1/60. Camptocormia (bent spine) in patients with Parkinson's disease--characterization and possible pathogenesis of an unusual phenomenon.Camptocormia is characterized by severe forward flexion of the thoracolumbar spine which increases while walking and disappears in the recumbent position. We describe for the first time eight patients with presumed idiopathic Parkinson's disease (mean age 66 /-5 yrs; mean symptom duration 13.1 /-5.1 yrs) who developed camptocormia. This impressive abnormal posture emerged 4-14 years from disease onset, and in some patients stooped posture was the prominent symptom at diagnosis. There was no clear correlation between camptocormia and levodopa treatment. In some patients the camptocormic posture improved, and in others it was unchanged or even aggravated following levodopa administration. Three patients reported worsening of this symptom during "off" periods and also with fatigue. The pathogenesis of this phenomenon is unknown but might represent either a rare type of dystonia or an extreme form of rigidity.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
2/60. Deterioration in parkinsonism with low-dose pergolide.The administration of dopamine agonists can have a role early in the course of Parkinson's disease, in an attempt to reduce the frequency of long-term motor complications associated with the use of levodopa. After treatment with dopamine agonists has begun, gradual dose escalation is recommended to reduce the incidence of side effects; at low doses, parkinsonian symptoms significantly decline in some patients, only to improve as the dose increases. We report a number of such patients and discuss the possible pathogenesis of this motor deterioration.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
3/60. Treatment with AC pulsed electromagnetic fields improves olfactory function in Parkinson's disease.Olfactory dysfunction is a common symptom of Parkinson's disease (PD). It may manifest in the early stages of the disease and infrequently may even antedate the onset of motor symptoms. The cause of olfactory dysfunction in PD remains unknown. Pathological changes characteristic of PD (i.e., lewy bodies) have been demonstrated in the olfactory bulb which contains a large population of dopaminergic neurons involved in olfactory information processing. Since dopaminergic drugs do not affect olfactory threshold in PD patients, it has been suggested that olfactory dysfunction in these patients is not dependent on dopamine deficiency. I present two fully medicated Parkinsonian patients with long standing history of olfactory dysfunction in whom recovery of smell occurred during therapeutic transcranial application of AC pulsed electromagnetic fields (EMFs) in the picotesla flux density. In both patients improvement of smell during administration of EMFs occurred in conjunction with recurrent episodes of yawning. The temporal association between recovery of smell and yawning behavior is remarkable since yawning is mediated by activation of a subpopulation of striatal and limbic postsynaptic dopamine D2 receptors induced by increased synaptic dopamine release. A high density of dopamine D2 receptors is present in the olfactory bulb and tract. Degeneration of olfactory dopaminergic neurons may lead to upregulation (i.e., supersensitivity) of postsynaptic dopamine D2 receptors. Presumably, small amounts of dopamine released into the synapses of the olfactory bulb during magnetic stimulation may cause activation of these supersensitive receptors resulting in enhanced sense of smell. Interestingly, in both patients enhancement of smell perception occurred only during administration of EMFs of 7 Hz frequency implying that the release of dopamine and activation of dopamine D2 receptors in the olfactory bulb was partly frequency dependent. In fact, weak magnetic fields have been found to cause interaction with biological systems only within narrow frequency ranges (i.e., frequency windows) and the existence of such frequency ranges has been explained on the basis of the cyclotron resonance model.- - - - - - - - - - ranking = 2keywords = administration (Clic here for more details about this article) |
4/60. 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.- - - - - - - - - - ranking = 4keywords = administration (Clic here for more details about this article) |
5/60. amantadine-induced peripheral neuropathy.We report a 48-year-old woman with a 17-year history of PD who developed a peripheral sensory-motor neuropathy secondary to chronic administration (8 years) of amantadine. Discontinuation of amantadine resulted in resolution of trophic skin ulcers, paresthesias, and distal weakness. amantadine may be hazardous to patients with severe and chronic livedo reticularis.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
