Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The averaging of the ongoing activity of the electroencephalogram (EEG) allows extracting the potentials that are time-locked and phase-locked to an event. These potentials are described as evoked potentials. There is another type of change in the ongoing EEG, which is time-locked but not phase-locked to an event: the EEG rhythm reactivity, also called "Event-Related Desynchronization and Synchronization" (ERD/ERS) by Pfurtscheller. These changes are often visible to the naked eye but they cannot be extracted by the averaging technique. Their quantification requires another method, which was suggested by Pfurtscheller and Aranibar in 1977. This method consists in measuring the temporal evolution of the power of EEG signal within a given frequency band before, during, and after an event. ERD corresponds to the decrease in power of an EEG rhythm related to an event. Conversely, ERS corresponds to an increase in amplitude of an EEG rhythm related to the event. ERD represents the activation of the subjacent cortical areas. ERS would partly traduce the setting at rest of the cortex; it would also be related to the somesthetics afferents inputs. This method can be applied to the study of cortical activation in many situations: memory tasks, auditory processing, attention, anticipatory behavior, and voluntary movement. Thus, a voluntary self-paced movement of the dominant hand is preceded by an ERD of mu and beta rhythms occurring respectively 2 000 and 1 500 ms before the movement onset. This ERD is recorded over the contralateral central region. It becomes bilateral at the movement onset and reaches its maximum at the movement offset. It is then followed by an ERS of the beta rhythms. We show that ERD/ERS phenomena vary with the type of movement, and that their study allows exploring the modifications of cortical excitability that are observed in Parkinson's disease and in epilepsy with focal motor seizures.
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PMID:Event-related variations in the activity of EEG-rhythms. Application to the physiology and the pathology of movements. 1178 Dec 1

SCH 23390, the halobenzazepine (R)-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5- tetrahydro-1H-3-benzazepine, is a highly potent and selective dopamine D1-like receptor antagonist with a K(i) of 0.2 and 0.3 nM for the D1 and D5 dopamine receptor subtypes, respectively. In vitro, it also binds with high affinity to the 5-HT2 and 5-HT1C serotonin receptor subtypes. However, the doses required to induce a similar response in vivo are greater than 10-fold higher than those required to induce a D1-mediated response. Previous in vivo pharmacological studies with SCH 23390 have shown it to abolish generalized seizures evoked by the chemoconvulsants: pilocarpine and soman. These studies provide evidence of the potential importance of D1-like dopaminergic receptor mechanisms in facilitating the initiation and spread of seizures. The inference from a majority of studies is that the activation of dopamine D1 receptors facilitates seizure activity, whereas activation of D2 receptors may inhibit the development of seizures. SCH 23390 has also been used in studies of other neurological disorders in which the dopamine system has been implicated, such as psychosis and Parkinson's disease. Apart from the study of neurological disorders, SCH 23390 has been extensively used as a tool in the topographical determination of brain D1 receptors in rodents, nonhuman primates, and humans. In summary, SCH 23390 has been a major tool in gaining a better understanding of the role of the dopamine system, more specifically the D1 receptor, in neurological function and dysfunction.
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PMID:SCH 23390: the first selective dopamine D1-like receptor antagonist. 1183 Jul 57

Clinicians become concerned when ECT is contemplated in an individual with a neurological disorder. In this review, the authors summarize the reports on the use of ECT in the presence of neurological disease. Because blood pressure, cerebral blood flow, and intracranial pressure rise with ECT, space-occupying lesions with increased intracranial pressure, cerebral aneurysm, recent head trauma, or active CNS infection pose special concerns for ECT treatment. In this review, we conclude that epilepsy and states with lowered seizure threshold may predispose to prolonged seizures. A history of head injury or stroke probably does not increase risk. Toxic/metabolic disorders are not contraindications to ECT, although correction of the underlying imbalance is a first priority. Extrapyramidal, demyelinating, and neuromuscular disorders pose little increased risk. Indeed, in Parkinson's Disease, ECT may be beneficial for the motor symptoms. As a general rule, it seems advisable to treat the underlying disorder prior to beginning ECT.
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PMID:ECT and Neurological Disorders. 1194 Sep 5

