Hypokinetic Movement Disorders Research Articles

Gastrointestinal disorders in hyperkinetic movement disorders and ataxia

Disorders of the gastrointestinal tract in patients suffering from hypokinetic movement disorders, and in particular Parkinson's disease, have increasingly been the subject of more intensive neuromedical research. So far, few data are available for patients with hyperkinetic movement disorders and ataxias. This review article summarizes the currently available and relevant publications on this topic. The particular focus is on essential tremor, restless legs syndrome, Huntington's disease and the group of hereditary ataxias. Further intensive research will be necessary in the future to collect detailed information also for these disease symptoms about specific disturbance patterns, in order to understand the underlying pathological pathways and to derive specific treatment approaches.

Movement Disorders in Patients with Subacute Sclerosing Panencephalitis: A Systematic Review.

Subacute sclerosing panencephalitis (SSPE) is a complication of measles, occurring after a latency of 4-10 years. It continues to occur in developing countries although resurgence is being reported from developed countries. Characteristic features include progressive neuropsychiatric issues, myoclonus, seizures, movement disorders and visual impairment. Electroencephalography (EEG) typically shows periodic generalized discharges, and elevated CSF anti-measles antibodies are diagnostic. Movement disorders are being increasingly recognized as part of the clinical spectrum, and range from hyperkinetic (chorea, dystonia, tremor, tics) to hypokinetic (parkinsonism) disorders and ataxia. This article aims to comprehensively review the spectrum of movement disorders associated with SSPE. A literature search was conducted in PubMed and EMBASE databases in December 2023 and articles were identified for review. Movement disorders reported in SSPE included hyperkinetic (chorea, dystonia, tremor and tics), hypokinetic (parkinsonism), ataxia and extraocular movement disorders. Myoclonus, a core clinical feature, was the most frequent "abnormal movement." Movement disorders were observed in all clinical stages, and could also be a presenting feature, even sans myoclonus. Hyperkinetic movement disorders were more common than hypokinetic movement disorders. An evolution of movement disorders was observed, with ataxia, chorea and dystonia occurring earlier, and parkinsonism later in the disease. Neuroradiological correlates of movement disorders remained unclear. A wide spectrum of movement disorders was observed throughout the clinical stages of SSPE. Most data were derived from case reports and small case series. Multicentric longitudinal studies are required to better delineate the spectrum and evolution of movement disorders in SSPE.

Neurophysiology of hypokinetic movement’s disorders: New insights in daily clinical practice

Hypokinetic movement disorders encompass a group of clinically similar diseases that present challenges in discrimination during neurological examinations. Characterizing a specific hypokinetic disorder is necessary for the diagnosis and treatment in daily clinical practice. Neurophysiological tools, such as electromyography (EMG) combined with accelerometry, motor-evoked potentials (MEPs), electroencephalographic recording (EEG), Bereitschaftspotential (BP), auditory-evoked cognitive potential (P300), blink reflex (BR), and R2 blink reflex recovery cycle (R2BRRC), are useful in the differential diagnosis of movement disorders due to the common clinical features. However, neurophysiological assessments of movement disorders, especially hypokinetic diseases, are currently underutilized in clinical practice as compared to a few decades ago. This review aims to summarize practical insights gleaned from reported studies over the past 5 years (i.e., 2019 – 2023) regarding neurophysiological assessments of hypokinetic movement disorders, emphasizing the importance of their routine application. In particular, the methodology of the electrophysiologic evaluations pertaining to hypokinetic movement disorders is assessed. Moreover, a practical approach for the differential diagnosis of similar movement disorder syndromes based on specific neurophysiological features is proposed. Collectively, this review of the most recent neurophysiological implications in hypokinetic movement disorders highlights the practicality of these methods. Despite the advancement of other diagnostic techniques (e.g., neuroradiological methods), neurophysiological assessments may be a promising tool for clinical diagnoses, due to their high accuracy and ability to categorize and manage movement disorders (e.g., hypokinetic movement disorders) in daily clinical practice.

