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H Altenkirch

Publications and source records attributed to H Altenkirch.

At least 19 recordsLinked to original sources

Multiple chemical sensitivity (MCS)--differential diagnosis in clinical neurotoxicology: a German perspective.

The multiple chemical sensitivity syndrome (MCS) is a new cluster of environmental symptoms which have been described and commented on for more than 15 years now in the USA. In the meantime it has also been observed in European countries. The main features of this syndrome are: multiple symptoms in multiple organ systems, precipitated by a variety of chemical substances with relapses and exacerbation under certain conditions when exposed to very low levels which do not affect the population at large. There are no lab markers or specific investigative findings. In our view, MCS is not a separate clinical syndrome but a collective term. A very small part of the patients in question may actually exhibit a somatic or psychosomatic response to low levels of a variety of chemicals in the environment. For another part, even if the MCS symptoms are induced by chemical substances in the environment, the basic hypersensitivity is a psychological stress reaction. In the third and largest group, the patients have been misdiagnosed, i.e. a somatic or psychiatric disease has been overlooked. There is a fourth group of patients in whom there is no evidence of any exposure at all but instead a belief system installed by certain physicians, the media and other groups in society. This paper tries to describe the neurological and neurotoxic aspects of MCS problems and to illustrate it with examples of an alleged outbreak of chronic neurotoxic disease caused by pyrethroids in Germany. Research strategy should establish clearly determined diagnostic criteria, agreement on the use of specific questionnaires as well as clinical and technical diagnostic procedures, prospective clinical studies of MCS patients and comparative groups as well as experimental approaches.

Adolescent↗

[Multiple chemical sensitivity syndrome].

The multiple chemical sensitivity syndrome (MCS) is a novel constellation of symptoms in environmental medicine that has been extensively described and commented on in the USA. The main features of this syndrome are: multiple symptoms in different organ systems triggered by a variety of chemical substances, with relapses and exacerbations under certain precipitating circumstances at very low levels which do not cause any reactions in the population at large. There are no lab markers or specific investigative findings. This paper describes the historical development of the term MCS, its diagnostic criteria and pathophysiological aspects using 10 patient histories from our hospital.

Adult↗

PCBs have a predominantly neurotoxic effect on dissociated cultures of the nervous system.

Although their manufacture and use have been restricted or banned in Europe and the United States since the 1970s, polychlorinated biphenyls (PCBs) are still an ubiquitous environmental contaminant whose low-term effects are as yet not completely clear. Clinical case studies of patients with occupational exposure report cognitive impairment and peripheral neuropathy. In our defined nerve cell culture models in which we use pure neurons, pure glia and mixed cultures prepared from dorsal root ganglia of chick embryos we observed a neurotoxic effect after the application of a PCB compound (Clophen). It was only at higher concentrations that an additional gliatoxic effect could be observed.

Animals↗

2,5-Hexanedione is a potent gliatoxin in in-vitro cell cultures of the nervous system.

Of the metabolites of hexane, 2,5-hexanedione (2,5 HD) has the strongest neurotoxic effect. There is a wealth of experimental studies in animals showing an axonotoxic mechanism consisting of an accumulation of 10 nm neurofilaments. Only few studies deal with a possible action of 2,5-HD on Schwann cells, glia cells or both. Pure neurons, pure glia and mixed cultures prepared from dorsal root ganglia (DRG) of chick embryos were studied in this model. DRG were chosen because they constitute a linkage between the peripheral and central nervous system and provide the additional advantage of containing only few defined glial and neuronal cell types. Additionally, pure neuronal cultures of sympathetic ganglia and mixed cultures of spinal cord and brain were prepared. In cultures of the different parts of the nervous system investigated, we observed at a concentration of 0.25% 2,5-HD massive toxic alterations of glial cells, whereas neurons and neurites were virtually unaffected.

Animals↗

Specific neurotoxic effects of different organic solvents on dissociated cultures of the nervous system.

Pure neurons were prepared from dorsal root ganglia (DRG) of 8 day old chick embryos (E8). The substances tested in this model were pure n-hexane, 2.5-hexanedione (2.5 HD) and methyl-ethyl-ketone (MEK). Differentiated cultures were exposed to these neurotoxins after two days in culture and then examined over a period of up to one week. For all three substances a specific neurotoxic effect could be demonstrated: (i) n-Hexane mainly altered the neurites, leading to focal swellings and in a second step to degenerative changes in glial cells; (ii) 2.5 HD had a minor effect on neurons and proved to be mainly gliatoxic; (iii) MEK primarily affected the neurons by swelling and disintegration of the cell body.

Animals↗

Type 2a fibre rhabdomyolysis in myoadenylate deaminase deficiency.

