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Biomedical subjects

Paul Krack

Publications and source records attributed to Paul Krack.

10 recordsLinked to original sources
PubMed2003

Acute psychotropic effects of bilateral subthalamic nucleus stimulation and levodopa in Parkinson's disease.

High-frequency deep brain stimulation (DBS) of the subthalamic nucleus (STN) improves the motor symptoms of Parkinson's disease (PD). Opposite changes in mood, such as mania or depression, have been reported after surgery, but it is not known whether these side effects are specifically related to STN DBS. To learn whether STN DBS also influences the limbic loop, we investigated acute subjective psychotropic effects related to levodopa or bilateral STN DBS. After a median postoperative follow-up of 12 months, 50 PD patients completed the Addiction Research Center Inventory (ARCI), assessing subjective psychotropic effects in four conditions: off-drug/on-stimulation; off-drug/off-stimulation; on-drug/off-stimulation; and on-drug/on-stimulation. Both levodopa and STN DBS improved all the ARCI subscales, indicating subjective feelings of well being, euphoria, increase in motivation, and decrease in fatigue, anxiety, and tension. A suprathreshold dose of levodopa was significantly more effective than STN DBS, using the same electrical parameters as for chronic stimulation, on four of the five ARCI subscales. We concluded that 1) both STN DBS and levodopa have synergistic acute beneficial psychotropic effects in PD, 2) the psychotropic effects of both treatments need to be considered in the long-term management of chronic STN DBS, and 3) the results indicate an involvement of the limbic STN in mood disorders of PD.

Activities of Daily Living↗
PubMed2002

Dyskinesias and grip control in Parkinson's disease are normalized by chronic stimulation of the subthalamic nucleus.

Deep-brain stimulation of the subthalamic nucleus appears to reduce levodopa-induced dyskinesias, but whether this effect is caused by the reduction of the total levodopa ingestion or represents a direct effect on the motor system is unknown. Precision grip force of grasping movements and levodopa-induced dyskinesias was analyzed in 10 parkinsonian patients before and after 3 months of deep-brain stimulation of the subthalamic nucleus. Peak grip force was abnormally increased before surgery in the off-drug state and, particularly, in the on-drug state (sensitization). This grip force upregulation normalized with chronic deep-brain stimulation in both conditions (desensitization). Peak-dose dyskinesias also improved, and off-dystonia was completely abolished. Mean dosage of dopaminergic drugs was reduced, but force overflow and dyskinesias were equally improved in 2 patients without a reduction. Despite the same single levodopa test dose, force excess and levodopa-induced dyskinesias were drastically reduced after 3 months of deep-brain stimulation of the subthalamic nucleus. This indicates that direct effects of deep-brain stimulation of the subthalamic nucleus on levodopa-induced dyskinesias are likely to occur. Grip force overflow is a promising parameter to study the desensitizing effect of chronic deep-brain stimulation on levodopa-induced dyskinesias.

Dose-Response Relationship, Drug↗
PubMed2002

Surgery of the motor thalamus: problems with the present nomenclatures.

The literature on thalamic surgery is difficult to read because different nomenclatures are in use. Neurosurgeons mostly use the stereotactic atlas of Schaltenbrand with Hassler's nomenclature of the thalamus. Neuroanatomists use different nomenclatures for the primate thalamus. The cytoarchitectonic definition of nuclei is difficult in the motor thalamus, and it would be best to define the nuclei based on their subcortical afferents. However, tracing studies are not available in humans. Thus, human thalamic nomenclature is based entirely on cytoarchitectonic subdivisions and transfer of knowledge by analogy from monkey to man. Problems arise when trying to transfer the detailed knowledge from monkey to the human brain. By doing so, different authors have come to different conclusions concerning the subcortical afferents of Hassler's motor nuclei, which inevitably leads to confusion when attempting neurophysiological interpretations of the surgical data. The present review draws attention to the discrepancies and open questions in the literature. There is a need to better define the limits of the sensory and cerebellar afferent receiving thalamic nuclei as well as those of the cerebellar and pallidal afferent receiving territories in humans.

Animals↗
PubMed2002

Treatment results: Parkinson's disease.

Deep brain stimulation (DBS) is a neurosurgical treatment of Parkinson's disease that is applied to three targets: the ventral intermediate nucleus of the thalamus (Vim), the globus pallidus internas (GPi) and the subthalamic nucleus (STN). Vim DBS mainly improves contralateral tremor and, therefore, is being supplanted by DBS of the two other targets, even in patients with tremor dominant disease. STN and GPi DBS improve off-motor phases and dyskinesias. There is little comparative data between these procedures. The magnitude of the motor improvement seems more constant with STN than GPi DBS. STN DBS allows a decrease in antiparkinsonian drug doses and consumes moderate current. These advantages of STN over GPi DBS are offset by the need for more intensive postoperative management. The DBS procedure has the unique advantage of reversibility and adjustability over time. Patients with young-onset Parkinson's disease suffering from levodopa-induced motor complications but still responding well to levodopa and who exhibit no behavioral, mood, or cognitive impairment benefit the most from STN DBS. Adverse effects more specific of the DBS procedure are infection, cutaneous erosion, and lead breaking or disconnection. Intracranial electrode implantation can induce a hematoma or contusion. Most authors agree that the benefit to risk ratio of DBS is favorable.

Electric Stimulation Therapy↗
PubMed2002

Results of deep brain stimulation for dystonia: a critical reappraisal.

