Scientific Basis for
Ayurvedic Therapies
edited by
Brahmasree Lakshmi Chandra Mishra
10.3.3 Treatment
Because ama is
not involved, the treatment of OA is simpler than RA. On the basis of the
constitution and involvement of other dosas, herbs and herbal preparations that alleviate
vitiated vata are
selected to treat OA. Because muscle atrophy commonly accompanies
OA, the treatment also involves an adequate
exercise program. Both muscle strength and
range of motion can be improved with
appropriate physical exercise. Regular bench-press
and leg-press exercises with a certain amount
of weight may slow down or even stop the
progress of OA in early stages and may even
help in later stages in some patients. Adequate
amount of rest is also an important adjunct
and should be included in the daily routine
of OA patients.
Basically, the drug treatments for OA and RA
are very similar because both have a
that are commonly used to treat RA are also
applicable to treat OA. In addition, Kishore
guggul from the Ayurvedic Formulary of India is also
used for OA. Singh53 reported a case
study showing usefulness of guggul (C. mukul) in
treating OA of the knee. In a larger study
in 30 OA patients, guggul extract (500 mg, three times/day for 2 months) provided
significant
relief in signs and symptoms of OA.54,11
In conventional medicine, the treatment of OA
includes a proper exercise program, rest,
NSAIDs, and newer NSAIDs (COX-2 inhibitors).
Intra-articular injections of steroids and
hyaluronan and joint replacement surgery are
also used to treat OA. It is interesting to
note that the NSAIDs and newer NSAIDs are the
drugs also used to relieve pain and
inflammation in RA.
10.4 Gout (Rakta Vata)
10.4.1 General Description
In Ayurveda, the origin of gout is believed
to be in blood. When functionally impaired
(vitiated) vata invades
the blood and bone joints, it produces gout. It is characterized by
acute excruciating pain (worse at night) and
inflammation of the joints, which generally
begins from a toe or finger and then
gradually spreads to the other joints of the body. The
affected joints are warmer than the body,
swollen, extremely tender with a burning sensation,
and have shiny overlying skin and dilated
veins. The other symptoms are excessive
sweating, rigidity, numbness, and
discoloration of the skin on the affected joints. The joints
return to normal after a few days with
desquamation of the overlying skin. An acute attack
may cause fever, anorexia, and general
malaise.
In conventional medicine, gout is known as an
inflammatory arthritis induced by
the pathogenic deposition of aggregated
monosodium urate monohydrate crystals
(tophi),
which deposit in various tissues and joints. Urate crystals can also deposit in
kidneys. Chronic high levels of uric acid in
the blood are necessary for the development
of gout, although some other factors may be
involved. This etiology points in the
direction of the Ayurvedic etiology that
indicates that blood is involved in this disease.
If untreated, it can cause painful,
destructive arthropathy and urolithiasis resulting in
renal failure.
common cause, vitiated vata. Single herbs and formulas listed in Table 10.1 to Table 10.3
10.4.2 Treatment
Ayurvedic treatments include the following:
1. Guduchi (T. cordifolia) decoction of 14 to 28 ml made from 6 to 8 g
of powder of
leaves and stem to be ingested with purified guggul (2 to 4 g, three times/day)
2. Decoction of equal parts of vasa (Adhatoda vasica) leaves, stem of guduchi, and fruit
pulp of Aaragvadha (Cassia) of 14 to 18 ml taken with castor oil (7 to
14 ml two
times/day)
3. Kishora guggul and Punarnavadi guggul (3 g/day)
4.
To apply the treatment on the affected
joints, a poultice of black sesame seeds is prepared
in milk.
Guda (Jaggary), rice, wheat, gram, pigeon peas, spinach,
black coffee, ripe fruit of white
gourd, Guduchi, Deodar (Cidrus deodar) are useful articles of diet. The food articles to avoid
are seeds of Masa (black phaseolus bean), Kulattha (dolichos
beans), pea, legumes, radish,
sugarcane products, wine, and yogurt. Because
uric acid is the end product of protein
metabolism, it is important to avoid
high-protein diet. Sleeping during the day, exposure
to heat, and excessive exercising should be
avoided.
10.5 Spasmodic Torticollis, Lockjaw (Hanu-Stambha), Lumbago (Kati Shula),
and Fibromyalgia
10.5.1 General Description
Vitiated vata is
the cause for torticollis (Manya-stambha),
lockjaw (Hanu-stambha), and
lumbago (kati shula). When the vitiated vata invades
the neck muscles it causes muscle
rigidity and immobility of the neck and pain
in the neck muscles. Similarly, when it invades
jaw muscles and joints, it causes lockjaw.
