Post-stroke aphasia severely impacts communication and quality of life. Aerobic exercise enhances learning and memory in healthy adults, with evidence suggesting benefits for verbal tasks. Research exploring its effects in stroke patients with aphasia is minimal. This case study investigated the effects of combining speech and language therapy (SLT) with high-intensity aerobic exercise on speech performance in post-stroke aphasia. Over 4 weeks, two participants with post-stroke anomic aphasia engaged in daily 20-min SLT sessions focused on naming activities. Speech training was followed by 20-min of high-intensity interval exercise on alternate days (Tuesday, Thursday). Speech performance was assessed daily, and the Western Aphasia Battery was used to assess expressive and receptive language skills before and after the intervention. Participants demonstrated greater day-to-day speech performance gains the following days when exercise was performed immediately after speech training (Cohen's range: 2.40-2.59), suggesting that exercise enhanced consolidation of learned speech skills. Participants also demonstrated improved aphasia quotient scores via the Western Aphasia Battery following completion of the intervention. Results suggest potential benefits of combining SLT with aerobic exercise for rehabilitation of anomic aphasia. Findings may contribute to the development of novel approaches to facilitate response to post-stroke language rehabilitation.

Creutzfeldt - Jakob disease (CJD) is a subacute spongiform encephalopathy characterised by rapidly progressive dementia and is difficult to diagnose antemortem. We present the case of a 21-year-old woman with a family history of early-onset neurological disease of unclear aetiology. She had a 2-year history of rapidly progressive cognitive decline, cogwheel rigidity in all four limbs and ataxia. After initial evaluation, she was referred to the nuclear medicine centre for Tc-TRODAT SPECT, which revealed mildly reduced uptake of the presynaptic radiotracer in the right caudate and left putamen, consistent with dopaminergic dysfunction. Tc-ECD perfusion SPECT showed widespread cortical hypoperfusion, including involvement of the right thalamus and cerebellum, indicative of global neuronal dysfunction. MRI revealed high signal intensity on diffusion-weighted imaging, and C-deuterium-L-deprenyl PET/CT demonstrated reactive astrocytosis. The final diagnosis was probable CJD according to the Centers for Disease Control and Prevention criteria. Follow-up revealed that the patient belonged to a family carrying a missense mutation in the PRNP gene (G114V). These findings describe the neuroimaging phenotype of an early-onset familial CJD and highlight the role of multimodal brain imaging in both the diagnosis and pathophysiological understanding of movement disorders in this condition.

Fahr syndrome is a rare neurological condition characterized by idiopathic bilateral basal ganglia calcifications. It often presents psychiatric symptoms that may precede neurological signs, especially in adolescents, making early diagnosis a challenge. We report the case of a 17-year-old male who exhibited treatment-resistant psychotic symptoms including aggression, paranoia, and auditory hallucinations beginning at age 12. Extensive bilateral calcifications in the basal ganglia and subcortical regions were identified via cranial CT, with no evidence of metabolic or infectious etiology, confirming the diagnosis of idiopathic Fahr syndrome. Treatment with clozapine and brexpiprazole led to rapid and sustained symptom remission. This case emphasizes the importance of neuroimaging in adolescents with atypical psychiatric presentations and suggests that combined antipsychotic therapy may be effective in managing Fahr syndrome-related psychosis.

We reviewed the performance of global episodic amnesic patient H.M. Although he was affected by severe anterograde and retrograde amnesia (i.e. global amnesia), he occasionally showed some "islands" of residual intact memory. Therefore, we also searched for the presence of islands of memory in other global amnesic patients with the aim of comparing their performance with that of H.M. We sustain that islands of memory might be guided by residual brain structures and memory mechanisms that are not affected by lesions causing global episodic amnesia. Finally, we considered some possible cues for the treatment of amnesia guided by the presence of islands of memory.

