Parkinsonism as a neurologic manifestation of dengue infection is rare with only 1 reported case in an adult patient. We report a case of a 6-year-old child with self-limiting post-dengue encephalopathy and Parkinsonism. This is the first reported pediatric case of post-dengue Parkinsonism and expands the neurologic manifestations associated with dengue infection in children. Clinicians should consider the possibility of post-dengue Parkinsonism in children with a history of pyrexia from endemic areas of dengue.
BACKGROUND: Dengue is a common illness in the tropics. Equally common are neurological complications that stem from dengue infection. However, to date, parkinsonism following dengue has not been reported in medical literature.
CASE PRESENTATION: A previously well 18-year old man developed parkinsonism, in addition to other neurological symptoms following serologically confirmed dengue fever. Alternative etiologies were excluded by way of imaging and blood investigations.
CONCLUSIONS: The authors detail the first reported case of parkinsonism complicating dengue fever. Keeping rare presentations of common illnesses in mind, it behoves clinicians to consider parkinsonism as a complication following dengue infection. This would prevent injudicious treatment with L-dopa and dopamine agonists. Immunosuppression with steroids has been shown to be helpful in certain cases.
Parkinson's disease (PD) is a member of a larger group of neuromotor diseases marked by the progressive death of dopamineproducing cells in the brain. Providing computational tools for Parkinson disease using a set of data that contains medical information is very desirable for alleviating the symptoms that can help the amount of people who want to discover the risk of disease at an early stage. This paper proposes a new hybrid intelligent system for the prediction of PD progression using noise removal, clustering and prediction methods. Principal Component Analysis (PCA) and Expectation Maximization (EM) are respectively employed to address the multi-collinearity problems in the experimental datasets and clustering the data. We then apply Adaptive Neuro-Fuzzy Inference System (ANFIS) and Support Vector Regression (SVR) for prediction of PD progression. Experimental results on public Parkinson's datasets show that the proposed method remarkably improves the accuracy of prediction of PD progression. The hybrid intelligent system can assist medical practitioners in the healthcare practice for early detection of Parkinson disease.
Catatonia may concomitantly occur with other psychiatric diagnoses such as
Major Depressive Disorder, however problem in diagnosis may arise due to
the overlapping features with other problems such as serotonin syndromes,
neuroleptic malignant syndromes and Parkinsonism. Despite the diagnostic
dilemma and lack of diagnostic tools, the clinical correlation between the
carbon monoxide poisoning and the late-onset development of the
Parkinsonian features is the highlight of this report.
Osmotic demyelination syndrome commonly affects the pons and infrequently involves the extrapontine region. We report a patient with severe hyponatraemia who developed osmotic demyelination syndrome as a consequence of rapid sodium correction. The condition manifested as acute severe parkinsonism, bilateral ptosis and gaze impairment. MRI revealed typical features of central pontine and extrapontine myelinolysis. The patient improved gradually after treatment with a combination of levodopa, intravenous immunoglobulin and dexamethasone. However, it is important to emphasise that the improvement of neurological symptoms is not necessarily causal with these experimental therapies.
Parkinson's disease (PD), the second most common neurodegenerative disorder, is characterized by cardinal motor impairments, including akinesia and tremor, as well as by a host of non-motor symptoms, including both autonomic and cognitive dysfunction. PD is associated with a death of nigral dopaminergic neurons, as well as the pathological spread of Lewy bodies, consisting predominantly of the misfolded protein alpha-synuclein. To date, only symptomatic treatments, such as levodopa, are available, and trials aiming to cure the disease, or at least halt its progression, have not been successful. Wong et al. (2019) suggested that the lack of effective therapy against neurodegeneration in PD might be attributed to the fact that the molecular mechanisms standing behind the dopaminergic neuronal vulnerability are still a major scientific challenge. Understanding these molecular mechanisms is critical for developing effective therapy. Thirty-five years ago, Calne and William Langston (1983) raised the question of whether biological or environmental factors precipitate the development of PD. In spite of great advances in technology and medicine, this question still lacks a clear answer. Only 5-15% of PD cases are attributed to a genetic mutation, with the majority of cases classified as idiopathic, which could be linked to exposure to environmental contaminants. Rodent models play a crucial role in understanding the risk factors and pathogenesis of PD. Additionally, well-validated rodent models are critical for driving the preclinical development of clinically translatable treatment options. In this review, we discuss the mechanisms, similarities and differences, as well as advantages and limitations of different neurotoxin-induced rat models of PD. In the second part of this review, we will discuss the potential future of neurotoxin-induced models of PD. Finally, we will briefly demonstrate the crucial role of gene-environment interactions in PD and discuss fusion or dual PD models. We argue that these models have the potential to significantly further our understanding of PD.