The authors described the first cases in Senegal (West Africa) of the association Parkinson's disease and epilepsy. Almost studies on this feature, stressed on their different pathophysiology basis epilepsy is related on excess of neuronal excitation, and Parkinson disease is an expression of lack of motor neuromodulation. The diagnosis has been done because of the coming out two seizures in the year on two patients one 59 years old and the other 70 years old experiencing Parkinson disease well documented before and treated. Biological study, ultrasonography and Doppler, CT Scan lead to rule out a vasculopathy. Good outcome with antiparkinsonian and anticonvulsant medications confirm the diagnosis.
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PMID:[Anatomophysiologic and clinical study of the association of epilepsy and Parkinson's disease: apropos of 2 cases]. 1195 96

In recent years, oxidative stress has been implicated in a variety of degenerative processes, diseases, and syndromes. Some of these include atherosclerosis, myocardial infarction, stroke, and ischemia/reperfusion injury; chronic and acute inflammatory conditions such as wound healing; central nervous system disorders such as forms of familial amyotrophic lateral sclerosis (ALS) and glutathione peroxidase-linked adolescent seizures; Parkinson's disease and Alzheimer's dementia; and a variety of other age-related disorders. Among the various biochemical events associated with these conditions, emerging evidence suggests the formation of superoxide anion and expression/activity of its endogenous scavenger, superoxide dismutase (SOD), as a common denominator. This review summarizes the function of SOD under normal physiological conditions as well as its role in the cellular and molecular mechanisms underlying oxidative tissue damage and neurological abnormalities. Experimental evidence from laboratory animals that either overexpress (transgenics) or are deficient (knockouts) in antioxidant enzyme/protein levels and the genetic SOD mutations observed in some familial cases of ALS are also discussed.
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PMID:Role of superoxide dismutases in oxidative damage and neurodegenerative disorders. 1219 1

A 59-year-old man, who was diagnosed as having Parkinson's disease and depression seven years ago and was on oral antiparkinsonian agents, antianxiety agents, and antidepressants, developed a high fever, disturbed consciousness, and marked muscle rigidity after discontinuation of etizolam and amitriptyline. He was admitted to a nearby hospital. Hypothyroidism had been noted two months before admission. Marked muscle rigidity and increased serum CK were observed. Since discontinuation of benzodiazepine has been known to rarely trigger a neuroleptic malignant syndrome (NMS), he was diagnosed as having NMS. After receiving dantrolene and bromocriptine, these symptoms temporarily improved but he again developed consciousness disturbance, and convulsive seizures associated with an elevated serum CK. He was transferred to our hospital. On admission, the CK level was normal at 168 IU/l, while free T4 was 0.6 ng/dl (normal range, 0.9-2.3) and TSH was 108.7 mU/ml (normal range, 0.2-4.2) in serum, indicating the presence of primary hypothyroidism. As an increase in thyroid hormone dosage improved the thyroid function to normal level, his disturbed consciousness and muscle rigidity gradually improved. Convulsive seizure and recurrence of NMS in a short interval are unusual in neuroleptic malignant syndrome. In this patient, hypothyroidism may have contributed to the development of malignant syndrome through metabolic changes of the central dopaminergic system, and discontinuation of etizolam, a kind of benzodiazepine, may have triggered NMS, since there has not been reported that discontinuation of antidepressants including amitriptyline triggers NMS.
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PMID:[A patient with Parkinson's disease complicated by hypothyroidism who developed malignant syndrome after discontinuation of etizolam]. 1242 63

