Clinical Neuroscience

[Parkinson's syndrome and cognitive disorders]

SZIRMAI Imre, KOVÁCS Tibor

AUGUST 20, 2002

Clinical Neuroscience - 2002;55(07-08)

[The cognitive (executive) ability of patients with Parkinson’s-disease (PD) deteriorates gradually during the progression of the disease. Fluency of speech, word finding, working memory, ability to plan the future and flexibility decline. Cognitive disturbance was found to be proportional with the speech, posture, gait and balance problems and can not be influenced by L-dopa substitution. Apart the dorsal and ventral mesolimbic dopaminergic systems the coerulo-cortical noradrenergic, serotoninergic and cholinergic systems are also impaired in PD. Subcortical dementia in PD can also be explained by the functional dysability of dorsolateral and anterior cingular circuits. Attention deficit can be explained by the dopamine depletion of cingular cortex. Cortical Lewy bodies, neurofibrillary tangles, neurit plaques and additional vascular pathology should also play a role in cognitive impairment of PD. In several systemic degenerative diseases associating with Parkinson’s syndrome (PS) ie. progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA) dementia can be detected with various severity, therefore the question arises concerning the correlation between cognitive disability and PS. Parkinson syndrome can also develop in frontotemporal dementias (FTD), Alzheimer’s disease and cortical Lewy body disease (CLBD) but no correlation exists between motor disability and severity of dementia. In CLBD dementia can be the initial symptom in 18% of cases but PS can also preceedes the dementia. In PSP profound depletion of other monoaminergic neurotransmitter system was also reported. In FTDs associated with PS degeneration of substantia nigra, locus coeruleus and basal nucleus of Meynert has been reported with increased number of neurofibrillary tangles. In patients with vascular PS (VP) there is generally no tremor and rigidity, but pseudobulbar palsy, dementia, gate disturbance, incontinency appeares; L-dopa treatment is generally ineffective. In VP no cellular loss can be found within the substantia nigra, but leukoaraiosis, lacunae in the white matter and basal ganglia are commonly demonstrated.]

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[The molecular genetic control of bony developmental malformations affecting the craniocervical junction and the cervical spine]

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[In this review a new interpretation of the origin of bony developmental malformations affecting the craniocervical junction and the cervical spine is presented based on recent advances in the understanding of embryonic development of the spine and its molecular genetic control. Radiographs, CT and MRI scans or CT myelograms of patients with Klippel-Feil syndrome were used for demonstration. Detailed clinical and radiologial analysis of these patients was published earlier [David KM, Stevens JM, Thorogood P, Crockard HA. The dysmorphic cervical spine in Klippel-Feil syndrome: interpretations from developmental biology. Neurosurg Focus 1999;6(6):1.]. Homeotic transformation due to mutations or disturbed expression of Hox genes is a possible mechanism responsible for C1 assimilation. Notochordal defects and/or signalling problems, that result in reduced or impaired Pax-1 gene expression, may underlie vertebral fusions. This, together with asymmetrical distribution of paraxial mesoderm cells and a possible lack of communication across the embryonic mid-line, could cause the asymmetrical fusion patterns. The wide and flattened shape of the fused vertebral bodies, their resemblance to the embryonic cartilaginous vertebrae and the process of progressive bony fusion with age suggest that the fusions occur before or, at the latest, during chondrification of vertebrae. The authors suggest that the aforementioned mechanisms are likely to be, at least in part, responsible for the origin of the bony developmental malformations affecting the craniocervical junction and the cervical spine.]

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Clinical Neuroscience

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