Amyloid-lowering therapy via administration of monoclonal antibodies against amyloid beta has been previously associated with the formation of cerebral edema and/or microhemorrhage. These changes are often picked up on MRI and referred to as amyloid-related imaging abnormalities, or ARIA. Cerebral ischemia has not been systematically reported in clinical trials involving amyloid-lowering therapy but has been reported in case reports. Here we describe an additional case of a patient with Alzheimer's Disease treated with the amyloid-lowering drug Lecanemab who developed both ARIA-H and ARIA-E, as well as multiple asymptomatic ischemic infarctions. Extensive workup did not reveal another clear cause for infarction. These infarcts, in conjunction with previous reports of ischemic infarction in the setting of anti-amyloid therapy, suggest that amyloid-lowering therapy may predispose individuals to both hemorrhagic and ischemic infarction. This result is discussed in the context of microvascular pathology known to occur in the setting of Alzheimer's Disease.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOG AD) is a rare autoimmune demyelinating condition typically presenting with optic neuritis, transverse myelitis, or encephalitis. Its occurrence in immunocompromised individuals, particularly those with human immunodeficiency virus (HIV), is rare and presents unique diagnostic and therapeutic challenges. We report the case of a 70-year-old HIV-positive man who developed alexia without agraphia following treatment for opportunistic infections, including pneumonia and cytomegalovirus. Brain MRI revealed a non-enhancing hyperintense lesion in the medial left occipital lobe extending into the splenium of the corpus callosum. MOG-IgG was positive at a titer of 1:30, while aquaporin-4 antibodies and paraneoplastic panels were negative. Neuropsychological assessment confirmed selective impairment in visual word recognition with preserved writing ability, consistent with alexia without agraphia. The patient was treated with intravenous immunoglobulin (IVIG) without corticosteroids due to immunosuppressive concerns and demonstrated approximately 40% improvement in visual word recognition accuracy. At six months follow-up, no relapse was observed, and reading ability remained stable. This case represents the first reported instance of MOGAD presenting with alexia without agraphia in an HIV-positive individual, underscoring the importance of considering autoimmune demyelination in immunosuppressed patients with focal neurological deficits.

We describe a case of supernumerary phantom limb (SPL) persisting into the chronic phase of a right putaminal hemorrhage. The individual, a forced right-handed female in her 40's, was admitted to the hospital 9 months after onset with clear consciousness, well-preserved cognitive function, severe left hemiparesis, and deep sensory impairment. When attempting to move the paralyzed upper limb, she perceived an SPL and felt as if it assisted the motion. Subsequently, the perceived SPL became associated with pain in the paralyzed upper limb. She reported that the SPL wrapped and tightened around her left arm. In another situation, she described the SPL as protruding from the back of her left shoulder and hurting when she lay on her back. Previous reports noted that hemiparesis and deep sensory impairment may be necessary for SPL's to appear. Staub et al. (2006) associated SPL to motor intention, suggesting that motor imagery triggers the feeling of movement in SPL. Our case shares these conditions with the previous reports. Pain and deep sensory impairment may contribute to SPL development. This case is interesting because SPL's with different triggers emerged at various times during the long-term course after cerebral hemorrhage onset.

Peak focal atrophy in the anterior temporal lobe (ATL) highlights the critical role of this area for word comprehension in semantic variant primary progressive aphasia (svPPA). However, the assumption that peak atrophy sites are specific markers of dysfunctional brain sites, and therefore reliable variables for clinicopathologic correlations, has not been rigorously tested. Using structural MRI and FDG-PET, we assessed atrophy and hypometabolism in 32 individuals with PPA (11 svPPA) and 10 healthy controls. Word comprehension was measured using the Peabody Picture Vocabulary Test. Voxel-based morphometry and standardized uptake value ratios were used to generate atrophy and hypometabolism maps. Two-sample t-tests compared svPPA and controls, and regression analyses evaluated the relationship between imaging metrics and word comprehension. Findings revealed significant bilateral ATL atrophy and hypometabolism (left > right). Structural and metabolic measures were independently associated with impaired comprehension. There was substantial overlap between atrophy and hypometabolism within the ATLs, with dysfunction extending into posterior temporal regions. However, there was no evidence of peak hypometabolism in traditional Wernicke's area. Degeneration - both anatomical and metabolic - of the ATL serves as a robust predictor of comprehension impairment, highlighting its role a critical locus for word comprehension.

