Neurological Signs Research Articles

7668 Rhabdomyolysis Associated with Severe Hypothyroidism

Abstract Disclosure: H. Soe: None. P. Mikkilineni: None. Background: Over 70% of the patients with newly diagnosed hypothyroidism can present with muscle complaints such as weakness, fatigability, cramps, myalgia. However, rhabdomyolysis, which is the rapid breakdown of skeletal muscle cells, is the rare presentation. Clinical Case: A 70-year old male patient with history of rheumatoid arthritis, hyperlipidemia, prior CVA (left hemispheric subcortical stroke) 6 months ago without residual deficit presented to the hospital with poor oral intake and generalized muscle weakness for 3 weeks. He was unable to get out of bed without assistance and also needed adult diapers. Found to have new-onset severe hypothyroidism with TSH 228 uIU/ml (Ref: 0.350-4.940) and FT4 <0.40 ng/dL (Ref: 0.70-1.50), positive TPO antibody 197 IU/ml (Ref: 0-34). No prior thyroid labs were available and no known history of thyroid disorder was recorded. He has never been on Amiodarone or Lithium before. On physical exam, he was alert and oriented. There was no goiter or palpable thyroid nodule. There was no focal neurological deficit and no peripheral edema. There were no other signs and symptoms pertinent to hypothyroidism except mild bradycardia (HR 56-60) and borderline low blood pressure. AM cortisol was 10.1 ug/dL (Ref: 3.7-19.4). EKG showed low-voltage sinus bradycardia. Echocardiogram was normal. Urinalysis was positive for large blood but only 3 RBCs were present which raised the suspicion of rhabdomyolysis. Creatinine kinase (CK) was 15,584 IU/L (Ref: 30-200). Other laboratory studies were significant for acute renal failure with mild hyperkalemia and mild hypocalcemia, also transaminitis; BUN 130 mg/dl (Ref: 8-26), Creatinine 9.51 mg/dl (Ref: 0.72-1.25), eGFR 5 ml/min/1.73 m2 (Ref: >59), AST 435 IU/L (Ref: 5-34), ALT 269 IU/L (Ref: <55), ALP 171 IU/L (Ref: 40-150). On medication review, he was started on Atorvastatin 80 mg daily during prior admission for CVA 6 months ago. He received IV fluids, s/p 1 dose of Hydrocortisone 100 mg IV, Levothyroxine IV 200 mcg, followed by Levothyroxine IV 50 mcg daily x 3 days and switched to Levothyroxine PO 100 mcg daily (weight-based dose). Atorvastatin was on hold. He became anuric during the hospital course and received 2-3 sessions of hemodialysis. 3-4 days later, CK was trending down to 3000 IU/L, FT4 improved to 0.54 ng/dl and there was also significant improvement in kidney and liver functions. The patient was diagnosed with acute renal failure secondary to rhabdomyolysis associated with severe hypothyroidism caused by Hashimoto's thyroiditis, in the setting of high dose statin use. Conclusion: Clinicians should raise the suspicion of rhabdomyolysis in a patient with severe hypothyroidism, especially in patients with recent high dose statin use as rhabdomyolysis can be a rare and fatal complication of severe hypothyroidism, in the presence of precipitating factors. Presentation: 6/2/2024

