Secondary Atrophy Research Articles

Hypothalamic atrophy and structural covariance in amnestic mild cognitive impairment and Alzheimer’s dementia

BackgroundAlzheimer’s disease (AD) is characterized by progressive cognitive decline and specific brain atrophy patterns, primarily involving the medial temporal lobes. A number of studies have discussed hypothalamic involvement in AD with consecutive metabolic and/or autonomic disturbances yet only few studies have investigated hypothalamic atrophy in AD and its early stages in particular. Methods: We applied semi-automated volumetry of the hypothalamus (HTH) in 3 T MRI in a sample N = 175 participants [age 74.9 ± 7.22; gender 85 m/90f; cognitively normal controls (CN; N = 56); amnestic mild cognitive impairment (MCI; N = 78); AD (N = 41)] from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). In addition, we used voxel-based morphometry (VBM), cortical thickness (CTH) analyses and source-based morphometry (SBM) derived networks of structural covariance to investigate brain structural covariance patterns of the HTH under consideration of diagnostic groups, β-amyloid (AB) positivity and apolipoprotein E (APOE) ε4 status. Results: Hypothalamic atrophy was observed in both early and advanced disease stages (i.e. hypothalamic volume CN > MCI > AD). VBM, CTH analysis and SBM revealed positive associations between hypothalamic volume (HV) and AD-vulnerable regions, largely corresponding to the Papez circuit and brain regions implicated in autonomic regulation, however, group differences regarding HTH structural covariance were not observed. Similar observations were made in carriers and non-carriers of the ε4 allele, yet more pronounced in ε4 carriers. Although not reaching significance, comparisons of AB positive vs. negative subjects indicated stronger HTH atrophy in biomarker positive participants. HV was not associated with body mass index or longitudinal weight change. Conclusions: Our findings support early structural changes of the HTH in AD. HV covaries with regional volumes of AD-vulnerable regions. This could point to secondary atrophy of the HTH following atrophy of the hippocampus and other structures of the Papez circuit in AD.

Clinical and magnetic resonance imaging features of unilateral thalamic porencephaly in a dog

AbstractA 1‐year‐3‐month‐old, female, neutered labrador retriever was presented with a history of circling behaviour since 2 months of age and a recently detected blindness affecting its right eye. Neurological examination revealed a left‐sided head tilt, compulsive tight circling towards the left, postural reaction deficits in the right thoracic and pelvic limbs, absent menace response in the right eye and ventral positional strabismus of the left eye. The neurological examination findings were localised to the left thalamus. Magnetic resonance imaging of the head revealed porencephaly involving the left dorsal aspect of the thalamus. Furthermore, reduced volume of the left rostral colliculus, crus cerebri and optic chiasm, alongside marked thinning of the left cerebral hemispheric white matter tracts with associated left lateral ventriculomegaly, were present. Based on magnetic resonance imaging features and clinical history, a congenital or perinatal encephaloclastic porencephaly with secondary hypoplasia or atrophy of the associated thalamic projection pathways was prioritised.

Epigenetics of Skeletal Muscle Atrophy.

Skeletal muscle atrophy, characterized by diminished muscle strength and mass, arises from various causes, including malnutrition, aging, nerve damage, and disease-related secondary atrophy. Aging markedly escalates the prevalence of sarcopenia. Concurrently, the incidence of muscle atrophy significantly rises among patients with chronic ailments such as heart failure, diabetes, and chronic obstructive pulmonary disease (COPD). Epigenetics plays a pivotal role in skeletal muscle atrophy. Aging elevates methylation levels in the promoter regions of specific genes within muscle tissues. This aberrant methylation is similarly observed in conditions like diabetes, neurological disorders, and cardiovascular diseases. This study aims to explore the relationship between epigenetics and skeletal muscle atrophy, thereby enhancing the understanding of its pathogenesis and uncovering novel therapeutic strategies.

