Lesions Of Nucleus Research Articles

Aesthetic Surgical Treatment of Large Xanthelasma palpebrarum.

Xanthelasma palpebrarum (XP) is a common eyelid condition. Various treatment modalities exist, each with its own merits and drawbacks. Managing larger lesions poses increased challenges. This study aims to explore the aesthetic surgical management of large xanthelasma palpebrarum. Patients with xanthelasma palpebrarum presenting to our department underwent partial excision of the lesion and debridement of the medullary nucleus under local anesthesia for lesions with a diameter of 6mm or more. Microsurgical scissors were utilized to remove residual subcutaneous lesions. Postoperatively, tie-over bolster dressings were applied. Patients with lipid and glucose abnormalities received corresponding therapy. Bolster dressings were removed on the third postoperative day, with suture removal seven days later. All flaps subjected to subcutaneous medullary debridement exhibited complete viability, with minimal localized eyelid depression early postoperatively and inconspicuous scarring three months post-surgery. No instances of lid ectropion were observed. The eyelid maintained a natural appearance, with a low recurrence rate of xanthelasma palpebrarum. Surgical intervention involving partial excision of the lesion and medullary nucleus debridement offers a satisfactory approach for managing large xanthelasma palpebrarum. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Unilateral Magnetic Resonance-Guided Focused Ultrasound Lesion of the Subthalamic Nucleus in Parkinson's Disease: A Prospective Study.

Unilateral subthalamic nucleus (STN) ablation using magnetic resonance-guided focused ultrasound (MRgFUS) is being explored as a new treatment for asymmetric Parkinson's disease (PD). The aims were to study the efficacy and safety of this treatment in asymmetric PD patients and to characterize the lesions. This prospective, single-center, open-label study evaluated asymmetric PD patients at 6 (n = 20) and 12 months (n = 12) after MRgFUS lesion of the STN. The primary outcome was the change in the Movement Disorders Society-Unified Parkinson's Disease Rating Scale, Part III (MDS-UPDRS III), score in off medication on the treated side and the adverse events (AEs) at 6-month follow-up. We also evaluated cognitive-neuropsychological changes, self-assessment of clinical improvement, and the correlation of the lesion volume with the motor outcomes. On the treated side, the MDS-UPDRS III score (mean difference = 13.8) and the scores in rigidity, bradykinesia, and tremor improved (P < 0.001) throughout the follow-up compared to baseline (at 6 months: rigidity mean difference = 2.8, improvement: 83.5%; bradykinesia mean difference = 6.0, improvement: 69.4%; tremor mean difference = 4.7, improvement: 91.5%). One patient had severe weakness in the treated hemibody, 1 had moderate dyskinesia, and 1 was in moderate confusional state that became mild (weakness) or completely resolved (dyskinesia and confusional state) at 6 months. The rest of the AEs were mild. We observed no clinically relevant changes in cognitive-neuropsychological tests. The percentage of ablation of the STN correlated with the improvement in the total MDS-UPDRS III and contralateral tremor scores (P < 0.05). Unilateral MRgFUS lesion of the STN resulted in a significant motor improvement. We observed no persistent severe AEs, although mild, mostly transient AEs were frequent. © 2024 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

A double CYP27A1 gene mutation in spinal cerebrotendinous xanthomatosis in a patient presenting with spastic gait: a case report

BackgroundCerebrotendinous xanthomatosis (CTX, OMIM #213700) is a rare inherited metabolic disease caused by the mutation in the CYP27A1 gene. Spinal CTX is a rare clinical subgroup of CTX which lacks typical symptoms seen in classical CTX. Here we report a spinal CTX case revealed double mutation of CYP27A1 gene.Case presentationA 42-year-old Asian man visited our hospital with spastic gait started at 35. Physical examination showed bilateral masses on his Achilles tendons and were identified as xanthoma on ankle magnetic resonance imaging (MRI). Brain and spinal cord MRI revealed high signal lesions in bilateral cerebellar dentate nuclei and long tract lesions involving lateral corticospinal and gracile tracts. Gene analysis revealed double heterozygous mutation, c.223C > T (p. Gln75Ter) and c.1214G > A (p. Arg405Gln).ConclusionsWe believe that novel mutation detected in our case might have a role in the pathomechanism in CTX. Moreover, spinal CTX should be considered in the patients only presenting with pyramidal symptoms, as CTX shows good prognosis in early treatment with chenodeoxycholic acid.

