LAUSR

Dear Editor, Acute disseminated encephalomyelitis (ADEM) is an immune-medicated condition usually affecting children and younger adults, characterized by multiple demyelinating CNS lesions with a variable presentation of neurological symptoms such as encephalopathy, headache, and different focal neurological symptoms [1]. There is no specific test, and the diagnosis is based on clinical reasoning helped by neuroimaging, and exclusion of other relevant differential diagnosis. The most common causes suggested are recent infections and vaccinations. Monophasic clinical course is most common and associated with good prognosis. Higher age and recurrent episodes tends to be associated with higher morbidity and mortality. Steroids, immunoglobulin, plasmapheresis, and immunosuppressive medications are the most common treatment alternatives. A possible link between glutensensitivity and neurological symptoms has been suggested [2]. Here, we report the first case of ADEM possibly associated to late onset coeliac disease (CD) in a woman > 50 years old. A 59-year-old Caucasian woman was admitted to the neurological department due to acute onset of severe headache 3– 4 days earlier. The headache was frontal, bilateral with a pressing and tightening nature. The pain had moderate to severe intensity with co-occurring nausea and photophobia. Previous medical history included hypertension and anemia due to B12 and iron deficiency. Clinical and a complete neurological examination, initial blood tests (hemoglobin 14.1 (ref 11.7– 15.3), leucocytes 6.7 (ref 3.5–8.8), thrombocytes 234 (ref 145–490) and C-reactive protein 2 (ref < 5), iron, ferritin, transferrin, vitamin B12, electrolytes, kidney and liver) and head CT scan were all normal. Lumbar puncture showed elevated lumbar pressure (32 cm H2O), increased leucocytes (241 10/L, ref. 0–5), 97% mononuclear cells, elevated spinal protein (1.8 g/L, ref. < 0.5) and CSF/serum albumin ratio (23, ref. 0–9). Cerebrospinal fluid (CSF) PCR was negative for the most common neurotropic viruses (Herpes simplex virus type 1 and 2, Enterovirus and Varicella Zoster virus). CSF spectrophotometry analysis was negative for xantochromia; thus, subarachnoid hemorrhage was excluded. Her condition was better the next day, and she was discharged from the hospital with a diagnosis of possible aseptic meningitis. However, 6 days later, the patient was re-hospitalized due to worsen more intense headache. A new clinical and neurological examination was normal and did not reveal any new signs of a severe underlying condition. The history was not typical for post-lumbar puncture headache, blood tests still normal and the patient had not had any fever. A new head CT including cerebral venography were normal. Therefore, aseptic meningitis was still suspected. Shortly after, she got a worsening in cognitive functions including problems recognizing family members, reduced concentration and a loss of memory. She scored 21/30 on mini mental status (MMS). Electroencephalography (EEG) showed a nonspecific pattern with generalized slowing in terms of frequent paroxysmal high-voltage slow-wave theta/delta activity over both hemispheres with a maximum over frontal and occipital regions. A few epileptiform discharges were seen. In conclusion, the EEG showed a general nonspecific pattern that may be seen with encephalitis or encephalopathies. Brain MRI showed multifocal white matter high signal abnormalities on T2 in both cerebral and cerebellar hemispheres which were suspected for encephalitis (Fig. 1). The lumbar puncture was repeated. The new CSF analysis showed lumbar pressure * Espen Saxhaug Kristoffersen [email protected]