Journal Banner

Pain: A patient with painful diabetic neuropathy and post herpetic neuralgia: A review report

Mehboob Matteo Manuelli Haque1*, Tan GLC2

1Department of Public Health, Experimental and Forensic Medicine, Unit of Human Nutrition, University of Pavia, Italy

2Department of Neurology and Psychiatry, University of Santo Tomas, Manila, Philippines

Corresponding Author:
Mehboob Matteo Manuelli Haque
Department of Public Health
Experimental and Forensic Medicine
Unit of Human Nutrition, University of Pavia, Italy
Tel: +91-9007322346
E-mail: [email protected]

Received date: January 04, 2017; Accepted date: January 28, 2017; Published date: February 04, 2017

Citation: Haque MMM, Tan GLC. Pain: A patient with painful diabetic neuropathy and post herpetic neuralgia: A review report. Insights Nutr Metabol 2017;1(1):01-09.

Copyright: © 2017 Haque MMM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Insights in Nutrition and Metabolism


State-of-the-art information shows that the incidence of diabetes mellitus will expand via the 12 months 2030, where as much as 50% increase neuropathy and about a quarter will strengthen neuropathic pain. The purported immunocompromised diabetic state makes them additionally prone to various infections, for illustration, herpes zoster illness. Presented on this record is a case of a sixty three-12 months ancient Filipino with painful diabetic neuropathy and who due to this fact developed publish herpetic neuralgia. A pain regimen with pregabalin at the start at one hundred fifty mg/day ultimately attaining 600 mg/day decreased pains, however needed an augmentation with lidocaine patch (5%) utility, and tramadol plus paracetamol fixed dose mixture as rescue medication, for higher manipulate.


Diabetic polyneuropathy; Post herpetic neuralgia; Neuropathic pain; Pregabalin


Neuropathic soreness is outlined as “agony coming up as an immediate outcome of a lesion or disorder affecting the somatosensory procedure” [1]. This can be brought on by using foremost lesions in the crucial fearful system (e.g. Stroke more than one sclerosis spinal wire damage or trauma) and peripheral nervous approach (e.g. Diabetes mellitus [DM], toxins, accidents and varicella-zoster infections and HIV). The scientific confident signs would incorporate spontaneous affliction, paraesthesia’s and dysesthesia (hyperalgesia and allodynia) at the same time the negative signs would comprise hypoesthesia weak point and loss of steadiness. At the same time rough to estimate painful diabetic neuropathy (PDN) could occur in up to 25% of sufferers with DM [2] and that DM is related to an elevated risk of power submit-herpetic neuralgia (PHN) [3-25].

Neuropathic pain is a complex chronic pain state that usually is accompanied by tissue injury. With neuropathic pain the nerve fibers themselves may be damaged dysfunctional or injured. These damaged nerve fibers send incorrect signals to other pain centres. The impact of nerve fiber injury includes a change in nerve function both at the site of injury and areas around the injury [26-30].

One example of neuropathic pain is called phantom limb syndrome. This rare condition occurs when an arm or a leg has been removed because of illness or injury but the brain still gets pain messages from the nerves that originally carried impulses from the missing limb. These nerves now misfire and cause pain [31-35].

Causes of Neuropathic Pain

Neuropathic pain often seems to have no obvious cause but some common causes of neuropathic pain include:

• Alcoholism

• Amputation

• Back leg and hip problems

• Chemotherapy

• Diabetes

• Facial nerve problems

• HIV infection or AIDS

• Multiple sclerosis

• Shingles

• Spine surgery

• Symptoms of Neuropathic Pain

Neuropathic pain symptoms may include

• Shooting and burning pain

• Tingling and numbness

• Diagnosing Neuropathic Pain

To diagnose neuropathic pain, a doctor will conduct an interview and physical exam. He or she may ask questions about how you would describe your pain when the pain occurs or whether anything specific trigger the pain. The doctor may also request both blood and nerve tests.

Neuropathic Pain Treatment

Some neuropathic pain studies suggest the use of non-steroidal anti-inflammatory drugs such as Aleve or Motrin may ease pain. Some people may require a stronger painkiller such as those containing morphine. Anticonvulsant and antidepressant drugs seem to work in some cases.

