The cerebral tissues of the human brain are comprised of two hemispheres, consisting of subcortical (beneath grey matter) white matter fibres, which project as an extensive array into the grey matter of the cortical (outermost) layer. Inferior to these hemispheres, the configuration of grey and white matter inverts within the inferior medulla as the brainstem descends, and the fibre tracts become continuous with the cervical spinal cord as levels C1 to C8: yielding grey matter interiorly, and white exteriorly as it descends, and throughout the spinal cord until the grey matter tapers into the conus medullaris.

The spinal cord mediates an array of sensations which are crucial for survival and relation to the outside world, itself containing tracts of grey and white matter that are interlinked and compartmentalised with precision signals, each transmitted by dedicated fibres and codified appropriately so they may be conveyed to and from the brain / periphery to provide information.

Within the spinal cord grey matter, the upper half of the butterfly like shape is referred to as the dorsal horn, and it is in this tissue that a variety of 1st order nerve fibres synapse from outside the spinal cord with a vast array of interneurons. The interneurons are fundamental to how physical pain is gated within the spinal cord, as they relay codified signals into 2nd order fibres, exciting or inhibiting ascent to the supraspinal pathways (the brain/stem), thus determining if the pain becomes conscious.

This LV article will focus on the nerves and tracts of the spinal cord in terms of sensation and how losses and gains in neuronal structure can cause nociceptive and peripheral neuropathies.

On Pain

‘I can't tell you how
I knew - but I did know that I had crossed
The border. Everything I loved was lost
But no aorta could report regret.

A sun of rubber was convulsed and set;
And blood-black nothingness began to spin
A system of cells interlinked within 
Cells interlinked within cells interlinked
Within one stem. 

And dreadfully distinct
Against the dark, a tall white fountain played’.

~ Vladimr Vladimirovich Nabokov.

Nabokov’s verse implies the experience of a heart attack, using visceral language to evoke a sense of sudden dread and vascular trauma. In terms of neural sensation, experience of pain within the viscera is led by interoceptive sensation, and due to the chemical signalling and structure of specific C-fibres which codify this pain, tending by default to have a more dull, burning and poorly localised codification when compared to exteroceptive sensations we experience. Visceral pain quite often will refer sensation, inducing ‘referred pain’, to the dermatome (the network of sensory nerves in the skin) or myotome (in the muscle).

Referred pain is induced by the convergence of cutaneous with visceral afferent nociceptive fibres onto the same (ascending) 2nd order neuron, via interneuronal synapsing in the laminae of the dorsal horn. We experience this as either sharp or dull pain referred from the organs or muscles of the torso, due to the distribution of fibres in the visceral and parietal peritonea (the membrane lining the abdominal cavity) of the abdomen. The pain described in the above poetry alludes to the effect of cardiovascular nociception, which can incidentally manifest as referred pain from vagal nerves which innervate the teeth and lower jaw, but is more often present as pain in the chest (via T1 to T4 sympathetic nerves) and numbness or pain in the left arm due to loss of circulation.

To understand these different fibres and how they shape the reality of our sensations relative to the extrinsic world on a more daily basis, as well as in pathophysiology, we must first understand each sensation as an adaptive function. For this article we will look mainly at peripheral rather than visceral sensation.

Anatomical terms and labels are key indicators of structure, function and location. Neurologists and neuroscientists use the terms nociception, thermoception and pruriception to denote physical pain, thermal sensation and itch respectively. The crucial distinction between these terms is that they delineate sensations which each confer a survival benefit, unlike pathological sensation, which confers no benefit and instead is an affliction. These discrete sensations also indicate the organisation of nervous tissues and their development across natural history, largely in response to change in the external environment, but also to perceive the state of oneself, as bodily internal tissues (the interoception aforementioned).

Sensation and affect are also worth delineating. Pain includes nociception, but also assumes a range of sensations which can be more affective, coinciding with emotion. In terms of clinical neuroanatomy, the limbic system of the brain can itself induce nociception in conditions such as somatisation, where mental anguish brings about physical pain, fatigue and discomfort.

Structures of Sensation: Nerve Fibres

As humans, we intuit from experience that nociception is not absolutely equivalent to ‘pain’. For something to be a sensation of pain, it is the nervous transduction of a noxious (harmful) stimulus, that is, the transdermal action of a pin perforating the skin damages / causes chemical attack of the free nerve endings of primary afferent fibres (the 1st order nerves of peripheral sensation) calibrated and oriented to detect this damage, largely classified as Aδ and C-fibres.

We can specify the functions of each so that their differences are clear. In the broadest terms, there are two types of sensory receptors in the skin, the mechanical and the chemical. Thermoreceptors respond to thermodynamic states, which is a little more nuanced, but part of chemistry.

The Aδ fibres are myelinated, 1-5 micrometres in diameter and project as mechanically sensitive free nerve endings into the epidermal skin cell layer, and in circumference around various hair follicles in the dermal layer (1), relaying signals at a speed of 5 to 30 m/s.

The Aδ nociceptive fibres are all reliant on peptides to chemically signal that something sharp has come into contact with the skin or that a hair follicle has been damaged; but the free nerve endings which are in the epidermis of both glabrous and haired skin are high-threshold, requiring a noxious stimulus well beyond the low-threshold fibres that detect the movement of both villus and terminal hairs.

All nociceptors respond to stimuli at a high enough threshold to ensure they are only activated if tissue damage occurs, and Aδ fibres by necessity relay highly localised and sharp nociception to the spinal cord as one complete 1st order neuron, conducting the signal via the dorsal root ganglion. This ensures an instantaneous aversion to pain through the sensation of sharp objects that can damage cutaneous and subcutaneous tissues.

The C-fibres are unmyelinated, 0.2-1.5 micrometres in diameter, and are slower by a factor of 10 or 15 ( at 0.5 to 2.0 m/s). Some use peptides to mediate chemical signals (called peptidergic fibres) and some do not.

Peptidergic C-fibres induce a dull, persistent ache, lasting beyond any initial stimulation of Aδ fibres (see Table 1.). They are calibrated to chemically receptive sensation, having evolved to transduce an array of signals via discriminative receptors. These include ATP receptors (the energy molecule adenosine triphosphate is inherent to all cells and is released during cellular trauma) and TRPV1 (Transient Receptor Vanniloid 1), which, even if its name does not roll off the tongue, does reside within it, codifying heat through the increased acidity caused by inflammation trauma. This includes the capsaicins, which evolved initially among certain plants to deter predators that present a cost of energy to the plant. The TRPV1 receptors can detect noxious levels of heat directly, but the binding of capsaicins to the active site of the receptor stimulates the same thermo-nociceptive pathways in mammals. As in human neuroanatomy, nature conserves adaptive functions across different stimuli, allowing for both clinical and lived inferences to be made because of the consistency of these stimuli in the context of everyday life.

As tabulated above, C-fibres provide us with a reminder of the event which caused tissue damage, alongside a codified sensation, memorable enough to improve association and avoidance of the stimulus in future. A cut to the skin feels like a sharp and very defined pain (A-delta fibres), whereas there may be a general pain in the area which persists that is burning (nociceptive C fibres). A bruise tends to be the result of deeper tissue damage, and so results in a dull burning ache, but may also include abrasion of the skin. The neurotransmitter glutamate is responsible for mediating the high-speed, sharp, well localised pain, lasting for only a few milliseconds via peptidergic A-delta fibres. In contrast the neurotransmitter coined as, 'Substance P’ (the pain substance) is released slowly and builds in concentration, which induces the slow chronic pain we experience following an injury.

The lower velocity of nerve conduction in nociceptive C-fibres relative to Aδ reinforces the functional role of this reminder pain, as nerve conduction velocity is most important in terms of preventing contact with noxious stimuli from entering the skin, as the most peripheral tissue layer, and thus causing a physical withdrawal from the stimulus that is reflexive rather than conscious. Hence most organisms have their own reflex arc, which in humans enters via the dorsal horn and proceeds directly through the ventral horn to elicit a nocifensive (withdrawal, jumping, contracture) motor response. This can also take the form of immobilisation, where we perceive pain from proprioceptive sensory organs, and are prevented from moving by either reflex or conscious pain, in order to avoid further damage by our movements.

Once the damage has occurred however, nociceptive pain plays a crucial role in initiating the immunological and inflammatory responses that precede healing. This for example is why non-steroidal anti-inflammatory drugs (NSAIDS) can inhibit healing, especially of tendons and ligaments, as they block the enzymatic production of prostaglandins that cause inflammation. This inflammation also initiates the cellular signalling cascades crucial for repair. Inflammatory pain is also crucial in that it lowers the nociceptive threshold significantly, making any tactile or mechanical stimulation to an inflamed area much more painful in order to prevent literal insult to injury.

The 1st order sensory neurons which provide sensation by synapsing in the spinal cord are unlike neurons of the central nervous system (protected by the blood-brain barrier) in that they are readily exposed to the extravasation of substances through the endothelium of fenestrated capillaries. Capillaries are microvascular, and have evolved these fenestrations (‘little windows’ if taken literally from the original latin) in order to allow gases to diffuse via their walls. This means that circulating inflammatory signalling molecules, drugs and toxins can make contact with these first order sensory neurons via interstitial diffusion from capillary beds of the deep, papillary and superficial layers of the skin, eliciting physical pain we associate with its injury. In terms of human evolution, and the complex nutrients, drugs, and analgesic behaviours which we have the capacity to engage in, these mechanisms have allowed us to survive, grow larger brains, and mitigate pain, as well as expand pleasure and evolve bonding mechanisms which are socially and biologically complex. We can see this evolution in terms of the chemical, mechanical and tactile sensory organs themselves, and the unique tract which evolved to allow their signalling of the brain.

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The Elder & Younger Tracts

The Dorsal Column Medial Lemniscal tract was discussed in the previous article, mentioning its key functions and that it evolved far later in vertebrates than the sensations of the Ventrolateral (anterior lateral) System. It is composed of two columns (tracts), the fasciculus gracilis (the tract of Goll) and the fasciculus cuneatus (the tract of Bardach), which carry sensory input from the lower and upper body respectively. The columns are positioned in the dorsal half of the spinal cord, hence the name dorsal column, with the medial lemniscal tract forming from the decussation (crossing over) of 2nd order ascending internal arcuate (‘arching’) fibres in the medulla, which then synapse with a 3rd order neuron in the thalamus. The DCML thus takes its name from the ascending synaptic path of these fibres into the somatosensory gyrus of the cerebrum, the outer cortical layer of the brain, where each area of the body is topographically represented across the grey matter of this gyrus.

The distribution of ascending spinothalamic fibres (part of the Ventrolateral System) indicates its earlier evolution within nervous system, with only 10 to 25% of its fibres ascending as 2nd order neurons into the thalamus of the midbrain, the majority project into the mesencephalon, pons and medulla of the brainstem. These fibres first cross-over to the contralateral section of the spinal cord via the ventral white commissure (Figure 2), then in ascent, eventually project into the midbrain regions known as the tectal area and the periaqueductal grey (surrounding the aqueduct of Sylvius, and which circulates cerebrospinal fluid into the cord) because the fibres convey information about pain, temperature and crude touch which the brainstem and midbrain are configured to manage by analgesic response (enkephalins and endorphins).

The Spinoparabrachial and Spinomesencephalic tracts for example, are part of the Ventrolateral System along with the Spinothalamic tract, and respectively have aversion and analgesic roles relative to nociceptive stimuli, especially for the peptidergic C-fibres that detect thermally related pain.

• Within the Ventrolateral System, the lateral spinothalamic area (Figure 2) predominantly contains the spinomesencephalic, spinotectal, and spinoparabrachial tracts.

• In the ventral area of the spinothalamic tract reside the spinoreticular and spinohypothalamic tracts.

• The spino-olivary and spinocerebellar tracts are not part of the Ventrolateral System, ascending their 2nd order fibres instead (respectively) in the dorsolateral (funiculi) white matter, and ventromedial white matter anterior to the ventral spinothalamic tract.

