ABSTRACTBackgroundTo investigate the relevance of hyperperfusion on computerised perfusion imaging (CTP) in the emergency setting in people with non‐convulsive status epilepticus (NCSE) and previous stroke, to derive relevant aspects on the epileptogenic focus and the network recruited for NCSE propagation.MethodsWe enrolled consecutive adult patients with acute‐onset NCSE and a previous stroke at a single institution undergoing CTP and EEG during symptoms. All patients underwent standard imaging including CT, CTP, CT angiograms and standard EEG within 30 min from hospital arrival. Age‐/sex‐matched NCSE without previous stroke cases and recurrent ischaemic stroke cases were included to test for accuracy of hyperperfusion rates.ResultsOverall, 15 patients had a previous stroke and developed NCSE (mean age 78 years, 46.7% female). All patients had hyperperfusion on CTP imaging (mean onset‐to‐CTP 184 min). Only one case showed hyperperfusion limited to the previous stroke lesion, and one had a combination of lesional and peri‐lesional hyperperfusion. All remaining cases (n = 13) had exclusive extra‐lesional involvement. Five cases had multiple separated hyperperfused areas, and five had ipsilateral intra‐thalamic hyperperfusion. No correlation emerged between onset‐to‐CTP timing and hyperperfusion (p value for CTP = 0.66, CBV = 0.28, MTT = 0.28, reverse Tmax = 0.66). Hyperperfusion was present in NCSE cases only and in none of age‐/sex‐matched ischaemic stroke cases (n = 18).ConclusionsHyperperfusion involves cortical areas external to the previous lesion site during NCSE, supporting the relevance of networks for the spatial evolution of epileptic activity and limited relevance of the lesion site for the propagation of the epileptiform activity.

BackgroundNon-convulsive status epilepticus (NCSE) is a time-dependent neurological disorder often misdiagnosed in the emergency setting. Electroencephalography (EEG) is often not available on a 24/7 basis, and Salzburg criteria may at times miss the diagnosis. Here, we tested the accuracy of hyperperfusion on CT perfusion imaging (CTP) in the identification of NCSE against Salzburg criteria, to define its potential role in a pragmatic diagnostic workflow.MethodsWe enrolled consecutive patients with suspected acute seizure or seizure disorder undergoing brain imaging with CTP and EEG from January 2021 to March 2023. EEG recordings, Salzburg criteria and CTP hyperperfusion were rated and adjudicated by two independent experts blinded to patient status. A reference standard including all clinical, lab, imaging, EEG and therapeutic data was used to adjudicate NCSE diagnosis. Sensitivity, specificity, diagnostic accuracy, positive and negative predictive values (NPV) were calculated for CTP hyperperfusion and Salzburg criteria versus NCSE adjudicated according to reference standard.ResultsSeventy-seven patients were enrolled. Among 21 NCSE cases, 17 were adjudicated according to Salzburg criteria (81%) and 4 received NCSE diagnosis according to reference standard. Agreement between EEG and CTP emerged in 16/21 NCSE cases, reaching sublobar level in 37.5% of cases. Receiver operator curve analysis suggested good accuracy for CTP hyperperfusion for the diagnosis of NCSE (AUROC 0.79, 95% CI 0.69 to 0.89). CTP hyperperfusion had a high NPV for NCSE (NPV 0.97, 95% CI 0.86 to 1).ConclusionCTP hyperperfusion may be implemented in the emergency fast-track to rule out NCSE, given very high NPV. Further validation studies are needed to evaluate CTP application in real-world setting for NCSE codes.

