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1/9. Rhodesian trypanosomiasis in a splenectomized patient.

    We report the first apparent case of a splenectomized individual who developed severe trypanosomiasis with central nervous system involvement. The patient was a 41-year-old man who participated in an east African safari. Upon his return to the united states, the patient presented with an infection with trypanosoma brucei rhodesiense that was treated successfully with suramin and melarsoprol. The onset of symptoms, laboratory studies, and disease progression did not differ from previously reported cases in the literature. The role of the spleen in trypanosomiasis is not well understood and the few reports available describe only animal models. This report suggests that asplenia had no apparent effect on the onset of symptoms and overall severity of illness. Further studies are necessary to ultimately define the role of the spleen in trypanosomiasis.
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2/9. central nervous system magnesium deficiency.

    The central nervous system concentration of magnesium (Mg ) appears to have a critical level below which neurologic dysfunction occurs. Observations presented suggest that the interchange of the Mg ion between the cerebrospinal fluid, extracellular fluid, and bone is more rapid and dynamic than is usually believed. This is especially so when the hypertrophied parathyroid gland is associated with significant skeletal depletion of Mg as judged by history rather than serum level. Magnesium, much like calcium, has a large presence in bone and has a negative feedback relationship with the parathyroid gland. A decline in central nervous system Mg may occur when the skeletal buffer system orchestrated largely by the parathyroid glands is activated by an increase in serum calcium. Observations in veterinary medicine and obstetrics suggest that the transfer of Mg from the extracellular fluid into bone during mineralization processes may be extensive. If the inhibition of the hypertrophied parathyroid gland is prolonged and the skeletal depletion of Mg extreme, serious neurologic symptoms, including seizures, coma, and death, may occur. noise, excitement, and bodily contact appear to precipitate neurologic symptoms in Mg ( )-deficient human subjects as it has been documented to occur in Mg ( )-deficient experimental animals. The similarity of the acute central nervous system demyelinating syndromes with reactive central nervous system Mg deficiency is reviewed.
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3/9. Childhood giant axonal neuropathy. Case report and review of the literature.

    giant axonal neuropathy (GAN) is a rare autosomal recessive childhood disorder characterized by a peripheral neuropathy and features of central nervous system involvement. Typically seen are distal axonal swellings filled with 8-10 nm in diameter neurofilaments in central and peripheral axons, and intermediate filament collections in several other cell types. Many neurotoxins produce a morphologically similar neuropathy in humans and experimental animals. Defective nerve fiber energy metabolism has been postulated as a cause in these toxic neuropathies. It is possible that GAN represents an inborn error of metabolism of enzyme-linked sulfhydryl containing proteins, resulting in impaired production of energy necessary for the normal organization of intermediate filaments.
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4/9. Potroom palsy? Neurologic disorder in three aluminum smelter workers.

    We studied three patients with a progressive neurologic disorder, all of whom had worked for over 12 years in the same potroom of an aluminum smelting plant. All had incoordination and an intention tremor. Two of the three patients had cognitive deficits, and the most severely affected patient also had spastic paraparesis. None had involvement of the peripheral nervous system. Despite extensive evaluations, the cause of these patients' problems remains obscure. It is tempting to implicate one of the numerous substances to which the patients were exposed in the potroom, but none is known to cause the neurologic problems seen in these patients. Neurotoxic effects of aluminum in animals are directed at the central nervous system, and theoretically long-term low-level exposure to aluminum in the potroom could explain the findings in our patients.
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5/9. paraparesis following intrathecal chemotherapy.

    We studied a case of flaccid paraplegia that immediately followed intrathecal injection of cytosine arabinoside diluted in 1.5% bacteriostatic water (1.5% benzyl alcohol in H2O). The complication was reversed by rinsing the CSF space with saline. autopsy showed fibrosis and remyelination of lumbosacral nerve roots. In acute and chronic animal experiments, we showed that benzyl alcohol in commercially used concentrations can have a local anesthetic and an irreversible toxic effect on nerve fibers. This provides a sufficient explanation for many cases of paraparesis following intrathecal chemotherapy.
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6/9. central nervous system and facial defects associated with maternal hyperthermia at four to 14 weeks' gestation.

    An analysis of 28 dysmorphic offspring with a retrospectively ascertained history of maternal hyperthermia during the first trimester of pregnancy showed a similarity in their pattern of CNS dysfunction and facial dysmorphogenesis. All survivors had mental deficiency and most of them demonstrated altered muscle tone, including hypotonia with increased deep tendon reflexes. Those exposed at four to seven weeks' gestation showed an increased prevalence of facial dysmorphogenesis. The duration of the high fever was usually one or more days, an unusual occurrence during the first trimester of pregnancy. The nature of these defects in relation to the relative timing of hyperthermia exposure is similar to that previously noted in animal studies. The morphogenetic implications of these findings are explored and the need for larger, controlled studies is suggested.
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7/9. central nervous system disorders and possible brain type carnitine palmitoyltransferase II deficiency.

    We describe two male infants with central nervous system disorders, i.e. infantile spasms in one and athetotic quadriplegia in the other, and with recurrent attacks of high plasma creatine kinase levels induced by viral infections. Although carnitine palmitoyltransferase I (CPT I) activity in biopsied muscle was normal in both cases, that of carnitine palmitoyltransferase II (CPT II) was decreased to 37% and 25% of the control value, respectively. Meanwhile, to determine whether or not and how CPT exists in the central nervous system (CNS), we studied animal brain tissues. CPT activity was demonstrated in almost all regions, especially in the brainstem, cerebellum and spinal cord. Although CPT deficiency can be classified into hepatic (CPT I) and muscular (CPT II) presentations, these data suggest that another symptomatology of CPT II deficiency with CNS involvement (brain type?) might exist.
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8/9. Combined central and peripheral acute demyelination.

    We describe a patient with multiple sclerosis who had a bout of central demyelination associated with an acute inflammatory demyelinating polyneuropathy. The contemporary involvement of central and peripheral nervous system due to a demyelinating disease has been reported anecdotically in humans, and can be induced experimentally in animals. It may be sustained by a common pathogenetic factor.
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9/9. Compulsive targeted self-injurious behaviour in humans with neuropathic pain: a counterpart of animal autotomy? Four case reports and literature review.

    Four cases of compulsive self-injurious behaviour (SIB) with variable degrees of tissue damage targeted to the painful body part are reported in humans with neuropathic pain. review of human literature revealed several cases, primarily after central nervous system (CNS) lesions, during which non-psychotic verbally communicating humans (mostly with intact mental status) target specifically the painful part which is usually analgesic or hypoalgesic. In few instances, however, the involved part is not only sentient but also hyperalgesic in part or as a whole. The act is characterized by uncontrollable urge and compulsion, aggravated under conditions of stress, isolation, confusion or depression, and occasionally occurring in patients with personality disorders, ongoing drug abuse and pre-existing compulsive habits (i.e., habitual nail biting or picking). It fails to be deterred by the appearance of the injured part, social mores or even the experience of pain. Successful treatment of underlying painful dysesthesiae with specific medications, neurostimulation or surgery has resulted in marked improvement of dysesthesiae accompanied by wound healing in several cases. The four presented cases and the human literature experience provide evidence that compulsive targeted SIB in humans with neuropathic pain and painful dysesthesiae is consistent with the concept that animal autotomy may result from chronic neuropathic pain after experimental peripheral or CNS lesions.
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