If another condition such as diabetes is involved better management of that disorder may alleviate the pain. Effective management of the condition can also help prevent further nerve damage.

In cases that are difficult to treat a pain specialist may use an invasive or implantable device to effectively manage the pain. Electrical stimulation of the nerves involved in neuropathic pain may significantly control the pain symptoms [36-60].

Other kinds of treatments can also help with neuropathic pain. Some of these include:

• Physical therapy

• Working with a counsellor

• Relaxation therapy

• Massage therapy

• Acupuncture

Unfortunately neuropathic pain often responds poorly to standard pain treatments and occasionally may get worse instead of better over time. For some people it can lead to serious disability. A multidisciplinary approach that combines therapies however can be a very effective way to provide relief from neuropathic pain [61-75].

Patient Information and Clinical History

The patient is a 63-12 month-ancient male, Filipino identified with variety 2 DM 12 years in the past. He got here in complaining of reasonable to severe (7-8/10 VAS) spontaneous pricking pains over each toes for the past 4 months. He famous that the pains would also show up when he walked and when his feet touched the cold ground. Eventually there used to be noted accompanying numbness that involved now not best each his feet but also both of his arms. Even though he claimed that he had quite excellent glycaemic manipulate (latest regimen: weight loss program, exercise, sitagliptin or metformin 5/500 mg/tab 1 tab BID and gliclazide 60 mg/tab 1 tab OD) with an HbA1c 6.1%, his pains endured inflicting impaired sleep anxiety symptoms and recurrent work absenteeism.

In the final 6 months he developed varicella zoster lesions located on the proper T9-12 dermatome levels accompanied with the aid of power stabbing pains (VAS 7/10) 2 months after. The agony would additionally show up at any time when cloth would touch the affected body components.

Likewise he had a body Mass Index (BMI) of 40 and a known dyslipidemia on healing with a statin. He had no earlier varicella zoster vaccinations. He is negative for HIV and there is no consumption of medicinal drugs that could cause neuropathies (e.g. Colchicine amiodarone and isoniazid among others). Household historical past is likewise unremarkable for any neuromuscular ailments.

As a part of his earlier scientific historical past he was once given from somewhere else a routine for his PDN with vitamin B16, B12 and naproxen (more often than not prescribed for nociceptive ache). Despite 2 months into the routine these didn't alleviate his PDN pains.

He was earlier given a prognosis of “claudication” considering the fact that the suffering was noted more upon ambulation. Nonetheless the dorsalis pedis pulses and ankle-brachial index (1-ranking on the test) have been usual. Upon further historical past taking and examination it was once noted to be considering the fact that of mechanical allodynia (i.e., Affliction occurring on movement).

Clinical Findings and Diagnostic Assessment

On neurologic examination his cognitive repute was average and there have been no cranial nerve deficits. Motor examinations didn't show any atrophy fasciculation’s and ataxia. He used to be competent to ambulate good together with a just right toe and heel walking. Deep tendon reflexes were symmetric and graded +2 in all extremities. Sensory examination was once natural for testable modalities (pinprick, light touch, monofilament and role/ vibration senses focusing on distal limbs (chiefly the enormous toe). However, he had allodynia upon cotton and cold utility typically over the edges of his shingle-affected areas over the proper T9-12 dermatomes (Figure 1).


Figure 1: Affected areas over the right T9-12 dermatomes.

Activities Nerve Conductions experiences (NCS) revealed usual latencies conduction velocities and amplitudes of evoked motor and sensory nerves (together with emphasis over the sural and superficial fibular nerves). The late response stories (i.e., F-waves and tibial H-reflexes) have been likewise common and aspect-part similar. The electro-physiologic Sympathetic skin Response (SSR) was once absent in the scale down limbs but could be elicited on the upper limbs.

Therapeutic Intervention

The sufferer was once at the beginning started on pregabalin at a hundred and fifty mg/day which was slowly titrated up to 600 mg/day in three weeks. The PDN improved with VAS lowered to 2/10. For the reason that of the PHN the remedy finally needed an augmented cure with lidocaine patch (5%) applied 12 hours per day plus rescue remedy of tramadol+paracetamol combination. With these multi-modal medicines, there was an over-all famous 70% anguish discount and patient have been able to sleep higher think better and return to work more conveniently. Sufferer informed consent was secured as good as Ethics approval [76-85].


