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Trigeminal neuralgia: no laughing matter
  1. Daniel Blackburn1,2,
  2. Marc Stewart Randall2,
  3. Nigel Hoggard3,
  4. Robin Highley4,
  5. Kirsty Harkness5
  1. 1Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UK
  2. 2Department of Neurology, Royal Hallamshire Hospital, Sheffield, UK
  3. 3Academic Unit of Radiology, Royal Hallamshire Hospital, Sheffield, UK
  4. 4Department of Neuropathology, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UK
  5. 5Department of Neurology, Royal Hallamshire Hospital, Sheffield, S.Yorks, UK
  1. Correspondence to Dr Daniel Blackburn, Sheffield Institute of Translational Neuroscience (SITraN), University of Sheffield—385a glossop Road, Sheffield s10 2hq, UK; d.blackburn{at}sheffield.ac.uk

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Case history

A 21-year-old right-handed man was referred to neurology in autumn 2009. He had been a university student for 1 year, with his studies progressing well until Easter 2009, when his work had deteriorated. His writing had become muddled with frequent spelling mistakes and he was diagnosed with dyslexia. In June, he developed severe generalised headaches, which did not respond to simple analgesics. The pain progressed to a right-sided facial pain with a sharp electric shock quality and was diagnosed as trigeminal neuralgia: his general practitioner started carbamazepine, which was ineffective. The pain had been constant for the previous 8 weeks, with no nausea or vomiting.

Question 1

What are the causes of acquired dyslexia and how would you investigate it?

Comment

‘Dyslexia’ is commonly used to refer to a developmental reading disability. In contrast, acquired dyslexia, sometimes termed ‘alexia’ to highlight the distinction, indicates a difficulty in reading in someone who previously read normally.

Acquired dyslexias can be divided into:

  • peripheral dyslexia, where there is a defect in the visual processing of written material with intact language centres

  • deep/central dyslexia, where there is a breakdown of the normal linguistic processing.

The deep dyslexias are seen in semantic dementia and with lesions (strokes and tumours) affecting the dominant hemisphere temporal and parietal lobes. A non-dominant hemisphere lesion can cause alexia by two mechanisms.

  • A lesion in the right parietal lobe can cause ‘neglect alexia’ due to a failure to read the left half of words correctly.

  • A lesion in the non-dominant splenium can prevent transfer of visual information to the primary language centres in the temporal and parietal lobes. Classically these patients can write but cannot read (alexia sine agraphia). They can recognise letters but not words and hence are very slow to read long words.

Question 2

What are the typical symptoms of trigeminal neuralgia …

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