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The glossopharyngeal nerve is a mixed ninth cranial nerve: it carries pharyngeal and lingual sensation, posterior tongue taste, carotid sensory input, motor fibres to stylopharyngeus, and a secretomotor route to the parotid gland. Its connections explain why its name alone understates its functions.

Rootlets leave the lateral medulla oblongata, behind the olive and above those of the vagus nerve. They cross the posterior cranial fossa and leave through the jugular foramen. Superior and inferior sensory ganglia lie at or near that passage. The cervical trunk descends in relation to the internal carotid artery and internal jugular vein, then turns forwards around stylopharyngeus. It reaches the pharyngeal wall between the superior and middle constrictors and divides towards the posterior tongue, tonsillar region and pharynx. Its topographical association with the vagus does not make the two nerves functionally identical.

The tympanic branch returns through the inferior tympanic canaliculus into the middle ear. Its tympanic plexus supplies the mucosa of the tympanic cavity, auditory tube and related air spaces and communicates with carotid sympathetic fibres. Preganglionic parasympathetic fibres continue through the lesser petrosal nerve to the otic ganglion. Postganglionic fibres then reach the parotid gland with the auriculotemporal nerve, a branch of the mandibular division of the trigeminal nerve. This is a useful example of fibres originating in one cranial outflow and travelling for their last segment with another nerve.^[ref]

The branch to stylopharyngeus is motor; contraction elevates and expands the pharynx during swallowing. Pharyngeal branches contribute to the pharyngeal plexus, together with the vagus nerve and sympathetic connections. The principal motor supply of the pharyngeal constrictors is vagal: membership of a mixed plexus does not justify assigning every fibre or every pharyngeal muscle to the ninth nerve. Tonsillar branches supply the palatine tonsil and neighbouring mucosa. Lingual branches carry ordinary sensation and taste from the posterior third of the tongue, including the vallate papillae even though these lie just anterior to the terminal groove.

The carotid sinus nerve carries information from pressure-sensitive endings in the carotid sinus and from the carotid body's chemical sensors. The first contributes to regulation of blood pressure; the second responds especially to arterial oxygen deficiency, with responses also influenced by carbon dioxide and acidity. These are afferent functions, distinct from the motor and secretory branches.^[ref]

In the modern central account, branchial motor fibres arise from the nucleus ambiguus, parasympathetic fibres from the inferior salivatory nucleus, visceral and taste afferents project towards the solitary nucleus, and relevant general sensory fibres project to the spinal trigeminal system. These nuclear and reflex distinctions refine the gross anatomical description available in 1864. Pharyngeal touch can initiate swallowing and contributes to the afferent limb of the gag reflex, whose principal motor limb is vagal. Ordinary sensation, taste, pharyngeal movement and secretion therefore need separate observations; the absence of one response does not by itself prove loss of every ninth-nerve function.^[ref]

The two pneumogastric nerves are the right and left vagus nerves, the tenth cranial nerves: mixed sensory, branchial motor and parasympathetic pathways from the medulla oblongata to the neck, thorax and abdomen. A useful description separates their apparent origin at the surface of the brain from the origins and terminations of their component fibres.

Rootlets emerge in the groove behind the inferior olive, between the glossopharyngeal nerve above and the accessory rootlets below. Branchial motor fibres arise chiefly in the nucleus ambiguus; preganglionic parasympathetic fibres arise in the dorsal motor nucleus of the vagus and, particularly for cardiac control, the nucleus ambiguus. Visceral sensory fibres have their cell bodies chiefly in the inferior vagal ganglion and terminate centrally in the nucleus of the solitary tract; somatic sensory fibres associated with the superior vagal ganglion project to the spinal trigeminal nucleus. Consequently a sensory fibre is not accurately described as originating in a motor nucleus simply because its peripheral nerve emerges nearby.^[ref]

Each vagus nerve leaves the skull through the jugular foramen, with the glossopharyngeal nerve and accessory nerve. It bears the small superior vagal ganglion at the foramen and the larger inferior vagal ganglion below it. Connections include communications with adjacent cranial nerves and the cervical sympathetic nervous system. Traditional descriptions assign fibres joining the vagus nerve from the cranial part of the accessory nerve to the latter peripheral nerve; their modern classification is more nuanced and does not change the peripheral branches being described. In the neck the vagus nerve descends in the carotid sheath, behind and between the internal jugular vein and the internal, then common, carotid artery.

