The evaluation of a patient with peripheral neuropathy starts with simple blood tests, including a complete blood count, comprehensive metabolic profile, and measurement of erythrocyte sedimentation rate and fasting blood glucose, vitamin B 12 , and thyroid-stimulating hormone levels 5 Figure 1.

Additional tests, if clinically indicated, may include a paraneoplastic panel to evaluate for occult malignancy; antimyelin-associated glycoprotein antibodies to evaluate for sensorimotor neuropathies; antiganglioside antibodies; cryoglobulins; cerebrospinal fluid CSF analysis to evaluate for chronic inflammatory demyelinating neuropathy; antisulfatide antibodies to evaluate for auto-immune polyneuropathy; and genetic testing if hereditary peripheral neuropathy is suspected Table 3.

Lumbar puncture and CSF analysis may be helpful in diagnosing Guillain-Barré syndrome and chronic inflammatory demyelinating neuropathy; CSF protein levels may be elevated in patients with these conditions. Electrodiagnostic studies are recommended if the diagnosis remains unclear after initial diagnostic testing and a careful history and physical examination.

Nerve conduction studies assess the shape, amplitude, latency, and conduction velocity of an electrical signal conducted over the tested nerve. Axonal loss leads to lower amplitudes, and demyelination causes prolonged latency and slow conduction velocity.

EMG can detect active axonal damage, as evidenced by the presence of spontaneous muscle fiber activity at rest resulting from the absence of neuro-regulation denervation.

The motor unit action potential on voluntary muscle contraction also is assessed. In neuropathic conditions, reinnervation changes are recorded, the details of which are beyond the scope of this article.

Electrodiagnostic studies can help determine whether the neuropathy is the result of damage to the axons axonal neuropathy or the myelin demyelinating neuropathy , or both mixed. Normal nerve conduction studies and needle EMG significantly decrease the likelihood of peripheral neuropathy, whereas abnormal nerve conduction findings confirm the diagnosis.

A potential limitation of electrodiagnostic studies is that they are able to test only the large, myelinated nerve fibers. This limits their sensitivity in detecting neuropathies of the small nerve fibers i. In these cases, a specialized test directed at autonomic functions, and other non-electrodiagnostic tests e.

Nerve biopsy should be considered when the diagnosis remains uncertain after laboratory and electrodiagnostic testing, or when confirmation of the diagnosis is needed before initiating aggressive treatment e.

Sural and superficial peroneal nerves are preferred for biopsy. When all investigations fail to identify a cause and electrodiagnostic studies show axonal-type symmetric peripheral neuropathy, idiopathic peripheral neuropathy is the presumptive diagnosis.

Epidermal skin biopsy can be performed in patients with burning, numbness, and pain, and in whom small, unmyelinated nerve fibers are suspected to be the cause. Small nerve fiber damage may constitute the earliest stages of some peripheral neuropathies and cannot be detected by electrodiagnostic studies.

Treatment of peripheral neuropathy has two goals: controlling the underlying disease process and treating troublesome symptoms. The former is usually achieved by eliminating offending agents, such as toxins or medications; correcting a nutritional deficiency; or treating the underlying disease e.

Acute inflammatory neuropathies require more urgent and aggressive management with intravenous immunoglobulin 9 or plasmaphereis. Mechanical ventilation should be considered in patients whose forced vital capacity is less than 20 mL per kg or is reduced by more than 30 percent of baseline, or if maximal inspiratory pressure is less than 30 cm of water.

It is important to help patients control troublesome symptoms of peripheral neuropathy, such as severe numbness and pain, as well as to alleviate disability resulting from weakness. A second opinion regarding the patient's diagnosis and management also should be considered before initiating long-term opioid therapy.

Martyn CN, Hughes RA. Epidemiology of peripheral neuropathy. J Neurol Neurosurg Psychiatry. Davies M, Brophy S, Williams R, Taylor A. The prevalence, severity, and impact of painful diabetic peripheral neuropathy in type 2 diabetes.

Diabetes Care. England JD, Gronseth GS, Franklin G, et al. Distal symmetric polyneuropathy: a definition for clinical research. Willison HJ, Winer JB. Clinical evaluation and investigation of neuropathy.

Dyck PJ, Lais AC, Ohta M, Bastron JA, Okazaki H, Groover RV. Chronic inflammatory polyradiculoneuropathy. Mayo Clin Proc. Lewis RA. Sympathetic skin responses were also normal. Therefore, electrophysiological evidence of large sensory fibre deficits or impaired sympathetic efferent function was not present at the sites tested.

