Central nervous system secondary disease

In addition to its role in the development of the secondary sex characteristics in females, estrogen has important physiological functions in the cardiovascular, immune, and central nervous systems, as well as its effects on the growth and maturation of the long bones. It is also implicated in a number of diseases (including breast and uterine cancers) and in... 

Patients with preexisting tumors or growth hormone deficiency secondary to an intracranial lesion should be examined routinely for progression or recurrence of the underlying disease process. In pediatric patients, clinical literature has revealed no relationship between somatropin replacement therapy and central nervous system (CNS) turmor recurrence or new extrracranial tumors. However, in childhood cancer survivors, an increased risk of a second neoplasm has been reported in patients treated with somatropin after their first neoplasm. Intracranial tumors, in particular meningiomas, in patients treated with radiation to the head for their first neoplasm, were the most common of these second neoplasms. In adults, it is unknown whether there is any relationship between somatropin replacement therapy and CNS tumor recurrence... 

In contrast to T cells, in different immunopathologies, the brain provides a fostering envkonment to B cells. Primary central nervous system (CNS) lymphomas are usually of B cell origin. The cerebrospinal fluid (CSF) of patients with chronic infections and autoimmune diseases of the CNS typically contains remarkably stable oligoclonal Ig bands. In the CNS of multiple sclerosis patients, clonally expanded B cells and plasma cells persist. Ectopic B cell follicles develop in the meninges of patients with secondary progressive MS, and B cell differentiation may be recapitulated in the CNS of MS patients (Krumbholz et al., 2006) (see Chapters 18-24). 

PrP " deposition in the central nervous system is also a hallmark feature of prion disease (Prusiner, 1991). The type of Prpsc cleposit and its location varies among the human prion diseases. PrP is also a component of amyloid plaques. A characteristic of vCJD and kuru is florid amyloid plaques, which is a large cluster of PrP aggregates interspersed with vacuolar pathology. PrP deposition is also present in peripheral tissues of patients with vCJD, primarily in secondary... 

Deaths from consumption of methylmercury-contaminated foods are well documented in outbreaks in Japan and Iraq, and lethal doses of 10-60 mg Hg/kg have been estimated from tissue concentrations (Bakir et al. 1973 Tsubaki and Takahashi 1986). Fatalities were attributed to central nervous system toxicity (Bakir et al. 1973 Tamashiro et al. 1984). Pneumonia and nonischemic heart disease were prominent secondary causes of death in the Japan epidemic (Tamashiro et al. 1984). Case reports of deaths associated solely with dermal mercury exposure to inorganic mercury are limited to a woman who died after inserting a mercuric chloride tablet into her vagina (Millar 1916) and a man who died after a 2-month treatment with a topical medicine containing mercurous chloride (Kang-Yum and Oransky... 

Clinicians most often confuse botulism with a polyradiculoneuropathy, such as Guillain-Barre or Miller Fisher syndrome, myasthenia gravis or central nervous system disease (36) (see Table 2.14). In the United States, a cluster of cases of flaccid paralysis is more likely secondary to botulism than to GuiUain-Barre syndrome or polio. In addition, compared to other causes of flaccid paralysis, unique features of botulism include (36) ... 

The mechanisms by which PTH might impair central nervous system function are only partially nnderstood. The increased calcium content in such diverse tissues as skin, cornea, blood vessels, brain, and heart in patients with hyperparathyroidism suggests that PTH may somehow facilitate the entry of Ca into such tissues. The finding of increased calcium in the brains of both dogs and humans with either acute or chronic renal disease and secondary hyperparathyroidism is consistent with the conception that part of the central nervous system dysfunction and EEG abnormalities found in acute renal failure or chronic renal failure may be due in part to a PTH-mediated increase in brain calcium. Calcium is essential for the function of neurotransmission in the central nervous system and for a large number of intracellular enzyme systems. Thus, increased brain calcium content could disrupt cerebral function by interfering with any of these processes (Rasmussen, 1986). It is also possible that PTH itself may have a detrimental effect on the central nervous system. 

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