8472 A Little Too Much Of Tums: A Unique Presentation Of Milk Alkali Syndrome

Abstract Disclosure: Z. Al-Hiti: None. A. Misbah: None. Milk-Alkali Syndrome is characterized by a triad of hypercalcemia, metabolic alkalosis, and renal dysfunction. Historically associated with the excessive consumption of milk and alkali-containing antacids, it has re-emerged in recent years due to the widespread use of calcium and vitamin D supplements. It primarily results from an imbalance between calcium intake and renal excretion, leading to elevated calcium levels in the bloodstream. We present a case of milk-alkali syndrome with persistent renal dysfunction after normalizing calcium levels. We present the case of a 65-year-old male who presented to the emergency department with generalized weakness, poor oral intake, and confusion for 3 days. He was noted to have been more adherent with taking his prescribed medications over the last 2 weeks, which include calcitriol 0.5 mcg BID, calcium acetate 667 mg TID, and calcium carbonate 800 mg TID. On admission, he was afebrile and hemodynamically stable. . On examination, he had dry mucous membranes. He had no focal neurological deficits but he was confused and lethargic, and was only oriented to self. Other examination was noncontributory. Complete blood count and urinalysis were largely unremarkable. Chemistry demonstrated an elevated calcium level of 16.0 (8.3-10.6 mg/dL), ionized calcium of 7.3 (4.6-5.3 mg/dL), sodium of 134 (135-145 mmol/L), potassium of 5.4 (3.5-5.1 mmol/L), high phosphorus of 5.3 (2.4-5.1 mg/dL), and bicarbonate of 36 (20-31 mEq/L). Creatinine was elevated at 2.9 (0.6-1.1 mg/dL) from baseline of 1.3 to 1.4 mg/dL, and he had a BUN of 40(9-23 mg/dL). Venous blood gas showed a pH of 7.54( 7.32-7.42), pCO2 of 56 (40-52 mm Hg), and bicarbonate of 38 (23-28 mEq/L), indicating metabolic alkalosis. TSH was elevated at 36.15 (0.55- 4.78 uIU/mL) with a level of 140 two weeks back. Chest X-ray, renal ultrasound and CT head all showed no acute disease. Further work-up revealed a low PTH level of 6.3 (18.4-80 pg/mL), normal PTHrP level and 25-OH Vitamin D. There was no monoclonal gammopathy. Management included aggressive IV fluid resuscitation and IV calcitonin. However, no zoledronic acid was given due to a history of parathyroidectomy and risk of hypocalcemia. His serum calcium improved and eventually normalized. His confusion resolved. However, his creatinine and BUN increased to 3.4 mg/dL and 77, respectively, and did not improve to his baseline. This case highlights the importance of recognizing Milk-Alkali Syndrome as a potential consequence of over-the-counter calcium supplementation and highlights the potential for acute kidney injury which could be irreversible. Healthcare providers should be vigilant in identifying patients at risk, which includes older patients and patients with chronic kidney disease. Early recognition and appropriate management are crucial to prevent further renal deterioration and improve outcomes in individuals with Milk-Alkali Syndrome. Presentation: 6/2/2024

6928 Vitamin D excess in a patient with hypoparathyroidism after parathyroidectomy

Abstract Disclosure: Z. Zavgorodneva: None. A. Barsegian: None. F. Zhang: None. Introduction. We describe a case of a patient with mild persistent hypoparathyroidism after parathyroidectomy with autotransplantation, which was indicated for ESRD-related secondary hyperparathyroidism. The patient presented with nonspecific complaints and was found to have a high Vitamin D level after long-term moderate-dose Vitamin D supplementation. Case report. A 71-year-old male with a past medical history of end-stage renal disease (ESRD) undergoing hemodialysis for the past 18 years, as well as a history of parathyroidectomy with autoimplantation of parathyroid glands in the forearm in 2010 due to severe secondary hyperparathyroidism, presented to the hospital complaining of generalized weakness and lower extremity cramps that had been ongoing for a few weeks. Further investigations did not reveal evidence of infectious processes. A review of medications indicated the absence of statins among his outpatient medications. No focal neurological deficits or objective signs of muscle weakness were identified. Laboratory findings showed no significant metabolic derangements or haematological abnormalities. Inflammatory markers and creatine phosphokinase were within normal ranges. As part of the workup for generalized subjective weakness and ESRD, Vitamin D levels were checked, revealing a result of of120 ng/mL. The patient reported taking over-the-counter 2000 IU of Vitamin D twice daily for the past six years despite having a normal level of Vitamin D checked five years prior to admission. Calcium supplements were initiated in the postoperative period and continue to be administered at a dose of 600 mg daily. Analysis of the PTH-calcium axis demonstrated persistent mild hypoparathyroidism with hypocalcemia since the time of the surgery. However, there was an observed tendency for calcium levels to improve, especially in the last six years. Vitamin D supplement was discontinued, and the patient was subsequently discharged home with the continuation of physical therapy. Discussion. Explaining the origin of the high level of Vitamin D in this patient poses a challenge. There is limited data in the literature regarding the long-term effects of vitamin D use when the initial Vitamin D levels are normal. Additionally, there are numerous abstracts suggesting significantly higher doses of Vitamin D received for up to 6 years without any evident biochemical or clinical consequences. Moreover, the typical consequences of Vitamin D toxicity, such as hypercalcemia, can not be present in patients who underwent parathyroidectomy. Therefore, it is possible to consider that the severe generalized subjective weakness may be a sign of Vitamin D toxicity itself. Presentation: 6/1/2024

