Wernicke encephalopathy (WE) is a rare but known complication of severe hyperemesis gravidarum caused by thiamine deficiency. This article presents an unusual case that occurred at our institution and reviews the 48 previously published cases of WE in pregnancy. Considering all the 49 cases, the mean (+/-standard deviation) patients' age was 26.7 +/- 4.9 years, the mean gestational age when WE manifested was 14.3 +/- 3.4 weeks, and the mean duration of vomiting and feeding difficulties was 7.7 +/- 2.8 weeks. Wernicke's classic triad (confusion, ocular abnormalities, and ataxia) manifested in only 46.9% (23 of 49) of the patients. Confusion affected 63.3% (31 of 49) of the patients, ocular signs 95.9% (47 of 49) and symptoms 57.1% (28 of 49), and ataxia 81.6% (40 of 49). Deterioration of consciousness affected 53.1% (26 of 49) of the subjects and memory impairment 61.2% (30 of 49). Complete remission of the disease occurred in only 14 of 49 cases. Symptom resolution required months and permanent impairments were common. The overall pregnancy loss rate, directly (spontaneous fetal loss) and indirectly (planned abortion) attributable to WE, was 47.9% (23 of 49). The diagnosis of WE is clinical and can be rapidly confirmed by magnetic resonance imaging. We emphasize the importance of thiamine supplementation to women with prolonged vomiting in pregnancy, especially before intravenous or parenteral nutrition. We also underline the necessity to promptly replace vitamin B1 when neurologic symptoms and/or signs develop in a patient with hyperemesis gravidarum.

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The effects of an anesthetic dose (100 mg/kg) of ketamine, a phencyclidine derivative, on local rates of cerebral glucose utilization (LCGU) and CBF (LCBF) have been investigated by the quantitative [14C]2-deoxy-glucose and [14C]iodoantipyrine techniques in the unparalyzed, spontaneously breathing rat. In ketamine-injected animals, LCGU was significantly increased in some limbic structures and decreased in inferior colliculus, vestibular, and cerebellar nuclei. The degree and spatial distribution of drug-induced changes was similar for local blood flow rates, LCBF being increased in limbic regions and decreased in the inferior colliculus. Although Paco2 values were higher in anesthetized animals, the pattern of LCBF/LCGU ratios was not significantly affected by ketamine in the 36 brain regions examined in this study. So, at least in the rat and at the anesthetic level studied here, a net vasodilatory in vivo effect was not observed. These results support the hypothesis that CBF changes induced by the drug in animals and man are primarily related to the metabolic effects exerted by ketamine on cerebral structures.

Local cerebral blood flow (LCBF) was measured autoradiographically in newborn puppies by an indicator fractionation technique using 4-iodo-[14C]antipyrine as the diffusible indicator. Measurements were obtained in unanesthetized, normotensive animals, and the sensitivity of blood flow to hypercapnia and acute hypoxia was determined in 32 brain structures. LCBF in normal and hypoxic puppies was correlated with local cerebral glucose utilization (LCGU) obtained under the same experimental conditions (Duffy et al, 1982). In normocapnic (PaCO2 33 mm Hg) control animals, highest rates of blood flow were found in gray matter nuclei of the brainstem, in the medulla oblongata, and in the posterolateral nucleus of the thalamus (50 to 77 ml/100 gm/min); far lower flows were recorded among white matter structures (5 to 11 ml/100 gm/min). The vasodilatory response to both hypercapnia and hypoxia was greatest among brainstem gray matter structures, intermediate among cortical and diencephalic gray matter structures, and least in white matter. When LCBF was plotted as a function of LCGU for control animals, a positive linear correlation was obtained for all structures (p less than 0.001), implying that in newborns, as in adults, cerebral blood flow and metabolism are physiologically coupled. In hypoxic puppies, no consistent relationship between LCGU and LCBF could be demonstrated; however, there was suggestion that the two measurements correlated inversely, presumably reflecting enhanced anaerobic glycolysis in structures (e.g., hemispheric white matter) that were not adequately protected by compensatory hyperemia. White matter damage, a frequent complication of perinatal hypoxia-asphyxia, may be a consequence in part of the limited capacity of white matter to vasodilate in response to te chemical "signals" of hypercapnia and lactic acidosis.