Diabetic Neuropathy and Clinical Practice

By Sanjeev Kelkar

Diabetic Neuropathy and Clinical Practice aims to improve the pathophysiological understanding of the entire spectrum from sensory motor to autonomic diabetic neuropathy, its correlation with the symptoms, improving thereby the communication with the patient including prognostication and other tools that one should utilize to better management. It also emphasizes the need to regain the grip on the basic sciences of clinical medicine to deal with it better - Anatomy, Physiology, Biochemistry and Pathology and gives the necessary details. The volume aims at explaining what the clinicians need most to help patients and may not possess.

• Language: English
• Publisher: Springer
• Release date: Feb 29, 2020
• ISBN: 9789811524172

Book preview

Part IAnatomy and Pathophysiology of Diabetic Nerves

© Springer Nature Singapore Pte Ltd. 2020

S. KelkarDiabetic Neuropathy and Clinical Practicehttps://doi.org/10.1007/978-981-15-2417-2_1

1. Introduction

Sanjeev Kelkar¹  

(1)

Independent Health Researcher, Pune, Maharashtra, India

Sanjeev Kelkar

This book is about Diabetic Neuropathy AND Clinical Practice and not Diabetic Neuropathy IN clinical practice. The title first places any neuropathic elements with or without diabetes which must be attended to. This in itself is a large area even without diabetes. If the Great Peter Dyck has to be quoted 40% of all neuropathies is likely to have an autoimmune origin, eclipsing the toxic-, alcohol-, and vitamin deficiency-induced neuropathies with other neuropathies associated with neurological syndromes. Managing neuropathy with close listening to the symptoms, an examination, diagnosis, investigation, explanation, and therapeutics are rudimentary in today’s practice.

A detailed clinical examination even at the specialty level today may have got transferred to an Electromyography and Nerve conduction studies, foraying into the evoked potentials at times. Such recordings not corresponding with disordered nerves, imperfect conclusions, and confusions with no particular benefit to the patient to understand of his problems or to the specialist in terms of diagnosis. The same problems will get more confusing if diabetic neuropathies get added to the above scenario. Thus it is not a strong element in practice.

A title of Diabetic Neuropathy IN Clinical Practice would have limited the scope and would have taken the learning and practice away from the rest of the non diabetic spectrum. Diabetic Neuropathy also placed within the same clinical practice, has in itself a much larger spectrum and scope than consciously recognized by the physicians. The foundational ideas of these depressing and fatiguing conditions are far from clear in their minds. That the physician thus needs to pay special attention to it while dealing with diabetes is wanting. The big issues in diabetes—glucose, heart, and kidneys, sometimes eyes dominated the era from nineties till middle of the first decade of the new millennium. Promptly, the burden of being abreast with these systems was gleefully shared by the referral culture of today’s practice with unenviable results. Lately it is the diabetic foot movement which has caught up well with much less understanding and hence without engagement with diabetic neuropathy as a whole.

If at all diabetic neuropathy is clearly defined in practice, from clinical to final well laid out diagnosis, separating the nondiabetic nerve involvement from diabetic nerve involvement in practice is still more crucial. That is because at least 10% people with diabetes will have this dual pathology. Treating them in an undifferentiated way leads to many unsavory clinical situations. Unfortunately, the complex diabetes disorder has come to be equivalent to a sugar-only problem, the management of which is far from optimal. Even after so many advances if it comes to any surgery, including foot, the pandemonium over it breaks lose.

Diabetic Neuropathy and its relationship to the symptoms it produces are considered somewhat complex to understand and explain or diagnose. If the basic pathophysiology and anatomy is well understood, it is quite dimple. This negative attitude or belief results in inadequate or unsatisfactory explanation to the patients about the situation. The potential and limitations of treatment remain unclear. There is a need to understand the pathogenetic mechanisms in broad terms also so that the treatment will have a well-calibrated approach. This approach reduces the anxiety and relieves their depression common in severe forms of Diabetic Neuropathy. More often than not this remains an unmet need.

