Case Reports in Neurology最新文献

{"title":"Sildenafil-Associated Anterior Ischemic Optic Neuropathy with Optic Nerve Enhancement in Brain Magnetic Resonance Imaging and Pleocytosis in Cerebrospinal Fluid: A Case Report.","authors":"Ghazale Molaverdi, Nahid Abbasi Khoshsirat, Shirin Mavandadi, Matineh Heidari","doi":"10.1159/000552502","DOIUrl":"10.1159/000552502","url":null,"abstract":"<p><strong>Introduction: </strong>Anterior ischemic optic neuropathy (AION) is characterized by an acute, painless decrease in visual acuity due to restricted blood flow to the optic nerve. It is categorized into two types: arteritic AION and non-arteritic AION, which is more prevalent and is also associated with the use of sildenafil.</p><p><strong>Case presentation: </strong>The patient was a 64-year-old male who presented with sudden, painless, blurred vision in both eyes, progressing to near blindness with minimal light perception. The patient had taken sildenafil the night before symptom onset. A thorough workup, including history-taking, laboratory tests, and imaging, revealed no alternative etiology for the vision loss other than sildenafil use. Nevertheless, he presented atypical features, such as optic nerve enhancement in brain contrast-enhanced magnetic resonance imaging and pleocytosis in cerebrospinal fluid, which are uncommon in sildenafil-associated AION cases.</p><p><strong>Conclusion: </strong>This case contributes to the growing literature on sildenafil-associated AION, underscoring the importance of raising awareness about this potential side effect. These findings highlight the importance of appropriate management and evaluation of patients with sudden visual loss. The improvement in symptoms with corticosteroid therapy in the acute phase suggests that some patients may benefit from early intervention.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"386-393"},"PeriodicalIF":0.4,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13427029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influenza-Triggered Seronegative Myasthenia Gravis in an Anaplastic Lymphoma Kinase-Positive Lung Cancer Patient on Chronic Alectinib: A Case Report.","authors":"Michael Motoc, Sand Mastrangelo, Sruthi Valluri, Carrie J Li, Edison K Miyawaki","doi":"10.1159/000552849","DOIUrl":"10.1159/000552849","url":null,"abstract":"<p><strong>Introduction: </strong>Seronegative myasthenia gravis is an under-recognized cause of acute neuromuscular respiratory failure, and its convergence with infection and targeted oncologic therapy, specifically anaplastic lymphoma kinase inhibition, is poorly characterized, underscoring the importance of vigilance in oncologic patients presenting with respiratory failure.</p><p><strong>Case presentation: </strong>A 51-year-old man with anaplastic lymphoma kinase-positive non-small-cell lung cancer on long-term alectinib presented with fever, cough, and progressive generalized weakness. He tested positive for influenza A and rapidly developed respiratory failure requiring intubation. Neurological examination demonstrated ptosis, oculobulbar involvement, and proximal weakness. Repetitive nerve stimulation showed a decremental response, while assays for acetylcholine receptor, anti-muscle-specific kinase, and anti-lipoprotein receptor-related protein 4 antibodies were negative. A diagnosis of seronegative myasthenia gravis was established. The patient received intravenous immunoglobulin, plasma exchange, pyridostigmine, corticosteroids, and azathioprine with gradual clinical improvement.</p><p><strong>Conclusion: </strong>Early recognition of myasthenia gravis in this population is critical to initiate appropriate immunotherapy and supportive management. This case illustrates the difficulty of distinguishing underlying disease and treatment-related effects from new-onset neurological syndromes. It highlights the importance of neurological considerations in cases of progressive respiratory difficulty and posits a putative link between chronic immunosuppression and subsequent susceptibility to autoimmune insult, as well as the need for more aggressive treatment in the setting of immunosuppression.