Acute Parkinsonism Research Articles

Pathophysiology of COVID-19-Related Extrapyramidal Disorders.

Coronavirus disease 2019 (COVID-19) has been associated with a variety of neurological manifestations (i.e., anosmia, ageusia, myalgia, headache) and neurological syndromes (i.e., encephalopathy, ischemic and hemorrhagic stroke, myelitis, encephalitis) underlying different pathogenetic mechanisms. COVID-19 has also been associated with various movement disorders including acute or subacute parkinsonism. However, to date, only few cases of parkinsonism linked to COVID-19 have been reported, nevertheless raising the possibility of a post-viral parkinsonian syndrome. Furthermore, various studies in vitro and in animal models have highlighted a close relationship between SARS-CoV-2 virus and α-synuclein, leading to the hypothesis that COVID-19 could represent a factor favoring the long-term development of α-synucleopathies. In this chapter, we will discuss the pathophysiological mechanisms related to movement disorders' manifestations of COVID-19 focusing on the possible overlap between pathogenetic mechanisms of Parkinson's Disease and COVID-19.

Acute parkinsonism secondary to SARS Cov 2 infection

SARS Cov 2 or Corona virus is a respiratory virus, responsible for a new pandemic since 2019. Main symptoms revolve around respiratory manifestations. Nevertheless, many extra-respiratory attacks are attributed to it. Among these impairments, neuropsychiatric disorders are frequently reported. They are manifested by cerebral vascular accidents, myelitis and mainly Guillain Barré syndromes. We report in this work the case of a patient who presented an acute Parkinsonian syndrome following COVID 19 infection. Brain MRI objectified lesions of the basal ganglia. The evolutionary consequences were favorable after treatment targeting covid 19 infection’s encephalopathy and Parkinsonian symptoms. This extremely rare clinical case enriches the very broad spectrum of neurological manifestations of SARS Cov 2 infection.

Partially reversible bilateral Lenticular fork sign and acute Parkinsonism in diabetic uremic syndrome (P5-11.005)

<h3>Objective:</h3> Not applicable <h3>Background:</h3> Diabetic uremic syndrome is a concept that has been increasingly recognized since it was proposed in 2003. It differs from uremic encephalopathy. Hereby, we describe the first case of North African Arab descent with end-stage renal disease and diabetes who developed acute Parkinsonism with bilateral lenticular fork sign and uremia that partially resolved after extensive dialysis therapy. <h3>Design/Methods:</h3> Not applicable <h3>Results:</h3> <h3>Case Description:</h3> 65 years old man with end-stage renal disease on peritoneal dialysis and newly diagnosed diabetes millets presented with a 3-day history of unsteady gait, generalized weakness, mild dysarthria, mild dysphagia, drowsiness, and changes in concentration. Examination revealed a mask face, dysphagia, absent gag reflex, dysphonia, generalized motor weakness more prominent in lower limbs, bradykinesia, absent knee reflexes, and myoclonic jerks. Laboratory studies showed urea 25 mmol/L, Creatinin 922 umol/L, arterial pH 7.25, and normal lactate. The lumbar puncture study was unremarkable. CT head showed swollen hypodense bilateral lentiform nuclei with a hypodense rim delineating the basal ganglia and giving the appearance of a lentiform fork sign. MRI showed bilateral T2 and FLAIR putamen and globus pallidus hyperintensity and significant lactate peak in the bilateral basal ganglia on MR spectroscopy. EMG study was evident of axonal polyneuropathy. IVIG course was commenced, and motor weakness improved. The peritoneal dialysis was intensified, and later treatment was switched to hemodialysis. Acidemia resolved, and uremia significantly improved. Two weeks post-admission, the fork sign on MRI significantly regressed, and the patient’s Parkinsonian symptoms partially improved. <h3>Conclusions:</h3> Development of acute or subacute extrapyramidal movement disorder in end-stage renal disease associated with diabetes should promote the possibility of diabetic uremic syndrome with bilateral basal ganglia lesions forming fork sign appearance that occurs early on brain imaging. Usually, extensive dialysis, preferable hemodialysis, leads to a total resolution of brain imaging and partial resolution of clinical findings. <b>Disclosure:</b> Dr. Nofal has nothing to disclose. Dr. Noorain has nothing to disclose. Dr. Safan has nothing to disclose. Dr. Adeli has nothing to disclose. Dr. Sokrab has nothing to disclose.