The spectrum of symptoms arising from many organ systems, its pathogenesis, and evaluation methods admittedly is large. However a unifying approach, over which this book is built the matters will be far simpler to understand and manage. As important as evaluating diabetic foot at risk of ulceration are other forms of neuropathies commonly met with in clinical practice if one pays attention to. The treatment options also therefore are many. The diabetes consultant or physician who manages it therefore needs a complete picture of this disorder. These two factors point to a need to have a usable, sufficiently detailed, and easily available single volume on this subject to fulfill this need. It is with this purpose this monograph is prepared.

Before going in to the details of the book, one question that looks legitimate and should be answered is—how much should a specialist know and undertake about so many complex disorders with so much advanced knowledge available? Why should she get burdened by it when subspecialists are abundantly available, particularly if one’s own practice is quite busy? The answer is as much more as possible. When any patient comes for consultation, the detailed definition of all problems must be made by spending time for it and communicating more immediate elements and what is required to be done. It is a skill to impart more details of less urgency over time in repeat visits. Once this is done, the rest of the time one needs to spend with the patient in follow-up visits is much less and far more meaningful. This is possible when any issue that concerns either the physician or the patient is understood in anatomical and pathophysiological basis.

There is another reason for undertaking this burdensome-looking exercise. The less one refers the more unified and unitary the treatment becomes with numerous benefits following it. Today if an internist tries to do as less as possible and depend on the specialties all the time, a time will come when he will become the post office directing all the mail to this or that place never dealing with anything at all. The enormous consequences of this type of practice are detailed in the two volumes mentioned earlier. The last and not the least are to understand correctly and as less frequently as possible when a person needs institutional support and matters cannot be handled in the office.

Turning to the book itself it may be said that it is constructed and written to precisely overcome all the objections, limitations, and for physician benefits in understanding this subject. The book covers the entire spectrum of diabetic neuropathy with sufficient detail which can be remembered without feeling burdened over it. The author has long believed that medicine is not to be practiced by remembering ten million random data points. It should be practiced by using a framework of logic for every organ, organ system, and the whole body as such. It is possible to do so by retaining some basics of cellular physiology and anatomy of tissues. The second and the third chapters, Functional Anatomy of the Peripheral, Autonomic, and Cranial Nerves and Pathogenesis of Diabetic Neuropathy, cover the most relevant information precisely in this manner. Once this basic logic is consolidated, the door to proper diagnosis and evaluation of the neuropathic element opens in a well-lit manner. This also gives an ability to think of diseases or disorders as they affect the cells and tissues and then organs, etc.

The section that follows next is the Dysfunctions of the Diabetic Autonomic Neuropathy. This is the least understood part of the diabetic spectrum and within the Diabetic Neuropathy itself. These neuropathic abnormalities are also loaded with troublesome and debilitating symptomatic elements for which little explanations are offered by the clinicians, often pushing these aside as functional disorders without any organic basis. Considerable work and awareness have developed about the sensory neuropathies. Hence what is likely to be new and beneficial to the internist is first placed here. No doubt this will give so much information that a much better assessment of this spectrum will improve the diagnosis and the communication to alleviate the anxieties even if there is no possibility of completely eliminating the hardships in all cases.

The sections Diabetic Peripheral Neuropathy with Clinical and Laboratory Measurements, Small Fiber and Painful Neuropathy, Motor Neuropathy, and Diabetic Hand Syndrome followed by Electrophysiology in Diabetic Neuropathy will bring the internist to a more familiar ground systematizing the logic-based understanding. These chapters like the earlier sections are closely connected and well separated for the clarity of understanding.

The next section, Therapeutics of Diabetic Neuropathies, once again will bring enhancement and precision for the ideas of how to reduce the patient burden of the neuropathy itself and postpone or prevent altogether the disastrous consequences arising there from. Treatment of Painful Neuropathy essentially discusses the oral medications and other physical methods of treating this depressing condition with as great a success as possible. What is particularly interesting in this section is the chapter on Insulin which plays a great role in the preservation of integrity of function and structure of the diabetic nerves. This information surely brings home the judicious, early use of this wonderful and purely anabolic hormone to great benefit of people suffering from diabetes and its complications.