8186 Hypoglycemia as an Unusual Presentation of Panhypopituitarism

Abstract Disclosure: P. Chalasani: None. M. Asfaw: None. M. Mansour: None. M. Hammoud: None. T. Altaweel: None. H. Ilyas: None. L. Lawrence: None. Introduction: Hypopituitarism refers to the diminished or complete absence of anterior pituitary function, which may arise from acquired or congenital factors. The symptoms depend on the patient’s age and the hormones affected. We report a case where hypoglycemia led to a new diagnosis of panhypopituitarism in an adult patient. Clinical Case:A 53-year-old female with a past medical history of hypertension was brought to the emergency department after syncope. Patient experienced diaphoresis and loss of consciousness associated with urinary incontinence. She did not have confusion, tongue biting, or muscular weakness after the episode. On presentation, the patient was hypoglycemic with blood glucose of 39 mg/dl and received IV dextrose. No focal neurologic deficits were noted on physical examination. She was mildly hypotensive with blood pressure 98/66 mmHg, and received hydrocortisone 100 mg IV once, and started on IV dextrose infusion. Hypoglycemia workup revealed elevated insulin 16.6 uIU/mL and C-peptide 4.8 ng/mL (1.1-4.4) levels for a blood glucose level of 132 mg/dl, with normal beta-hydroxybutyrate of 0.14 mmol/L (0.02-0.27). Sulfonylurea screen was negative. CT abdomen revealed no pancreatic lesions or abnormalities. Hyperinsulinemia was attributed to insulin resistance in this patient with a BMI of 34 kg/m2. CT head revealed a heterogeneous low-density expansile mass in the sella/suprasellar region measuring approximately 2.5 x 2.3 x 2 cm. MRI brain confirmed a heterogeneous sellar mass with suprasellar extension measuring 3.4 x 2.3 x 2.1 cm abuting the optic chiasm without displacement. Biochemical workup revealed panhypopituitarism with secondary adrenal insufficiency ACTH < 1.5 pg/mL (7.2-63.3) and cortisol 3.63 ug/dL (3.70-19.40); secondary hypothyroidism TSH 0.84 mIU/mL (0.27-4.20) and FT4 < 0.50 ng/dL (0.70-14.8); growth hormone deficiency with low IGF-1 23 ng/mL (65-216); secondary hypogonadism FSH < 1 mIU/mL (46-177), LH < 1 mIU/mL (7.7-59) and estrone < 6 pg/mL (0-125); with normal prolactin 14.1 ng/mL (4.8-23.3). Patient revealed she had been amenorrheic since 23 years old and conceived one child prior. Patient was transitioned to oral hydrocortisone 20 mg AM and 10 mg PM, and started on levothyroxine 50 mcg PO daily. No neurosurgical intervention was recommended. Subsequently, patient requested a second opinion and was transferred to a tertiary center. Conclusion: The link between hypoglycemia and hypopituitarism, may be attributed to hypocortisolism and growth hormone / IGF-1 deficiency. Intriguingly, this patient's initial clinical presentation centered around hypoglycemia, and further evaluation led to the identification of a sellar mass and new diagnosis of panhypopituitarism. This case demonstrates the need to include hypopituitarism in the differential when evaluating hypoglycemic patients. Presentation: 6/2/2024

Autoimmune and infectious encephalitis: development of a discriminative tool for early diagnosis and initiation of therapy.

Encephalitis originates from diverse autoimmune and infectious etiologies. Diagnostic challenges arise due to the spectrum of presentation and the frequent absence of specific biomarkers. This study aimed to comprehensively characterize and differentiate autoimmune encephalitis (AE) from infectious encephalitis (IE) in adults, and disentangle clinical, paraclinical, and therapeutic differences. A cohort study spanning 10years was conducted across three Austrian tertiary care hospitals. Inclusion criteria comprised adults with probable or definite encephalitis. Demographics, clinical features, technical findings, treatment modalities, and outcomes were collected from the electronic patient files. A follow-up was performed via telephone interviews and clinical visits. Of 149 patients, 17% had AE, 73% IE, and 10% encephalitis of unknown etiology. Significant differences between AE and IE included the prevalence of acute symptomatic seizures (AE: 85% vs. IE: 20%, p < 0.001), fever (8% vs. 72%, p < 0.001), headache (15% vs. 61%, p < 0.001), and focal neurological deficits (56% vs. 23%, p = 0.004), respectively. Paraclinical differences comprised lower CSF pleocytosis in AE compared to IE (median 6 cells/µl vs. 125 cells/µl, p < 0.001). Epileptic discharges on EEG and MRI lesions were more prevalent in AE than IE (50% vs. 14%, p < 0.001; 50% vs. 28%, p = 0.037). The modified Rankin Scale scores at discharge and last follow-up (median duration 2304days, IQR 1433-3274) indicated favorable outcomes in both groups. This comprehensive analysis provides insights into the epidemiology, clinical, paraclinical, and therapeutic aspects and the outcomes of AE and IE in adults. We developed a diagnostic tool that facilitates early differentiation between AE and IE, aiding in timely therapeutic decision-making.

