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Psychosis is a common and often debilitating non-motor symptom of Parkinson’s disease (PD). It typically manifests in the form of well-formed visual hallucinations and minor hallucinations, and, at times, can present with delusions and nonvisual hallucinations. Psychosis is associated with many adverse outcomes in PD, and for that reason, it is essential to recognize and treat the symptoms early. The objective of this review article is to highlight the phenomenology, diagnosis, and pathophysiology of PD-associated psychosis (PD-P) and discuss a step-by-step approach to its management. One of the critical steps in managing PD-P is the identification of potential non-PD causes of psychosis, which often require conservative measures. If no secondary causes are identified, pharmacotherapy should be considered. Role of several drugs including pimavanserin (the only FDA-approved agent for the treatment of PD-P), atypical antipsychotics such as quetiapine and clozapine, and cholinesterase inhibitors such as rivastigmine and donepezil are discussed in this review. In addition, we also highlight the potential role of noninvasive brain stimulation (electroconvulsive therapy and transcranial magnetic stimulation) for the treatment of medication-refractory psychosis.

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Bupropion (BPP) was originally an antidepressant, but now it is also used for seasonal affective disorder and smoking cessation. The aim of this systematic review was to evaluate the clinical epidemiological profile, pathological mechanisms, and management of BPP-associated movement disorders. Relevant reports in six databases were identified and assessed by two reviewers without language restriction. A total of 63 reports of 710 cases from 16 countries were assessed. The movement disorders associated with BPP found clearly defined were: dyskinesia (8), dystonia (7), parkinsonism (7), myoclonus (6), tic (6), stuttering (3), rapid eye movement sleep disorders (2), and ballism (1); the not clearly defined cases included 488 tremors, 80 slurred speech, 48 ataxia, 20 abnormal movements, 19 falls, 4 akathisia, 3 dyskinesia, 2 hyperkinesia, 2 poor coordination, and the rest was only reported once (dystonia, myoclonus, motor tic, and rigidity). The mean age was 46 years (7–85 years). The male was predominant sex (52.77%). The mean BPP dose was 248.38 mg, and the most common indication was a major depressive disorder (73.68%). The average time of onset was 3.47 weeks and of recovery was 2.71 weeks. The most common management was BPP withdrawal. In the literature, the majority of the cases did not clearly report the clinical neurological examination and lacked electrodiagnostic studies. Future studies about adverse effects with BPP should describe at least the clinical characteristics and the physical exam of the individuals, especially when fall and slurred speech are observed.

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Movement disorders following stroke is a well known phenomena both during acute stage as well as in later phases. The type of movement depends on the site of involvement, it is however not uncommon to have more than one type of movement disorder following a stroke. We present a patient with combined dystonia and asterixis following a unilateral thalamic infarct, whose dystonia persisted on follow up while the asterixis faded away with time.

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Hypoglycemia is associated with adrenergic and various neurological symptoms including hemiparesis. Though not common, movement disorders such as chorea and ballism have been reported in hypoglycemia. This case was of an elderly lady, a known diabetic, who developed two episodes of hemiparesis and single episode of jerky head movement with preserved sensorium lasting for few seconds, associated with hypoglycemia on different occasions, 1 week after increasing the dosage of oral hypoglycemic agent with complete recovery each time with correction of sugar levels. Magnetic resonance imaging showed transient bilateral diffusion restriction in posterior limb of internal capsule.

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Mirtazapine (MTZ) is an atypical antidepressant frequently prescribed for the management of major depressive disorder. It has multiple mechanisms of action, which probably contribute to the several side effects encountered with this medication. Hyperkinetic movement disorders induced by MTZ have been rarely reported in the literature. To the best of authors’ knowledge, there are five cases of dystonia (DTN) secondary to MTZ use, but this study reports the youngest individual in a nonpsychiatric MTZ indication. We report a case of an adult woman who presented with axial and cervical DTN-type laterocollis after 5 days of MTZ use, which was indicated for hot flashes. A comprehensive review of the cases and a mechanism assumption are performed.

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Hashimoto’s encephalopathy (HE) commonly presents with two types of neurological presentation: recurrent stroke-like episodes or seizures and progressive cognitive decline. Being a treatable disorder, one cannot afford to miss the diagnosis. We report a female with HE who presented with a history of recurrent episodes of catatonia, recovering completely with steroids. The diagnosis of the primary disease got delayed for 5 months. HE presenting as catatonia has been reported rarely. A high degree of suspicion in appropriate clinical settings, resulting in early diagnosis, is rewarding as HE usually show good response to corticosteroids.