The chapter on Treatment of Cardiovascular Autonomic Dysfunction is purposely separated from the discussions of its pathophysiology so that all aspects of therapeutics hang together. It may be mentioned that one cannot do much about causal cure of Cardiovascular Autonomic Dysfunction, but much can be achieved by mitigating the high frequency of cardiovascular deaths in diabetes, by reducing the consequences of the same.

Every bit of information provided in this volume is aimed at improving the communication from the doctor to the patient about what is the issue, its cause, effects on the body and life, the investigation—necessary and unnecessary, the treatment and its potential for cure, and limitations thereof. The author hopes that this aspect is kept in mind while going through the book.

Let us move on to the book.

© Springer Nature Singapore Pte Ltd. 2020

S. KelkarDiabetic Neuropathy and Clinical Practicehttps://doi.org/10.1007/978-981-15-2417-2_2

2. Functional Anatomy of the Cranial, Peripheral, and Autonomic Nerves

Sanjeev Kelkar¹  

(1)

Independent Health Researcher, Pune, Maharashtra, India

Sanjeev Kelkar

2.1 Introduction

System entails classification. In science information is consolidated to make it understandable and easier to refer to. One of the main instruments used for that is classification. In this volume a formal classification is partially set aside and presented as descriptive functional anatomy for many reasons. The diabetic neuropathy is essentially quite varied as it relates to many types of nerves, all in the same human body. The target organs, the functions regulated by each type, the physical, biochemical, and electrophysiological characteristics are different for each set. Within each set there are at least two divisions. The development of abnormalities in each set and different types of many such sets also affect a single organ system or participate in affecting other, different systems with an overlap. This cannot be viewed in isolation from each other and in the context and perspective of varied pathophysiological changes it brings about in the body.

In addition, the changes in one or all subgroups in one set can and do occur in temporally separated sequences. In most cases not just one set but several sets of neural networks are present simultaneously, with varying degrees of abnormalities, appearing at various times and affecting each other or working in concert with each other, the effects of which are composite. In view of this the author considers that a formal and somewhat rigid system of classification of diabetic neuropathy would be more an academic and conventional way of starting a monograph on this subject, of little practical significance. Instead a descriptive functional anatomical approach would be more helpful in understanding the neuropathic symptom/signs/effects, and pathologies emanating from it.

The three main divisions are the Cranial Neuropathies, the Somatic Neuropathies, and the Autonomic Neuropathies. In cranial neuropathies dominant segments which subserve autonomic functions along with the other sensory motor function are also present. The noncranial Somatosensory and Somatomotor neuropathies subserve the rest of the body. This system also offers the delicate autonomic nerves (see later) an anatomical support pathway till these reach their target organ or nearby it.

2.2 Cranial Nerves

2.2.1 General Features

Wide variations on incidence/prevalence are reported. There is little universally applicable hard data about prevalence, or gender ratios. It is generally agreed that some of the palsies or neural afflictions are commoner in diabetes or at times highly specific to it. Near complete recovery over few days to few months is a definitive characteristic, but recurrence is frequent. In somatic nerves during axonal regeneration after injury or praxis or disruption of axons, aberrant regeneration is common. Aberrant regeneration of cranial nerve fibers is uncommon, except in case of Bell’s palsy, considered more frequent to occur in diabetes (discussed later).

Laboratory findings, all cranial imaging, and CSF are mostly normal. Nerve conduction velocity studies however do offer some clues discussed later. Hence it is important to make an astute diagnosis of cranial neuropathies in diabetes and avoid unnecessary, essentially fruitless and expensive investigations. This will be repeated elsewhere also in the context of other neuropathies. Treatment consists of good diabetes control, pain relief, stopping smoking, vasodilators, omega fatty acids, anticonvulsants, or antidepressants, antioxidants.

