J K Curé

Medical University of South Carolina, Charleston, SC, United States

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Publications (30)156.4 Total impact

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    ABSTRACT: The epidermal nevus syndrome (ENS) is an unusual neurocutaneous disorder consisting of the combination of an epidermal nevus and a central nervous system (CNS), ophlhalmological, and/or skeletal abnormality. The study reports four new patients with ENS. Each had a confirmatory biopsy of the epidermal nevus, abnormal neurological examination findings, and documented CNS anatomical studies by imaging or autopsy. The paper also reviews the literature in English to determine neurological abnormalities found in skin-biopsy-proven cases of ENS. Hemi-atrophy, hemimegalencephaly, migrational abnormalities and vascular anomalies were found to be the most frequent intracranial abnormalities associated with ENS. Seizures and/or disabling moderate to severe developmental delays were present in a majority of patients. Seizure onset during the neonatal period or early infancy was associated with major hemispheric malformations. Neuroectodermal-derived ocular lesions were often bilateral. No consistent relation between laterality of the nevus and laterality of CNS abnormalities was found, supporting the gene mosaicism theory of pathogenesis. Anomalies neurologic/tie de développement et crises dans un syndrome de naevtis épidermique Le syndrome du naevus épidermique (ENS) est un trouble neurocutané inhabituel associant un naevus épidermique et des anomalies du système nerveux central (SNC), ophtalmologiques et/ou du squelette. Ľarticle rapport quatre nouveaux cas ďENS. Pour chacun, il y a une confirmation biopsique, des donnees anormales àľexamen neurologique et des études anatomiqucs bien documented sur le SNC par imageries et autopsie. Ľarticle fait également un relevé de la littérature dc langue anglaise sur les anomalies neurologiques trouvées en cas ďENS prouvé par biopsie. Les plus fréquentes anomalies intracrâniennes trouvées associées àľENS étaient ľhémiatrophie, ľhémimégalencéphalie, les anomalies de migration et les anomalies vasculaires. Des crises comitiales et/ou un retard de développement de modéréà sévère existaient chez la majorité des patients. Un début de crises durant la périodc néonatale ou la première enfance était associéà des malformations hémisphériques majeures. Les lésions oculaircs ďorigine neuro-ectodermique étaient souvent bilatérales. Aucune corrélation entre la latérulifi du naevus et la latéralité des anomalies du SNC n'a été trouvée, ce qui favorise la thèse pathogénique ďune mosaïque génétique. Entwicklungsbedingte neurale Miβbildungen und Anfälle beim epidermalen Nävus-Syndrom Das epidermale Nävus-Syndrom (ENS) ist einc ungewöhnliche neurocutane Erkrankung, die aus einer Kombination von epidermalem Nävus mit Mißbildungcn des Zentralnervensystems (ZNS), ophthalmologischcn Veränderungen und/oder Skelettanomalien besteht. Diese Studie berichtet über vier neue Patienten mit ENS. Bei alien war eine Biopsie des Nävus durchgeführt, waren abnorme neurologische Untersuchungsbefunde erhoben und anatomische ZNS Untersuchungen durch bildgebende Verfahren oder Autopsie dokumentiert worden. Die Arbeit enthält außerdem einen öberblick über die cnglische Literatur im Hinblick auf neurologische Anomalien bei bioptisch gesicherten Fällen mit ENS. Hemiatrophie, Hemimegalenzephalie, Migrationsanomalien und Gefaßveranderungen waren die häuflgsten intrakraniellen Mißbildungcn beim ENS. Krampfanfälle und/oder einschränkende mäßige bis schwere Entwicklungsverzögerungen waren bei den meisten Patienten vorhanden. Wenn die Anfälle in der Neonatalperiode oder im frühen Kindesaltcr begannen, konnten erhebliche cerebrate Mißbildungen nachgewiesen werden. Neuroektodermal bedingte Augenläsionen traten häufig bilateral auf. Es fand sich keine Relation zwischen der Seite des Nävus und der Seite der ZNS Mißbildungen, was für die Gen Mosaik Theorie zur Pathogenese spricht. Anomalías en el neuro-desarrollo y convulsiones en el síndrome de Nevus epidérmico E sindromes de nevus epidérmico (SNE) es una rara alteración neuro-cutánea que consisten en la combinación de un nevus epidérmico y una anomalía del SNC, oftalmológica y/o esquclética. El presente estudio aporta cuatro nuevos pacientes con SNE. Todos tenían una biopsia conftrmatoria del nevus epidérmico. hallazgos anómalos en el examen neurológico y estudios anatómicos de su SNC con imágencs o autopsia.La comunicación también revisa la literalura inglcsa para dcterminar ias anomalías neurológicas en casos de SNE con biopsia cutánea positiva. Se halló que las anomalías intracraneales más frccuentes asociadas al SNE eran la hemiatrofia, la hemimegaloencefalia, las anomalías migracionales y las anomalías vasculares. En la mayoría de los pacientes había también convulsiones y/o retrasos moderados o graves en el desarrollo discapacitantes. El inicio de las convulsiones en el periodo neonatal o precozmente durante la lactancia iba asociado a malformaciones hemisfericas importantes. Las lesiones oculares derivadas de la situación neurocctodérmica a menudo eran bilaterales. No se halló ninguna relación consislente entre la lateralidad del nevus y la de las anomalías del SNC, lo que apoya la teoría patogenética de un mosaicismo genético.
