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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although, in the course of the last 50 years, the achievements in the medical field have been astonishing, at the beginning of the third millennium a number of clinical pictures are still left without a precise nosographic origin. In the past, the delay in scientific communication was the main explanation presented for the lack of understanding of clinical pictures of unknown nosographic origin. The history of medicine provides excellent examples of this dispersion of human capital, even if the history of clinical neurology presents "exceptions" (the pictures that we now call de la Tourette's syndrome and Parkinson's disease) that indicate that major clinical syndromes could be clearly detected and relatively rapidly diffused even in the 19th century. Contrary to the past, the delay in scientific communication no longer seems an obstacle to the sharing of medical knowledge. Nevertheless, the problem of the in-depth comprehension of clinical pictures of unknown nosographic origin still remains dominant, mainly because of the limited spread of ample and flexible online accessible databases of unknown nosographic origin clinical syndromes. The need for interactive electronic archives and other artificial intelligence resources in order to promote progress in clinical knowledge is discussed in this paper.
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PMID:Clinical pictures of unknown origin in neurology: past, present and future usefulness of artificial intelligence. 1605 45

Originally considered a psychogenic disorder, camptocormia, an abnormal posture with marked flexion of thoracolumbar spine that abates in the recumbent position, is becoming an increasingly recognized feature of parkinsonian and dystonic disorders. Prior reports were limited by sample size, short follow-up, and paucity of data on response to therapy. The authors reviewed 16 patients evaluated in their PD Center and Movement Disorders Clinic diagnosed with camptocormia. In addition to detailed neurologic assessment all patients were videotaped. The mean age was 64.9 +/- 17.4 years, mean age at onset of neurologic symptoms was 51.5 +/- 19.9 years, duration from onset of neurologic symptoms to development of camptocormia was 6.7 +/- 7.6 years, and the mean duration of camptocormia was 4.5 +/- 3.9 years. Of the 16 patients, 11 (68.8%) had Parkinson disease (PD); others had dystonia (n = 4) and Tourette syndrome (n = 1). Twelve patients received levodopa, with minimal or no improvement in the camptocormia. Nine patients received botulinum toxin type A injections into the rectus abdominus, with notable improvement in their camptocormia in four. One patient underwent bilateral subthalamic nucleus deep brain stimulation for PD, but there was no improvement in camptocormia. Based on this series and a thorough review of the literature of camptocormia, head drop, and bent spine syndrome, the authors propose etiologic classification of camptocormia and conclude that this heterogeneous disorder has multiple etiologies and variable response to systemic and local therapies.
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PMID:Camptocormia: pathogenesis, classification, and response to therapy. 1663 62

Movement disorders such as Parkinson's disease and Tourette's syndrome, primarily manifest during wakefulness, intrude into sleep. There are some disorders, however, such as periodic limb movements in sleep, restless legs syndrome, paroxysmal nocturnal dystonia, bruxism, and somnambulism, which occur primarily during sleep. The diagnosis and management of these disorders pose a challenge to neuropsychiatric practice, not only because they may be difficult to distinguish from other neuropsychiatric disorders, but also because psychiatric disorders are often co-morbid with them. Study of these disorders is necessary for an understanding of the interaction of sleep and movement, and how disturbance in one may affect the other.
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PMID:Periodic limb movements and other movement disorders in sleep: neuropsychiatric dimensions. 1619 1

