Cerebrus

Click "Search" to find an article
PHOSPHATE PRECIPITATION - keywords
phosphate precipitation r e f e r e n c e s n a v i g a t o r phosphate precipitation: references < Abuelo  DN,  Barsel-Bowers  G,  Tutschka  BG,  Ambler  M,  Singer  DB  (1981)  Symmetrical  infantile  thalamic degeneration in two sibs. J Med Genet  18:448-450.  Ambler M, O’Neill W (1975) Symmetrical infantile thalamic degeneration and focal cytoplasmic calcification. Acta Neuropathologica 33:1-8. Anderson C, Eggert L, Fitzgerald K, Jackson D, Farr F. Calcium and Phosphate Solubility Curve Equation for Determining Precipitation Limits in Compounding Parenteral Nutrition. Hosp Pharm. 2022 Dec;57(6):779-785.  Ansari MQ, Chincancham CA, Armstrong DL (1990) Brain calcification in hypoxic-ischemic lesions: an autopsy review. Pediatr Neurol 6:94-101.  Bekiesinska-Figatowska M, Mierzewska H, Jurkiewicz E. Basal ganglia lesions in children and adults. Eur J Radiol. 2013 May;82(5):837-49.  Boltshauser E, Steinlin M, Boesch C, Martin E, Schubiger G (1991) Magnetic resonance imaging in infantile encephalopathy with cerebral calcification and leukodystrophy. Neuropediatrics 22:33-35. Chen SY, Ho CJ, Lu YT, Lin CH, Lan MY, Tsai MH. The Genetics of Primary Familial Brain Calcification: A Literature Review. Int J Mol Sci. 2023 Jun 29;24(13):10886. Cheng X, Zhao M, Chen L. Astrocytes modulate brain phosphate homeostasis via polarized distribution of phosphate uptake transporter PiT2 and exporter XPR1. Neuron 2024; 112, 3126-3142.e8 Dykes FD, Ahmann PA, Lazzarra A (1982) Cranial ultrasound in the detection of intracranial calcification. J Pediatrics 100:406-408. Embleton ND, van den Akker CHP, Johnson M (2025) Parenteral nutrition for preterm infants: benefits and risks in 2025. Seminars in Fetal and Neonatal Medicine, Volume 30, Issue 2. Grant EG, Williams AL, Schellinger D, Slovis TL (1985) Intracranial calcification in the infant and neonate : evaluation by sonography and CT. Radiology 157:63-68. Hutchinson M, O’Riordan J, Javed M (1995) Familial hemiplegic migraine and autosomal dominant arteriopathy with leukoencephalopathy (CADASIL). Ann Neurol 38:817–824. Illum N, Reske-Nielsen E, Skovby F, Askjaer SA, Bernsen A (1988) Lethal autosomal recessive arthrogryphosis multiplex congenita with whistling face and calcifications of the nervous system. Neuropediatrics 19:186-192. Kalyanasundaram S, Dutta S, Narang A, Katariya S (2002) Microcephaly with plate-like cortical calcification. Brain Dev 25:130–132. Knowles JB, Cusson G, Smith M, Sitrin MD. Pulmonary deposition of calcium phosphate crystals as a complication of home total parenteral nutrition. JPEN J Parenter Enteral Nutr. 1989 Mar-Apr;13(2):209-13.  Livingston JH, Mayer J, Jenkinson E, Kasher P, Stivaros S, Berger A, Cordelli DM, Ferreira P, Jefferson R, Kutschke G, Lundberg S, Ounap K, Prabhakar P, Soh C, Stewart H, Stone J, van der Knaap MS, van Esch H, van Mol C, Wakeling E, Whitney A, Rice GI, Crow YJ. Leukoencephalopathy with calcifications and cysts: a purely neurological disorder distinct from coats plus. Neuropediatrics. 2014 Jun;45(3):175-82. McCartney E, Squier W (2014) Patterns and pathways of calcification in the developing brain. Dev Med Child Neurol 56(10):1009-15. Melchior JC, Benda C, Yakovlev PI (1960) Familial idiopathic cerebral calcifications in childhood. Am J Dis Child 99:787–803. Mihatsch W, Fewtrell M, Goulet O, Molgaard C, Picaud JC, Senterre T; ESPGHAN/ESPEN ESPR/CSPEN working group on pediatric parenteral nutrition. ESPGHAN/ESPEN/ESPR/CSPEN guidelines on pediatric parenteral nutrition: Calcium, phosphorus and magnesium. Clin Nutr. 2018 Dec;37(6 Pt B):2360-2365.  Nellhaus G, Haberland C, Hill BJ. Sturge-Weber disease with bilateral intracranial calcifications at birth and unusual pathologic findings. Acta Neurol Scand. 