Background: Symptomatic intracerebral hemorrhage (sICH) and major bleeding can be fatal complications of intravenous thrombolysis (IVT) for acute ischemic stroke. We investigated the impact of early fibrinogen depletion after IVT on major bleeding events. Methods: This multicenter observational prospective cohort study enrolled 1678 consecutive patients receiving IVT for acute ischemic stroke at 6 Italian centers, undergoing fibrinogen concentration assessment at baseline, 2 hours and 6 hours after IVT. Fibrinogen depletion was defined as a reduction below 200 mg/dL after 2 hours from IVT, or as a reduction below 50% of baseline fibrinogen levels after 2 hours from IVT. Main outcomes were (1) sICH (National Institute of Neurological Disorders and Stroke criteria) and (2) major bleeding defined as fatal bleeding, decrease in the hemoglobin level>2 g/dL/>1 unit transfusion, or bleeding at critical site. Additional outcomes were (1) any ICH, (2) any bleeding, (3) fatal ICH, and (4) sICH according to ECASSII definition. Good functional recovery was defined as modified Rankin Scale score 0 to 2 at 3 months. Results: Overall, 1678 patients were included (mean age 72 years, 46% female). sICH (n=116) and major bleeding (n=297) were associated with lower rate of good functional recovery (P<0.001). Despite similar fibrinogen levels at admission, fibrinogen depletion after 2 hours from IVT was more common in people with sICH, major bleeding and all additional bleeding outcomes. In the backward stepwise multivariable logistic regression model, fibrinogen depletion remained a significant predictor of sICH (OR, 1.55 [95% CI, 1.04–2.32]) and major bleeding (OR, 1.36 [95% CI, 1.03–1.8]). Thirty-one percent of sICH could be attributable to fibrinogen depletion. The association between fibrinogen depletion and worse clinical outcome at 3 months after stroke (P=0.012) was attributable to the higher risk of major bleeding/sICH. Conclusions: Fibrinogen depletion significantly increases the risk of sICH and major bleeding after IVT for acute ischemic stroke. Fibrinogen depletion represents an independent risk factor for bleeding, and routine assessment could be considered to stratify the risk of ICH. Trials on early fibrinogen repletion are needed to investigate mitigation of bleeding risk.

Objective Nonconvulsive status epilepticus (NCSE) is misdiagnosed in >50% of cases in the emergency department. Computed tomographic perfusion (CTP) has been implemented in the hyperacute setting to detect seizure-induced hyperperfusion. However, the diagnostic value of CTP is limited by the lack of thresholds for hyperperfusion and high interrater variability. This pilot case-control study aims at identifying the diagnostic value of reverse Tmax (rTmax) in differentiating NCSE from acute ischemic stroke in the hyperacute setting. Methods We enrolled patients with NCSE (Salzburg criteria-based diagnosis) and stroke cases 1:1 matched for clinical features and time of presentation. CTP standard maps (mean transit time [MTT]-cerebral blood volume-cerebral blood flow [CBF]) and rTmax maps were elaborated and rated by two experts in CTP blinded to the final diagnosis. Hyperperfusion was adjudicated for standard CTP maps as an increase in CBF and a decrease in MTT, and for rTmax as the presence of a black area on 3-, 2-, and 1-s threshold maps. Cronbach alpha was used for interrater agreement; receiver operating curve analysis was run to measure accuracy with area under the curve. Results Overall, 34 patients were included (17 NCSE, 17 stroke; time from onset to imaging = 2 h for both groups). People with NCSE were older and more frequently had a history of epilepsy. NCSE patients had hyperperfusion on rTmax maps in 11 of 17 cases versus zero of 17 in stroke. Intra- and interrater reliability was higher for rTmax than for standard CTP maps (kappa = 1 vs. kappa = .6). rTmax was 82% (95%CI = 67-97%) accurate in predicting NCSE versus stroke in the hyperacute setting. Agreement between neuroimaging and electroencephalography (EEG) was limited at a hemispheric level for standard CTP maps, whereas rTMax had agreement with EEG largely reaching the sublobar level. Significance rTmax mapping might represent a reliable tool to spot NCSE-induced hyperperfusion with a threshold-based reproducible approach. Further studies are needed for validation and implementation in the differential diagnosis of focal neurological deficit in the hyperacute setting.

Autoimmune encephalitis (AE) associated to antibodies against GABA A R is a rare form of encephalitis. On the other hand, thymoma has been linked to antibodies against both muscular and neuronal epitopes, even if concurrent positivity for more than one antibody is exceptional, and their contribution to the clinical course and treatment decision is unclear. We report a case of a 73-year-old male with AE associated with thymoma secreting both anti-GABAaR and anti-titin antibodies. Clinical presentation included status epilepticus, behavioural changes and cognitive decline. While the status was stopped with lacosamide, AE treatment included first- and second-line immunomodulation, in addition to thymoma's removal. Nonetheless, the patient experienced a worsening in cognitive and behavioural status.