Vertigo as Initial Symptom of Cerebellar Hemorrhage in Adult Woman : A Case Report

Vertigo, difficulty walking, and loss of balance/coordination are among the symptoms of stroke in 50% of stroke cases. Vertigo due to cerebrovascular disease is generally associated with other neurological signs such as cranial nerve abnormalities, hemiparesis, facial weakness, diplopia, hyperesthesia, and Horner's syndrome. A 42-year-old woman came to the emergency department with complaints of dizziness, nausea, and frequent vomiting for the previous 4 hours. The symptoms are also accompanied by a feeling of tingling on the left side of the face, and the left eyelid cannot open optimally. The patient has a history of uncontrolled hypertension. The HINTS test revealed central vertigo, and the patient also found dysdiadochokinesis, ataxia, and dysmethria. A non-contrast head CT scan showed ICH in the left cerebellum with a volume of 6.9 cc. Based on the results of these examinations, the patient was diagnosed with cerebellar hemorrhage. The blood supply to the brainstem, cerebellum, and inner ear comes from the vertebrobasilar vascular system. Blockage or rupture of blood vessels in one of the main branches of this system can cause symptoms of vertigo. Symptoms of vertebrobasilar stroke vary widely and depend on which of the three main circumferential branches is affected; posterior inferior cerebellar artery, anterior inferior cerebellar artery, or superior cerebellar artery. Vertigo in patients who have risk factors for stroke accompanied by other neurological symptoms should be considered for a thorough neurological examination to evaluate the possibility of cerebrovascular disease.

Transverse and oblique course of the vertebral artery over the medullospinal junction.

The vertebral artery (VA) pierces the dura mater and continues with the intradural V4 segment. Once entered into the dura mater, the VA ascends from the infero-lateral to the antero-superior side of the medulla. Scarce reports of VAs compressing the medullospinal junction (MSJ) are available. We therefore aimed to determine the incidence of a course of the AV over the MSJ. One hundred sixty-two archived CT angiogram files were documented in the study. We recorded the cases in which the VA crossed the MSJ. We assessed the VA as dominant, non-dominant or co-dominant. In 32 cases (19.75%), we identified intradural AVs on the ventral side of the MSJs. The incidence of this course of the VA was 17.1% in males and 23.81% in females. Of the 32 cases, the VA was non-dominant in 6, dominant in 14, and co-dominant in 12. The VA course over the MSJ is not rare. Therefore, when specific neurological signs of MSJ or medulla compression are found, the course of the VA should be documented on CT or MRI angiograms.

Treatment-Related Reversible Cerebral Vasoconstriction Syndrome

Reversible cerebral vasoconstriction syndrome (RCVS) is a rare but significant cause of intracranial arteriopathy and stroke in young adults. The syndrome encompasses a spectrum of disorders radiologically characterized by reversible narrowing and dilation of intracranial arteries, often triggered by vasoactive drugs or the postpartum period. The hallmark clinical feature of RCVS is thunderclap headache with or without other neurological signs. Though endothelial dysfunction and sympathetic hyperactivation are hypothesized to be key mechanisms, the exact pathogenesis of RCVS is still unclear. RCVS’s diagnosis could be challenging, since vasospasm proceeds centripetally, initially involving distal small pial and cortical arteries, and angiographic studies, especially brain magnetic resonance angiography (MRA) and computed tomography angiography (CTA), may miss it in the early phase of the disease, while early signs such as vascular hyperintensities may be visible on T2/FLAIR sequences before vasospasm onset. Catheter angiography is the gold standard and it could be used to assess vasospasm reversibility post-intra-arterial vasodilator administration. Treatment is mainly symptomatic, and nimodipine is the most commonly administered therapy, given orally or intra-arterially in severe cases. Since many aspects of RCVS remain partially known, further research is needed to better understand the complex pathophysiology of this unique clinical condition and to optimize specific management strategies.

A 10-year cross-sectional study showed that anti-coagulation therapy was not always of value when treating paediatric cases with septic cerebral venous thrombosis.

Cerebral venous thrombosis (CVT) is a rare complication of ear, nose and throat (ENT) infections. Although recent guidelines recommend the systematic use of anti-coagulation therapy (ACT) in the treatment of these CVT, literature data are scarce. The present study's objective was to determine the value of ACT in achieving recanalisation after thrombosis and its effect on patient outcomes. All paediatric patients with CVT and a concomitant ENT infection who attended Lille University Hospital (Lille, France) between January 2012 and December 2021 were retrospectively included. We included 43 children (63% boys), with a mean age of 4 years. The most frequent infection was mastoiditis (54%). ACT was initiated in 23 patients (53%), one of whom had an intracranial haemorrhage. Partial or full recanalisation was observed in 33 (80%) of the 41 survivors. In patients with no neurological signs and symptoms on admission and in patients with mastoiditis-related CVT, the clinical and radiological outcomes were favourable and did not differ according to the administration of ACT. Likewise, ACT did not appear to influence the recanalisation rate or sequelae. ACT was not necessary for all patients with mastoiditis-related CVT and those with no neurological signs and symptoms on admission.