Deep brain stimulation for severe dystonia is still in the very first stage of development. Only single case reports or small case series have been reported to date. Best results have been obtained with pallidal stimulation in patients with primary generalised dystonia, especially in DYT1 mutation carriers. In secondary dystonia, conflicting results were reported. However, there is today enough promising evidence for a striking efficacy of pallidal stimulation in dystonia, supporting the need for further investigations in the field, with collaborative projects (regarding to the limited number of eligible patients); double-blind studies, including a consensus about surgical method; and a precise anatomic analysis of the position of the electrode. A careful assessment of the efficacy by using improved clinical scale is also warranted.

Dystonia↗
PubMed2002

Intraoperative microrecordings of the subthalamic nucleus in Parkinson's disease.

Microelectrode recordings of single unit neuronal activity were used during stereotactic surgery to define the subthalamic nucleus for chronic deep brain stimulation in the treatment of Parkinson's disease. By using five parallel trajectories, often two to three microelectrodes allow us to recognize subthalamic nucleus (STN) neuronal activity. STN neurons were easily distinguished from cells of the overlying zona incerta and the underlying substantia nigra. During a typical exploratory track, we can observe a very low background noise in the zona incerta and almost complete absence of single cell recording. Penetration of the electrode tip into the STN is characterized by a sudden increase in background activity and single cell activity of spontaneously active neurons. The exit of electrode tip out of the STN corresponds to a decrease in background noise and a loss of single cell activity. Spontaneous neuronal activity increases again when the electrode tips enters the substantia nigra pars reticulata (SNr); however, the activity is less rich than in the STN, indicating a more cell-sparse nucleus. STN neurons are characterized by a mean firing rate of 42.30 +/- 22.00 spikes/sec (mean +/- SD). The STN cells exhibited irregular or bursty discharge pattern. The pattern of single cell activity in the SNr is a more regular tonic activity that can easily be distinguished from the bursting pattern in the STN. The most useful criteria to select a trajectory are (1) the length of an individual trajectory displaying typical STN activity, (2) the bursting pattern of activity, and (3) motor responses typical of the sensorimotor part of the nucleus. In conclusion, microelectrode recording of the subthalamic area improves the accuracy of targeting the STN.

Brain Mapping↗
PubMed2002

Intraoperative micro- and macrostimulation of the subthalamic nucleus in Parkinson's disease.

Studying the clinical effects induced by electrical stimulation of the subthalamic nucleus (STN) area in a parkinsonian patient under local anesthesia is a mandatory step to determine the precise location of the final chronic electrode. Using multiple microelectrodes, preferably in a concentric parallel array allows a precise mapping of the STN region. The most reliable features to determine the suitable target are stimulation-induced dyskinesias and rigidity decrease at a low intensity without adverse effects or only at far higher intensities. New skills are needed to assess all stimulation-induced effects and interpret them in anatomo-functional terms.

Brain Mapping↗
PubMed2002

Postoperative management of subthalamic nucleus stimulation for Parkinson's disease.

The postoperative neurologic management of patients with deep brain stimulation (DBS) of the subthalamic nucleus (STN) for Parkinson' s disease is a complex dynamic process that involves a progressive increase in stimulation intensity and a parallel decrease in antiparkinsonian medication while assessing the interactions of both treatments. Neurologists responsible for postoperative management of patients receiving STN DBS must have expert knowledge of the electroanatomy of the subthalamic area and be familiar with the medical treatment of motor and nonmotor symptoms, including the management of long-term complications of levodopa treatment. Neurosurgeons who perform DBS need to understand the principles that guide the postoperative adaptation of treatment. This article defines guidelines for setting stimulation parameters, adapting drugs and managing adverse effects.

Antiparkinson Agents↗
PubMed2002

Force overflow and levodopa-induced dyskinesias in Parkinson's disease.

We assessed force coordination of the hand in Parkinson's disease and its relationship to motor complications of levodopa therapy, particularly to levodopa-induced dyskinesias (LID). We studied two groups of Parkinson's disease patients with (Parkinson's disease + LID, n = 23) and without levodopa-induced dyskinesias (Parkinson's disease - LID, n = 10), and age-matched healthy controls. The motor score of the Unified Parkinson's Disease Rating Scale, a dyskinesia score and force in a grip-lift paradigm were assessed ON and OFF levodopa. A pathological increase of forces was seen in ON-state in Parkinson's disease + LID only. In Parkinson's disease + LID, the force involved in pressing down the object before lifting was significantly increased by levodopa (by 61%, P < 0.05). An overshooting of peak grip force by 51% (P < 0.05) and of static grip force by 45% (P < 0.01) was observed in the ON- compared with the OFF-drug condition. In contrast, no excessive force was found in Parkinson's disease - LID. Peak grip force in ON-state was 140% (P < 0.05) higher in Parkinson's disease + LID than in Parkinson's disease - LID, while static grip force was increased by 138% (P < 0.01) between groups. Severity of peak-dose dyskinesias was strongly correlated with grip force in ON-state (r = 0.79 with peak force, P < 0.01). No correlation was observed between forces and the motor score as well as with the daily dose of dopaminergic medication. Force excess was only observed in patients with LID and motor fluctuations. A close relationship was seen between the overshooting of forces and dyskinesias in the ON-drug condition. We postulate that both LID and grip force excess share common pathophysiological mechanisms related to motor fluctuations.

Aged↗