NEUROPROTECTIVE POTENTIAL OF ALOGLIPTIN IN LIPOPOLYSACCHARIDE INDUCED EXPERIMENTAL MODEL OF PARKINSON’S DISEASE

AbstractBackgroundParkinson’s disease is a hypokinetic movement disorder characterized by selective loss of dopaminergic neurons in the substantia nigra. Dopaminergic degeneration of neurons is considered to be due to oxidative stress, neuroinflammation, mitochondrial dysfunction etc. Thus therapies that could alter all the pathologies linked with the disease and produces less or minimal side effects may work as better therapeutic target than the existing one.MethodThe intranigral LPS (5µg/μl) administration was used to induce PD like symptoms in rats. LPS‐infused rats were treated with alogliptin (10, 20 and 40 mg/kg/day/p.o.) for 21 days. Behavioral parameters and body weight analysis were performed on weekly basis to examine the movement disabilities in rats. On 21st day, animals were sacrificed; biochemical and histological assessment was done to evaluate role of alogliptin in LPS‐infused rats.ResultIt has been observed that Alogliptin at significant dose level attenuates movement disabilities in LPS induced in PD rats. Alogliptin significantly reduces malondialdehyde, nitrites levels and raises glutathione levels. These suggest that neuroprotective action of alogliptin is due to its anti‐oxidant activity. Moreover, histomorphological assessment confirms the neuroprotective activity of alogliptin.ConclusionAlogliptin has neuroprotective potential and observed increment in the motor activity of LPS‐infused rats following alogliptin treatment may be due to its antioxidant potential and ability to prevent the morphological alterations in brain cells.

IMMU-45. REVERSIBLE PARKINSONISM AFTER BCMA-DIRECTED CAR T CELL ADMINISTRATION

Abstract B-cell maturation antigen (BCMA)-targeting chimeric antigen receptor (CAR)T cell therapy has revolutionized the treatment of patients with relapsed or refractory multiple myeloma (MM), resulting in FDA-approval of two products, idecabtagene vicleucel (ide-cel) and ciltacabtagene autoleucel (cilta-cel). In addition to immune effector cell associated neurotoxicity syndrome (ICANS), a novel hypokinetic movement disorder resembling parkinsonism has been reported with BCMA-targeting CAR. Cases reported to date have been irreversible or fatal, and guidance on how to manage this complication is limited. Here we describe a patient with MM who developed features of parkinsonism on day 24 post ide-cel infusion which were apparently reversible with supportive care and dexamethasone. A 77 year-old man with MM received standard lymphodepletion followed by ide-cel. He developed grade 1 cytokine release syndrome (CRS) for which he received tociluzumab, followed by transient expressive aphasia (grade 2 ICANS) on day 23. Brain MRI showed no structural abnormality. On day 24 he developed new tremor and gait impairment. Neurologic examination revealed cogwheeling in bilateral wrists, hypomimia, soft speech, and slowed gait. Lumbar puncture and electroencephalogram were unremarkable. FDG-PET brain did not show basal ganglia hypometabolism or abnormal avidity. Lymphocyte percentage was elevated and correlated with a high level of circulating CAR+ T cells. He was started on dexamethasone 10 mg q day, receiving a total of 17 days of steroids with improvement in symptoms. At day 60, ambulation was improved and cogwheeling and hypomimia resolved. By day 90, all neurological symptoms had resolved. Improvement remained sustained as of last follow up day 120. To our knowledge, this is the first case report of steroid responsive parkinsonism after BCMA-CAR therapy. Our report supports close neurological monitoring of patients beyond 30 days after BCMA-CAR and suggests that intervening early in the setting of hypokinetic movement disorders may lead to sustained reversal of symptoms.

Features of drug therapy for functional gastrointestinal disorders in children of preschool and primary school age

The article explores modern concepts about functional gastrointestinal disorders in children, considers features of the classification according to the Rome criteria and Russian clinical guidelines, and presents the evolution of views in the context of understanding the general pathophysiological mechanism as impaired “gut-brain” interactions, which leads to dysmotility in different parts of the gastrointestinal tract, visceral hypersensitivity, changes in the local immune system functions, dysbiosis of the gut microbiota and a failure of the central nervous system to process signals. Dysregulation of the central nervous system and the enteric nervous system causes functional gastrointestinal disorders with pain syndrome: irritable bowel syndrome, functional dyspepsia and centrally mediated abdominal pain syndrome. In addition, the article discusses the Russian version of the guidelines due to differences in the diagnostic instrumental and laboratory facilities, as well as national peculiarities of marketing authorization, indications and contraindications for drug use in children. Subject to understanding of the mechanisms of functional gastrointestinal disorders in children, the authors presented information on the role of trimebutine, a universal motility regulator of different parts of the gastrointestinal tract, in the development of functional gastrointestinal disorders, as well as modern approaches to their prevention and correction using a drug of proven efficacy. Numerous national and foreign studies proved the efficacy of trimebutine in hyperkinetic and hypokinetic movement disorders, decreased gastric evacuation function, and impaired gallbladder contractile function in patients with both hypomotor and hypermotor types of functional disorders. The accumulated experience determines the prospects for its use in pediatric practice.

