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The neurological symptoms and signs appear when the nerve injury involves the axons, and this is often some days after the beginning of the pain depending on the aetiology of the injury and the speed of progression. For the somatotopical organization of the peripheral and central nervous systems, all neuropathic pains are perceived within the innervation territory of the damaged structure.

A neuro-anatomical distribution of pain and sensory alteration supports the diagnosis [ 23 ] that relies on the medical history and bedside examination. The evaluation aims at correlating sensory, motor and autonomic signs with the detailed medical history. Electromyography, nerve conduction studies, evoked potentials, infrared tele-thermography and quantitative sensory testing support the clinical diagnosis allowing better definition of nerve fibres or central sensory pathways involved.

In plexo pathy, pain might be a medical emergency by itself, before neurological signs appear. In the acute polyradiculoneuropathy, pain might shortly herald the explosion of the disease and it is typically localised in the back, coinciding with the anatomical location of the affected rootlets. At times nociceptive nerve pain and neuropathic pain coexist and last together for a long time. In carpal tunnel syndrome there is often a combination of focal nociceptive pain in the wrist, and neuropathic projected sensory disturbances and pain in the fingers.

Radiculopathy in spondyloarthritis also often combines nerve trunk pain in the back and neuropathic pain in the radicular sensory territory.

Lumbosacral Plexopathy – Causes and Management

In contrast, in peripheral neuropathy associated with leprosy the axonal damage usually causes painless sensory loss, while the pain is nociceptive, due to the combination of nerve inflammation and entrapment.

A comprehensive epidemiology of painful peripheral neuropathies is not yet available [ 56 ], although, as a whole, pain is a relevant problem in peripheral nerve diseases and injury, because of its frequency and resistance to treatment.

There is information on prevalence and incidence of some peripheral nerve diseases; however, the same neuropathy may be painful in some cases and painless in others. The most common painful neuropathies are diabetic neuropathy and postherpetic neuralgia, for which epidemiological data are available [ 7 , 33 , 49 ].

In describing the clinical classification of painful peripheral neuropathies we begin with hereditary neuropathies, which are seldom painful but are of great interest because they allow a correlation between the involvement of selective nerve fibres and the presence of pain. In most of the cases, they evolve slowly over many years, with a severity ranging from mildly disturbing to invalidating.

As a group, hereditary neuropathies are common disorders, and likely many patients affected by mild forms remain undiagnosed [ 46 ]. Hereditary neuropathies may affect predominantly motor fibres, or sensory and motor fibres or sensory and autonomic fibres. The genetic abnormality may involve primarily the myelin or the axon.

The chief complaint in hereditary sensory-motor demyelinating neuropathies is usually weakness. Patients also complain of numbness that is a positive sensory phenomenon originating from spontaneous large fibres activity. Sensory loss preferential for low threshold mechanical stimuli is more often a clinical finding than a spontaneous complaint.

Sensory demyelinating neuropathies provide clinical evidence against the inhibitory role of large peripheral nerve afferents proposed by the gate control theory. In demyelinating sensory neuropathies small fibres are spared, and there is no loss of pain sensation.

Contrary to what one would have expected if activity in large fibres had inhibitory effect on small fibres input, there is not spontaneous pain or hyperalgesia. The few hereditary polyneuropathies that are painful primarily affect small fibres.

The hereditary sensory and autonomic neuropathies with abnormality in the axonal structure are subdivided in five groups.

In these severe unmyelinated axonal neuropathies there is insensitivity to pain and major dysautonomia, often incompatible with survival. The hereditary sensory and autonomic neuropathy type II shows clinical symptoms in the infancy, there is loss of pain and warm sensation to such extent that hands, feet and tongue are at risk of spontaneous or traumatic mutilation. In this neuropathy, spontaneous pain is not a chief complaint. In the hereditary sensory and autonomic neuropathy type I, which has clinical manifestation of small fibres sensory loss, leading to cutaneous ulcers and spontaneous stress fractures around the second decade of life, severe lancinating pain is the main complaint.

Thus, the hereditary small fibres sensory neuropathy is painful in adults, but not in neonates, a condition rekindling the effects of capsaicin treatment in neonates and adult mice [ 53 , 25 ].

Small sensory and autonomic fibres are affected in other hereditary diseases in which the genetic abnormality leads to accumulation of substances in or around small neurons of sensory and autonomic ganglia.

