BLOCK B - PAIN

8/7/2019 BLOCK B - PAIN

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Saint Louis University

Baguio City

Pain, Numbness and Other Sensory Modalities

Group 6

Andres, Xyrose

Bangloy, Michael

Batino, Laurence Kristoffer

Hullon, Timothy James

Artienda, Aubrey

Bolislis, Mellicent

Chan, Jacqeline

Reginaldo, VenusSicat, Sheena Marie


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Pain Receptors

Meissners Corpuscle

Dendrites enclosed in CT in dermal papillae of hairless skin

Discriminative touch & vibration-- rapidly adapting

Generate impulses mainly at onset of a touch

Hair Root Plexus

y Free nerve endings found around follicles, detects movement of hair

Merkels Disc

Flattened dendrites touching cells of stratum basale

Used in discriminative touch (25% of receptors in hands)


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y Ruffinis Corpuscle

Found deep in dermis of skin

Detect heavy touch, continuous touch, & pressure

Pacinian Corpuscle

o Onion-like connective tissue capsule enclosing a dendrite

o Found in subcutaneous tissues & certain viscera

o Sensations of pressure or high-frequency vibration

Spinal Trigeminal Tract

The spinal trigeminal tract involves Cranial Nerves V, VII, IX, X as primary neuron for the

tract. The cell body of the receptive fiber is considered a psudounipolar type. These cell bodies

are localized in a ganglion, the trigeminal ganglion for CN V located in proximity to the pons; the

Geniculate ganglion for CN VII, and the Superior ganglion for CN IX and X located near the

medulla.

Cranial nerves V, VII, IX, and X serve the cutaneous receptors of the face, the oral cavity,

and the dorsum of the head except for the area served by the cervical nerves. In addition to

cutaneous structures, the trigeminal nerve also innervates deep tissues, including the

temporomandibular joint, the meninges, and the peridontium. The primary sensory fibers of


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these nerves have their cell bodies in the trigeminal ganglion, the geniculate ganglion of cranial

nerve VII, and the superior ganglia of cranial nerves IX and X.

The central processes of small and large trigeminal ganglion cells are part of the

trigeminal sensory root, which attaches to the pons. The bifurcating small-diameter axons

course posteromedially into the pontinetegmentum, sending an ascending branch to the

principal sensory nucleus. The descending branch of these fibers joins with numerous other

unbranched small-diameter fibers to form a prominent fiber bundle in the posterolateral

brainstem, the spinal trigeminal tract. Through the caudal pons and the rostral medulla, this

tract is internal to the restiform body. However, in the lower medulla caudal to the obex, it

forms a superficial landmark lateral to the cuneate tubercle, known as the trigeminal tubercle

(tuberculumcinereum). This landmark served as a useful reference point for surgeons, who

discovered that sectioning the spinal tract of the trigeminal nerve at this level (tractotomy)

provides substantial relief from facial pain on the operated side.

In addition to the large contributions from the trigeminal nerve, small numbers of fibers

conveying general somatic afferent information from the ear on cranial nerves VII, IX, and X

also enter the spinal trigeminal tract and terminate in the spinal nucleus. The primary afferent

neurons associated with cranial nerves VII, IX, and X have cell bodies in their respective ganglia,

enter the medulla, and take a position adjacent to those of the mandibular division in the spinal

trigeminal tract.

The peripheral distribution of the branches of the trigeminal nerve (V1, V2, and V3)

delineates the facial dermatomes. Unlike the spinal segmental dermatomes, which partially

overlap, the boundaries between adjacent facial dermatomes are sharply defined. This

segregation of trigeminal branches is maintained by their central processes in the spinal

trigeminal tract. An unfortunate clinical condition that illustrates the divisional pattern of the

trigeminal system is herpes zoster, or shingles. Patients with shingles have a characteristic rash

that outlines the affected dermatome or spinal cord segment; the ophthalmic or maxillary

division is usually affected, and the rash is unilateral

Injury to trigeminal nerve fibers produces a paresthesia restricted to specific regions of the

face. The pain oftic douloureux (trigeminal neuralgia) produces episodic "paroxysmal" pain

usually restricted to the peripheral distribution of the maxillary or mandibular division on oneside.