1967;43(3):314-47. Newton DW, Driscoll DF. Calcium and phosphate compatibility: revisited again. Am J Health Syst Pharm. 2008 Jan 1;65(1):73-80.  Patel PJ (1987) Some rare causes of intracranial calcification in childhood : computed tomographic findings. Eur J Pediatr 146:177-180. Perez-Fontan JJ, Herrera M, Fina A, Peguero G (1982) Periventricular calcifications in a newborn associated with aneurysm of the great vein of Galen. Pediatr Radiol 12:249-251. Ramonet D, Pugliese M, Rodríguez MJ, de Yebra L, Andrade C, Adroer R, Ribalta T, Mascort J, Mahy N. Calcium precipitation in acute and chronic brain diseases. J Physiol Paris. 2002 Apr-Jun;96(3-4):307-12. Rickert CH, Rieder H, Rehder H, Hülskamp G, Hörnig-Franz I, Louwen F, Paulus W. Neuropathology of Raine syndrome. Acta Neuropathol. 2002 Mar;103(3):281-7.  Rosales  RK,  Riggs  HE  (1962)  Symmetrical  thalamic  degeneration  in  infants.  J  Neuropath  Exp  Neurol 21:372-376.  Sabatino G, Domizio S, Verrotti A, Ramenghi LA, Pelliccia P, Morgese G (1994) Fetal encephalopathy with cerebral calcifications: a case report. Child’s Nervous System 10:195-197. Samson JF, Barth PG, de Vries JIP, Menko FH, Ruitenbeek W, van Oost BA, Jakobs C (1994) Familial mitochondrial encephalopathy with fetal ultrasonographic ventriculomegaly and intracerebral calcifications. Eur J Pediatr 153:510-516. Schell-Feith EA, Kist-van Holthe JE, van der Heijden AJ. Nephrocalcinosis in preterm neonates. Pediatr Nephrol. 2010 Feb;25(2):221-30.  Schiffmann JH, Wessel A, Bruck W, Speer CP (1992) Idiopathic infantile arterial calcinosis. A rare cardiovascular disease of uncertain etiology. Case report and a review of the literature. Monatsschr Kinderheilk 140:27-33. Shefer-Kaufman N, Mimouni FB, Stavorovsky Z, Meyer JJ, Dollberg S (1999) Incidence and clinical significance of echogenic vasculature in the basal ganglia of newborns. Am J Perinatol 16(6):315-9.  Shaw WW, Cohen WA (1993) Viral infections of the CNS in children : imaging features. Am J Roentgenol 160:125-133.  Stippel, G. (2004). Speckle Suppression, Segmentation and Registration of Medical Ultrasound Images. PhD thesis, Ghent University, Belgium.  Takashima S, Becker LE (1985) Basal ganglia calcification in Down’s syndrome. J Neurol Neurosurg Psychiatr 48:61-64. Thijssen J Oosterveld B (1990). Texture in tissue echograms: Speckle or information. Journal of Ultrasound Med, 9:215–229.  Thomas-Sohl KA, Vaslow DF, Maria BL. Sturge-Weber syndrome: a review. Pediatr Neurol. 2004 May;30(5):303-10. Vansteenkiste E (2007) Quantitative Analysis of Ultrasound Images of the Preterm Brain. PhD thesis at Gent University, dept. Telecommunication and Information Processing, Faculty of Engineering. Venkatesh S, Coulter DL, Kemper TD (1994) Neuroaxonal dystrophy at birth with hypertonia and basal ganglia mineralization. J Child Neurol 9:74-76. Voit T, Lemburg P, Neven E, Lumenta C, Stork W (1987) Damage of thalamus and basal ganglia in asphyxiated full-term neonates. Neuropediatrics 18:176-181. > speckle imaging The quality of cranial ultrasound differs per neonatal unit, because machines differ in resolution and doppler quality, and because interpretation is by variably experienced raters. Entities often described in VLBW infants are germinal matrix and intraventricular haemorrhage, white matter injury, arterial infarction, sinovenous thrombosis, germinolysis and fetal infection. This describes a new entity, cloudy precipitation of phosphate and calcium (P/Ca) specifically affecting VLBW infants and only diagnosed by targeted serial CUS, for now a pure sonographic entity. The relevance of the situation may have an impact on care in units where parenteral nutrition is provided according to guidelines, because experience suggests it is a recent abnormal finding and there seem to be no alternative explanations than fine