When it invades the lower part of the back it
causes lumbago, and when it invades all body
muscles it causes fibromyalgia (Sarvang
shula). Pain and stiffness of the muscles are the main features of these
diseases.
Specific etiology of these diseases is not
known at this time. Ayurvedic etiology of these
diseases refers to food and lifestyle habits
that can aggravate vata.
10.5.2 Treatment
Because the causative dosa is vitiated vata, single herbs and formulas for the treatment
of
these tables but also used for these diseases
are Kishora guggul and Triphala guggul from
the Ayurvedic Formulary of India. Both
formulas are given at a dose of 3 g/day. It is
interesting that there are so many choices of
treatments in Ayurveda. A physician needs
to assess the body constitution, diagnose
accompanying diseases, and determine the
predominance of other dosas in order to select suitable herbal formulas and other components
of the management regimen.
Additional single herbs and formulas used for
RA (see Table 10.1 to Table 10.3)
RA listed in Table 10.1 to Table 10.3 for RA
are applicable. Additional formulas not in
10.6 Future Research on Ayurvedic Herbal
Fomulas for Musculoskeletal
Disorders
Because the efficacy of many Ayurvedic herbs
has been shown in animal models, the next
step is to investigate the mechanism of
action so that effective combination of herbs can
be formulated. It is likely that these herbs
may have selective inhibitory activity on COX-
2 because they have not been known to cause
any toxicity in the stomach or intestine.
Ergolide, a sequiterpine lactone from Inula britanica, has been shown to inhibit the COX-
2 activity.49 Semicarpous anacardium has been shown to bring back the levels of
altered AO
defense system in adjuvant-induced arthritic
rats.41
These and other biochemical mechanisms of
action of these herbs should be further
investigated.
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Ayurvedic Therapies of Sciatica (Gridhrasi)
Subhash Singh
11.1 Introduction
Neuropathic pain due to injury or dysfunction
of the nervous system is a difficult therapeutic
challenge in the treatment of chronic pain.
The pain of sciatica
is typically a radiating
pain that usually is related to a specific
nerve root. Nerve dysfunction may be present in
both motor and sensory modalities. The
response of neuropathic pain to conventional
analgesics has been in many cases
disappointing. Several studies have suggested that
spinal clonidine may be effective in treating
some forms of neuropathic pain; some of the
authors do not advocate such procedures
because of its major complications. Thousands
of years ago, Charaka
,
a great physician and Susruta
(800
B
.
C
.), the father of the surgery,
identified the disease and named it
gridhrasi.
This recent research was aimed to establish
the ancient ayurvedic therapeutic values
among the people of modern era, evaluating
fundamental principles by scientific
parameters. In this chapter, the current knowledge
about pathophysiologic mechanism, diagnosis,
and management of sciatica is reviewed
and discussed in relation to its prognosis.
11.2 Epidemiology
Lower back pain (LBP) is the most common
presentation of lumbar spine disorders.
Reports from various research institutes
(Central Council for Research in Ayurveda
and Siddha [CCRAS]), different modern
class-three level hospitals, and referral centers
show that 3 to 5% of the patients visiting
annually in India present with LBP. Of them,
1.5% have features of sciatica, in which 62
to 69% are males and 31 to 38% are females.
Sciatica affects mostly adult males,
particularly those 41 to 60 years old. The ratio of
incidence is similar in the people of low
income as well as in higher income groups.
It is more prevalent in the month from May to
July (rainy season) in which
vata dosa
naturally gets vitiated and people become
sick. People of
vataj prakriti
are more prone
to the disease. Annual incidence of LBP in
the U.S. is 2 to 5%, and annual cost of direct
medical care for LBP has been estimated at
$13 to $16 billion. Total annual societal
costs are estimated at $20 to $50 billion.
1
Incidents are the same among heavy, light,
and sedentary workers, although a higher
proportion of heavy workers are incapacitated
with LBP. Sciatic pain is common in people
who either sit or stand for prolonged
periods of time.
11.3 Definition
When tendons of the toes and heel become
paralyzed due to vitiated
vata
and confine the
extension of the leg, the disease is known as
sciatica
.