    No preview · Article · Nov 2008 · Developmental Medicine & Child Neurology
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    ABSTRACT: Sturge-Weber syndrome is characterized by a facial port-wine nevus, leptomeningeal angiomatosis, and glaucoma; it is commonly complicated by epilepsy and hemiparesis. We present a patient with a head and neck port-wine nevus, glaucoma, abnormalities of the intracranial deep veins, and untreated communicating hydrocephalus. The patient lacks any radiologic or clinical evidence of cerebral leptomeningeal angiomatosis. Considering that intracranial venous anomalies also are likely compatible with the embryologic explanation of Sturge-Weber syndrome, this child can serve as an unusual example of Sturge-Weber syndrome type II.
    No preview · Article · Mar 2006 · Journal of Child Neurology
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    ABSTRACT: We compared magnetic resonance imaging (MRI), magnetic resonance angiography, and transcranial Doppler ultrasonography as predictors of specific neurocognitive functions in children with sickle cell disease. Participants were 27 children with sickle cell anemia (hemoglobin SS) who were participants in the Stroke Prevention Trial in Sickle Cell Anemia (STOP) and had no documented history of stroke. Children's MRIs were classified as normal or silent infarct, and their magnetic resonance angiograms were classified as normal or abnormal. The highest time-averaged mean flow velocity on transcranial Doppler ultrasonographic examination of the major cerebral arteries was analyzed. Age and hematocrit also were analyzed as predictor variables. The battery of neurocognitive tests included measures of intellectual functioning, academic achievement, attention, memory, visual-motor integration, and executive functions. MRI, magnetic resonance angiography, transcranial Doppler ultrasonography, age, and hematocrit were analyzed as predictors of participants' performance on the various measures of neurocognitive functioning. Age and hematocrit were robust predictors of a number of global and specific neurocognitive functions. When age and hematocrit were controlled, transcranial Doppler ultrasonography was a significantly unique predictor of verbal memory. We found an association between low hemoglobin and neurocognitive impairment. We also found that abnormalities on transcranial Doppler ultrasonography can herald subtle neurocognitive deficits. (J Child Neurol 2006;21:37-44).
    Full-text · Article · Feb 2006 · Journal of Child Neurology
  • AV Yallapragada · JK Cure · KR Holden
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    ABSTRACT: Sturge-Weber syndrome is characterized by a facial port-wine nevus, leptomeningeal angiomatosis, and glaucoma; it is commonly complicated by epilepsy and hemiparesis. We present a patient with a head and neck port-wine nevus, glaucoma, abnormalities of the intracranial deep veins, and untreated communicating hydrocephalus. The patient lacks any radiologic or clinical evidence of cerebral leptomeningeal angiomatosis. Considering that intracranial venous anomalies also are likely compatible with the embry-ologic explanation of Sturge-Weber syndrome, this child can serve as an unusual example of Sturge-Weber syndrome type II.