We present a patient with recurrent attacks resembling epileptic seizures but ultimately shown to be life-threatening insulinoma-related hypoglycemic attacks.

Incidence of neuroepithelial Primary Brain Tumors (nPBT) varies, ranging from 7.3 to 11.6 cases/100,000/year across Europe. We present incidence and survival of nPBT in the Emilia-Romagna region (ER), Italy. This study is the largest in Southern Europe. Specialists in neurosurgery, neurology, neuroradiology, oncology, radiotherapy, genetics, and pathology of ER notified all suspected nPBT adult cases residing in ER (4,337,966 inhabitants) observed during 2009. Furthermore, through ICD-9 discharge codes, we identified and reviewed all possible cases. Neuroepithelial PBT diagnosis was based on histological or radiological findings. We included 400 incident nPBT cases, of which 102 (25%) were retrospectively identified. These latter were significantly older. The standardized incidence was 10.5/100,000/year (95% CI 9.4–11.5), higher for men. It was 9.2/100,000/year (95% CI 8.3–10.2) for astrocytic tumors, 0.6/100,000/year (95% CI 0.4–0.9) for oligodendroglial tumors, and 7.1 (95% CI 6.3–8.0) for glioblastoma (GBM). Among GBM patients, median survival was 249 days if prospectively identified vs. 132 days when identified through ICD-9 codes (p < 0.0001). The incidence of nPBT in the ER region is among the highest in the literature. Older patients were more likely to escape an active surveillance system. This should be considered when comparing incidence rates across studies, giving the increasing number of elderly people in the general population.

A missense mutation in ATP2A1 gene, encoding sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA1) protein, causes Chianina cattle congenital pseudomyotonia, an exercise-induced impairment of muscle relaxation. Skeletal muscles of affected cattle are characterized by a selective reduction of SERCA1 in sarcoplasmic reticulum membranes. In this study, we provide evidence that the ubiquitin proteasome system is involved in the reduced density of mutated SERCA1. The treatment with MG132, an inhibitor of ubiquitin proteasome system, rescues the expression level and membrane localization of the SERCA1 mutant in a heterologous cellular model. Cells co-transfected with the Ca(2+)-sensitive probe aequorin show that the rescued SERCA1 mutant exhibits the same ability of wild type to maintain Ca(2+) homeostasis within cells. These data have been confirmed by those obtained ex vivo on adult skeletal muscle fibers from a biopsy from a pseudomyotonia-affected subject. Our data show that the mutation generates a protein most likely corrupted in proper folding but not in catalytic activity. Rescue of mutated SERCA1 to sarcoplasmic reticulum membrane can re-establish resting cytosolic Ca(2+) concentration and prevent the appearance of pathological signs of cattle pseudomyotonia.

Elisa Bianchini, Stefania Testoni, Arcangelo Gentile, Tito Calì , Denis Ottolini , Antonello Villa**, Marisa Brini , Romeo Betto, Francesco Mascarello, Poul Nissen, Dorianna Sandonà, and Roberta Sacchetto From the Departments of Biomedical Sciences and Biology, University of Padova, 35131 Padova, Italy, the Departments of Animal Medicine Production and Health and Comparative Biomedicine and Food Science, University of Padova,35020 Legnaro (Padova), Italy, the Department of Veterinary Medical Sciences, University of Bologna, 40064 Bologna, Italy, the **Consorzio M.I.A., University of Milano Bicocca, 20900 Monza, Italy, the Neuroscience Institute, Consiglio Nazionale delle Ricerche Padova, 35131 Padova, Italy, and the Department of Molecular Biology and Genetics, Centre for Membrane Pumps in Cells and Disease, Aarhus University, 8000 Aarhus, Denmark

Veterinary RecordVolume 170, Issue 1 p. 22-22 Research Renal dysplasia in grey Alpine breed cattle unrelated to CLDN16 mutations S. Testoni DVM, PhD, Corresponding Author S. Testoni DVM, PhD stefania.testoni@unipd.it Department of Veterinary Clinical Sciences, University of Padua, Via Dell'Università 16, 35020 Legnaro (Padua), ItalyE-mail for correspondence stefania.testoni@unipd.itSearch for more papers by this authorS. Mazzariol DVM, S. Mazzariol DVM Department of Public Health, Comparative Pathology and Veterinary Hygiene, University of Padua, Via Dell'università 16, 35020 Legnaro (Padua), ItalySearch for more papers by this authorC. Drögemüller DVM, PhD, C. Drögemüller DVM, PhD Institute of