The lateral tracts is not as old as the ventral tract regions, and so the ventral is sometimes referred to as the paleo-spinothalamic tract, having a majority of C fibres configured to transmit crude touch and pain.

Both the DCML and VLS tracts are shown in cross-section of their fibre density area in Figure 2. Metabolically, the human central nervous system (brain and spinal cord) utilise 20 to 30% of the basal metabolic rate (caloric use at rest). The clinical symptoms of vitamin B12 deficiency reveal that the sensory fibres of the DCML are degenerated, by virtue of the fact that myelination is similar to the principle of insulating a wire, save that, nerve fibres are complex living cells that rely on saltatory (salt) conduction and ionic electrochemistry, not the electrical conduction of solid elemental metals. Myelin is itself a membrane rich layer, and all membranes are phospholipids.

The speed of nerve conduction is higher in some nerve fibres, with the fastest being those of proprioceptors in skeletal muscle at 80 - 120 m/s, with 13 - 20 micrometres of myelin in diameter (see A-alpha fibres in Table 2), which ensure muscles are not overstretched, and indicate to us the position of our limbs without visual confirmation. The next fastest are the mechanoreceptors of the skin, at 35 - 75 m/s, with 6 - 12 micrometres of myelin, and which include all of the A-beta low-threshold mechanoreceptors shown in Table 2.

When B12 becomes deficient, two production pathways necessary for myelination are affected: 1. is that lipid synthesis for incorporation into myelin by the enzyme methylmalonyl-CoA is not converted correctly, resulting in the abnormal accumulation of fatty acids in neuronal lipids, and 2. the hinderance of oligodendrocyte growth (the support cells which actually myelinate neuronal axons of the central nervous system), as B12 is a key biochemical step in DNA synthesis. Vitamin B12 deficiency can also be secondary to folate (vitamin B9) deficiency, or can induce microcytic anaemia (abnormally small red blood cells) due to its influence on protein synthesis and lipid incorporation (2). In terms of the evolution of the human nervous system, the requirement for B12 in sufficient quantities would have been essential for survival and reproductive capacity, allowing the dorsal column medial lemniscal tract and its sensory organ inputs to have evolved.

The skin itself is full of these sensory organs, each specialised with its own receptive (cutaneous) field, an area of skin yielding the response of a specific organ, and each its own elegant result of evolutionary research and development (in a manner of speaking). The low-threshold A-beta fibres (Table 2) innervate these organs and lanceolate (‘lance-like’) nerve endings in the epidermal, dermal and hypodermal layers. This is how vitamin B12 deficiency gradually induces paraesthesias, loss of vibratory sensation, and loss of proprioception.

A loss of vibratory sensation in this context indicates neurodegeneration in the DCML. Paraesthesias denote ‘any abnormal sensation, spontaneous or evoked, but not unduly painful or unpleasant’ (5), and if unpleasant are termed dysaesthesiae. If any pain is delayed following stimulation it can be distinguished as hyperpathia, which usually indicates that the spinal cord / supraspinal pathways have acquired an abnormal temporal and spacial summary of sensory signals, and that some form of neuropathic remodelling has occurred. These peripheral neuropathies can also be symptomatic of shingles, Lyme disease and diabetes.

If we look at Table 2, we can see each of these sensations is contributed by the 1st order afferent neurons listed. Their nerve endings and sensory organs transduce the stimulus into a signal, then into the spinal cord via the dorsolateral fasciculus (of Lissaur, Figure 2.), and synapse within the grey matter of the spinal cord before their signal ascends to the brain via 2nd order projection fibres in the white matter.

We see listed above the diverse fibres which conduct signals from these sensory organs, with their functions in the last column. The Ruffini nerve endings (sensing ‘kinaesthetic’ limb movement), Merkel cells (an adapted form of epithelial cell not derived from neurons, sense skin indentation) as well as the corpuscles of Meissner and of Pacini.

The C-fibre low-threshold mechanoreceptors are particularly interesting in terms of their evolutionary development and role in our relationships, for they transduce the sensation of hair deflection in a linear path across the skin, as the affective component of light touch (caress). Instead of spatial acuity, these fibres subserve tactile interactions in a receptive field of 1 to 10 centimetres, conducting at speeds of only 1 m/s. This relatively slow speed is conducive to sustained emotional touch as distinct from fast A-beta fibres and their discriminative sensation. Synapsing in lamina II, the afferent signal ascends via the spinoparabrachial tract, terminating in the insular cortex rather than the somatosensory, implying their role in interoceptive and emotional awareness. They are likely to have evolved, as they function similarly now, in order to codify slow-nurturing signals, promoting social cohesion, buffering of stress, and emotional regulation (3). Although they can also be stimulated under the right circumstances, by a gentle breeze.

The Islets of Gobel & Chronic Neuropathic Pain

Interneurons are grey matter intermediaries, which serve to either inhibit or excite signals between white matter nerve fibres. Because the majority of neurons in laminae I-III (Figure 2) have nerve axons which remain intrathecal (within the dura mater but outside the meninges, of the spinal cord) they are interneurons.

These axons arborise within the same lamina in which their soma (cell body) resides, but some fibre types cover a larger range of laminae within the dorsal horn. In murine models, A-beta and A-delta fibres span every lamina from I to V, respectively being more medial and lateral in their position in the dorsal horn. The peptidergic and non-peptidergic C-fibres are relegated only to laminae I and II (4).

With the exception of the C-LTMR fibres, which provide us with the aforementioned sensations that codify the caress experience, the distribution of the A fibres reflects their wide dynamic range; - a term used to denote that A-delta functions include a nociceptive range (Table 1), and A-beta provide an expansive range of non-nociceptive specialised sensations via the sensory organs and nerve endings (Table 2).

Inhibitory interneurons prevent signals from these fibres being transmitted to the brain, but the default distribution of fibres in the dorsal horn has been implicated as a contributing factor in neuropathic pain, wherein pathological arborisations may allow for signals to cross-talk between non-nociceptive and nociceptive fibres. The reality of neuropathogenesis in every neuropathic setting, from acquired physical trauma to inherited ion channelopathies, has revealed that there are numerous points of failure and need not be mutually exclusive. What is well established is that a changes in neuronal morphology chemical neurotransmission, and synaptic connectivity occur.

The Islets of Gobel are a type of interneuron residing in the deep half of II, with very significant responsibilities in the gating of nociceptive signals from the peripheral sensory organs and nerve endings of the skin. They utilise Gamma Amino Butyric Acid (GABA is the prevailing inhibitory neurotransmitter throughout the human nervous system) and / or glycine in order to propagate signals from one neuron to another.

The Islets have a wide spanning dendritic form which can ascend and descend longitudinally through up to 9 segments of the spinal cord, meaning that if their inhibitory functions are compromised, then the inhibition of pain at points of entry surveilled by this cell is reduced. Experimental evidence suggests that chronic neuropathic pain is not primarily the result of inhibitory interneuron cell death, although this is more so the case when contusive / ischaemic trauma to the spinal cord is involved. Instead the synthesis of the enzymatic precursor to GABA, Glutamic Acid Decarboxylase (GAD) has been shown to downregulate when 1st order afferent nerve signals to lamina II of the dorsal horn are compromised.

When nerve damage occurs, if secondary to a primary bodily trauma for example, the 1st order nerve signals which maintain inhibitory (GABA/Glycinergic) signals among the Islet cells can be diminished. This is a process where peripheral sensitisation leads to central sensitisation of the spinal cord, however, instances of spinal cord injury can lead to direct sensitisation of the spinal cord pathways without peripheral trauma. Ectopic sensitisation occurs when the abnormal arbors of a free nerve ending (see Table 1) can lead to arborisation of the fibres projecting from the soma of the nerve cell body into the dorsal horn lamina, arborising their also, and increasing synaptic connectivity with excitatory interneurons that function to propagate nociceptive signals into the Ventrolateral System (ascending pain tracts, Figure 2).

The complexity of response to injury within the axonal and nerve cell bodies of 1st order afferent fibres can also result from the invasion of afferent action potentials (the depolarisation of a nerve cell resulting in it ‘firing’ a signal) into other terminal branches of the efferent terminal axon, which can cause the release of neuroinflammatory substances (peptides for example), affecting both nearby neuronal and vascular tissues. Inflammation is a mechanism which has evolved to protect damaged tissues, but in neural cellular environments can also lead to abnormal functions with disproportionate effects on physiological functions.

Under similar conditions, the A-beta fibres we know the non-nociceptive functions of from Table 2 can gain access in some form to the superficial laminae I/II, see Figure 2), inducing allodynia.

Allodynia is a nociceptive pain evoked by a normally innocuous stimulus. The neurochemical and morphological changes to inhibitory and excitatory neurons are focal to the pathogenesis of allodynia, in which the functional distinction between innocuous and noxious signalling is compromised. Tactile allodynia is a mechanical form of the condition, as the loss of differentiation by a fibre type results in distinct symptoms of disease or injury. Most forms can result from central (spinal cord) sensitisation as primary injury, or peripheral sensitisation from primary injury (leading to central sensitisation as a secondary effect), the neuroanatomical crux is that each indicates an underlying difference in the nerve fibre types affected, and how the relevant tissues or neurochemistries have changed.

Persistent cutaneous mechanical allodynia often involves the wide dynamic range of A-beta fibres, but also the A-delta and C fibre types due to interneuronal circuit changes in the dorsal horn, and thus patients may experience pain in haired and glabrous skin as a result of nociception in subcutaneous tissues such as muscle. In tactile allodynia, abnormal nociception is induced by the A-beta low-threshold mechanoreceptive fibres, which are activated by various forms of light touch (Table 2).

The tragedy of chronic pain neuropathies is they recruit pathways which evolved for the adaptivity and specialised sensation of our species. It can be said of many diseases of course, that the tissues which have evolved as layers of many parts to make us human are all susceptible to disease. But for sensation to itself become the affliction marks a unique limitation on quality of life.

In either case, research has shown points of failure in hyperalgesic and allodynic states to be numerous. In central sensitisation of the dorsal horn, GABA interneurons can become less excitable due to the microglial (a support cell of the central nervous system) release of neuroinflammatory cytokines, which reduce their synaptic functions of pain inhibition. The function of ion channels can be disrupted, leading to abnormal anion gradients (differences in charge) which renders interneuronal dysfunction in lamina I. It has also been shown that a potassium cotrasporter (a kind of finely tuned toll gate in the membrane of interneuronal axons which exchanges potassium cations (+) and chloride anions (-) proportionately) can lead GABA / Glycinergic interneurons to change phenotype entirely, from being inhibitory interneurons to excitatory glutamatergic interneurons, inducing hyperalgesia.

Since the seminal initiatives of Ramón y Cajal at the turn of the 20th century, structure-function classifications have been attempted. Lamina I, through which the majority of nociceptive transmissions are relayed for either inhibition or ascent, contains fusiform, pyramidal and flattened cells, each having dendritic trees restricted to that lamina of the dorsal horn in order to isolate the codification of pain. The pyramidal cells for example, have (unsurprisingly) a pyramidal soma (cell-body) in all planes of section, and their arbors (dendrites) tend to remain in lamina I. There is a fourth class, the multipolar cells, which penetrate into the deeper laminae of the dorsal horn. If nothing else, the description of these differences in morphology reveal to us the sheer variety of interneuronal cells and their synaptic configurations, required to act by coordination of their circuitry and their timing, to maintain a clear and adaptive impression of the world within and the world without.

Lamina II, also known as the substantia gelatinosa (Figure 2) because of its low myelination, appears translucent in living tissue, and relays signals from C (caress) and A-delta LTMRs, and peptidergic (nociceptive) C fibres. In the remaining lamina, populations include the following key classes of interneuronal cell morphology: the central interneurons (elongated, similar to the Islets of Gobel, in the longitudinal axis), radial (with radiating dendrites through lamina II) and vertical (cone-like, with arbors through the dorso-ventral axis of lamina II).