A dynamic computational model of the parallel circuit on the basal ganglia-cortex associated with Parkinson's disease dementia.

The cognitive impairment will gradually appear over time in Parkinson's patients, which is closely related to the basal ganglia-cortex network. This network contains two parallel circuits mediated by putamen and caudate nucleus, respectively. Based on the biophysical mean-field model, we construct a dynamic computational model of the parallel circuit in the basal ganglia-cortex network associated with Parkinson's disease dementia. The simulated results show that the decrease of power ratio in the prefrontal cortex is mainly caused by dopamine depletion in the caudate nucleus and is less related to that in the putamen, which indicates Parkinson's disease dementia may be caused by a lesion of the caudate nucleus rather than putamen. Furthermore, the underlying dynamic mechanism behind the decrease of power ratio is investigated by bifurcation analysis, which demonstrates that the decrease of power ratio is due to the change of brain discharge pattern from the limit cycle mode to the point attractor mode. More importantly, the spatiotemporal course of dopamine depletion in Parkinson's disease patients is well simulated, which states that with the loss of dopaminergic neurons projecting to the striatum, motor dysfunction of Parkinson's disease is first observed, whereas cognitive impairment occurs after a period of onset of motor dysfunction. These results are helpful to understand the pathogenesis of cognitive impairment and provide insights into the treatment of Parkinson's disease dementia.

Post-stroke hemiballismus: a series of two cases

Background. Hemiballismus is a rare hyperkinetic movement disorder characterized by irregular, poorly patterned, high amplitude involuntary movements of the limbs on one side of the body. While being usually a consequence of subthalamic nucleus lesions, hemiballismus is uncommonly associated with stroke in adults. Moreover, many debates remain regarding the physiopathology behind post-stroke hemiballismus and its optimal treatment. Case reports. In this context, the article aims to present two intriguing cases of hemiballismus arising from ischemic stroke, illustrating the intricate interplay between vascular pathology and movement disorders. Case 1 involves a 72-year-old female presenting with sudden onset left hemiballismus following incomplete right middle cerebral artery infarction, who received intravenous thrombolysis and had a good outcome. Case 2, an 80-year-old female presenting with abrupt onset right hemiballismus, with a suboptimal therapeutic response but self-remission after three months. Considering the inconclusive imaging results, this case highlights the diagnostic challenges and dilemmas encountered in the management of post-stroke hemiballismus. Conclusions. The authors propose a discussion by comparing the selected case reports with currently available data from the literature, focusing on the diagnosis and possible therapeutic strategies. These two cases underscore the importance of early recognition and tailored management of post-stroke hemiballismus, enriching the understanding of this movement disorder.

Giant Left Atrial Myxoma Revealed by Neurological Manifestation in a Young Female Patient

Cardiac myxoma is a prevalent benign neoplasm that arises inside the cardiac tissue and exhibits a gradual growth pattern. The annual incidence rate of cardiac myxoma is approximately 0.5–1 cases per 1,000,000 persons. The fragmentation of a cardiac tumor may be influenced by cerebrovascular events. Ischemic stroke is a relatively infrequent occurrence in pediatric populations and can occasionally be attributed to cardiac myxoma. In instances of ischemic stroke, neurological impairments are observed as a result of emboli or thrombi originating from the myxoma. Echocardiography is a valuable tool for promptly diagnosing myxoma and facilitating immediate surgical removal of the myxoma. We report a 17 years old female with neurological deficit weakness in the upper and lower right extremities since 2 months ago as the chief complaint with intermittent shortness of breath. Haemodynamic parameters was stable. The patient underwent brain imaging with result a lesion of the left lentiform nucleus, transthoracic echocardiography and trans esophageal echocardiography with oscillating septated mass on left atrial, attached to the anterior mitral leaflet (AML). Primary cardiac tumors are a very uncommon cause of cardiac embolic events. An atrial myxoma, a benign growth, can form on either the left or right side of the upper part of the heart. Untreated atrial myxoma can lead to adverse effects such as arrhythmia, pulmonary edema, and emboli formation that obstruct blood flow in the heart's veins. Ischemic stroke causes a specific functional impairment. Neurological symptoms in stroke can be an extra cardiac manifestation of atrial myxoma. The use of transthoracic and tran seso phageal is important in diagnosing atrial myxoma.

