Klinische Neurophysiologie 2014; 45 - P108
DOI: 10.1055/s-0034-1371321

Cerebellar atrophy due to recurrent electrical injury as the result of torture

NB Kipke 1, R Brüning 2, PP Urban 1
  • 1Asklepiosklinik Barmbek, Neurologie, Hamburg, Deutschland
  • 2Asklepiosklinik Barmbek, Radiologie, Hamburg, Deutschland

We report on a 26-year-old male Libyan who was imprisoned over a 28-day period in Libya, where he was beaten and tortured with electrical current of 380 V several times a day. The cable was attached to the median upper back. The electrical shocks frequently caused loss of consciousness, and after release from prison the patient was neither able to stand or walk, nor speak and swallow without regurgitation, especially after the intake of fluids. Over the past two years the symptoms improved slightly. Both the patient's medical history before imprisonment and the family history revealed no prior neurological or psychiatric findings.

The patient currently presented with saccadic pursuit movements of the eyes, dysarthria, slight dysphagia, limb and truncal ataxia and astasia. Several scars on the skin of his upper back were identified. Neuropsychological evaluation of the patient demonstrated deficits of cognitive function including memory, processing speed, attention and numerical exercises. The patient further showed irritability, anxiety, depression and posttraumatic stress disorder. MRI of the brain demonstrated isolated cerebellar atrophy. Other causes of acquired ataxia were excluded.


The close temporal relationship, the potentially adequate electrical current to induce CNS injuries, and the tendency of improvement argue in favor of an electrically induced cerebellar atrophy. We found no indications of an alternative cause of the cerebellar syndrome. Although cerebellar symptoms prevail, the presence of dysphagia and initial regurgitation leads us to postulate additional brainstem involvement. To our knowledge only four patients with cerebellar atrophy following electric trauma (lightning injuries) have thus far been described in the available literature. The pathogenetic mechanisms are still unclear. Cellular mechanisms, e.g. heat induced protein degradation, might therefore be assumed.