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DRPLA (dentatorubral–pallidoluysian atrophy) is a neurodegenerative disorder caused by cytosine-adenine-guanine (CAG) trinucleotide repeat expansion (>48) in ATN1 gene at 12p13.31 locus inherited in an autosomal-dominant manner. The key clinical manifestations of DRPLA are ataxia, dementia, and myoclonic epilepsy and have variable association with intellectual disability, behavioral changes, epileptic seizures, and choreoathetosis. It is most commonly reported in Japanese population with a prevalence of 0.2–0.7/100,000. Here we report a three-generation first Indian family identified to carry a pathogenic CAG expansion in ATN1 and clinical features conformed to its key manifestations.

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The objective of this paper was to report on a case of steroid-responsive chorea in a patient with κ light-chain monoclonal gammopathy. In addition to subacute-onset generalized chorea, evidence of peripheral neuropathy in this elderly gentleman led us to investigate for paraproteinemia. We treated the patient with intravenous steroids in view of elevated κ light-chain assay and bone marrow biopsy, suggestive of monoclonal gammopathy of undetermined significance. There was a remarkable improvement of paresthesias and chorea at 6 months follow-up with no evidence of evolution to malignancy at 1 year. Autoimmune chorea is a treatable condition if identified and treated timely.

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OBJECTIVES: To compare the sleep profiles of genetically proven cases of Huntington’s disease (HD) with healthy controls and to correlate the results of various sleep-related parameters with disease severity, duration, and length of cytosine–adenine–guanosine repeats.METHODS: This prospective study was conducted at the National Institute of Mental Health and Neurosciences (NIMHANS), Bengaluru, India, which included 31 genetically confirmed patients with HD and 50 controls. All the subjects were evaluated for sleep disturbances using standardized sleep questionnaires (Pittsburgh Sleep Quality Index [PSQI] and Epworth Sleepiness Scale [ESS]).RESULTS: The mean age of the patients during the first consultation was 46.0±12.7 years (range: 28–80). The mean age at onset of symptoms was 40.5±13.8 years. Nineteen patients (61.2%) gave history of sleep disturbances. Symptom suggestive of rapid eye movement sleep behavior disorder was present in 8 patients (25.8%). Difficulty in falling asleep was the most common sleep-related disturbance reported by 16 patients (51.6%). The mean ESS score of the patients was 6.22±2.89 and that of the control population was 3.00±2.8 (P value < 0.001). The mean PSQI score of the patients was 8.90±3.50 and that of the control population was 3.3±2.9 (P value < 0.001).CONCLUSIONS: This study demonstrates sleep disturbances in patients with HD compared to healthy controls and the sleep disturbances correlated significantly with the disease duration, severity, and coexistent anxiety and depression.

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BACKGROUND: The role of deep brain stimulation (DBS) of bilateral subthalamic nuclei (STN) in motor improvement of patients with Parkinson’s disease (PD) is well proven. But, the effect DBS has, on non-motor symptoms (NMSs), is still debatable. There are few studies, which have attempted to address this issue, though it also has significant effect on the quality of life of patients. PURPOSE: To study the impact of bilateral STN-DBS on NMSs in patients with PD. SUBJECTS AND METHODS: A prospective study was constructed from a center in South India. Thirty-five patients with PD who underwent bilateral STN-DBS were assessed preoperatively and 6 months postoperatively for NMSs with two well-established questionnaires: Non-motor Symptoms Questionnaire (NMS Q) and Non-motor Symptoms Scale (NMSS). The significance of improvement in scores was assessed with McNemar’s test, chi-square test, and paired two sample t-test for correlated samples. P value significance was set at <0.05. RESULTS: NMSs were seen in all patients. The most frequent symptoms preoperatively were insomnia (66%), nocturia (63%), urgency, and constipation (49% each). Statistically significant reduction after STN-DBS in overall NMSs was noted in both NMS Q (by 2.83, P = 0.008) and NMSS (by 17.40, P = 0.0013). Among the various domains, a significant reduction was observed in cardiovascular and sleep domains with improvement in individual questions on mood, insomnia, and light-headedness. Weight gain was more common after STN-DBS. CONCLUSION: Subthalamic nucleus stimulation causes significant improvement in NMSs with significant improvement in cardiovascular and sleep domains.