Lobar and Segmental Atrophy of the Liver: Differential Diagnoses and Treatments

Segmental or lobar liver atrophy is a common but not well-understood clinical condition. Hepatic atrophy can be classified into hepatic atrophy secondary to other pathologies and primary segmental hepatic atrophy, which is a benign intrahepatic lesion (pseudotumor) not associated with any other pathology. The pathophysiological mechanisms underlying atrophy can be divided into three main situations: obstruction of biliary outflow, obstruction of the systemic venous outflow, and obstruction of incoming portal venous flow. For what may concern secondary hepatic atrophy, there are many pathologies that could underlie this condition, ranging from benign to intrahepatic malignancies, with particular reference to particularly hepatocellular carcinoma and biliary duct carcinoma. An accurate and prompt differential diagnosis between the various forms and causes of atrophy is important for early identification and adequate treatment of underlying pathologies. A comprehensive review of the literature on the etiology and the radiological and histological characteristics of different types of hepatic atrophy is currently unavailable. Therefore, the aim of this review is to summarize the primary and secondary causes of segmental or lobar liver atrophy (excluding forms involving the entire liver parenchyma) and to provide practical tools for clinical and radiological differential diagnosis.

Иридокорнеальный эндотелиальный синдром. Клинические случаи

Iridocorneal endothelial syndrome is a rare disorder characterized by increased proliferation and migration of corneal endothelial cells to the iris and anterior chamber angle, leading to secondary angle-closure glaucoma, corneal edema, and iris atrophy. This condition is often associated with secondary glaucoma due to obstruction of the trabecular meshwork and formation of peripheral anterior synechiae. Vision loss usually occurs due to progression of secondary glaucoma and corneal decompensation. Key words: iridocorneal endothelial syndrome; secondary glaucoma; endothelial keratoplasty.

Cerebral venous thrombosis and the eye: the neuro-ophthalmology of cerebral venous blood clot

Introduction: Cerebral venous thrombosis (CVT) is a form of venous thromboembolism which has varied clinical presentation. Ocular clinical features are quite common in CVT and may be the sole presenting feature and often tend to get misdiagnosed. This study was conducted to analyse clinical features especially neuro ophthalmological manifestations in CVT patients. Materials and Methods: In this prospective study 60 patients were enrolled in a study period of 3 years at tertiary care hospital. Follow up visits were performed at 1 month, 3 months, 6 months and 12 months after the initial diagnosis. We analysed the clinical features as well as aetiology of CVT, special focus was on the ocular symptoms and signs. Results: Headache was the most common clinical symptom with 93.33% patients. Among ocular symptoms 43.33 % patients presented with complaint of blurring of vision. Among ophthalmological signs papilledema was reported in 40.0 % patients, cranial nerve involvement in 10.0 % patients, diplopia was seen in 6.66 % patients. In patients with papilledema the intensity reduced as time progressed. Vision loss was seen in 2 patients who had secondary optic atrophy. Conclusion: To avoid misdiagnosis and for the prevention of vision deterioration the ophthalmologist must pay attention to CVT symptoms and signs when patients present with ocular symptoms as the initial manifestation.

Visual evoked potential evaluation following brain injury in school-aged children.

Aim: The research aimed to establish reference values of visual evoked potentials among school-aged children after brain injury. Methods: Eighteen patients with persisting visual symptoms after brain injury have been examined. A pattern-VEP test has been used during the examination. Results: The prolongation of the N2 wave in 55,6%-66,6%, P wave in 55,7%-66,7%, and N3 wave in 16,7%-22,2% was determined in the research group. Likewise, the decrease in the amplitude of the P wave was determined in the case of 16,7%-33,3%. According to the topography, we concluded that the prechiasmatic alteration was predominantly determined as bilateral in the optic pathways, with emphasis equally on the right and left. Conclusions: VEP evaluation remains one of the most credible methods of examination. In the case of moderate or severe traumatic optic neuropathy, it allows the detection of damage to the optic pathways before the appearance of organic changes that are often irreversible. The possibility of early detection of such modifications could justify the initiation of a dosed stimulatory treatment, to avoid damage to the optic pathways that would induce secondary optic atrophy. Abbreviations: VEP = visual evoked potentials, MRI = magnetic resonance imaging.

Dose-Dependent Progression of Chorioretinal Atrophy at the Injection Site After Subretinal Injection of rAAV2/8 in Nonhuman Primates