LPS Triggers Acute Neuroinflammation and Parkinsonism Involving NLRP3 Inflammasome Pathway and Mitochondrial CI Dysfunction in the Rat

Whether neuroinflammation leads to dopaminergic nigrostriatal system neurodegeneration is controversial. We addressed this issue by inducing acute neuroinflammation in the substantia nigra (SN) with a single local administration (5 µg/2 µL saline solution) of lipopolysaccharide (LPS). Neuroinflammatory variables were assessed from 48 h to 30 days after the injury by immunostaining for activated microglia (Iba-1 +), neurotoxic A1 astrocytes (C3 + and GFAP +), and active caspase-1. We also evaluated NLRP3 activation and Il-1β levels by western blot and mitochondrial complex I (CI) activity. Fever and sickness behavior was assessed for 24 h, and motor behavior deficits were followed up until day 30. On this day, we evaluated the cellular senescence marker β-galactosidase (β-Gal) in the SN and tyrosine hydroxylase (TH) in the SN and striatum. After LPS injection, Iba-1 (+), C3 (+), and S100A10 (+) cells were maximally present at 48 h and reached basal levels on day 30. NLRP3 activation occurred at 24 h and was followed by a rise of active caspase-1 (+), Il-1β, and decreased mitochondrial CI activity until 48 h. A significant loss of nigral TH (+) cells and striatal terminals was associated with motor deficits on day 30. The remaining TH (+) cells were β-Gal (+), suggesting senescent dopaminergic neurons. All the histopathological changes also appeared on the contralateral side. Our results show that unilaterally LPS-induced neuroinflammation can cause bilateral neurodegeneration of the nigrostriatal dopaminergic system and are relevant for understanding Parkinson's disease (PD) neuropathology.

Acute Parkinsonism with West Nile Virus Infection.

Acute Parkinsonism with West Nile Virus Infection.

Acute Parkinsonism and basal ganglia lesions after wasp sting.

Acute Parkinsonism and basal ganglia lesions after wasp sting.

SARS-CoV-2 Infection-Related Acute Parkinsonism and Encephalitis

COVID-19 infection can cause neurological manifestations as early and late complications (chronic COVID syndrome). These include headache, dizziness, confusion, acute cerebrovascular problems, ataxia, and seizures. COVID-19-related encephalopathy, encephalitis, and parkinsonism have been reported earlier; however, the possible links and pathophysiological mechanisms are unclear. In this report, we report a series of patients (n = 5) presenting with acute severe neurological syndromes such as parkinsonism, focal status epilepticus, or acute ataxia as a part of long-hauler COVID-19 infection. We categorized the clinico-radiological and electroencephalographic features in our cases to understand the clinical patterns in SARS-CoV-2 related brain cortex involvement. This might help in future for better clinical categorization for these COVID-19-related neurological manifestations.

Neuronal intranuclear inclusion disease in patients with adult-onset non-vascular leukoencephalopathy.

