Low back pain is a common neurological problem with a variety of underlying causes. Pain results from complex interactions between sensory input and neural networks in the spine and brain. Central sensitization can cause disproportionate pain responses and chronic pain even after the original injury has healed. Tramadol is well-suited for treating back pain involving central sensitization due to its effects on opioid, serotonin, and norepinephrine systems in the brain. Proper treatment requires targeting medications to individual symptoms and regularly evaluating patients.

1. Low Back Pain
Neurologist’s perspectives
Dr.A.V.Srinivasan

2.  Back pain is a common cause of referral to
the neurology clinic
 Pain experience is the result of a multitude
of processes, whereof the sensory input is
one, that interact in a proposed neural
network, the neuromatrix.
Progress in Neurobiology August 2001; 64 (6): 613-637
Best Practice & Research Clinical Rheumatology Vol. 21, No. 1, pp. 153e166, 2007

3. Low Back Pain is more common

4. Prevalence of chronic pain
Best Practice & Research Clinical Rheumatology Vol. 21, No. 1, pp. 153e166, 2007

5. Best Practice & Research Clinical Rheumatology Vol. 20, No. 4, pp. 707-720, 2006

6. Differential diagnosis of low back pain
Am Fam Physician 2007;75:1181-8, 1190-2

7.  The lumbar disc herniation is the most
frequent disease of the spinal degenerative
processes, and they cause of 30% to 80% of
the low back pain cases
Medicina (Kaunas) 2007; 43(8)

9. Cauda equina syndrome
 Single or double-level compression of the lumbosacral
nerve roots located in the dural sac results in a
polyradicular symptomatology clinically diagnosed as
cauda equina syndrome.
 The cauda equina nerve roots provide the sensory and
motor innervation of most of the lower extremities, the
pelvic floor and the sphincters. Therefore, in a fully
developed cauda equina syndrome, multiple signs of
sensory disorders may appear such as low-back pain,
saddle anesthesia, bilateral sciatica, then motor
weakness of the lower extremities or chronic
paraplegia and, bladder dysfunction.
Progress in Neurobiology August 2001; 64 (6): 613-637

11. CES - Etiology
 Non-neoplastic compressive etiologies
 Herniated lumbosacral discs
 Spinal stenosis
 Spinal neoplasms
 Non-compressive etiologies
 Ischemic insults
 Inflammatory conditions
 Spinal arachnoiditis
 Other infectious etiologies.
Orendacavo J et al. Progress in Neurobiology August 2001; 64 (6): 613-637

12. Failed Back Syndrome
• Failed back syndrome (FBS) is a well-
recognized complication of surgery of the
lumbar spine. It can result in chronic pain
and disability, often with disastrous
emotional and financial consequences to
the patient.
• "spinal cripples"
Onesti ST. Failed back syndrome. Neurologist 2004 Sep; 10(5): 259-64.

15. Consequences of Untreated & Under treated
Acute Pain
Extensive and Persistent cascade of
neurochemical mediators triggered by tissue
injury leads to a long-term, permanent,
neurological change that can lead to
SENSITIZATION
ALLODYNIA
HYPERALGESIA
MAY evolve into chronic pain

16. Progression of Acute Pain to
Chronic Pain
Chronic pain appears
Because of an expression of the presence
of
Central Sensitization

17. Sensitization
Sensitization is a phenomenon of
inappropriate or disproportionate
response to normal stimulus

18. Types of Sensitization
Peripheral & Central

19. Peripheral Sensitization
Occurs at the site of injury
Primary afferent neurons are involved
Exposure to prostaglandins
Increased pain sensation at the site of injury

20. Central Sensitization
 Increased excitability of pain neurons
(nociceptor neurons) in the dorsal horn of the
spinal cord.
 Neurons detecting and transmitting pain display
‘plasticity’
• progressive increase in the response to repeated
painful stimuli
• all contribute to altered sensitivity to pain