ObjectiveProgressive retinal atrophy has been described after subretinal gene therapy utilizing the adeno-associated virus (AAV) vector platform. To elucidate whether thIS atrophy is a consequence of inherent properties of AAV, or if it is related to the surgical trauma of subretinal delivery, we analyzed data from an IND-enabling study for PDE6A gene therapy in non-human primates. DesignAnimal study (non-human primates), retrospective data analysis SubjectsForty eyes of thirty healthy non-human primates (macaca fascicularis) were included in the analysis. Two AAV dose levels (low: 1x10E11, high: 1x10E12) were compared to sham-injection (balanced saline solution; BSS). Twenty untreated eyes were not analysed. MethodsAnimals were treated with a sutureless 23G vitrectomy and single subretinal injections of AAV.PDE6A and/or BSS. The follow up period was 12 weeks. Atrophy development was followed using fundus-autofluorescence (AF), optical coherence tomography (OCT), fluorescence angiography (FA) and indocyanine green angiography (ICGA). Main Outcome MeasuresArea [mm2] of retinal pigment epithelium (RPE) atrophy on AF. Presence of outer retinal atrophy on OCT. Area [mm2] of hyperfluorescence in FA and hypofluorescence in ICGA. ResultsProgressive atrophy at the injection site developed in 54% of high dose, 27% of low dose, and 0% of sham-treated eyes. At the end of observation, the mean±SD area of atrophy in AF was 1.19±1.75 mm2, 0.25±0.50 mm2 and 0.0±0.0 mm2 respectively (sham x high dose: p=0.01). Atrophic lesions in AF (p=0.01) and FA (p=0.02) were significantly larger in high dose eyes, compared to sham-treated eyes. Rate of progression in high dose eyes was 4.1x higher compared to low dose eyes. ConclusionSubretinal injection of AAV.PDE6A induced dose-dependent, progressive retinal atrophy at the site of injection. Findings from multimodal imaging were in line with focal, transient inflammation within the retina and choroid and secondary atrophy. Atrophic changes after gene therapy with AAV-based vector systems are not primarily due to surgical trauma and increase with the dose given.

Anosmia due to bilateral papillary atrophy : a case report

Abstract
 Introduction : Papillary atrophy refers to degeneration of the optic nerve, which occurs as an end result of a pathological process that damages the axons, with ophthalmoscopic observation showing pallor of the optic nerve papillae which generally accompanies permanent damage to the optic nerve.
 Case Illustration : It was reported that a 36 year old woman came to the polyclinic with complaints of not being able to see in both eyes since 8 months ago. Complaints of blurred vision in both eyes are followed by smell that cannot smell. This complaint has been getting worse for the past 2 weeks. On brain MRI examination, results were obtained with SOL impressions in the midline frontalis area with perifocal edema ec, suspected olfactory groove meningioma.
 Discussion : In this case SOL is located in the midline frontal area so that the patient complains of loss of smell sensation (anosmia). The presence of a frontal or subfrontal tumor can compress the optic tract and optic nerve together. Optic tract compression will cause anosmia. Olfactory disturbances are strongly associated with anterior cerebral fossa tumors.
 Conclusion : Secondary papillary atrophy is caused by increased intracranial pressure caused by a mass tumor which is preceded by papilledema signs and eventually becomes papillary atrophy, and gives a pale optic papillae with blurred boundaries. Brain CT scan examinations are important to estimate the location of the lesion.

Association between skeletal muscle and left ventricular mass in patients with hyperthyroidism.

This study aims to investigate the relationship between skeletal muscle and left ventricular mass (LVM) in patients with hyperthyroidism, providing theoretical and data-based foundations for further research on the interaction between secondary muscle atrophy and cardiac remodeling. A retrospective data collection was conducted, including 136 patients with hyperthyroidism (Study group) and 50 healthy participants (control group). The Study group was further divided into Group A (high LVM) and Group B (low LVM) based on LVM size. Multiple linear regression analysis was performed to examine the correlation between skeletal muscle and LVM, with model evaluation. Based on the results, further nonlinear regression analysis was conducted to explore the detailed relationship between skeletal muscle and LVM. Compared to the control group, the Study group exhibited significantly lower LVM, skeletal muscle mass index (SMI), and skeletal muscle mass (SMM) (P<0.05). Within the subgroups, Group A had significantly higher SMI, SMM, and hand grip strength compared to Group B (P<0.05). The results of the multiple linear regression showed a certain correlation between SMI (β=0.60, P=0.042, 95% CI=0.02~1.17) and hand grip strength (β=0.34, P=0.045, 95% CI=0.01~0.67) with LVM. However, the residuals of the multiple regression did not follow a normal distribution (K-S=2.50, P<0.01). Further results from a generalized linear model and structural equation modeling regression also demonstrated a correlation between SMI (β=0.60, P=0.040, 95% CI=0.03~1.17) (β=0.60, P=0.042, 95% CI=0.02~1.17) and hand grip strength (β=0.34, P=0.043, 95% CI=0.01~0.67) (β=0.34, P=0.045, 95% CI=0.01~0.67) with LVM. Patients with hyperthyroidism may exhibit simultaneous decreases in LVM, SMM, and SMI. The LVM in patients is correlated with SMM and hand grip strength, highlighting the need for further exploration of the causal relationship and underlying mechanisms. These findings provide a basis for the prevention and treatment of secondary sarcopenia and cardiac pathology in patients with hyperthyroidism.