    No preview · Article · Feb 2006 · Journal of Child Neurology
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    ABSTRACT: The stroke prevention study in sickle cell disease (STOP) demonstrated a 90% reduction in stroke risk with transfusion among patients with time-averaged mean cerebral blood velocity (TAMV) of 200 cm/s or more as measured by transcranial Doppler (TCD). In STOP, 232 brain magnetic resonance angiograms (MRAs) were performed on 100 patients, 47 in the transfusion arm and 53 in the standard care arm. Baseline MRA findings were interpreted as normal in 75 patients and as indicating mild stenosis in 4 patients and severe stenosis in 21 patients. Among 35 patients who underwent magnetic resonance angiography within 30 days of random assignment, the TAMV was significantly higher in 7 patients with severe stenosis compared with 28 patients with normal MRA findings or mild stenosis (276.7 +/- 34 vs 215 +/- 15.6 cm/s; P<.001). In the standard care arm, 4 of 13 patients with abnormal MRA findings had strokes compared with 5 of 40 patients with normal MRA findings (P=.03). In this arm, TAMV became normal (less than 170 cm/s) or conditional (170-199 cm/s) in 26 of 38 patients with normal or mildly abnormal baseline MRA but remained abnormal in 8 of 10 patients with severely abnormal baseline MRA. These results suggest that TCD often detects flow abnormalities indicative of stroke risk before MRA lesions become evident. Furthermore, patients with abnormal MRA findings and higher TCD velocities are at higher risk for stroke, and their cerebral TAMVs are unlikely to decrease without transfusion.
    Full-text · Article · Apr 2004 · Blood
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    ABSTRACT: We conducted a retrospective study to determine whether the presence of moyamoya collaterals influenced the risk of recurrence of cerebrovascular events (CVEs: stroke or transient ischemic attack) in patients with sickle cell disease placed on chronic transfusions after a stroke. Forty-three patients with homozygous sickle cell anemia (HbSS) and 1 with HbSO(Arab) (16 females, 28 males) who had suffered strokes while under the age of 18 were studied. All patients had been on transfusions aimed at maintaining the sickle hemoglobin (HbS) level below 30%. They were followed for a mean of 6.6 years (2.2 to 20.4 years). The presence of collaterals was diagnosed based on either magnetic resonance angiography or conventional angiography. Eighteen (41%) of the 44 patients suffered recurrent CVEs. Nineteen (43%) (6 females, 13 males) patients had moyamoya collaterals. Eleven (58%) of these 19 experienced 21 total recurrent CVEs, including 4 strokes in 4 patients (21%). In comparison, 7 (28%) of 25 patients without moyamoya collaterals experienced 9 recurrent CVEs (P <.05) with only 1 recurrent stroke (4%). Moyamoya patients were also more likely to have 2 recurrent CVEs (42% vs 8%, P <.05) as well as poorer neuropsychological testing results. A proportional hazards regression analysis indicated that patients with moyamoya were more than twice as likely to incur a subsequent CVE (hazard ratio, 2.40; 95% confidence interval, 0.85, 6.75). We conclude that up to 41% of patients with sickle cell disease experience recurrent CVEs after an initial stroke despite chronic transfusions and that the risk of recurrence is significantly higher for those who have moyamoya collaterals.
    Full-text · Article · May 2002 · Blood
  • C D Cunningham · P C Weber · J Curé

    No preview · Article · Dec 2000 · Otolaryngology Head and Neck Surgery
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    D Gajjar · B Egan · J Curè · P Rust · P VanTassel · S J Patel
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    ABSTRACT: The pathophysiological factors of neurogenic or sympathetically mediated essential hypertension are unknown. Neurons close to the surface of the ventrolateral medulla (specifically, in the retro-olivary sulcus [ROS]) are integrally involved in the control of blood pressure by means of efferent connections to presympathetic neurons in the spinal cord. It is hypothesized that vascular contact with the ROS is pathogenically involved in neurogenically mediated hypertension. We evaluated that theory in 20 subjects with uncomplicated stage 1 to stage 2 essential hypertension (EHTN) (18 of whom completed the study). The baseline supine plasma norepinephrine level served as an index of central sympathetic outflow. The response of blood pressure to clonidine was used as a surrogate marker for neurogenically mediated hypertension. We also examined the relationship between those markers and evidence of anatomic abnormalities in the area of the ROS that was provided by magnetic resonance imaging. A vessel contacted the left ROS in 5 of the 18 subjects. Those 5 subjects had higher plasma norepinephrine concentrations than did the 13 subjects without this vascular contact (358+/-46 versus 76+/-43 pg/mL, P<0.001). These 5 subjects also exhibited a significant depressor response to clonidine that tended to be greater than that seen in the 13 subjects without vascular contact (-20.6+/-3.2 versus -13.6+/-9 mm Hg). Both race and baseline mean blood pressure had only an independent effect on the depressor response to clonidine. The findings are consistent with the theory that vascular contact with the left ROS may contribute to neurogenically mediated "essential" hypertension in some patients.
