Dural Calcification Research Articles

Extensive dural calcification in a young female patient: A case report

Introduction: Dural calcification is most observed in older adults. However, idiopathic extensive dural calcification is rare in young individuals, often raising concerns for potential underlying secondary diseases or disorders. Dural calcification is typically categorized into physiological (age-related and idiopathic) and pathological types (associated with underlying conditions) linked to metabolic and genetic factors. Case Report: We report distinctive idiopathic extensive dural calcification in an asymptomatic young adult female with no known pathological or metabolic predispositions. Conclusion: The presence of this condition in young, healthy adults without any identifiable etiologies is exceptionally uncommon. This case represents a rare instance of such extensive dural calcification in a healthy young adult, contributing a unique addition to the medical literature on this rare entity.

Diffuse incidental dural calcifications.

Diffuse incidental dural calcifications.

Compressive myelopathy from diffuse spinal dural calcifications in a patient with end-stage renal disease: illustrative case.

Diffuse spinal dural calcification is a rare disorder associated with hyperparathyroidism, including the secondary forms associated with renal failure, osteodystrophy, and chronic hypocalcemia. Here, the authors report a rare case of diffuse dural calcification causing spinal cord compression with myelopathy, requiring decompressive surgery with duraplasty to achieve adequate decompression. A 46-year-old male with a history of renal failure on dialysis presented with 2 months of progressive neuropathic pain, lower-extremity weakness, and nonsustained clonus. Spine imaging showed severe renal osteodystrophy with multilevel compression fractures and diffuse dural calcifications with areas of invagination causing severe spinal cord compression. Decompressive surgery was recommended. In surgery, a thickened and calcified dura was encountered with areas of buckling causing spinal cord compression. The invaginated area of the dura was resected and reconstructed with patch duraplasty. The patient's neurological status remained unchanged postoperatively, and at the 6-month follow-up, the patient reported significant improvement in pain and muscle spasms. Diffuse dural calcifications are a rare complication of prolonged dialysis and secondary hyperparathyroidism. When there is resultant spinal cord compression, this condition requires an intradural approach that addresses the thickened, calcified dura directly to obtain adequate spinal cord decompression.

Unusual neuroimaging findings in spontaneous intracranial hypotension

The most common neuroimaging manifestations of patients suffering from spontaneous intracranial hypotension (SIH) include subdural fluid collections, enhancement of the pachymeninges, engorgement of venous structures, pituitary hyperemia, sagging of the brainstem, and cerebellar hemosiderosis. However, infrequently patients may present with separate neuroradiological findings which could be easily mistaken for other pathology. We describe patients who presented with unique neuroimaging findings who were eventually found to have a spinal CSF leak or venous fistula. Relevant clinical history and neuroradiology findings are presented, and a relevant review of the literature is provided. We present six patients with a proven CSF leak or fistula who presented with dural venous sinus thrombosis, compressive ischemic injury, spinal hemosiderosis, subarachnoid hemorrhage, pial vascular engorgement, calvarial hyperostosis, and spinal dural calcifications. Radiologists should be familiar with atypical neuroimaging manifestations of SIH in order to avoid misdiagnosis and guide the clinical trajectory of the patient towards accurate diagnosis and eventual cure.

Mineralizing microangiopathy: radiological features of a "not uncommon" complication of chemoradiotherapy in pediatric cancer patients