MNGA-08 SKULL BASE TUMOR RESECTION IN LOW-RESOURCE SETTINGS: A REVIEW OF THREE CASES AT THE KENYATTA NATIONAL HOSPITAL

Abstract Skull-based tumors are challenging to treat surgically due to their proximity to vital structures and the risk of complications. In low-resource settings, the availability of advanced neurosurgical equipment and expertise is limited, which may affect the outcomes of these patients. We report the outcomes of three patients with skull base tumors who underwent surgery at the Kenyatta National Hospital, Kenya. We retrospectively reviewed the medical records and followed up with three patients who underwent surgery for skull base tumors between October and November 2023. We collected data on their demographic characteristics, clinical presentation, imaging findings, surgical procedures, histopathological diagnosis, and postoperative course. The three patients were male, aged 42, 40, and 36 years. The common presentation was with headache, but dizziness and other cerebellar deficits were common. Imaging revealed defined lesions in the posterior fossa, involving the cerebellum and brainstem. The differential diagnosis included hemangioblastoma and meningioma. The surgical approach with anatomically-specified craniotomy with resection of the tumor and decompression. The postoperative course was uneventful for the first and third patients, who showed improvement in their neurological symptoms and signs. The second patient had repeat surgery. Skull base tumor surgery in a low-resource setting can achieve favorable outcomes with careful patient selection, meticulous surgical technique, and multidisciplinary care. However, the challenges of limited resources and high complication rates remain. Further studies are needed to evaluate the long-term outcomes and quality of life of these patients.

Refining criteria for a neurodevelopmental sub-phenotype of bipolar disorders: a FondaMental Advanced Centers of Expertise for Bipolar Disorders study

Bipolar disorder (BD) is a complex and heterogeneous psychiatric disorder. Neurodevelopmental factors were suggested to contribute to the etiology of BD, yet a specific neurodevelopmental phenotype of the disorder remains unidentified. Our objective was to define and characterize a neurodevelopmental phenotype (NDP) in BD and validate its associations with clinical outcomes, polygenic risk scores (PGS), and treatment responses. We analyzed the FACE-BD cohort of 4,468 BD patients, a validation cohort of 101 BD patients, and two independent replication datasets of 274 and 89 BD patients. Using factor analyses, we identified a set of criteria for defining NDP. We next developed a scoring system for NDP-load and assessed its association with prognosis, neurological soft signs, polygenic risk scores for neurodevelopmental disorders, and responses to treatment using multiple regressions, adjusted for age and sex with bootstrap replications. Our study established a NDP in BD consisting of nine clinical features: advanced paternal age, advanced maternal age, childhood maltreatment, attention deficit hyperactivity disorder (ADHD), early onset of BD, early onset of substance use disorders, early onset of anxiety disorders, early onset of eating disorders, specific learning disorders. Patients with higher NDP-load showed a worse prognosis and increased neurological soft signs. Notably, these individuals exhibited a poorer response to lithium treatment. Furthermore, a significant positive correlation was observed between the NDP-load and PGS for ADHD suggesting potential overlapping genetic factors or pathophysiological mechanisms between BD and ADHD. The proposed NDP constitutes a promising clinical tool for patient stratification in BD.

Episodic mandibular tremor in dogs: an idiopathic movement disorder or a manifestation of pain.

Episodic mandibular tremor (EMT), manifested as teeth chattering, is not well described in dogs. The aim of this study was to describe clinical signs, MRI findings, and outcome of dogs with EMT. 11 dogs retrospectively and 31 dogs in an online survey. A retrospective multicenter study of dogs with EMT between 2018 and 2023 and prospective online questionnaire open to owners of pets with teeth chattering. All dogs had rapid and short-lasting (< 1 minute) episodes of EMT in the absence of other neurological signs. Lip smacking occasionally accompanied the tremor in 5 of 11 (45.5%) hospital dog cases. Excitement was a common trigger in 14 of 31 (45.2%) dogs from the survey. Cavalier King Charles Spaniel was the most common breed in both clinical and survey populations. Median age at presentation was 3 years for both hospital cases and the survey dogs. A concurrent medical condition was present in 8 of 11 (72.7%) hospital cases and 20 of 31 (64.5%) survey dogs. In 3 hospital dogs that underwent further investigations, no brain disease was present. EMT and its clinical features are presented for the first time, shedding light on a clinical sign that might resemble an idiopathic movement disorder or a manifestation of pain in dogs.

Acute disseminated encephalomyelitis (ADEM) in a patient with post streptococcal glomerulonephritis (PSGN): A case report.

