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Patients with decompensated congenital fourth nerve palsy generally have a better progno- sis after surgery than patients with acquired fourth nerve palsy, because they often have increased vertical fusional amplitude that reduces the likelihood of postoperative diplopia. Postoperatively, the patient had 1 diopter right hypertropia in primary and eccentric gaze, measured by Maddox rod testing. Head position-dependent changes in ocular torsion and vertical misalignment in skew deviation. A new classification of superior oblique palsy based on congenital variations in the tendon. The correct explanation should read as follows (revisions in italics): "According to the Parks-Bielschowsky three-step test, right hypertropia suggests weakness of the right superior oblique, right inferior rectus, left inferior oblique, or left superior rectus muscles. Next, increased right hypertropia in contralateral gaze narrows the possibilities to right superior oblique or left superior rectus weakness. Fluorescein angiogram (B, D) shows optic nerve hyperfluorescence bilaterally (arrows) with left stippled hypofluorescent spots representing choroidal leakage with nonfilling infiltrates (D, asterisk). He denied any symptoms of raised intracranial pressure including headSupplemental data at Two months prior, he developed pain in his lower back radiating into both legs and an associated band-like sensation around his waist. Ophthalmoscopy showed marked bilateral optic disc swelling (figure 1, A and C) and macular edema in the left eye. Visual field testing showed a small inferotemporal scotoma in the right eye, with a larger central scotoma in the left eye. There was subjective decrease in light touch and pinprick sensations up to the midshin level bilaterally. However, uncomplicated papilledema is not typically associated with reduced visual acuity or dyschromatopsia. Lymphoma can also invade the meninges, producing multiple cranial neuropathies and polyradiculopathies. This patient had a history suggestive of prior polyradiculopathy, but the spontaneous resolution of his symptoms was atypical of lymphoma. Infections such as cryptococcus, toxoplasmosis, tuberculosis, herpes zoster, cytomegalovirus, and herpes simplex virus can also affect the optic nerves or the retina. There was no evidence of venous sinus thrombosis or abnormal meningeal enhancement. Lumbar puncture yielded a slightly high opening pressure (27 cm H2O), high white cell count (21. However, the opening pressure associated with these conditions is typically much higher than that observed in this case. To better tailor further workup, reconsideration of the localization of the problem is important. Processes affecting the afferent visual pathway posterior to the chiasm should produce visual field deficits that respect the vertical meridian in both eyes. The field defects in this case crossed the vertical meridian, indicating a process affecting the visual pathway anterior to the chiasm. Therefore, given the lateralizing defects in visual acuity, visual field sensitivity, and color vision in the left eye, further assessment of the anterior and posterior segments, with focused examination of the macular regions, is necessary to identify any pathology and to elucidate the mechanism of vision loss in this case. In addition to the optic disc edema, there was a slightly creamy appearance to the choroid around the disc, greater in the left than the right eye. Fluorescein angiogram showed an infiltrative process around the optic nerves in both eyes, and extension through the macula in the left eye (figure 1, B and D). Further testing showed a reactive plasma syphilis antibody that was confirmed with enzyme immunoassay. Although syphilis serology does not differentiate active disease from previous infection, this man was known to have unreactive syphilis testing in the recent past. He was treated with parenteral penicillin with significant improvement in his visual symptoms. When assessed in follow-up after 2 months, his visual acuity was 20/20 in both eyes. Fundus examination demonstrated mild optic disc hyperemia bilaterally (figure e-1 on the Neurology Web site at In the early infection phase, acute meningitis, meningovasculitis, and myelitis have been described.