A 69-year-old Japanese man presented with prosopagnosia, visual form agnosia for line drawings of objects, as well as alexia and agraphia for Kanji after infarction in the right fusiform gyrus and occipitotemporal lobe. In contrast, the verbalization of real objects and line drawings of actions was good. Visual recognition disorders that affect the identification of faces, line drawings, and Kanji suggest impaired processing related to multielement integration. Real objects and line drawings of actions, which are easy to process as visual units and tend to evoke kinesthetic images, were less affected after damage in the right occipital-inferior temporal pathway, suggesting that cognitive processing is possible via the dorsal pathway.

A 63-year-old woman presented with gait disturbance, progressive hearing loss, and sensory dominant polyneuropathy. Brain MRI mainly revealed midbrain tegmental atrophy (hummingbird sign). Genetic testing identified a heterozygous exon 21 mutation, previously linked to autosomal dominant cerebellar ataxia, deafness, and narcolepsy (ADCA-DN), although her clinical presentation resembled hereditary sensory and autonomic neuropathy type 1E (HSAN1E). A review of previously published cases with the same mutation revealed variability in sensory involvement, cerebellar signs, and sleep disorders, supporting the existence of a wide disease spectrum of -related disorders. This case illustrates the phenotypic and radiological overlap within -related disorders and supports the concept of a disease spectrum, rather than discrete syndromes, highlighting the diagnostic value of combining neuroimaging with genetic analysis.

This study centers on a 44-year-old right-handed Japanese male with moderate Broca's aphasia. During a confrontation-naming task (CNT) during therapy, the person expressed that it was "easier to speak when I recall (in my mind) the Kana (Hiragana and Katakana) characters." To investigate this claim and its relationship to language impairment, this study sought to determine the effect of character type on the CNT, focusing on the person's perceived difference between Kanji and Katakana. We selected pictures corresponding to highly orthographically plausible Kanji and Katakana (more appropriate for comparison than Hiragana) words for CNT and oral reading tasks that the patient performed. The results revealed more correct responses in CNT in the Katakana stimulus group than in the Kanji one; the latency in oral reading was shorter in the Katakana group as well. The results suggest that words written in Katakana have a better naming performance than those in Kanji because of the influence of the characters as represented in the mental imagery of Katakana. A possible reason for this is that, for our respondent, Katakana is more likely to activate phonological information than Kanji. Additionally, the writing and reading training for confrontation-naming may have implicitly influenced the tasks.

Corticobasal syndrome (CBS) is a rare neurodegenerative disorder characterized by asymmetric motor symptoms, cognitive impairment, and cortical dysfunction. While gene mutations have been reported in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), their role in CBS spectrum remains unexplored. This study aimed to investigate a 48-year-old patient of South Asian origin, presenting with progressive cognitive decline, behavioral disturbances, and asymmetric motor symptoms characteristic of overlap CBS syndrome. Detailed cognitive and behavioral assessments were conducted, along with brain imaging and whole-exome sequencing. Structural modeling was performed to assess the functional impact of the novel variant. The family history indicated an autosomal dominant inheritance pattern of progressive cognitive decline, further suggesting genetic predisposition. Brain imaging revealed asymmetric atrophy and hypometabolism in the left temporoparietal and prefrontal regions. Genetic analysis identified a novel heterozygous missense variant (p.Met394Leu) in the gene. Structural modeling and in-silico prediction tools suggested deleterious effects, though its functional significance remains uncertain. The study reports a potential link between variants and CBS in a South Asian family, expanding the genetic spectrum of overlap CBS. While the findings suggest potential pathogenicity, further research is required to confirm this association and elucidate the underlying mechanisms.

