Callosal Lesions Research Articles

Intrinsic organization of the corpus callosum.

The corpus callosum-the largest commissural fiber system connecting the two cerebral hemispheres-is considered essential for bilateral sensory integration and higher cognitive functions. Most studies exploring the corpus callosum have examined either the anatomical, physiological, and neurochemical organization of callosal projections or the functional and/or behavioral aspects of the callosal connections after complete/partial callosotomy or callosal lesion. There are no works that address the intrinsic organization of the corpus callosum. We review the existing information on the activities that take place in the commissure in three sections: I) the topographical and neurochemical organization of the intracallosal fibers, II) the role of glia in the corpus callosum, and III) the role of the intracallosal neurons.

Etiologic factors and imaging features of cytotoxic lesions of the corps callosum (Cloccs): A series of 5 patients

Cytotoxic Lesions of the Corpus Callosum (CLOCCS) are secondary lesions associated with various etiologies, including trauma, infection, and metabolic disorders. Recognizing these lesions is crucial as they can mimic primary callosal lesions such as ischemia. This retrospective study presents a series of five patients with CLOCCS, evaluating their clinical and radiological characteristics over a one-year period. Imaging, particularly MRI, plays a pivotal role in diagnosis, with diffusion-weighted sequences revealing characteristic features of cytotoxic edema. Clinical context, additional imaging findings, and patient history aid in distinguishing CLOCCS from other pathologies. The study highlights diverse etiologies contributing to CLOCCS, including trauma, infection (e.g., Malaria, COVID-19), and metabolic disorders. Treatment strategies depend on addressing the underlying cause. Understanding the spectrum of etiologies and imaging features of CLOCCS is vital for accurate diagnosis and appropriate management.

Clinico-radiologic subtypes and therapeutic observation of acute Marchiafava-Bignami disease

We aimed to investigate the clinico-radiologic features of acute Marchiafava-Bignami disease (MBD) and its evolutionary process after effective treatment through subgroup comparison. The clinical and MRI data of 23 patients with acute MBD were retrospectively analyzed and divided into type A (12 cases, with entire callosal involvement) and type B (11 cases, with focal callosal involvement). The clinical assessments and MRI findings (before and after treatment) were compared between the two subtypes. Compared with type B, type A had lower MoCA (Montreal Cognitive Assessment) scores at admission (16.50 ± 1.73 vs 18.27 ± 1.68, P = 0.021) and were more common with extracallosal involvement (66.67% vs 18.18%, P = 0.036) and longer illness duration (18.3 ± 2.1 days vs 15.6 ± 2.4 days, P = 0.012). During the treatment, the residual lesion in the splenium was more common in type A (58.33% vs 9.09%, P = 0.027). After treatment, the MoCa scores of both subtypes gradually increased (P < 0.001), and the callosal and extracallasal lesions disappeared completely. Clinico-radiologic typing of acute MBD is related to the severity of early symptoms, but not to the prognosis. Complete clinico-radiologic recovery is possible for both subtypes with combined treatment. The clinico-radiologic reversibility is helpful for accurate diagnosis and therapeutic evaluation.

Susac syndrome: neurological update (clinical features, long-term observational follow-up and management of sixteen patients)

Susac syndrome is a likely autoimmune microangiopathy affecting the brain, retina and inner ear. Due to the rarity of this condition, diagnosis and treatment can be challenging. Diagnosis is based on the presence of the clinical triad of central nervous system dysfunction, branch retinal artery occlusions and sensorineural hearing loss. Typical MRI findings of callosal and peri-callosal lesions may assist in diagnosis. Clinical course can be monophasic, polycyclic or chronic continuous. It is important to look out for red flags to attain an accurate diagnosis and follow a therapeutic algorithm based on severity of the disease and response to treatment. Patients are treated with steroids and immunosuppressive agents with a variable response. Early aggressive treatment especially in severe cases, may help in preventing relapses and morbidity/disability. This study highlights important diagnostic features and proposes a treatment algorithm based on clinical experience from management of 16 patients from 2 neuroscience centres in the UK since 2007, who were followed up over a long period of 3–15 years.

