Cerebral Function of the Guinea Pig Neonate after Chronic Intrauterine Exposure to Khat &lt;i&gt;(Catha edulis &lt;/i&gt;Forsk.)

Thordstein, Magnus; Jansson, Thomas; Kristiansson, Bengt

doi:10.1159/000243339

Cited by 4 publications

(2 citation statements)

References 21 publications

(28 reference statements)

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“…In animal models, brain damage induced by poisonous substances in rodents during pregnancy causes a higher vulnerability to the effects of CNS stimulants in animal models of psychosis (Lipska, Halim, Segal & Weinberger, 2002; for a review see Thompson, Pogue-Geile & Grace, 2004). In a study with guinea pigs, prenatal exposure to khat caused EEG changes that were measured in the neonatal period (Thordstein, Jansson & Kristiansson, 1991). Additionally, from laboratory studies, evidence for the neuro-toxic effects of khat is growing (for a review see Carvalho, 2003).…”

Section: (D) Can Khat Use Increase Vulnerability To a Schizophrenia Smentioning

confidence: 99%

Chronic khat use and psychotic disorders: A review of the literature and future prospects

Odenwald¹

2007

SUCHT

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Aims: In recent decades, the traditional habit of chewing the khat leaves, which contain the amphetamine-like cathinone, has undergone profound changes in African and Arab countries, from a socially regulated use pattern to uncontrolled consumption. This is of special public mental-health concern. In this article, a review of the scientific literature on the relationship between khat use and psychosis is provided. Results: Several case studies, but only a few group and community-based studies, have addressed this topic. The studies show inconsistent results, have methodological problems, and fail to report quantitative results. Many important questions remain unaddressed. Conclusions: The frequently stated association between khat use and psychosis contrasts with the small number of sound studies. Currently, only a few conclusions can be drawn, that excessive khat use can cause brief psychotic disorders and that people with a preexisting vulnerability should be discouraged to use it. The direction of causality between general psychopathology and khat use remains unclear. This review confirms the need for quantitative, controlled, and longitudinal studies,

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Section: (D) Can Khat Use Increase Vulnerability To a Schizophrenia Smentioning

confidence: 99%

Chronic khat use and psychotic disorders: A review of the literature and future prospects

Odenwald¹

2007

SUCHT

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“…In the second series [9] pregnant does were fed leaves from the shrub Catlta edulis Forsk. (Khat or quat) as used on the Arabian peninsula as a central stimulant because of its amphetamine-like effect.…”

Section: Methodsmentioning

confidence: 99%

Cerebral Function in the Gowth-Retarded Fetus and Neonate

Kjellmer

Thordstein²,

Wennergren³

1992

Neonatology

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Intrauterine growth retardation is associated with increased risks for permanent neurological disabilities. A series of studies was undertaken to elucidate whether fetal growth retardation causes a primary perturbation of brain function and development and whether an increased vulnerability for periods of oxygen lack exists. In two groups of neonates who were small for gestational age (SGA) evoked potentials were investigated. A high frequency of abnormal recordings were obtained in SGA babies. SGA babies had significantly longer latency periods for the primary evoked potentials than appropriately grown controls. In guinea pigs and rats growth retardation was induced by reducing the placental blood flow during late gestation. Growth retarded guinea pups demonstrated a considerable reduction of the ability to retain normal somatosensory evoked response during hypoxia compared to appropriately grown littermates. Growth retarded rat fetuses exhibited marked changes of the monoamine metabolism in the brain inasmuch as basal levels of serotonin and its main metabolite were low while an inappropriate acceleration of the serotonin synthesis rate took place during hypoxia. The tissue concentrations of aspartate were also significantly lower in growth retarded fetuses than normally grown littermates. Finally, lipid peroxidation was assessed. During adequate oxygenation no difference was observed when lipid peroxidation was assessed. During adequate oxygenation no difference was observed when lipid peroxidation in brain tissue of growth retarded and appropriately grown fetuses was compared but during mild-moderate hypoxia lipid peroxidation was significantly more intense in the growth retarded group. In conclusion, studies on SGA babies bring forward primary consequences of growth retardation on cerebral function and animal studies provide evidence both for a deficiency of factors that support brain growth and for some mechanisms that may be related to a decreased tolerance towards oxygen deficiency.

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