Recent discoveries have shown that some of these interneuronal cell types are phasic, only depolarising into an action potential (conductive signal) as a phase; whereas others are tonic, firing slowly and continuously. It has been shown that in neuropathic states, pain signals are constantly active in the superficial laminae of the dorsal horn, with lowered inhibition by the responsivity of interneurons, like the Islets of Gobel.

Absent pathology, there is a constant balance between neurotransmissions made by inhibitory and excitatory interneurons, regulating the flow of codified signals into the supraspinal regions of the brainstem and brain. Pain, thermal sensation and crude touch came first in the lineage of vertebrate sensation, with more refined forms of sensation coming later.

Being able to experience and detect pain is however, crucial to what it means to be human and to our understanding of stimuli and hazards in the world.

Worth mentioning in closing, is the counter extreme to conditions of acquired pain, a condition known as Congenital Insensitivity to Pain Syndrome; a rare genetic disorder in which individuals are largely if not entirely anaesthesic in their cutaneous and subcutaneous tissues. The early development and survival of nociceptive fibres in this condition are compromised, and as such burns, cuts and fractures elicit no conscious reaction. Joints can become easily damaged, infections can go unnoticed, and on occasions where it develops in impoverished locations, at least one child with the disorder was known to perform an act to entertain. Some people considered the boy to be superhuman, blessed or immune to injury.

Understanding the nature of human sensation in both dysfunction and health, helps us to understand the underlying reality of phenomena we would otherwise deem strange. We better understand ourselves as a species, and our own individual experiences as part of a long continuum.

References:

1. Crawford, L.K. & Caterina, M.J., 2020. Functional anatomy of the sensory nervous system: Updates from the neuroscience bench. Toxicologic Pathology, 48(1), pp.174–189. https://doi.org/10.1177/0192623319869011

2. Al‑Chalabi, M., Reddy, V. & Alsalman, I., 2023. Neuroanatomy, Posterior Column (Dorsal Column). In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. Available at: https://www.ncbi.nlm.nih.gov/books/NBK507888/ [Accessed 2 Aug. 2025]

3. Marshall, A.G. & McGlone, F.P., 2020. Affective Touch: The Enigmatic Spinal Pathway of the C‑Tactile Afferent. Neuroscience Insights, 15, p.2633105520925072. doi:10.1177/2633105520925072

4. Li, L., Rutlin, M., Abraira, V.E., Cassidy, C., Kus, L., Gong, S., Jankowski, M.P., Luo, W., Heintz, N., Koerber, H.R., Woodbury, C.J. ​ and Ginty, D.D., 2011. The functional organization of cutaneous low-threshold mechanosensory neurons. ​ Cell, 147(7), pp.1615-1627. ​

5. Manji, H., Connolly, S., Kitchen, N., Lambert, C. & Mehta, A., 2014. Oxford Handbook of Neurology. 2nd ed. Oxford: Oxford University Press. p. 270.

• the architecture of nerves as a mechanical means of drawing human beings towards advantage and away from danger,

• the control that chemical and neuronal structures have in maintaining vital functions in everyday human life,

• and how the known signs and symptoms of neuropathy are caused by abnormal alterations to these.

The cord proper…

At a diameter of only 10 to 13.5mm, the human spinal cord is widest at the neck (1). This remarkably small area houses a vast collection of nerve fibres, with approximately half their sum needed to convey sensations from the outward surface of the skin, as well as the fascia, muscles, joints and viscera which lie deep to it.

Human spinal nerves ramify through 31 levels in order to reach the tissues they innervate via electrochemical transmissions to and from the cord. With each ramified nerve projecting laterally, the width of the spinal cord diminishes as it descends from the brain. In both humans and our mammalian relatives the spinal nerves continue to ramify until they cease as the cauda equina, ‘the horse’s tail’, where the remaining nerve roots branch at the level of the sacrum, and descend into the pelvic cavity and lower limbs. All the sensations, reflexes and movements of our lower body, including the sexual organs which allow us to reproduce, are made possible through these nerve branches and the organisation of tracts within the spinal cord from which they flow. Our sense of stability in relation to the surface on which we stand is likewise a function of sensation conducted by the lower body and allows for us to orient our position, brace ourselves physically and adapt to almost any surface.

Broad comparison can be made between neural tissues at every level (whether of cells or of nerve fibres visible to the naked eye) and the function of many forms which branch in order to glean information, distribute vital fluids or gather resources. The morphology of a tree e.g. is not dissimilar to neural cells in basic shape, and the descriptive terms ‘branched’, ‘dendritic’ or ‘arborised’ have been applied to neural tissues by the earliest scientific pioneers of neuroanatomy in the 19th to 20th century, these individuals being the first to observe neural cells directly through microscopy, including Heinrich Waldeyer and Santiago Ramón y Cajal.

Such terms are still used today by anatomists and surgeons especially, as they often imply a structure relatable to the underlying functions of the tissue. A loss of this structure will result in a loss of its function, prompting the inchoate question of neurology and neuroscience at their inception: how humanity is maintained by a selective current of millivolts, controlled across multitudes of cells, signalling in sequence at the appropriate time, and ceaselessly regulating every cubic inch of organic matter in response to changes within and changes without.

Alongside sensory fibres the spinal cord contains the tracts responsible for outgoing motor signals into peripheral tissues, providing a means for both voluntary and involuntary movements, secretions, contractions and so on. Despite such limited space, vast yet highly selective signalling is made possible by the sheer organisation of nerve fibres into dedicated functions, as determined by their structure, their calibre of myelination (for electrical insulation & propagation), their situation in the body and the chemical neurotransmitters they utilise. These features dictate which tissues and other neurons will be targeted, and how electrochemical signals are codified for the brain to interpret, maintaining tone and initiating phasic responses in some instances, whilst inducing long-term transformation (such as growth) in others.

Transmissions are separated from one another much in the same way an electrical wire is insulated, where with nerves the upmost importance of this feature is in preserving the fidelity and reliability of each signal. The fibres are compartmentalised into fasciculi (bundles) and funiculi (larger bundles), with those responsible for conveying prolonged physical pain being separated from those responsible for the sensation of non-noxious stimuli, such as tactility. The loss of this compartmentalisation contributes to a variety of neurological dysfunctions which articles in this Lucida Visionis series will follow, such as hyperalgesia, allodynia and paraesthesia.

At each level of the spinal cord (the illustration above e.g., shows a cross section of the cord from the 8th cervical level) the grey matter assumes a horn like symmetry either side of the midline, comprising a dorsal (posterior) horn and a ventral (anterior) horn. The dorsal horn is populated by a majority (>90%) of dense interneuronal networks. The arborised axons of these neurons are restricted to the dorsal horn, where they serve to promote or inhibit sensory transmissions to the brain, limiting or enhancing the long distance transmissions conveyed by 1st order projection neurons which target tissues peripheral to the cord (via the dorsal root ganglion shown) and 2nd order projection neurons that project from within the cord to the brain. These include those signals from free nerve endings which convey painful or pleasurable sensations, or general tactile, follicular (hair) and thermal sensations from bodily surfaces, being at their most distal and numerous from the brain in the glabrous skin that is found overlying the palm of the hand, including the skin overlying the palmar aspect of the fingers. This applies also to the soles of the feet.

Human dexterity allows us the use of endlessly varied tools, and to experience uniquely diverse sensations, both in response to our environment and in social activities. The importance of context in allowing us to define all these neurosensory signals as we experience them cannot be understated. This is itself achieved through separation of the sensory fibres into 2 key spinal tracts with discrete yet overlapping functions. Within these tracts, the configuration of interneurons into localised circuits inhibit certain signals transmitted through fibres of varying myelination towards the brain, whilst allowing the excitability to remain in others when the scenario demands.

Take the edges of a 50p coin, having a distinct equilateral curve heptagon which can be discerned by the coordination of sensory information from the fingertips. The surface features of the coin face likewise stimulate the pathways of the brain which integrate the subtle features of an object, allowing for it to be identified without audible or visible recognition. This stereognosis precedes removal of the object into view, allowing its suspected identity to be confirmed, but becomes especially beneficial to individuals with visual impairment who rely greatly on this sense to read brail and so on. An adaptive compensation for loss of sight through heightening of tactile sensation is one example among many which the human nervous system is capable of.

The spinal cord tract responsible for transmitting these specialised sensations from the periphery of the body (the Dorsal Columnar Medial Lemniscal tract), which also provides us with the ability to sense fine touch and vibration, is hypothesised to have evolved after the spinal tract dedicated to crude tactile sensation, thermal sensation and pain (the Spinothalamic tract). Homeostasis and survival are the first functions of the nervous system in all species, and consequently, the almost endless adaptivity provided by the human brain and nervous system have allowed for the fruition of both survival and the range of high precision senses through which we comprehend our physical world. The cumulative development of these senses, such as our ability to determine the identity of an object through touch alone, has thus come to inform what makes us human.

Sensing & Sensibility…

Although the natural history of human life is echoed in the lengthy development of our nervous system, from its foetal to infant and adult form, it can be said in the wake of technology today that we are seldom exposed to the diverse ecology of materials and textures we evolved to detect, interpret and manipulate, by handling, shaping or otherwise learning to avoid if hazardous. We vie now for abstract information, at times broadcast at a global scale, and which can shape our thoughts, working lives and perceptions of the world at large. This is perhaps the inevitable conclusion of our being the most social species on Earth. As a result of what can be an excessive strain on our decision-making capacity, our attention is redirected increasingly to deal with this mass of information (2), often leaving the cognitive processes which would otherwise be dedicated to the sensation of our immediate world and situation, quite overwhelmed.

The nervous system has come frequently to forgo the sensation of other living things which exist beyond the infrastructure we have created. This itself may impinge our capacity to engage in our own emotions, and consequently, the emotions of others.

Within clinical aspects of anatomy and medicine this prompts some reflection: Do we humanise the cadaver of a donor beyond basic respect? How does the clinician approach a patient with empathy in a sustainable fashion, and whilst remaining objective? What potentiates the reciprocation of this empathy by a patient?

At a rudimentary level, we can reasonably say that the opportunity to communicate both shared and unshared experiences can foster trust in such scenarios. Our consideration of the first and foremost infrastructure in human life, the neuroanatomy on which our experiences and interactions depend, would necessarily seem to be conducive to this shared understanding.

Dexterity Within & Dexterity Without

The combined development of the upper limbs into highly dextrous and sensible (in the archaic sense of the word) appendages, and also of the lower limbs into weight-bearing and bipedal structures e.g., have had immense influence on the evolution of the axial skeleton (the skull, vertebrae and rib cage) and on the manner in which the nervous system maintains vital functions throughout the body. Sensation has also been pivotal to the expansion of the human brain, both in its processing and connections. Due to the ever increasing benefits of integrating select yet diverse sensory experiences, the course of vertebrate and mammalian evolution have been shaped by sensation, providing a foundation for the refined actions we use to respond to what we sense, whether in conscious reply to a question or as the typically unnoticed and unconscious reflexes which maintain the circulation of vital fluids.

That we are upright for example, has required a more complex array of mechanisms to maintain blood flow to our metabolically demanding brains, with all the conscious sensations we process, whether cutting wood, playing an instrument, writing, typing, driving and so on. Circulatory reflexes which maintain pressure and flow evolved initially at a lower centre of gravity in quadrupedal mammals, at their origin being more akin to the morphology of dogs, including those domesticated and selectively bred into various (and at times regrettably unhealthy) shapes and sizes.

Our nervous system however, being wired for bipedalism, and an upright centre of gravity, is calibrated to sense changes in blood pressure more acutely, and adapts the diameter of blood vessels more locally in order to accommodate blood flow to the brain and vital organs. Alterations to blood pressure e.g. are closely monitored and adjusted, especially in situations where the plane of gravity changes rapidly. Here the nervous system must prevent an average of ~800 ml of blood from pooling in the abdominal cavity and lower limbs; first by sensing the loss of pressure in the major veins and arteries adjacent to and above the heart, then initiating reflexes to correct the disparity in pressure and flow. Failure of this reflex is typically due to dysfunctions of the autonomic nervous system responsible for the reflex, leading to faintness brought on by low blood pressure and dysreflexias of the nerve impulses that elicit a complete cycle of blood in and out of the heart (normal sinus rhythm).

