Tacrolimus treatment is associated with a range of neurological adverse effects. Neurotoxicity caused by tacrolimus may result in subacute onset of tremor in a subset of patients. The commonly reported tremor phenomenology associated with tacrolimus neurotoxicity is the action tremor of bilateral upper limbs with or without rest tremor. Tremor may occur even if the plasma concentration of tacrolimus is within the therapeutic range. In this report, we highlight a case of tacrolimus-induced tremor, in which, in addition to having action and rest tremor of the upper limbs, the patient had vocal, lingual, and lower limb tremor. We demonstrate how drug cessation and temporary administration of primidone remarkably improved the tremor.

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Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder. Eye movement abnormalities are characteristic manifestations of HD. The clinical manifestations and eye movement disturbances progress with the natural course of illness. Eye movement abnormalities evolve in HD from the premanifest stage to the early-manifest and late-manifest stages. In the premanifest stage, voluntary saccades, i.e., memory-guided saccades and anti-saccades are predominantly affected. There is an increase in latency and error rates of voluntary saccades. Early-manifest stage of HD is characterized by abnormality in reflexive saccades, with decrease in saccadic amplitude and velocity and slow broken pursuits. In the late-manifest stage, initiation of voluntary saccades in all directions is slow, leading to difficulty in initiating voluntary eye movements. The rate of progression of the saccades, pursuits, and other ocular movement correlate with the disease progression; monitoring this helps in early disease evaluation and in evaluating novel therapies to modify the disease. In this article, we systematically review the available literature on the patterns and progression of eye movement abnormalities, from the premanifest, to manifest, and advanced stages of HD.

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Botulinum neurotoxin (BoNT), produced by spore-forming anaerobic bacteria, is the most potent biological toxin and is a powerful therapeutic tool for several clinical indications in neurology and beyond. BoNT inhibits the release of acetylcholine from the presynaptic terminals of the neuromuscular junction by interfering with the normal process of vesicle–plasma membrane fusion. The spectrum of indications for the use of BoNT in the treatment of various disorders in neurology, ophthalmology, gastroenterology, urology, autonomic, and dermatology is widening. The major indications for BoNT are in hyperkinetic movement disorders. Because BoNT must be injected locally, neurologists should possess the appropriate expertise to effectively deliver the therapy. Although it is considered to be effective and safe, there are many limitations to its use such as the therapeutic effect wearing off and high cost. Here, we review the indications, techniques of muscle selection, and administration of BoNT for maximum benefit in various movement disorders.

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Context: Communication plays a fundamental role in life as an essential aspect of relationships, personal development, identity, and social interaction. Parkinson’s disease (PD) gradually affects the ability of individuals to effectively communicate, affecting the abovementioned factors; therefore, it severely affects their quality of life. Aim: To compare the impact of communication difficulty on quality of life between individuals with PD and neurologically healthy (NH) individuals. Methods and Material: A total of 15 individuals with PD and 15 NH individuals, between the ages of 45 and 85 years, participated in this study. Quality of communication life (QoCL) was estimated using the Tamil version of the American Speech-Language-Hearing Association–Quality of Communication Life scale. Results: The Mann–Whitney U test was performed to verify significant differences in the QoCL scores between PD and NH individuals. The mean QoCL scores were observed to be lower in the PD group than those in the NH group across the following three domains: socialization/activities, confidence/self-concept, and roles and responsibilities. However, the QoCL score was significantly different for only two domains: roles and responsibilities (p = 0.00) and socialization/activities (p = 0.00). Conclusion: Identifying the impact of communication difficulty in daily life will help speech–language pathologists in planning communication rehabilitation, prioritization of goals, counselling, structuring client-centered therapeutic strategies, and documenting outcomes to improve the QoCL in individuals with PD.

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Movement disorders are relatively sparse amongst COVID-19 patients. However, in the setting of large number of COVID-19 cases, relatively rare acute to subacute onset, para-infectious or post-infectious movement disorders such as myoclonus and myoclonus-ataxia with or without opsoclonus have increasingly become more evident. Our objective of writing this paper is to summarize the available evidence documenting new onset hyperkinetic movement disorders associated with COVID-19. Myoclonus is the most frequently reported movement disorder associated with COVID-19 alone or in combination with ataxia and tremors. Apart from isolated myoclonus, myoclonus with ataxia, opsoclonus myoclonus ataxia syndrome have been reported post COVID. Isolated cerebellar ataxia is the other most commonly described movement disorder post COVID. Tremors, Chorea and dystonia are rarely described hyperkinetic movement disorders in association with COVID. Treatments being offered for hyperkinetic movement disorders consists of symptomatic treatment with benzodiazepine, anti-seizure drugs, immunomodulatory treatment with steroids, intravenous immunoglobulin and rehabilitative therapies. In this review we summarize the neurological features, investigations, treatments, and outcomes of all the published cases of hyperkinetic movement disorders associated with COVID-19.