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"370-379"},"PeriodicalIF":0.4,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13427028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Weight Drop-Foot Drop: A Case Series of Peroneal Nerve Palsy from Leg Crossing after Tirzepatide-Mediated Weight Loss.","authors":"Ann I Tanyous, Jacob Oren Levitt","doi":"10.1159/000552890","DOIUrl":"10.1159/000552890","url":null,"abstract":"<p><strong>Introduction: </strong>Common peroneal nerve palsy, termed \"slimmer's palsy,\" is a recognized complication of rapid weight loss. This case series describes 2 patients who developed foot drop following tirzepatide-induced weight loss precipitated by habitual leg crossing.</p><p><strong>Case presentations: </strong>Peroneal neuropathy secondary to compression from habitual leg crossing developed in 2 male patients during tirzepatide therapy for weight loss. Patient 1 was a 55-year-old with severe hidradenitis suppurativa on multiple immunosuppressive medications who started on tirzepatide and lost 50 pounds over 5 months. Patient 2 was a 71-year-old with insulin resistance who lost 30 pounds over 3 months on tirzepatide. Both patients developed foot drop over 24-72 h. Treatment was behavioral modification to avoid leg crossing, supplemented by physical therapy, and, in patient 1, ankle bracing. Foot drop signs resolved over 3 to 4 months.</p><p><strong>Conclusion: </strong>Clinicians prescribing tirzepatide should counsel patients about peroneal nerve palsy risk during rapid weight loss. Patients should avoid prolonged leg crossing. Early recognition enables timely intervention and favorable outcomes.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"364-369"},"PeriodicalIF":0.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Korsakoff Syndrome in a Late Adolescent with Wernicke Encephalopathy: A Case Report.","authors":"Dax Bourcier, Joanna Holland, Andrew Veysey, Naeem Khan, Selene Etches","doi":"10.1159/000552504","DOIUrl":"10.1159/000552504","url":null,"abstract":"<p><strong>Introduction: </strong>Wernicke encephalopathy (WE) is a neurological emergency characterized by acute encephalopathy, oculomotor dysfunction, and ataxia, and may progress to Korsakoff syndrome - a disorder characterized by irreversible global episodic amnesia. Although classically linked to alcohol misuse, WE also arises in medical and psychiatric conditions associated with nutritional deficiency.</p><p><strong>Case presentation: </strong>We report an 18-year-old male with schizophrenia, non-adherent to antipsychotic treatment, who was admitted with disorganization, catatonia, and dehydration. After several days of minimal nutrition (including dextrose-containing fluids), oral lorazepam, and intramuscular olanzapine, he developed acute WE with worsening catatonia. Intravenous thiamine and continued lorazepam rapidly improved his level of consciousness. Laboratory testing revealed undetectable thiamine, and MRI findings were consistent with WE. Despite oral multivitamin supplementation, catatonia improved only after escalation to intravenous lorazepam and electroconvulsive therapy. As catatonia improved, symptomatology of schizophrenia emerged and improved significantly with paliperidone therapy. As schizophrenia symptoms improved, complete anterograde and partial retrograde amnesia, apathy, and anosognosia emerged, consistent with Korsakoff syndrome. He continued to meet diagnostic criteria at 3-year follow-up.</p><p><strong>Conclusion: </strong>This complex case demonstrates the importance of maintaining a suspicion of thiamine deficiency in patients with a history of nutritional depletion of greater or equal to 2 weeks. Prompt initiation and continuation of thiamine therapy while investigating and treating concurrent diagnoses can reduce the risk of WE and Korsakoff syndrome.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"356-363"},"PeriodicalIF":0.4,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148583679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chorea as a Non-Thrombotic Manifestation in an Adolescent with Systemic Lupus Erythematosus, Antiphospholipid Syndrome and Heterozygous Prothrombin G20210A Gene Mutation: A Case Report.","authors":"Rosa Amorim-Figueiredo, Carla Mendonça, Teresa Morais, Inês Madureira, Carla Conceição, Rita Lopes da Silva","doi":"10.1159/000552585","DOIUrl":"10.1159/000552585","url":null,"abstract":"<p><strong>Introduction: </strong>Chorea is a rare movement disorder in the context of systemic lupus erythematosus (SLE). Although basal ganglia thrombosis, autoimmune injury or neuronal direct lesion have been proposed as possible explanations, its mechanism is still unknown. It is important to understand its pathogenesis so that the best treatments can be identified.