One EPS finding in the brain stem detectable is the interrupted R1 and R2 reflex arcs in the pontine region in brain stem strokes which are far more frequent than in persons without diabetes. Evoked potentials from the scalp have also been recorded. Visual and auditory evoked potentials have also been recorded but are found to be normal. Some abnormalities may be detectable in long duration of diabetes but mostly recordings are normal.

2.2.2 Afflictions of Optic Tract

It is afflicted by certain autoimmune abnormalities not necessarily in diabetes which will be discussed in the section on autoimmunity in Pathogenesis of Diabetic Peripheral Neuropathies. The garden variety of diabetic retinopathy does have much to do with neuropathic abnormalities since these appear together too often.

2.2.3 Oculomotor Nerves III, IV, and VI in Diabetes

The symptoms of oculomotor nerve afflictions are acute ipsilateral head ache which is refractory to analgesics and diplopia that occurs on account of the oculomotor nerve lesions giving rise to muscle palsies. Ptosis is caused by total ophthalmoplegia or selective damage to the orbicularis oculi muscle and is unilateral, unlike myasthenia gravis where it is bilateral. In both diabetic and nondiabetic population, the VIth nerve is often affected leading to reduced unilateral lateral eye ball movement, whereas the IVth nerve causing medial movement of the eye ball probably is less common.

2.2.4 Pupillary Abnormalities

These are a part of the autonomic nerve supply to the pupillomotor muscle component. The ciliac ganglion is close to the pupillary muscle, characteristics of parasympathetic nerve supply. Ipsilateral pupil is smaller; it is a tonic small-sized pupil with reduced light reflex.

A self-limiting often detected abnormality of eye movements occurs in small embolic/ischemic lesion in the medial lemniscus in the midbrain pontine area with characteristic abducting eye nystagmus, not necessarily a diabetic abnormality.

2.2.5 Facial Neuropathy

Bell’s is a complete paralysis reportedly more common in diabetes, with clinical unilateral weakness on the face, both upper and lower. In facial palsies not involving the nucleus but on account of an upper pyramidal lesion, the upper face remains mobile, an important point of differentiation. Sensory symptoms in ear, pain and hyperacusis, are present much less often. There is often a lagophthalmos which may result in exposure keratopathy and dry cornea. Gustatory disturbances are variable. The facial nerve recovery more often results in aberrant regeneration of the axons which may innervate different axonal sheaths to give rise to unilateral sweating of face due to its stimulation while eating.

2.2.6 Treatment and Prognosis of Facial Neuropathy

It consists of control of diabetes. Steroids do not help but merely destabilize diabetes control. Dry cornea should be treated with appropriate lubrication; night eye taping is advisable to prevent injuries during sleep. In severe cases a marginal tarsorrhaphy is undertaken till recovery, to prevent dryness as well as injuries. Assumed to be due to Herpes like nuclear affliction, it is also treated with anti-retroviral drugs. Prognosis is proportional to the initial deficit; recovery is nearly complete in 80–90% cases although some residual damage may be seen.

2.2.7 Tenth Cranial Nerve Vagus

A large nerve trunk is populated with large numbers of parasympathetic fibers which has widespread effects on the body as a whole and will be discussed at many places in this monograph.

2.3 Diabetic Peripheral and Autonomic Neuropathies

2.3.1 Diabetic Sensory Neuropathies

The sensory nerves have nerve fibers of varying sizes each of which carry out specific sensory function/s in all parts of the body except those served by the cranial nerves for somatic sensations. The most prevalent is the distal symmetric sensory polyneuropathy involving lower limbs. Within it, the spectrum consists of distal but asymmetric sensory polyneuropathy to start with, which may or may not become fully symmetric. The sequence in which different fibers may get affected varies temporally. The smallest unmyelinated C or thinly myelinated A delta fibers are now known to precede the abnormalities in larger and thicker fibers. These sensory neuropathies are also not necessarily the first to appear as compared to the diabetic (somatic) motor neuropathies which may as well precede these or develop with these. The symptom spectrum thus is extremely wide and difficult to group into any one type.