Neuronal intranuclear inclusion disease (NIID), caused by an expansion of GGC repeats in the 5'-untranslated region of NOTCH2NLC, is an important but underdiagnosed cause of adult-onset leukoencephalopathies. The present study aimed to investigate the prevalence, clinical spectrum and brain MRI characteristics of NIID in adult-onset nonvascular leukoencephalopathies and assess the diagnostic performance of neuroimaging features. One hundred and sixty-one unrelated Taiwanese patients with genetically undetermined nonvascular leukoencephalopathies were screened for the NOTCH2NLC GGC repeat expansions using fragment analysis, repeat-primed PCR, Southern blot analysis and/or nanopore sequencing with Cas9-mediated enrichment. Among them, 32 (19.9%) patients had an expanded NOTCH2NLC allele and were diagnosed with NIID. We enrolled another two affected family members from one patient for further analysis. The size of the expanded NOTCH2NLC GGC repeats in the 34 patients ranged from 73 to 323 repeats. Skin biopsies from five patients all showed eosinophilic, p62-positive intranuclear inclusions in the sweat gland cells and dermal adipocytes. Among the 34 NIID patients presenting with nonvascular leukoencephalopathies, the median age at symptom onset was 61 years (range, 41-78 years) and the initial presentations included cognitive decline (44.1%; 15/34), acute encephalitis-like episodes (32.4%; 11/34), limb weakness (11.8%; 4/34) and parkinsonism (11.8%; 4/34). Cognitive decline (64.7%; 22/34) and acute encephalitis-like episodes (55.9%; 19/34) were also the most common overall manifestations. Two-thirds of the patients had either bladder dysfunction or visual disturbance. Comparing the brain MRI features between the NIID patients and individuals with other undetermined leukoencephalopathies, corticomedullary junction curvilinear lesions on diffusion weighted images were the best biomarkers for diagnosing NIID with high specificity (98.4%) and sensitivity (88.2%). However, this diffusion weighted imaging abnormality was absent in 11.8% of the NIID patients. When only fluid-attenuated inversion recovery images were available, the presence of white matter hyperintensity lesions either in the paravermis or middle cerebellar peduncles also favoured the diagnosis of NIID with a specificity of 85.3% and sensitivity of 76.5%. Among the MRI scans of 10 patients, performed within 5 days of the onset of acute encephalitis-like episodes, five showed cortical hyperintense lesions on diffusion weighted images and two revealed focal brain oedema. In conclusion, NIID accounts for 19.9% (32/161) of patients with adult-onset genetically undiagnosed nonvascular leukoencephalopathies in Taiwan. Half of the NIID patients developed encephalitis-like episodes with restricted diffusion in the cortical regions on diffusion weighted images at the acute stage. Corticomedullary junction hyperintense lesions, white matter hyperintensities in the paravermis or middle cerebellar peduncles, bladder dysfunction and visual disturbance are useful hints to diagnosing NIID.

Parkinsonism in multiple sclerosis patients: A prospective observational study

Background. Rare cases of coexisting multiple sclerosis and parkinsonism have been reported in the literature. However, the true prevalence, clinical characteristics, and causal relation between the two entities have not been systematically evaluated.Objective. To evaluate the prevalence of parkinsonism in patients with multiple sclerosis and examine the causal relationship, if any.Methods. Consecutive patients referred to the multiple sclerosis clinic were evaluated by a neurologist with double training in both neuroimmunology and movement disorders. All patients were specifically screened for movement disorders via a movement disorder survey and a focused exam. Video samples were independently rated by two blinded movement disorder raters. Pre-specified criteria were developed for five potential clinical scenarios: incidental idiopathic Parkinson's disease, incidental Parkinson-plus syndrome, drug-induced parkinsonism, acute symptomatic parkinsonism, and chronic symptomatic parkinsonism.Results. From 2016 to 2021, 336 patients were evaluated. Of those, 12 patients (3.6%) had clinical parkinsonism (average age 68 years, 66% females). Nine patients (75%) were deemed to have incidental Parkinson's disease, 2 (17%) had drug-induced parkinsonism, and 1 (8.3%) was deemed to have demyelination-related chronic symptomatic parkinsonism. The latter presented with gradual and progressive parkinsonism without prodromal symptoms. Both blinded raters agreed with the parkinsonism phenomenology. In addition to typical enhancing and non-enhancing demyelinating lesions, the patient had lesions bilaterally in the basal ganglia. She had positive oligoclonal bands in the cerebrospinal fluid. DAT scan was normal. She was diagnosed with PPMS with activity and progression manifesting solely with secondary parkinsonism. Her disease stabilized with ocrelizumab. There were no cases of acute symptomatic parkinsonism or co-existing Parkinson-plus syndrome over the five-year duration of the study. Three of the incidental idiopathic Parkinson's disease cases had radiologically isolated syndrome.Conclusion. Parkinsonism in MS is rare and most cases are incidental. However, clinicians need to recognize the entity of demyelination-related chronic symptomatic parkinsonism in patients with progressive MS phenotypes and demyelinating lesions in the basal ganglia and/or upper midbrain. Parkinsonism may be the sole clinical presentation of progressive MS and the only indication for DMT initiation or escalation. There is an over-representation of radiologically isolated syndrome in patients with presumptive incidental demyelination and idiopathic Parkinson's disease. Prospective studies utilizing high-field MRI and longitudinal DAT scans are needed to better characterize the complex relationship between demyelination and parkinsonism.