Optic canal stenosis in Crouzon syndrome: a case report and literature review

Incidence of Crouzon syndrome is 1 per 25.000-31.000 newborns. This syndrome is extremely rarely accompanied by optic canal stenosis. To present a patient with Crouzon syndrome and optic canal stenosis, to discuss the management of such patients considering own and literature data. A 6-year-old boy presented with Crouzon syndrome (verified by molecular genetic research, i.e. FGFR2 gene mutation). The patient underwent 3 surgeries for craniosynostosis and hydrocephalus. Nevertheless, visual acuity progressively decreased despite patent ventriculoperitoneal shunt. Examination revealed severe decrease in visual functions with optic disc congestion under secondary atrophy. MRI data on subarachnoid CSF accumulation over both optic nerves potentially indicated optic canal stenosis. This assumption was confirmed by 3D CT. The patient underwent decompression of both optic canals with subsequent improvement of visual functions. Vision decrease following Crouzon syndrome may be due to optic canal stenosis. Decompression may be effective, even in long-term course of disease, and improve visual functions.

Optic nerve sheath fenestration for salvaging acutely threatened vision in Idiopathic Intracranial Hypertension - A two-year completed follow up

Objectives: To determine the efficacy and safety of Optic Nerve Sheath Fenestration (ONSF) for salvaging acutely threatened vision in patients of Idiopathic Intracranial Hypertension (IIH).&#x0D; Methods: This retrospective, interventional case series study was performed at Institute of Ophthalmology Mayo Hospital Lahore from September 2017 to September 2019. Nine patients diagnosed with Idiopathic Intracranial Hypertension as per Modified Dandy Criteria, underwent medial trans-conjunctival ONSF. Pre-operative and 1st day, 1st week, 1st month, 1st year, and 2nd year postoperative best-corrected logMAR visual acuities (BCVA) were recorded. Mean BCVA were calculated and compared using paired t-test. P-value &lt;0.05 was taken as significant.&#x0D; Results: All nine patients were female with a mean age of 24 years. The average best-correctedpre-operative logMAR visual acuity (BCVA) in the better eye was 0.5 ± 0.28 and in the worse eye was 1.0 ± 0.57. After the worse eye ONSF, at 1st week mean BCVA in better eyes was 0.27 ± 0.32 (p-value=0.001), while it was 0.43 ± 0.63 (p-value=0.006) in the worse eyes. At 2nd year follow-up after optic nerve sheath fenestration mean BCVA in better eyes was 0.30 ± 0.30 (p-value=0.002) and in worse eyes was 0.44 ± 0.63 (p-value=0.007). Four patients (44.4%) had a subconjunctival hemorrhage, two patients (22.2%) had binocular diplopia, one patient (11.1%) pre-septal cellulitis, and one patient (11.1%) had no improvement in vision because of pre-operative secondary optic atrophy. All patients had unilateral fenestration and bilateral improvement, six patients (66.67%) reported improvement in headache and successful tapering of medical therapy.&#x0D; Conclusion: Optic nerve sheath fenestration is effective as well as a safe surgical procedure to salvage acutely threatened vision in patients of Idiopathic Intracranial Hypertension on maximal medical treatment.&#x0D; doi: https://doi.org/10.12669/pjms.39.6.6441&#x0D; How to cite this: Latif S, Rizwan A, Khan AA, Zahra S. Optic nerve sheath fenestration for salvaging acutely threatened vision in Idiopathic Intracranial Hypertension - A two-year completed follow up. Pak J Med Sci. 2023;39(6):---------. doi: https://doi.org/10.12669/pjms.39.6.6441&#x0D; This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Development of idiopathic intracranial hypertension on the background of zoledronic acid therapy in Gorham-Stoat syndrome