Role of interhemispheric connectivity in recovery from postoperative supplementary motor area syndrome in glioma patients.

Surgical resection of gliomas involving the supplementary motor area (SMA) frequently results in SMA syndrome, a symptom complex characterized by transient akinesia and mutism. Because the factors influencing patient functional outcomes after surgery remain elusive, the authors investigated network-based predictors in a multicentric cohort of glioma patients. The participants were 50 patients treated for glioma located in the SMA at one of the three centers participating in the study. Postoperative functional outcomes (motor deficits, mutism) and duration of symptoms were assessed during hospitalization. Long-term outcome was assessed 3 months after surgery. MRI-based lesion-symptom mapping was performed to estimate the severity of gray matter damage and white matter disconnection. The median duration of acute symptoms was 3 days (range 1-42 days). Long-term deficits involving fine motor movements and speech were found at follow-up in 27 patients (54%). Disconnection of the central callosal fibers was associated with prolonged acute symptoms (p < 0.05). Postoperative mutism was significantly related to disconnection severity of the left frontopontine tract, frontal aslant tract, cingulum, and corticostriatal tract (p < 0.05). Disconnection of midposterior callosal fibers and lesion loads within the left medial Brodmann area 4 were associated with long-term motor deficits (p < 0.05). This study provides evidence for the pathophysiology and predictive factors of postoperative SMA syndrome by demonstrating the relation of the disconnection of callosal fibers with prolonged symptom duration (central segment) and long-term motor deficits (midposterior segment). These data may be useful for presurgical risk assessment and adequate consultation for patients prior to undergoing resection of glioma located within the SMA region.

Stroke-like presentation of acute toxic leukoencephalopathy due to capecitabine treatment with extensive intramyelinic edema.

Stroke-like presentation of acute toxic leukoencephalopathy due to capecitabine treatment with extensive intramyelinic edema.

Reversible Splenial Lesion Syndrome (RESLES) in Sickle Cell Crisis Mimicking Marchiafava-Bignami Disease (P10-7.001)

<h3>Objective:</h3> N/A <h3>Background:</h3> Reversible Splenial Lesion Syndrome (RESLES) is characterized by the presence of transient lesion involving the splenium of corpus callosum in patients with encephalopathies of various cytotoxic etiologies. One of which is Marchiafava-Bignami Disease(MBD), which could manifest with sudden stupor or coma in alcohol use disorder (AUD) or malnutrition with severe demyelination of splenium. Here we report a case of MBD-like presentation in a patient with vaso-occlusive sickle-cell crises. <h3>Design/Methods:</h3> NA <h3>Results:</h3> A 46-year-old male with sickle-cell disease and no history of AUD presented with acute chest syndrome with pain crisis. He was treated with blood transfusion and analgesics. Two days later, he became acutely unresponsive with right-sided hemiparesis, requiring intubation. MRI brain showed numerous punctate infarcts in the watershed areas bilaterally, along with symmetric diffusion restriction in the splenium of corpus callosum, respecting its anatomic boundary. Exchange transfusion was initiated and maintained his hemoglobin &gt;10 g/dL and Hb-SS &lt; 30%, but he remained comatose (GCS 6). Electroencephalogram showed diffuse cerebral dysfunction without epileptogenicity. His extensive infectious workup was unremarkable. Other laboratory tests including electrolytes, liver function tests, ammonia, thyroid function tests, vitamin B12, B6, folic acid, and thiamine levels were normal. He was empirically treated with intravenous thiamine. One week later, his mental status improved to following commands. MRI brain two weeks after showed a near-complete resolution of the callosal lesion. The patient’s acute stupor/coma and MRI findings were attributed to hypoxic watershed infarcts and RESLES due to hypoxic stress from vaso-occlusive sickle cell crisis, leading to a transient coma, mimicking MBD. <h3>Conclusions:</h3> RESLES is a distinct syndrome with characteristic radiographic finding of diffusion restriction in the splenium of corpus callosum due to cytotoxic edema of various etiologies. MBD is one such example, presenting with stupor/coma. This case emphasizes the importance of identifying reversible metabolic stressors, including sickle cell crisis. <b>Disclosure:</b> Dr. Mulatu has nothing to disclose. Dr. Yoon has received personal compensation in the range of $500-$4,999 for serving as a Consultant for ECHAS. Dr. Ramaswamy has nothing to disclose. Dr. Mulatu has nothing to disclose. Cappi C Lay has received publishing royalties from a publication relating to health care.