Parkinsonism caused by infection is uncommon in children. We report 2 previously healthy children with acute self-limiting parkinsonism following Mycoplasma pneumoniae infection, with normal brain magnetic resonance imaging (MRI). Our case report expands the phenotype of parkinsonism associated with M. pneumoniae infection. We recommend that children with acute parkinsonism preceded by a period of febrile illness, even with a normal brain MRI, should be investigated for M. pneumoniae infection.
Reactive oxygen species (ROS) play an important role in ageing and age-related neurodegenerative changes including Parkinson's disease (PD). PD is characterized by signs of major oxidative stress and mitochondrial damage in the pars compacta of the substantia nigra. Present study was designed to investigate whether the Centella asiatica extract (CAE) would prevent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in aged Sprague-Dawley rats. Adult, male Sprague-dawley rats of 300-350 g were divided into control, C. asiatica alone, MPTP alone (20 mg/kg, for 21 days) and MPTP with C. asiatica (300 mg/kg for 21 days) groups. Effect of aqueous extract of C. asiatica on oxidative biomarker levels in corpus striatum and hippocampus homogenate was examined. MPTP-challenged rats elicited a significant increase in lipid hydroperoxides (LPO) (p < 0.01), protein-carbonyl-content (PCC) (p < 0.01) and xanthine oxidase (XO) (p < 0.01) when compared with control rats. There was a significant decrease in total antioxidants (TA) (p < 0.001), superoxide dismutase (SOD) (p < 0.001), glutathione peroxidase (GPx) (p < 0.01) and catalase (CAT) (p < 0.001) levels with MPTP treatment. Supplementation of CAE reduced LPO and PCC and significantly increased (p < 0.01) TA and antioxidant enzyme levels (p < 0.01) in corpus striatum and hippocampus. These results show that administration of C. asiatica was effective in protecting the brain against neurodegenerative disorders such as Parkinsonism.
Accumulating evidence strongly suggests that gamma amino butyric acid (GABA) receptors play a crucial role in the pathogenesis of Parkinson's disease (PD). Therefore, the present study was designed to investigate the role of GABA-B receptor modulation in experimental models of MPTP-induced PD. MPTP was administered repeatedly on 1st, 7th and 14th day intranigrally for the induction of PD in Male Wistar rats. Baclofen (10 and 20mg/kg) and GABA-B antagonist CGP35348 (10mg/kg) were given after induction of PD for 14 days. Different behavioural tasks were performed during 1st, 14th, 21st, 28th days after MPTP injection and biochemical parameters were estimated on day 28th. Central administration of MPTP showed significant impairment of motor behaviour and marked increase of oxidative damage LPO and GSH in striatum and cortex. Pro-inflammatory cytokines like TNF-α and IL-β were significantly increased in striatum region of MPTP treated rats. However, post treatment with baclofen significantly improved the motor abnormalities and attenuated the oxidative damage and neuro-inflammation in MPTP treated rats. CGP35348, GABA-B receptor antagonist, reversed the protective effect of baclofen GABA-B receptor play role in the neuroprotection. The present study concluded that baclofen produce beneficial effect against MPTP induced PD like symptoms rats through GABAergic mechanism.
The proper diagnosis of parkinsonian disorders usually involves three steps: identifying core features of parkinsonism; excluding other causes; and collating supportive evidence based on clinical signs or investigations. While the recognition of cardinal parkinsonian features is usually straightforward, the appreciation of clinical features suggestive of specific parkinsonian disorders can be challenging, and often requires greater experience and skills. In this review, we outline the clinical features that are relevant to the differential diagnosis of common neurodegenerative parkinsonian disorders, including Parkinson's disease, multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration. We aim to make this process relatable to clinicians-in-practice, therefore, have categorised the list of clinical features into groups according to the typical sequence on how clinicians would elicit them during the examination, starting with observation of facial expression and clinical signs of the face, spotting eye movement abnormalities, examination of tremors and jerky limb movements, and finally, examination of posture and gait dysfunction. This review is not intended to be comprehensive. Rather, we have focused on the most common clinical signs that are potentially key to making the correct diagnosis and those that do not require special skills or training for interpretation. Evidence is also provided, where available, such as diagnostic criteria, consensus statements, clinicopathological studies or large multi-centre registries. Pitfalls are also discussed when relevant to the diagnosis. While no clinical signs are pathognomonic for certain parkinsonian disorders, certain clinical clues may assist in narrowing a differential diagnosis and tailoring focused investigations for the individual patient.
Parkinson Disease (PD) is a neurodegenerative disorder of the central nervous system that often impairs the patient’s motor skills, speech and other functions. The four cardinal signs of parkinsonism are resting tremor, bradykinesia, cogwheel rigidity and postural instability. The prevalence of depression in PD ranges from 4% to 75%. However depression in PD is often mistakenly as the presentation of the disease itself. Therefore this paper reviewed the clinical feature of depression in PD and explored the aetiology of depression in PD.
