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Published by: Pikachu on Sep 21, 2008
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Sagar Naik,
TENS (Transcutaneous Electrical Nerve Stimulation)
Sagar Naik,
 By definition, any stimulating device, which delivers electrical currents across the intact surface of the skin, is TENS. TENS is low-intensity, short impulses applied largely for pain relief.
TENS is the application of a pulsed rectangular wavecurrent via surface electrodes on the patient’s skin.Transcutaneous electrical nerve stimulation (TENS) is a simple, non-invasive analgesic technique that is used extensively in health-care settings byphysiotherapists, nurses, and mid-wife’s. TENS is mainly used for
 the symptomatic management of acute and non-malignant chronic pain
. However, TENS is also usedin
 palliative care to manage pain caused by metastatic bone disease and neoplasm
. Itis also claimed that TENS has
 antiemetic and tissue healing effects
although it is usedless often for these actions.Small battery operated machines in which circuits modify the battery’soutput in such a way that it will have a stimulatory effect often generate TENS. Manydifferent types of TENS apparatus are manufactured on the basis of followingparameters:
Pulse Shape
– Usually
Pulse Width
– Measured in microseconds (
s) and is often fixed at
 s or 200
. Other units can vary the pulse width from 50
s through to 300
– Can be
 as low as 2 Hz or as high as 600 Hz
. A frequency of 150 Hz iscommonly used.
– Can be varied from
0 to 60 milliamperes (mA)
.The wide range of variation in pulse width, frequency, and intensity givesgreat flexibility in terms of the treatments applied to patients with chronic painsyndromes.
To be effective it is necessary for TENS to be able to affect conducting afferent nerves.
It is thus appropriate to ensure that there is some cutaneous sensationand that this is sufficient to provide protection against the application of excessivecurrent.
Advantages of TENS: 
In medicine, TENS is the most frequently used
electrotherapy for producing pain relief 
Sagar Naik,
It is popular because
it is non-invasive, easy to administer and has few sideeffects or drug interactions
 As there is no potential for toxicity or overdose, patients can administer TENS themselves
and titrate the dosage of treatment as required.
TENS effect are rapid in onset for most patients so benefit can be achievedalmost immediately.
TENS is cheap when compared with long-term drug therapy.
Pain Transmission
The fibres of lateral spinothalamic tract origin from
 substantia gelatinosa of Rolando (SGR)
situated in the posterior gray column. The first order neuronsare in posterior nerve root ganglia.
 Axons from second order neurons mostly cross to the opposite side and  reach the lateral column of same segment.
Few fibres may ascend one or twosegments and then cross to the opposite side and ascend in the lateral column. Allthe fibres pass through medulla, pons, and midbrain towards thalamus along withthe fibres of anterior spinothalamic tract. The fibres of lateral spinothalamic tractfrom
 spinal leminiscus
along with the fibres of anterior spinothalamic tract at thelower part of medulla. Some of the fibres of lateral spinothalamic tract formcollaterals and reach the reticular formation of brain stem.
The fibres of lateral spinothalamic tract terminate in the
ventral  posterolateral nucleus of thalamus
. From here, third order neuron fibres relay tothe
 somesthetic area of cerebral cortex
The fibres of this tract carry impulses of pain and thermal sensations.
 The unilateral lesion or sectioning of the lateral spinothalamic tract causes loss of pain (
) and temperature (
) below the level of lesionin the opposite side. The bilateral section of this tract leads to loss of pain andtemperature sensations on both the sides below the level of lesion.
Pain Gate Theory: 
Afferent input is predominantly via the posterior root of the spinal cord and allafferent information must pass through synapses in the
 substantia gelatinosa
 nucleus proprius
of the posterior horn.
Sagar Naik,
 It is at this level that the pain gate first postulated by Melzack and Wall in 1965 operates. They proposed the existence of a gating mechanism at the spinal level  that could alter ascending transmissions of nociceptive input.
The mechanism by which the gate influences afferent transmission is based on the quantity of input between A
and C fibres to the dorsal horn of the spinal  cord.
The substantia gelatinosa consists of a group of cells located in the dorsal horn of the spinal cord.
The A
and C fibres project to, and synapse on, both the substantia gelatinosaand the first central
 transmission (T) cells
in the dorsal horn.
It was thought that the T cells, when sufficiently stimulated, activated an actionsystem that is responsible for response and perception.
The T cells are, in turn, excited by the A
and C fibres.
Melzack and Wall felt that
 the substantia gelatinosa modulated the transmission from peripheral (A
& C) fibres to central (T) cells by presynaptically inhibiting the fibres from stimulating the T cells
The gate is “closed” by high levels of activity in the A
Using the negative feedback system, the A
fibres exert presynaptic on the T  cells via facilitation of the substantia gelatinosa.
The gate is “opened” with high levels of activity from the C fibres, preventing the substantia gelatinosa from exerting its inhibition on the T cells.
This results in T cell excitation by either spatial or temporal summation.
The net result is the perception of pain.
If nociceptive information is allowed through the gate then this traffic willcontinue up the lateral spinothalamic tract of the spinal cord to the thalamus, andfrom here to the cerebral cortex.
As this stimulus passes through the brainstem it may cause an interactionbetween the
 periaqueductal area of grey matter (PAG)
and the
 raphe nucleus
inthe midbrain.
These nuclei form part of the descending pain suppression system and theirdescending neurons can release an endogenous opiate substance into thesubstantia gelatinosa at the spinal cord level.
The chemical nature of this endogenous opiate, which may be
, is such as
 to cause inhibition of transmission in the nociceptive circuit synapses
This is achieved y blocking the release of the chemical transmitter (substance P) in the pain circuit.

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