Silent findings: Examination of asymptomatic demyelination in a pediatric US cohort.

Limited data is available on children with evidence of silent central nervous system demyelination on MRI. We sought to characterize the population in a US cohort and identify predictors of clinical and radiologic outcomes. We identified 56 patients such patients who presented with incidental MRI findings suspect for demyelination, enrolled through our US Network of Pediatric Multiple Sclerosis Centers, and conducted a retrospective review of 38 patients with MR images, and examined risk factors for development of first clinical event or new MRI activity. MRI were rated based on published MS and radiologically isolated syndrome (RIS) imaging diagnostic criteria. One-third had a clinical attack and ¾ developed new MRI activity over a mean follow-up time of 3.7 years. Individuals in our cohort shared similar demographics to those with clinically definite pediatric-onset MS. We show that sex, presence of infratentorial lesions, T1 hypointense lesions, juxtacortical lesion count, and callosal lesions were predictors of disease progression. Interestingly, the presence of T1 hypointense and infratentorial lesions typically associated with worse outcomes were instead predictive of delayed disease progression on imaging in subgroup analysis. Additionally, currently utilized diagnostic criteria (both McDonald 2017 and RIS criteria) did not provide statistically significant benefit in risk stratification. Our findings underscore the need for further study to determine if criteria currently used for pediatric patients with purely radiographic evidence of demyelination are sufficient.

A case of possible Susac syndrome with avascular necrosis of hip

Susac syndrome (SuS) is a rare autoimmune micro-angiopathic endotheliopathy. The diagnosis of SuS is a challenge to neurologists because of the diversity of symptoms and rarity of occurrence of classical triad of SuS. In this context, a plethora of immunological/demyelinating disorders can mimic the features of neurological manifestations of SuS. The detection of snowball corpus callosal lesion is unique to SuS. A high degree of suspicion is the key to diagnosis and early immunomodulator therapy can prevent catastrophic disabilities. The use of steroid-sparing medications should be advocated wherever possible. In this case report, we tried to explore a 20 year old female with headache, seizure, irritability, blurring of vision with right hip pain and emphasize the need for awareness of this rare entity along with high element of suspicion for detection of such disorders.

Corpus callosum involvement in MOG antibody-associated disease in comparison to AQP4-IgG-seropositive neuromyelitis optica spectrum disorder and multiple sclerosis

Background: Data on corpus callosum involvement in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are limited. Objective: The objective of the study was to compare callosal lesions in MOGAD, multiple sclerosis (MS), and aquaporin-4-IgG positive neuromyelitis optica spectrum disorder (AQP4+NMOSD). Results: Callosal lesion frequency was similar in MOGAD (38/171 (22%)), MS (24/72 (33%)), and AQP4+NMOSD (18/63 (29%)). Clinical phenotypes included encephalopathy (47%) and focal supratentorial (21%) or infratentorial (45%) deficits. None had callosal-disconnection syndromes. Maximal callosal-T2-lesion diameter (median (range)) in millimeter was similar in MOGAD (21 (4–77)) and AQP4+NMOSD (22 (5–49); p = 0.93) but greater than in MS (10.5 (2–64)). Extracallosal extension (21/38 (55%)) and T2-lesion resolution (19/34 (56%)) favored MOGAD. Conclusions: Despite similar frequency and imaging overlap, larger lesions, sagittal midline involvement, and lesion resolution favored MOGAD.