Neurologic toxicities following adoptive immunotherapy with BCMA-directed CAR T cells

In 2 complementary Letters to Blood, Karschnia et al and Graham et al provide new insights into the neurological toxicities that are observed with B-cell maturation antigen–directed chimeric antigen receptor T-cell treatment for multiple myeloma, identifying a frequency of immune effector cell–associated neurotoxicity syndrome (ICANS) that exceeds 40%. Severe ICANS is identified in 8% of patients in this real-world series. Outcomes were generally favorable, although the authors describe rare, late Parkinsonism-like hypokinetic movement disorders (also known as movement and neurocognitive toxicities) post-ICANS in 2 patients.

Chemotherapy-induced reversal of ciltacabtagene autoleucel–associated movement and neurocognitive toxicity

In 2 complementary Letters to Blood, Karschnia et al and Graham et al provide new insights into the neurological toxicities that are observed with B-cell maturation antigen–directed chimeric antigen receptor T-cell treatment for multiple myeloma, identifying a frequency of immune effector cell–associated neurotoxicity syndrome (ICANS) that exceeds 40%. Severe ICANS is identified in 8% of patients in this real-world series. Outcomes were generally favorable, although the authors describe rare, late Parkinsonism-like hypokinetic movement disorders (also known as movement and neurocognitive toxicities) post-ICANS in 2 patients.

Parkinson's Disease: From Genetics and Epigenetics to Treatment, a miRNA-Based Strategy.

Parkinson's disease (PD) is one of the most common neurodegenerative disorders, characterized by an initial and progressive loss of dopaminergic neurons of the substantia nigra pars compacta via a potentially substantial contribution from protein aggregates, the Lewy bodies, mainly composed of α-Synuclein among other factors. Distinguishing symptoms of PD are bradykinesia, muscular rigidity, unstable posture and gait, hypokinetic movement disorder and resting tremor. Currently, there is no cure for PD, and palliative treatments, such as Levodopa administration, are directed to relieve the motor symptoms but induce severe side effects over time. Therefore, there is an urgency for discovering new drugs in order to design more effective therapeutic approaches. The evidence of epigenetic alterations, such as the dysregulation of different miRNAs that may stimulate many aspects of PD pathogenesis, opened a new scenario in the research for a successful treatment. Along this line, a promising strategy for PD treatment comes from the potential exploitation of modified exosomes, which can be loaded with bioactive molecules, such as therapeutic compounds and RNAs, and can allow their delivery to the appropriate location in the brain, overcoming the blood-brain barrier. In this regard, the transfer of miRNAs within Mesenchymal stem cell (MSC)-derived exosomes has yet to demonstrate successful results both in vitro and in vivo. This review, besides providing a systematic overview of both the genetic and epigenetic basis of the disease, aims to explore the exosomes/miRNAs network and its clinical potential for PD treatment.

COVID19-associated new-onset movement disorders: a follow-up study

BackgroundNeurological symptoms are common manifestation in acute COVID-19. This includes hyper- and hypokinetic movement disorders. Data on their outcome, however, is limited.MethodsCases with new-onset COVID-19-associated movement disorders were identified by searching the literature. Authors were contacted for outcome data which were reviewed and analyzed.ResultsMovement disorders began 12.6 days on average after the initial onset of COVID-19. 92% of patients required hospital admission (mean duration 23 days). In a fraction of patients (6 of 27; 22%; 4 males/2 females, mean age 66.8 years) the movement disorder (ataxia, myoclonus, tremor, parkinsonism) was still present after a follow-up period of 7.5 ± 3 weeks. Severe COVID-19 in general and development of encephalopathy were risk factors, albeit not strong predictors, for the persistence.ConclusionsThe prognosis of new-onset COVID-19-associated movement disorder appears to be generally good. The majority recovered without residual symptoms within several weeks or months. Permanent cases may be due to unmasking of a previous subclinical movement disorder or due to vascular/demyelinating damage. Given the relatively low response rate of one third only and the heterogeneity of mechanisms firm conclusions on the (long-term) outome cannot, however, be drawn.