BackgroundMineralizing microangiopathy represents one of the delayed complications of radiotherapy and chemotherapy. We reviewed clinical and radiological data of pediatric cancer patients who presented with mineralizing microangiopathy. This is a retrospective analysis of the medical records of 37 cancer children treated with chemoradiotherapy presented with imaging criteria suspected of mineralizing microangiopathy admitted to our hospital during the period 2015–2020. The CT was reviewed for distribution of calcification and MRI for signal criteria.This study aims to raise awareness among radiologists about radiological features of mineralizing microangiopathy during the sequential routine follow-up brain scans of pediatric cancer patients who received chemo, radio, or combined chemoradiotherapy and to identify changes as a long-term delayed complication of therapy and avoid misdiagnosis.ResultsThirty-seven pediatric cancer patients (17 female and 20 males, aged 1.5–18 years) who had mineralizing microangiopathy were thoroughly investigated. Most of them (32 patients) had brain tumors and 5 patients had leukemia. Cranial radiotherapy and systemic chemotherapy were given to 33 patients, while nine patients received intrathecal chemotherapy. The interval needed to develop mineralizing microangiopathy ranged from 1 to 10 years after the end of treatment. CT detected calcification in the basal ganglia, being the most common location (32 cases), followed by cerebral gray–white matter interface in 26 patients, cerebellum (18), brain stem (13), thalamus (5), and caudate nucleus (4), while dural calcifications were found in only one patient. MRI was considered “positive” when T1 hyperintensity was noted in the anatomical location of CT detected calcification; it was positive in 29 cases.ConclusionMineralizing microangiopathy is one of the delayed complications of chemoradiotherapy among pediatric cancer patients. The awareness of its radiological criteria is essential to avoid misdiagnosis. Early detection can alert pediatric oncologists to monitor neurotoxicity and help prevent long-term neurological sequels.

Physiologic intracranial calcifications incidentally detected on cone beam computed tomography

This study aims to determine the incidence of physiologic intracranial calcifications on cone beam computed tomography (CBCT) and to contribute to the differentiation between physiologic and pathologic intracranial calcifications by sharing their characteristic appearances, with the largest number of patients in the literature and many different types of physiologic calcifications. CBCT images of 996 patients admitted to the clinic between 2018 and 2019 were scanned retrospectively. Petroclinoid (PCL) and interclinoid ligaments (ICL), pineal gland, coronoid plexus, falx cerebri, tentorium cerebelli, and other dural calcifications were evaluated in each radiograph. Physiologic calcification was present in 49.4% of the cases, and pineal gland calcification was the most common (47.6%) type. PCL calcification was detected in 22.1%, and it was mostly bilateral partial. There were complete ICL in 1.2%, coronoid plexus in 11.3%, falx cerebri in 6.3%, tentorium cerebelli in 1.1%, and other dural calcifications in 3.6%. Only PCL calcifications differed between sexes and were more common in males. PCL, pineal gland, and coronoid plexus calcifications were most detected in the third decade of the cases. Intracranial calcifications are detected incidentally in CBCT examinations. Some calcifications may indicate pathologic conditions, and patients may need to be referred for further evaluation.

CARDIAC FIBROMA AS MANIFESTATION OF NEVOID BASAL CELL CARCINOMA SYNDROME

Cardiac fibromas occur in 3% of patients with nevoid basal cell carcinoma syndrome (NBCCS), an autosomal dominant disorder characterized by multiple basal cell carcinomas, intracranial dural calcifications (Figure 1A), and odontogenic keratocysts (Figure 1B-C). Early diagnosis is essential for

Cranial Intraosseous Meningiomas: CT and MRI Findings.

To evaluate computed tomography (CT) and magnetic resonance imaging (MRI) findings of cranial intraosseous meningiomas (IOMs). This study included ten patients (six females and four males) with IOMs who underwent cranial CT and/ or MRI examinations during May 2009?June 2018. Lesions were classified based on the following locations: the sphenoid ridge, the calvarial convexity, other skull base bones, and the sphenoid ridge + calvarial extension. Bony extension, contour irregularity or radial bone spiculation, bony changes (hyperostotic, lytic, or mixed patterns), dural calcification, cerebral edema, and the presence of soft tissue were evaluated. A total of eleven IOMs were identified in ten patients. The age of patients was 46?80 (mean: 55.30 ± 9.84) years. Five of the lesions were located in the sphenoid ridge + calvarium, three in the sphenoid ridge, two in the skull base, and one in the calvarial convexity. Seven lesions exhibited radial bone spiculation. Moreover, nine lesions exhibited hyperostotic CT pattern; while, two exhibited a mixed pattern. Three IOMs were accompanied with dural calcification, and peritumoral edema was observed in six IOMs. IOMs are predominantly low-grade tumors, commonly located in the periorbital area and often accompanied by soft tissue components and dural infiltrations. They most commonly lead to radial bone spiculation and bone expansion. Patients primarily have single lesions but may occasionally have multiple ones.

Imaging Appearances and Pathologic Characteristics of Spinal Epidural Meningioma.

