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Subependymal thalamic haemorrhage due to a thalamoperforating artery aneurysm
  1. JOANNA D KOWNACKI
  1. Department of Neurosurgery
  2. Department of Neuroradiology
  3. Department of Neurosurgery, Inselspital, University of Berne, 3010 Berne, Switzerland
  1. Dr Joachim K Krauss, Department of Neurosurgery, Inselspital, University of Berne, 3010 Berne, Switzerland. Telephone 004131 6323444; fax 004131 3822414.
  1. LUCA REMONDA
  1. Department of Neurosurgery
  2. Department of Neuroradiology
  3. Department of Neurosurgery, Inselspital, University of Berne, 3010 Berne, Switzerland
  1. Dr Joachim K Krauss, Department of Neurosurgery, Inselspital, University of Berne, 3010 Berne, Switzerland. Telephone 004131 6323444; fax 004131 3822414.
  1. NELSON GODOY,
  2. JOACHIM K KRAUSS
  1. Department of Neurosurgery
  2. Department of Neuroradiology
  3. Department of Neurosurgery, Inselspital, University of Berne, 3010 Berne, Switzerland
  1. Dr Joachim K Krauss, Department of Neurosurgery, Inselspital, University of Berne, 3010 Berne, Switzerland. Telephone 004131 6323444; fax 004131 3822414.

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A 49 year old woman was admitted because of sudden onset of severe headache, followed by double vision shortly thereafter. Her medical history was unremarkable. On clinical examination she had mild meningism. She was alert and fully oriented. Arterial blood pressure was 150/90 mm Hg. Neurological findings included a left trochlear nerve palsy, an incomplete Parinaud’s syndrome with difficulty on convergence, delayed pupil reaction, and restriction of upward gaze. Brain CT disclosed a small subependymal left thalamic haemorrhage partially occluding the posterior third ventricle. There was minor intraventricular bleeding in the third and fourth ventricles and the posterior horns of the lateral ventricles. Cerebral four vessel digital subtraction angiography showed a left fusiform thalamoperforating artery aneurysm with a 3 mm diameter (figure, A and B). There were no other abnormalities. An MRI was obtained four days after the bleeding and confirmed the paraventricular location of the haemorrhage (figure C). During her stay in hospital repeated blood pressure measurements were normal. Echocardiography was unremarkable. Erythrocyte sedimentation rate was 30/75. Laboratory studies disclosed a titre of antibodies to native DNA of 86 IU/ml (normal range <40 IU/ml) and an antiparietal cell antibody titre of 21 U/ml (normal range<10 U/ml). The HBsAg was positive with 128 IU/ml (normal range<1 IU/ml). All other tests, including antinuclear antibodies, were unremarkable. The patient was managed conservatively. There was a gradual improvement in her neurological deficits. Four months later she still complained of double vision, but refused further diagnostic or therapeutical interventions.

Cerebral artery aneurysms usually develop at bifurcating branches of the arteries of the circle of Willis. Perforating artery aneurysms have been described only in occasional patients. There were no findings suggesting a “mycotic” aneurysm due to an infectious aetiology in our case. Before the advent of contemporary diagnostic and therapeutic techniques “microaneurysms” were described occasionally in patients with arterial hypertension.1 2 The diameter of these “miliary” aneurysms usually ranged between 0.3 and 0.9 mm. By definition, the perforating artery aneurysm described in our patient clearly differs from such “microaneurysms”. Small aneurysms of perforating arteries might represent a congenital abnormality. Alternatively, autoimmune processes could be involved in their pathophysiology.

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