This particular mutation has been called the first example of a "carcinogen-specific" biomarker that remains fixed in human tissue. This biomarker has been used in epidemiologic studies to establish the link between aflatoxins and hepatic cancer and also to show that cofactors such as infection with hepatitis B virus increase the risk of hepatocellular cancer substantially. Fumonisins, especially fumonisin B1, interfere with sphingolipid metabolism and cause leukoencephalomalacia (severe necrotizing brain disease) in horses, pulmonary edema and hydrothorax in pigs, and hepatotoxic and carcinogenic effects in the liver of rats. Fumonisin B1 has been associated with a higher incidence of esophageal cancer in people living in South Africa, China, and Italy. Although this evidence is intriguing, multiple factors, including other mycotoxins, have been implicated in the etiology of human esophageal cancer. Acute intoxication with fumonisin B1 has been observed in India, where consumption of unleavened bread made from moldy corn caused transient abdominal pain and diarrhea. Fumonisins have also been shown to cause neural tube defects in experimental animals and may have a role in human cases. Fumonisins have been classified as group 2B carcinogens (probably carcinogenic) by the International Agency for Research on Cancer. All the infants in this cluster also were exposed to certain environmental factors that might have affected their lungs, including environmental tobacco smoke, particulate matter. Cladosporium and Penicillium, the molds most commonly identified in each of the homes, typically are the most abundant fungal genera in indoor air. Total fungal spore counts in two of the homes were at concentrations that have been associated with increased risk for lower respiratory illness, and all four infants were treated presumptively for respiratory infections before their hemorrhagic episodes. Although the full significance of spore counts is not known, toxic and other non­ immunoglobulin (Ig)E-mediated health effects that have been hypothesized to occur with exposure to S. It has been implicated in porcine nephropathy, as well as urinary tract tumors, and may cause cholinergic responses such as bronchospasm, vasodilation, and smooth muscle contraction. Regardless, its acute nephrotoxicity, immunosuppressive action, and teratogenic effects in animals, coupled with its propensity to be carried through the food chain, merit concern and further investigation. There are more than 148 natural trichothecenes, of which at least 40 are mycotoxins. Trichothecenes act by inhibiting various aspects of protein synthesis in eukaryotic cells. These mycotoxins are commonly found as food and feed contaminants, the consumption of which can result in gastrointestinal hemorrhage and vomiting; direct contact causes dermatitis. So-called moldy grain intoxication of humans and animals is well documented in Japan. Akakabi-byo toxicosis, or red mold disease, is believed to be caused by ingestion of grain contaminated with Fusarium graminearum (see Table 67-1). Symptoms produced by these agents include effects on almost every system of the vertebrate body. When ingested in high doses, it causes vomiting and diarrhea; at lower doses, farm animals exhibit weight loss and food refusal. Thousands of people became sick after eating overwintered grain contaminated with Fusarium sporotrichioides and Fusarium poae. The disease was characterized by several stages, with initial oral mucosal ulceration and gastroenteritis followed by pancytopenia, bleeding from the nose, mouth, and vagina, hypotension, and vertigo. The high acute mortality rate was augmented by opportunistic bacterial infections during the later neutropenic stages of the disease. Although the two species of Fusarium that were isolated from the moldy grain were subsequently shown to be able to produce T-2 toxin and other trichothecenes, no attempt was made to document the presence of these mycotoxins in the grain or the affected people. Stachybotryotoxicosis is a well-described disease among horses and cattle consuming moldy straw and hay contaminated with Stachybotrys. Equine stachybotryotoxicosis is characterized by acute neurologic signs such as tremors, incoordination, and loss of vision and more chronic manifestations such as dermonecrosis, leukopenia, and gastrointestinal bleeding. Humans handling moldy hay have exhibited contact dermatitis, as well as mucosal inflammation, fever, chest pain, and leukopenia secondary to inhalation of dust from the hay. Given these findings, and because Stachybotrys grows well on wet building materials. Stachybotrys has also been associated with idiopathic pulmonary hemorrhage of infants; however, a cause-and-effect relationship has not been proven. Critical evaluation of the available literature has failed to find supportive evidence for serious human illness caused by Stachybotrys exposure in the contemporary human environment. Consumption of millet that was heavily contaminated with molds and contained high levels of cyclopiazonic acid produced a condition known as Kodua poisoning, characterized by giddiness and nausea (see Table 67-1).