Over the past 20 years, new methods have been developed that have allowed scientists to visualize the human brain in action. Initially positron emission tomography (PET) and now functional magnetic resonance imaging (fMRI) are causing a paradigm shift in psychiatry and the neurosciences. Psychiatry is abandoning the pharmacological model of 'brain as soup', used for much of the past 20 years. Instead, there is new realization that both normal and abnormal behavior arise from chemical processes that occur within parallel distributed networks in specific brain regions. Many of these pathological circuits are becoming well characterized, in disorders ranging from Parkinson's disease, to obsessive-compulsive disorder, to depression. Most recently, there has been an explosion of new techniques that allow for direct stimulation of these brain circuits, without the need for open craniotomy and neurosurgical ablation. The techniques include transcranial magnetic stimulation (TMS), magnetic seizure therapy (MST), vagus nerve stimulation (VNS), and deep brain stimulation (DBS). This review will describe these new tools, and overview their current and future potential for research and clinical neuropsychiatric use. The psychiatry of the future will be better grounded in a firm understanding of neuroanatomy and neurophysiology (as well as pharmacology). These brain stimulation tools, or their next iterations, will play an ever-larger role in clinical neuropsychiatric practice.
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PMID:New methods of minimally invasive brain modulation as therapies in psychiatry: TMS, MST, VNS and DBS. 1245 3

This article attempts an overview of the clinical and electrophysiological evidence supporting the involvement of the basal ganglia in epileptic seizures. In contrast to animal data, evidence for a role of these structures in human epilepsies is lacking. However, from the theoretical point of view, it remains conceivable that, given their strong interconnectivity, basal ganglia could be functionally linked to the cerebral cortex during an epileptic seizure. Several clinical ictal aspects have been suggested to be compatible with the involvement of basal ganglia, namely, ictal dystonic posturing during temporal lobe seizures, rotatory seizures and paroxysmal dyskinesia-like seizures. On the other hand, basal ganglia dysfunction may also influence some aspects of epilepsy, as suggested by pure basal ganglia pathology such as Parkinson's disease, or the described effect of an acute basal ganglia lesion in epileptic patients. The data discussed in this review may stimulate further research to link basic scientific data to human epilepsies, and lead to the development of novel therapeutical solutions.
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PMID:Seizures and the basal ganglia: a review of the clinical data. 1249 74

Inwardly rectifying potassium (Kir) channels have long been regarded as transmembrane proteins that regulate the membrane potential of neurons and that are responsible for [K(+)] siphoning in glial cells. The subunit diversity within the Kir channel family is growing rapidly and this is reflected in the multitude of roles that Kir channels play in the central nervous system (CNS). Kir channels are known to control cell differentiation, modify CNS hormone secretion, modulate neurotransmitter release in the nigrostriatal system, may act as hypoxia-sensors and regulate cerebral artery dilatation. The increasing availability of genetic mouse models that express inactive Kir channel subunits has opened new insights into their role in developing and adult mammalian tissues and during the course of CNS disorders. New aspects with respect to the role of Kir channels during CNS cell differentiation and neurogenesis are also emerging. Dysfunction of Kir channels in animal models can lead to severe phenotypes ranging from early postnatal death to an increased susceptibility to develop epileptic seizures. In this review, we summarize the in vivo data that demonstrate the role of Kir channels in regulating morphogenetic events, such as the proliferation, differentiation and survival of neurons and glial cells. We describe the way in which the gating of Kir channel subunits plays an important role in polygenic CNS diseases, such as white matter disease, epilepsy and Parkinson's disease.
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PMID:Kir channels in the CNS: emerging new roles and implications for neurological diseases. 1259 33

Since Yakovlev's contribution in 1928, very few cases with parkinsonism and epilepsy have been reported in the literature. While antagonism has been claimed between the two conditions, little is hypothesized about the pathophysiological mechanisms involved. We report the case of a patient with both temporal lobe epilepsy and Parkinson's disease, who presented with a dramatic decrease in seizure frequency when the parkinsonian signs developed and disappearance of motor fluctuations following recurrence of seizures. On the basis of recent knowledge regarding both pathologies we propose new insights into this old question.
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PMID:Parkinsonism and Epilepsy: Case Report and Reappraisal of an Old Question. 1260 42


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