Spinal epidural meningioma is an uncommon tumor. This study aimed to analyze the imaging and pathologic characteristics of this rare tumor. Fourteen confirmed cases of epidural meningioma were retrospectively reviewed, and imaging characteristics and pathologic findings were analyzed to identify the typical features. The mean age of the patients (4 men, 10 women) was 44.9 years. Twelve tumors were in the cervical spinal canal, and 2, in the thoracic spinal canal. There were 9 en plaque meningiomas, 4 dumbbell-shaped meningiomas, and 1 fusiform/ovoid meningioma. The epidural meningiomas extended over 2-5 spinal segments (mean, 3.2 spinal segments). A soft epidural mass was seen in 12/14 (86%) patients. Dural calcification was seen in 8/14 (57%) tumors. Tumor caused intervertebral foramen enlargement in 10/14 (71%) patients and adhered to the nerve roots in 11/14 (79%) patients. Intradural invasion was seen in 8/14 (57%) patients. The dural tail sign was present in 13/14 (93%) tumors on contrast-enhanced T1WI. Regarding pathologic type, 10 of 14 (71%) were psammomatous, 2 of 14 (14%) were meningothelial, 1 of 14 (7%) was angiomatous, and 1 of 14 (7%) was transitional. During follow-up (mean follow-up, 73.4 months; range, 4-192 months), 7 patients had recurrence. Recurrences were between 4 and 192 months after the operation. Epidural meningioma has 3 different growth patterns. Dural thickening, calcification, invasion, and epidural mass formation are characteristic features of epidural meningioma. Regular follow-up imaging is required to detect recurrence.

Recognizing the clinical triad and dural calcification in adult hypophosphatasia.

Recognizing the clinical triad and dural calcification in adult hypophosphatasia.

Age and gender related prevalence of intracranial calcifications in CT imaging; data from 12,000 healthy subjects

PurposeLocation and extent of intracranial calcifications have been detected accurately with the use of CT technology and since, many clinical or pathological entities have been linked to these calcifications. Our purpose is to provide data regarding the prevalence of calcifications in various locations in brain. Material and methodsWe retrospectively examined 11,941 subjects who underwent non-contrast enhanced brain CT examination. We determined the prevalence of choroid plexus, pineal gland, habenula, dura mater, basal ganglia and vascular calcifications. ResultsOf 11,941 subjects, 70.2% had choroid plexus calcifications. Calcifications were most frequently seen in pineal gland and 71.6% of the study population had pineal calcifications. Habeluna and dural calcifications were present in 19.2% and 12.5% of the population respectively. Basal ganglia calcifications and vascular calcifications only constituted 1.3% and 3.5% of the study population respectively. Male dominance was present in all calcification types except basal ganglia calcifications. ConclusionsShowing associations and dissociations from the literature, our study provides a baseline data regarding the prevalence of various types of intracranial calcifications.

Hyperostosis cranii ex vacuo from ventricular shunting

A legally blind 24-year-old young man with a history of extensive traumatic brain injury due to a motor vehicle accident at age 5.5, status post childhood ventriculoperitoneal shunt placement for hydrocephalus and longstanding refractory epilepsy, was admitted for worsening of his seizures. Neurological examination showed a non-verbal patient, unable to follow commands and unable to track. Pupils were asymmetric (left fixed and dilated), eyes were dysconjugate with the right displaced superiorly and laterally, and no reaction to visual stimuli. Upper extremity was hypotonic and atrophic, and lower extremities were spastic with sustained clonus on the left. Plantar response was upgoing bilaterally. During the admission, the patient had multiple clinical seizures consistent with tonic seizures characterized by arm flexion and stiffening with episode of tonus and neck extension. Cranial computed tomography and magnetic resonance imaging of the brain were notable for extensive dural calcifications (white arrows, Fig. 1A) as well as calvarial thickening (Fig. 1B and white arrows, 1C on magnetic resonance imaging) in the relative absence of thickening of the facial bones and jaw (Fig. 1C, black arrows). A right frontal-approach ventricular catheter with its tip

Physiologic pineal region, choroid plexus, and dural calcifications in the first decade of life.