2.3.2 Diabetic Somatic Motor Neuropathies

These are common, may precede the sensory neuropathies or coexist with them. The maximum pathological effects are seen in diabetic foot where deformities are caused and alter the dynamics of walking greatly leading to diabetic ulcers, deep spreading infections and often fatality. These abnormalities also affect large muscle groups, sometimes symmetrically and sometimes asymmetrically, from various known or unknown etiologies with variable prognosis and management. All of these will be discussed in the separate chapter on Motor Neuropathy and Diabetic Hand Syndrome in this volume.

2.3.3 Diabetic Autonomic Neuropathies

These fall in the third major group which is paid much less attention to, in clinical practice, are widely prevalent as will be discussed throughout this volume and often have unseen or undiagnosed serious consequences. These neuropathies also do not necessarily occur separately without the others described above, rather with them. Anatomically and functionally the two major divisions are the Sympathetic and the Parasympathetic Nervous Systems under direct governance of hypothalamus most of the times, with strong cerebral influence intermittently. These two systems are partially antagonistic to each other thereby regulate all the autonomic functions in a balanced manner. Generally one of the two systems will degenerate more than the other and will dominate the symptom complex arising there from in diabetes. Hence a proper diagnosis of which one is dominantly affected and how it relates to the symptoms and what therapeutics should be applied must be clearly worked out.

Both these systems innervate all the organs, the functions of which are generally unnoticed, until the cerebral cortex intervenes. The principle organ systems discussed in this volume are the cardiovascular, gastrointestinal, genitourinary, and the sudomotor (sweating) systems. Each of these has profound effects on the quality of life and prognosis in a patient with diabetes.

In addition to above, the type of nerve fibers these two systems consist of are the thin unmyelinated small nerve fibers which are also present in the somatic sensory nerves. As a result, sensations like pain are shared by these two.

Hence, considering these factors it is probably easier to group the diabetic neuropathies separately but manage them together rather than worrying about classifying them with all the structural and functional overlaps discussed above.

2.4 Functional Anatomy of Diabetic Somatic Peripheral Neuropathy

2.4.1 Diabetic Somatic Sensory Peripheral Neuropathy

It has different kinds of peripheral cutaneous receptors to detect various sensations. From the impulse generated at the receptor level, mostly skin or mucous membranes in limited areas or in muscles themselves, it is carried by sensory nerves to the spinal cord and from there to different parts of brain stem and cerebral cortex. These fibers are called the afferent fibers. These action impulses are carried back to the motor organs through the motor or efferent fibers mainly through the anterior horn cells of the spinal cord. This sensory motor arc is governed by both reflex and conscious mechanisms. The differences arise because of the physical characters of the receptors, sensory nerves, their ganglionic connections, and projections.

2.4.2 Classification, Anatomy, and Functions of Sensory Receptors

1.

Mechanoreceptors carry superficial skin tactile sensibilities from epidermis and dermis. These have free nerve endings as well as Spray endings, Ruffini’s endings and expanded tip endings like Merkel’s discs with other variants.

2.

Deep tissue sensibilities also have free nerve endings, expanded tip endings, spray endings, and Ruffini’s endings. The fibers with expanded tip with encapsulations are the Meissner’s corpuscles, Krause’s corpuscles, and Pacinian corpuscles with some variants.

3.

Hair end-organs are supplied with a pilo-erector muscle stimulated by emotions or application of chemicals to a skin area.

4.

Muscle spindles and Golgi tendon receptors are essentially sensory and will be described later in motor neuropathy.

5.

Thermoreceptors for Cold, Cold pain, Warm, and Hot pain.

6.

Nociceptors for pain, free nerve endings will be discussed under the section of small fiber neuropathy.

7.