Postoperative aphasia is a significant complication following brain tumor resection, affecting both quality of life and prognosis. Currently, speech language therapy (SLT) is the primary approach for treating aphasia, with no alternative rehabilitation options available. However, rTMS has shown promise intreating stroke-related language impairments. In this case report, we applied bilateral rTMS to address aphasia following brain tumor resection. A 36-year-old man with a known diagnosis of an oligodendroglioma (WHO3°) at the temporo-parieto-occipital junction presented with initial mild aphasia. Preoperative diagnostics revealed language-relevant areas in the supramarginal gyrus and infiltration of the AF, ILF and IFOF, leading to the decision to perform an awake craniotomy fortumor resection. Following complete resection, ischemia medial to the resection cavity was observed, resulting in a worsening of aphasia (AAT score196/440). Over 7 days, continuous bilateral rTMS combined with SLT was administered without any severe side effects. The patient's aphasia significantly improved post-treatment (AAT score291/440; AAT score343/440; AAT score 386/440). Given the encouraging results, a potential beneficial effect of the additional rTMS therapy may be suggested. However, larger cohorts and randomized controlled trials are necessary to confirm these preliminary results.

Alzheimer's disease (AD) is the leading cause of cognitive decline, whereas primary familial brain calcification (PFBC) is rare. We analyzed the clinical and radiological findings of a 75-year-old man who presented with memory impairment. Brain imaging revealed bilateral basal ganglia calcification, severe white matter hyperintensities, and significant amyloid deposition. Genetic analysis identified a heterozygous c.1711 G > A variant in and a heterozygous c.166 G > A variant in . The patient was diagnosed with genetically confirmed PFBC due to a likely pathogenic variant, together with AD biology. The variant was classified as a variant of uncertain significance.

We summarize and review the clinical and genetic characteristics of four adolescents with Hyperhomocysteinemia. Four cases of adolescent-onset Hyperhomocysteinemia diagnosed at Qingdao University Affiliated Hospital were selected as research subjects. Clinical data, whole exome sequencing and Sanger sequencing information of the patients were collected, and gene variation analysis and literature review were conducted. The pathogenic variants carried by the four patients were MAT1A c.895C>T(p.Arg299Cys), CBS c.374G>A(p.Arg125Glu), CBS c.785C>T(p.Thr262Met), and MMACHC c.482G>A(p.Arg161Glu) and c.658_660del(p.Lys220del) along with other site mutations. There were three cases with epileptic seizures as initial manifestation, three cases with varying degrees of intellectual disability, two cases with lens dislocation, one case with cervical artery occlusion leading to cerebral infarction, and one case with extensive white matter lesions. Four patients showed relief of symptoms after treatment with vitamin B and necessary antiepileptic drugs. We combined the cases and relevant literature to retrospectively analyze the characteristics and treatment related to the disease. The onset of Hyperhomocysteinemia in adolescents is early, and the clinical manifestations are broad and atypical. At the same time, it has a significant impact on the growth and development of adolescents and can affect future life for a long time. Early detection and diagnosis have an important impact on prognosis.

Mills' syndrome is a rare motor neuron disease characterized by progressive upper motor neuron dysfunction. As the disease advances, there may be manifestations of bulbar involvement, such as dysarthria, dysphagia, and possibly pseudobulbar affect and progression to the contralateral side may occur lately in patients. Since it was first described by Mills in 1900, there are few cases of Mills' syndrome that have been reported in the literature. Here, we present a case, diagnosed as Mills' syndrome, with 5 years of gradually progressive weakness and stiffness in her left-side limbs with recently added difficulties in speech. Neurological examination revealed bilateral asymmetrical upper motor neuron signs, including increased tone, brisk reflexes, and muscle weakness with dysarthria and dysphagia. There was no sensory involvement as well as sphincter dysfunction and her cognition was contact.

Lewy body dementia (LBD), the second most common degenerative dementia after Alzheimer's disease, is frequently associated with neuropsychiatric symptoms such as depression, anxiety, and apathy. These symptoms may precede cognitive decline, often resulting in misdiagnosis and inappropriate treatment. Electroconvulsive therapy (ECT) has emerged as a promising option for treatment-resistant depression in LBD. This report describes a 68-year-old female patient with LBD who received multiple ECT sessions for persistent severe depression and suicidal ideation. ECT led to marked symptom improvement across several hospitalizations. This case underscores the diagnostic and therapeutic challenges of neuropsychiatric symptoms in LBD and highlights ECT as a potential alternative when pharmacotherapy is inadequate. Early identification of LBD in patients with late-onset depression is essential to guide individualized treatment strategies.