    Full-text · Article · Aug 2000 · Hypertension
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    ABSTRACT: X-linked adrenoleukodystrophy (X-ALD) is a progressive demyelinating disorder whose neurological signs and symptoms can manifest in childhood as cerebral ALD or in adulthood in the form of a progressive myelopathy (AMN). The consistent metabolic abnormality in all forms of X-ALD is an inherited defect in the peroxisomal beta-oxidation of very long chain (VLC) fatty acids (>C(22:0)) which may in turn lead to a neuroinflammatory process associated with demyelination of the cerebral white matter. The current treatment for X-ALD with Lorenzo's oil aims to lower the excessive quantities of VLC fatty acids that accumulate in the patients' plasma and tissues, but does not directly address the inflammatory process in X-ALD. We have previously demonstrated that lovastatin and other 3-HMG-CoA reductase inhibitors are capable of normalizing VLC fatty acid levels in primary skin fibroblasts derived from X-ALD patients. Lovastatin can block the induction of inducible nitric oxide synthase and proinflammatory cytokines in astrocytes, microglia, and macrophages in vitro. In a preliminary report, we demonstrated that lovastatin therapy can normalize VLC fatty acids in the plasma of patients with X-ALD. Here we report our clinical and biochemical observations on 12 patients with X-ALD who were treated with lovastatin for up to 12 months. Our results show that the high plasma levels of hexacosanoic acid (C(26:0)) showed a decline from pretreatment values within 1 to 3 months of starting therapy with 40 mg of lovastatin per day and stabilized at various levels during a period of observation up to 12 months. The percentage decline from pretreatment values varied and did not correlate with the type of ALD gene mutation (point mutation versus gene deletion). In 6 patients, in whom red cell membrane fatty acid composition was studied, a mean correction of 50% of the excess C(26:0) was observed after 6 months of therapy suggesting sustained benefit. In a few patients who discontinued lovastatin therapy plasma C(26:0) levels reverted to pretreatment values suggesting a cause and effect relationship between these events. Two patients dropped out of the study claiming no clinical benefit, 1 was withdrawn due to adverse effects, and an adult patient with cerebral involvement died during the study. A 10-year-old boy with severe cerebral involvement showed worsening of his neurological status. All patients with AMN remained neurologically stable or showed modest subjective improvement. All patients who did not have Addison's disease at the time of enrollment maintained normal adrenal function throughout the study. The implications of our findings for developing an effective therapy for X-ALD are discussed.
    No preview · Article · Apr 2000 · Molecular Genetics and Metabolism
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    J K Curé · L L Key · D D Goltra · P VanTassel
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    ABSTRACT: The purpose of this study was to describe the cranial MR imaging manifestations of osteopetrosis. These features have not previously been reported in the literature. Cranial MR studies, obtained with a uniform imaging protocol, were reviewed in 47 patients with osteopetrosis. Thirty-four patients had autosomal recessive (malignant) osteopetrosis (AROP), seven had intermediate osteopetrosis (IOP), and six had either type I or type II autosomal dominant osteopetrosis (ADOP I or II). The prevalence of abnormalities was tabulated and compared with the specific osteopetrosis variants. All patients with osteopetrosis had thickening and sclerosis of the calvaria. Ventriculomegaly, tonsillar herniation, proptosis, and dural venous sinus stenosis were observed in the majority of patients with AROP and ADOP I. Optic nerve sheath dilatation occurred in many of the patients with AROP and in all patients with ADOP I. Acquired cephaloceles were also observed only in these two groups. Optic nerve atrophy and optic canal stenosis were observed in a majority of patients with AROP, IOP, and ADOP II. Middle ear fluid was prevalent in AROP and IOP, present in over half the patients in each group. Features seen most prevalently, or exclusively, in AROP included stenosis of the internal carotid and vertebral arteries and extramedullary hematopoiesis. The cranial MR imaging features of osteopetrosis are both shared and unique among the various subtypes of the disease. The specific cranial and intracranial manifestations reflect the predominant calvarial or skull base patterns of bone thickening. The unique features seen in patients with AROP probably reflect the early age of onset and the greater severity of this form of the disease.
