A 66-year-old patient with diabetes mellitus and pulmonary malignancy presented with flaccid tetraplegia and urinary retention since the day before hospital admission. MRI (fig 1A) and cerebrospinal fluid (CSF) analysis suggested panmyelitis. PCR assays detected herpes simplex virus (HSV) type 1 in the CSF. Moreover, there was a marked CSF lymphocytosis with a raised total protein level of 65 mg/dl. Cytological studies for malignant cells were negative, and there were no onconeural antibodies. Infection with Epstein–Barr virus, varicella zoster virus, cytomegalovirus and HIV was rejected. The initial combined antiviral treatment with aciclovir (750 mg three times a day) and steroid treatment (50 mg daily) given immediately was followed by plasma exchange and immunoglobulin administration because the patient’s condition deteriorated continuously, despite use of the preferred treatment. At 5 days after hospital admission he exhibited disturbed consciousness and respiratory failure. Over the next 10 days he developed signs of widespread brainstem dysfunction. Repeated MRI investigations revealed a marked involvement of the brainstem, midbrain and thalamus expanding to the temporal region bilaterally (fig 1B). Finally, the patient died after 26 days of intensive care treatment; an autopsy was not performed.

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Figure 1

T2-weighted (turbo spin echo (TSE)) sagittal MRI on the day of admission showing signal increase and swelling of the spinal cord (A). Fluid-attenuated inversion–recovery (FLAIR) coronar MRI 3 weeks later revealed oedema involving brainstem, midbrain, thalamic and temporal regions (B).

Acute ascending myelitis due to HSV infection is a rare, usually monophasic, fatal disorder.1^,2 We could not prevent progression despite extensive treatment in our patient. Presumably, parainfectious mechanisms based on damage of myelin structures by cytokines and other immune mediators or molecular mimicry may have complicated the neural spread of HSV. The detailed immunological mechanisms remain to be identified.