Concurrent recurrence of acute disseminated encephalomyelitis (ADEM) and poststreptococcal glomerulonephritis (PSGN) in a thalassemia intermedia patient is rare and underscores the complexity of autoimmune disorders. This case emphasizes the importance of considering ADEM in the differential diagnosis of children presenting with PSGN accompanied by neurological symptoms. Post-streptococcal glomerulonephritis (PSGN) is a common group A streptococcal (GAS) infection sequela. The pathophysiology of PSGN involves immune complex deposition, with type 3 hypersensitivity reaction triggered by GAS. Certain neurological conditions may also arise following a GAS infection, possibly due to molecular mimicry in the brain, a pathophysiology similar to rheumatic fever, another common sequel of GAS infection. We present the case of a child with β-thalassemia intermedia who exhibited the classic triad (edema, hypertension, hematuria) of PSGN along with neurological manifestations, including a low glasgow coma scale (GCS) score and seizures. Magnetic resonance imaging (MRI) of the brain indicated changes consistent with acute disseminated encephalomyelitis (ADEM). Initially treated with methylprednisolone, the patient eventually received intravenous immunoglobulin (IVIG) due to lack of response. The patient had a good outcome, with complete resolution of all symptoms and no residual neurological deficits. This case underscores the importance of considering ADEM in the differential diagnosis for patients presenting with neurological signs and symptoms following a recent throat infection with GAS. Furthermore, given the increased risk of infection in thalassemia, patients with thalassemia who have a throat infection and neurological symptoms should be evaluated for the possible presence of ADEM.

A Histopathological Study on the Changes in the Central Nervous System of Dead Cats With Neurological Symptoms

Background: Neurological conditions constitute approximately 10% of feline cases referred to veterinary clinics. Such cases often present manifestations of central nervous system (CNS) damage, including inflammatory lesions, neoplastic growth and structural and cellular transformations. Objectives: This study aimed at identifying histopathological changes in the CNS of cats that had succumbed to neurological symptoms. Methods: Microscopic evaluation of different sections within the CNS was conducted on 20 cats that had either died naturally or were euthanized due to neurological signs. After performing a necropsy, we examined the CNS tissues and conducted PCR testing to screen for possible viral infections, including feline infectious peritonitis (FIP), feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV). Results: The majority of cases showed characteristic histopathologic lesions, notably mononuclear and suppurative meningoencephalitis, perivascular cuffing, disseminated intravascular coagulation (DIC), granulomatous meningoencephalitis, acute neuronal necrosis, liquefactive necrosis, epididymitis, thrombosis and demyelination. Among the 20 cats studied, 12 tested positive for FIP by PCR analysis, while 5 cats exhibited positive results for FIV. Also, FeLV PCR tests displayed positive results in 4 cats. No evidence of feline spongiform encephalopathy (FSE) was observed. Conclusion: This study is the first of its kind conducted in Iran. Based on the results, the most prevalent viral agents infecting cats’ CNS were FIP, FIV and FeLV. The investigation revealed no evidence of FSE in cats with neurological signs.

Neuro-Behcet's Masquerading as Status Epilepticus and Meningoencephalitis in the Emergency Department

BackgroundBehcet disease (BD) is a rare small vessel vasculitis that commonly manifests as recurrent painful oral or genital ulcerations, uveitis, and skin lesions. Some patients with BD develop neurological symptoms termed neuro-Behcet's disease. In the emergency department (ED) setting, these symptoms can be mistaken for other common acute issues including stroke, infection, epilepsy, multiple sclerosis, toxin ingestion, or psychiatric conditions. Case ReportWe present a case of a 28-year-old male with neuro-Behcet disease mimicking status epilepticus and meningoencephalitis. He was actively seizing on arrival and febrile at 103.8 F. The patient also had a history of vasculitis, uveitis and genital lesions which raised suspicion for a rheumatological process. Cerebrospinal fluid (CSF) samples were obtained and computed tomography (CT) of the head revealed no acute findings. The patient was started on treatment for seizure and meningoencephalitis and admitted to neurology for continuous electroencephalogram (EEG) monitoring with additional consults placed for rheumatology, ophthalmology, and infectious disease. The patient was ultimately diagnosed with neuro-Behcet's disease and treated appropriately.Why should an emergency physician be aware of this?: In a patient presenting with neurological symptoms and signs of rheumatological disease providers should consider neuro-Behcet's disease as a differential diagnosis. This case exemplifies the vital role of reviewing past medical history to expand differential diagnoses and early coordination with specialists so treatment can be initiated early to prevent morbidity and mortality. The case will also review different presentations of this unfamiliar diagnosis for a more comprehensive understanding.