The spinal trigeminal nucleus, located medial to the spinal tract, is the site of termination

for fibers of the spinal trigeminal tract. On the basis of cytoarchitecture, this nucleus is divided

into a pars caudalis, a pars interpolaris, and a pars oralis. The caudal subnucleus(pars

caudalis)extends from C2 or C3 rostrally to the level of the obex. This part of the spinal nucleus


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shares many cytoarchitectural similarities with the posterior horn. For this reason, it has been

termed the medullary posterior horn and has been divided into layers that correspond to Rexed

spinal cord laminae. The substantiagelatinosa is largely continuous with lamina II of the spinal

cord, and the magnocellularregion is continuous with laminae III and IV. The pars caudalis and

the posterior horn also show homology in the distribution of neurotransmitters.F

or example,substance P and calcitonin gene-related peptide (CGRP) are localized in nociceptive C fibers that

terminate in both of these areas.

The pars caudalis plays an important role in the transmission of nondiscriminative touch,

nociceptive, and thermal sensations. This role is reflected by the fact that central processes of

A and C fibers terminate somatotopically in this subnucleus. In addition to the somatotopy

within the pars caudalis, an onionskin pattern of facial pain representation is oriented along the

rostrocaudal axis of the subnucleus. The nociceptive fibers that innervate circumoral and

intraoral zones (teeth, gums, and lips) terminate rostrally, close to the obex at the interface of

the pars interpolaris with the pars caudalis. Fibers innervating progressively more caudal and

lateral regions of the face terminate in progressively more caudal regions of the spinal

trigeminal nucleus, pars caudalis. Many second-order neurons in the subnucleuscaudalis

receive convergent input from small-diameter fibers that innervate cutaneous and deep tissues

(jaw muscles and the temporomandibular joint). Convergence of information from different

regions is thought to contribute to the referral of pain and may be involved in the manifestation

of less well-understood clinical problems such as temporomandibular disorders and atypical

facial pain.

The interpolarsubnucleus(pars interpolaris) is located between the level of the obex and the

rostral pole of the hypoglossal (XII) nucleus. The most rostral subdivision is the oral

subnucleus(pars oralis), which extends from the level of the rostral pole of the hypoglossal

nucleus to the caudal end of the trigeminal motor nucleus. Some neurons in the pars

interpolaris and the pars oralis contribute to ascending somatosensory pathways, whereas

others project to the cerebellum. In addition to projection neurons, the spinal trigeminal

nucleus, particularly the subnucleusoralis, contains many local circuit neurons involved in

brainstem reflexes.

A particularly prominent target of some of these collaterals is the parabrachial nuclear

complex. Located adjacent to the superior cerebellar peduncle (brachium conjunctivum), the

parabrachial nuclei serve as an important relay for spinal and trigeminal pain fibers, as well as

for ascending axons carrying visceral sensory information. In addition to regulating oral and

facial reflexes, projections from the reticular formation terminate in the dorsal thalamus in the


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intralaminar nuclei and the medial region of the posterior nucleus. The intralaminar nuclei

project widely to the striatum and cortex, especially the frontal and somatosensory cortex. The

medial region of the posterior nucleus projects to the head representation in the secondary

somatosensory cortex.

Anterolateral System

The ALS is a composite bundle that includes spinothalamic, spinomesencephalic, spinoreticular,

spinobulbar, and spinohypothalamic fibers.Spinothalamic fibers project directly from the spinal

cord to the ventral posterolateral (VPL) nucleus, the posterior nuclear group, and intralaminar

nuclei (central lateral and centromedian-parafascicularis nuclei) of the thalamus. Collaterals to

the reticular formation arise from some of these axons. Spinomesencephalic axons project to

the periaqueductal gray (PAG) and to the tectum; the latter are spinotectal fibers. Although

spinoreticular fibers project to the reticular formation of the medulla, pons, and midbrain,

collaterals may ascend to other targets such as the thalamus. Projections of less relevance tothe somatosensory system, such as spino-olivary fibers, are grouped under the category of

spinobulbar fibers.Spinohypothalamic fibers terminate in hypothalamic areas and nuclei,

including some that give rise to hypothalamospinal axons.

