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1/10. amyotrophic lateral sclerosis: Lou Gehrig's disease.

    amyotrophic lateral sclerosis (ALS), commonly called Lou Gehrig's disease, is a progressive neuromuscular condition characterized by weakness, muscle wasting, fasciculations and increased reflexes. Approximately 30,000 Americans currently have the disease. The annual incidence rate is one to two cases per 100,000. The disease is most commonly diagnosed in middle age and affects more men than women. It usually presents with problems in dexterity or gait resulting from muscle weakness. Difficulty in speaking or swallowing is the initial symptom in the bulbar form of the disease. Over a period of months or years, patients with ALS develop severe, progressive muscular weakness and other symptoms caused by loss of function in both upper and lower motor neurons. Sphincter control, sensory function, intellectual abilities and skin integrity are preserved. patients become completely disabled, often requiring ventilatory support and gastrostomy. death usually occurs within five years of diagnosis and is attributed to respiratory failure or cachexia. The etiology of the disease is unknown. Current research is focused on abnormalities of neuronal cell metabolism involving glutamate and the role of potential neurotoxins and neurotrophic factors. New drugs are being developed based on these theories. Current management involves aggressive, individualized alleviation of symptoms and complications.
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2/10. diagnosis and treatment of multiple sclerosis and amyotrophic lateral sclerosis: neuropathies from bordetella pertussis.

    Having found positive the research for anti-Bordetella antibodies in the 95.47% of 92 patients affected by defined multiple sclerosis and in the 100% of 55 patients affected by non-patched neuropathies (amyotrophic lateral sclerosis and correlated neuropathies), I reassessed the pathogenesis of the neuropathies from bordetella pertussis. In the two categories of neuropathies (with and without patches), the beginning pathogenetic mechanisms are the same: 1) pertussis re-infection in patients with mucociliary barrier defect; 2) pertussis toxins passage in the blood; and 3) formation of circulating immune complexes. In multiple sclerosis, astrocytes produce class II human leukocyte antigens, the endothelia of the small brain vessels show the "adhesion molecules," and the immune complexes fall in the central nervous system (patches are formed). In amyotrophic lateral sclerosis and in the other non-patched neuropathies, the astrocytes do not produce the class II human leukocyte antigens, the endothelia do not show adhesion molecules, and immune complexes do not fall in the central nervous system; but they increase in blood until they inhibit the ulterior antibodies production. For relative antibodies lack, pertussis toxins fix directly on neuro-epithelia; their pathogenic power and physiopathologic astrocytes role in the central nervous system produce the damage. With a blood sample, we can assess Bordetella etiology. In all these neuropathies, an extended antibiotic therapy to clear mucosae and to prevent reinfections is necessary.
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3/10. Mechanical trauma as a risk factor in classic amyotrophic lateral sclerosis: lack of epidemiologic evidence.

    We have examined the relationship between mechanical injuries and the subsequent development of classic amyotrophic lateral sclerosis (ALS) through a critical review of the literature. Only prospective evaluation of a large cohort of trauma victims can provide an unbiased answer to this controversy. However, such an evaluation would be prohibitively expensive, and the results would not be available in our lifetime. The results of retrospective case-control studies are conflicting in part because of biases in the selection of patients and controls, poor definition of the nature and extent of the trauma and its chronological relationship to the onset of ALS, and a non-uniform approach to the collection of antecedent information. More rigorously designed studies show no association of ALS to antecedent trauma. The existing data thus do not suggest that mechanical trauma is a risk factor for ALS. Future case-control studies should conform to a standardized methodology. The critical analysis presented here of the research on the purported connection between mechanical injury and ALS may serve as a model for the evaluation of the role of trauma in other chronic diseases. Application of these methodological principles may bring increased scientific rigor to assessing the frequently litigated question of what constitutes a true trauma sequela.
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4/10. Early respiratory insufficiency in the ALS patient: a case study.

    respiratory insufficiency is a problem that develops in nearly all people diagnosed with amyotrophic lateral sclerosis (ALS). Noninvasive positive pressure ventilation (NIPPV) is the treatment of choice for ALS patients with respiratory insufficiency. Forced vital capacity (FVC) is the test most commonly used to qualify ALS patients for NIPPV; however, some research suggests FVC may not be the best tool to measure early respiratory insufficiency in all patients with ALS. This case study introduces an ALS patient who had normal FVC results, symptoms of respiratory insufficiency, and abnormal nocturnal oximetry. After NIPPV initiation, the patient reported improved sleep and less daytime fatigue, which he associated with the start of NIPPV treatment.
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5/10. Neural internet: Web surfing with brain potentials for the completely paralyzed.

