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By: S. Diego, M.A., M.D., M.P.H.
Professor, Texas Tech University Health Sciences Center Paul L. Foster School of Medicine
Mercury Poisoning Mercury (Hg) occurs naturally in three forms: elemental Hg treatment integrity checklist purchase sinemet 110 mg overnight delivery, mercury vapor treatment 3 degree heart block purchase sinemet online now, and organic/inorganic the treatment 2014 purchase sinemet american express. Although occupational exposures to Hg still occasionally occur in manufacturing and mining, most current cases are caused by dermal absorption from illegal skin-lightening cosmetic products or bioconcentration of inorganic methylmercury in the food chain. Seafood (fish, marine mammals) is especially Lead Poisoning Lead (Pb) is a potent and pervasive environmental neurotoxicant that is especially harmful during childhood development. Chronic Pb poisoning occurs in three forms: (1) a gastrointestinal form (anorexia, vomiting, lead "colic," etc. Gross pathology shows widespread cortical atrophy, white matter shrinkage, and thinning of the corpus callosum (3044). Severe spongiosis and gliosis with neuronal loss are seen on microscopic examination. Imaging findings of Minamata disease include atrophy of the calcarine (visual) cortex, cerebellar vermis and hemispheres, and the postcentral cortex. Decreased regional blood flow in the cerebellum can be demonstrated even in the absence of cerebellar atrophy. Here we discuss the most common disorders with a focus on treatment effects that must be recognized on imaging studies, namely radiation, chemotherapy, and surgery. Patients may have significant cognitive impairments even in the absence of detectable anatomic abnormalities. Pathologically, radiation injury varies from mild transient vasogenic edema to frank necrosis. Once considered relatively radioresistant, neurons are now known to respond negatively to radiation and probably play a significant but asyet-unidentified role in late radiation-induced cognitive impairment. These late delayed injuries are viewed as progressive and largely irreversible, resulting from loss of glial and vascular endothelial cells. Pathologically, coagulative necrosis in a "mosaic" pattern with coalescing foci produces a necrotizing leukoencephalopathy in the deep cerebral white matter. The subcortical association or U-fibers and corpus callosum are typically spared (30-45). Vascular changes include fibrinoid necrosis, hyalinization, and sclerosis with thrombosis. Late delayed radiation necrosis is initially expansile and mass-like, with necrosis largely confined to white matter. Later, volume loss, white matter spongiosis with confluent hyperintensity, and calcifications can be seen (30-46). Mineralizing microangiopathy generally does not appear until at least 2 years following treatment; it is then seen as calcifications in the basal ganglia and subcortical white matter (3048). Approximately 70% are meningiomas, 20% malignant astrocytomas or medulloblastomas, and 10% sarcomas. Meningiomas occur an average of 17-20 years after treatment, whereas gliomas occur at a mean of 9 years. The two most frequent abnormalities are posterior reversible encephalopathy syndrome and treatment-induced leukoencephalopathy. The occipital lobes are frequently spared whereas the cerebellum, brainstem, and basal ganglia are frequently involved. Acute neurotoxicity occurs in 5-18% of children treated for acute lymphoblastic leukemia. Effects of Surgery Interpreting imaging findings in the postoperative brain can be challenging. We focus on just two abnormalities that are important to recognize on imaging studies: retained surgical material ("textiloma") and sinking skin flap syndrome. Textiloma Textiloma-also known as muslinoma or gauzoma-is a foreign body reaction to retained surgical elements.