Acute Movement Disorders in Childhood: A Cohort Study and Review of the Literature.

Acute movement disorders (AMD) are frequent in neurological and pediatric emergencies. Few studies analyzed AMD in children, none in Tunisia or other African country. The purpose of this study was to describe the peculiarities of AMD in a Tunisian pediatric population with a literature review. We conducted a retrospective descriptive study over 8 years including 80 children (sex ratio, 1.05; mean age of onset, 4.8 years) with AMD, followed in tertiary referral Child Neurology Department in North Tunisia. Acute movement disorders were mainly hyperkinetic (n = 67 with dystonia (n = 33; mostly due to inherited metabolic diseases (IMD) in 11; with status epilepticus in 10 children), chorea (n = 14; with Sydenham chorea in 5); myoclonus (n = 14; mostly with opsoclonus-myoclonus syndrome in 10) and tremor (n = 6; of posttraumatic origin in half). Hypokinetic movement disorder (MD) included acute parkinsonism in 5 children of infectious (n = 3), postinfectious (n = 1, malaria) and posttraumatic origin (n = 1). Mixed MD, found in 8 children, were mainly due to IMD in half of them, and to familial lupus in two. Paroxysmal MDs were seen in 2 children, one with multiple sclerosis and one of idiopathic origin. Psychogenic MDs were found in 7 patients mainly of dystonic type. Management of AMD comprised symptomatic treatment according to the phenomenology of the MD and causative treatment depending on its etiology. Our study illustrated the broad range of AMD in children and the wide spectrum of their etiologies. In our series, we described some exceptional findings and etiologies of AMD in children. These findings may denote a specific profile in of AMD in our country with predominant infectious, postinfectious, and IMD.

Reversible Parkinsonism due to Chronic Subdural Hematoma: A Case Report

Although Chronic Subdural Hematoma (CSDH) is frequent in elderly patients, the CSDH can exceptionally cause a parkinsonism or aggravation of pre-existing parkinsonism. Only 27 cases reversible parkinsonism due to chronic subdural hematoma was reported in the literature. Disappearance of the extra pyramidal symptoms followed craniotomy and removal of the CSDH suggest a cause-and-effect relation between the haematoma and the clinical symptomatology. A case of a 62-year-old man with a two weeks history of parkinsonism caused by a CSDH reversible after surgery evacuation of the haematoma is reported. CSDH is a rare cause of reversible parkinsonism after surgery. CT scan must be recognized in any acute Parkinsonism or any deterioration of preexisting Parkinson disease to diagnose the Parkinsonism secondary to CSDH.

The extrapyramidal syndromes of chronic kidney disease and dialysis (EPS-CKDD): diagnostic criteria, risk factors and prognosis.