The IENFD measurements from the lower leg of our study participants showed evidence of small fibre pathology Fig. Compared to published age- and gender-matched normative data The remaining IENFD measurements, albeit above the 0. Small fibre pathology was demonstrated on skin biopsy.

Blue circles represent values below the 0. Green circles represent values at or above the 0. Red circles represent healthy African American study participants, whose IENFDs were all above the 0.

B Bright field images of skin biopsies taken from the leg of i a healthy study participant; and ii participant with NFCI demonstrating PGP 9.

There is a clear reduction in intraepidermal nerve fibres in the participant with NFCI. An example of a clinical assessment and patient narrative has been included in the Supplementary material. The mean z-scores for the cold and warm detection thresholds in the hand were reduced when compared to the DFNS normative range Fig.

This is indicative of thermal hypoaesthesia. The mean z-scores for cold and heat pain thresholds fell within the normative range. Worse neuropathy is associated with more recent injury and more severe pain. Sensory impairment was demonstrated on QST. By comparing participant data to normative data from the DFNS a z-score can be generated, which indicates the number of standard deviations from the mean control population.

Positive z-scores denote gain of function, whereas negative z-scores denote loss of function. There were significant reductions in the mean z-score in both the hand for CDT, WDT, TSL, MDT and VDT and foot MDT and VDT.

C Loss or gain of sensory function in the hand and foot. z-scores that were greater or less than two standard deviations from the mean. The mean z-scores for mechanical and vibration detection threshold in the hand were below the normative range, indicating hyposensitivity, when compared to the DFNS healthy control cohort.

The z-scores for all other mechanical parameters fell within the normative range of the DFNS control data. Hyposensitivity to thermal and mechanical stimuli is indicative of loss of function in both small and large fibre modalities in the hand. The mean z-scores for the cold detection thresholds and thermal sensory limen in the foot were at the lower limit of the DFNS normative range Fig.

The mean z-score for warm detection threshold, and cold and heat pain thresholds fell within the normative range.

The mean z-scores for mechanical and vibration detection threshold in the foot were below the DFNS normative range, indicating hyposensitivity, when compared to the DFNS healthy control cohort.

The z-scores for all other mechanical parameters fell within the normative range of the DFNS healthy control data. Thus, the QST data were almost the same in the hand and the foot, demonstrating distal loss of small and large fibre modalities.

Of the 42 study participants, 27 The remaining participants declined this investigation and were not required to provide a reason for this decision, consistent with the ethics protocol. Only a minority of study participants exhibited gain-of-function phenomena within the pain detection parameters.

Paradoxical heat sensations were elicited in Mean z-scores for the foot from our participants are compared to those of patients with small fibre neuropathy and diabetic neuropathy in Supplementary Fig. Data are from The Pain in Neuropathy Study Themistocleous et al.

All our participants reported chronic pain that was temporally related to an episode of cold exposure. Pain was localized to the hands and feet and all participants exhibited sensory examination abnormalities in these areas. Therefore, all study participants satisfied the criteria for probable neuropathic pain.

A diagnostic test confirmed a lesion of the somatosensory nervous system in The sensory sum score correlated positively with BPI pain severity and correlated negatively with time from injury to assessment Fig.

Therefore, study participants with a more severe neuropathy on clinical examination reported higher pain scores, and experienced their cold injury more recently than those with a less severe neuropathy on clinical examination.

The sensory sum score correlated negatively with certain QST scores for both the hand and foot Supplementary Table 4. Therefore, study participants with a more severe neuropathy on clinical examination showed greater loss of sensation on QST parameters.

IENFD did not correlate with the sensory sum score Supplementary Table 3. There were no significant correlations between BPI pain severity and IENFD, time from injury or QST Supplementary Tables 3 and 4. IENFD was negatively correlated with heat pain threshold recorded from both the hand and foot.

This suggests that participants with lower IENFD were more sensitive to heat. Time from injury to assessment was positively correlated with mechanical detection threshold. This suggests that participants with poorer light touch sensitivity had sustained their cold injury more recently.

those participants in whom a longer period of time has elapsed have less severe deficits. Spearman correlations. We have, for the first time, undertaken detailed neurological evaluation of patients with chronic NFCI defined as sensory symptoms usually pain in the extremities lasting at least 3 months after cold exposure.