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Multiple meningiomatosis is characterized by multifocal meningiomas without schwannomas medicine of the wolf buy cheap sinemet 300mg online. Congenital Malformations of the Skull and Brain 1254 (39-28) Gross pathology of schwannomatosis shows multiple eccentric medications 126 purchase 300 mg sinemet fast delivery, expanded foci along this peripheral nerve medicine 2015 song purchase sinemet 300mg line. Schwannomatosis Terminology Schwannomatosis, which is the third major form of neurofibromatosis, is a rare hereditary cancer syndrome in which patients develop multiple nonvestibular schwannomas. Schwannomatosis is a paradigm for a tumor predisposition syndrome caused by the concomitant mutational inactivation of two or more tumor suppressor genes. The rate of transmission to offspring is low, likely due to the high rate of genetic mosaicism in founder mutations. Nearly two-thirds of meningiomas in patients with this tumor predisposition syndrome are located at the falx cerebri. Clinical Issues Schwannomatosis is the rarest of the neurofibromatoses, affecting 1:40,000 births. Multiple schwannomas of the spine (75%), subcutaneous tissues (15%), and nonvestibular cranial nerves (10%) are characteristic (39-28). It is associated with autism, seizures, and neurocognitive and behavioral disabilities. Microscopically, cortical tubers consist of giant cells and dysmorphic neurons with foci of gliosis, disrupted lamination, and disordered myelin. Typical microscopic features are large (not truly giant), plump cells that resemble astrocytes and/or ganglion cells in a fibrillar background. Between 20 and 30% are diagnosed during the first year of life when infantile spasms are observed in the patients with a positive family history. The most common skin lesions are hypomelanotic macules, which are ovoid depigmented areas with irregular margins that are best visualized by ultraviolet light (Woods lamp). Other common cutaneous findings such as forehead plaques, shagreen patches, facial angiofibromas ("adenoma sebaceum") (39-32), and periungual fibromas (39-34) usually do not appear until after puberty. The classic triad of facial "adenomata sebaceum" (39-32), seizures, and mental retardation is seen in only 30% of patients. Although they can develop at any age, they are most frequent in patients between 5-19 years of age. Downregulation of general protein synthesis, upregulation of macroautophagy, and activation of stress-responsive anabolic proteins occur. Neonatal and infantile cortical tubers are initially seen as hypodense cortical/subcortical masses within broadened and expanded gyri (39-35B). The lucency decreases with age; tubers in older children and adults are mostly isodense with cortex. By 10 years, 50% of affected children demonstrate one or more globular or gyriform cortical calcifications. The walls of the atria and temporal horns of the lateral ventricles are less common sites. The periphery of the expanded gyrus is isointense with cortex while the deeper component is strikingly hyperintense. It is the interval change in size seen on serial examinations-not the degree of enhancement-that is significant. Streaky linear or wedge-shaped lesions extend along radial bands from the ventricles to the undersurfaces of cortical tubers (39-37). Cerebellar tubers can be identified in 10-40% of cases and are always associated with supratentorial lesions. Other uncommon abnormalities include hemimegalencephaly, cerebellar malformations, and linear, clump-like, or gyriform parenchymal calcifications.
The vermis is intact but rotated superiorly medications similar to lyrica buy generic sinemet on line, and the tegmentovermian angle is increased treatment 32 for bad breath cheap sinemet express. Posterior Fossa Malformations 1191 (36-44) Coronal graphic of rhombencephalosynapsis shows that no vermis is present in the midline of the cerebellum treatment abbreviation buy sinemet 110 mg low cost. Instead, the folia, interfoliate sulci, and cerebellar white matter are continuous across the cerebellar midline. Note absent vermis, transversely oriented folia, continuity of cerebellar white matter across the midline. It is a midline arachnoid-lined cyst located behind the vermis and fourth ventricle that does not communicate with the latter. Although there may be mass effect on the cerebellum, there is no associated hydrocephalus and no communication with the 4th ventricle. Coronal and axial images show transverse folia and continuity of the cerebellar white matter across the midline (36-45). Images through the rostral fourth ventricle may demonstrate a diamond or pointed shape. Other forebrain anomalies include absent olfactory bulbs and corpus callosum dysgenesis. We now discuss several of those in which the abnormalities are largely defined by imaging features: rhombencephalosynapsis, Joubert syndrome, cerebellar hypoplasias, and unclassified dysplasias. Rhombencephalosynapsis is a midline brain malformation characterized by (1) a "missing" cerebellar vermis and (2) apparent fusion of the cerebellar hemispheres (36-44). Severity ranges from mild (partial absence of the nodulus and anterior and posterior vermis) to complete (the entire vermis, including the nodulus, is absent). Molar tooth disorders are, at least in part, "ciliopathies" with mutations of ciliary/centrosomal proteins that affect cell migration. The classic clinical presentation is a child with developmental delay, ataxia, and oculomotor and respiratory abnormalities. The fourth ventricle appears deformed with a thin upwardly (36-46) Axial graphic shows Joubert malformation. Thickened superior cerebellar peduncles around an elongated 4th ventricle form the classic "molar tooth" sign. Posterior Fossa Malformations convex roof and loss of the normal pointed fastigium (3648A). Axial scans demonstrate the classic "molar tooth" appearance with foreshortened midbrain, narrow isthmus, deep interpeduncular fossa, and thickened superior cerebellar peduncles surrounding an oblong or diamond-shaped fourth ventricle. The superior vermis is clefted, and the cisterna magna may appear enlarged (36-48B). In rhombencephalosynapsis, the cerebellar hemispheres and dentate nuclei are fused across the midline, not split. Unclassified cerebellar dysplasias are not associated with other known malformations or syndromes such as molar tooth malformation or Dandy-Walker continuum. A variety of findings including enlarged, vertically oriented fissures or clefts (36-50), disordered or primitive foliation, lack of normal white matter arborization, gray matter heterotopias, and small cyst-like cavities in the subcortical white matter are some of the many abnormalities seen in such cases (36-51). Congenital Malformations of the Skull and Brain 1194 Hindbrain Malformations: Imaging Vermis Position Mega cisterna magna Blake pouch cyst Arachnoid cyst Vermian dysgenesis Dandy-Walker malformation Cerebellar hypoplasia Pontocerebellar hypoplasia Cerebellar disruption N Rotated Vermis Size N N Torcular Position N N Cerebellar Hemispheres N N N or compressed N Often small Small Small Asymmetric; one smaller, abnormal structure Fused with continuous horizontal folia Small Fourth Ventricle N Enlarged; communicates with posterior fossa via valleculae N or compressed Abnormal shape; lacks normal fastigial point Dilated, enlarged; lacks normal fastigial point N or small Pontine bulge missing Variable depending on part of cerebellum disrupted Small; lacks normal fastigial point May be displaced N or compressed N May be rotated Rotated N N N Small or absent Small or absent Small Small N or small N Elevated N N N Rhombencephalosynapsis N/A Absent N Joubert syndrome N Small or absent, clefted N Large (associated with elongated superior cerebellar peduncles and "molar tooth" sign) (Table 36-1) N = normal.
