A syndrome simulating encephalitis affecting childrenrecovering from malnutrition (Kwashiorkor)

Kahn, E.; Falcke, H. C.

doi:10.1016/s0022-3476(56)80054-1

Cited by 24 publications

(6 citation statements)

References 4 publications

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“…A similar situation of a tremor appearing after treatment has been seen in African children recovering from protein-calorie malnutrition, but this does not seem to be related to cobalamin deficiency (33,34).…”

Section: -Methylene-thf Sammentioning

confidence: 51%

“…Neurological deterioration after the commencement of cobalamin therapy has been reported in adult patients with pernicious anemia (19) and children with inborn errors of cobalamin metabolism. In the report of Hall (26) A similar situation of a tremor appearing after treatment has been seen in African children recovering from protein-calorie malnutrition, but this does not seem to be related to cobalamin deficiency (33,34).…”

Section: Discussionmentioning

confidence: 76%

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The neurological syndrome of infantile cobalamin deficiency: Developmental regression and involuntary movements

Grattan-Smith

Wilcken²,

et al. 1997

Movement Disorders

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Developmental regression is the presenting symptom of most infants with cobalamin (Vitamin B12) deficiency. We present a report of three infants with cobalamin deficiency in which the infants also developed a movement disorder. In each case the mother was a vegetarian and the infant was exclusively breast-fed. In two of the infants, a striking movement disorder consisting of a combination of tremor and myoclonus particularly involving face, tongue, and pharynx appeared 48 h after the initiation of treatment with intramuscular cobalamin. This was associated with marked changes in plasma amino acid levels. Paradoxically, the onset of the movement disorder coincided with overall neurological improvement. The third infant had a persistent focal tremor, which appeared before the commencement of treatment. The movements slowly abated during a 3-6 week period. The presence of a movement disorder in cobalamin deficiency has received less attention than other features, but in a mild form is probably common. It may offer an early clue to the diagnosis before the onset of profound neurological deterioration. The cause of the severe movement disorder that can appear after treatment is not known.

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Section: -Methylene-thf Sammentioning

confidence: 51%

Section: Discussionmentioning

confidence: 76%

The neurological syndrome of infantile cobalamin deficiency: Developmental regression and involuntary movements

Grattan-Smith

Wilcken²,

et al. 1997

Movement Disorders

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“…The transient pseudo-Parkinsonism seen in children during recovery from malnutrition (Kahn 1954, Kahn and Falcke 1956, Udani 1960 has not been observed in the pigs. Experiments with dogs indicate, however, that if the malnourished state is established at an early stage (intra-uterine or before weaning), such a syndrome may appear (Meyer et al 1961a).…”

Section: Discussionmentioning

confidence: 96%

“…Evidence of involvement of the central nervous system, other than mental changes, has been reported only rarely and then mainly during recovery from severe protein-calorie deficiency (Kahn 1954, Kahn and Falcke 1956, Udani 1960. Neuropathological observations in cases of marasmus and kwashiorkor are few , Trowel1 et al 1954, Udani 1962 and probably one of the best descriptions of the response of the central nervous system to severe protein-calorie deficiency is still that given by Jackson (1925) for inanition.…”

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confidence: 99%

Experimental Protein‐Calorie Deficiency Clinical, Electroencephalographic and Neuropathological Changes in Pigs

Piatt

Pampiglione

Stewart

1965

Develop Med Child Neuro

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SUMMARY A report is given of the clinical and electroencephalographic findings and the histo‐pathological changes observed in the spinal cords in pigs maintained from about 2–3 weeks of age on protein‐calorie‐deficient diets. The deficient animals were very small compared with normal pigs of the same age, their skin was dry, scaly, wrinkled and crackled, and their hair was coarse and long. Their hind legs became stiff and the pigs walked with a ‘hobble‐skirt’ gait. In the more severe examples appetite failed, the animals became listless, some inco‐ordination of the hind legs developed, and sudden collapse and death occasionally occurred. In the EEGS of the deficient pigs there was a marked decrease in the fast components, the dominant frequencies being 4–15 c/s instead of 20 to 40 c/s as in the normal animals. In the spinal cord the neuroglial cells were increased in number, their nuclei showed signs of activation, and in severe cases there was a proliferation of astrocytic fibres. Chromatolysis, pronounced satellitosis, reduced staining of the nuclei and occasionally Nissl's ‘severe change’ were seen in and around the motor cells. Many of the changes (clinical, EEG and histological) were reversible, but the possibility of permanent stigmata brought about by protein‐calorie‐deficient regimens in early life cannot be ignored. RÉSUMÉ Déficience experimentale en calories‐proteines Les auteurs exposent les résultats de leur étude clinique et encéphalographique, ainsi que les changements histopathologiques observés dans la moelle épinière de pores maintenus à des régimes déficients en calories‐proteines depuis l'âge de 2 à 3 semaines. Les animaux déficients étaient très petits en comparaison des pores normaux du même âge, leur peau était sèche, écailleuse, ridée et craquelée et leurs poils étaient gros et longs. Les membres postérieurs se raidissaient, leur démarche était comme entravée. Dans les cas les plus sévères l'appétit tombait, les animaux devenaient nonchalents, une certaine incoordination des membres postérieurs apparaissait, suivie parfois d'affaissement et mort soudaine. Dans les EEG des pores déficients il y avait une diminution marquée des composés rapides, les fréquences dominantes étant de 4–15 c/s au lieu de 20 c/s à 40 c/s comme chez les animaux normaux. Dans la moelle épinière les cellules de la névroglie étaient en nombre accru, leurs noyaux montraient des signes d'activité et dans les cas sévères il y avait prolifération de fibres astrocytiques. Chromatolyse, satellitose prononcée, faible coloration des noyaux et, à l'occasion, ‘changements sévères’ des corps de Nissl étaient décelés à l'intérieur et autour des cellules motrices. La plupart de ces changements étaient réversibles (changements cliniques, EEG et histologiques), mais la possibilité de stigmates permanents dûs aux régimes déficients en proteines au début de la vie ne peut être ignorée. ZUSAMMENFASSUNG Experimenteller Protein‐Kalorienmangel Darlegung der klinischen und elektro‐enzephalographischen Befunde sowie der histopathologischen V...