Emergencies in movement disorders

Movement disorders can be defined as the abnormality of the speed and form of body movements. Although movement disorders often occur chronically, they can sometimes develop acutely or sub-acutely, and some can be fatal if not diagnosed and treated early. Here, emergencies in movement disorders are discussed under two main headings as emergencies related to hyperkinetic movement disorders and emergencies related to hypokinetic movement disorders. This review draws attention to the importance of that accurate diagnosis and early treatment can be life-saving in emergencies in movement disorders. It also provides recommendations for diagnosis and therapy.

Psychomotor slowing alters gait velocity, cadence, and stride length and indicates negative symptom severity in psychosis

Schizophrenia is a severe mental disorder, in which 50% of the patients present with motor abnormalities such as psychomotor slowing. Slow spontaneous gait has been reported in schizophrenia. However, comprehensive objective instrumental assessments of multiple gait conditions are missing. Finally, the specific gait patterns of subjects with psychomotor slowing are still unknown. Therefore, this study aimed to objectively assess multiple gait parameters at different walking conditions in patients with schizophrenia with and without psychomotor slowing. Also, we hypothesised gait impairments to correlate with expert ratings of hypokinetic movement disorders and negative symptoms. We collected gait data (GAITRite®) in 70 patients with psychomotor slowing (SRRS (Salpetriere retardation rating scale) ≥15), 22 non-psychomotor slowed patients (SRRS < 15), and 42 healthy controls. Participants performed four walking conditions (self-selected speed, maximum speed, head reclined, and eyes closed) and six gait parameters were extracted (velocity, cadence, stride length, functional ambulation profile (FAP), and variance of stride length and time). Patients with psychomotor slowing presented slower velocity, lower cadence, and shorter stride length in all walking conditions compared to healthy controls, with the non-slowed patients in an intermediate position (all F > 16.18, all p < 0.001). Secondly, slower velocity was associated with more severe hypokinetic movement disorders and negative symptoms. In conclusion, gait impairments exist in a spectrum with healthy controls on one end and patients with psychomotor slowing on the other end. Patients with psychomotor slowing are specifically impaired when an adaptation of gait patterns is required, contributing to the deleterious effects of sedentary behaviours.

Reconsideration of the firing loop models for dystonia and Parkinson's disease

AbstractParkinson's disease (PD) is a hypokinetic movement disorder with degeneration of dopaminergic and other neurons, whereas dystonia is a hyperkinetic movement disorder caused by various pathogenesis, that is, sporadic, genetic, stroke, brain injury, and other diseases, such as PD. Dopamine receptor 1 (D1R) antagonist and dopamine receptor 2 (D2R) antagonist induce dystonic symptom in monkey. Consistently, D1R antagonist and D2R antagonist decrease locomotion in mice. Moreover, D1R knock‐out (KO) mice and D2R KO mice show motor deficits. In humans, dopa‐responsive dystonia (DRD) is caused by genetically defective dopamine (DA) synthesis. DYT1 dystonia and genetic mouse models show decreased striatal D1R and D2R. Therefore, PD, pharmacological dystonia models, DRD and DYT1 dystonia, have defective DA pathways. Firing of globus pallidus internus (GPi) neurons is increased in PD and dystonia with local anesthesia. However, the ordinary firing loop model cannot explain how defective DA pathways induce dystonia. PD shows thalamic neurodegeneration, whereas PD with dystonia has relatively intact thalamic neurons. Since thalamic GABAergic interneurons are innervated by GPi GABAergic neurons, here I propose to add thalamic GABAergic interneurons between GPi GABAergic neurons and thalamic glutamatergic neurons as thalamic inverse pathway for healthy condition and dystonia, whereas thalamic ordinary pathway due to degeneration of thalamic GABAergic interneurons is suitable to PD. On the contrary, PD with dystonia has both thalamic ordinary and inverse pathways. Although precise thalamic circuits have not been elucidated, discrepancy in the ordinary firing loop model for dystonia seems to be solved by the thalamic switch from dystonia to PD.

Presenting Patterns of Genetically Determined Developmental Encephalopathies With Epilepsy and Movement Disorders: A Single Tertiary Center Retrospective Cohort Study.

