• CLINICAL NEUROLOGY
• TUMOURS

A 55-year-old woman, previously well, attended the emergency department with a 1-year history of falls, increasing dizziness, memory loss, personality change and poor concentration affecting certain activities, such as reading and puzzles. She attended a psychiatric clinic because of panic attacks and depression relating to her husband's ill health and domestic flooding. The psychiatrist diagnosed post-traumatic depression and anxiety and prescribed medication. However, her cognitive symptoms progressed over time and she developed a new onset of weakness in her left arm and leg.

On admission to the Neurology Ward, she showed cognitive slowing, poor recent memory, horizontal nystagmus, moderate left hemiparesis, left hyperreflexia and left Babinski sign. While in the hospital, she had a complex partial seizure and so started an antiepileptic drug. Her routine blood tests were normal. We suspected a right hemisphere lesion and so requested brain imaging. However, her MR scan of brain (T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences) showed an extensive area of hyperintensity involving the left temporal lobe and insula, with mass effect on the left lateral ventricle; there was also a hyperintense lesion in right midbrain and pons (figure 1). A cerebral biopsy showed a high-grade astrocytoma.

• Download figure
• Open in new tab
• Download powerpoint

Figure 1

MR scan of brain (T2-weighted and fluid-attenuated inversion recovery) showing an extensive hyperintense area in the left temporal lobe and insula, with the mass effect on the left lateral ventricle; there is also a hyperintense lesion in right midbrain and pons.

The Kernohan's notch (or Kernohan–Woltman notch) phenomenon results from compression of the midbrain crus against the tentorium, due to an expansive lesion in the contralateral hemisphere. Damage of the descending corticospinal fibres above the decussation causes a hemiparesis ipsilateral to the hemisphere lesion.1 James Watson Kernohan and Henry William Woltman described the first case in 1929. Most reported cases have been due to haematomas (intracerebral, subdural or epidural), skull fracture and, in one case, nigrostriatal dysfunction causing parkinsonism.

The typical MR scan of brain shows T1-weighted hypointensity and T2 and FLAIR hyperintensity in the cerebral peduncle (anterolateral midbrain) involving the descending corticospinal fibres. Occasionally, the MR scan is normal.2