Genetics, Vetsuisse Faculty, University of Berne, Bremgartenstr, 109a, 3001, Bern, SwitzerlandSearch for more papers by this authorC. Piffer DVM, C. Piffer DVM Veterinary Services of Bolzano, Health Department of South Tyrol, Via Laura Conti 4, 39100 Bolzano, ItalySearch for more papers by this authorL. Aresu DVM, L. Aresu DVM Department of Public Health, Comparative Pathology and Veterinary Hygiene, University of Padua, Via Dell'università 16, 35020 Legnaro (Padua), ItalySearch for more papers by this authorA. Gentile DVM, DipECBHM, A. Gentile DVM, DipECBHM Department of Veterinary Medical Sciences, University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia (Bologna), ItalySearch for more papers by this author S. Testoni DVM, PhD, Corresponding Author S. Testoni DVM, PhD stefania.testoni@unipd.it Department of Veterinary Clinical Sciences, University of Padua, Via Dell'Università 16, 35020 Legnaro (Padua), ItalyE-mail for correspondence stefania.testoni@unipd.itSearch for more papers by this authorS. Mazzariol DVM, S. Mazzariol DVM Department of Public Health, Comparative Pathology and Veterinary Hygiene, University of Padua, Via Dell'università 16, 35020 Legnaro (Padua), ItalySearch for more papers by this authorC. Drögemüller DVM, PhD, C. Drögemüller DVM, PhD Institute of Genetics, Vetsuisse Faculty, University of Berne, Bremgartenstr, 109a, 3001, Bern, SwitzerlandSearch for more papers by this authorC. Piffer DVM, C. Piffer DVM Veterinary Services of Bolzano, Health Department of South Tyrol, Via Laura Conti 4, 39100 Bolzano, ItalySearch for more papers by this authorL. Aresu DVM, L. Aresu DVM Department of Public Health, Comparative Pathology and Veterinary Hygiene, University of Padua, Via Dell'università 16, 35020 Legnaro (Padua), ItalySearch for more papers by this authorA. Gentile DVM, DipECBHM, A. Gentile DVM, DipECBHM Department of Veterinary Medical Sciences, University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia (Bologna), ItalySearch for more papers by this author First published: 07 January 2012 https://doi.org/10.1136/vr.100209Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume170, Issue1January 2012Pages 22-22 RelatedInformation

Tendon injuries, degenerative tendinopathies, and overuse tendinitis are common in races horses. Novel therapies aim to restore tendon functionality by means of cell‐based therapy, growth factor delivery, and tissue engineering approaches. This study examined the use of autologous mesenchymal stromal cells derived from peripheral blood (PB‐MSCs), platelet‐rich plasma (PRP) and a combination of both for ameliorating experimental lesions on deep digital flexor tendons (DDFT) of Bergamasca sheep. In particular, testing the combination of blood‐derived MSCs and PRP in an experimental animal model represents one of the few studies exploring a putative synergistic action of these treatments. Effectiveness of treatments was evaluated at 30 and 120 days comparing clinical, ultrasonographic, and histological features together with immunohistochemical expression of collagen types 1 and 3, and cartilage oligomeric matrix protein (COMP). Significant differences were found between treated groups and their corresponding controls (placebo) regarding tendon morphology and extracellular matrix (ECM) composition. However, our results indicate that the combined use of PRP and MSCs did not produce an additive or synergistic regenerative response and highlighted the predominant effect of MSCs on tendon healing, enhanced tissue remodeling and improved structural organization. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 306–314, 2013

Bovine congenital pseudomyotonia (PMT) is a genetic disease in Chianina and other breeds of cattle that induces muscular stiffness. PMT in the Chianina breed is caused by a missense mutation in exon 6 of the ATP2A1 gene, which encodes the SERCA1 pump. In this study, the prevalence of PMT carriers and the frequency of the deleterious PMT allele in selected subpopulations of the Chianina breed were estimated. The prevalence of PMT carriers among ranked Chianina sires used for artificial insemination in the years 2007-2011 was 13.6%. The frequency of PMT carriers in young bull calves born in the period January 2007 to June 2011 selected for a performance testing programme was 13.4%. Selective breeding against this genetic defect is restricted to males only and therefore is predicted to require at least seven generations to eradicate PMT.