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Background: Motor and neuropsychiatric symptoms are the manifestations of Parkinson’s disease (PD), leading to poor quality of life of patients. Aim: This study aims to compare the benefits of yoga versus physiotherapy on motor and neuropsychiatric symptoms and health-related quality of life in patients with PD. Materials and Methods: Twenty-four patients with PD, Hoehn and Yahr disease severity rating scale of I–III, score of <3 on a pull test, and walking ability for 10 meters participated in this observer-blinded randomized clinical trial. The yoga group practiced asanas (postures), pranayama (breathing), and meditation. The comparator group underwent physiotherapy. All participants performed 60-minute training sessions a day, with two sessions per week for 12 weeks. The Parkinson’s Disease Questionnaire-39 (PDQ-39), Addenbrooke Cognitive Examination (ACE-R), Beck’s Depression Inventory (BDI), Unified Parkinson’s Disease Rating Scale (UPDRS) motor experiences, and Balance Evaluation System Test (BESTest) were the outcome measurements. Results: On comparing the groups using the Mann–Whitney U test, a statistical significance was observed in the overall quality of life (p = 0.008), emotional well-being (p = 0.008), and stigma (p = 0.048) domains of PDQ-39 and the memory (p = 0.025) and fluency (p = 0.003) domains of ACE-R, which were favorable for yoga. The BDI, UPDRS motor experiences, and BESTest measures were statistically significant (p < 0.05) for both the yoga and physiotherapy groups, only on within-group analysis. Conclusion: Psycho-spiritual yoga practice appears to promote emotional well-being and alleviate the stigma attached to PD; therefore, it improves the quality of life of PD patients compared to physical exercises. In addition, it is noted that patients taking antidepressants may experience less depressive symptoms, warranting a multi-arm parallel-group randomized trial. In conclusion, both yoga and physiotherapy appear to exhibit therapeutic potential in alleviating the motor and neuropsychiatric symptoms of PD and enhancing the balance performance in patients.

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Pisa syndrome (PS) is characterized by tonic flexion of the trunk and head to one side of the body and generally occurs in patients with Parkinson’s disease (PD) taking antipsychotic drugs. Recently, only a few cases of PS caused by normal pressure hydrocephalus (NPH) have been reported. Here, we report a case of PS associated with NPH. We believe that the presentation of this rare case may provide an interesting perspective regarding the pathophysiology of PS. Future studies involving a large number of patients are warranted to clarify the mechanisms underlying PS in distinct neurological diseases such as PD, NPH, and multiple system atrophy.

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Objectives: To highlight the clinical significance of de novo dystonia and its spontaneous resolution during pregnancy. Methods: Two patients were evaluated in a movement disorder clinic during their first trimester of pregnancy and followed up longitudinally. Results: Our first patient developed severe right torticollis and laterocollis during the sixth week of pregnancy. No etiology could be identified by a series of laboratory and imaging investigations for dystonia. The patient had near-complete resolution of cervical dystonia, without any therapeutic interventions. The second patient developed cervical dystonia and severe neck spasms during the eighth week of pregnancy, and no identifiable etiologies were found. Because of the extreme severity of dystonia, the patient had to undergo medical termination of pregnancy, after which the dystonia subsided. Discussion: The literature on de novo dystonia in pregnancy or “dystonia gravidarum” is limited. To date, only three such cases have been reported. Our report expands the literature on this rare phenomenon. The cases in our study highlight that new movement disorders during pregnancy may indicate aberrant dopamine receptor sensitivity in a hyperestrogenic environment and that they are often self-limiting.

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A 65-year-old man presented to us with a 6-month history of recurrent, bilateral, purposeless, arm-raising and lowering movements that fulfilled all criteria for stereotypy. He was on a dopamine blocking agent levosulpiride before the onset of the movements. After the diagnosis of tardive, levosulpiride-induced, armraising stereotypy was made, the offending drug was stopped. Tetrabenazine at 100 mg/day produced near-complete improvement at 3 months. Proximal limb involvement—such as arm-raising—is not reported as a phenotype in tardive stereotypy to date, with all cases having distal hand involvement. Furthermore, any limb stereotypy is not reported with levosupride to date.

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The novel coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with a myriad of potential neurological manifestations, with de novo movement disorders still being reported. There is growing concern about a possible new wave of neurological complications in the aftermath of the COVID-19 pandemic. The objective of our review is to summarize all available evidence documenting new-onset movement disorders associated with COVID-19, with focus on hypokinetic movement disorders and their pathogenesis. We identified 66 new-onset movement disorder cases from using the PubMed and Google Scholar databases. Myoclonus was the most frequently reported movement disorder associated with COVID-19 alone or in combination with ataxia and tremor, while parkinsonism was the most notable movement disorder associated with the pandemic. To date, only eight cases of de novo parkinsonism associated with COVID-19 have been reported in the literature. Their exact pathophysiology is not well-understood but can include viral neuroinvasion–neurodegeneration, central nervous system-specific immune activation, vascular damage, systemic inflammation, autoimmune mechanisms, hypoxia, or metabolic disturbances. Although it is difficult to point out the specific relationship between SARS-CoV-2 and movement disorders, in this brief review, we unfold various potential plausible mechanisms responsible for the pathogenesis of movement disorders, with focus on hypokinetic movement disorders. Clinicians should closely monitor patients who have recovered from COVID-19 for the possibility of new-onset COVID-19-associated movement disorders. Longitudinal follow-up studies are necessary to ascertain the long-term neurological and neuropsychological consequences of the disease and the associated evolution of movement disorders.

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