Cases reported "Parkinson Disease"

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1/16. AC pulsed electromagnetic fields-induced sexual arousal and penile erections in Parkinson's disease.

    Sexual dysfunction is common in patients with Parkinson's disease (PD) since brain dopaminergic mechanisms are involved in the regulation of sexual behavior. Activation of dopamine D2 receptor sites, with resultant release of oxytocin from the paraventricular nucleus (PVN) of the hypothalamus, induces sexual arousal and erectile responses in experimental animals and humans. In Parkinsonian patients subcutaneous administration of apomorphine, a dopamine D2 receptor agonist, induces sexual arousal and penile erections. It has been suggested that the therapeutic efficacy of transcranial administration of AC pulsed electromagnetic fields (EMFs) in the picotesla flux density in PD involves the activation of dopamine D2 receptor sites which are the principal site of action of dopaminergic pharmacotherapy in PD. Here, 1 report 2 elderly male PD patients who experienced sexual dysfunction which was recalcitrant to treatment with anti Parkinsonian agents including selegiline, levodopa and tolcapone. However, brief transcranial administrations of AC pulsed EMFs in the picotesla flux density induced in these patients sexual arousal and spontaneous nocturnal erections. These findings support the notion that central activation of dopamine D2 receptor sites is associated with the therapeutic efficacy of AC pulsed EMFs in PD. In addition, since the right hemisphere is dominant for sexual activity, partly because of a dopaminergic bias of this hemisphere, these findings suggest that right hemispheric activation in response to administration of AC pulsed EMFs was associated in these patient with improved sexual functions.
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2/16. hallucinations in Parkinson's disease: prevalence, phenomenology and risk factors.

    hallucinations, mainly of a visual nature, are considered to affect about one-quarter of patients with Parkinson's disease. They are commonly viewed as a side-effect of antiparkinsonian treatment, but other factors may be involved. The aim of this study was to determine the phenomenology, prevalence and risk factors of hallucinations in Parkinson's disease. Two-hundred and sixteen consecutive patients fulfilling clinical criteria for Parkinson's disease were studied. Demographic and clinical variables were recorded, including motor and cognitive status, depressive symptoms and sleep-wake disturbances. patients with and without hallucinations were compared using non-parametric tests, and logistic regression was applied to significant data. hallucinations had been present during the previous 3 months in 39.8% of the patients, and fell into three categories: minor forms, consisting of a sensation of a presence (person), a sideways passage (commonly of an animal) or illusions were present in 25.5% of the patients (an isolated occurrence in 14.3%), formed visual hallucinations were present in 22.2% (isolated in 9.3%) and auditory hallucinations were present in 9.7% (isolated in 2.3%). patients with minor hallucinations had a higher depression score than non-hallucinators but did not differ in other respects. Logistic regression analysis identified three factors independently predictive of formed visual hallucinations: severe cognitive disorders, daytime somnolence and a long duration of Parkinson's disease. These findings indicate that, when minor hallucinations are included, the total prevalence is much higher than previously reported. A simple side-effect of dopaminergic treatment is not sufficient to explain the occurrence of all visual hallucinations. The main risk factor in treated patients is cognitive impairment, although sleep-wake cycle disturbances, and possibly other factors related to the duration of the disease, act as cofactors.
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3/16. The protective role of levodopa in the human substantia nigra.

    Laboratory studies and studies of animal models of parkinsonism have produced contradictory evidence, but there is no evidence that LD is toxic to normal substantia nigra in animals. We have studied human subjects longitudinally to address that issue. A cumulative LD dose up to 24 kg was not toxic in one autopsied essential tremor (ET) case. Two other ET patients did not develop parkinsonism on 8.5 kg and 21 kg cumulative LD dose, respectively. One DOPA-responsive dystonia (DRD) case has no evidence of parkinsonism after 29 years and more than 17 kg of LD. A DRD patient who received 3 kg over 11 years had normal SN neuronal complement at autopsy. One patient who has clinical and laboratory evidence of nigral pathology as the basis of parkinsonism when untreated for 18 years had progressive disability. While on LD he has excellent symptomatic benefit and virtual cessation of progression of the disease. epidemiologic studies indicate that those prescribed LD at an early stage of illness and hence given larger cumulative lifetime doses have longer survival than those in whom LD is started late and who receive smaller total doses. Our observations and the available literature support that levodopa is not toxic to normal or diseased substantia nigra in human beings. Evidence presented here indicates that levodopa has a protective effect on the human substantia nigra neurons.
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4/16. Tactile hallucinations in Parkinson's disease.