Its meningeal and auricular branches supply small sensory territories of the cranial covering and external ear. Pharyngeal branches contribute to the pharyngeal plexus, supplying much of the soft palate and pharynx; the stylopharyngeus muscle belongs to the glossopharyngeal nerve and the tensor veli palatini muscle to the mandibular division of the trigeminal nerve. The internal branch of the superior laryngeal nerve supplies sensation above the vocal folds; its external branch supplies the cricothyroid muscle. The recurrent laryngeal nerve supplies the other intrinsic laryngeal muscles and sensation below the vocal folds. The right recurrent laryngeal nerve loops beneath the right subclavian artery; the left loops under the aortic arch beside the ligamentum arteriosum. Both return towards the larynx near the groove between trachea and oesophagus.^[ref]

In the thorax, both vagus nerves pass behind the roots of the lungs, contrasting with the anterior course of the phrenic nerves. Cardiac branches join the cardiac plexus; pulmonary branches join the pulmonary plexus. The trunks break up into the oesophageal plexus, then collect principally as an anterior trunk derived from the left vagus nerve and a posterior trunk derived from the right. Through the oesophageal hiatus they reach the stomach; hepatic and coeliac branches distribute to abdominal viscera. Their parasympathetic territory includes foregut and midgut derivatives, extending into the proximal colon, rather than every abdominal and pelvic organ.^[ref] This extensive distribution explains why the level of experimental section is indispensable information.

The main consequences of section can be organized by the interrupted functions:

A discriminating historical experiment would record respiratory movements and heart rate before and after section, distinguish unilateral from bilateral section, and compare an intact airway with an airway bypass. A tracheal cannula can separate obstruction at the glottis from changes in the respiratory rhythm, while the central-versus-peripheral stimulation comparison separates incoming reflex traffic from outgoing motor effects. Later separate-lung recordings confirmed that a change following unilateral section could affect both lungs, supporting a central reflex interpretation rather than simple local paralysis.^[ref] The gastric distinction is also borne out by measurements of persistent acidity after surgical vagotomy, despite major reductions in stimulated gastric acid secretion.^[ref]

The fourth ventricle is the cavity of the hindbrain between the dorsal surfaces of the pons and upper medulla oblongata anteriorly and the cerebellum posteriorly. It is continuous above with the cerebral aqueduct and below, at the obex, with the central canal of the spinal cord. Its floor is diamond-shaped when viewed from behind, while its roof rises dorsally towards the fastigium.

The floor, the rhomboid fossa, consists of an upper pontine triangle and a lower medullary triangle. Its upper apex points towards the cerebral aqueduct; its lower apex is the obex; the two lateral angles continue into the lateral recesses of the fourth ventricle. A median groove divides it into right and left halves. On each side, the medial eminence lies medial to the sulcus limitans, which separates predominantly motor territories medially from sensory territories laterally. The striae medullares of the fourth ventricle cross the floor near the junction of its pontine and medullary portions; their extent varies.

Several surface features identify deeper relations. In the pontine part, the facial colliculus overlies the abducens nucleus and the internal looping course of fibres of the facial nerve; it is not the exposed facial motor nucleus. The upper part of the sulcus limitans has the superior fovea, and near its rostral lateral region lies the locus coeruleus. Laterally, the vestibular area overlies the vestibular nuclei. In the lower triangle, the hypoglossal trigone overlies the hypoglossal nucleus, and the vagal trigone, lateral to it, overlies the dorsal motor nucleus of the vagus. The area postrema lies still farther caudolaterally, separated from the vagal trigone by the funiculus separans. These are landmarks and underlying relations, not claims that the cranial nerve nuclei lie loose within the cavity.^[ref]

The upper lateral boundaries are formed by the superior cerebellar peduncles. The lower lateral boundaries relate to the inferior cerebellar peduncles and adjacent dorsal medullary margins. The lateral recess on each side curves around the inferior cerebellar peduncle towards its external opening near the flocculus.

The roof has superior and inferior slopes. Superiorly the thin superior medullary velum spans the superior cerebellar peduncles, with the lingula of the cerebellum on its dorsal surface. Inferiorly, the roof relates to the inferior medullary velum, nodule of the cerebellum and thin tela choroidea. Vascular folds of the tela choroidea carry the choroid plexus of the fourth ventricle, with median and lateral extensions. The cavity has an ependymal lining; the choroid plexus has its specialized epithelial covering and produces cerebrospinal fluid.

There are three important exits to the subarachnoid space: one median aperture of the fourth ventricle through the inferior roof, opening towards the cisterna magna, and two lateral apertures of the fourth ventricle at the ends of the lateral recesses of the fourth ventricle. These must be distinguished from the inlet through the cerebral aqueduct and the inferior continuity with the central canal of the spinal cord. Most cerebrospinal fluid leaving the fourth ventricle reaches the subarachnoid space, not the narrow adult central canal of the spinal cord.