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BACKGROUND: There is an emerging role of various non-pharmacological strategies in the management of motor and non-motor symptoms of Parkinson’s disease (PD). OBJECTIVE: The aim of the study was to examine the effectiveness of Tai chi and Qigong on cognitive and motor functions, emotions, and quality of life in patients with PD. SUBJECTS AND METHODS: Seven subjects with mean age of 50.2 years, education of 11.71 years, and duration of PD of 6.03 years underwent four-week training of Qigong and Tai chi. They received one session per week under supervision and daily two 45-min practice sessions at home following instructions from the manual. Participants were assessed before and after intervention on neuropsychological tests, Unified Parkinson’s Disease Rating Scale (motor section), Hamilton Anxiety Rating Scale (HAM-A), Hamilton Depression Rating Scale (HAM-D), Epworth Sleepiness Scale (ESS), and Parkinson’s Disease Questionnaire (PDQ-39). RESULTS: There was a significant improvement in executive functions, verbal memory, and reduced scores on clinical scales (UPDRS III, HAM-A, PDQ-39). CONCLUSION: Combined practice of Tai chi and Qigong improves motor and non-motor symptoms of PD. However, well-designed randomized controlled trials and longitudinal studies are required to understand its full potential.

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Movement Disorders are currently growing to be one of the major subspecialties of neurology worldwide, primarily by developments of research and therapeutics in this field. As any specialty grows, it leads to the formation of its society and the publication of journal to disseminate the knowledge. The International Parkinson’s Disease and Movement Disorders Society (IPMDS, formerly known as Movement Disorders Society) played its role with inception since 1980s. Further development of Movement Disorders subspecialty leads each region and country to have their own national societies and publications. Similarly, the seeds of Movement Disorders were sown in India in mid-1980s but it took a major stride in last few years with the formation of Movement Disorders Society of India (MDSI) in 2014 and following this, it is now at the crux of starting its journal—Annals of Movement Disorders (AOMD). This would be a right time to look back into the history of Indian Neurology with specific reference to the Movement Disorders and pen down these chronicles since the inception of modern neurology in India. The current chronicles of Indian Movement Disorders is penned based on personal interviews with various senior Movement Disorder specialists of India. However, it should also be remembered that many of the chronicles are limited by the memories of people and their biases with whom the interviews are conducted.

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Syphilis is a well-known “great simulator/mimicker” of other diseases. Over the last decades, the clinical features of neurosyphilis have changed with an increasing percentage of atypical manifestations. In this context, movement disorders caused by neurosyphilis are rare and challenging to diagnose. This literature review aimed to evaluate the clinical epidemiological profile, pathological mechanisms, and historical features of neurosyphilis-associated movement disorders. Relevant reports in six databases were identified and assessed by two reviewers without language restriction. A total of 84 reports containing 168 cases who developed a movement disorder related to neurosyphilis were reported. The mean and the median reported ages were 40.50 (standard deviation [SD], 20.30) and 43 years (2.5–72.5 years). The predominant sex was male (79.16%). Argyll Robertson pupils were found in 54.90% of the individuals. The movement disorders reported were tremor, chorea, parkinsonism, ataxia, myoclonus, dystonia, athetosis, and ballism. In the literature, we have a large number of reports about movement disorder associated with neurosyphilis. But, in the majority of them, the individuals had the syphilitic diagnosis based on unspecific methods, electrodiagnostic studies were not performed, or penicillin therapy was unavailable. Also, we believe that any patient presenting with a movement disorder should have a thorough neurological examination of pupillary reflex, and if any abnormality is present, syphilitic laboratorial tests should be done.

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Thermoregulatory abnormalities, especially sweating disorders, are very common in Parkinson’s disease (PD). The estimated prevalence of sweating abnormalities ranges from 5.5% to 12.9% in de novo, newly diagnosed patients with PD and up to 64% during later stages of the disease. The range of thermoregulatory abnormalities in PD is broad, and includes hyperhidrosis, hypohidrosis, and hypothermia. In addition, the way in which these symptoms present themselves varies between patients and they can be chronic or fluctuating, local or generalized affecting the whole body, and related to motor complications or medication. Often there is a strong link to other autonomic symptoms, yet the exact pathogenesis behind these overlapping symptoms remains largely elusive, although current evidence points toward both central and peripheral involvement. Treatment remains difficult because of the lack of understanding of pathophysiology as well as specific clinical trials needed for evidence base. In this review, we have identified 43 studies in English language assessing sweating disorders in idiopathic PD. Here, we summarize knowledge gleaned from these reports and discuss current understanding of thermoregulatory dysfunction in PD, its phenomenology, pathophysiology, and management options.

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