книги студ / Color Atlas of Pathophysiology (S Silbernagl et al, Thieme 2000)

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Plate 10.18 Autonomic Nervous System: Disorders

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Lesions of the Hypothalamus

The hypothalamus integrates the body’s autonomic, endocrine, and somatomotor functions. Neurons in the hypothalamus are responsible for regulating various homeostatic functions such as food intake, electrolyte and water metabolism, temperature regulation, and circadian rhythm. In addition, the functions are adapted in the hypothalamus to the required behavioral patterns, such as the fight and flight reaction, nutritive or sexual behavior. The programs required for the particular behavioral patterns are stored in the hypothalamus and are called up as needed, in particular by the neurons of the limbic system.

Circumscribed lesions in the hypothalamus can occur as the result of tumors, trauma, or inflammation, and they can produce profound disorders of autonomic regulation (→A1).

A lesion in the anterior hypothalamus (including the preoptic region) leads to disturbances of temperature regulation and circadian rhythm (destruction of the suprachiasmal nucleus). It expresses itself, for example, in insomnia. Also, as a result of lesions in the supraoptic and paraventricular nuclei, the antidiuretic hormone (ADH) and oxytocin (see below) are no longer formed, and there is no sense of thirst.

A lesion in the medial hypothalamus also results in disorders of temperature control and the sense of thirst. At the same time there may be marked impairment of food intake. A lesion in the lateral part of the medial hypothalamus stops the sensation of hunger. Such patients no longer have the urge to eat (aphagia), their food intake is inadequate, and they lose weight (anorexia). Conversely, lesions of the medial hypothalamus cause a craving for food (hyperphagia) and, because of the intake of hypercaloric food, lead to obesity. However, obesity or anorexia are only rarely due to a hypothalamic lesion, but rather have psychological causes (→p. 26). Damage to the medial hypothalamus also brings about disorders of memory acquisition and emotions.

Lesions in the posterior hypothalamus lead to poikilothermia, narcolepsy and memory gaps, along with other complex autonomic and emotional disorders.

Abnormal release of hypophyseal hormones occurs with lesions in different parts of the hypothalamus. As a result, the peripheral functions regulated by the hormones are affected (→A2). When ADH is not released diabetes insipidus develops in which the kidney can no longer produce concentrated urine and may

cause hyperfunction or hypofunction of the peripheral hormonal glands. Increased release of sex hormones can result in premature sexual maturation (precocious puberty), while reduced release brings about delayed sexual maturity and infertility (→p. 272ff.).

Longitudinal growth is promoted by the sex hormones, somatotropin (→p. 262ff.), and the thyrotropin-regulated thyroid hormones (→ p. 280ff.). A reduced concentration of these hormones delays growth, reduced release of the sex hormones retarding the fusion of the epiphyseal plates which may eventually cause gigantism, despite the slower growth. Corticotropin inhibits longitudinal growth via the action of cortisol.

The main hormones that affect metabolism are somatotropin, thyroid hormones, and the adrenocortical hormones (→p. 268ff.) which are regulated by corticotropin. Abnormal release of the latter hormones can have massive metabolic effects. Thyroid and adrenocortical hormones also have a profound effect on the circulation. The adrenocortical hormones also have an influence on the blood cells. They cause an increase in erythrocytes, thrombocytes and neutrophils, while decreasing the number of lymphocytes, plasma cells, and eosinophils. They thus affect O2 transport in blood, blood clotting, and immune defenses (→p. 268 ff.).

Plate 10.19 Lesions of the Hypothalamus

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The Electroencephalogram (EEG)

The neurons of the cerebral cortex, when their membrane potential is changed, generate varying electrical fields on the surface of the skull that can be recorded with suitable leads. The EEG can provide valuable clues to neuronal functions and as a result has gained great clinical importance. Like the electrocardiogram ([ECG] →p.184), the EEG registers the summated activity of the cells that, projected onto the area of the recording lead, generates similarly directed dipoles.

The potential changes on the cortical surface largely depend on the postsynaptic potentials at dendrites of the pyramidal cells (→A). Although the postsynaptic potentials have a lower amplitude than the action potentials, they last significantly longer. Because the pyramidal cells are positioned at right angles to the cortical surface, their local activity generates dipoles in the direction of the surface much more easily than other cells in the cortex. They thus have a much greater impact on the surface potential than other neurons. Furthermore, they are all orientated in parallel to one another, so that equidirectional potential changes of neighboring pyramidal cells are summated. EEG deflections are to be expected only if (around the lead electrode) several pyramidal cells are simultaneously depolarized, i.e., there is a synchronized event.

During an excitatory postsynaptic potential, Na+ enters the cell and thus leaves behind a local negative extracellular potential (→A1). The depolarization promotes an efflux of K+ ions along the remaining cell membrane, this efflux in turn generating a local positive extracellular potential. If an excitatory synapse at the apical end of a dendrite is activated, the extracellular space in the area is relatively negative, but relatively positive at the base of the dendrite (→A1; to simplify matters the K+ efflux has been entered at only one site). As a result a dipole is generated that creates a negative potential at the surface. Commissural fibers from the other cortical hemisphere and nonspecific parts of the thalamus form excitatory synapses mainly at the surface; excitation via these fibers thus leads to a negative potential at the surface electrode (→A1). Conversely, activation of specific thalamocortical

fibers are more likely to lead to positive potentials at the surface (→A2) because they act near the cell body, i.e., deep in the cerebral cortex. Inhibition in the area of the cell body theoretically results in a negative potential at the surface, but it is not strong enough to be registered at the surface of the scalp (→A3).

The neurons in the thalamus that excite the cortical pyramidal cells undergo a rhythmical activity due to negative feedback (→A4). This rhythm is transmitted by the thalamocortical tracts to the pyramidal cells, with one thalamic neuron simultaneously exciting several pyramidal cells. Because of this, subcortical lesions are better registered in the EEG than small cortical ones.

The frequency of the recorded waves (deflections) is a diagnostically significant criterion when analysing the EEG (→B1). In adults who are awake with their eyes open it is predominantly β-waves (14 – 30 Hz) that are registered. With their eyes closed the somewhat slower α-waves (8 – 3 Hz) dominate. Yet slower waves such as the ϑ-waves (4 – 7 Hz) and the δ- waves (0.5 – 3 Hz) are not normally recorded in waking adults but only in children and adolescents. However, in adults the latter slow waves are recorded during the phases of deep sleep (→p. 340). Some diseases of the brain can result in slowing (sleeping-drug overdose, dementia, schizophrenia) or acceleration (alcoholism, manic-depressive illness) of the recorded frequency.

The EEG is of particular importance when diagnosing epilepsy, which is characterized by massive synchronized excitation of cortical neurons (→p. 338). It causes “spike” activity (“seizure spikes”; →B2) or “spike and wave” complexes (→B3).

In destruction of the cerebral cortex (brain death) all electrical activity will have ceased and the EEG tracing will therefore be isoelectric (“flat”), i.e., there will be no deflections.