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Biomedical subjects

P Krystkowiak

Publications and source records attributed to P Krystkowiak.

27 records · Page 2Linked to original sources
PubMed2000

[Chronic electric stimulation of the internal globus pallidus and subthalamic nucleus in Parkinson disease].

PATHOPHYSIOLOGY: In Parkinson's disease, the neurodegenerative process of the nigrostriatal dopaminergic pathways induces an increase in activity of the subthalamic nucleus and the medial globus pallidus, which cause inhibition of thalamo-cortical outputs explaining parkinsonism. HIGH-FREQUENCY DEEP BRAIN STIMULATION: The adverse effects induced by lesions of subcortical structures (thalamotomy, pallidotomy) have increased interest in chronic electrical stimulation proposed as a new therapy in Parkinson's disease. This technique is reversible and can be modulated with less adverse effects. TWO TARGETS: Two targets may be proposed in case of severe motor fluctuations: the medial globus pallidus and the subthalamic nucleus. Pallidial stimulation improves dramatically levodopa-induced dyskinesia and, with a variable degree, the parkinsonian triad. Subthalamic stimulation rapidly reverses akinesia, rigidity and tremor and also dyskinesias which progressively tend to diminish after decreasing L-dopa dosage. LONG-TERM EFFICACY: A follow-up period of a few years has confirmed that the beneficial effect is maintained. However, stimulation dose not prevent the development of certain symptoms (postural impairment, cognitive decline). LIMITED INDICATIONS: Chronic electrical stimulation of medial globus pallidus and subthalamic nucleus may be proposed for parkinsonian patients with severe motor fluctuations associated with abnormal involuntary movements which are not controlled by different medical therapies. Parkinsonian symptoms must still be levodopa responsive and cause severe clinical disability severely limiting daily living activities. Cognitive impairment and other severe pathologies are contraindications.

Electric Stimulation Therapy↗
PubMed2000

Thalamic tremor: correlations with three-dimensional magnetic resonance imaging data and pathophysiological mechanisms.

Tremor associated with a single focal thalamic lesion has rarely been reported. Furthermore, the exact localization of the lesions is difficult to determine because of the imprecision of "conventional" radiology (computed tomography scan and/or "standard" magnetic resonance imaging). The aim of this study was to identify which thalamic structures are involved in tremor associated with a single focal thalamic lesion. We selected two patients who presented with unilateral postural and kinetic tremor of the upper limb related to a localized thalamic infarction. Three-dimensional T1-weighted magnetic resonance imaging sequence (MP-RAGE sequence) was used to determine the precise topography of the lesions by stereotactic analysis using the atlas of Hassler. The lesions were located within the pulvinar, the sensory nuclei, the mediodorsal nucleus, and the ventral lateral posterior nucleus (according to the classification of Hirai and Jones), the latter including the ventral intermediate nucleus (Vim according to the classification of Hassler). However, the Vim was spared. The subthalamic area, which can induce tremor, was not involved. After having compared the topography of the lesions with the clinical findings, we suggest that thalamic tremors may result from the interruption of the cerebellar outflow tract to the Vim within the thalamus.

Adult↗
PubMed2000

A case of severe dysexecutive syndrome consecutive to chronic bilateral pallidal stimulation.

In treatment for severe Parkinson's disease (PD), a recent procedure was developed which consists of implanting electrodes in the internal Globus Pallidus (GPi) for chronic electrical stimulation. The consequences on cognitive function of such an intervention are quite variable. Although most group studies observed no significant post-operative change, individual cases of post-operative cognitive impairment were reported. The present study reports the case of a PD patient who underwent bilateral implantation of deep brain stimulation electrodes in the GPi and who, after surgery, suffered from a severe dysexecutive syndrome. An extensive neuropsychological examination showed a selective negative effect of pallidal stimulation on tests assessing executive function. When the stimulation was turned off, the impairment was partly reversible. This observation emphasizes the role of the GPi in executive function.

Attention↗
PubMed1998

Dystonia after striatopallidal and thalamic stroke: clinicoradiological correlations and pathophysiological mechanisms.

OBJECTIVE: To establish the pathophysiological mechanisms of striatopallidal and thalamic dystonia. METHODS: Five patients from among 26 who presented (between March 1987 and July 1996) with focal dystonia, segmental dystonia, or hemidystonia caused by a single localised vascular lesion, were selected. Patients with lesions with indefinite boundaries, and diffuse, or multiple, or large brain lesions were excluded. Three dimensional T1 weighted MRI (1.5 tesla) was performed to determine the topography of the lesions. The atlas of Hassler allowed the stereotactic localisation of the lesions to be specified exactly. RESULTS: Three patients had dystonic spasms associated with striatopallidal lesions and one with a thalamic and striatopallidal lesion. One other patient presented with a myoclonic dystonia related to a thalamic lesion. The striatopallidal lesions were located in the sensorimotor area with a somatotopical distribution. The pure thalamic lesion involved the centromedian nucleus, the sensory nuclei, and the pulvinar whereas the thalamic and striatopallidal lesion was located in the pallidonigral thalamic territory, which receives pallidonigral inputs. CONCLUSION: The striatopallidal dystonia might be the consequence of the interruption of the cortico-striato-pallido-thalamo-cortical loop induced by lesions located within the sensorimotor part of the striatopallidal complex. By contrast, it is suggested that thalamic dystonia might be caused by lesions located in the centro-median or the ventral intermediate nuclei, outside the pallidonigral territory, but leading also to a dysfunction of the cortico-striato-pallido-thalamo-cortical loop.

Adult↗
PubMed1998

[Collet-Sicard syndrome disclosing periarteritis nodosa].

An 82-year-old woman developed acute onset isolated paralysis of the right ninth, tenth, eleventh and twelfth cranial nerves (Collet-Sicard syndrome). The polynevritis was associated with major weight loss, increased blood pressure, nephropathy, distal arteriopathy and an inflammatory syndrome, suggesting panarteritis nodosa. Neuromuscular biopsy results confirmed the diagnosis. Collet-Sicard syndrome resulted from ischemia in the territory of the ascending pharyngeal artery.

Accessory Nerve↗
PubMed1997

[Regressive leukoencephalopathy in chronic brucellosis].

A 59 year-old-man had ataxia and hemiparesis of progressive onset which resolved in a few weeks. CT scan and magnetic resonance imaging showed white matter multiple lesions. The cerebrospinal fluid was consistent with an inflammatory disease. The diagnosis of multiple sclerosis was evoked. However, the patient had chronic brucellosis and serological rates increased and decreased according to the clinical and radiological signs. Thus, encephalitis caused by brucellosis was evoked. The mechanism is assumed to be a demyelinating process caused by a deep focus reactivation.

Brucellosis↗