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A CJD MIMIC; ‘FEEDING ICE–CREAM TO HER CATS’
  1. Cherry Shute,
  2. Ann Johnston,
  3. Jim Neal,
  4. Philip Smith
  1. University Hospital Wales, Cardiff

    Abstract

    Introduction Cognitive decline is a common presentation in general medicine and neurology clinics, however the case of a rapidly progressive dementia cues some very specific differential diagnoses. This case highlights the reality of rapid onset dementias and illustrates that in the elderly the classical diagnostic features may be missing or misleading. This case also serves to illustrate the difficulties in achieving a diagnosis, which sometimes may be illusive, and may only be revealed at post–mortem.

    Case History A 74–year–old woman presented in a confused and dishevelled state after being found at home by her daughter. She had inappropriate speech, was shivering, smelt strongly of urine and was behaving in an unusual manner; repeatedly folding and unfolding clothes and feeding ice–cream to her cat. She had previously been fiercely independent and in the preceding 6–months had lost a significant amount of weight, had a reduced appetite and had lost her sense of smell.

    On examination, she was apyrexial with no signs of meningism. There was a brisk jaw–jerk and she had a poor swallow. In her limbs there was increased tone with cog–wheeling, brisk reflexes, bilateral extensor plantars and prominent frontal–release signs.

    Her clinical condition rapidly deteriorated; became increasingly drowsy, mute, rigid and immobile and required NG tube feeding. She with treated with intravenous pabrinex and methylprednisolone without any benefit. She died of a lower respiratory tract infection prior to the planned brain biopsy. A neurodegenerative condition such as sporadic Creutzfeldt–Jakob disease (CJD) was suspected.

    Investigations Haematological investigations revealed an ESR of 65mm/hr and an LDH of 281 IU; all other haematological and biochemical indexes were within the normal range. Voltage–gated potassium channel and anti–NMDA receptor antibodies were negative. A CT scan of head showed extensive white matter change through the thalami into the dorsal brainstem. An electroencephalogram showed generalised slowing with several sharp waves in the vertex and the occiput, consistent with an encephalopathy. Cerebrospinal fluid analysis revealed normal constituents with a normal S–100 and a positive protein 14–3–3. Neuropathology after a post–mortem examination revealed a widely infiltrating B–cell Non–Hodgkin's lymphoma in the basal ganglia, frontal lobe, corpus callosum and hippocampus.

    Conclusions Primary CNS lymphoma is a rare cause of cognitive decline and most commonly affects individuals who are immunosuppressed, however in immunocompetent individuals, increasing age is a major risk factor. In the elderly most cases are diffuse large B–cell lymphoma which can present with a vast array of symptoms; seizures, neuropsychiatric symptoms, altered mental state, focal neurological deficits and systemic symptoms of weight loss, fever and night sweats. Neuroimaging is often highly variable and may differ between those who are immunocompetent or immunosuppressed. Ultimately, the gold–standard test is a brain biopsy. This case therefore illustrates that even in the elderly a brain biopsy should be pursued, and how even in death a post–mortem examination can be enlightening and provide answers for the neurologist and the grieving family.

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