This study presents a neuropsychological evaluation of a unique case of prosopagnosia (patient EP) with atypical lesion patterns, characterized by intact face-selective nodes but significant damage to the Vertical Occipital Fasciculus (VOF). Given the presumed interruption of ventral-parietal connectivity, we focused on assessing the potential presence of simultanagnosia and its potential relationship to his face recognition deficits. Our neuropsychological battery included tests of global and local processing, scene perception, and face recognition. Results revealed intact global processing abilities and no evidence of simultanagnosia, despite the patient's prosopagnosia. These findings suggest that EP's face recognition impairment is likely attributable to disrupted connectivity within the face processing network rather than a general deficit in global/holistic processing. This case highlights the importance of comprehensive neuropsychological assessments in atypical presentations of prosopagnosia and contributes to our understanding of the complex relationship between white matter integrity and face recognition abilities.

Frontotemporal dementia (FTD) is a rare and often hereditary type of dementia, usually developing under the age of 65 years. Mutations in the gene encoding the prion protein (), typically resulting in Creutzfeldt-Jakob disease, are an extremely rare cause of FTD phenotype. The clinical spectrum of this genetic form of FTD has not been fully elucidated, and no case carrying a PRNP gene mutation has been previously described in the Greek population.

Fahr's disease (FD) is a rare neurological disorder that causes abnormal, symmetrical, and bilateral calcification of the basal ganglia and other brain regions. Psychiatric symptoms are one of the many manifestations that guide FD diagnosis, with most usually occurring by ages 30-60 years. Herein, we report an incidental finding of bilateral basal ganglia calcification in a 14-year-old male teenager presenting psychotic characteristics, including schizophreniform and manic-like symptoms, who was initially investigated for mycoplasma infection. No similar study has been reported so far in the literature. Case report and literature review. Computed tomography (CT) revealed a calcification deposit in bilateral basal ganglia, thalamus, frontal cortex, and semioval center, magnetic resonance imaging detected a T1-weighted image and fluid-attenuated inversion recovery hyperintense signal abnormalities in the bilateral basal ganglia and thalami. Furthermore, the laboratory tests revealed no obvious abnormality except for hypocalcemia and low vitamin D levels with an elevated uric acid level. The gene test results confirmed the diagnosis of familial FD, which was caused by a mutation in the SLC20A2 gene (NM_001257180.2:c.551delC/p.Pro184Glnfs *8). The patient was prescribed oral medication, including olanzapine, sodium valproate extended-release tablets, lorazepam, and vitamin D drops. Additionally, individualized administration with therapeutic drug monitoring was recommended for the patient to enable dose adjustments. The patient experienced no new psychotic symptoms within the 6-month follow-up after discharge. Bilateral basal ganglia calcification may be a contributing factor to the sudden onset of psychiatric symptoms in children and adolescents.

Absolute pitch (AP) is the ability to identify the pitch of isolated tones without reference to an external pitch. A 21-year-old semi-professional musician with a previous ability for AP developed a left-hemispheric cerebral hemorrhage due to an arteriovenous malformation (AVM). One month after the hemorrhage, she underwent surgery to treat the AVM, resulting in the resolution of her aphasia and right upper limb clumsiness. However, her AP ability was lost. Before the hemorrhage, she could dictate complex music that she listened to, but afterward, she could no longer identify even a single tone. Neuropsychological assessments revealed a decreased retention span for auditory information, slight impairment of environmental sound and speech processing, and difficulty in understanding the auditory presentation of numbers with more than four digits. Neuromusicological assessments with an established battery of tests revealed impairments of chord and timbre perception, alongside the loss of AP ability. Brain computed tomography conducted 9 months after the hemorrhage revealed low-density areas in the middle longitudinal fasciculus, a region associated with language and auditory processing, including AP perception. To our knowledge, this is the first reported case of a patient with AP loss because of a focal brain lesion.

