Neurological Consequences of Starvation
January 1, 2007 4 minutes read
Neurological Consequences of Starvation
Abstract & Commentary
By Michael Rubin, MD, Professor of Clinical Neurology, New York-Presbyterian Hospital, Cornell Campus. Dr. Rubin is on the speaker's bureau for Athena Diagnostics, and does research for Pfizer and Merck.
Synopsis: Prolonged starvation causes Wernicke's encephalopathy in spite of oral thiamine supplementation, and permanent neurological deficits may result.
Source: Basoglu M et al. Neurological complications of prolonged hunger strike. Eur J Neurol. 2006;13;1089-1097.
Within the limits permitted by the declaration of Malta on Hunger Strikers as adopted by the 43rd World Medical Assembly in Malta and revised at the 44th World Medical Assembly in Spain, neuropsychological, neuroradiological, and electrophysiological studies were performed on 41 political prisoners in Turkey who participated in a prolonged hunger strike, ranging from 130-324 days (mean 199), between the years 2000 and 2002. Ages ranged from 22 to 43 years (mean 28.6) among the 22 men and 19 women, none gave a history of alcohol abuse, and all were in good general health except for peptic ulcer disease (n = 4), migraine (n = 6), or hypertension (n = 2). Daily oral thiamine tablets, 200-600 mg for 60-294 days, and a jug of tap water with a teaspoon each of sucrose and table salt dissolved therein, was the only intake and was administered by nurses. Weakness and instability resulted in all patients becoming bedridden, where twice-daily routine examinations were performed. Treatment could be legally instituted only when confusion set in, at which point intravenous fluids, electrolytes, and parenteral thiamine were administered for 5 days, followed by parenteral nutrition. By day 9, all tolerated an unrestricted general diet. No deaths occurred. Following resolution of the confusional state, informed written consent was obtained from all patients, and neuropsychological testing, including the Wechsler Memory Scale, verbal fluency and memory process testing, Stroop neuropsychological screening, Wisconsin card sorting, and Benton facial recognition tests were performed. All underwent brain magnetic resonance imaging (MRI). Electrophysiological studies, encompassing nerve conduction studies (NCS), needle electromyography (EMG), somatosensory and visual evoked potential studies (SEP, VEP), and electroencephalography (EEG) were performed on 32 prisoners who allowed them. Student's t-test and Spearman correlation test provided statistical analysis.
Altered consciousness, ranging from confusion to stupor, lasted from 3 to 31 days, with all patients showing gaze-evoked horizontal nystagmus (vertical in 9) and truncal ataxia. Limb ataxia was seen in 3, and 14 demonstrated nystagmus, ataxia, and lateral rectus palsy. Muscle atrophy was seen in all, but weakness or hyporeflexia was manifest in only 11. Paresthesiae was a complaint in 15, 17 had abnormal touch or pinprick sensation, and 10 had vibration and joint position abnormalities with a Romberg sign. All patients satisfied criteria for Wernicke's encephalopathy and all recovered following thiamine supplementation within 3 to 31 days. Nystagmus and ataxia resolved in 22 prisoners by one year, with 19 showing no change. Areflexia was permanent in 2, sensory function normalized in all, but amnesia, both anterograde and retrograde, remained in all. No correlation was seen between neuropsychological testing and loss of body mass index (BMI). Brain MRI was normal in 32, and 9 demonstrated cortical atrophy with dilated ventricles, sulci, and Sylvian fissures. EEG was normal in 35, with theta or nonspecific sharp waves seen in 3, each. Motor and sensory amplitudes were significantly reduced on NCS compared to controls, but, except for 2 patients, remained within the normal range. Needle EMG was mildly abnormal in only one. VEP P100 latency was prolonged in 22, with normal amplitude. SEPs were not significantly different compared to controls. Central, rather than peripheral, nervous system abnormalities are more common with prolonged hunger, despite thiamine supplementation, and prolonged deficits may be the result of permanent injury.
Commentary
Osmotic myelinolysis, with coma and radiographic changes, consequent to a shift from normo- to hypernatremia, has also been reported due to a hunger strike, in a 19-year-old Algerian asylum seeker whose application for residency status was rejected (Neurology 2005;64:574-575). After 5 days without food or drink, he developed confusion followed, 5 days later, by somnolence. Serum sodium was 187 mmol/L on admission to penitentiary hospital, but urine osmolality was not measured. Water, 2 L/day, by feeding tube was begun, but coma developed 2 days later, and, on admission to the intensive care unit, Glasgow Coma Scale score was 6, sodium was 152 mmol/L, brain CT and cerebrospinal fluid analysis were normal, EEG showed diffuse slowing, and chest radiograph showed bilateral infiltrates, consistent with aspiration pneumonia. Brain MRI 5 days after admission was consistent with pontine and extrapontine myelinolysis, acute hydrocephalus, and posterior fossa edema. Over the next few days the patient regained consciousness, but other than eye and slight finger movements, he was unable to move. Over several months, he recovered but required a cane for ambulation. Central pontine myelinolysis is linked to rapid correction of hyponatremia, but rapid increase of sodium from normal, as in this patient, may also rarely cause this syndrome.
Prolonged starvation causes Wernicke's encephalopathy in spite of oral thiamine supplementation, and permanent neurological deficits may result.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content