In the last decade breeders of Romagnola cattle observed an outbreak of a new congenital anomaly. This lethal multi-organ developmental dysplasia is mainly characterized by facial deformities, ascites and hepatic fibrosis. Affected stillborn calves were inbred to a single founder sire suggesting autosomal monogenic recessive inheritance. We localized the causative mutation to a 1.2 Mb interval on BTA 17 by genome-wide association and identical by descent mapping. A solution-based method for targeted DNA capture combined with massively parallel sequencing was used to analyze the entire critical region containing 24 genes. Homozygosity for two non-synonymous coding sequence variants affecting the RNF34 and KDM2B genes was detected by evaluating one affected calf. Here we show that the disease phenotype is associated with a KDM2B missense mutation (c.2503G>A) leading to an amino acid exchange (p.D835N) in an evolutionary strongly conserved domain. In addition, the genetic makeup of three inbred cattle strongly supports the causality of the KDM2B mutation. This report of a naturally-occurring spontaneous mutation of a JmjC domain containing histone demethylase gene provides evidence for their important role in the endo- and mesodermal organ development.

BACKGROUND:Bovine congenital pseudomyotonia (PMT) is an impairment of muscle relaxation induced by exercise preventing animals from performing rapid movements. Forms of recessively inherited PMT have been described in different cattle breeds caused by two independent mutations in ATP2A1 encoding a skeletal-muscle Ca2+-ATPase (SERCA1). We observed symptoms of congenital PMT in four related Romagnola beef cattle from Italy and evaluated SERCA1 activity and scanned ATP2A1 for possible causative mutations.RESULTS:We obtained four PMT affected Romagnola cattle and noted striking clinical similarities to the previously described PMT cases in other cattle breeds. The affected animals had a reduced SERCA1 activity in the sarcoplasmic reticulum. A single affected animal was homozygous for a novel complex variant in ATP2A1 exon 8 (c.[632 G>T; 857 G>T]). Three out of four cases were compound heterozygous for the newly identified exon 8 variant and the exon 6 variant c.491 G>A(p. Arg146Gly), which has previously been shown to cause PMT in Chianina cattle. Pedigree analysis showed that the exon 8 double mutation event dates back to at least 1978. Both nucleotide substitutions are predicted to alter the SERCA1 amino acid sequence (p.[(Gly211Val; Gly284Val)]), affect highly conserved residues, in particular the actuator domain of SERCA1.CONCLUSION:Clinical, biochemical and DNA analyses confirmed the initial hypothesis. We provide functional and genetic evidence that one novel and one previously described ATP2A1 mutation lead to a reduced SERCA1 activity in skeletal muscles and pseudomyotonia in affected Romagnola cattle. Selection against these mutations can now be used to eliminate the mutant alleles from the Romagnola breed.