Two-point discrimination is a test that is carried out by touching two nearby points on skin by an opened-up clip. It is a mixed sensation of very light touch and sight pressure. This sensation is most acute in fingertips and tips that are extremely sensitive areas of the body and can be within a couple of millimeters, whereas on dorsal back it may get detected 5 or even 10 cm apart.

8.

The importance of this sensation lies in fact that many parietal strokes may cause a loss of it or that of proprioception. It is also said that the closer the area of two points, the higher is the mobility of it. This element in general has not been investigated for any potential benefit for diagnosis or treatment.

2.5 Classification of Nerve Fibers: General

In the general classification, the fibers are divided into types A and C. C fibers correspond to the fibers which carry sensations of cold, cold pain, warmth and hot pain, and other pain sensations. Type C fibers are the small unmyelinated nerve fibers that conduct impulses at low velocities. The C fibers constitute more than one half of the sensory fibers as well as all the postganglionic autonomic fibers in most peripheral nerves.

Type A fibers are the typical large and medium-sized myelinated fibers of spinal nerves. The type A fibers are further subdivided into alpha, beta, and delta fibers and g fibers (discussed later). The different nerve fiber types are given in Fig. 2.1. Type A alpha are motor and carry the sensations of the touch, vibration, and position sense as well.

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Fig. 2.1

Peripheral and autonomic nerve fiber morphology. (Courtesy: Diabetic Foot Society of India from National Guidelines for Diabetic Foot Management 2nd edition 2017)

A delta and C fibers carry the sensation of pain and thermal stimuli. A delta fibers are also important since these with the autonomic fibers, both sympathetic and parasympathetic, are responsible for the regulation or modulation of organs with smooth muscle fibers like heart, gastrointestinal, and genitourinary tract and sweating, a vital function for thermoregulation.

The motor nerve fibers are the thickest. The axonal diameter is larger and the myelin sheaths are also thicker than others. The velocities of these fibers are as high as 120 m/s. Conversely, the smallest fibers which are unmyelinated with much smaller axonal diameter transmit impulses as slowly as 0.5 m/s, requiring about 2 s traveling from the big toe to the spinal cord. The velocities are thus proportional to both the diameter and the myelination.

The uniform diameter myelin sheaths constrict at many places called the nodes of Ranvier. The sensory or the motor impulses carried by these fibers have a Saltatory conduction. It jumps from one Ranvier node to the next which is why these impulses travel so fast. This mechanism is not available to C fibers hence their velocities being purely axonal are slower. The anatomical pathways and significance of each function and its neural distribution will be discussed later.

Thus, the more critical sensory signals, precise localization on the skin, minute gradations of intensity, or rapid changes in sensory signal intensity are all transmitted in more rapidly conducting types of sensory nerve fibers.

2.5.1 Alternative Classification Used by Neurophysiologists

Much refined techniques for action potential recordings separate the type A alpha fibers as A alpha and Ag fibers. Therefore, the following classification is frequently used by sensory physiologists:

Group I A alpha fibers arise from the annulospiral endings of muscle spindles embedded in the contractile muscle itself. It has an average diameter of 17 μm. These are type A fibers in the general classification carrying other sensations as well.

Group I beta fibers arise from the Golgi tendon organs with an average of 16 μm diameter; these also are like type A alpha fibers from the general classification.

Group II fibers arise from most discrete cutaneous tactile receptors as well as from the flower-spray endings of the muscle spindles. These average about 8 μm in diameter; these are beta and g-type A fibers in the general classification.

Group III fibers carrying temperature, crude touch, and pricking pain sensations average about 3 μm in diameter; these are the A delta fibers in the general classification.

Group IV unmyelinated fibers carrying pain, itch, temperature, and crude touch sensations have 0.5–2 μm diameter; (these are type C fibers in the general classification).

2.6 General Principles and Sensory Physiology

Intense stimulation of any sensory receptor leads to the continual reduction in the frequencies and magnitude of large action potentials once generated within it initially. The receptor thereby becomes sensitive even to weak stimulations without reaching the maximum action potential firing rate till the stimulation becomes extremely intensive. That facilitates the receptor recognition and response from weak to intense stimuli.

