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At least 1,369 records · Page 76Linked to original sources
PubMed1987

Cerebral glucose and dopa metabolism in movement disorders.

The development of positron emission tomography (PET) has enabled us to perform in vivo measurements of certain aspects of regional cerebral function. Regional cerebral glucose metabolism may be readily quantified with [18F] fluoro-2-deoxyglucose (FDG) and presynaptic dopaminergic function may be studied with the labelled dopa analog 6-[18F] fluoro-L-dopa. We have applied a model to the analysis of 6-FD/PET data with which in vivo age-related changes in dopaminergic function may be demonstrated in normal subjects. With this technique, we have studied a series of asymptomatic MPTP-exposed subjects and have shown evidence of subclinical nigrostriatal pathway damage. Studies of regional cerebral glucose metabolism with FDG in early Huntington's disease have shown a characteristic impairment in caudate function which precedes the development of caudate atrophy. In addition, some asymptomatic individuals who are at risk for HD have caudate hypometabolism. We feel that, at the present time, PET provides information which is complementary to the clinical examination in establishing a diagnosis of HD. In the future these studies may also help in the investigation of at risk individuals.

Animals↗
PubMed2000

A branch site mutation leading to aberrant splicing of the human tyrosine hydroxylase gene in a child with a severe extrapyramidal movement disorder.

We report a branch site mutation in the gene of the enzyme tyrosine hydroxylase (TH): a -24t > a substitution two bases upstream of the adenosine in the branchpoint sequence (BPS) of intron 11. As normal lariat formation is therefore prevented, alternative splicing takes place; use of the BPS of intron 12 results in skipping of exon 12, whereas the use of a cryptic branch site in intron 11 leads to partial retention of this intron in the mRNA. This leads in both cases to an aberrant protein product. In the one case, skipping of exon 12 results in the absence of 32 amino acids. In the other, retention of 36 nucleotides of intron 11 in the mRNA results in the incorporation of twelve additional amino acids. The functional consequences of this mutation for the patient, who is also heterozygous for another previously identified mutation, become apparent in a severe clinical phenotype.

Basal Ganglia Diseases↗
PubMedDate not supplied

[Fatigue fractures of the lower patellar pole in adolescents with cerebral movement disorders].

Changes at the apex of the patella, seen on X-rays of 4 children with cerebral motility disturbances, raise the question as to whether the changes seen in patella tip syndrome are an event typical for the underlying condition. The present authors are of the opinion that these changes, which resemble patella partita, Sinding-Larsen-Johansson disease and osteopathia patellae juvenilis (C. Mau), do not represent a separate syndrome. The authors believe that all these changes are merely variants of one and the same event, namely a disturbance of the balance between loading and loadbearing capacity of the insertion of the Lig. patellae, a balance which is evidently especially unstable at this age.

Adolescent↗
PubMedDate not supplied

[Etiology of hip dislocation in children with cerebral movement disorders and possibilities of conservative treatment using rotating and spreading plates and electrostimulation].

Dislocations of the hip associated with spastic paralysis are almost always found in severely disabled children. The onset is in infancy. Two methods, electrostimulation of the minor gluteal muscles and treatment with simple leg casts to correct the malposition, are described. Follow-up examinations showed that the treatment had had a positive effect on the hip condition in 33 of the 42 children treated with casts and 26 of the 32 children treated by electrotherapy. Electrotherapy is an innovation, since in the past it was considered contraindicated in these patients. However, it is based on the fact that the gluteal muscles do not normally show any spasticity. Irrespective of this, the treatment is long-term, and has to be continued for many years, a fact which makes greater demands on the cooperativeness of the family.

Adolescent↗
PubMed2002

Midbrain syndrome with eye movement disorder: dramatic improvement after cranioplasty.

BACKGROUND: Patients with skull defects sometimes develop neurological deficits, which have been grouped under "the syndrome of the trephined". The deficits are usually nonspecific or nonlocalizing, such as apathy or diffuse headaches. We report, to our knowledge, a first case of severe midbrain syndrome associated with a skull defect. Cranioplasty dramatically resolved the patient's symptoms. A midbrain syndrome represents the main manifestation of the syndrome of the trephined and can be corrected by cranioplasty. CLINICAL PRESENTATION: A 38-year-old man with head trauma and epidural hematoma initially had normal eye motility. He developed a skull defect after infection following cranioplasty. He presented with onset of neurological symptoms one year after head trauma with a skull defect, a small divergent and vertical strabismus, elevation deficit of both eyes, headaches and fatigue. Over several months he developed severe bilateral deficit of adduction, elevation, depression and convergence. He had neuropsychological deficits, fatigue, headaches and impaired coordination. Neuroimaging and lumbar puncture did not show evidence of increased intracranial pressure or hydrocephalus. INTERVENTION: Cranioplasty using Palacos was performed one-and-a-half years after trauma. Immediately after surgery, the patient noted remarkable improvement in his symptoms. Headaches and fatigue disappeared within two days. Two weeks after cranioplasty the patient had orthotropia and virtually normal ocular motility. Neurological symptoms completely disappeared. Recovery remained sustained for over 5 years after cranioplasty. CONCLUSION: To our knowledge, this represents the first case of the syndrome of the trephined in which the neurological deficits map primarily to the brainstem and show rapid improvement following cranioplasty. We show that cranioplasty in patients with large skull defects is indicated for more then cosmetic reasons and should be considered even after longer periods following a trauma.

Adult↗
PubMed2006

Essential tremor-the most common movement disorder in older people.

Essential tremor (ET) affects approximately 4% of the population above 65 years of age. The traditional view that ET is a familial monosymptomatic disorder with a benign prognosis has recently been challenged, as it is now known to be a progressive and clinically heterogeneous condition with sporadic and familial forms. The pathogenesis of ET is not fully understood, though a disordered central mechanism is the most likely site of origin with possible modulation by muscle adrenoreceptors. The limited post-mortem studies have not shown consistent abnormalities in the brains of ET patients. ET is often misdiagnosed as Parkinson's disease, particularly in the older population. Tremor amplitude increases with age, accounting for substantial disability in older people. Current therapy (drugs and neurosurgery) has significant limitations in older people. A better understanding of its pathophysiology in the future will help in developing more effective therapy, including neuroprotective strategies.

Adrenergic beta-Antagonists↗