Cerebral hyperplasia

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

Dexamethasone Synthetic glucocorticoid, lacks mineralocorticoid activity Used to treat range of inflammatory diseases. Used to treat some forms of asthma, also cerebral oedema and congenital adrenal hyperplasia... 

Substitution therapy for deficiency states acute or chronic adrenal insufficiency, congenital adrenal hyperplasia, and adrenal insufficiency secondary to pituitary insufficiency, nonendocrine disorders arthritis rheumatic carditis allergic, collagen, intestinal tract, liver, ocular, renal, shin diseases bronchial asthma cerebral edema malignancies PO 5-60 mg/day in divided doses. Intra-articular, Intralesional (acetate) 4-100 mg, repeated as needed. Intra-articular, Intralesional (sodium phosphate) 2-30 mg, repeated at 3-day to 3-week intervals, as needed. IM (acetate, sodium phosphate) 4-60 mg a day. 

CNS Copper deposits affect the whole CNS. Degeneration and tissue loss as well as atrophy of the lenticular nucleus prevail. Occasionally, there are also small necrotic foci with a diffuse spot-like distribution. Micro-cavernous lesions occur due to the destruction of nerve cells. Myelinized fibres and oligodendrocytes are present, but there is also cellular hyperplasia and hypertrophy of astrocytes rich in protoplasm. The cerebral changes detectable in CT scanning do not correlate with the degree of severity of the functional disturbances (320, 335) however, there is a close correlation between the lesions detected by MRI and certain neurological findings. (350, 366, 376, 388) (s. p. 615)... 

A variety of neuroanatomic differences have been observed in samples of autistic patients in comparison with controls. This topic has been reviewed in recent publications [43-45]. Magnetic resonance imaging (MRI) studies show that by 2-4 years of age, 90% of autistic children have an abnormal early brain overgrowth followed by abnormally slowed growth [45, 46]. The most common finding has been hyperplasia of cerebral gray matter and cerebral and cerebellar white matter in the early life of autistic patients [46]. 

Fig. 9.1 Alzheimer Type II astrocytosis in HE (chronic liver failure) (a) light micrograph of cerebral cortex from a cirrhotic patient who died in hepatic coma. Note prominence of pale, enlarged astroglial nuclei frequently occurring in pairs (anvw) suggestive of hyperplasia. A normal astrocyte nucleus is shown for comparison purposes (arrowhead). Bar = 20 pM. (b) Similar section showing intranuclear glycogen inclusions (arrow). Inset irregular lobular astrocyte in pallidum. Reproduced from Norenbeig (1987), with permission from Humana Press...

Histopathological and morphological findings with fatal encephalopathy presented in the form of cerebral edema, endothelial hypertrophy and hyperplasia, and perivascular glial proliferation. Various ischemic disorders were also reported cell necrosis and neuronal loss in isocortex and basal ganglia... 

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