Calcifications of the pineal, habenula, choroid plexus, and dura are often physiologic. In the modern CT era with thin-section images and multiplanar reformats, intracranial calcifications have become more conspicuous. We aimed to discover the CT prevalence of pineal region, choroid plexus, and dural calcifications in the first decade of life. Five hundred head CTs from different patients (age range, 0-9 years) encountered during a consecutive 6-month period at a single academic children's hospital were reviewed retrospectively after excluding examinations with artifacts and pineal region masses/hemorrhage. All studies were performed on a 320-detector CT, with 0.5-mm collimation and a 512 × 512 matrix. Five-millimeter reformatted axial, sagittal, and coronal images were analyzed for location and extent of intracranial calcifications. The mean age was 3.5 ± 5.7 years (range, 0-9 years). There were 285 males (57%) and 215 females (43%). Pineal calcifications were present in 5% (n = 25; age range, 3.2-8.9 years; median, 7 years). Habenular calcifications were found in 10% (n = 50; age range, 2.8-8.8 years; median, 7 years). Twelve percent (n = 58) had choroid plexus calcifications, (age range, 0.1-8.8 years). Dural calcifications were rare, present in 1% (n = 6; age range, 2.9-8.7 years). Physiologic intracranial calcifications may be found in the first decade, principally in children older than 5 years. Most epithalamic calcifications are habenular. Pineal and habenular calcifications were never present in children younger than 3 and 2 years, respectively. Choroid plexus calcifications may be present in the very young. Dural calcifications are rare.

Idiopathic Dural Optic Nerve Sheath Calcification Associated with Choroidal Osteoma

A 28-year-old woman presented with a choroidal osteoma in the right eye and optic atrophy in the left eye, associated with bilateral optic nerve sheath calcification and calcifications in the pineal, choroid plexus, and dura (falx and tentorium). Visual acuity, tumor size, and intracranial calcifications did not change over 16 years. The combination of bilateral optic nerve sheath calcification with multiple intracranial calcifications suggests an unexplained and generalized dural calcification process. To the authors' knowledge, this is the first case of choroidal ossifying tumor associated with calcified lesions of the optic nerves. Although the pathogenesis of bone formation in choroidal osteoma remains uncertain, intraocular inflammation might be one cause.

Epidural Fluid Collection after Cranioplasty : Fate and Predictive Factors

Infection and bone resorption are major complications of cranioplasty and have been well recognized. However, there are few clinical series describing the epidural fluid collection (EFC) as complication of cranioplasty. This study was planned to identify the predictive factors and fate of EFC after cranioplasty. We reviewed retrospectively the demographic, clinical, and radiographic data in 59 patients who underwent a first cranioplsty following decompressive craniectomy during a period of 6 years, from January 2004 to December 2009. We compared demographic, clinical, and radiographic factors between EFC group and no EFC group. The predictive factors associated with the development of EFC were assessed by logistic regression analysis. Overall, 22 of 59 patients (37.3%) suffered from EFC following cranioplasty. EFC had disappeared (n=6, 31.8%) or regressed (n=6, 31.8%) over time on follow up brain computed tomographic (CT) scans. However, 5 patients (22.7%) required reoperation due to symptomatic and persistent EFC. Predictive factors for EFC were male [odds ratio (OR), 5.48; 95% CI, 1.26-23.79], air bubbles in the epidural space (OR, 12.52; 95% CI, 2.26-69.28), and dural calcification on postoperative brain CT scan (OR, 4.21; 95% CI, 1.12-15.84). The most of EFCs could be treated by conservative therapy. Air bubble in the epidural space and dural calcification are proposed to be the predictive factors in the formation of EFC after cranioplasty.