The brain, heart, kidneys and lungs are privileged over other organs, both in states of acute change to blood pressure and emergency (such as haemorrhagic loss of blood). Blood pressure is monitored internally (at the level of the neck) via sensory organs within the carotid (artery) sinus, operating in tandem with chemosensory changes in O2, CO2 and H+ (hydrogen ion = pH) levels in the carotid sinus of the same artery. These signals are largely conveyed via the vagus and glossopharyngeal nerves into the brainstem, not via the spinal cord, thus sensation from the viscera is not always the remit of the spinal cord, but in many instances is the responsibility of the 12 cranial nerves which project directly from the brainstem into the viscera of the head and all tissues beneath these.

If at all, how do the sensory and motoric functions of the spinal nerve tracts differ in their relation of what we experience, and how our bodies understand the world around us? Or the interoception of bodily tissues within us?

In this series, the architecture of nerves as the mechanism by which human beings are drawn towards advantage and away from danger will be explored, as well as the control that chemical and neuronal structures have in maintaining vital functions in everyday human life, and on how the known signs and symptoms of neuropathy are caused by abnormal alterations to these.

1. Frostell A, Hakim R, Thelin EP, Mattsson P, Svensson M. A Review of the Segmental Diameter of the Healthy Human Spinal Cord. Front Neurol. 2016;7:238. Published 2016 Dec 23. doi:10.3389/fneur.2016.00238

2. Wiehler A, Branzoli F, Adanyeguh I, Mochel F, Pessiglione M. A neuro-metabolic account of why daylong cognitive work alters the control of economic decisions. Curr Biol. 2022;32(16):3564-3575.e5. doi:10.1016/j.cub.2022.07.010

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Meaningful communication is an absolute drive for human beings, one for which we have evolved a uniquely sophisticated capacity to produce language.

We develop our familiarity with patterns of linguistic structure so fluently within life however, that we may inevitably come to take this capacity for granted.

Human language is as much a process of information input as it is output. It requires sensory afference (neural conduction towards the brain) in the first instance, such as visual, auditory or tactile stimulation, followed by cognition in the second.

The synthesis of language requires a variety of discrete anatomical systems to perform across the human lifespan. These are presided over by the neural coordination of the brain, and the pulmonary (of respiration) anatomies, which are mainly the lungs, the pleura surrounding the lung, the rib cage surrounding this, and the diaphragm inferior to these.

Collectively these structures provide airflow for the laryngeal and orofacial structures to influence through dynamic changes to the potential space (the space which can occur within structures) of the larynx and oral cavity in order to produce an array of precise sounds. Via these structures, a fluid coordination occurs between the information we receive and the information we convey.

Linguistic cognition hinges on our comprehension of phonetic, lexical, grammatical, syntactic and semantic patterns. In this way, we can understand the layers of human communication as a living and breathing endeavour, made up of linguistic patterns, anatomical structures and physical forces acting in elegant coordination with one another.

The ease and utility of communication which language provides us, and the comprehension of meaningful language that our senses and nervous tissues mediate, have gradually become the cornerstone of human civilisation. We can easily make the case perhaps, that language is human civilisation, for nothing that is humanly societal, communal or familial, can exist without this simple and yet detailed means of communication we understand as our language.

The result of cumulative human experience, language is for us all an inheritance of a wider heritage and yet also an individuated art.

Consider the lexicography of Egyptian hieroglyphs, which communicate meaning through a language of symbolic imagery. When compared to the letters and numbers of today, to us they seem quite conspicuous, for the alphabets of many modern languages, those languages still ‘alive’ and in use today, are not pictographic, albeit they contain a residual pictography that has become part of a convention of lexical symbols. We can take Chinese calligraphy to be an example.

The alphabet used in English, is instead an organised set of simpler patterns which we seldom consider to have symbolic meaning individually. They have become such a standardised unit of symbol, that what individual meaning they had in signifying something beyond their phonetic sound has become secondary if not trivial.

In our early years of life, we consider these symbols to be devoid of any meaning other than what they are agreed to mean in order for a language to function. With time we discover that the combination of letters provides for their expansion into words and sentences. Years later, we utilise vocabulary or turn of phrase, and through these there come intonations, with subtle verbal and vocal cues nestling into their rise and fall. All told, these symbols which allow us to infer and relate patterns of sound become the providence of our communicable thoughts and feelings, and through them, our humanity is mediated.

We do not utilise the entirety of our linguistic heritage, because there is an economy of meaning to life. It is neither desirable nor practical to incorporate the whole vocabulary of English language into our communications, it does not allow us to achieve the purposeful aims of everyday life, despite it having the largest vocabulary of any language on Earth. The crux of human language lies in the purpose of the communications we make. The purposeful selection of words in any given language made by any individual using it is a fraction of those available. Language has the potential to frustrate when used to obscure on the one hand, or to imbue life with meaningful communication, musicality and poetry on the other. The right word in the right place then, allows us to specify that the sum words available to the speaker can be called the lexicon of their language.

Lexical selection is the remit of the neurolinguistic comprehension and interpretation of the words recorded within the mind; selection is also however, dependent on the context in which these words are to be used, and also on the intent of the user. Crucial aspects of language may change with the individual’s intent, and the context in which the candidate word is to be applied by the person in their use of language. 

All neurolinguistic functions combine in order to aid the selection of words during the life history of a human being. Even in infancy when we babble, the production of sound in and of itself is essential, as it aids our refinement of crude sounds into shaped sounds, known as phonemes, which are then combined into words. This process is entirely dependent on coordination of the orofacial, laryngeal and respiratory musculatures and their neural innervation.

Sound we at first only hear, yet then come to associate with aspects of the physical world, and finally, to imbue the information we sense with coherent meaning. We develop deep a bonding affection with our mother’s heart beat en utero, for example, and sense the world more and more as we develop.

Without these crucial neurolinguistic functions, a multitude of words may be at our disposal, but not necessarily put to use in a way that represents reality, or otherwise, concepts that are relatable by human beings to one another. 

In light of patterns we perceive in our environment, or from written language, we learn to recognise the world around us as perceptibly separate from ourselves, and to describe its features and effects on us.

The electrical and chemical patterns which signal within our bodies to coordinate our living functions and responses, including that of writing and speaking, are well observed in clinical evidence and neuroanatomy. This is the principle function of science, to observe without imposition.

Neurolinguistic and anatomical sciences are not the means through which we should understand ourselves, but they can help us to understand aspects of ourselves and of our nature which are confusing or intriguing; for instance, by offering insight into how and why the selection of words in order to convey information is so effective at converting real world patterns we sense through the nervous system, we understand that the electrochemical patterns in our neural tissues can be affected by factors beyond our control and by choices we make on a day to day basis. We can understand the nature of a neurological disorder, and suspend the judgement which as human beings with mechanistic fears and beliefs, we might otherwise be predisposed to.

These electrochemical patterns we sense are transduced (converted from a physical force into a codified neural pattern) then into information that can be interpreted by the brain, which may then be expressed by linguistic information within the networks of that organ. Sometimes we might not say, ‘Ow!’, when we are exposed to physical pain; and instead, ‘Agh!’, or with the emphatic disinhibition of adulthood, ‘F#£k!’, will suffice; - yet the word, Ow!, still forms a very early part of any English speakers vocabulary.

The neurally mediated process of language is, in its entirety, why specific words serve us so well when used with the precision of both verbal and written communication. Conversely then, if there is a loss of neural function due to an injury or disease which affects the temporoparietal or temporofrontal brain tissues (introduced in the 3rd article of this series), is significant enough, the individual would likely suffer a loss of linguistic functionality, including the recall of words.

Which words however, and in what manner the symptoms present, makes for the crucial distinction between which of the functional neurolinguistic tissues are being affected, and how best a clinical intervention can restore these functions.

SPACE, TIME & CLINICAL HISTORY of the LINGUISTIC BRAIN:

The process of learning a language requires the construction of new connections, represented spatially within the brain regions responsible for language and memory.

Linguistic patterns are made up of words, formed of verbs, subjects and objects; their meaning must be made available to conscious working memory in order for them to be compared and contrasted with those previously acquired. This is linguistic fluency in a nutshell.

By way of converse example, if we hear or read a language we do not understand, we have no prior record of the sounds or written words with which to compare, and thus to decodify their meaning.

The brain parenchyma - a useful anatomical word derived from the ancient Greek which means, ‘an infusion of that within which differs from that without’, admittedly gets somewhat lost in direct translation. Here we need only understand that this word specifies the functional tissue of an organ, as distinct from its supporting or connective tissues.

Within the parenchyma of the brain, we find the microstructure of neuronal networks establishes a vast array of functions that go well beyond the sum of their number, and in the case of language learning, that there is a relationship between physical space and time.

The spatial retention and processing of language within the brain has been revealed to some degree by contemporary neuroscientific research, in that a second language learned later than the first is situated in an adjacent space. Whereas the more simultaneously two languages are learned, the more spatially proximate their processing becomes within the microcosm of networked connections in the brain which are dedicated to language and memory. 

This illustrates again than the neuroanatomy of language is the result of a functional space that is stimulated by iterations of sensory experience.

To briefly reiterate, linguistic function is the result of sensation, cognition and affect; patterns of language become information because they are derived directly from auditory and visual sensations of the world, or from descriptions related by human beings to one another through language. Both of these activities require a synchronous and fluid continuity between neural comprehension and interpretation, which can be influenced by thoughts and emotion.

For example, we can understand what a specific word means, but not be able to successfully interpret its meaning in a specific context. We can likewise initially sense something in the world, and then our senses can organise this into information for transmission to the brain, but both these steps precede the cerebral level of organisation which allow us to comprehend and interpret the information. In other words, the information is not intelligible by virtue of sensation in and of itself.

Hence, the loss of one or more of our linguistic functions, i.e., of comprehension or interpretation during states of neurological disease, has offered medical practitioners and clinical anatomists opportunities to demarcate the neuroanatomical structures and connections responsible.

The first cerebral localisation of function is attributed to Thomas Willis in the 17th century; as an anatomist and physician he coined the term neurology, and attributed localised function to the cerebral cortex for the first time. Recall that ‘cortex’ means tree-bark, and is the outermost and most major layer of the brain.

Through the post-mortem dissection of individuals who had experienced a loss of speech function in life, the localisation of language to a specific part of the brain was demonstrated by Pierre-Paul Broca in the 19th century. In such cases Broca discovered a left frontal lobe lesion had induced a set of symptoms that were pre-emptively termed by him in 1861 as ‘aphemia’.

This term is now more readily differentiated from the term aphasia and its sub-classifications, where aphemia denotes a neurological speech dysfunction in which the ability to articulate ideas is lost, despite the capacity to comprehend and produce speech through coordination of the bucco-facial musculature being retained.

The buccinator muscle, derived from the Latin for trumpeter, is crucial to shaping the potential space within the oral cavity such that blowing air into wind instruments and whistling are possible.

The word buccal means ‘cheek’, a square bilateral muscle which forms part of the lower face; it is an accessory to the muscles of mastication when it aids the formation of a food bolus, from the ancient Greek meaning a ‘clod’ of soft material, until the bolus is liquified and compacted enough for it to be swallowed from the oral cavity into the oesophagus. The buccal muscle happens also to be utilised in certain orofacial expressions. 

The musculo-facial process of verbal expression is clinically termed, arthria, where respectively partial or complete loss of this function is termed, dys-arthria and an-arthria, where each prefix of, dys-, means ‘reduced’, and that of, an-, means ‘without’. Arthria is itself derived from the same root as articulacy and articulate, meaning to utter in distinct parts, but simultaneously from, compose, attach or separate by joints, whether the adjective or verb form of the word is being used.