Early cortico-muscular coherence and cortical network changes in Parkinson's patients treated with MRgFUS.

To investigate cortical network changes using Magnetoencephalography (MEG) signals in Parkinson's disease (PD) patients undergoing Magnetic Resonance-guided Focused Ultrasound (MRgFUS) thalamotomy. We evaluated the MEG signals in 16 PD patients with drug-refractory tremor before and after 12-month from MRgFUS unilateral lesion of the ventralis intermediate nucleus (Vim) of the thalamus contralateral to the most affected body side. We recorded patients 24 h before (T0) and 24 h after MRgFUS (T1). We analyzed signal epochs recorded at rest and during the isometric extension of the hand contralateral to thalamotomy. We evaluated cortico-muscular coherence (CMC), the out-strength index from non-primary motor areas to the pre-central area and connectivity indexes, using generalized partial directed coherence. Statistical analysis was performed using RMANOVA and post hoct-tests. Most changes found at T1 compared to T0 occurred in the beta band and included: (1) a re-adjustment of CMC distribution; (2) a reduced out-strength from non-primary motor areas toward the precentral area; (3) strongly reduced clustering coefficient values. These differences mainly occurred during motor activation and with few statistically significant changes at rest. Correlation analysis showed significant relationships between changes of out-strength and clustering coefficient in non-primary motor areas and the changes in clinical scores. One day after MRgFUS thalamotomy, PD patients showed a topographically reordered CMC and decreased cortico-cortical flow, together with a reduced local connection between different nodes. These findings suggest that the reordered cortico-muscular and cortical-networks in the beta band may represent an early physiological readjustment related to MRgFUS Vim lesion.

Dermatomal Dissociated Facial Sensory Loss due to a Partial Trigeminal Pontine Principal Sensory Nucleus Lesion.

Dermatomal Dissociated Facial Sensory Loss due to a Partial Trigeminal Pontine Principal Sensory Nucleus Lesion.

Etonogestrel promotes respiratory recovery in an invivo rat model of central chemoreflex impairment.

The central CO2 chemoreflex is a vital component of respiratory control networks, providing excitatory drive during resting conditions and challenges to blood gas homeostasis. The retrotrapezoid nucleus is a crucial hub for CO2 chemosensitivity; its ablation or inhibition attenuates CO2 chemoreflexes and diminishes restful breathing. Similar phenotypes characterize certain hypoventilation syndromes, suggesting underlying retrotrapezoid nucleus impairment in these disorders. Progesterone stimulates restful breathing and CO2 chemoreflexes. However, its mechanisms and sites of actions remain unknown and the experimental use of synthetic progestins in patients and animal models have been met with mixed respiratory outcomes. We investigated whether acute or chronic administration of the progestinic drug, etonogestrel, could rescue respiratory chemoreflexes following selective lesion of the retrotrapezoid nucleus with saporin toxin. Adult female Sprague Dawley rats were grouped based on lesion size determined by the number of surviving chemosensitive neurons, and ventilatory responses were measured by whole body plethysmography. Ventilatory responses to hypercapnia (but not hypoxia) were compromised in a lesion-dependent manner. Chronic etonogestrel treatment improved CO2 chemosensitivity selectively in rats with moderate lesion, suggesting that a residual number of chemosensitive neurons are required for etonogestrel-induced CO2 chemoreflex recovery. This study provides new evidence for the use of progestins as respiratory stimulants under conditions of central hypoventilation and provides a new testable model for assessing the mechanism of action of progestins in the respiratory network.