</p><p><strong>Case presentation: </strong>A 12-year-old female adolescent with choreoathetoid movements of the trunk and four limbs, slurred speech, hypophonia and orofacial dyskinesia with 14 days of evolution. Brain magnetic resonance imaging revealed recent subcortical ischemic lesions in both frontal and parietal lobes. Basal ganglia lesions were not found. She started acetylsalicylic acid (ASA) and tetrabenazine, with chorea improvement. Transcranial Doppler ultrasound identified a microembolic sign between the left middle cerebral and anterior cerebral arteries. Therefore, ASA was switched to enoxaparin. Antinuclear antibodies and lupus anticoagulant (LAC) antibody were positive, with heterozygous prothrombin G20210A gene mutation being found. Five-day methylprednisolone pulses 1 g/day were performed, followed by prednisolone 60 mg/day. Intravenous immunoglobulin was administered, and hydroxychloroquine was initiated. Due to progressive microscopic hematuria and non-nephrotic proteinuria, a kidney biopsy was performed, being compatible with class V lupus nephritis. Consequently, mycophenolate mofetil and enalapril were started. Chorea resolved 5 days later. After discharge, LAC remained positive, but no more neurologic symptoms occurred.</p><p><strong>Conclusions: </strong>Basal ganglia thrombosis does not seem to be the most likely mechanism of SLE-related chorea. Antiphospholipid antibodies alone do not seem to be enough to trigger chorea. Further studies are needed to clarify the mechanisms that trigger this movement disorder.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"347-355"},"PeriodicalIF":0.4,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13349368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relative Efficacy of Self-Managed Caffeine Supplementation in Maintaining Daily Activity in a Patient with ADCY5-Related Dyskinesia: A Case Report.","authors":"Kaori Kodama, Haruhiko Nakamura, Aritomo Kawashima, Yukimune Okubo, Wakaba Endo, Takehiko Inui, Noriko Togashi, Naoya Saijo, Jun Takayama, Atsuo Kikuchi, Kazuhiro Haginoya","doi":"10.1159/000552512","DOIUrl":"10.1159/000552512","url":null,"abstract":"<p><strong>Introduction: </strong>ADCY5-related dyskinesia is an autosomal dominant movement disorder with limited treatment options because many standard medications are ineffective. Caffeine has shown efficacy in ADCY5-related dyskinesia as an adenosine A2A receptor antagonist, but optimal dosing remains uncertain.</p><p><strong>Case presentation: </strong>We report a 24-year-old woman with paroxysmal dyskinesia since early childhood, consisting of chorea, dystonia, and myoclonus upon waking. More than 15 medications failed. Whole-exome sequencing identified a mosaic ADCY5 variant (p.R418Q, 7% variant allele frequency). Caffeine escalation from 100 to 600 mg worsened symptoms. Four months later, she found that unsweetened canned coffee containing approximately 100 mg of caffeine per can, taken 1-3 times daily, reduced her symptoms and helped her maintain daily employment. In a self-controlled analysis of 39 coffee-intake events, dyskinesia episodes during the 6 h after coffee intake were significantly fewer than during the preceding 6 h (<i>p</i> = 0.002).</p><p><strong>Conclusion: </strong>This case demonstrates successful symptom control in ADCY5-related dyskinesia using patient-directed, low-dose caffeine therapy. The striking response suggests a narrow therapeutic window for caffeine in this condition and that patient self-titration may be valuable in optimizing treatment response.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"325-329"},"PeriodicalIF":0.4,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13345610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute MOG-IgG-Associated Myelitis in a Patient with Long-Standing Multiple Sclerosis: A Case Report.","authors":"José Luis Sánchez-Menoyo, Miriam Cortés-Rubiales, Iñigo Vicente-Olabarría, Aranzazu Pacho de Lucas, Ana Cristina Pinedo-Brochado","doi":"10.1159/000552322","DOIUrl":"10.1159/000552322","url":null,"abstract":"<p><strong>Introduction: </strong>Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and multiple sclerosis (MS) are distinct inflammatory demyelinating disorders that may share overlapping clinical and imaging features, creating important diagnostic challenges.