Idiopathic intracranial hypertension (IVH) is a condition or a heterogeneous group of vessels characterized by an increase in intracranial pressure (ICP) without signs of mass formation, hydrocephalus, infection, venous thrombosis, and hypertensive encephalopathy. The term "pseudotumoral cerebral hypertension" is used to describe the secondary origin of ICP due to various causes and is a diagnosis of exclusion. One of the risk factors for the development of IVH are hypocalcemic conditions of the development of etiology, leading to the development of ICP. Long-term use of zoledronic acid, which is a risk factor for the development of hypocalcemia, can contribute to the occurrence and fluctuating course of IVH, requires monitoring clinical monitoring of the patient's condition in order to prevent the occurrence of secondary atrophy of the optic discs, with further progressive decline and loss of vision. The choice of vaccine for a 12-year-old child with a clinically-instrumentally-histologically confirmed diagnosis of Gorham-Stout syndrome, with progressive bone resorption, receiving zoledronic acid therapy. Attracting the attention and informing a wide range of specialists in various fields about the likelihood of IVH on the background of long-term use of bone and cartilage metabolism correctors can serve as an important factor in the timely diagnosis, prevention and correction of this pathological condition in childhood.

Linezolid induced toxic optic neuropathy in drug resistant tuberculosis-A case series

In developing countries like India, Linezolid is widely used for the treatment of Multi drug resistant tuberculosis (MDR-TB) and extensively drug resistant tuberculosis (XDR-TB). Long-term administration of Linezolid is reported to cause toxic optic neuropathy causing bilateral, progressive visual loss in patients. We report case details of three patients on anti-tubercular therapy presented to us with sudden, progressive, painless blurring of vision of both eyes the cause of which was confirmed to be toxic optic neuropathy due to linezolid. Subsequently, cessation of the drug resulted in complete visual recovery in two patients whereas one patient had minimal visual improvement due to secondary optic atrophy. Clinicians and health care workers need to be aware of sight threatening complications of Linezolid.

Glucocorticoid effects in the regenerating fin reflect tissue homeostasis disturbances in zebrafish by affecting Wnt signaling.

As a treatment for various immune-mediated diseases, the use of glucocorticoids as anti-inflammatory and immunosuppressive agents is common practice. However, their use is severely hampered by the risk of the development of adverse effects such as secondary osteoporosis, skin atrophy, and peptic ulcer formation. The exact molecular and cellular mechanisms underlying those adverse effects, which involve most major organ systems, are not yet fully understood. Therefore, their investigation is of great importance to improve treatment regimens for patients. Here, we investigated the effects of the glucocorticoid prednisolone on cell proliferation and Wnt signaling in homeostatic skin and intestinal tissue and compared them to the anti-regenerative effects in zebrafish fin regeneration. We also investigated a potential recovery from the glucocorticoid treatment and the impact of short-term treatment with prednisolone. We identified a dampening effect of prednisolone on Wnt signaling and proliferation in highly proliferative tissues, namely the skin and intestine, as well as reduced fin regenerate length and Wnt reporter activity in the fin. The presence of the Wnt inhibitor Dickkopf1 was enhanced in prednisolone treated skin tissue. A decreased number of mucous producing goblet cells was observed in the intestine of prednisolone treated zebrafish. Unexpectedly, proliferation in bone forming osteoblasts of the skull, homeostatic scales, as well as the brain was not decreased, opposite to the observed effects in the skin, fin, and intestine. Short-term treatment with prednisolone for a few days did not significantly alter fin regenerate length, skin cell proliferation, intestinal leukocyte number and proliferation of intestinal crypt cells. However, it affected the number of mucous-producing goblet cells in the gut. Likewise, discontinuation of prednisolone treatment for a few days saved the skin and intestine from a significant reduction of skin and intestinal cell proliferation, intestinal leukocyte number and regenerate length, but did not rescue goblet cell number. The suppressive effects of glucocorticoids in highly proliferative tissues may be relevant in the context of their therapeutic applications in patients with inflammatory diseases.

Surgical Management of Large (≥3 cm) Trigeminal Schwannomas: Functional Outcomes and Approach Selection in Multicompartmental Schwannomas.