BackgroundThis paper aimed to evaluate the frequency of observation of genetically determined developmental encephalopathies with epilepsy and movement disorders in a specialistic center, the distribution of etiologies and presenting clinical hallmarks, and the mean times for the achievement of molecular genetic diagnosis.Patients and MethodsRetrospective data about clinical phenotypes, etiology, and diagnostic pathways were collected in all the genetically confirmed patients with developmental encephalopathies with epilepsy and movement disorders referred to our institution between 2010 and 2020. The cohort was divided into two groups according to the predominant movement disorder type: 1) Group A: patients with hyperkinetic movement disorders; 2) Group B: patients with hypokinetic movement disorders. Both groups were analyzed in terms of developmental, epileptic, and movement disorder phenotypes.ResultsThe cohort included 69 patients (Group A = 53; Group B = 16). The etiological spectrum was heterogeneous with a predominance of Rett and Angelman syndrome in Group A and neurodegenerative disorders in Group B. A moderate/severe intellectual disability was assessed in 58/69 patients (mean age at the first signs of developmental impairment = 1,87 ± 1,72 years). Group A included patients with an earlier onset of epileptic seizures (2,63 ± 3,15 vs. 4,45 ± 5,55 years of group B) and a predominant generalized motor semiology of seizures at the onset. Focal seizures were the main initial epileptic manifestations in Group B. Seizures were noticed earlier than movement disorders in Group A while the opposite occurred in Group B. A higher increase in molecular genetic diagnosis was obtained in the last five years. Mean diagnostic delay was longer in Group B than in Group A (12,26 ± 13,32 vs. 5.66 ± 6.41 years). Chorea as an initial movement disorder was associated with a significantly longer diagnostic delay and a higher age at etiological diagnosis.ConclusionsThis study suggested: (a) a higher frequency of genetic defects involving neurotransmission, neuronal excitability, or neural development in patients with hyperkinetic movement disorders; (b) a higher frequency of neurodegenerative courses and a longer diagnostic delay in patients with hypokinetic movement disorders.

Apigenin Attenuates Functional and Structural Alterations via Targeting NF-kB/Nrf2 Signaling Pathway in LPS-Induced Parkinsonism in Experimental Rats : Apigenin Attenuates LPS-Induced Parkinsonism in Experimental Rats.

Parkinson's disease (PD) is a progressive hypokinetic movement disorder caused by selective degeneration of dopaminergic neurons in striatum and dopamine deficiency in a region of the midbrain. LPS is an endotoxin, used as animal model to induce microglial activation, neuroinflammation, oxidative stress, and neurotransmitter alteration with PD-like symptoms. Therefore, to prevent neuroinflammation and neurotransmitter changes and to restore normal brain physiology, we tried apigenin (AGN) alone and in combination with piperine (bioenhancer), in LPS experimental model of rats. In this study, rats were treated with single unilateral intranigral injection of LPS at a dose of 5 μg/5 μl on day 0. The oral administration of AGN (25 and 50 mg/kg; p.o.) alone, AGN (25 mg/kg; p.o.) in combination with piperine (2.5 mg/kg; p.o.), and bromocriptine (10mg/kg; p.o.) started from day 7th once in a day. Intranigral injection of LPS significantly altered body weight and behavioral parameters assessed on weekly basis. Furthermore, the biochemical and neuroinflammatory analysis confirmed (on day 22nd) increased level of nitrite, MDA, SOD, TNF-α, IL-1β, IL-6, and caspase-1, and decreased level of CAT, GSH, and complex-I. Furthermore, altered level of neurotransmitters (DA, GABA, and glutamate) and cellular changes were observed from histopathological and immunohistochemistry (NF-kB and Nrf-2) analysis. Treatment with AGN (25 and 50 mg/kg; p.o.) alone and AGN (25 mg/kg; p.o.) in combination with piperine (2.5 mg/kg; p.o.) significantly attenuated the alteration in body weight, motor impairments, oxidative stress, neuroinflammation, and neurotransmitters in rat brain. The neuroprotective effect of AGN against LPS-induced cell death is attributed by modulating NF-kB and Nrf2 signaling pathway in the striatum.

Skin Conditions and Movement Disorders: Hiding in Plain Sight.