</p><p><strong>Case presentation: </strong>We describe a 58-year-old woman with unequivocal long-standing relapsing-remitting MS fulfilling established diagnostic criteria, including typical periventricular and deep white matter lesions on magnetic resonance imaging (MRI) and clear dissemination in space and time, with characteristic brain and spinal MRI findings and more than a decade of clinical and MRI stability under extended-interval natalizumab therapy. Following a febrile prodrome, she developed acute severe myelitis with rapid progression from baseline paraparesis (Expanded Disability Status Scale [EDSS] 6.0) to near-complete paraplegia (EDSS 8.0) within 7 days. Cerebrospinal fluid analysis revealed marked pleocytosis, elevated protein levels, and absence of oligoclonal bands, findings atypical for MS relapse. Serum testing demonstrated high-titre MOG immunoglobulin G antibodies, which progressively declined and became negative during follow-up. Retrospective spinal cord MRI revealed transient central grey matter involvement with a characteristic H-sign on axial T2-weighted sequences, consistent with MOGAD-associated myelitis. The patient responded to high-dose intravenous corticosteroids and returned to baseline disability within 3 months.</p><p><strong>Conclusion: </strong>This case highlights that acute neurological deterioration in patients with established MS should not automatically be attributed to disease reactivation and supports careful consideration of alternative inflammatory demyelinating processes such as MOGAD when clinical, cerebrospinal fluid, and imaging features are atypical. Integration of clinical findings, cerebrospinal fluid analysis, MRI features, and antibody testing is essential to avoid diagnostic anchoring and ensure appropriate management.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"337-346"},"PeriodicalIF":0.4,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13345611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dyshidrotic Eczema following Intravenous Immunoglobulin Therapy in Guillain-Barré Syndrome: A Case Report.","authors":"Khuzama Alfalah, Khalid Nabil Nagshabandi, Abdullah M Shadid, Abdulaziz Almohanna","doi":"10.1159/000552513","DOIUrl":"10.1159/000552513","url":null,"abstract":"<p><strong>Introduction: </strong>Dyshidrotic eczema is an uncommon but recognized cutaneous adverse reaction to intravenous immunoglobulin (IVIG) therapy, particularly among patients treated for immune-mediated neurological disorders such as Guillain-Barré syndrome (GBS). The eruption typically consists of pruritic vesicles on the palms and soles, arising within days to weeks after infusion. Although usually self-limited, the reaction may recur with subsequent IVIG courses and can influence therapeutic decision-making.</p><p><strong>Case presentation: </strong>We report a 39-year-old man newly diagnosed with GBS who was treated with standard-dose IVIG (2 g/kg over 5 days). Three days after completing therapy, he developed intense pruritus and burning of the palms, followed by the appearance of numerous deep-seated vesicles symmetrically distributed along the lateral digits and central palms. There was no systemic involvement, pustulation, or exposure to irritants. A diagnosis of IVIG-induced dyshidrotic eczema was made based on the temporal association, typical morphology, and exclusion of alternative causes. The patient responded well to high-potency topical corticosteroids, antihistamines, and emollients, with complete resolution in 2 weeks and no recurrence at 1-month follow-up.</p><p><strong>Conclusion: </strong>This case highlights dyshidrotic eczema as a benign yet clinically relevant dermatologic complication of IVIG therapy in GBS. Prompt recognition allows effective management and helps avoid unnecessary diagnostic workup or treatment interruption. Awareness of this reaction is important when counseling patients and planning future IVIG use.