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A STROKE MIMIC; FOCAL NEUROLOGICAL DEFICITS IN BENIGN HEREDITARY CHOREA?
  1. Katie Maw,
  2. JA Johnston,
  3. C Rowntree,
  4. A Kalhan
  1. University Hospital of Wales; Department of Acute Medicine University Hospital Llandough

    Abstract

    Introduction Primary CNS lymphoma (PCNSL) is an aggressive brain tumour which, if left untreated, carries a high rate of rapid deterioration and death with a mean survival of just 1.5–3.3 months.1 Therefore it's recognition, investigation and prompt treatment is essential. PCNSL most commonly presents with headaches, confusion and focal neurological deficits such as hemiparesis and enhancing white matter lesions on MRI.

    Neurologists enjoy a diagnostic puzzle, none more so, when an individual with an existing neurological problem presents with symptoms and signs beyond the spectrum of their illness. Such cases frequently present to the medical assessment unit (MAU).

    We present a stroke mimic of focal neurological deficits in an individual with benign hereditary chorea. This case illustrates the diagnostic challenge and highlights an opportunity to rapidly investigate, diagnose and initiate treatment in the acute setting.

    Case history A 48–year–old woman presented to the MAU with progressive onset weakness of her left arm and leg. The deficit did not improve over days and resulted in the use of a wheelchair. She also complained of headaches, poor memory and decreased recall over several months. She had a history of benign hereditary chorea (all other potential causes had previously been excluded).

    She had previously been assessed in the community, upon which it was assumed her new deficit was due to vascular disease. Following an assessment at a rapid access stroke clinic she was referred to neurology on the basis that her symptoms were attributable to her pre–existing benign hereditary chorea. However due to worsening weakness she presently acutely to MAU.

    Investigations Haematological and biochemical initial investigations were unremarkable and a chest X–ray was normal. A CT scan of head demonstrated a large occipital mass with midline shift, thought to be consistent with glioma. MR imaging was arranged and following this surgical resection and biopsy were performed. Neuropathology revealed lymphoma cells. These results were discussed at The All Wales Lymphoma Panel upon which the diagnosis of PCNSL was confirmed and she was admitted under haematology for chemotherapy.

    Conclusion This case highlights the difficulties in assessing patients with new focal neurological symptoms in the presence of known, pre existing, neurological disease. It also serves to highlight how often erroneously progressive weakness is mislabelled as a ‘stroke’. Neurologists working together with acute physicians in liaison posts in MAU, provides a unique opportunity to improve overall recognition of neurological disease, and for patients potentially provides a more timely diagnostic work–up and the opportunity for early treatment.

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