Orofacial Dyskinesia in Elderly.
Ontology highlight
ABSTRACT:
SUBMITTER: Pandey S
PROVIDER: S-EPMC6353328 | biostudies-literature | 2015 Dec
REPOSITORIES: biostudies-literature
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Project description:We reported a case of a 33-year-old lady who was diagnosed with a Pineal tumor and underwent craniotomy and gross total surgical resection of the mass through a right occipital transtentorial approach. Immediately upon extubation, the patient started to have persistent chewing-like movements typical of orofacial dyskinesia that resulted later in buccal mucosal injury and swelling of the lips. The movements spontaneously resolved after 3 days. The patient was not taking any medications that were known to induce such movements. Literature review showed that one of the possible mechanisms could be that the suddenly reduced melatonin level in the acute postoperative period leads to dysregulation of dopamine secretion in the nigrostriatal and limbic system causing these abnormal movements. To the best of our knowledge, this is the first such reported complication of orofacial dyskinesia post craniotomy for resection of the pineal tumor in humans.
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Project description:1. Tardive dyskinesia (TD), a syndrome of potentially irreversible, involuntary hyperkinetic disorder occurring in 20 - 40% of the patient population undergoing chronic neuroleptic treatment is a major limitation of neuroleptic therapy. 2. Oxidative stress and products of lipid peroxidation are implicated in the pathophysiology of various neurological disorders including tardive dyskinesia. 3. Chronic treatment with neuroleptics leads to the development of abnormal oral movements in rats known as vacuous chewing movements (VCMs). Vacuous chewing movements in rats are widely accepted as an animal model of tardive dyskinesia. 4. All the antipsychotics were administered i.p. once daily for 21 days, whereas carvedilol (also i.p.) was administered twice daily. Rats chronically treated with haloperidol (1.0 mg kg(-1)) or chlorpromazine (5 mg kg(-1)) but not clozapine (2 mg kg(-1)) significantly developed vacuous chewing movements and tongue protrusions. Carvedilol dose dependently (0.5 - 2 mg kg(-1)) reduced the haloperidol or chlorpromazine-induced vacuous chewing movements and tongue protrusions. 5. Biochemical analysis revealed that chronic haloperidol or chlorpromazine but not clozapine treatment significantly induced lipid peroxidation and decreased the glutathione (GSH) levels in the forebrains of rats. Chronic haloperidol or chlorpromazine but not clozapine treated rats showed decreased forebrain levels of antioxidant defence enzymes, superoxide dismutase (SOD) and catalase. 6. Co-administration of carvedilol (0.5-2 mg kg(-1)) significantly reduced the lipid peroxidation and restored the decreased glutathione levels by chronic haloperidol or chlorpromazine treatment. Co-administration of carvedilol (1-2 mg kg(-1)) significantly reversed the haloperidol or chlorpromazine-induced decrease in forebrain SOD and catalase levels in rats. However, lower dose of carvedilol (0.5 mg kg(-1)) failed to reverse chronic haloperidol or chlorpromazine-induced decrease in forebrain SOD and catalase levels. 7. The major findings of the present study suggest that oxidative stress might play a significant role in neuroleptic-induced orofacial dyskinesia. In conclusion, carvedilol could be a useful drug for the treatment of neuroleptic-induced orofacial dyskinesia.
| S-EPMC1573352 | biostudies-other
Project description:Antipsychotics often cause tardive dyskinesia, an adverse symptom of involuntary hyperkinetic movements. Analysis of the US Food and Drug Administration Adverse Event Reporting System and JMDC insurance claims revealed that acetaminophen prevented the dyskinesia induced by dopamine D2 receptor antagonists. In vivo experiments further showed that a 21-day treatment with haloperidol increased the number of vacuous chewing movements (VCMs) in rats, an effect that was inhibited by oral acetaminophen treatment or intracerebroventricular injection of N-(4-hydroxyphenyl)-arachidonylamide (AM404), an acetaminophen metabolite that acts as an activator of the transient receptor potential vanilloid 1 (TRPV1). In mice, haloperidol-induced VCMs were also mitigated by treatment with AM404 applied to the dorsal striatum, an effect not seen in TRPV1-deficient mice. Acetaminophen prevented the haloperidol-induced decrease in the number of c-Fos+preproenkephalin+ striatal neurons in wild-type mice but not in TRPV1-deficient mice. Finally, chemogenetic stimulation of indirect pathway medium spiny neurons in the dorsal striatum decreased haloperidol-induced VCMs. These results suggest that acetaminophen activates the indirect pathway neurons by activating TRPV1 channels via AM404.