    Preview · Article · Nov 1999 · American Journal of Neuroradiology
  • M. T. Smith · J. K. Curé · K. R. Holden

    No preview · Article · May 1998 · Journal of Neuropathology and Experimental Neurology
  • M. Bhatia · J. Curé · P. Van Tassel

    No preview · Article · Jan 1998
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    P Van Tassel · J K Curé · K R Holden
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    ABSTRACT: To investigate the presence of small cystlike structures in the cerebral hemispheric white matter on MR images of patients with tuberous sclerosis. The MR images of 18 consecutive patients with tuberous sclerosis were reviewed retrospectively. Eight of the 18 patients were found to have cystlike structures in the cerebral white matter. The signal intensity of these lesions was isointense with cerebrospinal fluid on T1-, proton density-, and T2-weighted images. Four patients were imaged with a fluid-attenuated inversion recovery sequence, which in each case also showed fluid-type signal in these areas. Three of the patients had CT for correlation, and these scans supported the diagnosis of cystic lesions. Cysts ranged in number from one to 12 per patient and were usually smaller than 1 cm. The most common location was adjacent to the occipital horn or trigone of the lateral ventricle (six of eight patients). Less frequent sites were near the frontal horns, in the corpus callosum, and in the deep white matter near the body of the lateral ventricle. Cysts in five patients were either immediately adjacent to a cortical tuber or in the center of a white matter dysplastic lesion. A cyst in one patient had septa, and none of the cysts enhanced. Cystlike structures in the cerebral hemispheric white matter were seen on the MR images of 44% of 18 patients with tuberous sclerosis. Whether these findings represent cystic degeneration of dysplastic tissue or are unrelated to the disease process of tuberous sclerosis is unknown. More than one pathogenesis may exist.
    Preview · Article · Sep 1997 · American Journal of Neuroradiology
  • W B Naso · J Cure · B G Cuddy
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    ABSTRACT: We report two cases of retropharyngeal pseudomeningocele after atlanto-occipital dislocation. This is rare, with only one other reported case in the literature. We report two patients who presented after blunt cervical and head trauma. Plain films revealed that each patient had atlanto-occipital dislocation. Subsequent magnetic resonance imaging revealed the delayed development of retropharyngeal pseudomeningocele. Concomitant hydrocephalus was noted in both patients. The surviving patient showed marked neurological improvement and resolution of his pseudomeningocele after ventriculoperitoneal shunting. For patients with closed head injuries who develop posttraumatic pseudomeningocele, we recommend cranial computed tomography to assess for the presence of hydrocephalus. In patients with atlanto-occipital dislocation, delayed neurological deterioration warrants magnetic resonance imaging of the craniocervical junction to rule out posttraumatic pseudomeningocele.
    No preview · Article · Jul 1997 · Neurosurgery
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    ABSTRACT: OBJECTIVE AND IMPORTANCE: We report two cases of retropharyngeal pseudomeningocele after atlanto-occipital dislocation. This is rare, with only one other reported case in the literature. CLINICAL PRESENTATION: We report two patients who presented after blunt cervical and head trauma. Plain films revealed that each patient had atlanto-occipital dislocation. Subsequent magnetic resonance imaging revealed the delayed development of retropharyngeal pseudomeningocele. Concomitant hydrocephalus was noted in both patients. INTERVENTION: The surviving patient showed marked neurological improvement and resolution of his pseudomeningocele after ventriculoperitoneal shunting. CONCLUSION: For patients with closed head injuries who develop posttraumatic pseudomeningocele, we recommend cranial computed tomography to assess for the presence of hydrocephalus. In patients with atlanto-occipital dislocation, delayed neurological deterioration warrants magnetic resonance imaging of the craniocervical junction to rule out posttraumatic pseudomeningocele.
    No preview · Article · Jun 1997 · Neurosurgery
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    ABSTRACT: above the distal anastomosis. The patient was brought to the operating room for revision of the stenotic graft. An epidural anesthetic was once again planned. Coagulation variables were within normal limits. When an l&gauge Tuohy needle was inserted at the L3-4 level, black, tarry, liquefied blood returned under pressure from the epidural space. After re- moval of approximately 10 mL of old blood, no additional blood returned passively or with gentle aspiration. The nee- dle was withdrawn, and the anesthetic technique was con- verted to a spinal anesthetic at the L2-3 interspace. The surgery proceeded uneventfully. Computerized tomogra- phy (CT) without contrast was performed postoperatively. The CT scan was equivocal for the presence of epidural hematoma. Subsequent magnetic resonance imaging (MRI) revealed epidural hematoma at interspace L2-4. The patient remained neurologically intact and was discharged on the sixth postoperative day.