Spinothalamic tract

Fibers classically described as composing the lateral spinothalamic tract were considered to

carry onlypain and thermal information, whereas the anterior spinothalamic tract was

concerned onlywith nondiscriminative touch. Current thinking holds that all parts of the ALS

carry all modalities (pain, temperature, and touch) but that there are direct and indirect routes.(ALS) transmits nociceptive ,thermal, and non-discriminatory (crude) touch information to

higher brain centers, generally by a sequence of three neurons and interneurons . The neuron

sequence consists of:

1A first order neuron (pseudounipolar neuron) whose cell body is located in a dorsal

root ganglion. It transmits sensoryinformation from peripheral structures to the dorsal

(posterior) horn of the spinal cord.

2 A second order neuron whose cell body is located within the dorsal horn of the spinal

cord, and whose axon usuallydecussates and ascends:

in the direct pathway of the ALS (spinothalamictract) to synapse in the

contralateral thalamus, andsending some collaterals to the reticular formation;

in the indirect pathway of the ALS (spinoreticular tract) to synapse in the reticular

formation, and sending some collaterals to the thalamus; or as spinomesencephalic,

spinotectal, or spinohypothalamicfibers to synapse in several brainstem nuclei.

3 A third order neuron whose cell body is located in thethalamus, and whose axon


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ascends ipsilaterally to terminatein the somatosensory cortex.In some cases, the first

order neuron may synapse with aninterneuronthat resides entirely within the dorsal

horn, andwhose axon synapses with the second order neuron.

SPINOTHALAMIC FIBERS

project directly from the spinal cord to the

ventral posterolateral (VPL) nucleus,

the posterior nuclear group,

andintralaminar nuclei (central lateral and centromedian-parafascicularis nuclei)

of the thalamus.

Collaterals to the reticular formation arise from some of these axons

LATERAL SPINOTHALAMIC

- Carries pain and temperature

Primary fibers

- ascend or descend 1-2 spinal cord segments before synapsing with secondary fibers.

Secondary axons

- - decussate through anterior gray and white commissures.

- - make up the lateral spinothalamic tract traveling in the lateral column of the spinal

cord.

Secondary fibers

> joined in brainstem by fibers of the trigeminothalamic tract:

(Pain and temperature from face and teeth.)

> collaterals project to reticular formation:

(Stimulate wakefulness and consciousness)

>project to ventral posterolateral (VPL) nucleus of thalamus.

>synapse with tertiary fibers in VPL.

Tertiary fibers (corticopetal fibers)

synapse in postcentralgyrus:

Somatic sensory areas 3, 1, 2

form part of internl capsule.


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ANTERIOR SPINOTHALAMIC FIBERS

- Carries light touch (crude touch), pressure, tickle, itch

Primary neurons

may ascend 8-10 spinal cord segments before synapsing with secondary

neurons.

Secondary fibers

decussate in anterior gray or white commissures.

ascend to synapse with tertiary fibers in VPL nucleus of thalamus.

Tertiary fibers

ascend through internal capsule to primary sensory cortex.

The spinomesencephalic fibers terminate in the periaqueductal gray matter and the midbrain

raphe nuclei, both of

which are believed to give rise to fibers that modulate nociceptive transmission and are thus

collectively referred toas the descending pain-inhibiting system. Furthermore, some

spinomesencephalic fibers terminate in the parabrachial nucleus, which sends fibers to theamygdalaa component of the limbic system associated with the processing of emotions. Via

their connections to the limbic system, the spinomesencephalic fibers play a role in the

emotional component of pain.


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Spinoreticular tract

Pain modulation

Spinoreticulothalamic Tract

Input from Laminae VII and VIII

Mostly from C-fibers

A bilateral tract

From reticular formation to thalamus

Behavioral and emotional aspects of pain

Reticularformationof melulla

Dorsalhorn

DRG

Receptor

Reticularformationof pons

cortex

AssociationcortexMidline

Dorsalthalamus

SI


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SPINOHYPOTHALAMIC TRACT

The spinohypothalamic fibers ascend to the hypothalamus where they synapse with neurons

that give riseto the hypothalamospinal tract. This pathway is associated with the autonomic and

reflex responses (i.e., endocrine and cardiovascular) to nociception

Allows autonomic adjustment for effective response to injury and intense pain.