2,3
The pain arises in the gluteal region,
gradually spreads and radiates down the back
of the thigh and knee, and travels up to
the leg and foot. Perception of numbness,
excruciating pain, needling sensation, restrained
movement, and muscle spasm repeatedly in the
limb are the main characteristics of the
disease. Patients sometime feel lassitude,
heaviness in the body, and may also have lack
of appetite.
4
11.4 Clinical Description
Sciatica is a disease of the nerves. The
sciatic nerve is the largest nerve in the body and
has a long course. It is derived from fourth
and fifth lumbar (L
4
and L
5
) and first and
second sacral (S
1
and S
2
) roots. It provides motor innervation of the
hamstring muscles
and to all muscles below the knee. It carries
sensory impulses from the posterior aspect
of the thigh and the posterior and lateral
aspect of the leg and entire sole. Any pathological
process that impinges upon at this level may
cause pain associated with sciatica. The
mechanism involved in the disease process is
distortion; stretching; and irritation or
compression of the spinal root (most often
central to the intervertebral foramen), which
causes tingling, paresthesias and numbness or
sensory impairment of the skin, soreness
of the skin, and tenderness along the nerve.
It usually accompanies radicular pain, loss
of reflexes, weakness, atrophy, fascicular
twitching, and occasionally stasis edema if motor
fibers of the anterior root are involved.
Ayurveda divides this disease into two
categories:
vataj
and
vat-kaphaj
.
Vataj
disease is
caused by the vitiation of
vata dosa
alone and contains a needling sensation. The
body
becomes crooked and the joints of the thigh,
knee, and hip are rendered stiff.
5
Vata-kaphaj
disease is caused mainly by
vata
in company with
kapha dosa
. Numbness, excruciating
pain, paresthesias, restrained movement, and
repeated muscle spasms are distinguishing
features of
vataj
sciatica. It is characterized by lassitude,
heaviness in the body, and
anorexia, along with associated symptoms of
vataj
sciatica. Patients suffer from dyspepsia
and experience lassitude, anorexia, and
excessive salivation.
11.5 Etiology (
Vyadhi Haitu
)
The potential causes of sciatica are myriad,
but these account for only 15% of the total
cases. The mechanisms of underlying
neuropathic pain in 85% of the cases are still not
clear. Sciatica is one of the many
vataj
diseases
(nanatmaj vyadhis)
.
Vata dosa
is the main
culprit in the disease. The nucleus pulposus
of intervertebral disc is probably not pain
sensitive under normal circumstances but may
induce some changes in the nerve root.
6
The causes of sciatica may be classified in
to two main categories: pathology based and
injury based. Both categories are discussed
below.
11.5.1 Pathology Based
The common causes of sciatica are
vata
-aggravating factors, such as grief,
sorrowful
thought and sickness, sitting or sleeping on
uncomfortable beds, anger, day sleeping and
night awakening, apprehension, suppression of
natural urges, indigestion, injury, starvation,
and systemic disorders (e.g., osteomalacia,
hyperparathyroidism, hyperthyroidism,
multiple myeloma, and glucocorticoid use).
Osteoporosis may be associated with the
causes of disk fracture. These degenerative
changes may be considered under the cause
described in Ayurveda in terms of
dhatu sanchhayat,
meaning the degeneration of essential
constituents. Other causes of sciatica are
spondylolisthesis (a degenerative spine disease),
spinal stenosis resulting from bony
encroachment by osteoarthritis, lumbar adhesive
arachnoiditis (the result of a fibrotic
process following an inflammatory response to local
tissue injury within a subarachnoid space),
systemic cancer with epidural metastases of
tumor, diabetes mellitus (DM), and
polyarteritis nodosa.
True sciatica or radicular pain related to
nerve root compression occurs in a small
percentage of patients with LBP, roughly 1%.
Herniation of nucleus pulposus occurs in
95 to 98% of cases at the disc between the L
4
and L
5
vertebrae or between the L
5
and S
1
;
it sometimes plays an important role in
developing sciatica. One third of the patients with
undiagnosed LBP and known systemic cancer
have epidural metastasis of tumor and one
third have pain associated with vertebral
metastasis alone.
7
Increased levels of circulating
antibodies against one or more glycosphingo
lipids were detected in 72% of patients with
acute sciatica in 61% of sciatica patients at
a 4-year follow-up visit (eight antigens analyzed)
and in 54% in patients undergoing discectomy.