A 4-day-old, 33-kg female Holstein calf had not been able to stand since birth. The delivery, which was without complications, involved a primiparous dam. On general physical examination, the calf appeared bright, alert, and had a normal appetite. The calf was in sternal recumbency with the hind limbs stiffly extended laterally and the forelimbs normally positioned underneath. Despite repeated attempts, it was unable to stand up. If passively positioned in a quadrupedal stance, the calf immediately fell down. The muscles were atrophic. Clinical examination of the respiratory and cardiovascular systems did not identify abnormalities that could explain the calf's inability to assume or maintain a quadrupedal stance. A thorough neurological examination was carried out. Because of recumbency, postural reactions could not be tested. A delayed withdrawal reflex and absence of the patellar reflex were found in the pelvic limbs. The reflexes and musculature in the thoracic limbs were normal. There were voluntary tail movements, a normal perineal reflex, and normal anal tone. There were no signs of pain upon palpation of the vertebrae. Examination of the cranial nerves was normal. On the basis of the clinical and neurologic findings, the diagnosis was a paraparetic syndrome ascribed to a spinal lesion localized between the T3-S2 segments. Inflammatory processes of the spinal cord were excluded on the basis of normal cerebrospinal fluid obtained from the lumbosacral space. BVD virus and Neospora caninum-induced malformation were excluded owing to the absence of the relevant antibodies. A tentative diagnosis of myelodysplasia at the level of the T3-S2 spinal cord segments was made. No additional diagnostic conclusions were possible regarding different types of myelodysplasia, such as diastenomyelia/diplomyelia complex (duplication of the gray matter at ≥1 segments), rachischisis (incomplete closure of the neural tube, with the central canal remaining open and communicating with the integument), meningocele (herniation of the dura matter through a spinal column defect), hydromyelia (dilatation of the central canal), syringomyelia (longitudinal cavitations of the spinal cord parenchyma), and hypoplasia (anomalous development of ≥ 1 segments of the spinal cord).1, 2 Ultrasonography of the spinal cord was performed. The calf was placed in right lateral recumbency. No sedation was necessary. Only slight restraint was used to flex the pelvic girdle and the lumbosacral spine so as to enlarge the space between the vertebral arches for wider acoustic windows. Ultrasonographic examination was performed in sagittal and transverse orientations through the lumbosacral junction (L6-S1) as well as through more cranial lumbar intervertebral junctions (L5-L6, L4-L5, L3-L4, L2-L3). A 6–10 MHz linear 4-cm transducer1 was used. Ultrasonographic pathologic findings were observed only at the level of the L4-L5 and L3-L4 intervertebral junctions, whereas the L6-S1, L5-L6 and L2-L3 acoustic windows showed normal images of the spinal cord. At the level of the L6-S1 acoustic window, in the sagittal orientation, the spinal cord appeared as a thin hypoechoic conus, 0.47 cm in thickness, with hyperechoic margins referable to the pia mater, and a central hyperechoic single line referable to the central canal. An anechoic cerebrospinal fluid-filled subarachnoid space and a hyperechoic dura-arachnoid layer were evident dorsally and ventrally to the spinal cord. In the transverse orientation, the conus medullaris was round with a diameter of 0.47 cm; hyperechoic margins and a central hyperechoic dot also were visible, and again referable to the pia mater and the central canal, respectively. The spinal cord was surrounded centrifugally by an anechoic cerebrospinal fluid-filled subarachnoid space, and a hyperechoic dura-arachnoid layer. Two large hyperechoic nerve roots were evident, emerging symmetrically dorso-laterally and ventro-laterally. The aforementioned images were compatible with the normal features of the conus medullaris.3 At the level of the L5-L6 acoustic window, in the sagittal orientation, the spinal cord appeared as hypoechoic tube 0.90 cm in thickness, with hyperechoic margins (pia mater) and a central hyperechoic single line (central canal). An anechoic cerebrospinal fluid-filled subarachnoid space, and the hyperechoic dura-arachnoid layer were evident dorsally and ventrally to the spinal cord. In the transverse orientation, the spinal cord was ellipsoid (0.90 × 1.25 cm) with hyperechoic margins and a central hyperechoic dot. An anechoic cerebrospinal fluid-filled subarachnoid space, a hyperechoic dura-arachnoid layer, as well as the emergence of the hyperechoic dorsal and ventral nerve roots were visible as well. The findings were compatible with a normal lumbosacral intumescence, as confirmed by images obtained from a 7-day-old healthy Holstein calf (Fig 1). Contrary with what has been described above with respect to the L6-S1 and L5-L6 intervertebral junctions, the L4-L5 acoustic window, which also was expected to be consistent with the lumbosacral intumescence, generated abnormal images. In particular, in the sagittal orientation, the spinal cord had a sudden reduction in thickness, appearing as