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• Dopaminergic abnormalities after subarachnoid haemorrhage
  Matthieu Faillot, Jean-Marc Gurruchaga, Schahrazed Bouazza, Titien Tuilier, Celine Botella, Imen Megdiche, Emmanuel Itti and Stephane Palfi
  Published on: 3 December 2020

• Published on: 3 December 2020

  Dopaminergic abnormalities after subarachnoid haemorrhage

  • Matthieu Faillot, Neurosurgeon Department of Neurosurgery, Beaujon University Hospital,Greater Paris University Hospital (APHP), INSERM U955 IMRB
  • Other Contributors:
    • Jean-Marc Gurruchaga, Neurologist
    • Schahrazed Bouazza, Neurosurgeon
    • Titien Tuilier, Interventional Neuroradiologist
    • Celine Botella, Neurosurgeon
    • Imen Megdiche, Neuroradiologist
    • Emmanuel Itti, Nuclear Medicine Physician
    • Stephane Palfi, Neurosurgeon

  We read with great interest the study by Jenkins et al 1. Using dopamine transporter (DAT) 123I- Ioflupane SPECT imaging, the authors provide evidence for different patterns of dopaminergic abnormalities in patients with traumatic brain injury (TBI) and patients with Parkinson’s disease.
  We would like to report on the clinical observation of a 35-year-old patient who was admitted at our institution after an aneurysmal subarachnoid haemorrhage (SAH). The patient was initially comatose, and the CT-scan revealed an intraparenchymal haemorrhage associated with an intraventricular haemorrhage. The patient was treated with endovascular treatment and a ventricular catheter was inserted to treat SAH-associated hydrocephalus. There were no ischemic complications. Upon awakening, we observed a bilateral postural tremor affecting the upper limbs, which had already been noticed by the relatives before SAH. The patient’s father is deceased but also had a history of tremor. Our initial conclusion was that this tremor was compatible with essential tremor and required no further investigation.
  After ventriculoperitoneal shunting for hydrocephalus (complicated by overdrainage) the patient made a progressive recovery and returned to part-time work as a gardener despite the persistence of cognitive symptoms.
  One year after haemorrhage, the amplitude of the postural tremor decreased, and a dystonia affecting the right hand appeared. Upon examination 21 months after haemorr...

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  We read with great interest the study by Jenkins et al 1. Using dopamine transporter (DAT) 123I- Ioflupane SPECT imaging, the authors provide evidence for different patterns of dopaminergic abnormalities in patients with traumatic brain injury (TBI) and patients with Parkinson’s disease.
  We would like to report on the clinical observation of a 35-year-old patient who was admitted at our institution after an aneurysmal subarachnoid haemorrhage (SAH). The patient was initially comatose, and the CT-scan revealed an intraparenchymal haemorrhage associated with an intraventricular haemorrhage. The patient was treated with endovascular treatment and a ventricular catheter was inserted to treat SAH-associated hydrocephalus. There were no ischemic complications. Upon awakening, we observed a bilateral postural tremor affecting the upper limbs, which had already been noticed by the relatives before SAH. The patient’s father is deceased but also had a history of tremor. Our initial conclusion was that this tremor was compatible with essential tremor and required no further investigation.
  After ventriculoperitoneal shunting for hydrocephalus (complicated by overdrainage) the patient made a progressive recovery and returned to part-time work as a gardener despite the persistence of cognitive symptoms.
  One year after haemorrhage, the amplitude of the postural tremor decreased, and a dystonia affecting the right hand appeared. Upon examination 21 months after haemorrhage, in addition to the bilateral postural tremor, we observed a rest tremor affecting the right hand when the patient was sitting and when the patient was walking. Froment maneuver facilitated rigidity in the right hand. There was no bradykinesia. A discrete cervical dystonia was observed (with right laterocolis). There were no cerebellar syndrome and no oculomotor abnormalities.
  An 18F-DOPA-PET/MRI was performed 22 months after haemorrhage. There was a clear asymmetry in striatal uptake which was below normal values in the left caudate and the left putamen. At our institution, normal values for 18F-FDOPA imaging were established in 10 patients with essential tremor. Fixation of the caudate could hardly be seen, and fixation was mostly visible in the anterior left putamen creating a radish-like appearance. Analysis of the susceptibility weighted imaging (SWI) sequence showed an hyposignal of the left substantia nigra.

  The interpretation of these clinical findings is not unambiguous. One could argue that the tremor and asymmetry in striatal uptake observed on DAT-scan are directly related to the nigral damage (as evidenced by hypodensity on SWI). A second interpretation, which is not incompatible with the former, is that the subarachnoid haemorrhage worsened a preexisting pathology affecting the nigrostriatal dopaminergic projections. We acknowledge that this observation does not allow to draw definitive conclusions since the dopaminergic system has not been investigated before injury in this patient. However, the progressive worsening of extrapyramidal signs is evocative of a continuous degenerative process affecting the nigrostriatal pathway. These clinical findings are reminiscent of a previously published observation of rest tremor and hemiparkinsonism which occurred seven months after mesencephalic haemorrhage 2. In this observation, the authors also report an asymmetry of 18F-FDOPA striatal uptake. Their conclusion is that the delayed onset of symptoms is compatible with nigrostriatal degeneration caused by nigral damage.
  Overall, we believe that our observation is in accordance with the results presented by Jenkins et al. It supports the idea that different patterns of dopaminergic abnormalities can account for some of the neurological signs observed after acute brain injury. The diversity of observed patterns could be the result of a complex interplay between structural damage to the nigrostriatal pathway and patient’s susceptibility to nigrostriatal degeneration. Early detection of dopaminergic abnormalities with nuclear imaging could help identify patients who are likely to benefit from dopaminergic treatment after acute brain injury.

  1. Jenkins, P. O. et al. Distinct dopaminergic abnormalities in traumatic brain injury and Parkinson’s disease. J Neurol Neurosurg Psychiatry 91, 631–637 (2020).
  2. Defer, G. L. et al. Rest tremor and extrapyramidal symptoms after midbrain haemorrhage: clinical and 18F-dopa PET evaluation. J Neurol Neurosurg Psychiatry 57, 987–989 (1994).

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  Conflict of Interest:
  None declared.

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