Circadian Rhythm and Leptin Hormone Responses to Nutritional Restriction in Gerbils (Meriones unguiculatus) with Suprachiasmatic Nucleus Lesions

Rhythmically-regulated feeding behavior is in harmony with physiologic and metabolic activities in mammals. This rhythmic regulation is orchestrated by Suprachiasmatic Nucleus (SCN). However, it is not entirely clear how the SCN, which generates endogenous (internal) rhythms, influences body weight and serum leptin profile with activity rhythms in relation to feeding timing. In this study, animals in long photoperiod (14L:10D) were divided into two groups as control (sham-SCNx) and SCN lesions (SCNx). Then, these groups were split into four separate subgroups: a) ad libitum feeding; b) feeding only during the dark phase; c) feeding only during the light phase; and d) feeding during a specific period of the day (11:00-14:00 h). Locomotor activity and leptin hormone changes were observed in animals fed in cages attached to activity wheels for one month. Under the conditions of food restriction, the locomotor activities of the groups with SCNx and sham-SCNx demonstrated a phase shift toward the time of feeding. Serum leptin level did not change with feeding conditions but decreased in lesioned groups (SCNx). In conclusion, nutritional restriction caused phase shifts in activity rhythms and it was found that the SCN in gerbils was in charge of these rhythmic changes in the presence and absence of nutrients.

Polioencephalopathy in Eurasier dogs.

Polioencephalopathies secondary to inborn errors of metabolism have been described in dogs, but few genetically characterized. Clinically and genetically characterize polioencephalopathy in a family of Eurasier dogs. Three Eurasier dogs (littermates) presented with early onset movement disorders (9 weeks in 2, 4-6 months in 1). Progressive gait abnormalities were detected in 2 of the dogs, persistent divergent strabismus in 1, whereas consciousness and behavior remained intact in all dogs. One dog was euthanized at 25 months. Video footage was assessed in all dogs, and Dogs 1 and 2 had examinations and investigations performed. Whole genome sequencing of Dog 1 and further genetic analyses in the family were performed. A cohort of 115 Eurasier controls was genotyped for specific variants. Episodes were characterized by generalized ataxia, as well as a hypermetric thoracic limb gait, dystonia, and irregular flexion and extension movements of the thoracic limbs. Magnetic resonance imaging of the brain in Dogs 1 and 2 identified symmetrical, bilateral T2 and fluid attenuated inversion recovery hyperintense, T1 hypo to isointense, nonenhancing lesions of the caudate nucleus, lateral and medial geniculate nuclei, thalamus, hippocampus, rostral colliculus and mild generalized brain atrophy. Genetic analyses identified a homozygous mitochondrial trans-2-enoyl-CoA reductase (MECR) missense variant in all 3 dogs, and a homozygous autophagy-related gene 4D (ATG4D) missense variant in Dogs 1 and 2. We describe a presumed hereditary and progressive polioencephalopathy in a family of Eurasier dogs. Further research is needed to establish the role of the MECR gene in dogs and the pathogenic effects of the detected variants.

Abstract 265: A Curious Case Of Acute Binocular Diplopia, Ischemic Stroke Of The Interstitial Nucleus Of Cajal