    hallucinations occur in up to 40% of patients with Parkinson's disease (PD) and are mainly of a visual nature. We prospectively studied 8 patients with PD and tactile hallucinations (TH). TH occurred with a clear sensorium, and were long-lasting. In most cases they involved animals, were combined with other types of hallucinations occurring simultaneously (mainly formed visual hallucinations), and predominated in the evening and/or at night. Pharmacological and disease-related factors, including a disorder in rapid-eye-movement sleep mechanisms, could play a part in the pathophysiology of these hallucinations.
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5/16. Weak magnetic fields in the treatment of Parkinson's disease with the "on-off" phenomenon.

    Application of external weak magnetic fields recently has been reported to be efficacious in the treatment of a 62-year-old patient with idiopathic Parkinson's disease (PD) complicated by levodopa-induced fluctuations in motor response ("on-off"). I report an additional case of a 67-year-old man with idiopathic PD and levodopa-related motor fluctuations who likewise experienced marked and sustained improvement in Parkinsonian symptoms and amelioration of "on-off" symptoms following the application of external weak magnetic fields. Based on these observations it is concluded that artificial weak magnetic fields may be beneficial for the treatment of PD complicated by levodopa-related "on-off" phenomenon. Furthermore, since in experimental animals external magnetic fields alter the secretion of melatonin, which in turn has been shown to regulate striatal and mesolimbic dopamine-mediated behaviors, it is proposed that the antiParkinsonian effects of weak magnetic fields are mediated via the pineal gland.
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6/16. Magnetic fields mimic the behavioral effects of REM sleep deprivation in humans.

    The discovery of rapid eye movement (REM) sleep by Aserinsky and Kleitman in 1953 initiated the impetus for sleep research and specifically the investigations of the effects of REM sleep deprivation (RSD) on animal and human behavior. The behavioral effects of RSD include the enhancement of motivational and "drive"-related behaviors. In laboratory animals, RSD has been reported to increase appetite, sexual behavior, aggressiveness, and locomotor activity. Moreover, RSD reportedly improves mood in patients with endogenous depression and heightens appetite and sexual interest in normal subjects. Since "drive"-related behaviors are thought to involve activation of limbic dopaminergic reward sites, RSD may enhance motivational behaviors through an action on limbic dopaminergic functions. In the present communication, we present two patients (one with multiple sclerosis and the other with Parkinson's disease) in whom treatment with magnetic fields produced behavioral effects which paralleled those observed in REM-sleep-deprived animals and humans. We propose, therefore, that the behavioral and mental effects of treatment with magnetic fields may be mediated via RSD and, by inference, involve activation of limbic dopaminergic reward sites.
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7/16. Magnetic fields in the treatment of Parkinson's disease.

    levodopa-induced dyskinesias are a common complication of chronic dopaminergic therapy in patients with Parkinson's disease (PD). The overall prevalence of levodopa-induced dyskinesias ranges from 40%-90% and is related to the underlying disease process, pharmacologic factors, and to the duration of high dose levodopa therapy. The mechanisms underlying the emergence of levodopa-induced dyskinesias are unknown, although most investigators favor the theory that striatal dopamine receptor supersensitivity is directly responsible for the development of these abnormal movements. In laboratory animals, the pineal hormone melatonin has been shown to regulate striatal dopaminergic activity and block levodopa-induced dyskinesias (Cotzias et al., 1971). Since the pineal gland is known to be a magnetosensitive organ and as application of external magnetic fields has been shown to alter melatonin secretion, we studied the effects of application of external artificial weak magnetic fields in a Parkinsonian patient with severe levodopa-induced dyskinesias ("on-off"). Application of weak magnetic fields with a frequency of 2 Hz and intensity of 7.5 picotesla (pT) for a 6 minute period resulted in a rapid and dramatic attenuation of Parkinsonian disability and an almost complete resolution of the dyskinesias. This effect persisted for about 72 hours after which the patient regressed to his pretreatment state. To ascertain if the responses elicited in the laboratory were reproducible, the patient was instructed to apply magnetic fields of the same characteristics daily at home. These subsequent treatments paralleled the initial response with a sustained improvement being maintained during an observation period lasting at least one month. This case demonstrates the efficacy of weak magnetic fields in the treatment of Parkinsonism and motor complications of chronic levodopa therapy.
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8/16. Unilateral transplantation of human fetal mesencephalic tissue into the caudate nucleus of patients with Parkinson's disease.