Acute extrapyramidal movement disorders in dialysis patients are rare, inconsistently defined and have uncertain aetiology and prognosis. Define diagnostic criteria, prognosis and risk factors. Retrospective case series review of 20 patients (14 female, mean age 62 years) receiving dialysis for a median of 15 (interquartile range 4-35) months who presented with acute parkinsonism (AP = 11) or chorea/athetosis (CA = 9). All patients had type 2 diabetes (HbA1c 6.8 ± 1.0) and had received metformin. Lactic acidosis was present in 2 patients at presentation and serum lactate was elevated in 7/15 patients tested. No patient had abnormal copper or thyroid metabolism and 5/8 patients tested returned marginal abnormalities in heavy metal screening. Magnetic resonance imaging (MRI) revealed characteristic bilateral symmetric T2 hyperintensity of the basal ganglia (BG), predominantly putamen and globus pallidus (the lentiform nucleus) and more extensive involvement of the external and internal capsules in patients with AP presentation. Post-mortem demonstrated cytotoxic necrosis of the BG. Therapy included thiamine, intensive dialysis and cessation of metformin. Two patients died acutely, nine recovered and nine had residual symptoms. Median survival did not differ by presentation: AP 24 [95% confidence interval (CI) 21-27] and CA 33 (95% CI 32-35) months, P = 0.21. There are two distinct clinical extrapyramidal movement disorders associated with specific diagnostic MRI imaging that support the diagnosis of the extrapyramidal syndromes of chronic kidney disease and dialysis. The associations with diabetes, metformin and metabolic acidosis suggest a common pathogenic mechanism but require additional study. Early recognition and treatment may improve outcomes.

Organothiophosphate Induced Acute and Reversible Parkinsonism: Case Report and Literature Review

Introduction: Organophosphate compound poisoning is one of the most common causes for admission to the Medical Intensive Care Unit. Parkinsonism is a primary neurotoxic manifestation of organophosphate intoxication. In this case report, we present the case of a 26 year old man who had the experience of organothiophosphate poisoning. Case presentation: A 26 year old man was admitted with tremors in upper and lower limbs together with the rigidity of all 4 limbs as well as difficulty in swallowing and in daily activities like walking, rising from chair, and turning on bed. He had consumed organophosphorus compound quinalphos, 15 days before. The basal ganglia changes were documented radiologically by Magnetic Resonance Imaging (MRI). Gradual recovery was observed by treatment with dopaminergic agents and central anticholinergics over few weeks. Only 0.5% of organophosphate poisoning patients develop neurotoxic manifestations in the form of extrapyramidal syndromes such as Parkinsonism. Discussion: The occurrence of Parkinsonism as a complication of organophosphate poisoning raises safety concerns, especially in developing countries. Yet, this study is the first case report on Organothiophospahate induced Parkinsonism. Conclusion: Clinicians should be aware of the possibility of extrapyramidal manifestations following organophosphate poisoning and the patients should be asked for regular follow-ups as the symptoms may appear even 1 month after the poisoning.

Acute Parkinsonism in Young Adult Following Streptococcal Infection

Acute parkinsonism following streptococcal infection is rarely reported. To date, there is paucity of literature of post streptococcal immune mediated acute parkinsonism and dyskinesia among adult. We report a case of 18 years old woman, who presented with acute parkinsonism after streptococcal tonsillitis. The patient who was previously well presented with a two-month history of intermittent fever, associated with sore throat and sudden onset of behaviour changes. She has been found to be quieter and respond slowly to questions and commands in the preceding one week prior to admission. Features of secondary parkinsonism was noted during examination. Her blood counts, viral screenings and anti-NMDAR were unremarkable. Her lumbar puncture revealed an opening pressure of 10 cm CSF with normal constituents. The ASO titre was raised up to 400IU/ml. Electroencephalogram (EEG) shows mild encephalopathy changes and MRI brain shows normal finding. She was initially treated initially for meningoencephalitis with intravenous acyclovir 500mg q8h and ceftriaxone 2g q12h, concomitant with intravenous methylprednisolone 1g daily for 3 days. Intravenous immunoglobulin was started on her in view of poor response to the above treatment, which later resulted in significant and rapid clinical improvement. Upon clinic review at 3 months, her tremor, bradykinesia, and rigidity resolved. Her medication was able to be weaned off and she was referred to the ENT team for further evaluation for tonsillectomy. This case illustrates the importance of recognising post-streptococcal infection as aetiology of acute parkinsonism in young adults, to avoid treatment delay. As illustrated in our case, the prognosis was excellent with prompt immunomodulatory therapy.&#x0D; Bangladesh Journal of Infectious Diseases 2020;7(2):110-112