We see that the language of anatomy is itself an elegant composition of forms that can be used to describe the elegant composition of forms. It is a language which has the potential to be used artfully when describing features and functions of the human form in life, and in specifying the loss of those functions in a meaningful way. Being able to use language to make these distinctions in a meaningful way, means that the functions are represented accurately by the language used to describe them, and that the partial or complete loss of them can be differentiated or compared.

The word root of arthria is interesting in relation to further derivations from its root. In fact this word and its clinical counterparts have other distant relatives which we include more often in everyday language, including alarm, article, armour, order, harmony, artist and arm - all derived from an indo-European root word, ar, which became their prefix, and means simply - to fit together. Thought and art can be understood principally as ways of fitting things together.

Broca also observed the effects of the brain lesions he investigated, and attempted to fit together how these symptoms might indicate a physical source of linguistic processing. He articulated his hypothesis through cogent and precise language. In doing so, he ultimately contributed to humanity’s understanding of ourselves as a highly expressive species in a wider continuum of life.

The loss of speech function observed by Broca and others was sometimes coincident with right-side hemiplegia, a complete paralysis of the side of the body which is contralateral to the damaged somatomotor area of the brain, where the functions that are local to the precentral gyrus discussed in article 3 are processed by its cortical grey matter.

This hemiplegia occurs in the event that pathways of the middle and front of the brain, known anatomically as the left parietal and frontal lobes, are damaged. If this damage includes Broca’s area, then the somatomotor cortex may also be affected.

This is simply because the opercular part of the inferior frontal gyrus that contributes to Broca’s area, abuts the precentral gyrus, and in doing so forms the lower third of the precentral sulcus.

It is the opercular part to which our ability to recognise tone of voice in our spoken native language is attributed.

Due to the decussation (crossing-over) of somatomotor efferent fibres from the left brain hemisphere to the contralateral side of the body, the patient under the same effects that Broca initially observed presents with a loss of speech function and right side paralysis.

Once again, the neuroanatomical specificity of terms is crucial. The loss of function is attributable to the 1st order neuron because the patient presents with a loss of speech and right side hemiplegia, with no peripheral injury to 2nd order neurons of the paralysed side (see article 2 in this series for an explanation of 1st and 2nd order neurons).

This paralysis is defined neuroanatomically as a central plegia because the 1st order (in this case the upper) motor neuron is affected. This diagnostic term is in contrast to a peripheral plegia, wherein the 2nd order neuron is affected, and paralysis is being caused outside of the central nervous system.

A case of partial denervation is termed hemiparesis, rather than hemiplegia, where the word denervation itself means the loss of nerve function without a qualifying cause. 

A secondary influence on the spinal plexi (from the latin pletere, meaning ‘of plaited structure/pattern’) may occur in cases of peripheral plegia.

This results from partial or complete denervation of the cervical, brachial, thoracic, lumber or sacral outflow of nerve plexi, where ‘outflow’ denotes how these nerves diverge from the spinal cord to form the main branches of the peripheral nervous system.

The cauda equina for example, the ‘horses tail’, is that outflow of nerves which innervate the pelvic region and the lower limb.

We will explore in the next article how meaningful differences between the presentation of linguistic ability and understanding come to inform diagnoses made by clinicians and inferences made by scientists.

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Neurolinguistic pathways are localised yet connected:

The first distinction we make now in this article series on language, is that our senses provide us with information but not with comprehension or interpretation of it.

Neither do our senses prioritise certain aspects of information over others, although they may be sensitised or change modes, such as during the adjustment of the human ear to low volume sounds, or of the eye to darkness.

This distinction shows that the human nervous system is fundamentally wired for the adaptive gathering of information prior to the prioritisation of certain objectives over others, whether or not we are consciously aware of these objectives. Our brains for example, know we are thirsty or fatigued before we become consciously aware of the process.

Like the cerebral functions of linguistic comprehension and interpretation, the general somatic sensations discussed in the previous article are a function of the brain itself, not of the tissue which comes into contact with the stimulus. When the hand is dipped in cold water, the sensation is decodified by the brain, not by the peripheral nerves which codify cold and wetness.

Suffice it to say, linguistic specificity is dependent on the comprehension, interpretation, and fluency of language. As such the codification of language must be learned, but the human brain nonetheless has a neurological predisposition for it. 

Linguistic functions are localised to the temporoparietal region of the cerebrum shown above, where the temporal and parietal lobes abut each other, and are separated by an oblique sulcus (a narrow groove), known as the fissure of Sylvius.

The neural function of the gyri that are responsible for language, are topographically labelled the inferior frontal and the superior temporal gyri, but are functionally known as Broca’s and Wernicke’s areas respectively. They serve as adjunct parts of the cerebrum, that outer tissue which makes up the majority of our brain, and among many functions provides us with the capacity to organise and integrate our conscious thoughts, to exercise reasoning and judgement, engage in learning, problem solving, and much else besides.

These latter functions are most directly the remit of the frontal lobes, but require interconnectivity with other brain regions to operate at an optimum. This includes language, speech, articulation, comprehension, interpretation and audition, which are distinct yet continuous in terms of their neuroanatomical functions during human communication. 

The inferior medial gyrus is responsible for verbal expression, and contains Broca’s area. It forms part of the cortices, the ‘outer bark’, as below.

Visual sections through the brain, as seen on an imaging scan, are referred to as planes of section. When looking at any plane of section through the brain, it becomes evident that a significant proportion of the cerebrum is dedicated to the white matter fibres which fan upward into the outermost layer of grey matter. These fibres are responsible for mediating neural transmissions which originate in the peripheral nervous system, the brainstem nuclei or contralateral hemisphere.

This white matter makes up approximately half of any human cerebrum, with the remaining cerebral grey matter being distributed throughout the gyral exterior. If we consider also that the cerebrum comprises ~82% of the brain’s overall mass, we find that a vast amount of the neural real estate is dedicated to connection between modular functions within brain tissue.

As the repository of all language, the brain in and of itself has much to teach us about how and why language functions as it does, including the selection of words to solve problems of description and categorisation, and how the application of language in everyday life forms the structure of our thoughts and ideas.

The observation of neurolinguistic capacity in health relative to disease is primarily concerned with comprehension and speech production. It has led to direct clinical observations of how the function of language is influenced by change due to trauma or neurodegeneration. Through this we can gain very robust and cohesive insight into what language is objectively, and all the more intriguing is the measure of why it exists as a means of communicating with other members of our species in the first place. 

We can deduce that the specificity of language in terms of words that we choose to use, and even the creation of language itself, is not just an abstraction, but rather, entails a unique dynamic between real world stimuli and physiological functions.

Recall that information may be sensed directly as a stimulus, such as light or sound, or a codification of sounds and somatic cues that we interpret and decode via language. Body language for example, is a form of somatic cue. If language ultimately represents the most highly functional means of contextualising, retaining, associating and expressing information, we might then ask, what nuances do neurolinguistic functions reveal about the human capacity for language, and language itself?

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Patterns are sensed, comprehended & interpreted:

When viewed as a functioning whole, the auditory and visual systems convert audible and visible patterns of language into electrical signals, becoming a codified forms of information. This information is organised by highly configured structures within the brain which allow the transmission of the information to its appropriate place.

Tactile sensation can of course also be used to infer or to read information, whether linguistic, or as a physical stimulus which indicates a change in the environment, such as vibration or temperature. In this way, patterns from the outside world are codified into electrical transmissions. A specific pattern is made to represent a specific stimulus, and consistency between the outside world and internal response is maintained.

This consistency is crucial because the fidelity of information conveyed to the mind and body, informs the response, whether this comes from voluntary or involuntary branches of the nervous system, or indeed both. The precision with which we understand the world through the senses is a necessary precursor to our being able to describe ourselves and our situation in it.

In the event of neuropathology, neural tissues will always attempt to compensate when and wherever possible, by way of regeneration in some cases, but in cases of severe tissue damage, most often through the rerouting of the localised function to another region of tissue.

This rerouting occurs within residual tissues of the region that has been spared from damage, but may also harness the symmetry of the brain in order to compensate. The anatomical function of the brain is patently symmetrical, and as we explored in the previous part of this article series (part 2), this provides for the division of motoric and sensory functions of the nervous system into two bodily halves.

Yet not all of these brain functions are distributed in this bilateral way. With regards to language for instance, the left hemisphere is the dominant language centre among the majority of human populations.

Despite the neurolinguistic functions of the brain being dominant in the left hemisphere over the right, the two hemispheres can in certain cases, such as when the temporo-parietal area is affected by stroke, allow for damage in one hemisphere to be compensated for.

Although language networks of the brain are left hemisphere dominant in the majority of the population, this function can be reorganised into undamaged regions of the network in the ipsilateral (same side) hemisphere which have not been affected, or rerouted to the contralateral (other side) cortices of the right hemisphere.

Another compensatory mechanism which has been posited is functional reserve, which describes the recruitment of neural tissue that is unrelated to the damaged tissue in terms of function, but may nevertheless adapt to new demands placed upon it.

The brain's modular functions are numerous and their connections between each other prolific, yet this connectivity must also remain specific in order to allow for functions to occur in an appropriate way.

In processing sensory information and affecting movement to produce linguistic and lexical output for example, functions of the temporoparietal cortices are coordinated to produce forms of communication that are selective and replicable. This is yet another direct example of form preceding function.

As nerve tracts ascend and descend via grey matter into and from the brainstem, the crossing over of neural pathways from one half of the body to the other often occurs. This depends on the function of the tract and the connections it makes within the central nervous system. These innumerable connections made between nerves that innervate certain tissues are crucial to the integration of codified electrical stimuli, providing neural sensation and motor control.

The specificity of neuroanatomical terms we require in order to differentiate between common and more precise forms of neural connections are important, and the following are two principle examples:

The first is a more general term, anastomosis, which denotes an interconnection between adjacent nerve fibres, and allows a redundancy of connections to occur in the event that any are damaged. For instance if a connection between nerve A and B1 and B2 exists, then the loss of innervation to B1 can be compensated for by a connection that exists between B2 and A.

Because vascular tissues anastomose far more frequently than nerves do, the word anastomosis is more often used in relation to blood vessels. This occurs because neurobiological control over the physical dynamics of a liquid differs greatly to that of the dynamics of electric conduction.

Second is the word, decussation, which is similar in its base definition, yet is more exactly applied for example, to the crossing of connections between the hemispheres of the brain, known as the commissural nerve fibres, which travel between hemispheres through the region known as the corpus callosum.

Similarly, the optic chiasm (cross) for example, transmits the nasal (medial) half of the retinal field from one eye to the apposite (contralateral) hemisphere of the brain.

During this process the visual field is converted into electrical patterns, and is then separated into intercalated quadrants by the configuration of the fibres.  Decussations also occur between the brain and the ascending and descending spinal tracts, and within the tracts themselves as they are found within the spinal cord.

Given all these interconnections, it is clear why delineating them in terms of their form has everything to do with the function of neural innervations they make. It follows that being able to specify their form is conducive to communicating their role in living tissue.

As explored previously, in some but not all cases, the crossing of nerve channels may allow for neural function to continue in the event of its loss (denervation), so that if one nerve branch is compromised, there may be a partial if not completely innervating nerve available to compensate.

When a nerve is not branched into another via anastomosis, then this nerve is said to be autonomous, and is more readily identifiable as a contributor to afferent sensation or efferent action as a result of its autonomy; this is because damage to a nerve of this kind will not be compensated for beyond the point at which it maintains lateral connection with other nerves.

Variation in how the anastomosis of a nerve occurs, if it occurs at all, can present differently in one individual when compared to the next. This is a caveat to the consistency of anatomy mentioned previously. The real world consequences of neuroanatomical variation are very real, but highly contextual. Suffice to say however, that the consistency in neuroanatomy and anatomy across populations in general, predominates because the functionality and adaptivity of the structures do.

Adapted Sensations:

At the outermost periphery of the nervous system, where the dermal layers of the skin and the muscle which lies deep to it are found, sensations may differ despite their being mediated by the same type of nerve ending.

