile, alert and orientated, with normal observations and no meningism. Examination showed a right hemiparesis with a brisk right knee jerk, equivocal plantars and right-sided ataxia. Tone, sensation and cranial nerves were intact. Blood investigations showed an erythrocyte sedimentation rate (ESR) of 22 mm/1st hour, with an otherwise negative vasculitis screen.
What is the differential diagnosis?
A new progressive headache with abnormal neurological signs on examination raises suspicion of a secondary cause. The ataxic hemiparesis may localise to the contralateral ventral pons, posterior limb of the internal capsule or corona radiata. We considered the possibility of an inflammatory process or neoplasia. An acute vascular insult seemed less likely. Unremarkable inflammatory markers and the absence of fever or meningism were against an infective cause.
What investigations would you recommend?
Serum ACE was normal, and virology and syphilis serology negative. MR scan of brain showed a lesion centred on the left cerebral peduncle, of high T2-weighted and fluid-attenuated inversion recovery, low T1-weighted and high diffusion-weighted signal, with a small focus of susceptibility artefact indicating haemorrhage (figure 1). This was associated with mild expansion of the left cerebral peduncle. The signal abnormality extended to the left brainstem, thalamus and right pons, left optic radiation and chiasm, and left mesotemporal lobe (figure 2). There was patchy postcontrast and perivascular enhancement, in keeping with an active process. We considered the clinical presentation to be consistent …
Footnotes
Contributors SEG: writing of first draft and subsequent revisions; final approval of manuscript. NEF: conception; review of the radiological images; revision of manuscript for intellectual content; final approval of manuscript. JRN: care of the patient; revision of manuscript for intellectual content; final approval of manuscript. CG: care of the patient; revision of manuscript for intellectual content; final approval of manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed by Desmond Kidd, London, UK.
Read the full text or download the PDF:
Other content recommended for you
- Cerebral venous thrombosis is associated with major vessel disease in Behçet’s syndrome
- Prevalence and patterns of neurological involvement in Behcet’s disease: a prospective study from Iraq
- Immune-mediated conditions affecting the brain, eye and ear (BEE syndromes)
- Neurological involvement by Behçet’s syndrome: clinical features, diagnosis, treatment and outcome
- Brainstem astrocytoma as a neuro-Behçet’s disease mimic
- Diagnostic dilemma in CNS Behçet's disease
- Herpes simplex virus (HSV) encephalitis in a young man: an unusual course
- Pharmacovigilance during treatment of multiple sclerosis: early recognition of CNS complications
- Asymptomatic spinal cord lesions in clinically isolated optic nerve, brain stem, and spinal cord syndromes suggestive of demyelination
- Cerebral venous thrombosis: a practical guide