The three-dimensional arrangement explains the method of examination: reflecting the cerebellum and opening the delicate roof exposes the rhomboid fossa, but destroys part of the structure one is trying to describe. Studying an intact roof, then the exposed floor, and using a median section to locate the fastigium avoids interpreting a dissected cavity as naturally open behind. The modern nomenclature is useful here; not every fine landmark or physiological interpretation in this account should be read as an assertion about what an 1867 examiner required.^[ref]

There is no single constant anatomical lesion of epilepsy. A sound autopsy answer separates an underlying brain lesion, changes associated with longstanding epilepsy, and the consequences of the final seizure or death.

The potentially causal group includes healed traumatic scars, old cerebral infarctions or intracranial haemorrhages, developmental abnormalities of the cerebral cortex, brain tumours, and inflammatory or infectious destruction of brain tissue. Such abnormalities can leave an enduring network capable of generating recurrent seizures. Their importance depends on location and the lifetime history; an incidental abnormality is not automatically the cause. A modern acute symptomatic seizure during a transient metabolic disturbance should also not automatically be called epilepsy.^[ref]

In longstanding cases one may find atrophy or scarring of particular brain regions. Hippocampal sclerosis is an important modern example: loss of neurons with gliosis in the hippocampus, associated especially with temporal-lobe epilepsy. Association does not settle whether a particular lesion preceded the first seizure, resulted from repeated seizures, or shares another cause with them. Conversely, genetically determined disturbances of neuronal excitability can produce recurrent seizures without a grossly visible destructive lesion.^[ref]

For the historical question, vascular redness or congestion and alterations around the medulla oblongata deserve mention as contemporary observations rather than established universal causes. A January 1864 report describes microscopic examination of fourteen longstanding cases, including dilated blood vessels and altered nervous material in that region. Its proposed localization of epilepsy to the medulla oblongata is a historical theory; modern epilepsy is not defined by that site or by those vascular appearances.^[ref]

The terminal group includes cerebral oedema, hypoxic-ischaemic brain injury, and pulmonary oedema or aspiration in some deaths. Congestion is nonspecific and may be terminal; injuries can result from a fall during a seizure. None of these alone establishes that epilepsy was the original cause. A modern autopsy study of sudden deaths in people with epilepsy found both structural abnormalities and nonspecific changes; exclusion of another anatomical or toxicological cause remains central to classifying sudden unexpected death in epilepsy.^[ref]

The appropriate investigation is therefore inspection followed by systematic histology, especially of the cerebral cortex and hippocampus on both sides, interpreted alongside the recorded seizure history and examination of other organs. A normal-looking brain does not exclude epilepsy, and a congested one does not prove it.

Vomiting is a coordinated nervous motor act that can be initiated from the digestive system, circulating emetic substances, the vestibular system, or higher and lower brain pathways. A cause need not lie in the stomach.

Local causes include irritant food or poisons, gastritis, gastroenteritis, gastric outlet obstruction and intestinal obstruction. Chemical irritation, inflammation or distension activates visceral sensory pathways, notably afferents of the vagus nerve, which relay to the medulla oblongata. In obstruction, retention and distension provide continuing stimulation; merely seeing food return does not imply excessive gastric contractile strength. Peritonitis and painful disease elsewhere in the abdomen can also recruit visceral afferent pathways.^[ref]

Circulating emetic agents, including some drugs and metabolic products accumulating in kidney failure, act partly through the area postrema, a chemosensitive region with unusually direct access to substances in the blood. Gastrointestinal and blood-borne inputs converge through the nucleus tractus solitarius and connected medullary networks. It is more accurate to describe interacting groups of neurons than one isolated “vomiting centre”.^[ref]

Other important groups are motion sickness, where information from the vestibular system conflicts with other sensory information; migraine and intracranial disease, including raised intracranial pressure from a brain tumour or intracranial haemorrhage; and higher-centre influences such as a repulsive sight, smell, fear or learned association. Pregnancy-associated vomiting belongs in the differential, with endocrine and central contributions rather than an explanation that it is simply mechanical pressure by the uterus upon the stomach. These causes engage different inputs to an overlapping final motor programme.^[ref]

The act itself requires several coordinated changes. The proximal stomach and lower oesophageal sphincter relax; retrograde activity can bring contents of the upper intestine into the stomach; the diaphragm and abdominal muscles generate a pressure gradient that expels the contents. During expulsion the upper passage opens while coordinated laryngeal closure helps protect the airway. Retching and actual expulsion are related stages, and neither should be confused with effortless regurgitation.^[ref]

This mechanism explains the diversity of causes: many sensory and chemical inputs can recruit the same coordinated output. A pressure recording and observation of gastrointestinal movements during an emetic response can distinguish the patterned act from a simple spontaneous return of contents; they would not, without further evidence, identify the original cause in an individual.

The diamond-shaped floor of the fourth ventricle, formed by the dorsal pons and upper medulla oblongata.