Neurology. Charles H. Clarke

bodies lie posteriorly. The reticular nucleus surrounds each thalamus laterally, separated by an external medullary lamina traversed by thalamo‐cortical fibres. The three groups of thalamic nuclei, somewhat uninformatively named are:

       Relay (specific) nuclei

       Association nuclei

       Non‐specific nuclei.

      Thalamic nuclei connect to most areas of the cortex, cerebellum and cord. The neurology of thalamic damage is confined largely to central post‐stroke pain, a.k.a. thalamic pain, and sensory loss (Chapters 6 and 23).

      Hypothalamus and Pituitary

      Hypothalamic Region

The multiple paired nuclei of each hypothalamus lie each side of the third ventricle (Figure 2.14).

      The hypothalamus is a central neural effector of basic survival, with roles in:

       Temperature homeostasis, regulation of food and water intake;

       Defence, arousal and sleep–wake cycles, sexual, endocrine and autonomic activity.

Figure 2.14 (a) Hypothalamic & pituitary region: sagittal – from right (b) Partial coronal section through A‐A. DN – dorsal nucleus; PN – posterior nucleus; LN – lateral nucleus; TMN – tuberomamillary nucleus; MB – mamillary body; PAR – paraventricular nucleus; DMN – dorsomedial nucleus; VMN – ventromedial nucleus; PER – periventricular nucleus; Arc – arcuate nucleus; GPL – globus pallidus lateral; GPM – globus pallidus medial; MFB – medial forebrain bundle; ZI – zona incerta.

      Source: Fitzgerald (2010).

For an area so intimately involved in essential activities, lesions of the hypothalamus are unusual. One reason is simple – bilateral destruction is necessary to produce clinical effects.

       Neuroendocrine Cells

      These neurones, specific to the region, both conduct action potentials and also liberate into the bloodstream peptide and other hormones, the latter having been synthesised in the endoplasmic reticulum and stored in Golgi complexes. The peptides are attached to long‐chain polypeptides – neurophysins. Cell bodies lie in the region of the preoptic nuclei and tuber cinereum. The principal nuclei that contribute to this system are the supraoptic, paraventricular, ventromedial and arcuate nuclei.

      Small neurone (parvocellular) axons in the tubero‐infundibular tract reach the median eminence, where releasing and inhibiting hormones are liberated. Large neurone (magnocellular) axons form the hypothalamo‐hypophysial tract→ posterior pituitary.

       Sympathetic and Parasympathetic Hypothalamic Activity (See Chapter 24)

       Water Intake, Thirst, Appetite and Satiety

      Zona incerta cells beside each lateral nucleus of the hypothalamus control thirst. Lesions lead to neglect of drinking. Other mechanisms contribute to osmotic homeostasis, for example serum sodium and glucose levels, and renal function.

      Balance between lateral and ventromedial hypothalamic nuclei constitutes a satiety control system.

       Lateral hypothalamic (feeding centre) stimulation leads to overeating

       Lateral hypothalamic destruction leads to lack of interest in food

       Ventromedial hypothalamic (satiety centre) stimulation inhibits eating

       Ventromedial hypothalamic destruction (bilateral) leads to gross obesity.

      Serotonin down‐regulates appetite. Selective serotonin reuptake inhibitors (SSRIs) and most antidepressants tend to increase appetite.

      Mood, Sexual Arousal, Wakefulness and Memory

      Aggression or docility are features of lateral/ventromedial hypothalamic imbalance. Obese animals with ventromedial lesions become aggressive. Underweight, ventromedially stimulated animals are docile. Hunger stimulates arousal. Maybe this explains why some people become grumpy when they are not fed at the time they expect to be.

      Sexual arousal: specific neurones (INAH3 cells) in each preoptic nucleus are more numerous in males than in females. This is an area rich in androgen receptors, activated by testosterone and induces male sexual activity. In females, neurones rich in oestrogen receptors are found in the ventromedial nucleus: stimulation induces sexual arousal.

      Sleep–wake cycles are set by the suprachiasmatic nucleus via pineal gland connections. Arousal is mediated via richly histaminergic neurones in the posterior hypothalamus (the tuberomammillary nucleus). These project widely (medial forebrain bundle, cortex, brainstem, cord). Hypersomnolence in Man is seen when the posterior hypothalamus is damaged bilaterally.

      Memory: the mammillary bodies are stations on Papez’s circuit (fornix → mammillary bodies → mammillothalamic tract → anterior nucleus of thalamus, Chapter 22). Mammillary body destruction produces a dramatic amnestic syndrome.

      Anterior/Posterior Pituitary Axes and Circumventricular Organs

      These are mentioned briefly. In the anterior pituitary, ACTH (corticotrophin), FSH/LH, GH, prolactin and thyrotropin have peptide releasing hormones. GH and prolactin also have inhibiting hormones – prolactin IH is dopamine.

      For the posterior pituitary, the hypothalamo‐hypophyseal tracts pass from large (magnocellular) neurones of the supraoptic nucleus and paraventricular nucleus. There are also contributions from periventricular neurones (opiate and peptide neurotransmission) and brainstem (aminergic) neurones. Vasopressin (antidiuretic hormone) and oxytocin are secreted by the supraoptic and paraventricular nuclei – hormones are housed in axonal secretory granules (Herring bodies) before release into the capillary system within the posterior pituitary.

      The circumventricular organs are neurones and glia adjacent to the ventricular system, each with an intimate relation to fenestrated capillaries:

       Neurohypophysis – ADH secretion

       Median eminence – anterior pituitary hormone release and inhibition

       VOLT (Vascular Organ of Lamina Terminalis) – feedback loop: low blood volume→renin→angiotensin II→VOLT/SFO→ADH

       SFO (SubFornical Organ)

       Area postrema – emetic centre, obex of 4th ventricle

       Pineal gland – melatonin, sleep‐wake cycles.

Acknowledgements

      I am most grateful to Professor Roger Lemon, UCL Institute of Neurology for his contribution to our neuroanatomy chapter in Neurology A Queen Square Textbook Second Edition upon which part of this text is based.

Professor Thomas Champney, Miller School of Medicine, University of Miami, Florida, USA was most helpful in providing new illustrations, from Champney, TH. Essential Clinical Neuroanatomy.