Cavernomatous malformation or vascular hamartomas show typical calcifications in "corn popcorn" with an incidence of 40-60%; the aneurysms may contain mural calcifications and more frequently if they are partially or totally thrombosed. Pathophysiologically, the mechanism of calcification of most of these lesions is secondary to chronic venous ischemia and formation of dystrophic calcifications by hemorrhage (23) (Figures 12 and 13). Intra-axial tumors are associated with hemorrhage by combination of neovascularization, arteriovenous shunts, and rapid tumor growth leading to necrosis and disruption of intracellular calcium regulation, which ultimately leads to calcium deposition. Within this group are the slow-growing oligodendrogliomas, located preferentially in the frontal lobe, show calcifications in a 40 - 90%, central, mirocalcifications or lumpy (23) (Figure 16). Other tumors do so in lesser percentages, such as those of the pineal gland and germ cells, in which it is rare for them to generate their own calcifications. Pineal tumors are believed to encompass existing calcifications, with the exception of pineablastoma that may have multiple and peripheral calcifications of its own. Other less frequent tumors that are calcified include primitive neuroectodermal tumor, dysembriogenic tumor, gangliogliomas, pilocytic astrocytoma and metastatic tumors of osteogenic sarcoma and mucinous adenocarcinoma or secondary to radiotherapy (24). Tumor calcifications have no pathological significance, but may suggest adequate response to treatment (25) (Figures 17 and 18). Extraaxial tumors, such as craniopharyngiomas occurring in adults, present with visual, Another possible aetiology of acquired calcifications is scarring, either by surgical treatment or by radiotherapy or post trauma, in which case it is of vital importance to know the antecedents and ideally to have the previous diagnostic images to assess if calcifications appear after the traumatic event or treatment, whether or not this type of tumor is associated with calcifications per se and evaluated in relation to the other findings in the image and clinical evolution (Figure 19). Residual calcifications posttreatment or posttrauma 4736 A Diagnostic Algorithm for Patients with Intracranial Calcifications. Topic review Diagnostic Algorithm (Correlate with clinical data and associated imaging findings) Intra-axial Unique Multiples Extraaxial Primary tumors and metastases Tuberculoma Distrophic Figure 20. Diagnostic Algorithm Vascular malformations Infections Metabolic Distrophic Metastasis Facomatosis Primary tumors and metastases Distrophic Vascular Conclusion For a correct approach of the intracranial calcifications it is necessary to define, in the first instance, if they are physiological or pathological; then, together with their location, pattern and morphology, clinical information and other findings in images, to approach possible differential diagnoses, in order to reduce the amount of them. Intracranial physiological calcifications in adults on computed tomography in Tabriz, Iran. A new concept for melatonin deficit: On pineal calcification and melatonin excretion. Physiologic pineal region, choroid plexus, and dural calcifications in the first decade of life. Physiologic calcification of the pineal gland in children on computed tomography: Prevalence, observer reliability and association with choroid plexus calcification. Intracranial hemorrhage revealing pseudohypoparathyroidism as a cause of Fahr syndrome. The frequency and determinants of calcification in intracranial arteries in Chinese patients who underwent computed tomography examinations. Correspondence Catalina Wilches Departamento de Radiologнa e Imбgenes Diagnуsticas Clнnica Reina Sofнa Bogotб, Colombia catalinawilches@yahoo. In diphtheritic neuropathy, the bacterium produces a toxin that inhibits Schwann cell synthesis of myelin constituents, producing severe weakness and large-fiber sensory loss. Neuronopathy: Selective involvement of the cell bodies of motor, sensory and autonomic nerves is the hallmark of this group of neuropathies. Amyotrophic lateral sclerosis and the spinal muscular atrophies are two examples of somatic motor neuronopathies. Somatic sensory neuronopathies result from disruption of the metabolism of sensory nerve cell bodies, followed by degeneration of their processes. Special permeability of the blood vessels in the dorsal root and Gasserian ganglia make these neurons particularly vulnerable to certain toxins. Autonomic Neuronopathy: this unusual group of neuropathies results from isolated involvement of post-ganglionic autonomic neurons and causes idiopathic orthostatic hypotension. The pathologic lesion in this group of neuropathies is confined to the cell bodies. Mixed-Modality Neuropathies: the majority of peripheral neuropathies is not modality-specific, and includes various combinations of motor, sensory and autonomic dysfunction. The reason for this finding is that most peripheral nerves include a mixture of motor, sensory and autonomic axons. Likewise, since most axons are myelinated to a greater or lesser extent, demyelinating neuropathies also produce a mixture of motor, sensory and autonomic symptoms. Electrodiagnostic studies are helpful in quantitating the neuropathy, while blood and urine studies are helpful in identifying an etiology.