Impaired hand function is a frequent finding in movement disorders. The skilled control of prehensile finger forces is an essential feature of tool use in daily life. In healthy subjects, grip force is precisely adjusted to the mechanical object properties, such as weight and surface friction. Grip force is accurately scaled to be only a small amount higher than the minimum necessary to prevent a hand-held object from slipping. When an object is lifted and moved around in space, grip force is modulated in parallel with the movement-induced fluctuations in load. The absence of a temporal delay between grip and load force profiles implies that the central nervous system is able to predict the load variations before the intended manipulation. Sensory information is used to adjust the level of applied finger forces efficiently to the requirements of the mechanical object properties and the task at hand. The characteristics of impaired finger force control include inefficient grip force scaling and imprecision of the temporal coupling between grip and load force profiles. Here, we review the characteristics of deficient grip force behavior in movement disorders, e.g. Parkinson's disease, task-specific dystonia, Gille de la Tourette's syndrome and cerebellar disease. Grip force analysis is a highly sensitive method to document even subtle impairments of finger force control and may be used both as a diagnostic tool and for the objective evaluation of treatment in neurological movement disorders.
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PMID:Objective evaluation of manual performance deficits in neurological movement disorders. 1635 52

Evidence supports the hypothesis that normalization of cholinergic tone by selective antagonism of neuronal nicotinic acetylcholine receptors (NNRs) may ameliorate the core symptoms of autism. As often is the case, epidemiology has provided the first important clues. It is well recognized that psychiatric patients are significantly more often smokers than the general population. The only known exceptions are obsessive-compulsive disorder (OCD), catatonic schizophrenia and interestingly, autism. In this regard, clinical studies with nicotine have demonstrated amelioration of symptoms of a number of diseases and disorders, including Alzheimer's disease, Parkinson's disease, ADHD and Tourette's syndrome. Nicotine's agonist properties at CNS NNRs have been implicated in these effects and support the concept of self-medication as a strong motivation for smoking in cognitively compromised individuals. On the other hand, the inverse correlation between autism and smoking suggests that smoking does not provide symptomatic relief and may actually be indicative of an active avoidance of nicotine's agonist effects in this disorder. Neuroanatomical evidence is consistent with this idea based on the presence of hypercholinergic architecture in the autistic brain, particularly during the first few years of development, making the avoidance of further stimulation of an already hyperactive cholinergic system plausible. This may also explain why stimulants (known to increase dopamine levels as do NNR agonists) appear to aggravate autistic symptoms and why studies with cholinesterase inhibitors that increase acetylcholine levels in the brain have yielded variable effects in autism. Taken together, the evidence suggests the possibility that nicotinic cholinergic antagonism may in fact be palliative. Pharmacological evidence supports this hypothesis. For example, antidepressants, many of which are now known to be non-competitive NNR antagonists, have been used successfully to treat a number of autistic symptoms. More specifically, there is anecdotal evidence from at least one medical practitioner that mecamylamine, a non-selective NNR antagonist, is effective in treating many autistic symptoms, particularly those that are refractory to most other treatments. Clearly there is a need for carefully controlled clinical studies with novel selective NNR antagonists to explore their potential as a new and exciting approach for the treatment of autism.
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PMID:Nicotinic cholinergic antagonists: a novel approach for the treatment of autism. 1640 87

The evidence for supramedullary influences on cough is largely indirect. Cough can be voluntarily induced or inhibited, functions usually thought to reside in the cerebral cortex. A sensation of 'urge-to-cough' usually precedes cough due to an airway irritant stimulus, and this may well involve the cerebral cortex. In conditions with interruption of the pathways between the cortex and the brainstem, such as strokes and Parkinson's disease, voluntary cough may be inhibited without disruption of reflex cough from the larynx or lower airways. 'Habit cough', like Tourette's syndrome, is assumed to be cortically mediated. Placebos and many treatments based on complementary medicine are effective in inhibiting clinical cough, and the site of action is likely to be the cerebral cortex. In sleep and in anaesthesia cough is depressed and, again, this seems likely to be at a cortical level. However there are few or no experimental or clinical observation as to the localization and functions of supramedullary areas responsible for cough. It is a field of research wide open for exploration.
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PMID:Supramedullary influences on cough. 1662 35