    Neural internet is a new technological advancement in brain-computer interface research, which enables locked-in patients to operate a web browser directly with their brain potentials. Neural internet was successfully tested with a locked-in patient diagnosed with amyotrophic lateral sclerosis rendering him the first paralyzed person to surf the internet solely by regulating his electrical brain activity. The functioning of Neural internet and its clinical implications for motor-impaired patients are highlighted.
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6/10. schizophrenia and amyotrophic lateral sclerosis.

    schizophrenia and amyotrophic lateral sclerosis (ALS) are central nervous system (CNS) disorders of unknown etiology. The association of these two disorders has been infrequently reported in the literature, but is not a rare occurrence. Various neuromuscular abnormalities involving the alpha-motor neuron have been described in some patients with schizophrenia. This report reviews the literature on schizophrenia, psychosis, and ALS and describes two additional cases of schizophrenia associated with ALS. The possibility that the neuromuscular dysfunction in schizophrenia may predispose to ALS and provide an explanation for the association of these two disorders is discussed. Additional research data are needed to test this hypothesis.
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7/10. Neuropsychological perspectives in amyotrophic lateral sclerosis.

    Three aspects of neuropsychological functioning in patients with ALS are examined. Contrary to previous research, a new psychometric study of psychological adjustment suggested significant depression-distress in this population and related psychological disturbance differentially to signs of upper versus lower motor neuron involvement and to respiratory failure. An association between ALS and impaired neuropsychological functioning is discussed through an examination of the clinical and pathologic literatures. ALS appears to be a multisystem degenerative disease with a variety of expressions that may frequently include loss of cognitive-behavioral competency with progressive involvement of the prefrontal cortex and, in a few instances, profound dementia. Finally, the article describes an analysis of trends in psychological adjustment and in the perception of physical capability over the course of a pilot clinical trial.
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8/10. carcinoma of the prostate and motor neuron disease.

    Non metastatic neurological concomitants of tumors are well known. They include an amyotrophic lateral sclerosis (ALS)-like syndrome in association with various tumors. The association with prostatic carcinoma is very rare. The case reported here seems to confirm the outcome of epidemiological research: the association is fortuitous.
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9/10. cognition, language, and speech in amyotrophic lateral sclerosis: a review.

    amyotrophic lateral sclerosis (ALS) is a progressive, adult-onset neurodegenerative disorder manifesting as a relentless loss of motor capabilities and, ultimately, death. Traditionally thought to affect solely the lower motor neurons and corticospinal tracts, recent studies suggest that the pathogenic process of ALS is more extensive, involving dysfunction of cortical grey and white matter with clinical correlates of impairment in cognition and language. The impact of speech and motor deficits are discussed in relation to the issues of assessment of cognition and language. Three case studies are presented for illustrative purposes. Finally, direction for future research to investigate cognitive dysfunction in ALS are presented.
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10/10. A clinicopathological study of a patient with familial amyotrophic lateral sclerosis associated with a two base pair deletion in the copper/zinc superoxide dismutase (SOD1) gene.

    The recognition of mutations in the copper/zinc superoxide dismutase (SOD1) gene in familial amyotrophic lateral sclerosis (FALS) has been a landmark in ALS research. We report a clinicopathological study of a female patient with FALS showing a two base pair deletion in exon 5 of the SOD1 gene. Her clinical course was rapid and she died 2 years after the onset. The SOD1 activity was down to 30% of the normal level. Western blot analysis did not reveal the mutant protein which was expected to be approximately 2.4 kDa smaller than normal SOD1 protein in molecular mass. In contrast to the neuropathological findings of the previously reported cases showing the same mutation, our case was characterized by sparing of the dorsal column and the presence of only a modest number of intracytoplasmic eosinophilic inclusions showing weak or partial immunoreaction for neurofilament and negative reaction for SOD1. Thus, the same mutation in the SOD1 gene does not necessarily induce consistent pathological changes in the central nervous system.
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