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PAIN PERCEPTION

Pain is not only a sensation, it also includes perception.

Generalizations:

y Vascular compromise of middle or anterior cerebral arteries produces a loss of

sensibility over contralateral regions of the body.

o Discriminative

o Nondiscriminative

o Thermal

o Nociceptive

Over time, appreciation of sensation may return (partially/totally).

Order of return of sensations:

o Pain sensations

o Nondiscriminativetactile and thermal sensations

o Discriminative tactile, vibratory, and proprioceptive sensations

y If occlusion of the middle cerebral artery affects most of the postcentralgyrus, sensation

begins returning first on the face and oral regions, then on the neck and trunk, and


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finally on the extremities and the distal parts of the limbs. This return of function

indicates that other cortical areas may partially take over the appreciation of

somatosensory stimuli.

y Pain is perceived at subcortical levels.

- Some forms of somatosensory stimuli can be perceived at subcortical levels.- Electrical stimulation of the primary somatosensory cortex does not result in a

complaint of pain, whereas thalamic stimulation may elicit paresthesia and

sensations of dull pain and pressure.

- Painful stimuli can be recognized and produce suffering without the presence of

primary and secondary cortices,

y Damage to specific cortical regions eliminates the ability to precisely localize pain,

suggesting that such localization is a function of the somatosensory cortex and its

lemniscal inputs.

y Pain perception and its affective component, suffering, are served by separate brain

regions.

o Neospinothalamic pathway to the primary somatosensory cortex is involved in

the localization of painful stimuli

o Paleospinothalamic pathways that access the hypothalamus and limbic system

via the reticular formation and PAG are involved in the suffering component of

the pain experience

This dissociation can be regulated pharmacologically, as some drugs eliminate suffering

without affecting pain perception.Ex. Patients taking benzodiazepines report that the pain is still present but that its

unpleasant nature is diminished.

Pain Perception in the Somatosensory Thalamus

Modern Procedures that provided tremendous insights to the role of the thalamus in pain

perception:

o Stereotaxic surgery for treatment of chronic pain or movement disorders

o Single-neuron recording and microstimulationhave demonstrated that:

y Neurons within the human Ventral Posteromedial (VPM) / Ventral Posterolateral

(VPL), collectively called ventrocaudal [Vc] nuclei by some neurosurgeons) are

involved with processing of tactile, thermal, and pain signals

y Microstimulation of Vc evokes:

o sensations of touch, warmth, coolness, tingling, burning, or pain localized

to specific body areas.


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o suggesting that these nuclei play a role in pain localization regardless of

its origin, that is, cutaneous or visceral

y A population of thalamic cells activated by innocuous tactile stimuli are mixed with

other neurons activated by mechanical and thermal stimuli in the painful range.

Generalizations:The human VPL/VPM (Vc) can undergo changes following deafferentation, which can occur

directly as a result of:

y damage to ascending pathways

y secondarily as a result of removing sensory inputs (e.g., amputation).

These changes may contribute to chronic pain or phantom limb pain.

Changes involve:

y theupregulation and downregulation of neurochemicals within the nucleus

y changes in local circuitry

y changes in the functional state of Vc neurons

Ex. in patients who have undergone leg amputation, single-neuron recordings reveal that the

thalamic region formerly receiving input from the lower leg and foot responded to stimulation

of the stump (thigh). These patients also described the presence of nonpainful tingling over the

stump in response to microstimulation in this same area.

Two therapies for chronic or neuropathic pain:

1. Thalamic lesioning

- Lesions have been centered in either the lateral thalamus or the medial thalamus.

a.) Lateral thalamic lesions involve the somatosensory thalamus (VPL/VPM).

- produces transient relief for pain

- produce unwanted side effects including:

loss of cutaneous and position sense in the affected limb

impaired motor function

b.) Lesions in the medial thalamus involve the centromedian-parafascicular (CM-PF) complex as

well as the central lateral nucleus (CL) and the medial dorsal nucleus.

