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OSCE 10A (card 1 of 2) – Examine for extrapyramidal side-effects
Published in Bhaskar Punukollu, Michael Phelan, Anish Unadkat, MRCPsych Part 1 In a Box, 2019
Bhaskar Punukollu, Michael Phelan, Anish Unadkat
3. General observation – comment on: Facial expression and evidence of oral-mandibular-lingual signs: chewing movements, rabbit syndrome, bon bon sign, grimacing, pouting, repetitive swallowing, trismus, mask-like facies.Signs of akathisia: legs shaking.Parkinsonian tremor: resting tremor.Limb movements: such as ballismus.Neck/spine signs: torticollis, antecollis, retrocollis, pleurothotonus, opisthotonus, axial hyperkinesias.Ocular signs: blepharospasm, oculogyric crisis.Vocal tics, dysphonia (from vocal cord spasm), stridor.Look for drooling, which may result from increased salivation and dysphagia.
Causes and Assessment of Dysphagia and Aspiration
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Parkinson’s disease is progressive and characterized by the triad of resting tremor, bradykinesia and rigidity, patients having difficulty in starting, performing and stopping a movement. The dysphagia is associated with changes in striated muscle under dopaminergic control and smooth muscle under autonomic control and is mostly due to abnormalities in the oral preparatory and pharyngeal phases of swallowing. The oral phase of the swallow is affected by rigidity of the tongue musculature with inefficient, non-propulsive, back and forth movement of tongue which prevents food being delivered into the oropharynx. In the pharyngeal phase there is delayed contraction of the pharyngeal muscles. Findings on VF include impaired motility, hypopharyngeal stasis, aspiration and poor movement of the epiglottis.
Twitching
Published in Wesley C. Finegan, Angela McGurk, Wilma O’Donnell, Jan Pederson, Elizabeth Rogerson, Care of the Cancer Patient, 2018
Wesley C. Finegan, Angela McGurk, Wilma O’Donnell, Jan Pederson, Elizabeth Rogerson
Resting tremor is seen in the following: extrapyramidal diseaseParkinson’s disease, including drug-induced Parkinsonism.
Cochlear implants and deep brain stimulators
Published in Cochlear Implants International, 2023
Zachary A. Kons, Kathryn L. Holloway, Daniel H. Coelho
Three years later, at age 50, the patient was noted to have bilateral resting tremor and was subsequently diagnosed with tremor-predominant Parkinson’s Disease. He was trialed on medical therapy with carbidopa-levodopa, but due to limited response and worsening quality of life, he was referred for DBS implantation of the subthalamic nucleus (STN). Despite significant artifact on preoperative MRI necessary for implantation of DBS (Fig. 2), an outside neurosurgical team proceeded with DBS implantation in two stages, first implanting the left STN (Fig. 3, panels a, b) followed by the right STN (Fig. 3, panels c, d). The extension was placed ipsilateral to the cochlear implant as there may have been sterility concerns about placing the extension in close proximity to the percutaneous Baha abutment. As of the patient’s most recent follow-up visit, he continues to experience adequate tremor control with his DBS while wearing both his CI and Baha. Of note, the neurosurgical service did not consult the CI team prior to implantation of his DBS. Fortunately, although the extensions passed directly over the CI receiver-stimulator, there was no injury to the device. In addition, he does not report magnet retention issues or phantom sounds when the DBS is in use. Retrospectively, a 3D reconstruction of the final postoperative CT scan was created using 3D Slicer to visualize the proximity of the DBS extension wires to the preexisting CI (Fig. 3, panel e).(Fedorov et al., 2012)
Acute parkinsonism in patients with systemic lupus erythematosus: a case report and review of the literature
Published in International Journal of Neuroscience, 2022
Chayasak Wantaneeyawong, Nuntana Kasitanon, Kullanit Kumchana, Worawit Louthrenoo
Of the 28 patients in this report, parkinsonism occurred in 90% of the SLE patients with active disease. Parkinsonism occurred together with other clinical manifestations that led to SLE diagnosis in approximately one-fourth of the cases, while it occurred in the remainder after SLE diagnosis. Resting tremor, bradykinesia and rigidity were among the main clinical features seen in parkinsonism in SLE patients, which was similar to those seen in non-SLE patients. Other neurological features, including seizures, psychosis, alteration of mental status, headache and focal neurological deficits, supported the fact that parkinsonism was part of CNS involvement in SLE patients. Of interest, SLE children with parkinsonism had significantly more psychosis, seizures/psychosis, mutism, brisk deep tendon reflexes and positive extensor response than adult patients.
The rs3129882/rs4248166 in HLA-DRA and rs34372695 in SYT11 are not associated with sporadic Parkinson’s disease in Central Chinese population
Published in International Journal of Neuroscience, 2021
Jie Li, Lubao Jian, Jinsha Huang, Nian Xiong, Tao Wang
Parkinson’s disease (PD) is the second common progressive neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra (SN). Clinical symptoms include resting tremor, rigidity, bradykinesia, postural instability and a variety of non-motor symptoms such as depression, visual hallucination and sleep disorders [1]. Most PD cases are sporadic and about 5-10% of the patients are genetic cases [2]. Over the past decades, it has been proved that at least 16 loci and 9 major pathogenicity genes are associated with PD in familial and sporadic cases such as alpha-synuclein gene (SNCA), leucine-rich repeat kinase 2 gene (LRRK2), microtubule-associated protein Tau gene (MAPT), PARK16, cyclin G-associated kinase gene (GAK/PARK17), HLA-DR (PARK18), and the bone marrow stromal cell antigen 1 gene (BST1) [3,4].