The codification of nociception (somatic pain) for example, is evidently different to that of pruriception - which we know colloquially as ‘itching’, and yet, both sensations may be transmitted through the same nociceptive nerve endings. The stimulus is differentiated only by its codification as a pattern, sensed from the outside world, and which the nerve ending is sensitised to, and in turn which the brain interprets as itch on the one hand, or pain on the other.

We shall return to nociception as a specifier of physiologically meaningful information later. Sufficed to state the obvious here again, that your body prefers you to experience the relative discomfort of sensing what for the majority of the time is something innocuous (a false positive), than not sensing it.

This is simply because the likelihood of surviving what could be a hazard is increased. For example, surface contact with an infectious or poisonous substance (the true positive scenario), as transmissible by an insect. By brushing the insect away before you experience the pain of it damaging bodily tissues, you limit the risk of damage before it occurs.

The sensation of itch and pain being codified by the same integumentary receptor seem both an efficient and more failsafe solution. This sensation preserves the consistency between reality and what we think is happening to our bodily surfaces, by leveraging the same nerves to codify a scale of differing sensations.

It is necessary that there be both specificity and priority of neural sensation. To achieve this, the same specificity and priority may also be expressed via the language we use to differentiate between these sensations.

Up to now in this article on the specificity of language, we have used neuroanatomical science to begin to explore some key aspects of how and why all language must begin as information that has been sensed directly from physical spaces, both within the body and without.

The neuro-affective states (of emotion) that interact dynamically with our thoughts are neurophysiological, and contribute constantly to the sum of those thoughts which we might (or might not) in turn communicate with others.

Yet we still articulate our thoughts and emotions through language to ourselves when we consciously engage with them, and as such, this quiet monologue is the intermittent yet everyday language of our inner lives.

We may even reply to those emotions with unspoken reason, or vice versa, to reason with emotions that turn over constantly beneath, as if our minds were a landscape of forests, all connected and talking to each other at the same time, coordinated into a series of driven interests, a single one in waiting whilst the other is winning out.

This quite human capacity allows us to specify our thoughts within our own minds through language, and apply linguistic precision to clarify our reasoning and to define our feelings. This is especially the case when the more cognitive may be in conflict with the more affective aspects of our experience.

Whether intrinsic or extrinsic to the body, evocative or calculative, both special, general and visceral forms of neuro-sensation provide us with information about our world. Their information is collated into a meaningful understanding, which may be formulated into a concept, relatable by us to another, or by another to us.

As readers, listeners and speakers, we are evidently familiar with language, but the patterns of the language we produce in writing or speech need be decoded first by the language centres and pathways of the brain. 

We shall explore this further as a combined process in the next article in this series.

Thank you for reading!

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By R. McMillan, with contributions from M. Mortimore, J.D., attorney at law.

This article challenges a premise - that the student of law, science or medicine, should only deal with ethical questions in a vacuum; where the details of the scenario itself are not available, and only ethical theory is.

Neuroethics is contingent on the reality of human anatomical functions, and medical and legal frameworks are likewise based on real world circumstances. This article operates as a case study, concerned with a medico-legal context and its neuroanatomical underpinnings to discuss where clinical anatomy is fundamental to discussing a dilemma in an informed way.

We start with our key definition:

An ethical dilemma is a choice between competing actions, none of which appear to offer a fully satisfactory moral outcome. The resolution of this conflict is rarely ever optimal, as the real world seldom allows it to be. 

In reality, facts are available to medical and legal practitioners which flow from actions and observations, as made by them in response to a given scenario.

Broadly, this is no different from decision making based on the discovery of information and its interpretation.

LUCIDA VISIONIS has produced an article on the Specificity of Words & Nerves which explores the interpretation of language at various levels of detail, and why these are significant to human perceptions and our sense of meaning.

The ethical question absent actions and observations however, is an exercise for the sake of exercise, and arguably it fails to take the case by case. In other words, it is a static question, absent the clinical reality needed to found, or to adjust it, how and when a patient’s status changes. 

It is crucial to medical and legal processes that information be as complete as possible. Unsurprisingly then, it is significantly more useful that practising for efficacy in the real world seek to flesh out the facts as a dynamic between patient status, clinical ethics and legal foundation. In effect, to think as if this were a real instance of medical or legal practice.

But why establish this in any detail, and at the cost of efficiency… In practice, the observations made by each discipline interact, and gaining mental practice under the assumption that they interact bears closer resemblance to reality. Of course, this is no different to weighing up the nuances of a decision in the real world when it has ramifications for one’s life, or the life of another.

Ethical questions as academic primers are of course just that, they prime discussion. That such details can wait until the student comes into contact with them in employment however, when the real world deals a baptism of fire, is a questionable ethos.

Fortunate medical students and anatomical students are challenged by their lecturers, so there may be continuity between their deliberative and deductive skills into clinical residency or education / research. This actively improves their diagnostic and educative abilities. Among clinicians, it is well known that the information concerning diagnosis is not limited only to symptoms.

For example, a complete history of the patient will ideally include the patient's occupation, simply because this may have implications for clinical status. Likewise students of science are directly challenged by those tutors who have a genuine interest in the deliberation of evidence and methods, and what can be deduced via experiment and dissection (e.g.) not only as a means of academic evaluation.

Scientific experiment and the diagnostic method are methodical tools, wherein information is derived from the real world, and which will almost always carry practical value, superseding information for information’s sake. This is arguably, equally true of tutoring medical sciences and legal study, as deliberation precipitates a careful and comprehensive consideration of the facts.

How Medicine & Medical Law Function:

Experience of the facts at hand in an ethical scenario, are dealt with in overlapping and yet also disparate ways within medical and legal practices. 

In legal practice, the analysis is dependent on the pattern of the facts as they have occurred, and to distinguish what their relevance is to an event that has also already occurred. Medicine is not dissimilar in these broad terms, but its analysis is made through scientific and clinical techniques. These of course are intended to infer, deduce and falsify the presence and particular presentation of a pathology or trauma, and how to manage this for the good of the patient. Precision and expertise which are conducive to a patient’s survival is the clinical concern, whilst the legal is how each party is protected, yet also where the exception to a legal rule is required.

Both practices consider the consequences of these factors, but never without the opportunity to derive more information than is immediately available. Doctors run tests, legal practitioners consider how the facts of the patient’s status might interplay with the law and warrant intervention. Law and fact are not synonymous. The scenario discussed here aims to describe how their interaction is of practical concern to the medical, scientific and legal process. The scenario is as follows:

A female patient is hit by a drunk driver and sustains substantial blood loss, several broken bones and a partially crushed skill with an intracranial bleed. Paramedics reported the patient as in and out of consciousness en route to the hospital, but by the time of her arrival she had regained full consciousness. The treating physician explains to the patient that their life is at risk and they need a blood transfusion and brain surgery immediately. However, the patient verbally communicates that they are a Christian Scientist, that they believe in the healing power of prayer, and that they wish to be discharged immediately so they can consult a Christian Science Healer.

An emergency conference room meeting by the surgical staff reveals a consensus - that failure to relieve pressure caused by her intracranial bleed will result in loss of consciousness within a few hours, and likely her death. When this information was provided to her, she remained steadfast in her desire to seek a Christian Science healer. When hospital staff inquire into next of kin, the patient explains that they are a widow with no living relatives except for seven dependent minor children, ages 1 through 15.

The patient’s faith remains subject to the underlying reality of their physiology, an ‘electric sea’, the term coined by the neurosurgeon Henry Marsh to describe the electrochemical landscape of brain tissue. These tissues underlie conscious and unconscious functions, and the metaphor is made by Marsh in light of the many patients which must undergo anaesthesia during surgery. Of note is that the scheduled excision of a tumour differs greatly when compared to surgical interventions for acute trauma. Especially when consent is ambiguous. 

At face value, the default legal basis for a scenario like this is simple…

As long as the patient understands the consequences of refusing treatment, informed consent is fulfilled. This satisfies the patient’s wishes within the medico-ethical requirement for autonomy. This is also however, where ethical theory comes into contact with clinical concern.

We know that the patient has requested to be discharged, and has communicated the conflict between the medical aid being offered to her and her religious beliefs.

However, the fact that she has no less than 7 dependents, aged 1 to 15, introduces uncertainty and room for deliberation regarding the best course of action. How the extent of her injuries may have impacted her capacity to make this decision also draws the weight of clinical analysis into the equation. Within these margins of uncertainty, ethical nuances are brought to the fore, becoming the only means of resolving the dilemma to within a reasonable and justifiable degree of certainty.

These margins are narrowed however, by clinical information, and how such information informs the legal basis of any medical decision.

The decision is of course time sensitive, and falls on whether or not to render aid when the patient loses consciousness, which is inevitable due to the severity of her injuries.

The main issue with the ethical question posited is that, if it is to be representative of reality, and so have practical value, it cannot be considered within an ethical vacuum.

This means that the weight of clinical evidence becomes of direct concern to any legal contingency, and any ethical argument which deviates from the protocol of medicine underwritten by law.

This article is a discussion of how clinical evidence and law cannot be considered ethically, without information pursuant to reality. This in no uncertain terms includes a relevant sample of scientific and legal precedent, because these respectively underlie the practice of medicine and law.

As we shall see, the medicine and law in such a scenario directly underlie and interact with each other.

In the UK the Mental Capacity Act of 2005 (the USA may vary marginally from consensus according to state law) if a patient is to either refuse or consent to treatment, they have to understand what the treatment entails. This means exactly that the patient is capable of retaining the information, able to weigh the consequence of their choice, and able to communicate this. Capacitous refusal of treatment is predicated on communication of consent, and that consent is based on a meaningful comprehension of the ensuing consequences.

Capacity is assumed unless there is clinically meaningful evidence to the contrary, such as an inability to communicate, which is by medical law equivalent to a loss of mental capacity. However, this does not mean that the patient’s communication of her wishes by means other than verbal, are not a demonstration of autonomy, pursuant to either consent or refusal of the patient to receive care.

In briefly differentiating the legality of patient capacity here, we can already see how the clinical scenario and its legislative detail are wholly necessary to practical ethics, wherein the ethical method is applied to a real world scenario in which there is high risk. In this vein also, the specificity of language in each domain focuses the issue at hand. Let’s explore how…

It would be a contravention of medical protocol and law to assume the patient does not have capacity only because their decision goes against their welfare, or is unwise.

However, if there is a consensus as to the unwise nature of a decision in this regard, it may be used in combination with evidence that the patient does not understand their status, or does not wish to understand, in order to argue the patient’s capacity is compromised. In this case, it could theoretically be argued, albeit with some difficulty, that the patient’s religious beliefs prevent them from being able to understand the inevitable outcome of the scenario, and that her situation is fatal if she does not receive immediate medical care.

Conversely however, the clinical evidence may be used to argue that the patient has capacity, despite the presence of a neurological disease which presents as cognitive impairment, providing the medical evidence demonstrates this…

Under the mental capacity act for example, a person cannot be said to lack capacity by default - solely because they have a diagnosis of dementia, and their capacity must be based on evidence derived from a neurological examination.

This does not mean of course that their capacity is not demonstrably impinged by dementia. The rub lies therefore, in the space between medical and legal concern. A space which cannot be reached in and of the ethical question.

The degree to which clinical evidence may affect the patient’s capacity becomes the key medical question, and will almost certainly aid the legal argument, whether it is for or against the patient’s choice. Time is also crucial however.

The acute nature of the patient’s trauma means that her consent needs to be expedient, and as such, there is little to no time available for her to reconsider, nor for the medical staff, who have a shared but limited duty to persuade her to receive care. However, the surgical staff may also conclude that surgical intervention is not ethical because with all the will in the world, the efficacy of care may not be capable of meeting her injuries.

The fact that the trauma is to her brain brings about the immediate need for surgery, and is the direct cause of any potential loss of her capacity. The question is to what extent, but there is no doubt as to the aetiology, that is, the causation and implications of impaired cognition by bleeding within the brain. 