granular precipitation of Ca with something else. Precipitation of Ca and P to particles of size similar to the brain speckles, was simulated in vitro. It is most likely that extra P injections near the tip of the line with parenteral nutrition led to precipitation and microembolism. The peculiar regional specificity (frontal white matter and thalamus) of the speckle clouds is unexplained. Either microemboli follow specific routes according to their nature and characteristics of regional brain perfusion, or the precipitation is triggered by some local brain factor encouraging P to precipitate. To turn this hypothesis into a genuine finding, postmortem confirmation is necessary. Alternatively the hypothesis can be tested in experimental settings. The potential of permanent injury to the brain (and other organs) by this event has to be considered. examples phosphate precipitation compare CMV calcification CaP precipitation in the lung of an adult, associated with chronic parenteral nutrition (Knowles et al. 1989) simulation of P precipitation  permanent other examples not on MRI lighthouse chracteristic phosphate precipitation: imaging The speckle clouds reported here have to be differentiated from dots creating the normal speckle pattern. The very nature of an ultrasound image is a collections of bright dots, organised in lines or blocks by specular reflection, organised in more or less structured speckle pattern in many areas of the brain parenchyma (Stippel 2004, Vansteenkiste 2007). The dots forming this speckle pattern are the result of constructive interference between phasors (backscattered rf-signals) that reach the sensing crystal at the same time. The distribution of the speckle peaks reveals info on the density of the scatterers, used more often in research than characterisation of individual speckle dots. A distinction is typically made between fully developed speckle, partially developed speckle and low scatter density speckle with structural components. Speckle that is formed from uniformly distributed backscattered amplitudes, reflecting of spatially uniformly distributed high density scatterers (> 10 per resolution cell), is called “fully developed” speckle.  Speckle size depends on the frequency (higher-frequency results in better spatial resolution), and the geometry of the employed transducer (linear or curvilinear) (Thijssen and Oosterveld 1990). Furthermore, attenuation by the insonated tissue yields a depth-dependent increase of mainly the lateral speckle size, in addition to the depth-dependency caused by the beam formation.  The main application of image speckle characterization is speckle reduction. Some well-known speckle reducing filters that either use the first- (of the rf signal) or second-order (of the image, about size and spatial correlations) speckle statistics are described (Stippel 2004).  This entire manipulaton, be it with Esaote machines or other, remains unaccessible to the clinical user. So comparison of speckle variation between vendors is not practical.   Preterm infants below 30 w PMA were reported on the basis of a chance detection of a specific lesion pattern in routine CUS. In the first days of life up to one scan per day can be done initially, but afterwards there is weekly follow up in VLBW infants until 34 w PMA. An infant was included in this cohort of patients when a group (cloud, usually more than 5) of very bright short linear or rounded hyperechoic cots (unusual speckles) was observed in either thalamus (9/36) or fronto-parietal white matter (35/36), in the second week after birth, standing out between normal ultrasound speckle. Speckle clouds were found in 36 VLBW infants in 10 years (2016-2025), a rough estimate suggests a prevalence of at least 8 % in that population (most likely an underestimation). In many infants