Acute parkinsonism in patients with systemic lupus erythematosus: a case report and review of the literature

Purpose of the study: Parkinsonism in patients with systemic lupus erythematosus (SLE) is rare. This study reported a case of parkinsonism in SLE and reviewed the clinical features and outcomes of parkinsonism in SLE patients. Methods: English language literature of parkinsonism in SLE patients was reviewed. Results: There were 28 patients (19 adults and 9 children) with SLE and parkinsonism. Twenty-three patients were female. Of 26 patients whose disease duration was available parkinsonism occurred at SLE diagnosis and after SLE diagnosis in 6 and 20 patients, respectively. Twenty-five patients had active SLE. Hematologic, mucocutaneous and musculoskeletal systems were the 3 most common organs involved in SLE during parkinsonism onset. Rigidity, bradykinesia and resting tremor were the 3 most common parkinsonian symptoms. Compared with adults, child cases had significantly more psychosis (4 in 9 vs. 1 in 19, p = .026), seizures or psychosis (6 in 9 vs. 2 in 19, p = .005) and mutism (6 in 9 vs. none, p < .001). Brain magnetic resonance imaging (MRI) was abnormal in 13 of 24 patients. Eight of nine patients had abnormal single-photon emission computed tomography (SPECT) and 5 and 3 showed hypoperfusion and hyperperfusion, respectively. The outcomes were resolution, partial response and persistent symptoms in 17, 7 and 4 patients, respectively. The outcome was no different whether or not dopamine therapy was included to corticosteroids and/or immunosuppressive drugs. Conclusions: Parkinsonism in SLE usually occurs during active SLE disease. Good response to corticosteroid and/or immunosuppressive drugs supports the immunologic mechanism in the pathogenesis.

Is COVID-19 a Perfect Storm for Parkinson’s Disease?

Three recent case reports (by Méndez-Guerrero et al.,Cohen et al., and Faber et al.) describe the development of acute parkinsonism following coronavirus disease 2019 (COVID-19). We discuss possible underlying cellular and molecular mechanisms, and whether COVID-19 might be associated with elevated long-term risk of Parkinson’s disease (PD).

Dyskinesia is most centrally situated in an estimated network of extrapyramidal syndrome in Asian patients with schizophrenia: findings from research on Asian psychotropic prescription patterns for antipsychotics

Background Network analysis provides a new viewpoint that explicates intertwined and interrelated symptoms into dynamic causal architectures of symptom clusters. This is a process called ‘symptomics’ and is concurrently applied to various areas of symptomatology. Aims Using the data from Research on Asian Psychotropic Prescription Patterns for Antipsychotics (REAP-AP), we aimed to estimate a network model of extrapyramidal syndrome in patients with schizophrenia. Methods Using data from REAP-AP, extrapyramidal symptoms of 1046 Asian patients with schizophrenia were evaluated using the nine items of the Drug-Induced Extrapyramidal Symptoms Scale (DIEPSS). The estimated network of the ordered-categorical DIEPSS items consisted of nodes (symptoms) and edges (interconnections). A community detection algorithm was also used to identify distinctive symptom clusters, and correlation stability coefficients were used to evaluate the centrality stability. Results An interpretable level of node strength centrality was ensured with a correlation coefficient. An estimated network of extrapyramidal syndrome showed that 26 (72.2%) of all possible 35 edges were estimated to be greater than zero. Dyskinesia was most centrally situated within the estimated network. In addition, earlier antipsychotic-induced extrapyramidal symptoms were divided into three distinctive clusters – extrapyramidal syndrome without parkinsonism, postural instability and gait difficulty-dominant parkinsonism, and tremor-dominant parkinsonism. Conclusions Our findings showed that dyskinesia is the most central domain in an estimated network structure of extrapyramidal syndrome in Asian patients with schizophrenia. These findings are consistent with the speculation that acute dystonia, akathisia, and parkinsonism could be the risk factors of tardive dyskinesia.