Accumulation of glycolipids causes association of kidney, myocardial, and brain disease. It is a painful small fibres neuropathy developing in childhood or adolescence. Lancinating burning pains are intensified by exertion, and hot environment likely related to a state of hyperalgesia to those stimuli. There is concomitant loss of autonomic fibres causing anhydrosis, impaired saliva and tear formation, decreased intestinal mobility and hypotension. The presence of severe burning pain with causalgic quality in people with complete loss of autonomic fibres provides also a case against a role of the sympathetic system in contributing to the pain, at least in this population of patients.

Familial amyloid neuropathy is a group of autosomal dominant disorders with extracellular deposition of amyloid in peripheral nerves and other organs. Amyloid is composed by many different types of fibrillar proteins [ 17 ]. The classification of amyloidosis, which was previously based on the clinical presentation, now relays on the protein composition and molecular genetics. The original description of familiarity was made in Portugal Andrade.

In this neuropathy a mutation of the plasma protein transthyretin is found. It is the most common form of familial amyloidosis.

The neuropathy begins insidiously around the age of 30 — 40 combining sensory loss for warm and pain, and spontaneous lancinating pain. There is also autonomic dysfunction. Treatment with enzyme replacement therapy improves pain to the extent that other pain medications can be discontinued [ 54 ]. Porphyric neuropathy is also a painful hereditary disease, usually autosomal dominant with incomplete penetrance, and occasionally autosomal recessive, which affects peripheral nerves, central nervous system and also the gastrointestinal and cardiovascular systems.

In Porphyric neuropathy there is a defect of the heme synthesis resulting in excessive accumulation of porphyrins and their precursor.

The typical clinical presentation appears as episodes of abdominal pain, nausea, vomiting and severe constipation. There might be tachycardia and orthostatic hypotension.

Some patients may have epileptic seizures due to central nervous system involvement. The neuropathy may have the feature of a distal sensory neuropathy with proximal and asymmetrical muscle weakness. At times the sensory loss affects the trunk and proximal limbs.

Pain used to be explained as a symptom of dysautonomia. In reality pain anticipates signs and other symptoms of neuropathy, last for a few days, and improves when the neuropathy becomes clinically evident.

It is most likely a nociceptive type of pain due to ischemia of nerve trunks that ultimately causes the neuropathy. This also explains the quite frequent asymmetrical and proximal distribution of sensory motor signs, typical of a multiple mononeuropathy [ 57 ].

According to Moulin et al. Pain is of two kinds: the most common is stabbing deep dorsal of low back pain, radiating into the limbs. Half of the patients report dysesthetic extremity pain with burning or tingling quality; a smaller number of patients report joint and muscle pain. It is likely that the back pain at onset is of nociceptive type and it is related to the radicular inflammation, while the distal extremity pain is neuropathic.

The symptom of tingling originates from large myelinated fibres and when intense it may be defined as a dysesthesia. Joint and muscle pain could be of neuropathic origin due to ectopic activity in nociceptive afferents subserving these tissues. Ganglionopathies or sensory neuronopathies are conditions in which the primary target is the sensory ganglion.

The most common is caused by herpes zoster infection. Herpes zoster almost constantly causes an acute neuralgia at the onset of inflammation. The acute pain is mediated by nociceptive and neuropathic mechanisms. Neuropathic pain is projected into the innervation territory of the sensory ganglion; the nociceptive pain is felt deeply in the paraspinal location of the ganglion.

After recovery from the acute phase that happens within a few weeks, a long lasting neuropathic pain might take over. This pain, arising or persisting in areas affected by herpes zoster at least three months after healing of the skin lesion, has been defined as post herpetic neuralgia [ 50 ]. Post herpetic neuralgia may last for many years, sometimes for the whole life. It causes a most disabling pain that combines spontaneous and evoked pain.

The sensory examination reveals areas of major, even complete sensory loss and areas of increased sensitivity hyperalgesia or allodynia to many different stimuli, particularly light stroking and warming. Pain in the area of sensory loss is caused by deafferentation of second order neurons, while evoked pain is caused either by irritable nociceptors or by sensitisation of central afferents [ 18 ].

This observation supports the hypothesis that one disease causing peripheral nerve injury might cause pain through more than one mechanism.

Post herpetic neuralgia is easy to diagnose and has relatively high prevalence [ 22 ] among the different painful neuropathies; for this reason, post herpetic neuralgia is commonly studied in clinical trials on neuropathic pain.

