• DOI:10.1007/s00415-006-0382-x
• Corpus ID: 32393176

Parietal proprioceptive loss with pseudoathetosis

@article{Salih2006ParietalPL,
  title={Parietal proprioceptive loss with pseudoathetosis},
  author={Farid Salih and Claus Zimmer and Hartmut Meierkord},
  journal={Journal of Neurology},
  year={2006},
  volume={254},
  pages={396-397}
}

• F. Salih, C. Zimmer, H. Meierkord
• Published 7 March 2007
• Medicine, Psychology
• Journal of Neurology

Sirs: Pseudoathetosis is an athetoid-like movement disorder [6] caused by impaired processing of proprioceptive information (i.e. joint position and movement sense) to the striatum, which consequently fails to integrate sensory and motor inputs [8]. Any lesion along proprioceptive pathways from muscle spindles and joint receptors to primary somatosensory cortex (S1) may produce pseudoathetosis. Nevertheless, pseudoathetosis is most often seen in peripheral neuropathies and in dorsal root ganglia or dorsal column disorders [2]. Because of the close spatial relation of deep sensation fibres from peripheral nerves to brain stem level pseudoathetosis usually presents with combined proprioceptive and vibration sense impairment [3]. Here we report a patient who presented with pseudoathetosis due to characteristic proprioceptive loss. Unusually, this was not associated with an impairment of vibration sense leading to the rare diagnosis of parietal pseudoathetosis. The 73-year-old male patient with a previous history of arterial hypertension and coronary artery disease suddenly noticed disturbed movement sense and difficulties in coordinating his left fingers 3–5. He experienced no pain or muscle weakness. On examination there was an impressive loss of joint position and movement sense of these fingers and a minor proprioceptive impairment at the level of the wrist. The patient was unable to maintain these fingers in a desired position. When asked to close his eyes the fingers started to wander with a low-amplitude positional drift. Further clinical examination including all other sensory modalities was normal. In particular vibration sense was unimpaired. MRI demonstrated confluent ischaemic lesions affecting cortical and subcortical parts of right S1 (Brodman areas 1,2,3). There were less pronounced lesions observed within other cortical and subcortical areas (e.g. area 6) of the right hemisphere (figure 1). There were no lesions in the basal ganglia, thalamus or the brain stem and no signs of cervical myelopathy. Ultrasound sonography of the extracranial arteries revealed slight artherosclerosis. Electrocardiographic monitoring and transoesophageal echocardiogramm did not reveal any cardiac sources of embolism. Full blood count and biochemistry were normal. Sensory neurography revealed normal conduction velocities and normal F-wave amplitudes und latencies. Recordings of sensory evoked cortical potentials (SEP) were absent after electrical stimulation of left fingers 3–5. SEPs of unaffected fingers were normal. Pseudoathetosis has been reported in various aetiological lesions along proprioceptive pathways, but is rarely seen in parietal lesions. Our patient differed from the previous case reported by Sharp et al. [8] who had an extensive haematoma involving the right parietal lobe leading to pseudoathetosis of the entire left arm accompanied by a left hand paresis. In a further patient with right parieto-temporal ischaemia pseudoathetosis occurred together with a ‘‘sensory cortical syndrome’’, including hyperpathy and astereognosis as well as slight hemiparesis [1]. Since pseudoathetosis with isolated proprioceptive impairment and sparing of vibration sense has only been reported as a supraspinal syndrome following parietal or thalamic lesions [8] the question is how can this phenomenon be F. Salih (&) Æ H. Meierkord Neurologische Klinik und Poliklinik Charité-Universitätsmedizin Berlin Germany, Augustenburger Platz 1 13353 Berlin, Germany Tel.: ++49 30 450660011 Fax: ++49 30 450560901 E-Mail: [e-mail]