Susac Syndrome: Description of a Single-Centre Case Series.

This study describes the clinical characteristics, diagnostic results, treatment regimens, and clinical course of a cohort of patients with Susac syndrome (SS). It is a retrospective observational study of all patients with the diagnosis of SS evaluated at the Hospital Clinic (Barcelona, Spain) between March 2006 and November 2020. Nine patients were diagnosed with SS. The median time from the onset of the symptoms to diagnosis was five months (IQR 9.0), and the median follow-up time was 44 months (IQR 63.5). There was no clear predominance of sex, and mean age of symptoms onset was 36 years (range 19-59). Six patients (67%) presented with incomplete classical clinical triad, but this eventually developed in six patients during the disease course. Encephalopathy, focal neurological signs, visual disturbances, and hearing loss were the most frequent manifestations. Brain magnetic resonance imaging showed callosal lesions in all patients. Most were in remission within two years. Only four patients met the proposed criteria for definite SS. When SS is suspected, a detailed diagnostic workup should be performed and repeated over time to identify the clinical manifestations that will lead to a definite diagnosis.

Differentiating central nervous system demyelinating disorders: The role of clinical, laboratory, imaging characteristics and peripheral blood type I interferon activity

Objective: While multiple sclerosis (MS) is considered the cornerstone of autoimmune demyelinating CNS disorders, systemic autoimmune diseases (SADs) are important MS mimickers. We sought to explore whether distinct clinical, laboratory, and imaging characteristics along with quantitation of peripheral blood type I interferon (IFN) activity could aid in differentiating between them. Methods: A total of 193 consecutive patients with imaging features suggesting the presence of CNS demyelinating disease with or without relevant clinical manifestations underwent full clinical, laboratory, and imaging evaluation, including testing for specific antibodies against 15 cellular antigens. Expression analysis of type I IFN-inducible genes (MX-1, IFIT-1, and IFI44) was performed by real-time PCR, and a type I IFN score, reflecting type I IFN peripheral activity, was calculated. After joint neurological/rheumatological evaluation and 1 year of follow-up, patients were classified into MS spectrum and CNS autoimmune disorders. Results: While 66.3% (n = 128) of the patients were diagnosed with MS spectrum disorders (predominantly relapsing–remitting MS), 24.9% (n = 48) were included in the CNS autoimmune group, and out of those, one-fourth met the criteria for SAD (6.7% of the cohort, n = 13); the rest (18.1% of the cohort, n = 35), despite showing evidence of systemic autoimmunity, did not fulfill SAD criteria and comprised the “demyelinating disease with autoimmune features” (DAF) subgroup. Compared to the MS spectrum, CNS autoimmune patients were older, more frequently females, with increased rates of hypertension/hyperlipidemia, family history of autoimmunity, cortical dysfunction, anti-nuclear antibody titers ≥1/320, anticardiolipin IgM positivity, and atypical for MS magnetic resonance imaging lesions. Conversely, lower rates of infratentorial and callosal MRI lesions, CSF T2 oligoclonal bands, and IgG-index positivity were observed in CNS autoimmune patients. Patients fulfilling SAD criteria, but not the DAF group, had significantly higher peripheral blood type I IFN scores at baseline compared to MS spectrum [median (IQR)]: 50.18 (152.50) vs. −0.64 (6.75), p-value: 0.0001. Conclusion: Our study suggests that underlying systemic autoimmunity is not uncommon in patients evaluated for possible CNS demyelination. Distinct clinical, imaging and laboratory characteristics can aid in early differentiation between MS and CNS-involving systemic autoimmunity allowing for optimal therapeutic strategies. Activated type I IFN pathway could represent a key mediator among MS-like-presenting SADs and therefore a potential therapeutic target.