8
Nerve ischemia may constitute an important
factor in the pathology of human peripheral
nerve injury and neuropathy.
9,10
Studies
on rats indicated that the circulating
monocyte and macrophages are well involved in the
development of hyperalgesia and wallerian
degeneration after nerve injury.
11
The idiopathic
mononeuropathy in young adults seems to occur
in 6 to 10% of cases of microneuropathies
of sciatic nerve.
12
11.5.2 Injury Based
Common injury-related causes of sciatica are
the unusual and excessive activities of the
lower body and legs, such as jumping,
climbing, stretching and other movements, and
spinal fracture or dislocation resulting from
compression (in 80%). The other causes are
flexion injuries presenting the features of
sciatica, neurologic impairment associated with
the injuries caused by falling from height or
sudden deceleration in an automobile accident,
disk herniation, or spondylolysis as a bony
defect of the pars interarticularis of the
lower lumbar vertebrae (probably caused by
stress fracture in the congenitally abnormal
segment). The causes of arachnoiditis are
myelography, multiple lumbar operations,
chronic spinal infections, spinal cord
injury, intrathecal hemorrhage, intrathecal injection
of steroids, and anesthetics, and sometimes
play an important role in producing sciatica.
Overweight individuals, especially females who
weigh >85 kg, occasionally present the
features of sciatica recurrently due to
abdominal muscle pressure on lumbosacral spine.
11.6 Pathogenesis
According to the
Ayurvedic
concept, vitiated
vata
dosa,
by its own aggravating factors,
strongly fills up the hollowed streams that
produce many kinds of diseases pertaining
to either all or one part of the body.
4,5,13
In this pathogenesis
vata dosa
, blood, muscle,
bone, ligaments, and tendons are involved.
In conventional medicine, the lumbosacral
nerve roots have been known for more
than 6 decades to be intimately involved in
sciatica. However, the basic pathophysiologic
mechanisms are still not well understood.
Intervertebral disk is a fibrocartilagenous
structure that lies between two vertebral
bodies. It consists of soft inner nucleus pulposus
surrounded by thicker fibrous tissue wall,
the annulus fibrosus. The nucleus pulposus
is a gelatinous structure and acts as a shock
absorber between adjacent vertebral bodies.
As age advances, the entire disc structure
becomes more susceptible to trauma and
compression. Tears develop in the annulus
fibrosus as a result of repeated minor trauma;
eventually, if the tears become large enough,
a portion of the soft nucleus pulposus
herniates through the annulus. Asymptomatic
herniation may occur into the center of
the vertebral bodies bordering the disc. When
disc material herniates into the vertebral
canal, it can compress nerve endings and
nerve roots, causing pain and other symptoms.
Generally, the disc herniates lateral to the
posterior longitudinal ligaments, compressing
spinal roots as they enter the intervertebral
foramen. Occasionally, the disc herniates
more centrally, compressing either the spinal
cord or the cauda equina.
An experimental study examined
compression-induced impairment of vasculature. It
was observed that sensory fibers are slightly
more susceptible to compression than are
the motor fibers and that nerve roots are
more susceptible to compression injury than are
the nerve fibers.
14
The study further suggests that nucleus
pulposus has the potential to
injure the nerve root. Proteoglycans and
tumor necrosis factors present in disc cells may
also be involved in early pathogenic process
of the nerve root.
6
11.7 Clinical Course and Prognosis
The clinical course of sciatic pain
associated with systemic illness is that of the underlying
disease. Excluding patients with local
infections, congenital anomalies, metastatic
neoplastic tumors, and cauda equina syndrome,
whose prognosis depends on the specific
cause and available treatment, the disease is
left with the score of the typical patient
with sciatica. From an Ayurvedic perspective,
the prognosis is good in patients with
vataj
sciatica; 70% of patients are relieved of
pain, enabling them to return to full activity
within a 3- to 4-week period, and complete
remission is observed in more than 90% of
cases within a 6- to 8-week period. Among the
patients who have the symptoms of
vatkaphaj
gridhrasi
, recurrence has been noted in 8% of cases 6
months to 5 years, after the
treatment. Recurrence is also observed in
those suffering from DM and herniated disc.
11.8 Clinical Examination and Diagnosis
11.8.1 History
History may provide a definite clue to set up
the diagnosis of the patient. A patient
presenting history of low back trauma with
inability to move the legs strongly suggests
either acute lumbar disc herniation or fracture.
