UNASSIGNED: Camptocormia is a postural deformity that is characterized by a markedly flexed lumbar spine, with symptoms that worsen with walking and standing. Here, we report a case of camptocormia associated with Parkinson\'s disease.
UNASSIGNED: A 70-year-old man with a 7-year history of Parkinson\'s disease presented with a fall injury that caused lower back pain for 3 months and was aggravated for 2 months. He had been diagnosed with a compression fracture after the fall and had undergone percutaneous kyphoplasty at a local hospital. MRI showed non-union of the L1 vertebra and compression fracture of L2. The patient underwent posterior osteotomy, canal decompression, and internal fixation of the T10-L3 intervertebral plate with bone graft fusion. Postoperative examination showed that the lumbar lordosis was corrected and sensation was restored in both lower extremities. However, after 1 month, the fixation was loosened and a correction surgery was performed at our hospital. At the most recent follow-up at 1.5 years, the patient was found to be in good general health and did not complain of lower back discomfort. He was also actively exercising according to the rehabilitation regimen and had resumed social life.
UNASSIGNED: This is a rare case of camptocormia in a Parkinson\'s patient that highlights the need for careful evaluation of whether internal spinal fixation surgery is beneficial in such patients.

UNASSIGNED: For safety reasons, both magnetic resonance-guided high-intensity focused ultrasound (MRgHiFUS) thalamotomy and pallidotomy are currently approved exclusively for unilateral treatment, but axial symptoms like levodopa-induced orofacial dyskinesia require a bilateral approach.
UNASSIGNED: We report the first case of successful bilateral MRgHiFUS pallidotomy for peak-dose dyskinesia in a patient with Parkinson\'s disease (PD).
UNASSIGNED: The treatment decision was based on the patient\'s reluctance toward brain implants and pump therapies and the fact that he had limited access to a deep brain stimulation center in his home country. The treatment was planned as staged procedure with an interval of 18 months because of travel restrictions because of the coronavirus disease (COVID)-19 pandemic.
UNASSIGNED: After the second treatment, levodopa-induced orofacial dyskinesia remitted and improved bradykinesia and rigidity with stable gait and good postural reflexes.
UNASSIGNED: This promising result suggests that in selected PD patients with dyskinesia, staged bilateral MRgHiFUS pallidotomy might be considered.

Lewy bodies (LBs) are usually detected in patients with idiopathic Parkinson\'s disease (PD), but there have been few reports of LBs in a familial form of early-onset PD associated with several mutations in parkin, a gene that encodes a ubiquitin E3 ligase involved in mitochondrial homeostasis, being also known as PARK2. Here, we report a case of PD with a PARK2 mutation characterized by a homozygous deletion of exon 2 and incidental LB pathology. A 60-year-old man developed tremor in the upper limbs. Although levodopa was initially effective, his symptoms slowly progressed. His cardiac uptake of 123 I-metaiodobenzylguanidine, as assessed by myocardial scintigraphy, decreased from an early stage after the onset. At the age of 81 years, he developed Legionella pneumonia and died of respiratory failure. Histopathological examination revealed a moderate loss of pigmented neurons, as well as gliosis in the substantia nigra and the locus coeruleus. Little LB-related pathology was found in the locus coeruleus, dorsal nucleus of vagal nerve, and basal nucleus of Meynert. The cardiac sympathetic nerve in the epicardium showed a reduction in the numbers of fibers immunoreactive for tyrosine hydroxylase and phosphorylated neurofilament protein. Genetic analysis of frozen brain materials revealed a homozygous deletion of exon 2 of parkin. To our knowledge, this is the first autopsy case with a homozygous deletion of exon 2 of parkin. The number of LBs was small, the age of disease onset was later than that in typical PARK2-associated PD patients, and cardiac sympathetic denervation was also present. Thus, we considered the LBs in our case as incidental and preclinical α-synucleinopathy.

The proverbial \"zebras\" in neurology are often times missed due to their low prevalence and incidence in the community. The number of misdiagnoses and improper therapeutic interventions that occur are further increased when patients with these rare diseases present with signs and symptoms of more common disorders. One such disease is sporadic Creutzfeldt-Jakob disease (sCJD), a prion disease that causes neuronal derangement and classically presents as a rapidly progressing dementia with extrapyramidal signs, ataxia, behavioural problems, and myoclonus in the advanced stage. It falls into the category of neurodegenerative disease, which also includes Alzheimer\'s disease, Huntington\'s disease, Parkinson\'s disease, and other Parkinson-related diseases. Though these diseases have overlapping symptomologies - such as cognitive impairment and neuromuscular dysfunction - they can be differentiated from one another based on the time course of the illness and the specific constellation of signs and symptoms. Our case report describes a patient who was found to have sCJD after months of treatment for Parkinson\'s disease and trigeminal neuralgia. Thus, we are highlighting the importance of recognizing rare diseases so that proper management can be initiated in a timely manner. Furthermore, we review the current literature on the diagnosis and management of sCJD.

The increasing use of herbal medicines calls for a heightened awareness of their potential side-effects. This especially pertains to western countries, where patients tend to use herbal medicine as self-medication, often alongside regular prescriptions, and physicians have less experience with their application. Here we report a case in which Parkinsonism, depression, and an atypical finding detected by dopamine transporter single-photon emission computed tomography were all belatedly recognized as side-effects of herbal medicine. This only occurred because one of its active ingredients, reserpine, has been extensively studied. For most other herbal medicines, however, knowledge about side-effects remains scarce or unavailable. Therefore, we suggest that physicians, when taking a medication history, should actively ask for the use of any herbal preparations.

