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J C Christensen

Publications and source records attributed to J C Christensen.

8 recordsLinked to original sources
PubMed1977

[Campimetric changes in optic radiation lesions].

Visual field defects may be congruous or not in lesions affecting the optic radiation. This fact, and the macular sparing found in some cases, can be explained if the optic radiation is envisaged as formed by three layers, the superficial corresponding to homolateral peripheral vision, the intermediate to contralateral peripheral vision, and the deepest to central vision from both hemimaculae. The fibers of all these layers fan out sequentially, first the more superficial, then the deeper, around the posterior part of the lateral ventricles, following a longitudinal plane of divergence in their way to area 17. The progressive displacement, upwards and downwards, of the thick fibers transmitting peripheral vision, leave out finally the thin fibers for central vision as the sole constituents of the central and terminal part of the optic radiation. As supporting evidence of this conception we have the fact that if the optic radiation is encroached on from its outer side (as it generally happens for reasons stated in the full text) visual field defects tend to be larger in the homolateral field. This holds true for temporal and parietal lesions, and to a lesser degree for occipital lesions. Deep lesions (for instance intraventricular tumours) tend to affect first the deeper strata of the optic radiation (macular vision and/or contralateral quadrants of peripheral vision). The schematic drawings presented allow us to understand how a temporal lesion may produce: a) no visual field defect, b) an upper homonimous quadrantopsia, c) a lower homonimous quandrantopsia, d) a homonimous hemianopsia; and that these field defects can be either congruent or uncongruous. Deep parietal lesions will produce visual field defects in the lower quadrants, which may be congrous or not. As the visual fibers for macular vision are deeply located in the optic radiation, forming a thin but wide layer in the vertical plane, they cannot be affected to a significative extent without the more superficial fibers for peripheral vision being also affected to an even greater extent. Due to the width and depth of this macular layer even in extensive lesions of the optic radiation some of its fibers can escape injury. This can explain macular sparing in some cases without resorting to hypothetical bilateral macular representation which is deemed unacceptable. Anatomical data and clinical examples are given which lend support to all these contentions.

Epilepsy↗
PubMed1976

After three years.

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Education, Nursing↗
PubMed1975

Multiple sclerosis: some epidemiological clues to etiology.

The diagnosis of multiple sclerosis is frequently made with undue haste and without a firm basis. A false positive diagnosis is made in about 20 to 30% of the cases originally labeled as multiple sclerosis. The proportion of false positive diagnosis is probably still higher in countries where this disease is less frequent. An exhaustive investigation (neurological, clinical, neurorradiological, isotopic, etc.) is necessary before accepting such a diagnosis. This is particularly important because many of the lesions which can masquerade as multiple sclerosis are amenable to medical or surgical treatment. The prevalence of multiple sclerosis varies widely throughout the world, with a very definite preference for the white race. This difference seems to be caused, at least in part, by dietary habits. Lack of breastfeeding and excessive consumption of cow's milk during infancy is postulated as an important factor in the appearance of multiple sclerosis later in life. A lack of essential fatty acids (and may be of certain minerals and vitamins) in such a diet during pregnancy and childhood may result in the synthesis of abnormally unstable myelin. This underlying deficiency in myelin composition may be the substrate on which immunological factors act to produce the disease. The breakdown of this unstable myelin may be initiated by a variety of factors; natural decay of abnormally weak bonds in proteolipids, viral infection, immune reactions or even trauma. Immune reactions can explain, at least in part, the onset and the course of the disease, and probably immunodeficiency is the most important factor. Demyelination, once it starts, may continue until all abnormally formed myelin is destroyed, or until the building up of immunological defenses can stop the process. It follows from this that prevention of multiple sclerosis should be based mainly on dietic measures which ensure a sufficient supply of essential fatty acids, minerals and vitamins, during pregnancy and childhood. Breast feeding is probably the most important preventive factor. Skin pigmentation, either natural or from exposition to sunshine also seems to act as a preventive factor, and its mode of action deserves further investigation. Treatment of multiple sclerosis should be based on the improvement of immunological defenses, the elimination of possible allergens and saturated fats from the diet, and on the administration of sufficient amounts of essential fatty acids and of other various elements.

Adolescent↗