In more severe trauma, the patient may
sustain a fracture, dislocation, or a burst
fracture that involves not only the vertebral body
but the posterior elements as well. Trauma
caused by falling from a height may be
associated with the fracture of pars
interarticularis of L
5
vertebra. Pain after a pure flexion
injury indicates a pathologic condition of
the disc end plates, whereas pain after torsional
is more often associated with disruption of
posterior structures (i.e., facet joint and ligament
injury). The duration, quality, severity and
location of pain all are important in a
detailed history.
An acute sciatic pain can last up to 6 weeks
in 90% of patients; if it persists beyond 2
months, specific diagnosis in most cases is
needed. Patients presenting a history of bowel
and bladder dysfunction (incontinence or
retention), perianal paresthesia, or pain are
usually associated with cauda equina
syndrome. Patients suffering from sciatica
symptoms
should be examined for the following
conditions: spondylosis, osteomyelitis,
osteoporosis, diskitis, spinal epidural
abscess, herniated lumbar disk, DM, metastatic
tumors, hyperparathyroidism, and neurological
diseases. Occupational, social, and psychological
factors also must be taken into account in
history taking. For example, job
dissatisfaction can sometimes adversely
affect the prognosis. All factors should be considered
in a proper manner.
11.8.2 Physical Examination
11.8.2.1 Spine Examination
A normal spine shows a thoracic kyphosis,
lumbar lordosis, and cervical lordosis in
sagital plain; exaggeration of these
alignments may result in hyperkyphosis (
lameback
)
of the thoracic spine or hyperlordsis (
swayback
) of the lumbar spine. A spasm of lumbar
paravertebral muscles results in the
flattening of the usual lumbar lordosis; examination
may reveal lateral curvature of the spine
(scoliosis) or an asymmetry in the appearance
of paraspinal muscles, suggesting muscle
spasm. Taut para spinal muscles limit the
motion of the lumbar spine. Back pain of bony
spine origin is often reproduced by
palpation or percussion over the spinous
process of the affected vertebrae. Nerve root
compression is indicated by radicular pain,
sensory disturbances, coarse twitching,
fasciculation, muscle spasm, and the
impairment of tendon reflexes. Motor abnormality
may also occur but is usually less prominent
than the pain and sensory disturbances.
Because the herniation of intervertebral
lumbar disc most often occurs between L
4
–L
5
and L
5
–S
1
with irritation and compression of L
5
and S
1
root, respectively, it is important
to recognize the clinical characteristics of
lesions of these two roots. If a patient complains
of pain in the hip region, groin,
posterolateral thigh, lateral calf radiating to the external
malleolus, or dorsal surface of the foot, the
first or second and third toes indicate L
5
nerve
root compression. Paresthesia may be in the
entire territory or only in the lateral calf, foot,
and toes. Tenderness is felt in lateral
gluteal region and near the head of fibula. If there
is muscle weakness, difficult dorsiflexion of
the great toe and, less often, of the foot is
shown. Moderately depressed ankle jerk may be
observed in some patients. Generally,
knee and ankle reflexes are not impaired but
may be observed in rare cases.
Walking on the heel may be more difficult for
a patient because of weakness of dorsiflexion
of the foot. In S
1
root compression, the patient feels pain in
the mid-gluteal region,
posterior part of the thigh, posterior of
calf to the heel, and the plantar surface of the foot
and fourth and fifth toes. Tenderness is most
pronounced over the mid-gluteal region
(sacroiliac joint), posterior thigh area, and
calf. It may sometimes extend to the rectum,
testicles, or labia. The patient’s complaint
of paresthesia and loss of sensation is more
likely in the lower leg and outer toes. If
nerve weakness is present, there is difficulty in
plantar flexion of the foot and toes. In this
nerve involvement majority of cases show
diminished or absent ankle reflex (Archilles
tendon reflex); walking on the toes is more
difficult because of the weakness of plantar
flexors.
Disc may herniate into the adjacent vertebral
body during the process of degeneration
and may give rise to a Schmort’s node. Such
cases often show no signs of nerve root
involvement, though the symptoms are same as
in sciatica. The lumbar disc syndrome is
usually unilateral. But sometimes massive
derangements of disc or the extrusion of the
large free fragment into the canal presents
lateral symptoms and signs of sciatica that may
be associated with the paralysis of the
sphincters. The infrequent occurrence of L
3
and L
4
disk herniation with L
4
root compression is manifested as a diminished
knee jerk (patellar
tendon reflex), quadriceps weakness, and
hypersthesia over the lateral aspect of the thigh.