The majority of paraneoplastic neuropathies are sensory, motor, axonal, or axonal and demyelinating polyneuropathies and they are seldom painful. Symptoms of paraneoplastic polyneuropathy often anticipate the symptoms of cancer.

When symptoms of polyneuropathy appear in patients with diagnosed cancer they are more likely caused by chemotherapy. The mechanisms producing nerve injury, and in particular neuropathic pain and sensory symptoms, are not clear. However, the severity of nerve damage appears to be directly proportional to drug dosage [ 2 , 9 , 12 , 29 ]. The widely used paclitaxel is known to provoke neuropathic pain and sensory dysfunctions mostly affecting hands and feet, related to a myelinated fibre neuropathy preferentially affecting the largest fibres, with sparing of C-fibres function at warm sensory testing [ 12 ].

Ascending distal paraesthesiae and dysesthesiae together with burning pain and allodynia to cold or mechanical stimuli in a stocking and glove-like distribution often appear after chemotherapy [ 62 ]. This finding of symptoms of small fibber neuropathy appearing in patients with predominantly large fibre sensory loss is contradictory with the evidence provided by the hereditary neuropathy that are painful when small fibre involvement prevail.

However, in isoniazid polyneuropathy, the sparing of small fibres is apparent and compulsive analysis of small fibre histogram shows a shift towards the left with increased number of small diameter axons, indicating loss of main small fibres and production of regenerating smaller sprouts [ 42 ]. In addition, there is no doubt that myelinated fibres are affected by chemotherapy because vibration, pin and cold perception are impaired. However, it is possible that small-fibre type of positive symptoms i.

In vincristine-induced polyneuropathy a small percentage of C-nociceptors respond in an exaggerated fashion to supra threshold heat stimulation [ 47 ].

Although modifications in threshold and spontaneous activity were not found in those cells, the finding supports a small-fibre generator of pain. Cisplatin causes mainly large fibre neuropathy leading more often to painless ataxia, and vincristine also causes large fibres sensory motor neuropathy. Pain caused by the use of these agents is relatively rare and has the quality of a muscle pain, and may be more related to a direct muscle toxicity [ 21 ]. Patients with pre-existing neuropathy of any kind are more prone to develop polyneuropathy while on chemotherapy [ 11 , 28 ], therefore, Sommer recommends to screen peripheral nerve function before initiating potentially neurotoxic chemotherapy [ 56 ].

Cancer patients often suffer also from painful invasion of peripheral nerves and plexus by cancer or from iatrogenic nerve injury,either due to radiotherapy or surgery [ 35 ].

Acute sensory polyganglionopathy is a rare autoimmune or paraneoplastic neuronopathy affecting sensory and autonomic ganglia. The most common cancer associated with acute polyganglionopathy is the small-cell lung cancer; in rare cases polyganglionopathy is associated with ovarian cancer, breast carcinoma or lymphoma.

The neuropathy causes major sensory loss for all sensory modalities with ataxia of lower and even upper limbs and loss of thermal sensation. Sensory loss rapidly involves the face and trunk, indicating direct neuronal cell involvement rather than axonal death. Pain is extremely intense, with stabbing and burning quality. Although paraneoplastic sensory neuropathy is related to an inflammatory, probably immune-mediated lesion of sensory neurons, usually it does not respond to plasma exchange, intravenous immunoglobulines, or immunosuppressants, but to the early treatment of the tumour [ 51 ].

Up to one third of patients with connective tissue disease develop a carpal tunnel syndrome , sometimes combined with a tenosinovitis. When these two conditions causing pain in the hand coexist, one of them may be missed. Connective tissue diseases are often associated with necrotising vasculitis of perineurial or endoneurial arterioles, and also with axonal damage due to secondary amyloidosis.

Lumbar and Sacral Plexus with Clinical Cases

The electromyographic findings in patients with vasculitic neuropathy show an axonal neuropathy of all fibres type, with the feature either of a symmetric polyneuropathy or asymmetric in patients with multiple mononeuropathy. Pain in inflammatory neuropathy may be the heralding symptom of vasculitis anticipating sensory motor symptoms and signs. Pain is also caused by axonal injury with altered distribution of sodium channels and increased release of inflammatory mediators in nerve fibres.

The expression of pro-inflammatory cytokines in peripheral nerves is increased in most vasculitic neuropathy [ 24 ] and in particular specimens from patients in whom pain is a prominent symptom [ 31 ].

Pain is at times severe; it has burning and stabbing quality, and is often associated with hyperalgesia and allodynia.