Therapeutic hypothermia: A descriptive, cohort study conducted over 10 years at a tertiary care public hospital.

Introduction. Therapeutic hypothermia (TH) reduces the risk of death or disability in children with moderate to severe hypoxic ischemic encephalopathy (HIE). Objective. To describe a population of patients with HIE that required TH and their course until discharge. Population and methods. Retrospective, descriptive, cohort study. All patients admitted to TH between 2013 and 2022 were studied. Epidemiological, clinical, monitoring, and treatment data were assessed, together with supplementary tests and condition at discharge. Risk factors were compared between deceased patients and survivors; and, among the latter, those requiring special healthcare needs (SHCN) at discharge. Results. A total of 247 patients were included. Mortality: 11%. Most common sentinel event: prolonged second stage of labor (39%). Treatment initiation: median of 5 hours of life. Seizures: 57%. Intravenous erythropoietin: 66.7%. Abnormal pattern in brain function monitoring: 52%. Normalization of monitoring: median of 24 hours. Pathological magnetic resonance imaging: 42%. Predictor variables of mortality: severe Sarnat and Sarnat staging and pathological ultrasound upon admission. Conclusion. The overall mortality rate was 11%. Referrals increased more markedly since 2018. The time of TH initiation was later than in previous reports. Severe neurological signs as per the Sarnat and Sarnat staging and a pathological baseline cranial ultrasound were independent predictors of mortality at discharge. Patients with SHCN at discharge showed a normalized tracing in the amplitude-integrated electroencephalography performed later. The most common finding in the magnetic resonance imaging was basal ganglia involvement. No statistically significant differences were observed in terms of clinical characteristics or complications among patients who received erythropoietin.

Structural and functional brain markers of cognitive impairment in healthcare workers following mild SARS-CoV-2 infection during the original stream.

Severe acute respiratory syndrome coronavirus 2 infection often involves the nervous system, leading to cognitive dysfunctions, fatigue and many other neurological signs that are becoming increasingly recognized. Despite mild forms of the disease accounting for most cases worldwide, research on the pathophysiology driving mild coronavirus disease 2019 (COVID-19) has received little attention. In this respect, recent evidence has pointed out that around 30-40% of non-critical, mild-to-moderate severity COVID-19 survivors may display cognitive disturbances several months post-illness. Hence, the impact of COVID-19 on the brain structure and function, through potential neuropathological mechanisms underpinning cognitive alterations in post-mild COVID-19 infections, remains largely unexplored. This retrospective multicentre observational cohort study, entirely based on a healthcare worker sample (n = 65; 55% females, aged 21-61), investigated the cognitive status and the structural and functional brain integrity among non-hospitalized individuals who developed mild COVID-19 symptoms during the occurrence of severe acute respiratory syndrome coronavirus 2 variants Alpha to Delta, compared with healthy controls tested before the pandemic onset. All evaluations were performed at an average of 9-month follow-up post-infection period. Participants completed a comprehensive neuropsychological assessment and structural and functional MRI exams. Radiological inspection sought to detect the presence of white matter hyperintensities on axial fluid-attenuated inversion recovery images. Global and regional grey matter integrity assessment, analysing changes in grey matter volumes and cortical thinning, and functional connectivity alterations of resting-state brain networks were also conducted. Regression analyses tested the relationships between the presence of specific cognitive impairments and potential structural and functional brain findings. Our results revealed that clinical, cognitive screening and neuropsychological examinations were average between both groups, except for specific impairments related to executive functions in the mild COVID-19. Compared to healthy controls, mild COVID-19 subjects exhibited increased juxtacortical white matter hyperintensities, thalamic and occipital volume loss and diminished resting-state functional connectivity involving the left precuneus and cuneus in default-mode network and affecting the right angular gyrus and left precuneus in the dorsal attentional network. Reduced thalamic volume was the only variable selected in the final model explaining the observed executive function impairment in mild COVID-19. The presence of cognitive, structural and functional brain abnormalities over time suggests that the action of widespread neurovascular and inflammatory phenomena on the nervous system might also occur in mild forms following COVID-19 infection rather than permanent brain damage linked to the direct or indirect action of the virus. Our findings emphasize the need to pay attention to the long-term brain-related consequences of mild COVID-19 infections during the original stream.

Seropositivity to louping ill virus in dogs in the UK.