In functional neurosurgery, there is a growing need for accurate localization of the functional targets. Since deep brain stimulation (DBS) of the Vim thalamic nucleus has been proposed for the treatment of Parkinson's disease, the target has evolved toward the globus pallidus and subthalamic nucleus (STN) and the therapeutic indications have enlarged to include psychiatric disorders such as Tourette syndrome or obsessive compulsive disorders. In these pathologies, the target has been restrained to smaller functional subterritories of the basal ganglia, requiring more refined techniques to localize smaller and smallerbrain regions, often invisible in routine clinical MRI. Different strategies have been developed to identify such deep brain targets. Direct methods can identify structures in the MRI itself, but only the larger ones. Indirect methods are based on the use of anatomical atlases. The present strategy comprised a 3D histological atlas and the MRI of the same brain specimen, and deformation methodology developped to fit the atlas toward the brain of any given patient. In this paper, this method is evaluated in the aim of being applied to further studies of anatomo-clinical correlation. The accuracy of the method is first discussed, followed by the study of short series of Parkinsonian patients treated by DBS, allowing to compare the deformed atlas with various per- and post-operative data.
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PMID:Retrospective cross-evaluation of an histological and deformable 3D atlas of the basal ganglia on series of Parkinsonian patients treated by deep brain stimulation. 1668 83

The present chapter reviews PET imaging in basal ganglia disorders; Parkinson's disease is used as a model of these disorders because the neurochemical pathobiology of this disease is well known and great advances in the imaging area have been achieved. Other basal ganglia disorders including Tourette's syndrome, dystonia, Huntington's chorea and Wilson's disease are also dealt with. With PET and SPECT techniques, the whole integrative dopaminergic network of neurons can be studied, which plays an important role in differential diagnostics. Furthermore, pharmacological effects of medication can be visualized and the role of stereotaxic neurosurgery can be evaluated. Finally, functional imaging gives clues about the prognosis and rehabilitation aspects of the basal ganglia disorders.
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PMID:PET imaging of the basal ganglia. 1672 12

The introduction of deep brain stimulation (DBS) as a treatment for medication-refractory essential tremor in the late 1980s revealed, for the first time, that "chronically" implanted brain hardware had the potential to modulate neurologic function with surprisingly low morbidity. Over time, the therapeutic promise of DBS has become evident in Parkinson's disease and dystonia. In some experienced centers, complex tremor disorders, such as posttraumatic Holmes tremor and the tremor of multiple sclerosis, are being increasingly targeted. More recently, other indications, including obsessive-compulsive disorder, Tourette's syndrome, major depression, and chronic pain, have been proposed. As the field has expanded, our knowledge about potential cognitive side effects of DBS has also expanded. This article reviews the current knowledge regarding the impact of stimulation of the subthalamic nucleus, globus pallidus internus, and ventralis intermedius nucleus of the thalamus on symptoms in essential tremor, Parkinson's disease, and dystonia. Also discussed are the emerging targets, what is known about the cognitive sequelae of DBS, and what has been learned about the complications and therapeutic failures.
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PMID:Lessons learned in deep brain stimulation for movement and neuropsychiatric disorders. 1681 92

Over the past two decades, deep brain stimulation (DBS) has supplanted lesioning techniques for the treatment of movement disorders, and has been shown to be safe and efficacious. The primary therapeutic indications for DBS are essential tremor, dystonia and Parkinson's disease. In the case of Parkinson's disease, DBS is effective for treating the primary symptoms--tremor, bradykinesia and rigidity--as well as the motor complications of drug treatment. Progress has been made in understanding the effects of stimulation at the neuronal level, and this knowledge should eventually improve the effectiveness of this therapy. Preliminary studies also indicate that DBS might be used to treat Tourette's syndrome, obsessive-compulsive disorder, depression and epilepsy. As we will discuss in this review, the success of DBS depends on an appropriate rationale for the procedure, and on collaborations between neurologists and neurosurgeons in defining outcomes.
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PMID:Surgery insight: Deep brain stimulation for movement disorders. 1693 75


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