Exchange blood transfusion has also been successful in patients who have had splenectomies and who have severe infections caused by B. The use of protective clothing and insect repellents can minimize tick exposure in endemic areas, which is critical for prevention of disease. Ticks must feed on humans for several hours before the organisms are transmitted, so prompt removal of ticks can be protective. These oocysts are similar to those of Cystoisospora belli, the human intestinal protozoan parasite, and can be ingested by mice and other animals (including humans) and produce acute and chronic infection of various tissues, including brain. Some infective forms (trophozoites) of the oocyst develop as slender crescentic types called tachyzoites. These rapidly multiplying forms are responsible for the initial infection and tissue damage. Slow-growing shorter forms called bradyzoites also develop and form cysts in chronic infections. The wide variety of animals that harbor the organism- carnivores and herbivores as well as birds-accounts for the widespread transmission. Humans become infected from two sources: (1) ingestion of improperly cooked meat from animals that serve as intermediate hosts and (2) ingestion of infective oocysts from contaminated cat feces. Serologic studies show an increased prevalence in human populations where the consumption of uncooked meat or meat juices is popular. It is noteworthy that serologic tests of human and rodent populations are negative in the few geographic areas where cats have not existed. Outbreaks of toxoplasmosis in the United States are usually traced to poorly cooked meat. Transplacental infection can occur in pregnancy, either from infection acquired from meat and meat juices or from contact with cat feces. Transplacental infection from an infected mother has a devastating effect on the fetus. The sharing of needles between intravenous drug users may also facilitate transmission of Toxoplasma. Although the rate of seroconversion is similar for individuals within a geographic location, the rate of severe infection is dramatically affected by the immune status of the individual. Illness in this setting is generally believed to be caused by reactivation of previously latent infection rather than new exposure to the organism. Only one species exists, and there appears to be little strain-to-strain variation. Physiology and Structure Organisms develop in the intestinal cells of the cat, as well as during an extraintestinal cycle with passage to the tissues via the bloodstream (Figure 74-7). The organisms from the intestinal cycle are passed in cat feces and mature into infective cysts within 3 to 4 days in the external environment. In humans, pigs, and other vertebrates Ingested In external environment Mature oocyst containing sporozoites Sporozoite Tachyzoites in tissue cell Oocyst with sporoblast Bradyzoite Cyst with bradyzoites Sporozoite Bradyzoite Infective stage Trophozoite Merozoite (Schizogony) Cat (definitive host) Diagnostic stage Immature oocyst Sexual reproduction Clinical Syndromes Most T. When symptomatic disease occurs, the infection is characterized by cell destruction, reproduction of more organisms, and eventual cyst formation. Shortly afterward, she became febrile and neutropenic, and treatment with broadspectrum antibiotics was started. After resolution of neutropenia (1 month post transplantation), confusion and lethargy developed. Imaging studies of the brain revealed microinfarcts in both hemispheres and the midbrain. When toxic epidermal necrolysis developed, the sulfadiazine was discontinued and clindamycin was begun. Histopathologic findings and immunohistochemical staining confirmed a diagnosis of disseminated toxoplasmosis. Disseminated toxoplasmosis is rare, especially after autologous stem cell transplantation.