Brain Magnetic Resonance Imaging Findings of Pediatric Hemophagocytic Lymphohistiocytosis Could Be Diagnostic and Life-Saving

BackgroundHemophagocytic lymphohistiocytosis (HLH) is a rare and fatal disease and may also present with central nervous system findings at the beginning without specific diagnostic criteria. Brain magnetic resonance imaging (MRI) findings are diverse and can also be diagnostic. We aimed to emphasize the importance of brain MRI findings in the early diagnosis of this fatal disease. MethodsMRI findings, clinical presentations, treatment response, and prognosis of seven patients with HLH were described. ResultsThere were seven pediatric patients who were initially diagnosed with HLH with neurological findings without systemic signs of HLH: four as primary, two as secondary, and one as possible primary HLH. All patients had contrast-enhancing diffuse cerebellar and brainstem lesions; patchy periventricular and callosal cerebral lesions were observed. Thalamus involvement was found in three (42.8%), corpus callosum involvement in six (85.7%), and cervical spinal involvement in one (14.2%). Patients were followed up with these MRI findings, with prediagnoses of toxic, metabolic, infectious, vascular, and demyelinating diseases. Not all patients met the HLH diagnostic criteria due to incomplete systemic/laboratory findings; therefore, only two were immediately directed for hematopoietic stem cell therapy. Four died shortly after admission, one patient could not be followed up after HLH treatment, and two patients who fulfilled the HLH diagnostic criteria underwent hematopoietic stem cell transplantation and survived. ConclusionsBrain MRI findings, especially in the presence of neurological findings, allow for early diagnosis, which can be life-saving. These common features in brain MRI findings should be evaluated with this suspicion and included in HLH diagnostic criteria.

Metronidazole-Induced Toxic Neuropathy With the “Boomerang” Sign: A Case Report

Metronidazole has been used to treat a broad range of infections over the decades, and its safety profile has been presumably well studied. However, neurological severe adverse events after prescription and nonprescription use of metronidazole is well recognized but underdiagnosed. We report the case of a 48-year-old Indian man who presented with unremitting symptoms of peripheral neuropathy along with a silent callosal lesion in the splenium ("boomerang" sign). Because he had visited 3 neurologists previously, there were many targeted and nontargeted investigations, which failed to reach an etiological diagnosis and hence to provide relief. The patient was questioned about a potential neurotoxin exposure, and at that point, he said that he had been taking metronidazole for a long time, without any supervision, as an over-the-counter remedy for self-diagnosed "chronic amebiasis." On stopping metronidazole, he recovered gradually. In the sixth month of follow-up, brain magnetic resonance imaging showed disappearance of the callosal lesion and significant improvement in the nerve conduction studies. Clinicians should keep metronidazole toxicity in mind while dealing with a case of cytotoxic lesion of the corpus callosum with splenium involvement and peripheral neuropathy.

Corpus callosum volumetrics and clinical progression in early multiple sclerosis.

Corpus callosum (CC) is commonly affected in multiple sclerosis (MS), with known association between CC atrophy and MS clinical activity. In this study, we assessed the association of callosal atrophy, lesions volume and residual CC volume with the clinical disability of early MS patients. Thirteen MS subjects (9 female, mean age 36.9 years), studied with magnetic resonance imaging (MRI) were selected. MRI scans were performed at baseline (T0), at 6 (T1), 12 (T2), and 24 months (T3) from baseline. CC was segmented into three sections (genu, body, and splenium); callosal boundaries were outlined and all CC lesions were manually traced. Normal CC and CC lesion volumes were measured using a semiautomatic software. From January 2014 to December 2016, all selected patients had confluent lesions on MRI at T3 with a significant increase in the size of confluent lesions compared to baseline (p=0.0007). At T1, a significant increase in the size of confluent (p=0.02) and single lesions located in the callosal body (p=0.04) was detected in patients with EDSS ≥1.5. Also, CC residual volume (CCR) rather than the whole CC volume (CCV) significantly correlated (p=0.03) with the clinical progression of MS in the whole cohort. In early MS patients with higher EDSS at baseline, a significant increase in confluent CC lesions size is evident, particularly in the callosal body. Also, median CCR is significantly associated with MS progression in the whole MS group, regardless of initial EDSS. Given their significant association with disability, we encourage measuring CC body lesions and residual CC size for therapeutic decisions and prognostic planning in early MS.