    BACKGROUND. Parkinson's disease is characterized by the loss of midbrain dopamine neurons that innervate the caudate and the putamen. Studies in animals suggest that fetal dopaminergic neurons can survive transplantation and restore neurologic function. This report compares the clinical results in four case patients with severe Parkinson's disease who underwent stereotaxic implantation of human fetal ventral mesencephalic tissue in one caudate nucleus with the results in a control group of similar subjects assigned at random to a one-year delay in surgery. methods. Each case patient received cryopreserved tissue from one fetal cadaver (gestational age, 7 to 11 weeks). Before implantation, adjacent midbrain tissue underwent microbiologic, biochemical, and viability testing. cyclosporine was administered for six months postoperatively. RESULTS. The procedure was well tolerated. Three case patients showed bilateral improvement on motor tasks, as assessed on videotape, and were more functional in the activities of daily living, as assessed by themselves and neurologists, during both optimal drug therapy and "drug holiday" periods. One case patient, who died after four months from continued disease progression, had striatonigral degeneration at autopsy. In the patients who received transplants, optimal control was achieved with a lower dose of antiparkinsonian medications, whereas the controls required more medication. positron-emission tomography with [18F]fluorodopa before and after surgery in one patient revealed a bilateral restoration of caudate dopamine synthesis to the range of normal controls, but continued bilateral deficits in the putamen. CONCLUSIONS. Although the case patients continued to be disabled by their disease, unilateral intracaudate grafts of fetal tissue containing dopamine diminished the symptoms and signs of parkinsonism during 18 months of evaluation.
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9/16. Experimental therapeutics of Parkinson's disease.

    1. The loss of central dopamine, which characterises Parkinson's disease, led to the main pharmacological strategy for treatment, namely levodopa, a dopamine-replacement therapy. Several years after treatment, the majority of patients experience dose-limiting side-effects and loss of symptom control. There is a resurgence of interest in neurosurgery for treating the Parkinson's disease, particularly in new techniques targeting the subthalamic nucleus (STN), which is overactive in Parkinson's disease and contributes to symptom development. 2. We performed unilateral subthalamotomy (lesioning the subthalamic nucleus via the toxin N-methyl-d-aspartate) in marmosets and rats with experimentally induced parkinsonism (induced using the toxin 6-hydroxydopamine). A range of similar behaviours common to both rodents and primates were evaluated before and after each type of surgery. Post-mortem histology was used to confirm the lesions. We also provide details of a case with Parkinson's disease who underwent high-frequency bilateral stimulation of the STN and in whom we analysed the STN post-mortem. 3. Unilateral subthalamotomy improved akinesia in parkinsonian primates. However, both monkeys and rodents showed postural abnormalities. The patient who underwent bilateral high-frequency stimulation showed improvement of akinesia and other disease symptoms and no postural abnormalities. Post-mortem analysis did not demonstrate substantial damage of the STN as a result of the electrodes. 4. Although unilateral subthalamotomy improves some aspects of parkinsonism, it causes postural abnormalities in animal models of Parkinson's disease. Because bilateral high-frequency STN stimulation improves disease symptoms, is reversible and is not reported to induce postural side-effects, it may be a better surgical therapy for Parkinson's disease than lesioning the STN.
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10/16. estrogens and the pathophysiology of Parkinson's disease.

    Two postmenopausal female Parkinsonian patients experienced exacerbation of symptoms including levodopa-induced "On-Off" following withdrawal or reduction of conjugated estrogen therapy. This report supports animal data implicating female sexual hormones in the pathophysiology of Parkinson's disease and levodopa-induced dyskinesias.
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