Introduction The nuclei in the periaqueductal gray of the midbrain are critical structures that coordinate and control vertical and torsional gaze, as well as crucial components of the vestibulo‐occular reflex. These structures are so fine that they may be missed on routine imaging however, they represent distinct localizations for the neurological exam, with lesions of these structures being important clinical considerations. The Interstitial Nucleus of Cajal (inC) coordinates signals from the saccadic burst neurons in the rostral interstitial nucleus of the medial longitudinal fasiculus (riMLF), vestibular projections (utricular and semicircular canal pathways from the vestibular nuclei via the MLF), and descending pursuit fibers, the paired interstitial nuclei of Cajal act as neural integrators for vertical gaze and torsion. These nuclei lie adjacent but dorsal and caudal to the riMLF, For upgaze, fibers from the inC cross via the posterior commissure, then connect to the contralateral superior rectus and inferior oblique subnuclei. For downgaze, fibers travel across the posterior commissure, then innervate the contralateral inferior rectus subnucleus and fourth nerve nucleus. Blood supply is derived from the terminal branches of the basilar artery. Lesions of these interstitial nuclei and their tracts may produce vertical and torsional gaze‐holding deficits such as impairments in the vertical vestibulo‐occular reflex, hypertropia, counter‐rolling of the eyes, superior oblique palsy, and see‐saw and torsional nystagmus. Methods Case report and review of literature Results 45‐year‐old, right‐handed woman with history of turner syndrome, anemia, nephrolithiasis, horseshoe kidney, premature ovarian failure on hormone replacement therapy (HRT), suspected adrenal mass of undetermined significant, and degenerative disk disease presented to the emergency department with complaints of acute binocular diplopia and dizziness clarified to be sensation of the ground/objects bobbing in visual field. Neurological exam significant for left hypertropia and exotropia in primary gaze, equal in right/left gaze and right/left head tilt, as well as large amplitude medium frequency (see‐saw) nystagmus characterized by upbeat nystagmus with intorsion on the right, and downbeat nystagmus with extorsion left. Visual fields were intact to finger count with binocular diplopia and oscillopsia noted in primary gaze. CT head and CT angiogram of the head and neck were unrevealing. Initial MRI brain negative for diffusion restriction but with flair hyperintensity in periaqueductal gray prompting repeat MRI brain without contrast with thin slices through the brainstem with showed infarct in periaqueductal gray within the region of the interstitial nuclei, with stroke etiology undetermined at the time of presentation but suspicion of small vessel disease vs hypercoagulability given propensity for thrombophilia in Turner syndrome and patient being on HRT. Full dose aspirin and high intensity statin therapy was initiated given presentation out of tPA window, and hypercoagulability workup initiated prior to discharge. Conclusion Acute ischemic stroke and lesions of the interstitial nuclei in the periaqueductal gray are important, under recognized considerations for the evaluation of binocular diplopia, that may represent an opportunity for thrombolytic administration if providers had a higher index of suspicion. Hypercoagulability and Turner syndrome are also unique qualifiers, underscoring a nuanced approach to determination of stroke diagnosis and etiology in cases of isolated ocular symptomology.

Stereotactic Staged Asymmetric Bilateral Radiofrequency Lesioning for Parkinson’s Disease

Introduction: Parkinson’s disease (PD) is one of the most common neurodegenerative progressive disorders. Despite the dominance of neurostimulation technology, stereotactic lesioning operations play a significant role in the treatment of PD. The aim of the study was to evaluate the effectiveness and safety of staged bilateral asymmetric radiofrequency (RF) stereotactic lesioning in a highly selected group of PD patients. Material and Methods: A retrospective review of 418 consecutive patients undergoing stereotactic ablation for advanced PD at our institution revealed 28 patients who underwent staged asymmetric bilateral ablation. In this subset, after initial RF thalamotomy, contralateral pallidotomy was performed in 16 (57.1%) patients (group Vim-GPi), and contralateral lesion of the subthalamic nucleus (STN) was performed in 12 (32.9%) patients (group Vim-STN). The mean duration of disease before the first surgery was 9.9 ± 0.8 years. The mean interval between the two operations was 3.5 ± 0.4 years (range, 1–10 years); in the Vim-GPi group, it was 3.1 ± 0.4 years; and in the Vim-STN group, it was 4.3 ± 0.1 years. After the second operation, the long-term follow-up lasted from 1 to 8 years (mean 4.8 ± 0.5 years). All patients were evaluated 1 year after the second operation. Results: One year after staged bilateral lesioning, the mean tremor score improved from baseline, prior to the first operation, from 19.8 to 3.8 (improvement of 81%), the overall mean rigidity score improved from 11.0 to 3.7 (improvement of 66%), and hypokinesia improved from 14.8 to 8.9 (improvement of 40%). One year after staged bilateral lesioning, the total UPDRS score improved in the Vim-GPi group by 47% in the OFF and 45.9% in the ON states. In the Vim-STN group, the total UPDRS score improved from baseline, prior to the first operation, by 44.8% in the OFF and 51.6% in the ON states. Overall, levodopa dose was reduced by 43.4%. Neurological complications were observed in 4 (14.3%) cases; among them, 1 (3.6%) patient had permanent events related to local ischemia after pallidotomy. Conclusion: Staged asymmetric bilateral stereotactic RF lesioning can be a safe and effective method in highly selected patients with advanced PD, particularly where deep brain stimulation is not available or desirable. Careful identification and selection of patients for ablative surgery allow achieving optimal results in the treatment of PD with bilateral symptoms.

