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Iron Deficiency

Iron deficiency is the most common nutritional deficiency in the world. Iron is an essential component of hemoglobin (55% of the total body Fe), myoglobin (15% of the total body Fe), and cytochromes. Iron deficiency leads to anemia, i.e., a reduction of the oxygen transport capacity in the blood. Moreover, iron is normally present in every griseum of the CNS as a component of certain enzymes and intracellular pigments (hemosiderin pigments). Some of it is unmasked and thus gives a positive reaction with Prussian Blue stain.

Definition and Clinical Features. Iron deficiency is defined as an abnormal value for at least two of the following three indicators: serum ferritin, transfer-rin saturation, and free erythrocyte protoporphyrin. Persons with iron deficiency and a low hemoglobin value are considered to have iron deficiency anemia. Although iron deficiency is more common in developing countries, a significant prevalence was observed in the United States during the early 1990s among certain populations, such as toddlers and females of childbearing age (Looker 2002). Iron deficiency can be caused by:

— Starvation

— Poor absorption

— Damage to the digestive system

Alcoholism

— Acute or chronic loss of blood (hemorrhages)

In adults, iron deficiency may be caused by acute hemorrhages, chronic blood loss, and disturbances of iron resorption. Biochemically, iron deficiency results in decreased heme proteins, iron-containing enzymes, and reactions in which iron is involved as a cofactor. Consequently, there are changes in nucleic acid biosynthesis, oxidative respiration and mitochondrial function, detoxification of metabolic byproducts and catecholamine metabolism (Prasad and Prasad 1991).

Pathophysiology and Neuroanatomy. Iron, transported by transferrin, enters brain endothelial cells via receptor-mediated endocytosis (Connor and Fine 1987). Iron is most commonly located in oli-godendrocytes of rat and human brains (Dwork et al. 1990). Iron-rich areas in the brain include the globus pallidus, ventral pallidum, substantia nigra reticulata, interpeduncular nucleus, cerebellar nuclei, facial nucleus, and the superior olive (Hill and Switzer 1984). Free iron has been implicated in the pathophysiology of several brain diseases, including Parkinson's and Alzheimer's disease, superficial sid-

erosis, and multiple sclerosis; excessive iron deposition in the already iron-rich basal ganglia has been demonstrated with Hallervorden-Spatz syndrome (Beard et al. 1993; Swaiman 2001).

Neurology and Neuropathology. Iron will be essential during the time of rapid development of the human fetal brain, i.e., from the 10th to 18th weeks of pregnancy. Malnutrition during these periods of rapid brain growth may have devastating effects on the nervous system and can affect not only neurons, but also glial cell development and growth. Effects on glial cells may change myelin development especially because myelin continues to form around axons for several years after birth (Back and Volpe 1997).

Babies born to mothers who had poor diets may have some form of mental retardation or behavioral problems. Also, children who do not receive adequate nutrition in their first few years of life may show delayed development. The following symptoms are seen in children: developmental delay, pediatric stroke, breath holding spells, pseudotumor cerebri, and cranial nerve palsies (Yager and Hartfield 2002). Often the effects of malnutrition and environmental problems, such as emotional and physical abuse, can combine to create behavioral problems. Therefore, the exact causes of behavioral disorders are difficult to determine (Brick and Erickson 1998). In adults, the most common sequelae are disturbances of at-tentiveness, concentration, and fatigue. Special neu-ropathological findings are not described.

23.2 Stroke

Incidence and Pathogenesis. Stroke in children is estimated at about 2.6 and 3.1 per 100,000 per year, in white and black children, respectively (Schoenberg et al. 1978; Broderick et al. 1993). The following essential risk factors should be mentioned (Nicolaides and Appleton 1996; Kirkham et al. 2000; Roach 2000; - for review: Sträter et al. 2002) in addition to so-called idiopathic ischemic strokes (Abram et al. 1996; Schievink et al. 1996; Kirkham 1999):

— Congenital heart malformations

— Hemoglobinopathies (sickle cell disease)

— Hematological and coagulation disorders (venous thrombosis or embolus from the heart)

— Infectious diseases (varicella zoster, HIV)

— Collagen diseases

— (Rare) inborn metabolic disorders

— Inborn abnormal respiratory control (Takashima and Becker 1989)

— Hereditary factors

— Dehydration

Fig. 23.2a-c. Generalized ischemic stroke. a Cardiac arrest in an 11 day old boy who survived for 10 days; b near SIDS with apnea and resuscitation in a 5-year-old girl who survived for about 5 years with bilateral cortical atrophy of the frontal lobes and cys tic alterations of the putamen (circles); c schizogyric alteration of the brain surface in a 3-year-old boy who survived the stroke for about 3 years

Fig. 23.2a-c. Generalized ischemic stroke. a Cardiac arrest in an 11 day old boy who survived for 10 days; b near SIDS with apnea and resuscitation in a 5-year-old girl who survived for about 5 years with bilateral cortical atrophy of the frontal lobes and cys tic alterations of the putamen (circles); c schizogyric alteration of the brain surface in a 3-year-old boy who survived the stroke for about 3 years

Neuropathology. The brain morphology commonly is characterized by the features of a pale, ischemic infarct (Fig. 23.2; see also Fig. 23.4a, b), while a hemorrhagic infarct occurs rarely (Humphreys 1991). The morphology and neurological features are comparable with stroke in adult brains which are described elsewhere (pp. 564 ff). The outcome is obviously dependent on the cause of stroke and the extent of brain damage. Idiopathic strokes in childhood were reviewed by Abram et al. (1996). Nearly half of their patients (n=42) had a poor outcome (43%) with moderate to severe hemiparesis (n=14), recurrent stroke (n=7), and death (n=1).

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