6/60. yawning and stretching induced by transcranial application of AC pulsed electromagnetic fields in Parkinson's disease.yawning is considered a brainstem regulated behavior which is associated with changes in arousal and activity levels. yawning and stretching are dopamine (DA) mediated behaviors and pharmacological studies indicate that these behaviors are associated with increased DA release coupled with stimulation of postsynaptic DA-D2 receptors. Despite their relation to the dopaminergic system, yawning and stretching are poorly documented in untreated or treated patients with Parkinson's disease (PD). A 49 year old fully medicated female patient with juvenile onset PD is presented in whom recurrent episodes of yawning and stretching developed during transcranial administration of AC pulsed electromagnetic fields (EM Fs) of picotesla flux density. These episodes have not been observed previously in this or other patients during treatment with levodopa or DA receptor agonists or in unmedicated PD patients during treatment with AC pulsed EMFs. It is suggested that yawning and stretching behavior resulted in this patient from a synergistic interaction between EMFs and DA derived from levodopa supplementation with EMFs possibly facilitating the release of DA and simultaneously activating postsynaptic DA-D2 receptors in the nigrostriatal dopaminergic pathways. In addition, it is postulated that the release of ACTH/MSH peptides from peptidergic neurons in the brain upon stimulation of the DA-D2 receptors reinforced the yawning and stretching behavior.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
7/60. Leucopenia induced by low dose clozapine in Parkinson's disease recedes shortly after drug withdrawal. Clinical case descriptions with commentary on switch-over to olanzapine.Four patients affected by severe Parkinson's disease developed leucopenia (900-1200 WBC) during treatment of psychosis (3) or untreatable insomnia (1) with clozapine (37.5-75 mg/day). clozapine withdrawal was followed by recovery of leucopenia (4000-6000 WBC) in two weeks with no need for the administration of leucokines. After 1-6 months olanzapine was administered (increasing the dose from 2.5 to 10 mg/day) to treat persisting disturbances, but the drug induced severe worsening of parkinsonism and also this drug had to be withdrawn.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
8/60. speech dysfluency exacerbated by levodopa in Parkinson's disease.The role of dopamine in the modulation of speech fluency is complex. In this report we describe two patients with Parkinson's disease whose speech dysfluency was exacerbated by the administration of levodopa. In doing so, we extend the observation that dopaminergic mechanisms may be involved in the regulation of speech fluency. It is important for clinicians to recognize that, in some instances, dopaminergic replacement therapy may exacerbate an underlying dysfluency syndrome in PD.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
9/60. Parasomnia as an occasion for the diagnosis of Parkinson's disease.We report a case of Parkinson's disease (PD) diagnosed by rem sleep behavior disorder (RBD). The patient was a 68-year-old man. On admission, rigidity in the left upper and lower extremities, bradykinesia, and gait disturbance were noted. In addition, polysomnography revealed REM sleep without atonia (RWA), and a diagnosis of untreated PD associated with RBD was made. Polysomnographic data showed that REM density decreased and RWA tended to increase after administration of a combination of L-DOPA and DCI (L-DOPA/DCI). Thus, we considered that the pathophysiological mechanism of RBD in this case was based not only on the dysfunction of the brainstem mechanism of RWA, but also on the impairment of dopaminergic neuron.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
10/60. Treatment of pathological crying with citalopram.Pathological laughing and/or crying may occur as a concomitant symptom of various diseases of the central nervous system. No known anatomical basis for any of these disorders exists at present. However, references to a disturbance in central serotoninergic neurotransmission have become frequent in the literature, implicating this as an important etiological factor. In the present communication three cases of successful treatment of pathological crying using the SSRI citalopram are reported. Besides the response of pathological crying in cerebral ischemia to SSRIs, which has already been described in earlier publications, this is the first report on the successful administration of citalopram for treating pathological crying in Parkinson's disease. Onset of response was very rapid in all cases.- - - - - - - - - - ranking = 1keywords = administration (Clic here for more details about this article) |
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