Fluorotic cervical compressive myelopathy, 20 years after laminectomy: A rare event

Background:Spinal cord compression in flourosis is a common complication. These complications are mainly due to compression of the spinal cord by thickening and ossification of posterior longitudinal ligament and ligamentum flavum. Surgical decompression is the treatment of choice for fluorotic spinal cord compression. The recurrence of spinal cord compression after surgical decompression in flourosis is a rare event.Case Description:We are presenting a case of a 63-year-old man who belonged to Kanpur, an endemic fluorosis region in India, with symptoms of cervical cord compression cranial to the operative site, 20 years after laminectomy for cervical fluorotic myelopathy. Urinary and serum fluoride levels were elevated. The patient underwent a skeletal survey: computed tomography and magnetic resonance imaging of the cervical spine showed a postoperative defect of laminectomy, osteosclerosis, osteophyte formation, calcification of the intraosseus membrane in the forearm, thickening and ossification of the posterior longitudinal ligament at C1, thickening and ossification of the residual ligamentum flavum at C1/C2, and dural calcification at the C2 vertebral level and compressive myelopathy. The patient refused surgical decompression and was managed with tizanidine HCl (an antispasticity medicine), a sublingual single night dose, 8 mg for symptomatic relief.Conclusion:The recurrence of spinal cord compression in the fluorotic spine 20 years after laminectomy is a very unusual event and hence the patient should be kept under observation for a long duration. This case report contributes to the literature associated with the management of fluorotic spine.

CT and MR Imaging of Progressive Dural Involvement by Nephrogenic Systemic Fibrosis

We present a patient with progressive dural calcifications, thickening, and enhancement presumably related to the development of nephrogenic systemic fibrosis (NSF). Head CT demonstrated progressive dural calcifications, whereas MR imaging demonstrated progressive dural thickening and enhancement during a 3-year period in which the patient received several gadolinium-enhanced MR imaging studies. To the best of our knowledge, dural calcifications are the only described intracranial finding of NSF.

Neurosurgical aspects of childhood hypophosphatasia

Hypophosphatasia (HPP; MIM241510) is a rare inborn error of bone metabolism of recessive inheritance. It is caused by mutations in the gene encoding the tissue-nonspecific alkaline phosphatase. Apart from problems in bone mineralization, growth failure, and premature loss of decidual teeth, the infantile and the childhood types of HPP are associated with premature fusion of cranial sutures. We report on seven children affected with infantile and childhood HPP who presented with craniosynostosis. Neurosurgical intervention was necessary in four of them because of intracranial hypertension. In one of these, severe dural calcification posed an unexpected problem during surgery. Secondary ectopia of the cerebellar tonsils were detected in five of the seven patients and caused hydrosyringomyelia in one of them. Since cranial sutures are frequently involved in infantile and childhood HPP, a multidisciplinary approach for the clinical care is necessary, including long-term neurosurgical surveillance.

Chronic Pachymeningitis and Bilateral Facial Paralysis Secondary to Renal Osteodystrophy

Heterotopic calcification can occur as a result of secondary or tertiary hyperparathyroidism. 1 Herein we describe a patient with end-stage renal disease who has had several episodes of facial palsy bilaterally. Clinical evaluation, medical testing, radiographic imaging, and, finally, surgery revealed facial nerve compression secondary to dural calcification. An extensive literature search demonstrated that dural calcifications resulting in facial paralysis has not been previously described to our knowledge.

Craniovertebral malformation complex in a child with Weismann-Netter-Stuhl syndrome

Bowing of the legs is usually thrown into the basket of vitamin D deficiency rickets; therefore, a significant number of affected children can be misdiagnosed and improperly managed. This case illustrates how the careful clinical and radiological assessment of such a case can lead to the adequate understanding of its etiology. We report a sporadic case of a 2-year-old male child who presented with radiological features that were compatible with Weismann-Netter-Stuhl syndrome. In addition, we observed craniovertebral malformation complex. He was of normal intelligence. To our knowledge, the combination of Weismann-Netter-Stuhl syndrome and presence of a hypoplastic occipitalized atlas and further C2-C3 fusion has not been reported before. The diagnosis of Weismann-Netter-Stuhl is discussed. Classically, Weismann-Netter-Stuhl syndrome is characterized by short stature, mental retardation (in some individuals), dural calcification, and anterior bowing of the tibiae. However, we believe that careful clinical and radiological examinations can reveal more striking data which might positively reflect on the whole process of management. We postulate that the congenital limitations in neck movements in our patient developed because of the marked fusion of the hypoplastic and occipitalized atlas and simultaneous C2-C3 fusion. Therefore, if this form of malformation is disregarded, there may be involvement of the atlantoaxial structure, and this can possibly lead to serious neurological and even life-threatening complications. The use of CT scanning for the detection of such abnormalities can be remarkably important.