11.8.2.2 Postural Examination
The fully developed syndrome of ruptured
lumbar disc consists of backache, abnormal
posture, and limitation of motion. Lateral
bending to the side opposite the involved spinal
element may stretch the affected tissue,
worsen pain, and limit motion. Reduction of the
lateral flexion is more suggestive of
spondyloarthropathy. Hyperextension of the spine
(with patient prone or standing) is limited
in nerve root compression, ligamentous or facet
joint injury, and bony spine disease.
Increased discomfort with spinal extension indicates
spinal stenosis. Forward bending in the
standing posture with legs straight stretches the
sciatic nerve and its root presenting pain.
Flexion of the hip is normal in patients with
lumbar spine diseases, but flexion of the
lumbar spine is limited and sometimes painful.
The manual internal and external rotation at
the hip with the knee and hip in flexion
(Patrick sign) may produce pain.
The most useful, simple maneuver in assessing
nerve root impingement is the straight
leg raising (SLR) test. In supine position, a
passive straight leg raising (possible up to 80
to 90°
in a normal individual without pain) or
passive dorsiflexion of foot during the
maneuver adds to the stretch of L
5
and S
1
nerve root and sciatic nerve, resulting in
pain
that is readily identified by the patient. If
this is the case, the test is positive. To exclude
false positive results, the physician should
attempt repeated trials. The angle associated
with pain should be reproducible when the
physician passively flexes the patient’s hip
with the knee in flexion, then slowly extends
the foreleg. An important supplement to the
direct SLR is the
crossed SLR
. The crossed SLR is positive when
performance of the
maneuver on one leg reproduces pain in the
opposite leg or buttock. The nerve root lesion
is always on the side of the pain. The
reverse SLR is a similar but less quantified provocative
test that is performed to detect L
2
and L
4
nerve root lesion. This sign is elicited by
making the patient stand next to the
examination table and passively extending each leg
while the patient continues to stand. This
maneuver stretches the L
2
and L
4
nerve roots
and the femoral nerve because the nerve
passes anterior to the hip.
11.9 Diagnosis
After taking a detailed history and
performing the complete physical examination of the
patient, diagnosis is made on the basis of
findings, subjective, and objective parameters
preceding laboratory studies for mere
confirmation. Examples of subjective parameters
include radiating pain starting from the
gluteal region toward the leg and foot, tenderness
along the course of nerve, severe pain when
squatting, sensory and motor changes,
sphincteric tone, and positive SLR signs.
Examples of objective parameters include pricking
and pulling pain, stiffness, ankle and knee
jerk, plantar and dorsal reflexes, pressing
power, muscle wasting, walking speed,
posture, and sensory impairment.
11.9.1 Laboratory Investigations
Investigations required for the patients are
always guided by the history taken, examination
performed, progress observed, and risk
factors to the underlying disease. A physician
has to decide what type of critical
investigation is required for his or her patient. Exhaustive,
hazardous, more expensive, and
complication-creating tests should always be
avoided. A patient having duration of illness
less than 2 weeks and presenting history of
no trauma or any serious disease without risk
factors for underlying disease needs no
investigation. Only conservative treatments
are required. If the patient does not respond
by the end of the second week, routine
laboratory studies such as routine and microscopic
urine examination; complete blood count;
percentage of hemoglobin; erythrocyte sedimentation
rate (ESR); chemistry panel; human leukocyte
antigen (HLA) B-27; rheumatologic
tests; immunoglobulin; calcium phosphate;
alkaline phosphatase; and a plain x-ray
of the lumbosacral part of the spine in
anteroposterior, lateral, and oblique planes are
required. Physician should keep in mind that
the lumbosacral spine radiographs are
abnormal in most persons over 50 years old
and are rarely helpful.
If the pain still persists for more than 4
weeks and the causative factor is not elicited,
the next option of choice is magnetic
resonance imaging (MRI) and computed tomography
(CT) scan-myelography. MRI is an excellent
noninvasive imaging method for the lumbar
spine. MRI elicites well the soft tissue such
as disc, nerve roots, thecal sac, and paraspinous
soft tissue. CT-myelography provides the
greatest information about osseous lesions in
the region of the lateral recess and
intervertebral foramen. CT-myelography is particularly
helpful in evaluating spondylolysis,
infection, or tumor associated with bony destruction.