    Preview · Article · Jun 1997 · Anesthesia & Analgesia
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    ABSTRACT: Spinal canal decompression at the most prominent of multiple posterior calcified thoracic lesions in a case of X-linked hypophosphatemia was undertaken for treatment and diagnosis purposes, as well as to assess possible nature of the pathophysiology underlying the presenting deficits. To discuss the clinical assessment diagnostic and treatment aspects of this rare coincidence of ossification of ligamenta flava in the patient with the skeletal deformities of X-linked hypophosphatemia. The patient with the stigmata and chemical findings of an X-linked hypophosphatemia presented with paraplegia and multiple calcified posterior spinal thoracic lesions. This was studied with magnetic resonance imaging and electrophysiologic studies of the spinal sensory pathways of the legs. These data constituted the preoperative information required to assess later results of surgical intervention. Presurgical clinical, imaging and electrophysiologic studies and laboratory and pathologic investigations of the surgical specimens. Resolution of the paraplegia with walking and return to work in a physically demanding job for the last 4 or 5 years of postoperative follow-up after surgical decompression of the spinal cord only at the worst and highest of the effected spinal levels. The coincidence of X-linked hypophosphatemia and ossification of ligamenta flava has been reported only in two or three cases in the literature. Removal of the offending ossifying lesion is known to result in resolution of the clinical deficits but similar lesions at other spinal levels are suspected of producing recurrences. The return of function and of the corresponding electrophysiologic correlates indicate a neurono-apractic nature of the neurologic symptoms.
    No preview · Article · Apr 1997 · Spine
  • P J Gurecki · K R Holden · E E Sahn · D S Dyer · J K Cure
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    ABSTRACT: The epidermal nevus syndrome (ENS) is an unusual neurocutaneous disorder consisting of the combination of an epidermal nevus and a central nervous system (CNS), ophthalmological, and/or skeletal abnormality. The study reports four new patients with ENS. Each had a confirmatory biopsy of the epidermal nevus, abnormal neurological examination findings, and documented CNS anatomical studies by imaging or autopsy. The paper also reviews the literature in English to determine neurological abnormalities found in skin-biopsy-proven cases of ENS. Hemi-atrophy, hemimegalencephaly, migrational abnormalities and vascular anomalies were found to be the most frequent intracranial abnormalities associated with ENS. Seizures and/or disabling moderate to severe developmental delays were present in a majority of patients. Seizure onset during the neonatal period or early infancy was associated with major hemispheric malformations. Neuroectodermal-derived ocular lesions were often bilateral. No consistent relation between laterality of the nevus and laterality of CNS abnormalities was found, supporting the gene mosaicism theory of pathogenesis.
    No preview · Article · Sep 1996 · Developmental Medicine & Child Neurology
  • J K Curé · L L Key · L Shankar · A J Gross
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    ABSTRACT: To study the association between petrous carotid canal (PCC) and internal carotid artery (ICA) stenoses in patients with malignant osteopetrosis. Mean and minimum PCC diameters obtained from cranial computed tomographic (CT) scans in 20 patients were compared with similar measurements in 52 control subjects. ICA caliber, evaluated with magnetic resonance (MR) arteriography, was correlated with age and PCC dimensions. There was a statistically significant difference between patient and control PCC diameters. There was a strong positive correlation between age and PCC diameter in the control subjects, but only a weakly positive correlation in the patients. One or both ICAs were stenotic on all patient MR arteriograms. MR angiographic stenosis grade correlated positively with age but not with PCC diameters. PCC and ICA stenoses occur frequently in patients with malignant osteopetrosis. Bony overgrowth or a "persistent fetal state" may produce the PPC stenoses. The findings do not support progressive PCC narrowing in these patients.
    No preview · Article · Jun 1996 · Radiology
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    J K Curé · J D Osguthorpe · P Van Tassel
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    ABSTRACT: We report the MR imaging findings in two cases of nasolabial cysts. Demonstration of their extraosseous location with cross-sectional imaging should prevent confusion with maxillary cysts and obviate unwarranted dental or maxillary surgery.
    Preview · Article · Apr 1996 · American Journal of Neuroradiology