The Pacinian corpuscle is a viscous and elastic structure which can instantly transmit any distorting force to the sensory fiber and recovers itself in just a few milliseconds to be able to generate another response as it has elicited before in the nerve fiber.

2.6.1 Adaptation, Accommodation, and Inactivation of the Stimulus and Impulse

In case of continuous significant stimulation, the initial response also withers away in a few milliseconds. This leads to adaptation to the continued sensory stimuli which in its turn do not bombard the central system unnecessarily. Otherwise there will be chaos. This is quick adaptation. The second adaptive mechanism is much slower. It occurs in the nerve fiber itself. Even if the central core fiber remains distorted, the tip of the nerve fiber slowly accommodates itself and inactivates response by the tip of the nerve fiber itself, gradually becomes accommodated to the stimulus. This probably results from progressive inactivation of the sodium channels stopping the sodium current.

2.6.2 Nerve Fibers, Transmission of Different Signals, and Their Physiologic Significance

Some signals must be rapidly transmitted due to fast changing body situation as in running. Unless the instantaneous position of the legs is not transmitted back and the motor order comes back equally fast, such activity will become unbalanced or uncoordinated. The sensory inputs in this example will be the pressure and position sense. These sensations are typically transmitted by the thickly myelinated sensorimotor nerve fibers with a velocity of 120 m/s.

Prolonged, aching pain sensations need not be transmitted fast. These sensations are thus transmitted by slowly conducting fibers. It will take even longer to reach the central system. The relevance of this will be clear in testing methods for heat cold hat pain and cold pain sensations in a later chapter. Type C unmyelinated fibers transmit impulses at velocities from a fraction of a meter up to 2 m/s. Type A delta thinly myelinated fibers conduct impulses at velocities of only 5–30 m/s.

2.7 Sensory Perception of Touch, Pressure, and Vibration and the Nerve Ending Distribution

Touch, pressure, and vibration are frequently considered as separate sensations. But all these are detected by the same types of receptors. The touch sensation generally results from stimulation of tactile receptors in the epidermis and dermis. Pressure sensation generally results from deformation of deeper tissues. The vibration sensation results from rapidly repetitive sensory signals in which instantaneous vibrations are like alternating pressure sensation. It causes deformation and reformation in the split second variation. The receptors used therefore are of the same type for touch and pressure.

In different areas even if there is a single type of sensory nerve distribution, it can sense different sensations. For example, in cornea there are only fine nerve endings present for pain; yet these can sense the touch as well as pressure even with a light touch.

2.7.1 Meissner’s Corpuscle

This is highly sensitive to touch sensation. These corpuscles are present in the non-hairy parts of the skin and are particularly abundant in the fingertips, lips, and other areas of the skin where one’s ability to discern spatial locations of touch sensations is highly developed. It is actually an elongated encapsulated nerve ending of large A beta type of myelinated nerve fiber. Inside the capsulation are many branching terminal nerve filaments. Meissner’s corpuscles adapt in a fraction of a second (see above) after they are stimulated. It is considered as being particularly sensitive to movement of objects over the surface of the skin as well as to low frequency vibration. Low frequency vibrations from 2 up to 80 cycles per second, in contrast, stimulate other tactile receptors also.

2.7.2 Merkel’s Discs

The fingertips and other areas have numerous Meissner’s corpuscles. These areas also have large numbers of Merkel’s discs. These are expanded tipped tactile receptors from the same type A beta single nerve fiber. The hairy skin also contains moderate numbers of these expanded tip receptors but hardly any Meissner’s corpuscles. Merkel’s discs are quick adapters to a strong stimulus (as discussed above) and continue to send weaker signals with continued stimulation with slower adaption. This is how a steady-state signal is transmitted that allows the perception of continuous touch of objects against the skin.

