Neuromuscular consequences of prolonged hunger strike: an electrophysiological study☆
Introduction
The neurological complications of nutritional deficiencies are well-known phenomena which occur in alcoholic individuals, in patients with diseases leading to impaired absorption of the dietary nutrients or in populations subjected to severe and long-term dietary restriction (Victor et al., 1971, Victor et al., 1971, Windebank, 1993, Adams et al., 1997). On the other hand, neurological manifestations of prolonged total fasting were rarely reported and there are only a few reports regarding electrophysiological studies performed after long periods of total starvation (Mattson and Lecocq, 1968, Peel, 1997).
Our country witnessed a long-term hunger strike (HS) between May 20 and July 27, 1996 which was performed by political prisoners (Beynon, 1996). There were 1500 strikers all over the country, 220 of whom went on the HS as ‘death fasting’. Twelve died between the 63rd and 69th days, and HS was terminated on the 69th day along with 208 surviving death fasters. We conducted electrophysiological studies on 15 of the strikers who presented with the clinical symptoms of central nervous system complications of the HS. Motor and sensory conduction studies as well as the somatosensory (SEP) and motor (MEP) evoked potentials were performed in order to find electrophysiological indications of neuromuscular and central nervous system involvement.
Section snippets
Patients
HS began in 41 prisons with 1500 performers who ingested water, salt and lemonade (or linden tea) in the first period of 45 days. In the second period, by the 46th day, having the strike changed into so called death fasting, 220 of them limited their daily intake to only 4 glasses of water and salt. HS was terminated on the 69th day after 12 deaths. A team of the physicians in this study (H.G., E.G., D.K., H.S.) examined 68 of the HS performers (64 from the same prison) in routine visits.
Results
Electrophysiological findings, which were considered as abnormal, are presented in Table 1. The most frequent abnormalities in this table are the low amplitude CMAPs elicited with stimulation at the wrists or ankles in motor NCV studies. Nine patients had at least one motor nerve with low amplitude CMAP. There was no significant difference between the BMI values of this group of patients (16±3.2 kg/m2) and those of the other 6 with normal amplitude CMAPs (17.3±2.3 kg/m2). As compared to the
Discussion
Nutritional deficiencies can damage both the central and peripheral nervous systems (Victor et al., 1971, Victor, 1984, Windebank, 1993, Adams et al., 1997). The presence of Wernicke's encephalopathy or Wernicke–Korsakoff syndrome in all of our patients suggests that deficiency of group B vitamins, particularly thiamine, was the major cause leading to neural damage (Victor et al., 1971, Adams et al., 1997). These syndromes are generally secondary to chronically insufficient supply of the
Acknowledgements
We thank Dr M. Ertaş for his help in the statistical analyses. The Department of Neurology, Istanbul Faculty of Medicine was awarded by the Istanbul Chamber of Physicians for its personnel's medical service to the hunger strikers with the 1997 Dt. Sevinç Özgüner Peace, Democracy and Human Rights Award.
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Presented as a poster at the 14th International Congress of EEG and Clinical Neurophysiology, Florence, Italy, August 24–29, 1997. Presented in part at the 16th World Congress of Neurology, Buenos Aires, Argentina, September 14–19, 1997.