Electromyography (EMG) is also useful to
assess the functional integrity of the peripheral
nervous system. In sciatica, sensory nerve
conduction studies are normal. Sometimes a
radionuclide bone scan is used to elucidate
sinester cause for sciatica, including occult
spondylolysis, primary and metastatic tumors,
diskitis and vertebral osteomyelitis, but
the technique is inferior to MRI and
CT-myelography.
11.10 Therapy (
Chikitsa
)
A comprehensive treatment plan should be made
keeping in view the duration, onset,
risk factors of the disease, and a goal of
early return of the patient to maximum routine
functions. The treatment of sciatica in
Ayurveda is based on a set of principles involving
palliative purification as well as enema
therapy (see Chapters 3 and 5). Preparations of
Commiphora mukul (guggul), Strychnos
nuxvomica
(
vistinduk), Ricinus communis
(erand),
Allium sativum
(garlic), and
Vitex
negundo
Linn.
(nirgundi)
are extensively recommended
for the treatment of
vat vyadhis
in general and sciatica in particular.
11.10.1 Shaman
Shodhan
Therapy
Palliative treatment (Shaman therapy)
includes guggul and vistinduk preparations orally
provides additional benefit to the patient.
More than 65% of patients have been benefited
within 2 to 3 weeks from this combination
therapy. The response of steam fomention with
rasnasaptak decoction has been proven better than
poultice or fomentation with hot sand
in bags. If the patient’s bowels are
constipated, he or she may be administered castor oil.
Garlic, castor, and vitex act against the
factors responsible for this disease. Trayodashang
and yogaraj are better formulations in guggul preparations. Punarnavadi
guggul is commonly
prescribed in the patients with stasis edema.
Common formulations used in the
treatment of sciatica are listed in Table
11.1.
Most of the Ayurvedic classics recommend
enema therapy in the management of sciatica.
The enema is an important part of
purification therapy that eliminates the waste materials
from channels. Palliative treatment given
after purification is believed to act more effectively
and disease is not relapsed once cured. If
the patient does not respond within 2
weeks of palliative treatment alone,
purification therapy should then be included in the
treatment. Purification procedures, in which
oleation, fomentation, purgation,
and enemas
panchakarma therapy).
When severe pain and neuromotor deficit from
sciatica persist despite 4 to 8 weeks of
appropriate conservative therapy,
bloodletting therapy is advised. Bloodletting provides
quick relief in pain and other inflammatory
conditions. Details of the procedure are
discussed in Chapter 4.
11.10.2 Cautery Therapy
If the pain and neurologic findings do not
disappear on these prolonged conservative
managements, or if the patient suffers
frequently recurring acute episodes, cautery may
be indicated. Cauterization
stimulates the nerve briskly like transcutaneous electrical
nerve stimulation (TENS) or percutaneous
electrical nerve stimulation percutaneous electrical
nerve stimulation (PENS). It is performed either
between the tendo calcaneous and
malleolus (in L5 impingement) or at the
plantar surface of the little toe (in S1 impingement)
in a peculiar marklike dot by a copper wire
of 4 mm diameter. The burnt place is smeared
with micro fine powders of Pterocarpus santalinus Linn. (rakt chandan) and Glycyrrhiza glabra
Linn. (yashtimadhu). Cauterization provides short-term relief to the patients. Occasionally,
some patients may receive a permanent cure.
In few studies, two to three burns on the
limb along the course of nerve were found to
be optimum. Cautery should be avoided in
children, the elderly, apprehensive patients,
patients with pittaj
prakriti,
pregnant women,
hemoptytic or hematemetic, diarrheic,
weakened, and leprotic patients.
A minor surgery for sciatica has been
suggested by Datta (11th century A.D.),16 but the
details are not clear. Patients impaired by
chronic sciatica pain also pose a special
challenge. Alcoholism, depression, headaches,
disruptions in family dynamics, unnecessary
regular medications and job dissatisfaction,
psychosocial issues, and narcotic
addiction may cause chronic pain condition in
sciatica. Attention must be focused on
these factors. Lifestyle changes,
reassurance, and education are important. If there is a
(Table 11.1) along with local massage and
fomention. Complete bed rest for 4 to 5 days
are used in the treatment of sciatica, have
been found most effective (see Chapter 4 on
TABLE 11.1
Formulations Used in Therapy of Sciatica,
Monoplegia, and Paraplegia
No. Name (Manufacturer*) Doses, Vehicle, and
Duration Ref.