The legislature bases itself on this premise.

That psychoneurological capacity forms the core of legal contingency in the UK is clear. But is based on clinical principles of analysis. Once more, we see the ethical reality is informed by a rich body of information, whereas the ethical idea is by itself an isolate.

Section 2(1) of the Mental Capacity Act stipulates that:

‘A person lacks capacity in relation to a matter if at the material time he is unable to make a decision for himself in relation to the matter because of an impairment of, or a disturbance to the functioning of, the mind or brain’.

Under UK law, mental capacity is demonstrable by way of medical examination, and comes down to the combination of these 2 tests.

These are the functional test and the diagnostic test. Dementia falls within the diagnostic test criteria for example, but does not include decisions based on religious beliefs. Under this test it must be shown that the patient has an impairment which affects the function of the brain. 

The functional test criteria have been mentioned in the rudiment of this article. They are that: the patient must understand the medical procedure at its most basic level and its purpose, must be able to comprehend the consequences of both the medical intervention and a decision to decline, must be able to retain this information, and communicate their decision.

All practical steps must be taken to allow the patient to communicate, and allow the criteria of each element to be fulfilled. Given the patient in our scenario is conscious, we can assume she is relatively lucid and capable of verbalising her thoughts.

It has been explained to the patient that her life is at risk. The potential gap in our information, albeit only potential, rests in part between the doctor’s communication of the patient’s circumstance to the patient, and the patient’s assertion that she does not want medical care. The rationalisation for rejection of care is her religious belief, but the declaration of her belief is no demonstration of diagnostic and functional competency in itself, yet neither is itself a legal basis for mental incapacity.

If however, the patient did not fully understand that they have suffered an inevitably fatal trauma, which in this scenario is to their central nervous system (the organ which defines medical and legal evidence of a person being alive), or their response implies that they do not wish to accept this fact, either of these could arguably serve as a justifiable basis for impaired capacity.

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Sensation precedes language:

By exploring examples of neural sensation, and the way in which our senses confer information about the world to us, not only can we explore how language is shaped before it is even uttered or written, we can also explore why human language and the neurosensory system are reflections of each other. In order to function, sensation and language must differentiate the reality of events and stimuli from one another in this way…

We know a human being is exposed to a wide variety of internal and external stimuli and physiological changes throughout a 24 hour period, and across a lifetime; our response to many of these changes requires us to be aware of them, on one level or another.

At the human scale, the world is especially complex, thus, our neural capacities allow us to meet the challenges of what we create, by observing their effect with assiduous measure, adjusting our designs or actions accordingly. 

Our functional neuroanatomy reflects this demand by its delineation into afferent and efferent transmission. This means respectively, those signals issued from more distal locations to the brain (sensation), and in the converse direction, those signals which operate from the brain to innervate the action of more distal (motoric) tissues such as muscles and glands. 

The spinal tracts which mediate all somatic (muscle, skin) and visceral (organs/glands) as sensations from the body to the brain for example, subserve the brain by transmitting afferent signals electrochemically, from the most peripheral to the most central neurons.

These nerve fibres are referred to as 1st order and 2nd order neurons, where respectively they define the first and second neuronal cells which synapse in the chain of transmission. This description of a stepwise process differs however, from the terms upper and lower motor neurons. These terms denote neurons which descend (efferently) from the brain to the spinal cord when upper motor neurons, and to complement this outflow, neurons which proceed from the spinal cord to the target musculature or organ are termed lower motor neurons. Lower motor neuron disease is then, a disease of the peripheral nervous system, affecting nerve fibres beyond the central nervous system, outside of the spinal cord.

The terms 1st, 2nd and 3rd order neurons, are useful, simply because they reflect the functional neuroanatomy of both afferent and efferent transmission. Our initial aim is to understand the specification of which order neuron operates during its functional role, and how it may be affected by injury or disease, and through which tissues each neuron travels, and how a loss in their function would present outwardly. This requires the use of specific terms, especially when the neural tissues in question are part of a branching complex, and this is almost always the case…

The trigeminal nerve, meaning the ‘threefold’ nerve, for example, issues general sensation from its 3 branches, which approximate to the upper, middle and lower face. For example then, symptoms of neuralgic pain in the temporomandibular junction, (where the jaw hinges to the the skull), indicate the mandibular branch of the trigeminal nerve is being affected. Whereas symptoms of headache would suggest the ophthalmic branch of the nerve, which innervates sensation to the forehead, eyes and midline of the nose, is the branch of concern.

Being able to distinguish the intrinsic structure of the trigeminal nerve through language is incredibly useful. But what about specifying different orders of neuron in relation to neurological dysfunction, what do the words actually provide us with here? We can use an example which deviates from afferent sensation momentarily to illustrate this by drawing on the efferent functions of the facial nerve.

Presentations of stroke must be differentiated from facial (Bell’s) palsy. An underlying understanding of which order of neuron and which branch of the cranial nerve in question is affected is clinically crucial, even though the facial signs may be sufficient to posit a diagnosis.

In terms of the muscles of facial expression which indicate these signs, by either losing or retaining their contractile innervation, these nerve branches function to confer muscle tone and contraction (and not sensation), therefore we ask which of 1. the upper (1st order) or lower (2nd order) motor neurons that descend from the somatomotor cortex have been affected, and 2. which subsequent subnuclear branch of the facial nerve is affected; - for it is these nerves which underly the neuroanatomical structures delineating a stroke from facial palsy. This is specifically because the 7th cranial nerve, the facial nerve, innervates the muscles of facial expression via 2 efferent neurons that synapse within its nucleus (the facial nucleus).

The diagnosis hinges anatomically on the synapsing of these 2nd order neurons where they proceed from the aptly named, pons verolli - i.e. ‘bridge of Verolli’ region of the brainstem, shortened usually to, the pons, and in which the facial nucleus is located, yet also where connections between the medulla and cerebellum are made. 

There are some specific terms here that help us delineate the connections and their states: first is the antonym of innervation, which is denervation, that denotes a loss of electrochemical activity in the nerve; second is the word ipsilateral, which in the context of brain hemispheres denotes the same side of the brain which has been damaged; finally their is contralateral, which is the antonym of ipsilateral, and simply means the adjacent hemisphere, which in this context has not been affected by damage. The potential space between them is the medial longitudinal fissure.

In the scenario of stroke or facial palsy, the stroke presents outwardly as a loss of tone in the muscles which the lower facial nerve innervates, hence the cheek and mouth sag. If the affected neuron is 2nd order from the facial nucleus, becoming the lower facial nerve branch, then the forehead is spared due to a backup nerve being available. This compensatory nerve is a 1st order neuron which also descends from the contralateral somatomotor cortex to synapse in the pons.

This nerve compensates for denervation of the somatomotor nerve affected in the ipsilateral hemisphere by maintaining innervation of the lower facial nerve branches; if however, both 2nd order neurons are affected, then complete denervation of the facial nerve will occur, presenting as paralysis (palsy) of one half the face (as seen in the facial presentation of 1) and an inability to wrinkle the forehead. 

The precision of these terms is elementary prima for any neurologist or keen neuroanatomist, because the wiring and the factors at play when denervation occurs, require knowledge of the underlying structures. This language must go beyond the interpretation of symptoms alone; especially when research on this mechanism is being conducted, communicated, or in the event that either the patient’s condition worsens despite intervention, or presents with more than one type of neural problem. 

How then do we infer the specific direction in which a 1st order neuron is transmitting its signal, whether toward or away from the brain, when compared to higher 2nd or 3rd orders which synapse in the brain?

A 1st order neuron is afferent when stimulated at a free nerve ending under the skin, and its transmission is directed towards the brain. Conversely, a 1st order neuron that descends from the brain to innervate a muscle say, courses towards that tissue in order to transmit efferently. Efferent nerves descend, afferents ascend.

An afferent transmission from the skin via the 1st order will subsequently synapse with a 2nd order neuron that transmits its signal up the spinal cord. This ascending fibre can be specified as an afferent post-synaptic neuron, as it is situated within the spinal cord, and is a functional structure in a 3 step process, ending in a 3rd (order) neuron of the brain. 

Ascending via the brainstem into the thalamus, the 2nd order neuron then synapses with a complex of modular nuclei (bundled synapses which represent functional units) before projecting via the 3rd order neuron into the higher order cortical tissues that receive specific somatosensory stimuli. 

Somatosensory afferent transmissions are issued from more peripheral locations via the spinal cord.

Where the term, viscera, is used to denote organ tissues, rather than somatic tissue, the word soma means ‘of the body’. Soma is in some way an etymological offshoot of the ancient Greek word demas, meaning ‘of the living body’; - a fact which may indicate that the majority of anatomical classifications made by early modern scientists were the result of observing cadavers more often than living patients, yet showing also how the specificity of a word’s meaning can develop over time. 

The term ‘somatosensory cortex’ denotes an area of cortical brain tissue which processes afferent sensations from somatic tissues. It is the complement of the motoric efferent processing which is provided by the adjacent somatomotor area of cortical tissue, that is precentral to the sulcus dividing each. The term ‘precentral gyrus’, denotes the anatomical relation of the somatomotor area to the central sulcus (of Rolando). The sulcus divides these two functional areas, as seen in the image below.

The somatomotor cortex dedicates a disproportionate area to the articulation of the mouth, lips and tongue through the descending nerve tracts. The situation of the tongue is not in the same area of the cortex as the mouth, hence its absence in the above image.

Fibres which descend from the inferior 3rd of the somatomotor cortex (precentral gyrus) originate from the laryngeal and orofacial motor cortices therein, and innervate these lower facial muscles. 

These efferent fibres terminate as 1st order neurons in the cerebral peduncles of the ventral midbrain, found within the brainstem. In brainstem nuclei which include the facial and trigeminal nuclei mentioned earlier, these descending fibres synapse with 2nd order neurons that contribute to the fine motoric control of speech. The course of these fibres collectively form the corticobulbar tract. Everything here is distinguishable in terms of locale and the flow of electric transmission. But with regards to language…

…the disproportionate representation of the orofacial musculature in the somatomotor cortex, evidently reflects how important linguistic precision is for our species. The production of speech requires the inclusion of the laryngeal complex (which is represented in the inferior 1/3rd of the somatomotor area, as above), and also requires the respiratory system in order to coordinate the passage of air necessary for vocalisation and phonation, which alongside the orofacial musculature, demands the precise coordination of more than 100 distinct muscles, 1/6th of those in the entire human anatomy.

Although each term, gyrus and cortex, may be used synonymously to denote this area of the parietal lobe of the brain, they have distinct meanings. The term ‘somatosensory cortex’, denotes the functional aspect of the cortical tissue; but the term ‘postcentral gyrus’ allows the area to be identified and located as a raised area of tissue when observing the exterior surface of the brain topographically.

The fact that this is the surface and not volume of a tissue, can be easily termed as a, pial surface. This parenchymal surface of the brain lies deep to the arachnoid mater that overlays the brain and allows for cerebrospinal fluid to be circulated. The specificity of how brain regions and areas relate to each other is built into the nomenclature so as to convey information, and in distinguishing each form and their positional relations, helps us to comprehend these complex structures more easily and yet also more completely. 

A useful takeaway here is that it pays not to avoid using specific terms when they describe something complex, or assume such terms are synonymous because they at face value describe the same thing. It is absolutely valuable to describe the simplest structures at their initial levels of detail, as in the hemispheres of the brain being divided into two, symmetrical and connected via the corpus collosum. But the more complex the structure is, the more specific the communication of its form and function need be.

Similarly, the term postcentral, obviously implying ‘posterior to the centre’, is used because the anterior-posterior axis clarifies the reference points for orientation of the brain in the cranial vault of the skull, whereas the word ‘behind’ does not specify anatomical orientation or relation. ‘Behind’ what?

As human beings, we sense the physical composition of our world through neural tissues, each relying on their own physical composition in order to confer function. 