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“…Brown (1965Brown ( , 1966 has collected data for Baganda children at autopsy and finds that, whereas the brain weight relative to bodyweight is high in the malnourished child, the weight for age is low. A transient 'pseudoparkinsonism', with tremors of the hands, has been described by Kahn (1954Kahn ( , 1957 and Kahn and Falcke (1956) in children recovering from kwashiorkor, and neurological manifestations have been described during the active phase of the condition by Udani (1960). Udani has found histological changes in the central nervous system very similar to those described in the malnourished pigs (Platt 19 and Stewart 1960, Platt et af.…”

Section: Discussionmentioning

confidence: 99%

Effects of Protein‐Calorie Deficiency on Dogs 1. Reproduction, Growth and Behaviour

Platt

Stewart

1968

Develop Med Child Neuro

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SUMMARY Dogs maintained from weaning on diets of low protein value grow slowly and develop changes in their bones, brains and behaviour. When they reach adulthood the protein‐calorie deficient bitches produce smaller and fewer pups per litter than do well‐nourished littermates. If the congenitally malnourished offspring are given diets of low protein value, they show more marked abnormalities than do pups born of normal mothers and given at weaning diets of similar protein value. The pups have an abnormal gait, especially of the hind legs, run and follow less readily and tire more easily than normal animals, and athetoid movements of the head and neck are common. Exercise exacerbates the abnormalities and in some instances convulsive seizures have occurred. The intensity of the changes reaches a peak at about 2 to 3 months of age and the more acute manifestations then recede but do not fully disappear. Many of the abnormalities of gait, growth and EEG pattern disappear when the deficient animals are given diets of high protein value. The most marked recovery occurs amongst animals born of normal mothers and subjected to a period of protein‐calorie deficiency after weaning. In contrast, congenitally malnourished puppies, even when they are given diets of high protein value from weaning, remain small and it is suggested that full recovery may never occur. Rehabilitated dogs, even when adult, are often obese, with short legs; they remain somewhat apprehensive and mix less well than normal dogs. The possible implications for man are discussed. RÉSUMÉ Les chiens maintenus à partir du sevrage avec des régimes pauvres en proteines grandissent lentement et subissent des changements dans leurs os, leur cerveau et leur comportement. Lorsqu'elles atteignent 1′âge adulte, les chiennes déficientes en calories‐proteiniques produisent des chiots plus petits et moins nombreux à chaque portée que leurs soeurs bien nourries. Si les descendants congénitalement mal‐nourris reçoivent des régimes de faible valeur proteinique ils ont des anomalies plus marquées que les chiots nés de mères normales et nourris depuis leur sevrage selon des régimes de valeur proteinique similaire. Les chiots ont une démarche anormale, affectant surtout les membres postérieurs, ils courent et suivent moins facilement et se fatiguent plus vite que les animaux normaux; les mouvements athétoides de la tête et du cou sont communs. L'exercice exagère les anomalies et des crises convulsives sont survenues quelques fois. L'intensité des changements atteint son maximum à environ 2 à 3 mois, puis les manifestations les plus aigues régressent mais ne disparaissent pas complètement. Beaucoup des anomalies de démarche, croissance et EEG disparaissent lorsque les animaux déficients reçoivent des régimes de haute valeur proteinique. Les guérisons les plus marquées se produisent chez les animaux nés de mères normales et soumis à une période de carence en proteine après leur sevrage. Au contraire, les chiots congénitalement malnourris, même s'ils reçoivent des régimes de ...

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A syndrome simulating encephalitis affecting childrenrecovering from malnutrition (Kwashiorkor)

Cited by 24 publications

References 4 publications

The neurological syndrome of infantile cobalamin deficiency: Developmental regression and involuntary movements

The neurological syndrome of infantile cobalamin deficiency: Developmental regression and involuntary movements

Experimental Protein‐Calorie Deficiency Clinical, Electroencephalographic and Neuropathological Changes in Pigs

Effects of Protein‐Calorie Deficiency on Dogs 1. Reproduction, Growth and Behaviour

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