We report that the pain is neuropathic in origin and is due to the development of a sensory neuropathy of the extremities. There has been conflicting evidence in the literature as to whether chronic NFCI is associated with a peripheral neuropathy. Studies have been hampered by a lack of clarity in terms of case definition and small study size Namer et al.

Persistent sensory symptoms pain, numbness, altered thermo-sensation and paraesthesia are the predominant cause of disability in patients with chronic NFCI. A number of our findings demonstrate that chronic NFCI is a sensory neuropathy.

In all of the participants there were sensory findings, most commonly impaired pin-prick sensibility in a symmetrical glove and stocking distribution and, in the more severe cases, impaired vibration sense and proprioception.

Ankle jerks were absent in only a minority of patients. There was a significant positive correlation between pain severity and neuropathy severity as elicited by deficits on clinical examination. In addition, there was a significant negative correlation between the time that had elapsed between injury and assessment and neuropathy severity.

It is possible that NFCI may improve with time. However, a longitudinal study is needed to verify such an observation. Consistent with these clinical findings there were marked abnormalities on QST of the hands and feet in the form of hyposensitivity relating to thermal parameters mediated by small fibres including temperature detection, as well as hyposensitivity to stimuli activating large myelinated sensory fibres such as mechanical detection and vibration sense.

A small subset of patients demonstrated hypersensitivity upon assessment of cold pain threshold or mechanical pain sensitivity. There was no significant correlation between QST findings and pain severity.

However, individual QST measures were related to IENFD and the time that had elapsed between injury and assessment. Heat pain threshold was negatively correlated to IENFD. This may indicate that in those with lower IENFD the remaining nociceptors are sensitized to heat with complex outcomes in terms of the final pain perception.

Mechanical detection threshold was positively correlated to the time that had elapsed between injury and assessment, thus the improvement in light touch sensitivity may be a surrogate for neuropathy recovery. It is plausible that in those patients who have severely impaired cold detection, the QST protocol may not be sufficiently sensitive to detect cold hypersensitivity.

We have used the DFNS database as a normative dataset for analysis of the QST data. This has advantages in terms of robust comparisons to a large gender- and age-matched control cohort. However, one potential disadvantage is that these normative data relate to Caucasians and many of the NFCI study participants are of African descent.

There have been few direct comparisons of QST from different ethnic groups. De Kruijf et al. In our experience, in a control Indian population unpublished data or mixed South American population von Bischhoffshausen et al. We do not feel, therefore, that such ethnic differences would be responsible for the large changes that we observed on QST.

A recent analysis of QST profiles in a large cohort of patients with peripheral neuropathic pain found that they could be broadly grouped into three clusters Baron et al.

The pattern of the QST profile in NFCI is distinct from small fibre neuropathy, given the involvement of large fibre modalities, and more closely resembles the pattern seen in diabetic neuropathy Supplementary Fig. Nerve conduction studies were normal and did not show a reduction in sensory nerve action potentials.

This seems a paradox given the clear sensory deficits described above. One potential explanation is that, given the superficial nature of NFCI, it is only the most distal sensory terminals that are affected, which are not interrogated by conventional neurophysiology.

This would also provide an explanation as to why ankle jerks were only absent in a minority of cases. Indeed a case report of NFCI sustained while mountaineering showed that the most marked changes were in the most distal segments of nerves that were either electrically stimulated on the dorsum of the foot or via activation of Pacinian corpuscles Carter et al.

When investigating potential NFCI the diagnosis of sensory neuropathy should not be discounted in the face of normal sensory nerve conduction studies. Additional investigations such as skin biopsy and QST should be performed. Furthermore, given that published normative data do not specify ethnicity and the majority of our patients were of West African or Caribbean ethnicity, we compared the IENFD in the NFCI cohort to healthy individuals of African American ethnicity and there was also a significant reduction.

These findings therefore confirm structural injury to small sensory nerve fibres predominantly nociceptors and thermoceptors that innervate the epidermis. IENFD was not related to time of injury from assessment, nor the clinical examination.

Therefore, histological assessment of small nerve fibres is helpful in confirming the diagnosis of NFCI, but does not relate to severity of neuropathy, pain nor clinical recovery in our cohort. The pain associated with NFCI was localized to the hands and feet and all study participants reported cold hypersensitivity.

