Abnormal development manifestations

Among both children and adults, panic attacks are associated with a set of respiratory abnormalities (Klein, 1993 Pine et ah, 2000). These abnormalities are found not only in panic disorder but also in a range of other conditions, such as separation anxiety disorder and isolated panic attacks, which show strong familial associations with panic disorder. It has been suggested that parents with panic disorder transmit a diathesis for certain forms of anxiety that is apparent in the respiratory system (Pine, 1999), may remain latent (Coryell, 1997), or may vary across development, manifested as separation distress during childhood or as panic attacks after puberty (Klein, 1993 Pine et ah, 2000). 

The final manifestations of abnormal development are death, malformation, growth retardation, and functional disorder. 

Another line of research is focused on the neurobiological development of the human brain in relation to schizophrenia. It has been hypothesised that schizophrenia is due to abnormal neurodevelopment, which results in a static encephalopathy that usually becomes manifest in adolescence. This abnormal development leads to morphological deviations such as enlarged or reduced brain structures, a disrupted communication between different brain structures, alterations in neuron density or decreased neuron size, and abnormal neuronal... 

In 2004 Okrm and colleagues studied the role of cytokines and growth hormone in the regulation of sleep and narcolepsy. Collectively, proinflammatory cytokines and human growth hormone (HGH), were found to be possibly involved in the development of or the exacerbation of narcolepsy (a disabling neurological sleep disorder characterized by excessive daytime sleepiness and abnormal sleep manifestations). As the role of the immune system in sleep becomes clearer, a better interpretation will be available to assess why narcoleptics have altered cytokine and HGH levels. Future studies should be conducted to fuUy characterize the sources, patterns, and significance of alterations in patterns of proinflammatory cytokines and HGH in narcolepsy. ... 

Congenital adrenal hyperplasia A rare inherited condition resulting from a deficiency in cortisol and aldosterone synthesis with resulting excess androgen production. The clinical presentation depends on the variant of the condition, but it typically manifests as abnormalities in sexual development and/or adrenal insufficiency. 

Atherosclerosis is a wide-spread pathology, manifested chiefly by the deposition of cholesterol in arterial walls, which results in the formation of lipid plaques (atheromas). Lipid plaques are specific foreign bodies around which the connective tissue develops abnormally (this process is called sclerosis). This leads to the cal-cification of the impaired site of a blood vessel. The blood vessels become inelastic and compact, the blood supply through the vessels is impeded, and the plaques may develop into thrombi. 

Patients who have received neuroleptics for long periods of time may develop a hyperkinetic disorder of the extrapyramidal system characterized by involuntary, purposeless movements affecting many parts of the body. This is known as tardive dyskinesia. Most commonly, these are manifested in a syndrome involving abnormal movements of the tongue, mouth and masticatory muscles. There are also choreoathetoid movements of the extremities. The mechanism by which these symptoms develop remains unknown. 

After incubation, initial clinical manifestations include fever, cough, chills, myalgia, headache, and sometimes pleuritic chest pain. Approximately 50% of patients show abnormal chest x-rays patchy infiltrates resemble viral disease. Uncommon complications include endocarditis, hepatitis, aseptic meningitis, encephalitis, and osteomyelitis. Most patients who develop endocarditis have preexisting valvular heart disease.3... 

Developmental toxicity, defined in its widest sense to include any adverse effect on normal development either before or after birth, has become of increasing concern in recent years. Developmental toxicity can result from exposure of either parent prior to conception, from exposure of the embryo or fetus in utero or from exposure of the progeny after birth. Adverse developmental effects may be detected at any point in the life span of the organism. In addition to stmcmral abnormalities, examples of manifestations of developmental toxicity include fetal loss, altered growth, functional defects, latent onset of adult disease, early reproductive senescence, and shortened life span (WHO/IPCS 2001b). 

Excessive estrogenic stimulation Certain patients may develop undesirable manifestations of excessive estrogenic stimulation (eg, abnormal or excessive uterine bleeding, mastodynia). Advise the pathologist of estrogen therapy when relevant specimens are submitted. 

Sheppard, A.M., and Pearlman, A.L. (1997) Abnormal reorganization of preplate neurons and their extracellular matrix an early manifestation of altered neocortical development in the reeler mutant mouse. / Comp Neurol 378 173—179. 

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