Introduction Trigeminal schwannoma surgery has shown a remarkable improvement in functional recovery and tumor resection. In the era of radiosurgery, these outcomes need to be characterized for tumors which are outside the realm of being treated with radiosurgery. We present a series of trigeminal schwannomas larger than 3 cm, surgical approaches used, and outcomes with an emphasis on functional recovery in a high-volume center with radiosurgery facilities. Method All consecutive cases of trigeminal schwannoma from January 2012 to May 2021 which were more than 3 cm in size and underwent microsurgery were included in this series. The surgical approach, neurological outcomes, and extent of resection were defined objectively with pre/postoperative magnetic resonance imaging. Results A total of 83 such cases (>3 cm) were found, with cranial nerve symptoms (5th most common) being the commonest. Twenty three percent cases had blindness due to secondary optic atrophy and eighteen percent had long tract motor symptoms signifying the tumor burden in our series. Radiological gross total excision was achieved in 75.9% cases. Conclusion Large-volume schwannomas present with cranial nerve involvement and may need extensive skull base approaches. Functional outcomes need to be prioritized and can be achieved albeit with lesser gross resection rates. Hearing and facial preservation in addition to relief of trigeminal symptoms should be the goal of resection with minimal additional morbidity.

Secondary sinusogenic neuritis and optic nerve atrophy

Secondary sinusogenic neuritis and optic nerve atrophy

Ductal Hyperkeratinization and Acinar Renewal Abnormality: New Concepts on Pathogenesis of Meibomian Gland Dysfunction.

Meibomian gland dysfunction (MGD) is a functional and morphological disorder of the meibomian glands which results in qualitative or quantitative alteration in meibum secretion and is the major cause of evaporative dry eye (EDE). EDE is often characterized by tear film instability, increased evaporation, hyperosmolarity, inflammation, and ocular surface disorder. The precise pathogenesis of MGD remains elusive. It has been widely considered that MGD develops as a result of ductal epithelial hyperkeratinization, which obstructs the meibomian orifice, halts meibum secretion, and causes secondary acinar atrophy and gland dropout. Abnormal self-renewal and differentiation of the acinar cells also play a significant role in MGD. This review summarizes the latest research findings regarding the possible pathogenesis of MGD and provides further treatment strategies for MGD-EDE patients.

Ocular gamut of neurofibromatosis type 1

Background: Neurofibromatosis type 1 (NF1) is a multi-system autosomal dominant disorder affecting 1 in 3000 individuals. The diagnostic criteria of NF1 includes ocular manifestations. Objective: To study the ophthalmic manifestations of neurofibromatosis type 1 and evaluate complications, if any. Methodology: A total of 30 eyes of 15 neurofibromatosis cases presenting to the ophthalmology outpatient department (OPD) underwent a detailed ocular examination, and clinical manifestations in each case were analyzed. Results: Lisch nodules were the most common presentation. Twenty-eight eyes of 14 patients had bilateral and one had unilateral presentation. Six eyes of three patients had ectropion uveae, one eye had plexiform neurofibroma, and one eye had pulsatile proptosis with absence of lesser wing of sphenoid. Other manifestations seen were optic nerve glioma, secondary optic atrophy, closed angles with raised intraocular pressure (IOP), medullated nerve fiber and retinal pigment epithelium (RPE) atrophic changes. Conclusion: This case series represents a spectrum of ocular manifestations of NF1 and highlights the importance of ocular examination and regular follow-up in these patients.

Secondary thalamic atrophy related to brain infarction may contribute to post-stroke cognitive impairment

Background and purposeThe thalamus is a key brain hub that is globally connected to many cortical regions. Previous work highlights thalamic contributions to multiple cognitive functions, but few studies have measured thalamic volume changes or cognitive correlates. This study investigates associations between thalamic volumes and post-stroke cognitive function. MethodsParticipants with non-thalamic brain infarcts (3-42 months) underwent MRI and cognitive testing. Focal infarcts and thalami were traced manually. In cases with bilateral infarcts, the side of the primary infarct volume defined the hemisphere involved. Brain parcellation and volumetrics were extracted using a standardized and previously validated neuroimaging pipeline. Age and gender-matched healthy controls provided normal comparative thalamic volumes. Thalamic atrophy was considered when the volume exceeded 2 standard deviations greater than the controls. ResultsThalamic volumes ipsilateral to the infarct in stroke patients (n=55) were smaller than left (4.4 ± 1.4 vs. 5.4 ± 0.5 cc, p < 0.001) and right (4.4 ± 1.4 vs. 5.5 ± 0.6 cc, p < 0.001) thalamic volumes in the controls. After controlling for head-size and global brain atrophy, infarct volume independently correlated with ipsilateral thalamic volume (β= -0.069, p=0.024). Left thalamic atrophy correlated significantly with poorer cognitive performance (β = 4.177, p = 0.008), after controlling for demographics and infarct volumes. ConclusionsOur results suggest that the remote effect of infarction on ipsilateral thalamic volume is associated with global post-stroke cognitive impairment