- produce transient relief from intractable pain but fail to produce loss of pain and thermal

sensations.

- do not produce the unwanted sensory loss seen with lateral thalamic lesions.

2. Deep brain electrical stimulation

- Stimulating electrodes centered in the somatosensory thalamus, the CM-PF complex, or theperiventricular gray (PVG)-PAG activateneurons within their vicinity and thus may contribute to

stimulus-induced analgesia.

- Cortical stimulation has also been shown to produce relief of chronic pain of neuropathic

origin.

*An evaluation of different brain regions that may contribute to the stimulus-induced analgesia

was carried out using PET.


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Following thalamic stimulation, increased regional cortical blood flow was noted in the rostral

insula, a region activated in studies of experimental pain, neuropathic pain, and warm and cool

innocuous stimuli, as well as in the anterior insular cortex. These results suggest that

stimulation of the somatosensory thalamus may activate a pain modulation circuit that involves

thalamocortical thermal pathways.

Centralor thalamic pain

- poorly understood sequela of natural or surgical lesions of structures involved in

somatic sensibility

- originally observed with thalamic lesions, but it can occur with lesions below the

level of the thalamus and from vascular lesions

- In central pain syndrome, the analgesia that initially results from the lesion is

replaced after a period of weeks, months, or years by:

y Paresthesia, An altered sensation often described as burning, tingling, or pin

prick

y

dysesthesia , sensations of numbness, tingling, burning, or pain felt below thelevel of the lesion that may or may not be characterized as pain

y Allodynia, pain resulting from a stimulus that does not normally evoke pain

y hyperalgesia, an increased response to a stimulus that is normally painful

y Patients often characterize central pain:

o burning, aching, pricking, or lacerating

o occurring in paroxysms that vary in intensity

o poorly localized

o last for years

o intractable to current analgesics

y Possible etiology:

This type of pain may represent a deafferentation phenomenon. This hypothesis is

supported by the time course and symptoms of central pain

o Changes may be:

sprouting of inappropriate connections of non-nociceptive or

nociceptive fibers

increased excitability of central pain neurons

removal of inhibitory influences on pain neurons.

y Treatment:

o Pharmacologic agents, such as antidepressants and antiepileptic drugs

o Transcutaneous electrical nerve stimulation (TENS) (electrical stimulation of

nerves through the skin), from electrical stimulation of the posterior columns,or from chronic deep brain stimulation

o Neuroablative surgical procedures that have been used in the treatment of

central pain include anterolateral cordotomy, trigeminal tractotomy,

thalamotomies, and cortical ablation.

- Unfortunately none of these procedures is successful in the long term.


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PAIN TRANSMISSION AND CONTROL

The relay of information from the spinal cord to the supraspinal centers is essential in

the higher-order processing of nociceptive sensory signals. Localization of putative

neurotransmitters and secondary messengers in the posterior horn includes peptides(calcitonin and substance P), glutamate and nitric oxide that may be involved in the process

underlying the central pharmacology of nocicceptive transmission.

Pain can be classified as acute or chronic, fast or slow, dull or sharp, or burning, or

aching.

The degree to which a person reacts to pain varies tremendously. Effective clinical

approaches include pharmacologic intervention and stimulation-produced analgesia.

Stimulation-produced analgesia

The capability of the brain itself to suppress input of pain signals to the nervous system

by activating a pain control system, called an analgesia system.

The analgesia system consists of:


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3 major components Location

periaqueductal gray and

periventricular areas of the

mesencephalon and upper pons

surround the aqueduct of Sylvius and

portions of the third and fourth ventricles

raphemagnus nucleus

nucleus

reticularisparagigantocellularis

lower pons and upper medulla

laterally in the medulla

pain inhibitory complex dorsal horns of the spinal cord

(dorsolateral columns)

In addition, central structures implicated in the descending control of nociceptive

transmission include also the somatosensory, frontal, and limbic cortices. Descending pathways

originating in these structures are activated by ascending afferent pain signals.

At this point, theanalgesia signals can block the pain before it is relayedto the brain.