a small hypoechoic tube 0.38 cm in thickness with hyperechoic margins (pia mater), but without the hyperechoic line of the central canal (Fig 2). In the transverse orientation, it appeared round and measured 0.40 cm with partial hyperechoic margins, but without evidence of a central hyperechoic dot, as expected. Dorsal and ventral nerve roots also were not evident. The L3-L4 acoustic window also indicated abnormal spinal cord features, but these were different from those described above. In fact, in the sagittal orientation, the spinal cord with its hyperechoic margins (compatible with the pia mater) regained the expected thickness, 1.0 cm, but showed a splitting of the central line into 2 hyperechoic lines, delimiting an anechoic space 0.30 cm in width (Fig 3), referable to a dilatation of the central canal (hydromyelia). In the transverse orientation, the spinal cord appeared ellipsoid (1.00 × 1.46 cm) with hyperechoic margins and, similar to what was observed in the sagittal orientation, a hypoechoic lumen confirmed the dilatation of the central canal, which measured 0.30–0.40 cm in diameter. The dorsal and ventral nerve roots were not evident. The L2-L3 acoustic window, in both the sagittal and the transverse orientations, again showed the characteristic features of a normal spinal cord. Therefore, the ultrasound findings localized at the L4-L5 and L3-L4 junctions were consistent with a diagnosis of lumbar hypoplasia (L4-L5 junction) and syringohydromyelia (L3-L4 junction) of the spinal cord. The calf was euthanized because of the poor prognosis, and a postmortem examination was carried out. The vertebral column, including the lumbar vertebrae, was normal. On the contrary, the segments of the spinal cord from L3 to L5 showed abnormal morphology. In particular, the lumbar intumescence had an hourglass appearance because of the presence of a 1.50 cm-long thinning at the level of the L4-L5 segment, up to 0.30 cm in diameter (Fig 4). Moreover, the segment of the spinal cord between L3 and L4 showed a fluctuation upon palpation. At this level, sagittal sectioning disclosed a fluid-containing 1.50 cm-long, 0.30 cm-wide, spindle-shaped cavity. Histological examination of the spinal cord at the level of the above-mentioned lesion (L3-L4) showed an optically empty cavitary lesion in the medial part of the gray matter. The cavity was lined by ependymal cells only in its ventral and caudal parts. The surrounding neuroparenchyma had architectural alterations caused by compression exerted by the above-mentioned space-occupying lesion. Blood vessels of the nervous tissue and meninges were congested. A progressive reduction of the dorsal column system, together with neuronal hypoplasia, gliosis, and an increased number of blood vessels, was evident caudal to the cyst. Moreover, there was a loss of the anatomical structure of the gray matter, which ended abruptly at a distance of 1.5 cm from the caudal blind sac of the cavity (L4-L5). More distally, the spinal cord contained only myelinic nerve fibers. The final diagnosis was syringohydromyelia associated with segmental hypoplasia of the lumbar spinal cord. Syringohydromyelia and segmental hypoplasia are 2 developmental disorders of the spinal cord rarely diagnosed in living calves. Myelography, MRI, or both are considered essential for diagnosing such conditions, but neither is readily available to bovine practitioners. This study showed that ultrasonography (an ancillary diagnostic technique that has been gaining wider use in bovine veterinary practice) is able to detect such congenital anomalies in living calves. Hydromyelia and syringomyelia constitute a complex of spinal cord abnormalities characterized by the presence of fluid-filled cysts. In particular, hydromyelia is a simple distension of the central canal, with the accumulation of cerebrospinal fluid. Therefore, it is lined by ependymal cells. On the contrary, syringomyelia is a neoformed, usually tubular, paracentral cavitation within the neuroparenchyma (syrinx). It is lined by glial cells and contains a liquid consistent with cerebrospinal fluid.4 The all-inclusive term syringohydromyelia has been proposed because hydromyelic cavities often include a contiguous pocket of neuroparenchyma lined by glial cells and, in addition, syrinxes within the neuroparenchyma often rupture into the central canal.5 However, the term syringomyelia also is generally accepted for all clinical conditions characterized by spinal cord cavitations containing fluid identical with or closely resembling cerebrospinal fluid.6 Moreover, hydromyelia and syringomyelia may be difficult to distinguish, even after detailed histologic examination. Segmental hypoplasia of the spinal cord is a rare dysraphism caused by an anomalous development of ≥1 segments of the spinal cord, generally associated with vertebral abnormalities.7, 8 Both syringohydromyelia and spinal segmental hypoplasia, along with associated congenital or progressive neurologic symptoms, have rarely been described in cattle.9, 10 Even rarer are reports on the use of ultrasonography in cattle for assessing myelodysplasia in general.3, 11 In fact, whereas in human medicine spinal ultrasound examination constitutes the initial screening test