In free-feeding animals, including humans, most daily water consumption is prandial, occurring during or soon after meals. In contrast to earlier interpretations, it now appears that this drinking has a systemic basis and is not purely anticipatory. Those systemic changes include small increases in osmolality, especially in hepatic portal regions, or decreased plasma volume with increase in plasma ANG II, and together these may be suprathreshold for initiation of drinking. In addition, release of histamine during eating may promote prandial drinking. Because feeding and thus associated drinking normally have a species-typical nycthemeral rhythm, studies of drinking at different times of day are potentially informative. Despite many studies in this regard, it is not fully clear whether osmotic (and/or volumetric) mechanisms for initiation of drinking and/or termination of drinking have different thresholds at different times of day. Recent work has shown a direct pathway from the suprachiasmatic nucleus (master clock) to the OVLT, which suggests at least the potential for direct clock influences on osmoregulation. I speculate that nycthemeral changes in body temperature may also affect the sensitivity of osmoreceptive and/or other elements of drinking circuitry in the brain.

Mechanisms of water acquisition, including drinking, are quite varied across species, reflecting their evolutionary and ecological histories. Increased osmolality seems to be a near-universal stimulus to water acquisition, but responsiveness to ANG II is considerably more restricted.

Cellular dehydration caused by stimuli such as hypertonic NaCl or mannitol cause a sustained shrinkage of osmosensitive cells, and in osmosensitive neurons this is transduced into a proportional change in firing rate. The basal firing rate of these neurons may encode an effective set point for osmoregulation. In the brain, these osmoreceptors seem to be predominantly in the SFO, MnPO, and OVLT. From selective lesion and other evidence, it appears that these regions act in a synergistic manner, such that optimal drinking and/or AVP secretion occurs when all three of these interconnected regions are functional. Some data suggest that there may be species differences in the details of this integrated functioning of the lamina terminalis.

Injection of solutes such as Na+ or mannitol, which initially elevate ECF osmotic pressure and then draw water from cells to dilute the load to near isotonicity, causes reliable drinking in all species studied. This osmoregulatory drinking is accompanied by report of thirst in humans and secretion of AVP. The threshold elevation of systemic osmolality to initiate these changes is in the range 1–3%. Regardless of whether drinking is allowed, the osmotic load is excreted by the kidney over the course of2–4 hours. From sham drinking and other studies, osmoregulatory drinking is satiated when osmotic pressure is normalized and cellular water is restored. Many studies have shown that osmoreceptors for drinking and AVP secretion are located in or near the CVOs of the lamina terminalis. In addition, peripheral osmoreceptors in the gut or splanchnic regions monitor the osmolality of fluids absorbed from the gut and are sufficient to stimulate drinking in the absence of systemic hyperosmolality.

Water deprivation or restriction is arguable the most natural of all dehydrations.The magnitude and rate of dehydration depends on the water and electrolyte content of available food, and the extent to which dehydration anorexia mitigates the net dehydrating effect of food.The early stages of water deprivation produce primarily intracellular dehydration, whereas longer durations of deprivation cause progressively greater extracellular fluid losses. Thus, the resulting stimulus to drink is a combination or hybrid of intracellular and extracellular drinking. There are considerable species differences in the rates of postdeprivation drinking and in the mechanisms that terminate such drinking, although in all cases some contribution of preabsorptive controls is evident. The principal structures of the lamina terminalis (OVLT, MnPO, SFO) collectively contribute to postdeprivation drinking, although the relative contribution of these structures may depend on the duration or degree of net dehydration and/or have species differences. Many neurons of the lamina terminalis are excited by both hyperosmolality and ANG II, and so act as integrators, but it has not been established whether the nature of that integration (or threshold) differs between cells within a region, or between regions.

Acute depletion of ECF volume without change in osmolality is sufficient to induce drinking in many species. However, the threshold for drinking appears to be quite large, of the order 10–20% loss of plasma volume. This change may occur without significant drop in arterial pressure, due to effective physiological counter-regulation, including secretion of renin from the kidneys and subsequent generation of ANG II. Under many conditions of actual or simulated hypovolemia, ANG II appears to be involved in the drinking response and probably by action on AT1a receptors in the SFO. However, interference with ANG II production and/or action does not uniformly disrupt all forms of hypovolemia-related drinking, and it appears that afferents from cardiopulmonary pressure receptors may also be involved. There may be strain differences in the relative contribution of these two mechanisms, or others, to extracellular dehydration drinking. Restoration of ECF volume requires ingestion of NaCl as well as water, and mechanisms for this are discussed briefly.