J Psychiatry Neurosci 25:446 458 Braunig P, Sarkar R, Effenberger S, Schoofs N, Kruger S (2009) Gender differences in psychotic bipolar mania. Biochem Pharmacol 68:1507 1514 Craddock N, Sklar P (2009) Genetics of bipolar disorder: successful start to a long journey. Lancet 361:1693 1699 Jaenisch R, Bird A (2003) Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Proc Biol Sci 263:689 696 Kieseppa T, Partonen T, Haukka J, Kaprio J, Lonnqvist J (2004) High concordance of bipolar I disorder in a nationwide sample of twins. Curr Opin Clin Nutr Metab Care 9:388 394 Lachner M, Jenuwein T (2002) the many faces of histone lysine methylation. Curr Opin Cell Biol 14:286 298 Lachner M, Sengupta R, Schotta G, Jenuwein T (2004) Trilogies of histone lysine methylation as epigenetic landmarks of the eukaryotic genome. Cold Spring Harb Symp Quant Biol 69:209 218 Lambert D, Gill M (2002) Evaluation of parent of origin effect in bipolar affective disorder relating to susceptibility loci on chromosome 18. J Nippon Med Sch 76:43 Moore T, Haig D (1991) Genomic imprinting in mammalian development: a parental tug of war. Cell 99:247 257 Ostrer H (1999) Sex based differences in gene transmission and gene expression. J Neurosci 26:9022 9029 Rakyan V, Whitelaw E (2003) Transgenerational epigenetic inheritance. Trends Genet 18:348 351 Reik W, Dean W, Walter J (2001) Epigenetic reprogramming in mammalian development. Am J Psychiatry 154:1641 1647 Sit D (2004) Women and bipolar disorder across the life span. Mol Psychiatry 13:558 569 St Clair D, Xu M, Wang P, Yu Y, Fang Y, Zhang F, Zheng X, Gu N, Feng G, Sham P, He L (2005) Rates of adult schizophrenia following prenatal exposure to the Chinese famine of 1959 1961. Curr Psychiatry Rep 4:130 133 Tochigi M, Iwamoto K, Bundo M, Komori A, Sasaki T, Kato N, Kato T (2008) Methylation status of the reelin promoter region in the brain of schizophrenic patients. Trends Biochem Sci 22:128 132 Watanabe D, Suetake I, Tada T, Tajima S (2002) Stage and cell specific expression of Dnmt3a and Dnmt3b during embryogenesis. Such endophenotypes are genetically correlated with disease liability, can be measured in all individuals (both affected and unaffected), and provide much greater power to localize and identify disease-related quantitative trait loci than affective status alone (Gottesman and Gould 2003). Clinical Endophenotypes for Bipolar Disorder 53 2 Defining Endophenotypes In the late 1960s, Gottesman and Shields coined the term "endophenotype" to describe traits that could be used as proxies for diagnosis in psychiatric genetics research (Gottesman et al. Furthermore, the term endophenotype was originally intended to denote a trait that was not an obvious manifestation of an illness. Instead, an endophenotype was defined as hidden or not discernible by clinical interview (Gottesman et al. Over the last 40 years, the definition of an endophenotype has become less precise and even a point of controversy (Insel and Cuthbert 2009). Indeed, the terms endophenotype, intermediate phenotype, risk factor, and (genetic) biomarker are all used to describe measures that are sensitive to liability for an illness but are not formally part of the illness itself. While these terms are used somewhat interchangeably in the literature, each has a different connotation (Bearden and Freimer 2006). The term endophenotype is specific to psychiatric genetics and tends to denote processes associated with psychiatric illnesses that are not readily observable. In addition, the study of endophenotypes for complex human psychiatric disorders could potentially be extended to animal models (Gould and Gottesman 2006), advancing our understanding of the neurobiology of psychiatric disorders, and furthering the development of novel medications (Nestler et al. Among the many recommendations, the workgroup pointed to the need for the widespread use of an endophenotype-based approach in order to facilitate the identification of susceptibility genes. Burdick co-segregate with the illness within a family, with nonaffected family members showing impairment relative to the general population (Gershon and Goldin 1986; Glahn et al. Twin, family, and adoption studies report heritability estimates of adult intelligence between 0. Endophenotypic measures must be associated with the illness being studied (Gottesman and Gould 2003). Furthermore, formal neuropsychological deficits have been documented in asymptomatic patients who do not complain of cognitive difficulties (Martinez-Aran et al. Endophenotypic markers should be somewhat independent of illness state (Gottesman and Gould 2003). A qualitative review concluded that although lithium had a negative effect on memory and speed of information processing, patients were often unaware of these deficits (Honig et al.