Several transmitter substances are involved in the analgesia system; especially involved

are enkephalin and serotonin. Fibers originating in this area send signals to the dorsal horns of

the spinal cord to secrete serotonin at their endings.The serotonin causes local cord neurons to

secrete enkephalin as well. The enkephalin is believed to cause both presynaptic and

postsynaptic inhibition of incoming type C and type Ad pain fiberswhere they synapse in the

dorsal horns.

About a dozen such opiate-like substances have now been found at different points of

the nervous system; all are breakdown products of three large protein molecules:proopiomelanocortin,proenkephalin,and prodynorphin.

Location

met-enkephalin Brain stem and spinal cord


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The PVG of the hypothalamus communicates with the PAG of the midbrain via an

enkephalinergic pathway. Descending PAG fibers exert an excitatory influence on serotonergic

neurons in the medullary nucleus raphe magnus, both directly and through interneurons in the

meduulalry reticular formation. The PAG to NRM projection uses serotonin, neurotensisn,

somatostatin, and glutamate. Raphespinal neurons project, in turn, to the posterior horn and

pars caudalis of the trigeminal nucleus. These raphespinal serotonergic axons terminate on

enkephalinergic interneurons in the laminae II and III, which act presynaptically andpostsynaptically to suppress incoming activity in the pain fibers. In addition, the hypothamus

projects directly to the medullary and spinal cord posterior horns to act on incoming

nociceptive signals.

In stimulation-produced analgesia relies on electrical stimulation on CNS to induce

release of endogenous chemicals such as enkephalins. Endogenous opiates such as enkephalin

inhibit pain transmission. Stimulation of PVG, PAG, or the nucleus raphe maagnus results in the

release of enkephalin or monoamines producing analgesia.

As with the pharmacologic aspect, systemic administration of pharmacologic opiates like

morphine excites periventricular and periaqueductal neurons supplementing their natural

activity. This increase in activity suppresses neurons in the spinal and medullary posterior horns

transmitting pain. The direct delivery of opioids to the spinal cord (epidural anesthetic

techniques) also is used to produce analgesia for surgical procedures.

leuenkephalin

b-endorphin Both hypothalamus and pituitary gland

dynorphin Brain stem and spinal cord but in lower

quantities


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Several clinical procedures have been developed for suppressing pain by electrical

stimulation. Stimulating electrodes are placed on selected areas of the skin or, on occasion,

implanted over the spinal cord, supposedly to stimulate the posterior columns. Posterior

column stimulation activates large-diameter myelinated fibers. Antidromic activation of thesefibers discharge collaterals in the posterior horn stimulating enkephalinergic interneurons

inhibitng transmission of signal. It explains why such simple maneuvers as rubbing the skin near

painful areas is often effective in relieving pain. And it probably also explains why liniments are

often useful for pain relief. This mechanism and the simultaneous psychogenic excitation of the

central analgesia system are probably also the basis of pain relief by acupuncture.

Some Clinical Abnormalities of Pain Other Somatic Sensations

Hyperalgesia

A pain nervous pathway sometimes becomes excessively excitable; this gives rise to

hyperalgesia, which means hypersensitivity to pain.Possible causes of hyperalgesia are (1)

excessive sensitivity of the pain receptors themselves, which is called primary hyperalgesia, and

(2) facilitation of sensory transmission, which is called secondary hyperalgesia. An example of

primary hyperalgesia is the extreme sensitivity of sunburned skin, which results from

sensitization of the skin pain endings by local tissue products from the burnperhaps

histamine, perhaps prostaglandins, perhaps others. Secondary hyperalgesia frequently results

from lesions in the spinal cord or the thalamus. Several of these lesions are discussed in

subsequent sections.

Herpes Zoster (Shingles)

Occasionally herpesvirus infects a dorsal root ganglion. This causes severe pain in the

dermatomal segment subserved by the ganglion, thus eliciting a segmental type of pain thatcircles halfway around the body.The disease is called herpes zoster, or shingles, because of a

skin eruption that often ensues. The cause of the pain is presumably infection of the pain

neuronal cells in the dorsal root ganglion by the virus. In addition to causing pain, the virus is

carried by neuronal cytoplasmic flow outward through the neuronal peripheral axons to their

cutaneous origins. Here the virus causes a rash that vesiculates within a few days and then


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crusts over within another few days, all of this occurring within the dermatomal area served by

the infected dorsal root.