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"311-316"},"PeriodicalIF":0.4,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13341101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABCA7 Mutation in Behavioral Variant of Frontotemporal Dementia: A Case Report.","authors":"Chloé Geron, Pierre Maquet","doi":"10.1159/000552305","DOIUrl":"10.1159/000552305","url":null,"abstract":"<p><strong>Introduction: </strong>Frontotemporal lobar degeneration (FTLD), a major cause of early-onset dementia, includes a heterogeneous group of neurodegenerative disorders with a strong genetic component. Mutations in <i>MAPT</i>, <i>GRN</i>, and <i>C9orf72</i> are found in about 40% of patients with the behavioral variant (bvFTD). More recently, rarer pathogenic variants have been identified in other genes, such as <i>ABCA7</i>, initially linked to Alzheimer's disease but increasingly implicated in other neurodegenerative conditions. Here we describe a specific variant which has not previously been reported in the literature.</p><p><strong>Case presentation: </strong>We report the case of a 42-year-old woman who presented with progressive behavioral changes and executive dysfunction, consistent with a bvFTD. A whole-exome sequencing was conducted in a family trio, revealing a heterozygous nonsense variant in the <i>ABCA7</i> gene (c.5260C>T, p.Arg1754*).</p><p><strong>Conclusion: </strong>This case highlights support the hypothesis of an ABCA7 loss-of-function associated with early-onset bvFTD. It contributes to expand the genetic spectrum of frontotemporal dementia and underscores the importance of broad genetic testing.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"317-324"},"PeriodicalIF":0.4,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13345613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"First Case of Creutzfeldt-Jakob Disease in Ghana: Diagnostic Challenge in a Resource-Limited Setting.","authors":"Vida Obese, Paulinus Domeh, Manolo Yao Agbenorku, Shiela Adamu, Benedict Kusi Ampofo, Priscilla Abrafi Opare-Addo, Kwaku Asare-Ankomah, Hanson Ababio, Andrew Jacobs Bilson, Fred Stephen Sarfo","doi":"10.1159/000552308","DOIUrl":"10.1159/000552308","url":null,"abstract":"<p><strong>Introduction: </strong>Creutzfeldt-Jakob disease (CJD) is a rare, but invariably fatal neurodegenerative disorder with multiple subtypes, region-specific prevalence patterns, and significant underreporting, particularly in resource-limited settings due to limited diagnostic infrastructure and surveillance capacity. We report what is, to the best of our knowledge, the first documented case of CJD in Ghana. This case highlights the importance of recognizing atypical neurodegenerative presentations and the critical role of neuroimaging in settings where access to advanced diagnostic tools is limited.</p><p><strong>Case presentation: </strong>The patient was a 47-year-old previously healthy Ghanaian woman who developed sub-acute rapidly progressive global cognitive decline, motor incoordination, visual hallucinations, myoclonus, and eventually akinetic mutism over a 4-month period. Initial evaluations, including routine metabolic and infectious panels, led to a misdiagnosis and treatment for acute ischemic stroke and neurosyphilis based on a positive syphilis test. Subsequent brain magnetic resonance imaging showed cortical ribboning and hyperintensity in the caudate nuclei. Electroencephalography revealed periodic sharp wave complexes and frontal intermittent rhythmic delta activity. Cerebrospinal fluid analysis was normal with negative viral testing. Based on clinical features and supportive investigations, a diagnosis of probable sporadic CJD was made in accordance with established diagnostic criteria.</p><p><strong>Conclusion: </strong>This case highlights the diagnostic value of neuroimaging in suspected prion diseases and highlights the importance of recognizing probable CJD in resource-limited settings where access to confirmatory assays is limited. It also emphasizes the need for improved surveillance systems and diagnostic capacity, as additional unreported cases may exist.</p>","PeriodicalId":9639,"journal":{"name":"Case Reports in Neurology","volume":"18 1","pages":"302-310"},"PeriodicalIF":0.4,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13341097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}