the initial scan on admission or on day 2 did not reveal this speckle cloud. In some infants there were only a few bright speckles, in others the cloud was more substantial. Isolated bright speckles were not included, there had to be some grouping. There was never progression in the number of abnormal speckles during weekly serial follow-up. The speckles had to be indepentent in location of GMH/IVH (typically around the caudothalamic groove) and of gliotic leukomalacia (typically around the atrium in the subcentral area). They were very bright from the first observation and remained so throughout neonatal follow-up in all. When there were was grouping the isolated speckles remained independently visible, unlike the contiguous hyperechoic change in focal arterial infarction with thalamic perforator stroke or medullary venous infarction. Speckles were not observed in caudate (one exception), putamen or pallidum. In thalamus (9/36) they were in the central part, perfused by PCA perforator arteries, neither in ventrolateral nor anterior thalamus. Although they could be suspected with a convex probe, the most convincing images were made by use of high frequency linear transducers (Esaote MyLab twice, LA435|18 MHz). Some speckles developed a twinkling quality (“lighthouse” with hyperechoic reflections spreading in the plane perpendicular to insonation) in the absence of doppler application. There were no acoustic shadows. Unlike haemorrhagic lesions these speckles remained unchanged in the weeks after detection. We had no follow-up scans after discharge near term.  Congenital CMV was excluded in all infants by early urine testing. The clinical context of non-bacterial infection, bacterial infection, neuro-ectodermal disorders, antepartum asphyxia, vascular anomaly and venous thrombosis is sufficiently clear and was absent in all instances. Unexplained brain abnormalities in such conditions are not chance findings. The speckle clouds in our cohort bear no resemblance to tumours, and metastases were excluded by serial scanning and clinical evolution. Exceptional disorders listed also present with specific findings, absent in our patients.  Near term the MRI was accompanied by a discharge ultrasound scan [T2 turbo spin-echo images (slice thickness of 4 mm, Echo time 99 ms, repetition time 7095 ms) and three-dimensional time-of-flight (TOF, slice thickness 1.2 mm, echo time 6.8 ms, repetition time 29 ms) angiographic sequences acquired using a 1.5 T GE Signa Artist MRI scanner (General Electrics, Boston, Massachusetts, USA)] .  In direct comparisons the speckle clouds were not observed with MRI.  phosphate precipitation: description of imaging findings speckle clouds versus CMV calcification typical examples of congenital CMV Non-bacterial fetal infection (Shaw and Cohen 1993). Deposition of calcium salts around the ependyma, in places where periventricular inflammation may lead to arteritis and phlebitis accompanied by necrosis. Typical of CMV, but periventricular localisation may be noted with toxoplasmosis, rubella, herpes simplex, LCM, parvovirus, zika and varicella. Meningitis and leptomeningeal thrombophlebitis and micro-arteritis are at the basis of superficial perisulcal calcification and calcium deposits in the hypothalamic region. Peripheral (not periventricular) calcification tends to suggest toxoplasmosis, but cytomegalovirus generates fine subcortical calcifications as well. Finally, many fetal brain infections are accompanied by hyperechoic striatal vasculopathy, also with mineralisation. Calcification in basal grey matter and in frontal and temporal lobes may follow neonatal HSV infection. Neonatal bacterial ventriculitis-meningitis may induce calcified lesions.  