Body water is contained in intracellular and extracellular compartments, in approximately a 2:1 ratio. The ionic concentrations are quite different between compartments and Na+, and the predominant cation in the ECF, Na+, is of particular significance with respect to maintaining the volume of the ECF. Several specialized organs and hormones for maintaining ionic and fluid balance are described.

During pregnancy in humans and rats, plasma osmolality is regulated at a level about 3% lower than in nonpregnant females (or males). This may be, in part, caused by reproduction-related hormonal changes. Late in gestation, fetal sheep show acute swallowing responses to some dipsogens, and the relevant CVOs in the brain appear to have full responsiveness to those dipsogens at this time. Postnatal development of independent drinking in rats shows that responses to hypovolemia are present and vigorous very soon after birth, whereas development of osmoregulatory drinking has a considerably slower ontogenetic trajectory. Further, this trajectory seems to be slower in mice than rats and requires further study. Some aspects of osmoregulatory drinking in rats, as well as food-associated drinking, appear to have an experiential component. Hypovolemia or other circulatory challenges before birth in rats cause alterations in the ontogenetic trajectory of drinking, although the limits and mechanisms of this phenotypic plasticity have not been fully elucidated.

Experimental analysis of drinking in humans has yielded inconsistent results, ranging from no deficits relative to young groups, to substantial deficits. It is possible that cognitive or other factors can account for some of these differences between studies. Age-related dehydration in at-risk human populations may be minimized by ensuring adequate food intake and meal-associated drinking and/or provision of foods with high fluid content. With the exception of hypotension-related stimuli, age-related declines in drinking by rats after about 25% of the life span are small. Increased drinking at younger ages (3–4 mo) seems to be the unexplained anomaly; a generic explanation would be maturation in late adolescence of an as-yet unrecognized inhibitory mechanism.

The definition of combined approaches is broad. This can include multiple portals to the same or different region in the skull base. The “pull-through technique is a versatile, dual-keyhole approach developed to attach tumors that extend between the temporal and occipital poles. This approach is complex, as it entails a knowledge of the intricate anatomy and eloquent cortical and subcortical structures in this region. This combined approach is tailed to minimize peripheral brain damage while providing a direct route to the pathology. This chapter discusses the indications, the anatomy, the patient selection, and the surgical nuances of this approach.

The combined petrosal approach (CTA) is one of the most complicated neurosurgical procedures. It is essential to learn and acquire the micro-anatomical key elements to complete a safe and less invasive CTA. The Fukushima lateral position can provide for an adequate surgical field and reduce the patient’s stress brought on by a long operative time. Three-layer scalp elevation including harvest of a vascularized flap is mandatory to carry out the closure. One should consider the bony landmarks to carry out the craniotomy safely and widely. The tentorial resection and dural incision are very important to secure the wide surgical field and to avoid complications. Closure with fat tissue and a vascularized flap is recommended to avoid postoperative CSF leak, deformity, and infection.

Intraventricular lesions are challenging pathologies in neurosurgery. Walter Dandy had a major impact in advancing our understanding of the management of these lesions. Furthermore, the introduction of the microscope and microsurgical techniques have improved the surgical outcomes of these lesions. Several approaches have been described to address ventricular lesions, and can be classified anatomically as anterior, lateral, or posterior. The operative corridor for each of these approaches transgresses unaffected neural tissues. Therefore, tailoring the approach to individual patient lesion characteristics and anatomy is crucial to maximize exposure and minimize morbidity. The majority of open and endoscopic approaches to the third ventricle use the interhemispheric anterior transcallosal, frontal transsulcal, or frontal transcortical corridor to access the lateral ventricle. Once inside the lateral ventricle, the operative corridors to the third ventricle include working through the foramen of Monroe (transforaminal approach) for small lesions located in the anterior superior part of the third ventricle, or through the choroidal fissure (transchoroidal or subchoroidal) which provide access to lesions located in, or extending into, the middle or posterior parts of the roof of the third ventricle. In this chapter, we will discuss the transchoroidal, subchoroidal, and combined transchoroidal and subchoroidal approaches to the third ventricle.

There is no single optimal approach for all skull base pathologies and locations. Skull base surgeons must tailor their surgery to both the tumor and the goals of care for the patient to optimize conditions for tumor removal while minimizing morbidity. Lateral skull base approaches are an attractive option to access the skull base given the direct surgical access to the lower cranial nerves, the intra- and extratemporal internal carotid artery (ICA), and the venous sinuses. These approaches can be broadly classified as otic capsule-sparing and otic capsule-sacrificing. These approaches are complex in nature, and patient selection on a case-by-case basis with multidisciplinary input is essential. Complex skull base tumors may not be adequately addressed with a single surgical approach and may require a combination or modification of these techniques. In this chapter, we will describe transcochlear approaches and how they can be modified to provide extended skull base access.