Louping ill virus (LIV) is a tick-borne flavivirus that can cause fatal meningoencephalomyelitis in dogs. Four dogs with confirmed LIV infection and a case series of dogs with suspected flavivirus infection have been reported in the UK. However, underreporting of LIV infection due to lack of testing is suspected. Surplus serum/plasma from 220 dogs was used to determine the seroprevalence of LIV by haemagglutination inhibition (HAI) test. Signalment and environmental factors were investigated for potential correlations with a positive titre (serum dilution of 1:20 or more). Two hundred and two dogs were suitable for inclusion in the study, nine of which (4.5%) were seropositive. Among the dogs investigated for neurological disease (40/202; 19.8%), six (15%) were seropositive. Ectoparasiticide use approached significance (p = 0.055) for being protective against LIV seropositivity. The main limitations were the specificity of the HAI test, the relatively small number of samples, the low number of seropositive dogs, the poor geographical distribution of the samples and the inherent limitations of questionnaire-based research. The seroprevalence of LIV in the UK dog population appears to be low. However, LIV should be considered in dogs presenting with unexplained acute or subacute progressive neurological clinical signs, especially because of the recent reports of several dogs with clinical flavivirus infections.

Cerebral Sinus Venous Thrombosis in Pediatric Acute Lymphoblastic Leukemia: Incidence, Clinical Characteristics, and Long-term Neurologic Outcomes.

To describe the incidence, clinical characteristics, and long-term outcomes of cerebral sinus venous thrombosis in children with acute lymphoblastic leukemia. This was a retrospective cohort study comprising pediatric patients with newly diagnosed or first-relapse acute lymphoblastic leukemia who developed cerebral sinus venous thrombosis at Texas Children's Hospital from 2002 to 2019. Nineteen cases (1.7%) with cerebral sinus venous thrombosis were identified in all pediatric patients with acute lymphoblastic leukemia (n = 1129). Increased risk of cerebral sinus venous thrombosis was observed with age >10 years (P = .006). Twelve cases (63%) occurred during the induction, 4 (21%) during maintenance, and 3 (16%) during the consolidation phases of leukemia therapy. Seizures (10/19) and headaches (9/19) were the most common presenting symptoms. After treatment with anticoagulation therapy, we observed full resolution of thrombosis in 10 (53%) and partial resolution in 8 patients (42%). Long-term neurologic outcomes at follow-up in the 14 patients who survived included normal neurologic examinations (n = 10), epilepsy (n = 3), and focal neurologic deficits (n = 2). The death occurred in 5 individuals. Cerebral sinus venous thrombosis is a notable complication of pediatric acute lymphoblastic leukemia therapy. Older age (>10 years) was a risk factor for developing cerebral sinus venous thrombosis. Despite variable patient presentations and treatment durations, favorable clinical outcomes were observed in most patients after the treatment with anticoagulation for a minimum of 3 months.

Clinical features, hemorrhage risk and epilepsy outcomes of familial cerebral cavernous malformation: A 20-year observational pragmatic single-center study

IntroductionFamilial Cerebral Cavernous Malformations (fCCMs) are rare, hereditary conditions characterized by multiple central nervous system lesions. Despite their rarity, CCMs can cause significant clinical challenges when symptomatic, manifesting as seizure and symptomatic hemorrhage (CASH). Guidelines suggest neurosurgical intervention for symptomatic or previously symptomatic lesions, while conservative management is recommended for new-onset epilepsy. However, the natural history and optimal management remain unclear, necessitating further research. ObjectiveThis study aims to provide a comprehensive analysis of the clinical features, hemorrhage risk, and epilepsy outcomes in fCCM patients over an extended follow-up period, offering a more precise estimate of CASH and epilepsy rates in this population. MethodsThis retrospective longitudinal cohort study included fCCM patients enrolled from 2001 to May 2024. Data collected included demographic information, new neurological symptoms, symptomatic hemorrhages, seizures, and modified Rankin Scale (mRS) scores. Incidence rates of first symptomatic events and Kaplan-Meier survival curves were calculated, with logistic and Cox-proportional hazard regression models used to evaluate outcomes. ResultsA total of 47 patients were included in this study, with a mean age at diagnosis of 37.51 years. At diagnosis, 68 % were symptomatic, with 30 % having CASH and 36 % experiencing seizures without CASH. During a median follow-up of 126.0 months (interquartile range, 110.5 months), 17 % had a new CASH event, 20 % had seizures without CASH, and 60 % remained asymptomatic. The bleeding rate was 1.02 % per patient-year, with new focal neurological symptoms at 2.045 per 1000 patient-years and new CASH at 10.225 per 1000 patient-years. Most patients maintained minimal or no disability (mRS 0 or 1). Presenting with epilepsy at baseline significantly increased the odds of future seizures (OR 18.13, p = 0.001). ConclusionThis study highlights the complex presentation and progression of fCCMs, emphasizing the necessity for long-term monitoring. Baseline epilepsy is a significant predictor of future seizures, underscoring the need for individualized management strategies. Future research with larger cohorts and standardized criteria is essential to refine the understanding and management of fCCMs.