Unilateral lesion of the suprachiasmatic nucleus impairs estradiol feedback, follicular development, estrous cycle and ovulation.

Ovulation is timed by neural signals originating at the suprachiasmatic nucleus (SCN) that trigger ovulation when converge with high estradiol levels, which indicates the maturation of ovarian follicles. We have shown that the hypothalamic regulation of ovulation is asymmetrical and we hypothesized that the paired SCN could contribute to such symmetries. We unilaterally lesioned the SCN of rats at each stage of the estrous cycle and evaluated the acute effects on the progression of their estrous cycle, follicular development and ovulation. Lesions disrupted the estrous cycle when performed in estrus/metestrus but not in diestrus/proestrus. Abnormalities in follicular development were observed in the non-ovulating lesioned rats and this was independent of the side of the SCN destroyed and the stage of the cycle when surgery was performed. Groups of lesioned rats were then hormonally primed with GnRH or estradiol to assess the neuroendocrine pathway altered by the treatment. GnRH restored ovulation, suggesting that both SCN are needed for proper triggering of the preovulatory surge of GnRH and that unilateral lesion does not impair the sensitivity of the pituitary or the ovary to GnRH and gonadotropins, respectively. Estradiol was asymmetrically effective to restore ovulation in rats lesioned in estrous, partially effective on rats operated at diestrus and ineffective on metestrus. Our results indicate that the SCN regulates the activity of the hypothalamic-pituitary-ovarian axis not only by modulating the preovulatory surge of GnRH/gonadotropins, but also by promoting the hypothalamic integration of estrogenic signals from the ovaries in an asymmetric and stage-dependent fashion.

Association of Circumscribed Subcortical Gray and White Matter Lesions With Apraxic Deficits in Patients With Left Hemisphere Stroke.

Apraxia is commonly attributed to left hemisphere (LH) lesions of the cortical fronto-temporo-parietal praxis networks or white matter lesions causing disconnections between cortical nodes. By contrast, the contribution of lesions to the subcortical gray matter, that is, basal ganglia or thalamus, to apraxic deficits remains controversial. Here, we investigate whether damage to these subcortical gray matter structures (i.e., caudate nucleus, putamen, globus pallidus, and thalamus) or the adjacent white matter tracts was associated with apraxic deficits. We identified patients with distinct subcortical lesions with and without apraxia from a large retrospective sample of subacute LH ischemic stroke patients (n = 194). To test which subcortical structures (caudate nucleus, putamen, globus pallidus, thalamus, and adjacent white matter tracts), when lesioned, contributed to apraxic deficits, we statistically compared the proportion of lesioned voxels within subcortical gray and white matter structures between the apraxic and nonapraxic patients. Of the 194 stroke patients screened, 39 (median age = 65 years, range 30-82 years; median time poststroke at the apraxia assessment = 7 days, range 1-44 days) had lesions confined to subcortical regions (gray and white matter). Eleven patients showed apraxic deficits when imitating gestures or pantomiming object use. Region-wise statistical lesion comparison (controlled for lesion size) revealed a more significant proportion of damage ('lesion load') in the caudate nucleus in apraxic stroke patients (mean difference = 6.9%, 95% CI 0.4-13.3, p = 0.038, η p 2 = 0.11). By contrast, apraxic patients had lower lesion load in the globus pallidus (mean difference = 9.9%, 95% CI 0.1-19.8, p = 0.048, η p 2 = 0.10), whereas the lesion load in other subcortical structures (putamen, thalamus, and adjacent white matter tracts) did not differ significantly between the apraxic and nonapraxic patients. These findings provide new insights into the subcortical anatomy of apraxia after LH stroke, suggesting a specific contribution of caudate nucleus lesions to apraxic deficits.

