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P J García-Ruiz

Publications and source records attributed to P J García-Ruiz.

12 recordsLinked to original sources
PubMed2001

Pharmacological options for the treatment of Tourette's disorder.

Tourette's disorder is a neuropsychiatric disorder characterised clinically by motor and vocal tics, which may be associated to conductual disorders such as obsessive-compulsive disorder (OCD) and attention-deficit hyperactivity disorder (ADHD). Although the neurochemistry of Tourette's disorder is not well known, there are some effective therapies for tics, OCD and ADHD. However, these are not devoid of adverse effects. Tics only require treatment when they interfere with the functioning of the patient. If therapy is needed, monotherapy at the minimal effective dose is desirable, but some patients may require two or more drugs. The most frequently used drugs for tics are antipsychotics (mainly pimozide and haloperidol) and clonidine. The potential usefulness of atypical antipsychotic drugs (risperidone, olanzapine, clozapine, ziprasidone) and other dopaminergic drugs (fluphenazine, sulpiride, tiapride, metoclopramide, piquindone, tetrabenazine), clonazepam, calcium channel antagonists, botulinum toxin, dopamine agonists, selegiline, and other drugs is discussed. The drugs of choice for OCD in patients with Tourette's disorder are the selective serotonin reuptake inhibitors (SSRIs), although the tricyclic antidepressant clomiplamine, which inhibits both serotonin and noradrenaline uptake, has also been found to be useful. ADHD can be treated with some psychostimulants, mainly methylphenidate, although these drugs must be used with caution. Other potentially useful drugs for the treatment of ADHD in patients with Tourette's disorder are clonidine, guanfacine, selegiline, some tricyclic antidepressants, sertraline, pimozide and clonazepam. Finally, the potential value of some nonpharmacological therapies (hypnotherapy, biofeedback, conductual therapies, electroconvulsive therapy, acupuncture and surgery) is briefly reviewed.

Adrenergic alpha-Agonists↗
PubMed1997

Drug-induced movement disorders.

Parkinsonism, tremor, chorea-ballismus, dystonia, tardive dyskinesia, myoclonus, tics and akathisia can be induced by many drugs. The drugs that are most frequently implicated in movement disorders are antipsychotics, calcium antagonists, orthopramides and substituted benzamides (e.g. metoclopramide, sulpiride, clebopride, domperidone), CNS stimulants, antidepressants, anticonvulsants, antiparkinsonian drugs and lithium. It is possible for a single drug to induce 2 or more types of movement disorders in the same patient. Movement disorders are not always reversible after drug withdrawal.

Akathisia, Drug-Induced↗
PubMed1997

[A comparative study of the effect of bromocriptine and pergolide on Parkinson disease].

INTRODUCTION: Bromocriptine and pergolide are the two dopamine agonists most often used in Parkinson's disease. Few comparative studies of the efficacy of both compounds are available. OBJECTIVE: To compare the relative efficacy of bromocriptine and pergolide in patients with Parkinson's disease and intermediate stages of evolution. METHODS: Open label study of 5-months of duration. The first agonist was given for two months and, after a period of substitution of one month, the second agonist was also maintained for two months. RESULTS: Pergolide was more effective than bromocriptine for global scores of the UPDRS, total motor scores, clinical symptoms, akinesia and rigidity. Both compounds were equal effective for the treatment of tremor and fluctuations. Both agonists produced similar side effects. CONCLUSIONS: At the ration 1/10 mg/day pergolide was more effective than bromocriptine in patients with Parkinson's disease at intermediate stages of evolution.

Aged↗
PubMed1996

[Calcium, neuronal death and neurological disease].

Calcium ion (Ca2+) plays a role in several important functions in the central nervous system such as production of action potentials, neurotransmitter release, or neuronal plasticity, etc. However, its excessive influx to neurons due to failure of the mechanisms implicated in the regulation of its intracellular concentration (Ca(2+)-channels, calcium binding proteins), leads to a cascade of events which causes cytotoxicity and neuronal death. Ca2+ mediated toxicity has been implicated in the pathogenesis of neurodegenerative diseases (Parkinson's, Alzheimer's, amyotrophic lateral sclerosis, Huntington's), brain ischemia, epilepsy, cranial trauma, and AIDS-dementia complex. In this article we review the current status of this topic.

Alzheimer Disease↗
PubMed1992

Parkinsonism associated with calcium channel blockers: a prospective follow-up study.

Parkinsonism is a well-known side effect of some calcium channel blockers (CCB). Its long-term evolution, however, is unknown. To clarify this issue, we performed a prospective follow-up study involving 32 patients diagnosed with CCB-induced parkinsonism. After the baseline examination, the CCB were discontinued and serial evaluations were carried out according to the same protocol. Despite a global improvement, cognitive and mood disturbances subsided slowly, and tremor persisted in most patients. After 18 months of CCB withdrawal, 44% of patients had depression, 88% had tremor, and 33% still had criteria for diagnosis of parkinsonism. During the survey, only three patients were found to be fully recovered. The improvement of some clinical symptoms was related to age: Patients younger than 73 years recovered better than older patients did. Our data indicate that CCB-induced parkinsonism is not the benign condition previously thought, and suggest an age-related prognosis of this entity.

Adrenergic beta-Antagonists↗
PubMed1992

Serum levels of alpha-tocopherol (vitamin E) in Parkinson's disease.

To elucidate the possible role of vitamin E in the pathogenesis of Parkinson's disease (PD), we compared serum levels of alpha-tocopherol (vitamin E), measured by high-performance liquid chromatography, and the vitamin E/cholesterol ratio of 42 Parkinson's disease (PD) patients using their spouses as the control group. The serum levels of vitamin E did not differ significantly between the groups (13.84 +/- 0.56 micrograms/ml for PD and 14.80 +/- 0.57 micrograms/ml for controls), nor did the vitamin E/cholesterol ratio (0.64 +/- 0.03 for both groups). There was no influence of antiparkinsonian therapy on vitamin E or the vitamin E/cholesterol ratio. Serum levels of the vitamin E and vitamin E/cholesterol ratio did not correlate with age, age at onset, scores of the Unified Parkinson's Disease Rating Scale or the Hoehn and Yahr staging in the PD group. These results suggest that serum vitamin E concentrations do not play a role in the pathogenesis of PD.

Aged↗
PubMedDate not supplied

[Abnormal movements. Historical notes].

Most of the knowledge about movement disorders comes from the last fifty years. However, the ancients made some remarkable neurological depictions. We still can find some neurological descriptions including Parkinson's disease in the Bible, and the ancient writings of Atreya and Susruta. In addition, classic tests provide us of valuable information on historical personages, including the dystonia of Alexander the Great.

History, 19th Century↗