21. Clinical Implications of Central
Sensitization
 Increased response to a noxious stimulus
(Hyperalgesia)
 Disproportionate response to pain syimulus
(Allodynia)
 Prolonged / Persistent pain
 Referred pain

22. Central sensitization in low back
pain
 In back pain patients, both hypoalgesia and
hyperalgesia to electrical cutaneous
stimulation is reported (Wilder-Smith et al.,
2002).
 Hyperalgesia to pressure on the thumbnail
was found in idiopathic chronic low-back pain
patients compared to controls indicating
generalized hyperalgesia (Giesecke et al.,
2004).
European Journal of Pain 11 (2007) 415–420

23. The distribution of experimental pain in controls and chronic low back patients
evoked by injection of hypertonic saline in infraspinatus and tibialis anterior
muscles. The evoked pain areas were significantly larger in the patients for both
muscles. Dark shading indicates overlapping pain areas among subjects.
European Journal of Pain 11 (2007) 415–420

24. Central Sensitization & Tramadol

25. Why Tramadol is Superior
In patients with Central Sensitization

26. Tramadol
An Atypical Centrally Acting Analgesic
5HT uptake
inhibition
NA
m-agonist uptake
inhibtion

27. Role of Tramadol
 Tramadol
• Centrally acting opioid analgesic, binds
to µ opioid receptors
• Inhibits reuptake of NE and serotonin
within pain pathways of CNS
• Contribute to enhancing the descending
pain inhibitory pathways

28. Role of Tramadol
 Down regulation of central sensitisation hence an
ideal drug for Neuropathic pain
 “Enhances” descending inhibitory pathways
 Excellent Analgesic Efficacy
 Tolerated well even in very high dosages

29. Tramadol
 Most Logical Choice for a variety of Chronic Pain
Conditions where central sensitisation plays a major role:
Our experience in INDIA :
OA /RA Flare Pain
Neuropathic Pain
Acute Radicular Back Pain
Chronic Back Pain
Fibromyalgia Pain
Cancer Pain

30. Tramadol – Central Sensitization
Inhibits reuptake of
Binds to Mu opiods
Serotonin and NE
Mimicks the effects More in qty at the
Enkephalins synapse
Reduce the effects of Reduce the effects of
Sub P Sub P
Reduce the intensity of Reduce the intensity of
the pain the pain
Pain relief Pain relief
Enhances descending inhibition

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32. Best Practice & Research Clinical Rheumatology Vol. 19, No. 4, pp. 609–621, 2005

33. Treatment choice
 Should be evidence based and tailored as much as possible
to suit the individual patient.
 Acetaminophen (paracetamol), mild opioids and NSAIDs
are the first-line drugs for low back pain but there is no
evidence that one is more effective than the others.
 Tramadol is proposed to be the better choice due to its
pharmacological profile and effect on pain in several
musculoskeletal disorders.
 Non-benzodiazepine muscle relaxants (with or without
pain medication) could be considered as second-line drugs
in acute low back pain, and cyclic antidepressants in
chronic low back pain.
 Strong opioids could be considered in musculoskeletal
pain when other treatment options have failed
Best Practice & Research Clinical Rheumatology Vol. 21, No. 1, pp. 153-166, 2007
Best Practice & Research Clinical Rheumatology Vol. 19, No. 4, pp. 609–621, 2005

35. Symptoms to be used to tailor choice
of treatment
Best Practice & Research Clinical Rheumatology Vol. 19, No. 4, pp. 609–621, 2005

36.  The benefits of medication in low back pain will
increase if:
 Medication is prescribed only for severe symptoms
 The choice of medication is targeted on the main
symptom
 Patients understand the aim of the medication and how
long it should be used before evaluation can take place
 Medication should be taken on a time-contingent basis;
this facilitates evaluation
 Evaluation is based on the aim
 The type of drug has been tailored on individual basis
 The dose has been tailored on individual basis.
Best Practice & Research Clinical Rheumatology Vol. 19, No. 4, pp. 609–621, 2005