| S-EPMC8262333 | biostudies-literature
Project description:Paroxysmal kinesigenic dyskinesia (PKD) is characterized by transient and recurrent involuntary movements that are triggered by a sudden movement. Here, we report an elderly female patient with a 1-month history of paroxysmal rigidity of the right limb. As the symptoms were characterized as paroxysmal, transient, and repetitive, her condition was initially thought to be epilepsy. Subsequent examinations showed no abnormality in the continuous video-electroencephalogram (EEG) monitoring, magnetic resonance imaging (MRI), fluorodeoxyglucose (FDG)-positron emission tomography (PET)/computed tomography (CT), and genetic testing. The final diagnosis was identified as clinically diagnosed PKD, and the symptoms were well controlled after oxcarbazepine treatment. To our knowledge, this is the first report to show elderly-onset PKD. This case expands our understanding of the age of onset of PKD. However, it is necessary to differentiate PKD from reflex epilepsy and hysteria attacks. For patients with typical clinical manifestations, we should adhere to the standard diagnostic workflow for the efficient diagnosis of PKD, aiming at avoiding misdiagnosis and mistreatment.
| S-EPMC9588133 | biostudies-literature
Project description:A 79-year-old man was admitted for 2 weeks of dizziness, followed by diplopia, involuntary movement and progressive gait disturbances. Neurologic examination revealed horizontal and vertical gaze paresis, bilateral choreiform movement with orofacial dyskinesia, and limb/truncal ataxia. MRI revealed fluid-attenuated inversion recovery image-hyperintense signal abnormalities in the dorsal midbrain, pontine and medulla. Within another few days, the patient developed type II acute respiratory failure requiring artificial invasive ventilation. Because autoimmune encephalitis was suspected, he received intravenous immunoglobulin therapy followed by intravenous methylprednisolone, but only his ophthalmoplegia improved minimally. Serological tests were positive for anti-Ri onconeural antibodies. CT-guided mediastinal lymph node biopsy was performed and revealed small cell lung carcinoma. We report the rare manifestation of anti-Ri antibody-associated paraneoplastic neurological syndrome (PNS), and this case can alert us to the importance of respiratory management in this diverse neurologic disease. Furthermore, PNSs positive for anti-Ri antibodies should be added to the list of differential diagnoses of chorea with orofacial dyskinesia.
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Project description:Clozapine is an atypical antipsychotic used in the treatment of refractory schizophrenia. It has a well-known side effect profile, including agranulocytosis, decreased seizure threshold, and tardive dyskinesia. In addition, numerous case reports have described clozapine-induced stuttering in adults. However, there has been only one previous case report describing it in the adolescent population. In addition, concurrent lithium therapy has been shown to enhance the neurotoxic effects of antipsychotics and lower the seizure threshold. Here, we report on the development of clozapine-induced microseizures, orofacial dyskinesia, and stuttering in a 17-year-old adolescent male with treatment of refractory early onset schizophrenia on clozapine and concurrent lithium therapy. The patient's symptoms of schizophrenia responded well to the clozapine regimen. However, with the escalating dose of clozapine, the patient developed speech dysfluency in the form of stuttering and perioral twitching. An electroencephalogram confirmed seizure activity. Due to similarities with tardive dyskinesia, symptoms of microseizures induced by atypical antipsychotics may not be accurately diagnosed. A multidisciplinary treatment of speech dysfluency is of particular importance in the adolescent schizophrenic patients, who are expected to have longer duration of lifetime exposure to antipsychotics and in whom peer group interaction is crucial for normal personal and social development.
| S-EPMC5556608 | biostudies-other
Project description:Developmental gene expression profiling of mammalian, fetal orofacial tissue Keywords = orofacial Keywords = embryo Keywords = development Keywords: time-course
2004-08-03 | GSE1624 | GEO
Project description:Achondroplasia (Online Mendelian Inheritance in Man [OMIM] 100800), is considered as a form of skeletal dysplasia dwarfism that manifests with stunted stature and disproportionate limb shortening. Achondroplasia is of special interest in the field of dentistry because of its characteristic craniofacial features which include relative macrocephaly, depressed nasal bridge and maxillary hypoplasia. Presence of large head, implanted shunt, airway obstruction and difficulty in head control requires special precautions during dental management. The current case report highlights the orofacial manifestations of Achondroplasia in a young pediatric patient, along with the multidisciplinary treatment (including the dental treatment) done for the patient which also might help the general practitioners in better understanding of the condition.
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