Diabetic polyneuropathy is one of the most fashioned longterm problems of DM. Most patients would present with distal symmetrical polyneuropathy by and large beginning at the toes and step by step ascending towards the palms. For both forms 1 and a couple of DM, the chance of constructing distal polyneuropathies – together with painful neuropathies – appears to be inversely involving the measure of glycaemic manipulate and is straight correlated with the duration of diabetes. Diagnosis of diabetic neuropathy is more commonly clinic-centred and neurophysiologic tests could also be applied where doubts exist (e.g. Uneven presentation motor weak point and atrophy “pink flags”) [86-100]. Activities NCS findings may yield common findings in those with PDN that will off with small nerve fiber involvement. NCS is a risk-free scan for tremendous fiber neuropathies. In the situations where NCS are average Quantitative Sensory testing, epidermal nerve fiber densities obtained from epidermis biopsies, confocal retinal microscopy and Laser evoked capabilities reviews will in this day and age provide documentation.

In this reward case the events NCS was no longer invaluable and now not unexpected in a sufferer with excellent tendon reflexes and proprioceptive assessments. The SSR an autonomic scan may function a surrogate scan for small nerve fibre neuropathy principally if absent in the lessen limbs (a case in factor for symmetric length-dependent diabetic neuropathy). While clinically ruled out on this present case one must be aware of differentials in small nerve fibre neuropathy that comprise the following: Metabolic issues (e.g. Porphyria and Fabray’s sickness) Infiltrative/Immune (e.g. Lupus, HIV Lyme’s ailment and Amyloidosis) and Toxins/drugs (e.g. Heavy metals, Metronidazole, Nitrofurantoin isoniazid and anti-cancer medications). These differential diagnoses have been ruled out in this present case with thorough historical past taking physical and neurologic examination and common laboratory examinations [101-112].

Prognosis administration and practice parameters for HZ and PHN have been systematically achieved prior to now [113]. In regard to DM and PHN regardless of usual potential that most beneficial glucose manipulate is sought new reports show that improved glucose control may have an impact on more in sufferers with style 1 diabetes than these with sort 2 DM [114,115].

DM patients are extra inclined to viral infections which may be of accelerated severity than in more immune competent subjects. Some measures of phone-mediated immunity are depressed in members with DM (for example T-Mobile deregulation attribute in DM would outcome in an increased incidence of HZ [116]. In one study [117] the cell-mediated immunity closer to HZ virus amongst sufferers with and without DM used to be analysed by means of the gamma interferon ELISPOT assay. Even though the learn did not show any gigantic variations it was once found that the ELISPOT rely was scale back for these with DM than the healthful topics in age-matched groups [118].

Guingard’s group estimated that the crude incidence of HZ infection was greater amongst kind 2 (4.59 per 1000 individual years) than style 1 DM (2. 13 per 1000 individual years). The magnitude of the threat is related to the sufferer’s age (≤ sixty five years old) and the presence of comorbid explanations comparable to (cardiac and power pulmonary disorder). A different workforce [119] recognized 4, 20, 515 cases of HZ (approximately 88 million man or woman-years). Participants with DM represented 8.7% of the individual years they analysed accounting for 14.5% of the patients with HZ contamination. Their incidence of HZ was once larger (78%) in DM and DM used to be related to a 45% adjusted threat of HZ. Additionally, they discovered greater premiums of PHN in individuals with DM than these without and that DM was once associated with an 18% adjusted danger of persistent PHN [120].

Hyperglycaemia used to be located to be a predictor for PHN in one more learns [14]. Despite the fact that they'd a small DM population it's of be aware that four out of 7 (57.14%) DM patients developed PHN compared to healthful topics (15.55%).

Enough pain manipulate is likely one of the targets of medication on account that affliction is probably the most debilitating symptom of PDN and PHN. There are more than one drugs used to deal with these agony syndromes and a discomfort practitioner must correctly weigh the treatment’s protection, efficacy, price and aspect outcome profile of the sufferer’s general knowledge tolerability and repute. For instance, antidepressants could take delivery of two patients who boost symptoms of melancholy, medicinal drugs will also depend on sufferer’s comorbidities like cardiac-hepato-renal impairments with a couple of drug regimens on board [121-125].