Sinonasal melanoma favors the lower nasal cavity as its site of origin (septum medicine 0031 cheap sinemet amex, turbinates) medications for rheumatoid arthritis discount sinemet 125 mg otc. Anterior skull base (cribriform plate) meningioma typically causes hyperostosis and exhibits a "sunburst" pattern of vascularity with the central tumor supplied by dural branches of the carotid arteries medicine 48 12 300 mg sinemet overnight delivery. Pedigree analysis supports an autosomal-dominant inheritance pattern with incomplete penetrance. Neoplasms, Cysts, and Tumor-Like Lesions 656 Enhancement on T1 C+ is strong but heterogeneous (21-26). Leptomeningeal spread is present in 15-20% of cases at the time of initial imaging. Most have high proliferative indices and exhibit other cytologic features of malignancy. Neoplasms, Cysts, and Tumor-Like Lesions 658 Selected References Medulloblastoma Borowska A et al: Medulloblastoma: molecular pathways and histopathological classification. Tumors of the cranial meninges are divided into three basic pathologic groups: (1) meningiomas and meningioma variants, (2) mesenchymal nonmeningothelial tumors, and (3) melanocytic tumors. Meningiomas (benign, atypical, and anaplastic) are by far the largest group of meningothelial neoplasms. Although meningiomas are physically attached to the dura, they actually arise from arachnoid "cap" cells rather than from the dura itself. These uncommon tumors correspond histologically to tumors of soft tissue or bone found elsewhere in the body. Solitary fibrous tumor/hemangiopericytoma, hemangioblastoma, and hemangioma are also now included in this subgroup. The third group features the rare primary melanocytic lesions of the cranial meninges, including focal melanocytoma and diffuse leptomeningeal melanocytosis. Anatomy of the Cranial Meninges Dura Arachnoid and Arachnoid Granulations Pia Mater Meningomas Meningioma Atypical Meningioma Anaplastic Meningioma Nonmeningothelial Mesenchymal Tumors Benign Mesenchymal Tumors Hemangioma Malignant Mesenchymal Tumors Solitary Fibrous Tumor/Hemangiopericytoma Primary Melanocytic Lesions Melanocytoma and Melanoma Diffuse Meningeal Melanocytosis/Melanomatosis Melanotic Neuroectodermal Tumor of Infancy Other Related Neoplasms Hemangioblastoma 659 659 660 660 660 661 670 673 674 674 676 679 683 686 686 687 687 688 688 Anatomy of the Cranial Meninges the cranial meninges consist of the dura mater, the arachnoid, and the pia. Dura the dura mater-also called the pachymeninx-is a continuous fibrous sheet that lines the calvaria and spine. As its name implies (Latin for "tough mother"), the dura is a comparatively tough covering that provides significant protection against injury and infection. Neurosurgeons traditionally view the cranial dura as a simple bilaminar structure with an outer ("periosteal") layer and an inner ("meningeal") layer. The periosteal layer is firmly attached to the cranial vault, especially at sutures. The inner (meningeal) layer folds inward to form the falx cerebri, tentorium cerebelli, and diaphragma sellae. The outer dural border layer, which is just 2 m thick, is the thinnest layer Neoplasms, Cysts, and Tumor-Like Lesions 660 (22-1) Close-up view of dura, opened to show the superior sagittal sinus with numerous arachnoid granulations protruding into the sinus. Its thickness varies according to location and patient age (more prominent in infants than in adults). This inner layer is 8 m thick and is composed of only cells that adhere to the arachnoid trabeculae. Scanning electron microscopy reveals that the dura actually consists of five layers, each with different constituents and patterns of organization.
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