A group of Merkel’s discs often protrudes underside of the epithelium of the skin to form domes on it. These domes are extremely sensitive receptors. With Meissner’s corpuscles, the domes play an extremely important role in localizing touch sensations to specific surface skin areas and determine the texture of what is felt.

2.7.3 Hair End Organ

The base of the hair entwined by a nerve fiber together is called hair end organ. Each nerve fiber ends in specific neuron of its own. This is also a readily adapting touch receptor and detects movement of an object over the skin or the initial contact with the body.

2.7.4 Ruffini’s End-Organs

These multibranched, encapsulated endings are located in the deeper layers of the skin and as well as the still deeper tissues. These endings adapt very slowly. It means that under a continuous state of deformation of tissues, it will continue to transmit the signals like heavy prolonged touch and pressure signals. These are also found in joint capsules and help to signal the degree of joint rotation.

2.7.5 The Pacinian Corpuscles

The corpuscle has a central nerve fiber extending through its core. Surrounding this are multiple concentric capsule layers so that compression anywhere on the outside of the corpuscle will elongate, indent, or otherwise deform the central fiber. The tip of the central fiber inside the capsule is unmyelinated, but the fiber become myelinated little before leaving the corpuscle to enter a peripheral sensory nerve. In capsule inclusion of myelin endows the corpuscle with Ranvier’s nodes thereby facilitating the fast conduction.

The Pacinian corpuscles lie immediately beneath the skin and deep in the fascial tissues of the body. They are stimulated only by rapid local compression of the tissues because they adapt in a few hundredths of a second. Therefore, they are particularly important for detecting tissue vibration or other rapid changes in the mechanical state of the tissues.

Pacinian corpuscles can detect signal vibrations from 30 to 800 cycles per second because they respond extremely rapidly to minute and rapid deformations of the tissues, and they also transmit their signals over type Ab nerve fibers, which can transmit as many as 1000 impulses per second.

The cruder types of signals, such as crude pressure, poorly localized touch, and especially tickle, are transmitted by way of much slower, quite small nerve fibers that require much less space in the nerve bundle than the faster myelinated ones. The signals sent by these localize into the spinal cord and lower brain stem, probably subserving mainly the sensation of tickle.

2.8 Transmission of Tactile Signals in Peripheral Nerve Fibers

Almost all sensory information from the somatic segments of the body enters the spinal cord through the dorsal roots of the spinal nerves. From there to the brain some signals are carried through the dorsal column–medial lemniscal system or the anterolateral system. These two systems then partially converge in the thalamus.

2.8.1 Anatomy and the Transmission of the Dorsal Column–Medial Lemniscal System

On entering the spinal cord through the spinal nerve dorsal roots, the large myelinated fibers from the specialized mechanoreceptors divide almost immediately to form a medial and a lateral branch. The medial branch runs in the dorsal column all the way to the brain.

The lateral branch enters the dorsal horn of the cord gray matter, then divides many times to provide terminals that synapse with local neurons in the intermediate and anterior portions of the cord gray matter. Majority fibers arising from these neurons enter the dorsal column to go to the cortex all the way. Many other fibers are short and terminate locally in the gray matter of the spinal cord to regulate the local spinal reflexes, and the remaining ones proceed up in the spino-cerebellar tract. That helps the coordination with the cerebellum and peripheral sensory outputs by connecting these two together.

After the nerve fibers synapse in medulla, these cross over to the opposite side in the medulla and continue upward through the brain stem to the thalamus by way of the medial lemniscus. Fibers from areas supplied by cranial nerves are added and from the thalamus these go to the postcentral gyrii of both the parietal lobe.

The dorsal column–medial lemniscal system is composed of large, myelinated nerve fibers that transmit signals to the brain at velocities of 30–110 m/s. It has a high degree of spatial orientation of the nerve fibers with respect to their origin. The sensory information that must be transmitted rapidly and with high degree of temporal and spatial accuracy is transmitted mainly in the dorsal column–medial lemniscal system. Thus, the more critical types of