Just as utilized in this gift case pregabalin unlike gabapentin (one more alpha-2 delta ligand) was the first option for healing in PDN [126] and it belongs to the tier of first line therapies derived from a couple of instructional materials. The common antagonistic results of pregabalin include somnolence, dizziness, peripheral edema and weight reap. At the same time pregabalin dose of one hundred fifty mg/day in two divided doses is encouraged as preliminary healing slowly augmenting the dose to 600 mg/day will obtain higher efficacy gleaned from this gift case. Algorithms for medication of PDN would start with choicest glycaemic manipulate and first line medication with anticonvulsant medicinal drugs (gabapentin and pregabalin) or antidepressants (duloxetine and tricyclic antidepressants). If these cures deem inadequate for right manipulate 2nd line agents (oxycodone, tramadol, topical and sodium channel blockers) or combination cures could also be used.

Brand new pooled reports, algorithms and instructions also point out that multimodal healing procedure in peripheral neuropathic soreness may be worthy [127,128] and to which can maintain actual with the extra use of lidocaine patch and opiates in PHN. Topical medicinal drugs provide curb facet result profiles and are useful for sufferers who are unable to tolerate oral medications. Lidocaine is a voltage-gated sodium channel antagonist and when applied on the dermis binds to the sodium channels on nociceptors stopping generation and conduction of neuronal motion potentials thereby reducing agony. Lidocaine patch (5%) is authorized each in US and Europe for the healing of PHN and has few regional side results (i.e., Erythema rash dermatitis skin irritation and hypersensitivity reactions). In keeping with Barbano et al. [18] up to four 5% lidocaine patches used for up to 18 h/day could tremendously reinforce pain and great of existence for patients with PDN.

As was once modelled in this present case a randomized manages study by using Baron et al. [129] recruited sufferers with each PDN and PHN. A colossal proportion of sufferers could not be handled with monotherapy. These patients have been then requested to take a combo of lidocaine patch and pregabalin. The addition of lidocaine patch supplied better ache discount. Furthermore, pregabalin would be titrated down to a scale back dose minimizing aspect effects. Use of oxycodone in combo with pregabalin has likewise been studied in PDN with PHN [130].

While we underscore the improved chance of PHN danger in sufferers with DM, the suffering symptomatology may even pose the better crisis to a struggling sufferer with PDN. The clinician must be able to respect the predicament and not depart the sufferer to “reside with discomfort.” The procedure of awareness by means of the application of validated screening tools is vital to a better care. Nonetheless, there are occasions when the clinician’s acumen on this state of affairs is also a mission as verbal exchange gaps may just exist between them and the sufferers. This used to be once more exemplified on this reward case wherein medicinal drug (vitamin B1, B6 B12 and anti-nociceptive medicine) with unproven advantages in neuropathic suffering had been initially given. Sooner or later “two” a lot of the pains the patient suffered has been noticeably managed with cause use of combo remedies [131-150].


Post herpetic neuralgia (PHN) is a common and often devastatingly painful condition. It is also one of the most extensively investigated of the neuropathic pains. Patients with PHN have been studied using quantitative testing of primary afferent function skin biopsies and controlled treatment trials. Together with insights drawn from an extensive and growing literature on experimental models of neuropathic pain these patient studies have provided a preliminary glimpse of the pain-generating mechanisms in PHN. It is clear that both peripheral and central pathophysiological mechanisms contribute to PHN pain. Some PHN patients have abnormal sensitization of unmyelinated cutaneous nociceptors (irritable nociceptors). Such patients characteristically have minimal sensory loss. Other patients have pain associated with small fibre differentiation. In such patients’ pain and temperature sensation are profoundly impaired but light moving mechanical stimuli can often produce severe pain (allodynia). In these patients allodynia may be due to the formation of new connections between no nociceptive large diameter primary afferents and central pain transmission neurons [151-155]. Other differentiation patients have severe spontaneous pain without hyperalgesia or allodynia and presumably have lost both large and small diameter fibres. In this group the pain is likely due to increased spontaneous activity in deafferented central neurons and/or reorganization of central connections. These three types of mechanism may coexist in individual patients and each offers the possibility for developing new therapeutic interventions.