Pain descriptors were typical for neuropathic pain and in all of our participants with chronic NFCI pain was either probably or definitely neuropathic in origin according to recently revised grading criteria Finnerup et al.

The cold hypersensitivity, which was reported by all participants and was also apparent on QST in a subset of patients, is a striking component of NFCI. One striking example is the cold pain induced by the chemotherapy agent, oxaliplatin, the sequel of which can be very reminiscent of NFCI for instance needing to wear gloves to remove objects from the fridge Ventzel et al.

The QST profiles for patients with NFCI and oxaliplatin-induced neuropathy are different Binder et al. Pain induced by NFCI was chronic and disabling. All participants had a change in employment status as a consequence of NFCI, usually due to their inability to tolerate a cold environment.

In addition, the chronic pain adversely affected their quality of life, a substantial impact in otherwise young and healthy individuals. The aetiology of NFCI has not yet been established. Our focus has been on neurological sequelae; however, abnormalities in vascular responsiveness to cold have also been reported in human NFCI Daanen, ; Golden et al.

Differences have also been noted in cold-acclimatized individuals versus non-acclimatized Daanen, It is striking that in some cases a single exposure to cold can lead to sensory afferent degeneration. Unlike frostbite, freezing does not occur in NFCI, so axon degeneration is not due to tissue disruption by ice crystals.

The vasoconstriction and vascular injury elicited by cold could have a role, for instance through causing ischaemia of axons Jia and Pollock, There have been attempts to develop preclinical animal models, for instance immersion of a limb in cold water, or exposure of a nerve trunk to cold.

It is not clear how well such models replicate human NFCI and reports that myelinated axons are particularly vulnerable are not consistent with the striking small fibre deficits that we found Nukada et al.

There are many factors that could contribute to the vulnerability of sensory afferents in NFCI. Many such afferents terminate superficially in skin in contrast to motor axons and they selectively express ion channels such as TRPM8 and TRPA1, which act as cold transducers Lolignier et al.

It has been shown in mice that the cold hypersensitivity resulting from oxaliplatin administration is subserved by enhanced responsiveness of TRPA1, the effect being abolished by administration of TRPA1 antagonists or TRPA1 deficiency Zhao et al.

However, one study in humans investigated the response to application of TRPA1 and TRPM8 agonists in individuals that had experienced NFCI and reported that there was no evidence of sensitization Namer et al.

Unlike other neuronal classes, nociceptors are activated by cold, which could potentially lead to excitotoxicity, as has been illustrated through the finding that sodium channel variants can lead to small fibre neuropathy Rolyan et al.

Nerve injury may bring about changes in the direct transduction of cold stimuli, but also in how resulting responses are modulated. For example the role of potassium currents in modulating the excitability of injured cold sensing neurons has been studied, recently, in a mouse model of neuropathic pain González et al.

Individuals of African ethnicity are particularly vulnerable to NFCI and the majority of participants in our cohort were African or Caribbean Burgess and Macfarlane, ; Nagarajan, The basis of this vulnerability is not yet clear. There are ethnic differences in vascular responses, for instance Africans show reduced cold-induced vasodilatation that may result in increased vulnerability to NFCI Daanen, ; Eglin et al.

There may be genetic differences in the complement of ion channels expressed in sensory neurons Kim et al.

Finally, there may be ethnic differences in the regenerative capacity of sensory neurons. For instance, following topical capsaicin treatment to the skin, sensory axon regeneration has been shown to be significantly slower in African Americans Polydefkis et al. All the patients that we reviewed experienced their injury while employed in the armed forces.

Armed service personnel may be particularly vulnerable to this form of injury because they are unable to remove themselves from the environment. None of our patients required surgical intervention and it is important to not only focus on tissue appearance or perfusion but also sensory symptoms when making an assessment of potential NFCI in the field.

Although all participants in the current study suffered from pain, it is possible that there are individuals who have acquired a small fibre neuropathy after cold exposure, but who do not experience pain.

Such individuals would not have been excluded, but none were referred. This may be because individuals with less distressing symptoms may not present or because such individuals are not referred. A prospective study may address this potential bias in recruitment.

Our finding that NFCI is a sensory neuropathy resulting in neuropathic pain enables the development of clear diagnostic criteria for chronic NFCI that can be applied to future prospective studies as well as being used in clinical practice.