Tumours may contain calcified foci: teratoma, lipoma, astrocytoma. Cerebral or cerebellar calcification often follows necrosis. Histopathology of samples from 28 autopsied brains aged from 22 weeks’ gestation to 14 years were selected because they showed calcification associated with a range of different diseases  (McCartney and Squier 2014). Calcification develops via two main pathways: dystrophic and vascular.  - Dystrophic calcification results from membrane disruption and uncontrolled calcium entry into necrotic cells in ischaemia and infections.  - Vascular calcification appears to be initiated in protein globules, sometimes intracellular, but outside the endothelium of small vessels (mutation of the occludin gene, implicating impaired endothelial integrity, showed this pattern (identical vascular calcification in Sturge–Weber syndrome)). Another form of vascular calcification involves the adventitia of arteries, the endothelium being spared. Reduced vascular compliance and altered permeability would explain associated atrophy, gliosis, and (in the developing brain) malformations of the cortex. Pericytes may also be involved in non-dystrophic brain calcification.  Precipitation with P is one of the mechanisms in Fahr disease (Chen et al. 2023, Cheng et al. 2024). Exceptional disorders. - Brainstem calcification typical of Möbius syndrome.  - Aicardi-Goutières syndrome and other pseudo-TORCH syndromes (Baraitser-Reardon).  - Brain disruption sequence.  - An hereditary disorder has been described by Illum et al. in 1988 and is accompanied by limb flexion-deformities, an immobile face with pouting mouth (‘whistling face’), early onset of convulsions together with fine diffuse intracranial calcifications (in the leptomeninges, penetrating from there along blood vessels into parenchyma, marking the ventricular borders by a fine line and highlighting the veins in deep gray matter).  - Generalised arterial calcinosis of infancy is accompanied by hypertension and hypertrophic cardiomyopathy, causing calcification in the walls of all major arteries but not always in brain arteries (Schiffmann et al. 1992).  - Mitochondrial disorders with congenital lactic acidosis (Samsom 1994, van Straaten et al. 2005).  - Mineralization in the basal ganglia may draw attention in cases of neonatal neuroaxonal dystrophy (Venkatesh 1994). - BLC-PMG Band-like calcification with simplified gyration and polymicrogyria. - Neu-Laxova syndrome. - Raine syndrome (lethal osteosclerotic bone dysplasia, facial dysmorphia, Binder phenotype: midface hypoplasia and small nose and brain calcification). - Norrie disease, Coats disease and other cerebroretinal angiopathies. - There are no neonatal presentations yet of Fahr disease (primary familial brain calcification)(Ramonet et al. 2002, Chen et al. 2023). - Leukodystrophy (Boltshauser et al. 1991). The only neuro-ectodermal disorders that may present with neonatal intracranial calcification, are Sturge-Weber syndrome (SWS) and tuberous sclerosis. Subependymal nodule calcification in the fetus has not been reported. Although SWS is associated with extensive calcification ater on, calcifications are absent or minimal in neonates and infants (Thomas-Sohl et al. 2004). The earliest report of calcification in SWS was in a 4-day-old neonate (Nellhaus et al. 1967) Established antenatal brain ischaemia with calcification in thalamic neurons (Ambler and O’Neill 1975, Voit et al. 1987, Ansari et al. 1990). ∆∆ [Symmetrical  infantile  thalamic  degeneration  (Ambler  and  O’Neil  1975). The varix wall and periventricular white matter may be calcified in vascular anomalies such as aneurysm of the vein of Galen (Perez-Fontan et al. 1982). During the organization of venous thrombosis, calcium deposit can be found in the affected vein. brain calcification in the newborn Mac OS X  2°âATTRâ¼&¼com.apple.TextEncodingËcom.apple.quarantineutf-8;134217984q/0082;69b84138;Hype4;