As established, the synapsing of 1st through to 3rd (and even 4th) order neurons, mediates the electrochemical transmission between body and brain, allowing the brain to process information that is afferently sensed within as well as without.

Worth noting is that there are 8 ascending spinal tracts, and 4 descending, which at least by number indicates there are twice as many ascending tracts, which are dedicated to transmitting sensation as afferent information towards the brain, than there are descending tracts dedicated to the efferent control of movement. We can to some degree infer then, that the nervous system assigns twice as much of its functionality to receiving information from the body and outside world as it does to movement. This has much to do with the dual imperative for us to move only when we have information which allows us to safely do so, and to issue close control over visceral and somatic functions via the autonomic nervous system.

For instance, the afferent spinal tracts known as the dorsal columnar medial lemniscal, and in partnership with them, the spinothalamic tracts, respectively mediate the sensation of both stereognostic (tactile detail) and crude forms of touch, with each transmitting the signal issued from integumentary (skin) nerves that detect an object held in the hand.

Like all anatomical labels, these nerve tracts are named to denote certain notable features, such as their shape, as in ‘columnar’, their position as in ‘dorsal’, and their course as being ‘spino-thalamic’, ascending through the spine and into the thalamus.

The dorsal columnar medial lemniscal pathway is so named because it is situated in the posterior half of the spinal cord, but on reaching the brainstem it decussates to the medial lemniscal tract.

The phylogeny of this tract (its evolutionary history) is relatively more novel in its evolution than the spinothalamic tract. It is responsible for our sense of fine touch, vibration (save for the head), conscious proprioception, and stereognostic touch - which discriminates complex objects, allowing us to identify them by prehensile (grasp) use of our hands, but without necessarily having to look at the object. 

The hand is a prehensile limb, that is by definition, ‘able to grasp’, and through which we can palpate, in order to sense the shape of an object with greater or lesser sensitivity.

Because the spinothalamic tract is far older than that of the dorsal columnar tract, it indicates that our evolutionary ancestors developed crude touch before that of the stereognosis which heavily contributes to the recognition of an object through touch alone.

Neuroanatomical mechanisms such as these are fundamentally how the sensation informing what we experience is mediated, to then directly inform what we describe of our sensory experience through language.

The tracts mediating the sensation of an object at hand in specialised degrees of detail; yet this process alone, as mediated by the spinal tracts specified above, does not allow us to successfully interpret what the object is, nor whether the object is of any value. This would require a range of modalities, including both comprehension and interpretation, each the remit of executive decision making in the brain itself.

In the next article, we shall explore the language making process as it proceeds from that of sensation.

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The nervous system is the repository and source of all language…

…It grows and develops to fulfil 4 fundamental functions: to sense, associate and discern between stimuli, and in processing the information, to then respond appropriately. 

These neurological functions are still emergent during the development of language postnatally, although they quickly become the absolute requirements for language synthesis in everyday infant life, progressing into adulthood. 

Where the anatomical functions of sensation, signalling pattern and processing combine, information is mediated through neuroanatomical mechanisms, revealing not only what language fundamentally is, but for human beings especially, why language has in turn become a tool of such precision.

As the first part of a series, this explorative science article looks at why the synthesis of thought into language occurs at its most fundamental level.

To describe complex structural functions is the aim of neuroanatomy as a medical science, and a mode of enquiry which directly observes this aspect of human nature.

Brain tissue consists of modular units connected by neural pathways, which are stimulated to function in a localised and yet integrated manner, connecting dynamically with other pathways within the cerebral hemispheres, brainstem and the wider nervous system. 

Before coming to how neurolinguistic functions can evince the nature of language, and why the power of descriptive communication through word composition is such a cornerstone of human existence, we can first explore examples of neuroanatomy outside of the brain to contextualise precision language, and in the same vein, draw on real world examples of neurolinguistic function, where neural structures underlie the process of language use in human life.

Through the specificity of words we can make distinctions, and within neuroanatomy, make scientific distinctions between human tissues and the forms they take; muscle for example is very distinct from bone, yet bone and muscle also vary within themselves, as also do neural structures. We can also make generalisations, such as the fact of nucleated cells being native to bone, muscle and nervous tissues all. This commonality between tissues is a fact of cell lineage, beginning from undifferentiated cells that become specialised into specific tissues. The differentiation of a cell’s form and function allow for these tissues to be generated, maintained and repaired in an organised manner. Not all cells are equally dedicated to these tasks within their respective tissues however.

Schwann cells of the peripheral nervous system, for example, differ greatly in morphology and location when compared to astrocyte cells, due to their respective functions. Both have primary yet differing roles in the support of neuronal axons, the neural conduits which conduct electrochemical signals. 

The eponymously named Schwann cell, is found enwrapping segments of neuronal axons that are local to the peripheral nervous system (distal to the brain), in a process known as myelination. Myelin acts as electrical insulation for select neural conduits, and thereby reduces the amount of axonal diameter (and overall space) that would otherwise be required for rapid conduction to be feasible over those distances found within human tissue. As well as the efficiency of space through form, the metabolic efficiency of our bodily tissues is likewise fundamental to retaining the energy needed to utilise higher brain functions.

By comparison, astrocytes are the most abundant cell in the brain, influencing the growth, metabolism and the protection of neuronal connections, yet surprisingly possess no direct neuronal functions in terms of electrical potential, although neither are they electrically silent. The astrocytes are found exclusively within the white and grey matter of the brain and spinal cord, and comprise fibrous and protoplasmic subtypes, designated respectively to more and less myelinated nerve fibre tissues of the central nervous system, which present respectively as the white and grey matter of the brain and spinal cord. We can intuit, being ‘star-like’ in appearance, that astrocytes differ greatly from the insulatory structure of Schwann cells, due to the radial processes which extend from their nucleated cell bodies. Within the category of astrocyte cells however, their namesake denotes an easily identifiable appearance, yet we cannot specify their subtype by it. 

The specificity of terms used to identify these cells and the living tissues they organise into is imperative, not only for their being the clinical and scientific means of delineating and labelling their microanatomy in a meaningful way, and for making neurological diagnoses and interventions in the presence of disease, but also in that the nature of language has deep implications for how we as human beings understand ourselves and the world around us. The functional differences between neural tissues such as these allow for the physical orchestration of the sensory when compared to the motoric (movement) functions, through which respectively we experience and engage in physical actions throughout life.

To expand on this further in living tissues, which by definition are neurally innervated, a general somatic sensation such as tactile sense via the skin - a fly landing on one’s arm say; - differs both in embryogenic derivation of its structure and its function, to that of the special senses - such as vision and audition; - which in health obviously allow us to see and hear the fly which has landed on us. Both our general and special senses evolved to avoid environmental hazards, seek both resource and advantage, to avoid predation and to participate in it. As we shall explore in further articles on this topic, the specificity of terms we use to communicate has become not just a recourse, but the mainstay of adaptations that contribute to human survivability and thriving. 

The form of living tissues and all their neural innervation, at the most fundamental level result from the demands for life to adapt to those physical forces that inform the world we inhabit. These include light, gravity, pressure, electric conductance, but also the elemental properties of calcium, sodium and potassium, to name a few. It is these forces which have stimulated the human form into being over deep time; and yet within a lifetime, also stimulate that same human form into growth and repair. All told, this has resulted in tissues which confer adaptive traits which in turn undergo genetic conservation, and subsequently, establish a continuity between the composition of tissues within and between species. All mammals for example, have skin, ears, eyes, limbs, mammary glands etc.

The epithelial cells of the skin for instance, which can be termed as the integumentary system when referring to the tissue as a cohesive anatomy, among other things serves to protect the deep tissues of the body, and to act as a medium for sensation. It is surprising to note that the cornea of the eye is composed of adapted epithelial cells on its interior and exterior surfaces, meaning these cells are ultimately of the same lineage as those of the skin, yet which in the cornea are transparent. There are cellular and acellular components to the cornea, and each contributes to the maintenance and function of its light refractive properties, allowing light to enter the eye, converge at a focal point through the crystalline lens, and for clear vision to be possible. All at once we find that this clear transparent exterior of the surface, a living tissue which resembles glass, is not as deceptively simple as it outwardly appears, but is a piece of precision, albeit blind engineering. 

We see in the cornea, and the eye in general, the wider principle of nature already mentioned; that when something works, and functions in the real world, nature conserves this functionality through the genetic expression of that trait across the generations - something which in a manner of speaking, requires an intensive specificity of language (in the form of protein coding genes). Another fact of evolution is its convergence, in that an adaptive anatomical form, such as a dorsal fin or the eye, has evolved many times over, with no genetic continuity of lineage between each instantiation, due simply to the consistency of demands placed by the physical and chemical world on the organism. The genetic specificity of language is one of nucleic acids, that allows for physical forms to be generated from the encoding of proteins into complex structures, with traits being adapted for other purposes, refined and optimised. A scientific understanding of nature means that we be able to directly observe its complexity as it is, requiring that we articulate the underlying reality of nature through language which holds true to what is specifiable. When meaningful, this gives us an opportunity to communicate the intricacy of how the world within the human body, and the world without, come to influence each other through sensation and language.

Life takes physical form, and in doing so meets the various demands needed to survive, thrive and operate in a complex world. In this task, form and function are essentially equivalent, simply because living tissues must answer the rigorous demands placed upon them, and pass on their genes. The evidence of this physical relationship is intuitive, but is overwhelmingly established in science, engineering, medicine and other fields of interest besides.

To describe the relative complexity of human tissues therefore requires a precision of language; one that through direct observation, can capture all of the most isolated to the most cohesive of morphologies across varying states and functions, from physical exertion to rest, from the cochleal hairs of the inner ear to the terminal hairs of the scalp.

This article series will orient its focus on language through the human nervous system, because it is this system which is responsible for language, and any specificity of communication through language. Language is after all, a physical form, as it assumes visual structure when written, and travels as sound when spoken in an atmosphere.

Taken as a whole, there is an intimate continuity between the development of our senses, and the ability to communicate experiences through verbal speech. As human beings, we can relate the reality of what we have experienced through our senses, but also, we are capable of displacing our account into tenses other than the present. We can relate an experience from the past, or posit another in expectation of the future. We can even convey concepts which may deviate from reality entirely, and produce works of imagination. The ability to specify our place in time’s constant through language, has allowed posterity, prescience, and presence of mind to be ever ready in our consciousness, such that tense is a norm of language.

Temporal processing is the responsibility of the brain, being both the remit of the dorsolateral prefrontal cortex, and the entrainment of circadian rhythms by the suprachiasmatic nucleus. Each of these brain structures form key parts of our neuro architectural inheritance in evolutionary terms, contributing to the electrochemical system as a modular yet integrated whole, allowing us to be cognisant and physiologically readied or resting. The brain is itself the most complex system known to our species, and these temporal processing units allow us to understand when we learned a fact such as this as listeners or readers, and approximately what time of day our body is most responsive to such information. Humanity has existed as the embodiment of this system, without any means of gaining direct observation of its function, and reflecting on its form, for the vast majority of human existence. We can now however, specify all of its elegant features and functions.

Through stimulation of the senses, we learn to differentiate those stimuli generated by our physical world, processing them through a combination of sensory, affective (emotional) and cognitive functions.

The influence of emotion is an especially nuanced process, one which is so dynamic and expansive in its interactions with general cognition that it deserves its own separate article. Suffice it to say that emotion, especially extremes of emotion, are the most potent in effect on neural pathways when it comes to their influence on the consolidation of memory, and have great bearing on how we develop and specify our experience of the world through language.

The next article will differentiate how and why sensation, which as a process is galvanised and cohered more immediately than cognitive and affective processes, informs the precision with which we think by providing us with information about the world, mediating our experience, for us to then differentiate consequences, and so establish what we value, such that we can communicate this through language.

Our focus shall primarily be on why language exists, and what the loss of language specificity in neural dysfunction reveals about this very human capacity. We shall start by describing the first means of exposure through which language is formed, that of sensation, and why the language used to describe neural sensation need itself be specific.

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