The impact of adding fetal MRI to sonographically diagnosed intrauterine ventriculomegaly: a prospective cohort study

Objective: Intrauterine fetal ventriculomegaly (IVM) is one of the most commonly detected fetal anomalies. Prenatal diagnosis in IVM is considered a challenge with a significant impact on management. The current study aims to evaluate the added value of performing fetal MRI to sonographically diagnosed IVM. Methods: A prospective cohort study was conducted at a tertiary University Hospital in the period between January 2017 and March 2019. We included pregnant women with a single fetus sonographically diagnosed IVM (symmetrical or asymmetrical). First, a basic obstetric sonographic examination was done, followed by a detailed (2D/3D) fetal CNS anomaly scan for the detection of other associated anomalies. A fetal MRI brain scan was performed for all cases. Results: Sixty women were included in the study. Of the 60 fetuses with IVM, additional findings were seen on MRI in 14 cases (23%), and most of these findings were identified in fetuses with severe IVM (about 50%). No additional abnormalities were identified in fetuses of less than 24 weeks gestation. Callosal and septum pellucidum lesions (29%), along with posterior fossa abnormalities (28%) and cortical malformations (21%) accounted for the most common additional significant fetal MRI findings. Fetal MRI sensitivity, specificity, and positive and negative predictive values in correlation with those of prenatal ultrasound turned out to be notably higher, approaching nearly 100 %. Conclusions: Fetal MRI for sonographically diagnosed moderate or severe IVM is recommended to guide clinical management.

Improvement in callosal disconnection syndrome with recovery of callosal connectivity

ABSTRACT Recent advancements in radiological techniques have enabled the observation of the topographic distribution of the human corpus callosum. However, its functional connectivity remains to be elucidated. The symptoms of callosal disconnection syndrome (CDS) can potentially reveal the functional connections between the cerebral hemispheres. Herein, we report a patient with CDS, whose callosal lesion was restricted to the posterior midbody, isthmus, and an anterior part of the dorsal splenium. A 53-year-old right-handed woman demonstrated CDS following cerebral infarction associated with subarachnoid hemorrhage. She exhibited CDS including ideomotor apraxia, and tactile anomia with the left hand, cross-replication of hand postures, cross-localization of the fingers, and constructional impairment with the right hand. Six months after onset, the left-handed ideomotor apraxia on imitation improved, but that to command did not, which indicated the difference in the nature of the transcallosal connections between ideomotor apraxia on imitation and ideomotor apraxia to command. Longitudinal CDS observation and corpus callosum tractography will prove useful in expanding our understanding of the nature of the organization of interhemispheric information transference.

Three cases of paroxysmal alien limb phenomena due to epileptic seizures and review of literatures

BackgroundThe alien hand phenomenon (AHP) is a rare disorder of involuntary limb movement together with a loss of sense of limb ownership. AHP occurs as a consequence of frontal, callosal, or posterior cerebral lesions. To characterize the phenomenon of AHP, three patients with paroxysmal AHP were described and proved to be focal seizures by using video-EEG monitoring.MethodClinical history of 3 epileptic patients with AHP was collected. EEG and MRI were performed in each patient. One patient completed EEG monitoring and postoperative pathological examination. We also review the recent literatures and summarize the characteristics, types and hypothetic mechanisms of epileptic AHP.ResultsCase 1 had AHP of the left arm followed by the left arm convulsion or AHP only. MRI imaging showed a lesion in the posterior parietal lobe. After complete resection of the lesion, he remained seizure free for 1.5 years. Cases 2 and 3 had AHP and convulsion. The three cases did not have auto-motor signs, so they were identified to be the posterior type of APH.ConclusionsThe mechanism underlying AHP remains poorly .understood. Currently, little is known for the epileptic paroxysmal AHP, a quite rare form of AHP. AHP can be represented before or immediately after convulsion, or be represented by the paroxysmal symptom only.