Playback of 50-kHz ultrasonic vocalizations overcomes psychomotor deficits induced by sub-chronic haloperidol treatment in rats

RationaleIn rodents, acute haloperidol treatment induces psychomotor impairments known as catalepsy, which models akinesia in humans and is characterized as an animal model of acute Parkinsonism, whereas sub-chronic haloperidol reduces exploratory behavior, which resembles bradykinesia. Haloperidol-induced catalepsy in rats can be ameliorated by playback of 50-kHz ultrasonic vocalizations (USV), an emotionally and motivationally relevant appetitive auditory stimulus, representing an animal model of paradoxical kinesia. In a condition like PD where patients suffer from chronic motor impairments, it is paramount to assess the long-term symptom relief in an animal model of Parkinsonism.ObjectivesWe investigated whether 50-kHz USV playback ameliorates psychomotor deficits induced by haloperidol in a sub-chronic dosing regimen.MethodsIn phase 1, distance traveled and number of rearing behavior were assessed in an activity chamber in order to investigate whether sub-chronic haloperidol treatment induced psychomotor impairments. In phase 2, we investigated whether 50-kHz USV playback could overcome these impairments by assessing exploratory behaviors and approach behavior towards the sound source in the 50-kHz USV radial maze playback paradigm.ResultsSub-chronic haloperidol treatment led to psychomotor deficits since the distance traveled and number of rearing behavior were reduced as compared to saline control group or baseline. These psychomotor impairments were ameliorated during playback of 50-kHz USV, with haloperidol treated rats showing a clear social approach behavior towards the sound source exclusively during playback.ConclusionsThis study provides evidence that 50-kHz USV playback induces paradoxical kinesia in rats exhibiting motor deficits after sub-chronic haloperidol, as we previously showed after acute haloperidol treatment.

Olive oil limited motor disruption and neuronal damage in parkinsonism induced by MPTP administration

Some vegetable oils show beneficial effects in modulating neurodegeneration; in this work, we evaluated the therapeutic potential of corn and olive oils against neurodegenerative processes using the acute parkinsonism murine model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL6 mice. The effects of corn and olive oils were quantified by the performance of mice in the open field and rotarod, and grasp strength tests and neuronal survival in the substantia nigra and striatum were determined by immunohistochemistry. Extra-virgin olive oil decreased the toxicity induced by MPTP administration judged by the performance in the behavioral motor tests and the number of total neurons in the analyzed brain regions. In contrast, corn oil only produced discrete changes in the behavioral and histological evaluations. Despite the numerous benefits of olive oil, its active substances that confer desirable effects and their mechanism of action remain unclear. Our observations can help to understand the ameliorative effects of some natural oils on neurodegeneration induced by some toxins, particularly the attenuation of neural damage related to toxin-induced parkinsonism or other pathologies that comprise neuronal death and motor disruption.

Extrapontinemyelinolysis (EPM) presenting as acute parkinsonism, successfully treated with immunomodulation therapy: Report of two cases

Extrapontinemyelinolysis (EPM) presenting as acute parkinsonism, successfully treated with immunomodulation therapy: Report of two cases