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At least 1,261 records · Page 70Linked to original sources
PubMed1983

[Pharmacologically-caused eye movement disorders--differential diagnosis and mechanisms of action].

The variety of drug induced patterns of pathological eye movements is reviewed with emphasis on hydantoins, barbiturates, carbamazepine, benzodiazepines, amitriptyline and alcohol. These different substances may be analogous or distinct in their site of action within the labyrinths, brain stem and cerebellum. Ocular oscillations are described in correlation to drug uptake or serum levels such as positional, downbeat, gaze evoked, periodic alternating nystagmus as well as saccadic pursuit, slowing down of saccades, alteration of VOR gain or suppression by fixation, internuclear and complete ophthalmoplegia. Most of the ocular motor disturbances are possibly due to a pharmacologically induced transient dysfunction of the vestibulo-cerebellar flocculus loop.

Alcoholism↗
PubMed1992

SCH 39166, a potential antipsychotic drug, does not evoke movement disorders in cebus monkeys.

Subchronic administration of a neuroleptic in cebus monkeys can reliably mimic the abnormal movements produced by these drugs in humans. SCH 39166 is the best candidate to test in this model to determine if selective antagonism at the dopamine D1 receptor is devoid of these side effects. It has superior selectivity for the dopamine D1 site versus several other sites and a significantly longer duration in primates than the prototypical D1 antagonist, SCH 23390. In contrast to haloperidol, weekly administration of SCH 39166 for 14 weeks did not produce abnormal movements but did produce equivalent sedative effects. Thus dopamine D1 antagonists are uniquely different from D2 antagonists with regards to the production of abnormal movements.

Animals↗
PubMed1985

Involuntary disorders of movement in chronic schizophrenia--the role of the illness and its treatment.

The prevalence and distribution of involuntary movements in age-matched chronic schizophrenics treated and not treated with neuroleptics were compared. While exposure to neuroleptic drugs in the past was important, high rates of movement disorder were associated with the severe, untreated illness. Ventricular enlargement correlated with severe movement disorder but not with past neuroleptic exposure. It is suggested that in the context of Schizophrenia neuroleptic drugs may act to promote what are features of the illness for some, and that in the search for predisposing factors illness, as well as treatment variables, is worthy of consideration.

Antipsychotic Agents↗
PubMed2001

Pharmacogenetic assessment of antipsychotic-induced movement disorders: contribution of the dopamine D3 receptor and cytochrome P450 1A2 genes.

Tardive dyskinesia (TD) is characterized by involuntary movements predominantly in the orofacial region and develops in approximately 20% of patients during long-term treatment with typical antipsychotics. The high prevalence of TD and its disabling and potentially irreversible clinical course is an important shortcoming for treatment with typical antipsychotics. The studies presented in this article evaluate the role of single nucleotide polymorphisms in dopamine D3 receptor (DRD3) and CYP1A2 genes for propensity to develop TD in patients with schizophrenia. In theory, a combined pharmacogenetic analysis of pharmacokinetic and pharmacodynamic targets for antipsychotics should improve our ability to identify subpopulations that differ in drug safety profile. This information may in turn contribute to the design of more efficient clinical trials and thus expedite the development and regulatory approval of newer antipsychotic compounds.

Antipsychotic Agents↗
PubMed1995

Eye movement disorders.

The ophthalmic, neurologic, and neuro-ophthalmic literature over the past year have included a wide variety of interesting case reports, patient series, and reviews involving eye movement abnormalities. This review highlights some of the more important articles and how they contribute to our understanding, diagnosis, and treatment of these disorders. A few topics will receive particular emphasis. In patients with sixth nerve palsies, botulinum toxin injection of the ipsilateral medial rectus muscle has been advocated. Recent results suggest that this treatment has no beneficial effect in acute sixth nerve palsies, but it may have a role in chronic cases. Two groups of authors, each supplying retrobulbar botulinum toxin injection for patients with acquired nystagmus and debilitating oscillopsia, obtained mixed results. One group of patients was moderately satisfied, whereas in the other group, no patients elected to repeat the treatment because of side effects such as ptosis, diplopia, or discomfort from keratitis. Finally, skew deviation is becoming a more recognized cause of vertical double vision from a central or peripheral basis. Articles published recently showed that cyclodeviation may be seen in skew deviation, and that binocular cyclotorsion distinguishes this motility abnormality from a fourth nerve palsy, which exhibits monocular excyclotorsion.

Botulinum Toxins↗
PubMed2000

The pedunculopontine nucleus: its role in the genesis of movement disorders.