Care pathways should be aimed at early recognition to prevent prolonged and repeated exposure, screening for neuropathic pain for instance using tools such as the DN4 questionnaire and finally provision of therapeutics targeting neuropathic pain. We would like to thank all the study participants.

We thank Dr John Scadding for his advice and guidance. We thank Dr Adrian Allsopp, Dr Daniel Roiz De Sa and Dr Rob Milner at the Institute of Naval Medicine, Alverstoke, Hampshire, UK for their assistance and advice.

We thank Dr Gabriele de Luca and Dr Olaf Ansorge for their assistance in the acquisition of the skin biopsy histology images.

This work was supported by grants from the UK Ministry of Defence and The Wellcome Trust. is a Senior Wellcome Trust Clinical Scientist ref. is supported by the International Diabetic Neuropathy Consortium IDNC research programme, and is an Honorary Research Fellow of the Brain Function Research Group, School of Physiology, Faculty of Health Science, University of Witwatersrand.

is supported by a grant from the UK Ministry of Defence. Neither the Wellcome Trust nor the UK Ministry of Defence played a role in the study design, patient recruitment, data analysis, data interpretation, or the preparation of the manuscript.

Supplementary material is available at Brain online. Baron R , Maier C , Attal N , Binder A , Bouhassira D , Cruccu G , et al. Peripheral neuropathic pain: a mechanism-related organizing principle based on sensory profiles.

Pain ; : — Google Scholar. Binder A , Stengel M , Maag R , Wasner G , Schoch R , Moosig F , et al. Pain in oxaliplatin-induced neuropathy—sensitisation in the peripheral and central nociceptive system.

Eur J Cancer ; 43 : — Bouhassira D , Attal N , Alchaar H , Boureau F , Brochet B , Bruxelle J , et al. Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire DN4.

Pain ; : 29 — Burgess JE , Macfarlane F. Retrospective analysis of the ethnic origins of male British army soldiers with peripheral cold weather injury. J R Army Med Corps ; : 11 — Buschbacher R , Orahlow N. Manual of nerve conduction studies.

New York, NY : Demos Medical Publishing ; Google Preview. Carter JL , Shefner JM , Krarup C. Cold-induced peripheral nerve damage: involvement of touch receptors of the foot.

Muscle Nerve ; 11 : — 9. Daanen HA. Finger cold-induced vasodilation: a review. Eur J Appl Physiol ; 89 : — de Kruijf M , Peters MJ , C.

Jacobs L , Tiemeier H , Nijsten T , Hofman A , et al. Determinants for quantitative sensory testing and the association with chronic musculoskeletal pain in the general elderly population.

Pain Pract ; 16 : — Denny-Brown D , Adams RD , Brenner C , Doherty MM. The pathology of injury to nerve induced by cold.

J Neuropathol Exp Neurol ; 4 : — Eglin CM , Golden FS , Tipton MJ. Cold sensitivity test for individuals with non-freezing cold injury: the effect of prior exercise. Extreme Physiol Med ; 2 : England JD , Gronseth GS , Franklin G , Miller RG , Asbury AK , Carter GT , et al.

Distal symmetric polyneuropathy: a definition for clinical research: report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation.

Neurology ; 64 : — Finnerup NB , Haroutounian S , Kamerman P , Baron R , Bennett DL , Bouhassira D , et al. Neuropathic pain: an updated grading system for research and clinical practice. Golden FS , Francis TJ , Gallimore D , Pethybridge R. Lessons from history: morbidity of cold injury in the Royal Marines during the Falklands Conflict of Blood flow slows in your outer extremities when your body is exposed to cold.

Nerve pain — especially in your hands and feet — increases as your circulation decreases. The change in barometric pressure — due to temperature drops — intensifies pressure on the nerves, which send pain signals to the brain.

Your perception of pain is increased as the nerve signals slow down because of the pressure. Also, soft tissues become firmer and tighten in the colder weather, thus resulting in painful muscle spasms.

Make sure to wear the winter essentials. A sturdy coat, hat, scarf, gloves and thick socks are helpful when going outside. These items will prevent your body heat from leaving and the cold temperatures from getting to you. Keep your body heated and covered to help blood flow and muscle stiffness.

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Signs and symptoms of peripheral neuropathy may include:. If autonomic nerves are affected, signs and symptoms may include:. Visit mayoclinic. org to read the complete article. If you suffer from any of these symptoms and would like to discuss a course of action call me at or contact me online here.

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