in infants suspected of spinal dysraphism,12 in veterinary medicine, especially in bovine medicine, it still is rarely used. Moreover, in young calves, the acoustic shadowing created by the ossified dorsal vertebral elements does not create the same favorable circumstances that are present in young human infants where the posterior arch of the spine only becomes ossified beginning at 6 months of age.12 Recently, 2 ultrasound acoustic windows for spinal cord examination have been proposed for calves: 1, cervical, is the atlanto-occipital junction11 and the other, lumbar, is the lumbosacral L6-S1 intervertebral space.3 In this study, despite the ossification of the spinous elements, in addition to the lumbosacral junction L6-S1, it was possible to use other new lumbar acoustic windows, namely the more cranial intervertebral lumbar spaces. The best sonographic images were obtained at the level of the L6-S1 and L5-L6 acoustic windows. However, the acoustic windows cranial to the L5-L6 junction also offered satisfactory images, enabling the detection of spinal cord segmental hypoplasia at the L4-L5 junction and of syringohydromyelia at the L3-L4 junction. In fact, all the above-mentioned acoustic windows allowed pattern recognition, as well as the assessment of abnormalities of the spinal cord (hypoechoic structure with no discernible interface between the gray and the white matter), the central canal (well-defined linear central echo or dot – depending on the scanning plan – hyperechoic to the surrounding spinal cord parenchyma), the pia mater (thin but strongly echogenic layer enveloping the cord parenchyma), the subarachnoid space (further peripheral anechoic zone), and the dura mater together with the arachnoid layer (a prominent echogenic line representing a combination of the 2 structures, superficial to the spinal cord). Moreover, in the transverse orientation, the nerve roots were evident as 2 large hyperechoic branches emerging symmetrically dorso-laterally and ventro-laterally. With respect to the central canal, the limited amount of cerebrospinal fluid in the unaffected portions of the spinal cord did not allow the central canal to have an anechoic appearance, as might be expected for a fluid-filled structure. Although still under debate in the literature, the central cord echo was attributed to the difference in acoustic impedance between the neural tissue of the cord and the fibrous ependyma lining the canal, or to the interface between the myelinated ventral white commissure and the central portions of the anterior median fissure.13 The increased amount of fluid filling the central canal in the spinal cord tract affected by hydromelia (L3-L4) allowed recognition of an anechoic lumen within a double-lined central canal. Similar considerations can be made with respect to the transverse orientation; a single echoic dot and a hypoechoic lumen, respectively, demonstrated the scant quantity and increased quantity of cerebrospinal fluid in the normal and in the hydromelia-affected spinal cord tracts, respectively. How much cerebrospinal fluid is necessary to ultrasonographically transform the echoic image into an hypoechoic lumen might be the subject of future investigation, but, currently, to the authors' knowledge, remains unknown. The hyperechoic aspects of the pia mater (the meningeal layer adhering to the surface of the spinal cord) were very useful in sagittal orientation for depicting the narrowing of the spinal cord at the L4-L5 acoustic window. The hyperechogenicity that delimits the dorsal and ventral borders of the spinal cord is, however, attributable to not only to the pia mater itself, but also to the acoustic impedance differences between the spinal cord parenchyma and the subarachnoid fluid. Because of the presence of the acellular cerebrospinal fluid, the subarachnoid space is seen as an anechoic zone between the pia mater and the more superficial dura-arachnoid layer. The thin net-like structure of the arachnoid cannot be detected ultrasonographically as a separate structure. Because of its close contact with the inner surface of the dura mater, it is ultrasonographically included in the prominent hyperechogenic line that defines the strong and dense structure of the most superficial meninge. With respect to the execution of the technique, the examination was favored by lumbosacral flexion, which enabled widening of the ultrasound windows. Unfortunately, the particular anatomical shape of the spinous processes of the thoracic vertebrae did not allow scanning the more cranial portions of the spinal cord. In conclusion, this study showed the ultrasonographical features of 2 rare spinal cord malformations that may be underreported because of the current lack of diagnoses made on living calves. This study, therefore, definitively demonstrated that ultrasound examination can be useful ancillary diagnostic tool for assessing diseases of the spinal cord in young calves. The case was evaluated at the Department of Animal Medicine, Productions and Health, University of Padua, via dell'Università 16, 35020, Legnaro (Padua), Italy. This study received no support from grants or any other financial source. Conflict of Interest: Authors disclose no conflict of interest.