Tic Douloureux

Lancinating pain occasionally occurs in some people over one side of the face in the sensory

distribution area (or part of the area) of the fifth or ninth nerves; this phenomenon is called ticdouloureux(or trigeminal neuralgia or glossopharyngeal neuralgia). The pain feels like sudden

electrical shocks, and it may appear for only a few seconds at a time or may be almost

continuous.Often it is set off by exceedingly sensitive trigger areas on the surface of the face, in

the mouth, or inside the throatalmost always by a mechanoreceptive stimulus rather than a

pain stimulus. For instance, when the patient swallows a bolus of food, as the food touches a

tonsil, it might set off a severe lancinating pain in the mandibular portion of the fifth nerve. The

pain of tic douloureux can usually be blocked by surgically cutting the peripheral nerve from the

hypersensitive area. The sensory portion of the fifth nerve is often sectioned immediately

inside the cranium, where the motor and sensory roots of the fifth nerve separate from each

other, so that the motor portions, which are needed for many jaw movements, can be spared

while the sensory elements are destroyed. This operation leaves the side of the face anesthetic,

which in itself may be annoying. Furthermore, sometimes the operation is unsuccessful,

indicating that the lesion that causes the pain might be in the sensory nucleus in the brain stem

and not in the peripheral nerves.

Brown-Squard Syndrome

If the spinal cord is transected entirely, all sensations and motor functions distal to the segment

of transaction are blocked, but if the spinal cord is transected on only one side, the Brown-

Squard syndrome occurs. The effects of such transection can be predicted from a knowledge

of the cord fiber tracts shown in Figure 488. All motor functions are blocked on the side of the

transaction in all segments below the level of the transection. Yet only some of the modalitiesof sensation are lost on the transected side, and others are lost on the opposite side. The

sensations of pain, heat, and cold sensations served by the spinothalamic pathwayare lost

on the opposite side of the bodyin all dermatomes two to six segments below the level of the

transection. By contrast, the sensations that are transmitted only in the dorsal and dorsolateral

columnskinesthetic and position sensations, vibration sensation, discrete localization, and

two-point discriminationare lost on theside of the transection in all dermatomes below the

level of the transection.Discrete light touch is impaired on the side of the transection

because the principal pathway for the transmission of light touch, the dorsal column, is

transected. That is, the fibers in this column do not cross to the opposite side until they reach

the medulla of the brain. Crude touch, which is poorly localized, still persists because ofpartial transmission in the opposite spinothalamic tract.


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Numbness/ Paresthesia

Paresthesia is a sensation of tingling, pricking, or numbness of a person's skin with no apparent

long-term physical effect. It is more generally known as the feeling of "pins and needles" or of a

limb "falling asleep"

The name comes from the Greekpara ("beside", i.e., abnormal) and aisthesia ("sensation").

Symptoms

Abnormal sensations in the absence of stimuli

y Numb sensation

y Cold, warmth or burning sensation

y Prickling, tingling or pins and needles sensation

y Skin crawling sensationy Pruritus

Transient


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Paresthesias of the hands and feet are common, transient symptoms of the related conditions

of hyperventilation syndrome, often open mouth, and panic attacks.

Other common examples occur when sustained pressure has been applied over a nerve,

inhibiting/stimulating its function. Removing the pressure will typically result in gradual relief of

these paresthesias, often described as a "pins and needles" feeling.

Chronic

Chronic paresthesia indicates a problem with the functioning of neurons.

Chronic paresthesia indicates a problem with the functioning of nerve cells, or neurons, in the

central nervous system.

This malfunction, which is especially common in older individuals, is often the result of poor

circulation in the limbs, or may be caused by atherosclerosis. Without a proper supply of blood

and nutrients, nerve cells can no longer adequately send signals to the brain.

Irritation to the nerve can also come from inflammation to the surrounding tissue. Joint

conditions such as rheumatoid arthritis and carpal tunnel syndrome are common sources of

paresthesia.

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