The pedunculopontine nucleus (PPN) is located in the dorso-lateral part of the ponto-mesencephalic tegmentum. The PPN is composed of two groups of neurons: one containing acetylcholine, and the other containing non-cholinergic neurotransmitters (GABA, glutamate). The PPN is connected reciprocally with the limbic system, the basal ganglia nuclei (globus pallidus, substantia nigra, subthalamic nucleus), and the brainstem reticular formation. The caudally directed corticolimbic-ventral striatal-ventral pallidal-PPN-pontomedullary reticular nuclei-spinal cord pathway seems to be involved in the initiation, acceleration, deceleration, and termination of locomotion. This pathway is under the control of the deep cerebellar and basal ganglia nuclei at the level of the PPN, particularly via potent inputs from the medial globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. The PPN sends profuse ascending cholinergic efferent fibers to almost all the thalamic nuclei, to mediate phasic events in rapid-eye-movement sleep. Experimental evidence suggests that the PPN, along with other brain stem nuclei, is also involved in anti-nociception and startle reactions. In idiopathic Parkinson's disease (IPD) and parkinson plus syndrome, overactive pallidal and nigral inhibitory inputs to the PPN may cause sequential occurrences of PPN hypofunction, decreased excitatory PPN input to the substantia nigra, and aggravation of striatal dopamine deficiency. In addition, neuronal loss in the PPN itself may cause dopamine-resistant parkinsonian deficits, including gait disorders, postural instability and sleep disturbances. In patients with IPD, such deficits may improve after posteroventral pallidotomy, but not after thalamotomy. One of the possible explanations for such differences is that dopamine-resistant parkinsonian deficits are mediated to the PPN by the descending pallido-PPN inhibitory fibers, which leave the pallido-thalamic pathways before they reach the thalamic targets.

Animals↗
PubMed1997

Slow saccades and other eye movement disorders in spinocerebellar atrophy type 1.

In order to study the relation between genotype and phenotype, a detailed study of the course of oculomotor deficits was performed in three patients with autosomal-dominant cerebellar ataxia, subtype spinocerebellar atrophy type 1 (SCA 1) using clinical testing and electrooculography. DNA analysis revealed a CAG repeat expansion of 65 in the SCA 1 gene on chromosome 6p in all patients. A progressive disorder of the saccadic system became obvious, leading to a marked slowing of saccadic eye movements and loss of pathological and physiological nystagmus. An upward gaze palsy developed early, followed by horizontal and downward gaze palsy at a later state of the disease. Smooth pursuit eye movements were disturbed to a lesser extent; the vestibulo-ocular reflex was reduced. As an additional feature, severe loss of visual acuity developed due to progressive optic nerve atrophy. The oculomotor deficits can be explained by progressive damage to the brain stem rather than to the cerebellum. Each combination of oculomotor deficits with or without optic atrophy may occur irrespective of the gene locus of the disease, making a correlation between clinical signs and genetic findings difficult.

Adult↗
PubMed2001

5: Movement disorders I: parkinsonism and the akinetic-rigid syndromes.

The major features of akinetic-rigid syndromes are bradykinesia (small, slow movements), rigidity and tremor, often summarised as "parkinsonism". Approximately 80% of akinetic-rigid syndromes are due to Parkinson's disease. Treatment of Parkinson's disease should be determined by level of disability and handicap. The combination of levodopa and peripheral dopadecarboxylase inhibitor is the most efficacious symptomatic treatment for Parkinson's disease. Motor fluctuations appear after 2-3 years of levodopa treatment, and affect at least 50% of patients after five years. Surgery can relieve refractory tremor and dyskinesias, but does not alter disease progression or need for drug therapy.

Aged↗
PubMedDate not supplied

[A study made on a data base of 2,471 patients with Parkinson disease and disorders of movement in Health District 1 of the autonomous region of Madrid. Observed demographic changes over 8 year-period].

INTRODUCTION: A specialised unit may influence favourably primary levels of health system by alerting physicians and patients on the existence of those pathologies most commonly seen. OBJECTIVES: To determine demographic changes and referral patterns observed in a hospital-based monographic outpatient clinic on Parkinson's disease and movement disorders along an eight-year period (1991-1998). PATIENTS AND METHODS: Database analysis of 2,471 patients attending a specialised unit covering an urban and rural population of 630,000 people in South-East Madrid city and county. RESULTS: We observed a slight, albeit non-significant reduction in the incidence of secondary parkinsonisms (40% of all parkinsonisms observed). This occurred despite a drastic reduction in drug-induced parkinsonisms, particularly those caused by cinnarizine/flunarizine and flupentixol. The reduction was balanced by a relative increase in neurodegenerative parkinsonisms, particularly Lewy body dementia. There was a sustained decrease in the time elapsed between onset of symptoms and identification of parkinsonisms as well as identification of its primary or symptomatic nature. The incidence of tardive dystonia (46.7%) of all symptomatic dystonias) remained unchanged. Essential tremor referrals markedly increased along the study period. CONCLUSIONS: Demographics features of patients attending a Parkinson's disease and movement disorder unit are submitted to changes over time. These probably reflect better awareness about these conditions by patients and physicians, ready access to hospital-based specialised units, and a greater demand for specialised care by the aged.

Adult↗