Modified models to distinguish central nervous system demyelinating diseases with brain lesions

BackgroundBrain lesions in patients with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are indistinguishable from those with relapsing-remitting multiple sclerosis (RRMS) and aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-Ab NMOSD). MethodsPatients with MOGAD, RRMS, and AQP4-Ab NMOSD with abnormal brain lesions were retrospectively reviewed and divided into training and validation sets. Discriminatory models using brain images and demographics were generated to identify optimal predictors using orthogonal partial least square discriminant analysis after principal component analysis (PCA) of clinico-radiological data without a diagnosis. Constructed models were tested in an independent cohort. ResultsPCA of 51 brain scans and demographics from patients (13 MOGAD, 24 RRMS, and 14 AQP4-Ab NMOSD) demonstrated that RRMS was distinct from antibody-mediated conditions. The best predictors between MOGAD and AQP4-Ab NMOSD were poorly demarcated lesions, large abnormalities (both predictive for MOGAD), female sex, disease duration, linear lesions adjacent to the lateral ventricle, and cerebellum involvement (all predictive for MOGAD). Periventricular, ovoid/round, juxtacortical, and callosal lesions; Dawson's fingers; T1 hypointensity (all predictive for RRMS); and fluffy as well as large lesions (for MOGAD) were the best predictors of MOGAD and RRMS. RRMS versus MOGAD and RRMS versus AQP4-Ab NMOSD models exhibited a high predictive value and perfect accuracy (100%), which was validated in an independent cohort. The model of patients with AQP4-Ab NMOSD and MOGAD exhibited lower predictive power but still achieved an accuracy of 90%. ConclusionsBrain MRI characteristics combined with demographics enables the distinction of MOGAD from RRMS and AQP4-Ab NMOSD. Fluffy and large lesions are relatively specific MRI characteristics in patients with MOGAD with brain abnormalities in Asian countries.

Interlimb Transfer of Reach Adaptation Does Not Require an Intact Corpus Callosum: Evidence from Patients with Callosal Lesions and Agenesis.

Generalization of sensorimotor adaptation across limbs, known as interlimb transfer, is a well-demonstrated phenomenon in humans, yet the underlying neural mechanisms remain unclear. Theoretical models suggest that interlimb transfer is mediated by interhemispheric transfer of information via the corpus callosum. We thus hypothesized that lesions of the corpus callosum, especially to its midbody connecting motor, supplementary motor, and premotor areas of the two cerebral hemispheres, would impair interlimb transfer of sensorimotor adaptation. To test this hypothesis, we recruited three patients: two rare stroke patients with recent, extensive callosal lesions including the midbody and one patient with complete agenesis. A prismatic adaptation paradigm involving unconstrained arm reaching movements was designed to assess interlimb transfer from the prism-exposed dominant arm (DA) to the unexposed non-dominant arm (NDA) for each participant. Baseline results showed that spatial performance of each patient did not significantly differ from controls, for both limbs. Further, each patient adapted to the prismatic perturbation, with no significant difference in error reduction compared with controls. Crucially, interlimb transfer was found in each patient. The absolute magnitude of each patient’s transfer did not significantly differ from controls. These findings show that sensorimotor adaptation can transfer across limbs despite extensive lesions or complete absence of the corpus callosum. Therefore, callosal pathways connecting homologous motor, premotor, and supplementary motor areas are not necessary for interlimb transfer of prismatic reach adaptation. Such interlimb transfer could be mediated by transcallosal splenium pathways (connecting parietal, temporal and visual areas), ipsilateral cortico-spinal pathways or subcortical structures such as the cerebellum.