Skin manifestations are well-recognized non-motor symptoms of Parkinson's disease (PD) and other hypokinetic and hyperkinetic movement disorders. Skin conditions are usually well visible during routine clinical examination and their recognition may play a major role in diagnostic work-up. In this educational review we: (1) briefly outline skin conditions related to Parkinson's disease, including therapy-related skin complications and their management; (2) discuss the role of skin biopsies in early diagnosis of PD and differential diagnosis of parkinsonian syndromes; and focus more on areas which have not been reviewed in the literature before, including (3) skin conditions related to atypical parkinsonism, and (4) skin conditions related to hyperkinetic movement disorders. In case of rare hyperkinetic movement disorders, specific dermatological manifestations, like presence of angiokeratomas, telangiectasias, Mongolian spots, lipomas, ichthyosis, progeroid skin changes and others may point to a very specific group of disorders and help guide further investigations.

Comparison of long-latency reflex and mixed nerve silent period responses in various hypokinetic movement disorders

Long-latency reflex and mixed nerve silent period responses are electrophysiological methods to study the sensorimotor functions of the central nervous system. Here we aimed to study long-latency reflexes and mixed nerve silent period responses in different types of hypokinetic movement disorders in order to find an electrophysiological landmark to distinguish them. We included 39 patients with idiopathic Parkinson's disease (IPD), 12 patients with multiple system atrophy (MSA), 10 patients with corticobasal syndrome (CBS), 5 patients with progressive supranuclear palsy (PSP) and 26 healthy participants. We recorded the segmental reflex, the long-latency reflexes and the mixed nerve silent period responses for each participant. C reflex, long-latency reflex-I and long-latency reflex-III responses were not obtained in any patients with PSP. Long-latency reflex amplitude/ F amplitude ratio was significantly lower in patients with IPD and PSP compared to healthy individuals (p=0.036, p=0.006 respectively). The mixed nerve silent period end latencies were significantly longer in IPD, MSA, CBS groups compared to the healthy individuals (p=0.026, p=0.050, p=0.008 respectively). We suggest that recording long-latency reflex, particularly C reflex responses may provide promising results in distinction of CBS and MSA from PSP. Prospective studies with clinical findings and brainstem reflexes may offer more information.

Spectrum of Movement Disorder Emergencies in a Tertiary Care Center in India: A Prospective Observational Study.

Movement disorders can present in emergency services in an acute severe form which can be life threatening if not recognized. The relative frequency and spectrum of movement disorder emergencies have not been studied extensively. We studied the frequency, spectrum, and outcome of patients presenting with movement disorders emergencies. This was a prospective, descriptive single center study. Patients presenting with acute movement disorders to the neurology emergency services of the institute during the study period from April 2019 to June 2021 were analyzed. A total of 71 patients presented with acute movement disorders during the study period. Out of them, 65 patients had hyperkinetic and 6 patients had hypokinetic movement disorders emergencies. Fifteen patients were below the age of 18 years. Chorea (59.1%) was the most common movement disorder emergencies followed by dystonia and myoclonus in adults. Dystonia (33.3%) was the common movement disorder emergencies in children. Hyperglycemia followed by stroke was the most common etiology of acute movement disorders. This study brings out some novel findings on the movement disorders emergencies in Indian scenario. Chorea was the most common movement disorder emergencies presenting to the neurology emergency services. Early recognition and management of movement disorders emergencies help in reducing morbidity.

Neurocognitive and hypokinetic movement disorder with features of parkinsonism after BCMA-targeting CAR-T cell therapy

Neurocognitive and hypokinetic movement disorder with features of parkinsonism after BCMA-targeting CAR-T cell therapy

Neurocognitive and hypokinetic movement disorder with features of parkinsonism after BCMA-targeting CAR-T cell therapy.

B-cell maturation antigen (BCMA) is a prominent tumor-associated target for chimeric antigen receptor (CAR)-T cell therapy in multiple myeloma (MM). Here, we describe the case of a patient with MM who was enrolled in the CARTITUDE-1 trial ( NCT03548207 ) and who developed a progressive movement disorder with features of parkinsonism approximately 3 months after ciltacabtagene autoleucel BCMA-targeted CAR-T cell infusion, associated with CAR-T cell persistence in the blood and cerebrospinal fluid, and basal ganglia lymphocytic infiltration. We show BCMA expression on neurons and astrocytes in the patient's basal ganglia. Public transcriptomic datasets further confirm BCMA RNA expression in the caudate of normal human brains, suggesting that this might be an on-target effect of anti-BCMA therapy. Given reports of three patients with grade 3 or higher parkinsonism on the phase 2 ciltacabtagene autoleucel trial and of grade 3 parkinsonism in the idecabtagene vicleucel package insert, our findings support close neurological monitoring of patients on BCMA-targeted T cell therapies.