1 Dwatrinshak guggul 3 g in the morning with cow’s ghrit or honey
(12 g)
13
2 Punarnavadya guggul (a, b, c) 3 g/day with lukewarm water 31
3 Pathyadi guggul 3 g/day with lukewarm water 32
4 Rasnadya guggul (a) 1 g three times/day with lukewarm water or
milk
13
5 Singhnad guggul (a, b, c) 3 g/day with lukewarm water 16
6 Trayodashang guggul (a, b, c, d, e) 1 g three times/day with milk or lukewarm
water
17
7 Yograj guggul (a, b, c, d, e) 1 g three times/day with lukewarm water 18
8 Vatari guggul 3 g/day with lukewarm water 34
9 Gorochanadi gutika (d) 250 mg three times/day for 60 days with
Ashwagandha decoction (60 ml)
21
10 Vistinduk vati (b, e) 250 mg three times/day with water 17
11 Ajamodadi churna (b) 3 g three times/day with lukewarm water 35
12 Krishna churna (b) 500 mg/day in addition to cow’s urine (50 ml)
and castor oil (15 ml)
32, 33
13 Dashmool, khireti, rasna leaves,
guduchi, and shunthi (powdered
and mixed in equal proportion)
3 g twice/day with castor oil (15 ml/day) 16
14 Mahanimb stem bark kalk 3 g three times/day with water 13, 32
15 Purified kupilu seed powder 100 mg twice/day with water for 15 days 18
16 Arusha, danti, and chirayata
(equal
parts) decoction
25 ml twice/day with castor oil (15 ml) 32
17 Erand mool twak, bilwagiri, brihati,
and chhoti kateri kwatha (equal
parts)
25 ml twice/day with black salt (kala namak as
per requirement)
32, 33
18 Gridhrasi decoction 20 ml twice/day with pushkar moola powder (3
g) and pure hingu powder (500 mg)
35
19 Maharasnadi kwatha (a, b, c, d, e) 50 ml twice/day with 1.5 g purified guggul or
adding shunthi/pippali powder (500 mg), or
with ajamodadi powder (3 g), or castor oil (15
ml)
35
20 Nirgundi leaves decoction 20 ml twice/day with dashmoola powder (3 g)
and pure hingu powder (500 mg)
16
21 Panchmooli decoction 50 ml/day with castor oil (15 ml) or nishoth mool
(bark) powder (3 g)
13
22 Rasnasaptak kwatha 20 ml twice/day with shunthi powder (1 g) 32
23 Shefalika leaves decoction 50 ml/day in two divided doses with castor oil
(12 ml)
33
24 Lahshun kalk 12 g with erand mool
twak kwatha (25
ml/day)
for 1 month
13, 16
25 Bala ashwagandha lakshadi taila
(b, d)
Apply to the affected parts of the leg 21
26 Hingu triguna taila (d) 5 ml two to three times/day orally with water
for 3 to 4 weeks
36
27 Mahavishagarbh taila (a, c, e) Apply to the affected parts of the leg 13
progressive neurologic deficit with
increasing weakness after 12 weeks of conservative
management with or without clinical evidences
of epidural abscesses, malignancy,
hematoma, nerve root compression with
persistent pain, spondylolysthesis or spinal
stenosis, surgery may be considered. Surgery
should be considered only in patients who
have clearly defined anatomic structural
abnormality and have failed from other therapeutic
treatments.
11.11 Strategy for Prevention of Sciatica
Changed dietary habits, rapid industrialization,
stress, pollution, and altered lifestyle have
made people prone to many serious diseases.
Sciatica may be one of them. Preventive
measures include avoiding fast food (little
food), starvation, regular and unnecessary
medication, frequent use of cold materials,
sleeping during the day and staying awake at
night, and strenuous stretching exercises.
The recurrences of pain can be reduced and
chronic disability can be prevented in
patients with mechanical sciatica due to lumbosacral
strain or sprain by using a properly
supervised exercise program, avoiding prolonged
sitting, prolonged standing, and improper
lifting.
Om Tat Sat
(Continued...)
(My
humble salutations to H H Maharshi ji, Brahmasri
Sreeman Lakshmi Chandra Mishra ji and other eminent medical scholars and
doctors for the collection)
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