ABSTRACT
Transcranial static magnetic field stimulation (tSMS) is a recent low-cost non-invasive brain stimulation technique that decreases cortical excitability in healthy subjects. The objective of the present study was to test the ability of tSMS to modulate cortical excitability in patients with Parkinson's disease. We performed a randomized double-blind sham-controlled cross-over study to assess cortical excitability before and immediately after tSMS (or sham) applied for 10 min to the more affected motor cortex of patients with Parkinson's disease. Cortical excitability was quantified by the amplitude of motor evoked potentials (MEPs) elicited by single-pulse transcranial magnetic stimulation (TMS). tSMS significantly decreased MEP amplitudes in patients OFF medication (after overnight withdrawal of dopaminergic drugs), but not ON medication (after an acute dose of levodopa). The between-patients variability of tSMS-induced changes was significantly greater ON medication. The variability ON medication could be partly explained by disease progression, i.e. the more advanced the patient, the more likely it was to observe a switch from inhibitory tSMS plasticity OFF medication to paradoxical facilitatory plasticity ON medication. These results suggest that tSMS induces dopamine-dependent changes of cortical excitability in patients with Parkinson's disease.
Subject(s)
Cerebral Cortex/metabolism , Cerebral Cortex/physiopathology , Cortical Excitability , Dopamine/metabolism , Parkinson Disease/metabolism , Parkinson Disease/physiopathology , Transcranial Magnetic Stimulation , Adult , Aged , Cerebral Cortex/drug effects , Dopamine Agents/pharmacology , Dopamine Agents/therapeutic use , Evoked Potentials, Motor , Female , Humans , Male , Middle Aged , Motor Cortex/metabolism , Motor Cortex/physiopathology , Parkinson Disease/drug therapyABSTRACT
INTRODUCTION: Huntington's disease (HD) is an autosomal dominant hereditary disease caused by triplet repetition in exon 1 of the huntingtin protein located in chromosome 4. Medium spiny neurons in the striatum are selectively affected. Clinical manifestations include progressive behavioural, motor and cognitive disorders. There is no treatment available today capable of modifying the natural course of the disease. A great amount of research work is being carried out, much of which involves animal models of the disease. DEVELOPMENT: We reviewed the articles published in PubMed on basic research into HD and analysed the most frequently used models. Transgenic mouse models, excitotoxic models, transgenic fly models and cell cultures are all used in studies into HD. The advantages and disadvantages of each of them are highlighted. CONCLUSION: The contribution made by each model of HD must be known in order to draw up a correct design in experimental studies of the disease.
Subject(s)
Disease Models, Animal , Huntington Disease , Animals , Cells, Cultured , Humans , Huntington Disease/pathology , Huntington Disease/physiopathology , Mice , Mice, Transgenic , PubMed , Review Literature as TopicABSTRACT
INTRODUCTION: We consider in this paper the applicability of the FAB in Spain, a battery at bedside devised to assess frontal lobe function and able to identify a dysexecutive syndrome, which takes few minutes to administer, and useful for neuropsychological diagnosis in diseases involving frontal lobe dysfunctions. PATIENTS AND METHODS: We study dual application of FAB and Folstein s MMSE to 195 subjects belonging to 11 subgroups (controls, neurodegenerative disorders and psychiatric conditions), and they were related to: cortical/subcortical normality, cortical/subcortical cognitive impairment, or cortical/subcortical dementia. STATISTICS: mean, standard deviation, U test (p< 0.05) and Pearson s correlation index. CONCLUSIONS: Data suggest FAB reflects in Spanish environment the reality of frontosubcortical deterioration in studied groups. FAB and MMSE showed a variable grade of positive lineal correlation in different diseases.
Subject(s)
Frontal Lobe/physiopathology , Nervous System Diseases/diagnosis , Neuropsychological Tests , Adult , Aged , Humans , Nervous System Diseases/physiopathology , Spain , Statistics as TopicABSTRACT
INTRODUCTION: Parkinson s disease (PD) is caused by an abnormal degeneration of the dopamine producing cells in the substantia nigra and ventral tegmental area. When PD advances, degeneration of the nigroestriatal tracts may expand and involve other pathways (mesolimbic and frontal), and also serotonergic and cholinergic systems. This degeneration leads to a multitude of motor and non motor behavioral disturbances. DEVELOPMENT: On the background of progressive degeneration, chronic levodopa and dopaminergic agonist administration may cause pulsatile non physiologic overstimulation of dopaminergic receptors. This may induce perturbations in limbic and frontal cortex structures and overstimulation of serotonergic, cholinergic and other neurotransmitter systems. These events are the basis of parkinsonian psychosis, perhaps in the setting of early dementia. The treatment of this psychosis is difficult. The reduction or withdrawal of dopaminomimetic agents may improve psychosis with worsening of parkinsonian disability. The recommended order to discontinue antiparkinsonian drugs, when is required, is anticholinergic, selegiline, amantadine and dopamine agonist. Levodopa should be reduced to a tolerable minimum to compensate the motor disturbances. At this point, it may be necessary to add an atypical neuroleptic such as clozapine, quetirapine or olanzapine to improve the symptomatology. CONCLUSIONS: More studies are needed to asses the relationship between parkinsonian psychosis and early dementia. Additional, the development of new drugs could be helpful to control these psychotic symptoms in PD without serious secondary effects.