Hemichorea secondary to isolated temporal infarction with severe middle cerebral artery stenosis: a case report and review of literature

BackgroundHemichorea typically results from a contralateral subthalamic nuclei (STN) lesion, although it has been reported in the cortex in a minority of cases. However, to our best knowledge, there are no documented cases in literature of hemichorea occurring as a secondary condition to an isolated temporal stroke.Case presentationWe present a case of an elderly female who sustained a sudden onset of hemichorea in her right extremities, predominantly in the distal region, lasting over a period of two days. Brain diffuse weighted image (DWI) demonstrated a high signal in the temporal region, while magnetic resonance angiography (MRA) revealed severe stenosis of the middle cerebral artery. During the symptomatic phase, computed tomography perfusion (CTP) revealed delayed perfusion in the left middle cerebral artery territory, characterized by the time-to-peak (TTP) measure. Based on the results of her medical history and laboratory tests, we were able to rule out the possibility of infectious, toxic, or metabolic encephalopathy. Her symptoms gradually improved with antithrombotic and symptomatic treatment.ConclusionsIt is important to recognize and consider acute onset hemichorea as an initial symptom of stroke to avoid misdiagnosis and delays in appropriate treatment. Further research on temporal lesion that lead to hemichorea is warranted to gain a better understanding of the underlying mechanisms.

Sex difference in the activation of central autonomic control regions in chronic intermittent hypoxia

Obstructive sleep apnea (OSA) results in sustained daytime hypertension. Chronic intermittent hypoxia (CIH) mimics the repetitive bouts of arterial hypoxemia associated with OSA. Male Sprague Dawley rats treated with CIH develop sustained hypertension and increased activation of central autonomic regions that regulate mean arterial pressure (MAP). However, gonadally intact female rats exposed to modest CIH treatment are not hypertensive. In male rats, lesions of the median preoptic nucleus (MnPO) prevent CIH-induced increase of MAP. We hypothesize that activation of MnPO and other autonomic control regions may contribute to the sex differences in the MAP response to CIH. To test this hypothesis, adult gonadally intact male and female rats (250-300 g bw) were exposed to either continuously normoxic (CON) or treated with CIH (10% O2 every 3 mins alternating with 21% O2 every 3 mins, 8 h/day) for 7 days. One week before the experiment started, some rats were instrumented with radiotelemetry transmitters to measure MAP and heart rate (HR). After one week of baseline recording, the rats were exposed to either normoxia or CIH and were euthanized (inactin 100 mg/kg ip) on the 8th day for immunohistochemistry. Forebrain and brainstem sections were stained for FosB/ΔFosB. Forebrain sections were also stained for neuronal nitric oxide synthase (NOS1) while brainstem sections were processed for dopamine-β-hydroxylase (DBH). The numbers of cells positive for NOS1 and FosB neurons in MnPO were counted and DBH and FosB positive neurons were counted in the hindbrain autonomic regions. CIH was associated with increased FosB staining in males but not females. Male exhibited an increase in the average number of FosB positive neurons (CON male 20 ± 2 cells/section, CIH male 35 ± 3; CON female 11 ± 1, CIH female 12 ± 2,) and colocalization of FosB and NOS1 (CON male 10 ± 1 cells/section, CIH male 18 ± 4; CON female 5 ± 1, CIH female 6 ± 1) in the MnPO. CIH females (n = 3) did not demonstrate increases in the numbers of FosB positive cells or DBH positive neurons in the commissural nucleus tractus solitarius (CON 7 ± 2, CIH 8 ± 2), rostral ventrolateral medulla (CON 2 ± 1, CIH 3 ± 1), caudal ventrolateral medulla (CON 5 ± 1, CIH 6 ± 2), and area postrema (CON 2 ± 1, CIH 2 ± 1) compared to CON females (n = 2). These preliminary results suggests that CIH is associated with increased FosB staining in the autonomic regions of male rats as opposed to female rats which is consistent with our working hypothesis. In addition, CIH was associated with increased FosB staining in NOS1 positive MnPO neurons suggesting that they may play a role in the sustained hypertension reported in male rats. The research is funded by NIH grant RO1 HL155977 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Cerebellar Transcranial Alternating Current Stimulation in Essential Tremor Patients with Thalamic Stimulation: A Proof-of-Concept Study.