Giggling incontinence(GI), although uncommon, can have a profound effect on a patient's quality of life, especially in adolescent females. A case study involving a 4-year-old girl who developed urinary incontinence symptoms following a traumatic brain injury from a motor vehicle accident and subsequent loss of her parents highlights the challenges in managing this condition after 4 months. Despite conventional treatments such as pelvic floor exercises and cognitive therapy, the patient's symptoms persisted. Unexpectedly, during facial expression recognition training, the guardian reported a notable improvement in the patient's symptoms. Following 45 days of specialized training in facial expression recognition, the patient experienced a complete resolution of GI symptoms. The initial objective of the intervention was to mitigate impairments in facial expression recognition, a social deficit that can have deleterious effects on development. However, the observed correlation between GI symptoms and regulation of brain areas was evident, compounded by the patient's concomitant frontoparietal brain injury and parental loss, which may have contributed to both GI symptoms and facial expression recognition impairments. This case report provides new insights into the intervention of GI symptoms and common emotional expression recognition disorders in the mental health field.

has been described in individuals, who show superior retrieval capacities in autobiographical memory. This condition differs from superior memory, which refers to the supranormal ability to acquire and recall new information but not autobiographical information. The process responsible for hyperthymesia is still largely unknown and most knowledge come from case studies, showing individual with impressive superior capacities to retrieve autobiographical memories. Here, we describe a case of hyperthymesia with an objective as well as a subjective assessment of mental time travel abilities in different temporal distances. This is the first observation of hyperthymesia with a full evaluation of mental time travel capacities in different temporal distances, encompassing the individual capacity to retrieve personal events from the personal past as well as to foresee personal events in the future. This observation could pave the way to further research on superior autobiographical abilities, studied in the context of personal temporality.

Variants in (encoding valosin-containing protein) lead to inclusion body myopathy, which is typically associated with Paget's disease of the bones and frontotemporal dementia (FTD). When symptoms of frontotemporal lobar degeneration (FTLD) develop in patients with pathogenic variants, the symptoms mainly present as behavioral-variant (bv) FTD and rarely as semantic dementia (SD). Various pathogenic variants have been reported to cause bvFTD, whereas the only variant previously linked to SD is p.Arg155Cys. Here, we report the case of a female Japanese patient with SD carrying the pathogenic variant p.Arg191Gln. The patient developed naming difficulties, word-finding difficulties, stereotypical behavior, decreased spontaneity, and executive dysfunction at 55 years old and was diagnosed with SD at our hospital at 56 years old. At 59 years, there were no clinical findings suggestive of myopathy, pyramidal signs, or bone involvement. Genetic analyses, including whole-exome and Sanger sequencing, identified the p.Arg191Gln variant in the patient with isolated SD. She required wheelchair assistance for 62 years and was mute. She later died from complications of malnutrition due to feeding difficulties. This case suggests that variants may result in not only bvFTD but also SD, indicating a broader spectrum of FTLD-related phenotypes linked to pathogenic variants.

Atypical frontotemporal lobar degeneration with ubiquitin-positive inclusions (aFTLD-U) is a rare subtype of Frontotemporal Lobar Degeneration. aFTLD-U is reported with a typically young onset behavioral variant of frontotemporal dementia syndrome, more specifically with younger age, predominant hyperorality, obsessive-compulsive features, and severe caudate atrophy. Very few cases have been reported with prominent language impairment with no major behavioral features. We present another such rare case of aFTLD-U presenting with prominent language impairment adding to the phenotypic spectrum, with language deficits observed primarily in spoken language seen in apraxia of speech associated with non-fluent primary progressive aphasia.