Typhoid fever is a systemic infection caused by Salmonella typhi, which may be associated with extra-intestinal
complications. Neurological manifestations, particularly Parkinsonism, are rarely reported. We report a
17-year-old patient with relapsed culture-proven Salmonella typhi infection who developed septic shock and
subsequently Parkinsonism. Lumbar puncture revealed acellular cerebrospinal fluid with raised protein level.
Magnetic resonance imaging revealed cerebral petechial haemorrhages resulted from small vessels vasculitis.
His symptoms resolved spontaneously after 3 months.
Acute mountain sickness is an illness caused by climbing to a high altitude without prior acclimatization. Neurological consequences, like parkinsonism following acute mountain sickness without lesion of brain MRI have been reported rarely. A healthy 56-year-old man presented with dysarthria and gait disturbance. Neurological examination revealed tremor of hands, limb rigidity, and bradykinesia. The symptoms developed approximately 30 days following a 3,500 m climb of the Annapurna in the Himalayas. Brain MRI did not reveal any abnormalities including globus pallidus. The parkinsonism symptoms persisted for about 3 months before a complete recovered was made. We suggest that parkinsonism can develop after climbing to a high altitude but that the symptoms can be transient if a brain MRI detects no abnormalities.
Zingiber zerumbet has been traditionally used as an anti-inflammation and antioxidant agent. The present study
investigates the neuroprotective effects of ethyl acetate extract of Z. zerumbet against oxidative stress on paraquat
(PQ)-induced Parkinsonism in rats. Forty male Sprague-Dawley rats were divided into five groups: Negative control
(normal saline), positive control (N-acetylcysteine, NAC 20 mg/kg + PQ 10 mg/kg), PQ only, 200 mg/kg Z. zerumbet +
PQ and 400 mg/kg Z. zerumbet + PQ. The extract was given orally for 19 consecutive days and PQ was administered
intraperitoneally on day 8-12th of the treatment regime. Both serum and fresh brains containing substantia nigra (SN)
region were taken for biochemical and histological analysis. Administration of both 200 and 400 mg/kg ethyl acetate
Z. zerumbet extracts to the PQ-treated groups have resulted in: Decreased levels of MDA and PC in the SN homogenates;
and increased SOD, GPx; and CAT activities in the SN and serum. Overall, ethyl acetate extract of Z. zerumbet reduced
oxidative stress in the SN of PQ-induced neuronal damages, therefore, has the potential to be developed as a preventive
agent for neurodegenerative disorders caused by environmental toxins.
The incidence of neurodegenerative diseases is directly proportional to age. The prevalence of non-communicable diseases, for example, Alzheimer's and Parkinson's, is expected to rise in the coming years. Understanding the etiopathology of these diseases is a crucial step that needs to be taken to develop drugs for their treatment. Animal models are being increasingly used to expand the knowledge and understanding on neurodegenerative diseases. Marine worms, known as polychaetes (phylum Annelida), which are abundantly and frequently found in benthic environments, possess a simple yet complete nervous system (including a true brain that is centralised and specialised) compared to other annelids. Hence, polychaetes can potentially be the next candidate for a nerve disease model. The ability to activate the entire nervous system regeneration (NSR) is among the remarkable features of many polychaetes species. However, the information on NSR in polychaetes and how it can potentially model neurodegenerative diseases in humans is still lacking. By exploring such studies, we may eventually be able to circumvent the developmental constraints that limit NSR in the human nervous system. This article is intended to briefly review responsible mechanisms and signalling pathways of NSR in marine polychaetes and to make a comparison with other established models of neurodegenerative disease.
Layered hydroxide nanoparticles are generally biocompatible, and less toxic than most inorganic nanoparticles, making them an acceptable alternative drug delivery system. Due to growing concern over animal welfare and the expense of in vivo experiments both the public and the government are interested to find alternatives to animal testing. The toxicity potential of zinc aluminum layered hydroxide (ZAL) nanocomposite containing anti-Parkinsonian agent may be determined using a PC 12 cell model. ZAL nanocomposite demonstrated a decreased cytotoxic effect when compared to levodopa on PC12 cells with more than 80% cell viability at 100 µg/mL compared to less than 20% cell viability in a direct levodopa exposure. Neither levodopa-loaded nanocomposite nor the un-intercalated nanocomposite disturbed the cytoskeletal structure of the neurogenic cells at their IC50 concentration. Levodopa metabolite (HVA) released from the nanocomposite demonstrated the slow sustained and controlled release character of layered hydroxide nanoparticles unlike the burst uptake and release system shown with pure levodopa treatment.