Impulse control disorders (ICDs) are nonmotor complications of dopaminergic medications characterized by problems in behavioral self-control. Common management involves discontinuing or lowering dopaminergic medication, often producing motor worsening. We performed a retrospective chart review of Parkinson\'s disease (PD) patients treated with clozapine for ICDs. Four patients treated with clozapine for ICD were identified. Three patients were men. All 4 took dopaminergic medications at the time that ICDs developed; all received dopamine agonist therapy. ICDs included compulsive shopping, binge drinking, and hypersexuality. All 4 patients had complete resolution of symptoms while taking clozapine (12.5-37.5 mg). Two patients discontinued clozapine because of side effects. Larger studies are needed to further evaluate clozapine\'s role in treating PD patients with ICD.

Thymoma is a tumor originating from thymic gland, frequently manifesting with paraneoplastic neurological disorders. Its association with paraneoplastic dysautonomia is relatively uncommon. Here, we describe the challenging case of a 71 year-old female who developed subacute autonomic failure with digestive pseudo-obstruction, dysphagia, urinary tract dysfunction and orthostatic hypotension complicating an underlying extrapyramidal syndrome that had started 3 months before hospital admission. Autonomic symptoms had 2-month course and acutely worsened just before and during hospitalization. Combination of severe dysautonomia and parkinsonism mimicked rapidly progressing multiple system atrophy. However, diagnostic exams showed thymic tumor with positive anti-Hu antibodies on both serum and cerebrospinal fluid. Complete response of dysautonomia to immunoglobulins followed by thymectomy confirmed the diagnosis of anti-Hu-related paraneoplastic neurological syndrome. With regards to extrapyramidal symptoms, despite previous descriptions of paraneoplastic parkinsonism caused by other antineuronal antibodies, in our case no relation between anti-Hu and parkinsonism could be identified. A literature review of published reports describing anti-Hu positivity in thymic neoplasms highlighted that a definite autonomic disease due to anti-Hu antibodies is extremely rare in patients with thymoma but without myasthenia gravis, with only one case published so far.

OBJECTIVE: The objective of this study was to report the first case of unilateral vocal fold paralysis in a patient with Parkinson disease (PD) and to review the literature.
METHODS: This is a case report and literature review following PubMed search using the keywords \"Parkinson,\" \"vocal fold paralysis,\" \"vocal fold palsy,\" \"vocal fold immobility,\" \"vocal fold adductor palsy,\" \"airway obstruction,\" and \"stridor.\"
RESULTS: A total of 18 subjects diagnosed with PD and vocal fold paralysis were described. In all cases, the vocal fold paralysis was bilateral and the main presenting symptoms were stridor and shortness of breath necessitating intubation and tracheostomy. This article describes the first case of PD presenting with dysphonia secondary to unilateral vocal fold paralysis (left). The management consisted of injection laryngoplasty for medialization of the paralyzed vocal fold.
CONCLUSIONS: Patients with PD can present with unilateral vocal fold paralysis. Early treatment is advocated in view of the advent of injection laryngoplasty as a safe office procedure.

[F-18]-AV-1451 is a novel positron emission tomography (PET) tracer with high affinity to neurofibrillary tau pathology in Alzheimer\'s disease (AD). PET studies have shown increased tracer retention in patients clinically diagnosed with dementia of AD type and mild cognitive impairment in regions that are known to contain tau lesions. In vivo uptake has also consistently been observed in midbrain, basal ganglia and choroid plexus in elderly individuals regardless of their clinical diagnosis, including clinically normal whose brains are not expected to harbor tau pathology in those areas. We and others have shown that [F-18]-AV-1451 exhibits off-target binding to neuromelanin, melanin and blood products on postmortem material; and this is important for the correct interpretation of PET images. In the present study, we further investigated [F-18]-AV-1451 off-target binding in the first autopsy-confirmed Parkinson\'s disease (PD) subject who underwent antemortem PET imaging. The PET scan showed elevated [F-18]-AV-1451 retention predominantly in inferior temporal cortex, basal ganglia, midbrain and choroid plexus. Neuropathologic examination confirmed the PD diagnosis. Phosphor screen and high resolution autoradiography failed to show detectable [F-18]-AV-1451 binding in multiple brain regions examined with the exception of neuromelanin-containing neurons in the substantia nigra, leptomeningeal melanocytes adjacent to ventricles and midbrain, and microhemorrhages in the occipital cortex (all reflecting off-target binding), in addition to incidental age-related neurofibrillary tangles in the entorhinal cortex. Additional legacy postmortem brain samples containing basal ganglia, choroid plexus, and parenchymal hemorrhages from 20 subjects with various neuropathologic diagnoses were also included in the autoradiography experiments to better understand what [F-18]-AV-1451 in vivo positivity in those regions means. No detectable [F-18]-AV-1451 autoradiographic binding was present in the basal ganglia of the PD case or any of the other subjects. Off-target binding in postmortem choroid plexus samples was only observed in subjects harboring leptomeningeal melanocytes within the choroidal stroma. Off-target binding to parenchymal hemorrhages was noticed in postmortem material from subjects with cerebral amyloid angiopathy. The imaging-postmortem correlation analysis in this PD case reinforces the notion that [F-18]-AV-1451 has strong affinity for neurofibrillary tau pathology but also exhibits off-target binding to neuromelanin, melanin and blood components. The robust off-target in vivo retention in basal ganglia and choroid plexus, in the absence of tau deposits, meningeal melanocytes or any other identifiable binding substrate by autoradiography in the PD case reported here, also suggests that the PET signal in those regions may be influenced, at least in part, by biological or technical factors that occur in vivo and are not captured by autoradiography.

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