Parkinson's disease (PD), a range of neuropsychiatric symptoms, including anhedonia, depression, emotional control, and cognitive deficits, may manifest. This study aims to investigate the impact of anhedonia, emotional regulation, and emotional expression on PD. The research included 68 PD patients and 60 healthy controls. Both groups were assessed using the Hospital Anxiety and Depression Scale (HADS), Emotional Expression Scale (EES), the Short Form of the Difficulties in Emotion Regulation Scale (DERS), and the Clinician-Administered Snaith-Hamilton Pleasure Scale (SHAPS), all administered by a psychiatrist. The PD group was evaluated by a neurology specialist using the Unified Parkinson's Disease Rating Scale (UPDRS). Results showed that the PD group scored significantly higher on the HADS ( < 0.01), DERS ( < 0.01), and SHAPS ( < 0.01), while their EES scores were significantly lower ( < 0.01) compared to the control group. Further analysis indicated that a one-unit increase in anhedonia scores corresponded to a 3.125 unit rise in non-motor symptom scores and a 5.034 unit rise in motor symptom scores. The findings suggest that anhedonia is a strong predictor of both motor and non-motor symptoms in PD. The data indicate that the link between anhedonia and PD exists independently of depression and anxiety, highlighting the necessity of addressing anhedonia as a distinct symptom in PD.

This case series elucidates pathological signs for diagnosis in two patients with Dementia. The first case highlights the term 'Smartphone sign', a novel psychopathology uncovered based on the existing 'TV sign', a rare type of delusional misidentification syndrome (DMS). The second case had symptoms consistent with the 'TV sign'. The possible underlying cause of these signs was hypothesized based on psychopathology, brain region, sensory system, cognition, and environmental factors. Moreover, the treatment outcome in terms of cognition and behavior on low doses of Risperidone and Escitalopram shows promising results and paves the way for the treatment of other DMS.

Catatonia may manifest as an independent entity or as a feature of a neuropsychiatric or medical illness. While electroconvulsive therapy (ECT) is the gold standard treatment for catatonia, it is typically administered if the patient's symptoms fail to respond to benzodiazepines. We describe the case of a 22-year-old male with Budd Chiari induced cirrhosis and no prior psychiatric history, who presented with symptoms of psychosis and hepatic encephalopathy, was treated in the ICU for multi-factorial delirium, developed symptoms of catatonia that failed to respond to lorazepam, ultimately requiring ECT with a favorable response. This report hopes to add to the literature by discussing potential etiologies of catatonia and by providing an illustrative example of the treatment of catatonia and its considerations in patients with hepatic impairment.

Alzheimer's disease (AD) symptomatology, while classically studied through the lens of amyloid-β and tau burden, is likely also influenced by multiple-interacting co-pathologies like vascular disease and dysmetabolism. These co-pathologies, especially vascular disease, occur disparately in the Chinese-American population and are often treatable via therapeutics and lifestyle modifications. Given this, we explored whether plasma biomarkers, including an array of vascular-related proteins, associate with cognition in a cohort of 34 Chinese Americans clinically diagnosed as cognitively normal, with mild cognitive impairment, or with AD. We found that a composite score of plasma angiogenesis biomarkers (MMP-1, bFGF, VEGF, and VEGF-C) were positively associated with total Mini Mental State Examination scores ( = 0.045) as well as memory performance ( = 0.006), and that this relationship was most pronounced in AD (biomarker composite score within AD vs MMSE & memory, both  < 0.001). To explore whether these findings were specific to the Chinese-American population, we repeated the above analyses in 73 demographically matched non-Hispanic White American participants and found no significant associations between angiogenesis biomarkers and MMSE or memory, highlighting the potential relevance of vascular dysregulation in Chinese Americans at risk for AD.

We report the case of a Japanese-speaking patient with semantic dementia who showed lower kanji visual performance than auditory performance in a lexical decision task (LDT), but better visual performance in a reading comprehension task (RCT). In the RCT, the patient presumed meanings from single-character kanji (e.g., "rescue" /kyuʀzyo/ → ける "help" /tasukeru/) or orthographic neighbors (e.g., "rest" /kyuʀsoku/ → "rest" /kyuʀkeʀ/). In the LDT, he misidentified non-words as real words by relying on semantic associations of individual kanji characters. The logographic characteristics of kanji may have facilitated RCT while complicating LDT performance.