A 31-year-old woman developed an acute, potentially fatal rhabdomyolysis of undetermined origin. Muscle biopsy revealed selective lysis involving exclusively type 2a fibers. Myoadenylate-deaminase (MAD) deficiency was proven by a negative histochemical reaction as well as by an enzymatic biochemical determination. The significantly greater energetic dependence of type 2a fibres on MAD explains their selective damage. The patient's mother also suffers from a similar muscle disease of still unclarified origin.

AMP Deaminase↗

The neurotoxicological aspects of the toxic oil syndrome (TOS) in Spain.

The pathomechanism of the Spanish mass oil poisoning, which affected more than 20,000 people in the spring of 1981 and has so far caused more than 500 deaths, has not yet been clarified. Subsequent to a toxic-allergic initial phase of the disease with fever as well as lung and skin manifestations, 10 to 20% of the patients, after passing through an interval of reduced symptoms, entered a second disease phase characterized by marked vasculitis and fibrosis in diverse organ systems. The most frequent manifestation type involved in this connection was a severe neuromyopathy with pronounced joint contractures and skin alterations. A survey of the disease course is presented on the basis of our own examinations at the Centro Especial Ramon y Cajal as well as morphological studies on nerve-muscle and brain tissue, chemical analysis studies with oil samples from affected families and the literature available so far.

Animals↗

Inhalant abuse and heroin addiction: a comparative study on 574 opiate addicts with and without a history of sniffing.

In the present study, a comparison relating to various social aspects was made between 74 opiate addicts who had abused or continued to abuse solvents and 500 fixers without sniffing experience (SE). The results show clear differences between the two groups with reference to age, sex, social status, socialization conditions, family structure, education, vocational training, drug sequence and criminality as well as attitude and motivation towards withdrawal therapy. Contrary to hitherto existing assumptions, solvent abuse among children and juveniles can lead to opiate addiction, given a certain set of social circumstances. Polytoxicomanic opiate addicts with sniffing experience can be differentiated as a marginal group with particularly unfavorable developmental conditions and a specific course of addiction. The results make it clear that a stronger differentiation is necessary within the group of heroin addicts, which has often been regarded as being homogeneous.

Adolescent↗

Ultrastructural alteration of intrapulmonary nerves after exposure to organic solvents. A contribution to 'sniffers disease'.

The effects of the solvents n-hexane, butanone (methyl-ethyl-ketone, MEK) and a mixture of both in the intrapulmonary nerve system of rats were studied by light and electron microscopy. The alteration in the fine structures of the tissue consisted in a disseminated swelling of axons due to a striking multiplication of neurofilaments. Nonspecific axonal alterations could be demonstrated as well. The latter consisted in clusters of phospholipid material within the axoplasm of nerve fibers and the cytoplasm of Schwann cells plus an accumulation of glycogen granules in the axoplasm. Additionally, single degenerative changes of Schwann cells were observed. An enzyme-associated metabolic damage with a concomitant impairment of axonal flow is discussed as a possible underlying pathomechanism.

Animals↗

Nervous system responses of rats to subchronic inhalation of N-hexane and N-hexane + methyl-ethyl-ketone mixtures.

The effects of long-term continuous and intermittent inhalation exposure to selected concentrations of n-hexane and mixtures of n-hexane and methyl-ethyl-ketone (MEK) on the nervous system of rats were investigated. Animals exposed continuously (24 h/d, 7 d/week) to 500 ppm n-hexane displayed complete hindlimb paralysis after 9 weeks. Histological examination showed hexacarbon-specific axonal lesions in peripheral nerves, particularly tibial branches to calf muscles, and in the gracile tract at cervical levels of the spinal cord. Similar clinical and pathological signs of neuropathy appeared one week earlier in animals treated with a mixture of 500 ppm n-hexane/MEK (4:1 or 3:2) and 5 weeks earlier with 700 n-hexane/MEK mixture (5:2) or 700 ppm of n-hexane alone. Rats exposed to the latter concentrations intermittently, 8 hours daily for 40 weeks, did not develop clinical or morphological signs of a hexacarbon neuropathy.

Animals↗

Ultrastructural alteration of the alveolar epithelium after exposure to organic solvents.

Adult rats were exposed to the solvents n-hexane and methylethylketone (MEK) in different concentrations. Lung tissue was examined systematically after various periods by electron microscopy. The direct toxic effect to pneumocytes could be demonstrated as definite regressive alterations, such as fatty degeneration and changes of lamellar bodies of type II pneumocytes as well as increased detachment of cells. Besides these findings, after chronic inhalation of solvents conspicuous aggregation of lamellar discharge material of type II pneumocytes can be seen, and probably, as a result of an irritated fat metabolism, large lysosome-like bodies with densely packed lipid material appear in type I pneumocytes. The most distinguished changes could be demonstrated after exposure to a mixture of n-hexane and MEK, while they were less obvious after n-hexane alone. The observation suggests a profound enzymatic irritation of metabolism.

Animals↗