Essential tremor (ET) is a disabling condition resulting from a dysfunction of cerebello-thalamo-cortical circuitry. Deep brain stimulation (DBS) or lesion of the ventral-intermediate thalamic nucleus (VIM) is an effective treatment for severe ET. Transcranial cerebellar brain stimulation has recently emerged as a non-invasive potential therapeutic option. Here, we aim to investigate the effects of high-frequency non-invasive cerebellar transcranial alternating current stimulation (tACS) in severe ET patients already operated for VIM-DBS. Eleven ET patients with VIM-DBS, and 10 ET patients without VIM-DBS and matched for tremor severity, were included in this double-blind proof-of-concept controlled study. All patients received unilateral cerebellar sham-tACS and active-tACS for 10min. Tremor severity was blindly assessed at baseline, without VIM-DBS, during sham-tACS, during and at 0, 20, 40min after active-tACS, using kinetic recordings during holding posture and action ('nose-to-target') task and videorecorded Fahn-Tolosa-Marin (FTM) clinical scales. In the VIM-DBS group, active-tACS significantly improved both postural and action tremor amplitude and clinical (FTM scales) severity, relative to baseline, whereas sham-tACS did not, with a predominant effect for the ipsilateral arm. Tremor amplitude and clinical severity were also not significantly different between ON VIM-DBS and active-tACS conditions. In the non-VIM-DBS group, we also observed significant improvements in ipsilateral action tremor amplitude, and clinical severity after cerebellar active-tACS, with a trend for improved postural tremor amplitude. In non-VIM-DBS group, sham- active-tACS also decreased clinical scores. These data support the safety and potential efficacy of high-frequency cerebellar-tACS to reduce ET amplitude and severity.

Mania and Hemiballismus: A rare presentation of subthalamic stroke (P12-5.008)

<h3>Objective:</h3> Mania and hemiballismus are rare presenting features of acute ischemic stroke. We present a unique case of acute subthalamic stroke presenting with mania preceding hyperkinetic movements by several days making the diagnosis challenging and precluding the patient from acute stroke care. <h3>Background:</h3> 66 year old patient presented with abnormal movements. The patient’s symptoms began with sudden onset of increased activity levels, pressured speech, and insomnia. Four days later he presented to the hospital with acute onset of uncontrolled flailing and pain in the left arm and leg. MRI brain revealed an acute right subthalamic infarct. He was diagnosed with post stroke mania and hemiballismus. <h3>Design/Methods:</h3> NA <h3>Results:</h3> NA <h3>Conclusions:</h3> Hemiballismus is a rare presenting symptom of acute stroke. Widely accepted pathophysiology behind hemiballismus is a structural lesion in the subthalamic nucleus. The subthalamic nucleus contains glutaminergic neurons with projections to the globus pallidus interna. The glutaminergic neurons increase the activity of the globus pallidus interna, which contains GABAergic neurons that, in turn, decrease the activity of the thalamus and inhibit movement. Lesions of the subthalamic nucleus can disrupt the inhibition of movement by the globus pallidus interna and results in hyperkinetic movements like hemiballismus. The subthalamic nucleus has a role is mood, memory and behavior. Studies have shown to have variable effects of subthalamic deep brain stimulation on working memory and response inhibition performance and some reported cases with aggressive impulsive episodes, suicide and suicidal attempts, apathy, severe depression, psychosis, and hypomania following bilateral sub thalamic nucleus DBS. Our patient presented with acute onset of mania preceding development of hemiballismus by several days making the case diagnostically challenging. On literature review, we could not find a case with this presentation. With this case, we add to the multitude of presentation of acute stroke since acute stroke is a medical emergency and requires prompt management. <b>Disclosure:</b> Dr. Mann has nothing to disclose. Dr. Kelly has nothing to disclose. Dr. Leichliter has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Neurocrine.

Contraversive Ocular Tilt Reaction, Body Lateropulsion and Gaze-Evoked Nystagmus After Inferior Cerebellar Peduncle and Dentate Nucleus Stroke

Contraversive Ocular Tilt Reaction, Body Lateropulsion and Gaze-Evoked Nystagmus After Inferior Cerebellar Peduncle and Dentate Nucleus Stroke