A sensory ataxia often complicates coexisting cerebellar deficits. Muscle strength is relatively spared. HIV infection causes several different types of peripheral nerve diseases, often superimposing one to the other in the same patient. At the time of death, 3 out of 4 HIV patients have a peripheral neuropathy, although clinical findings of polyneuropathy might be detected in about half to a third of the patients.

In the stage of seroconversion and early stages of the HIV disease, there is high incidence of inflammatory demyelinating polyradiculoneuropathy, multiple mononeuropathy and plexopathy with clinical features akin to the same diseases affecting non-HIV subjects.

In the advanced stages of the disease, the most common neuropathy is a distal axonal symmetrical mainly sensory polyneuropathy. A burning feet, with association of other painful and non-painful paraesthesiae is usually the symptomatic onset of this condition. The cause is unknown, and might include autoimmunity, nutritional deficiency, and drug toxicity. Direct viral invasion has never been proved. A recent study has reported that pain is a significant medical issue with a moderate-to-substantial impact on quality of life in some patients with diabetic neuropathy [ 19 ].

However, the definition of PDN does not take in account that there are several types of peripheral nerve damage in diabetic patients that can present as painful neuropathies.

The most common type of peripheral neuropathy in diabetic patients is the chronic distal symmetrical polyneuropathy [ 63 ] that is often associated to positive sensory symptoms, i. This condition represents the major source for PDN patients in clinical trials. However, several others types of painful nerve damage, with different medical history, clinical and neurophysiological examinations can be recognized in diabetic patients. In the pure form of small fibres neuropathy associated with diabetes, pain can be the major symptom being mainly distal in the lower limbs, long lasting, burning, shooting and unremitting, often combined with allodynia and hyperalgesia, alteration of thermal perception thresholds and autonomic dysfunctions.

Strength and reflexes are usually spared and sensory and motor conduction velocities and EMG remain within the normal range, generating sometimes diagnostic perplexity.

The clinical picture can be divided into an acute phase, lasting a few months, followed by a long phase of progressive pain reduction associated with impairment of small fibres function with hypaesthesia to cold, warm, and painful stimuli.

In rare cases, diabetic patients may complain of an extremely severe, diffuse neuropathic pain that can disrupt completely the life of the patient. Some authors refer to this neuropathy as diabetic neuropathic cachexia [ 16 ] or acute painful diabetic neuropathy [ 3 ]. At the beginning, the painful symptoms are localized in the lower extremities, later they spread to all the lower limbs, trunk, and hands, typically worsening at night.

The acute phase can last for a few months and then symptoms slowly subside in a time frame of 8—12 months. Treatment relays on aggressive glycemic control with insulin infusion, which provokes weight recovery and pain reduction. Acute nerve trunk pain is peculiar in the early phase of the painful lumbosacral radiculoplexus neuropathy [ 14 , 15 , 20 ], the focal and multifocal neuropathies [ 32 , 48 ] and the acute painful neuropathy precipitated by strict glycemic control [ 8 ].

All these forms of diabetic neuropathies are probably due to focal nerve ischaemia, thus combining a nociceptive origin for the pain in the beginning of the history to a typical neuropathic pain that takes place later on.

The painful lumbosacral radiculoplexus neuropathy is remarkable for the acute onset of a severe, often asymmetric, deep aching pain, localized proximally in the lower limb, subsequently associated with proximal weakness and wasting in the same area, without clear sensory loss.

Over time, the weakness may spread distally, sometime contra laterally and sensory loss often appears together with positive sensory symptoms [ 14 ]. From the beginning of the new millennium clinical research has been focused on neuropathy related to impaired glucose tolerance IGT.

The damage of peripheral nerve associated with IGT is described as a painful sensory neuropathy affecting primarily small calibre afferent fibres, associated with positive and negative sensory symptoms, typically located in the lower limbs [ 58 ]. In the early stages of the disease, tendon reflexes and muscle strength are spared, as well as EMG and nerve conduction studies. On the contrary, abnormalities in the sensory examination supported by quantitative sensory testing and intraepidermal nerve fibre density reveal the diagnosis.

In the clinical setting, it is crucial to identify the nociceptive and neuropathic components to quickly and effectively treat this painful complication of diabetes that may at times reach devastating intensity. The most common symptoms are cramps and restlessness in the legs. Dysesthesia may be present. Unfortunately many patients with renal failure do have coexisting diabetes and the combination of these two conditions might cause an unusually severe predominantly motor polyneuropathy with intense cramps.

Concluding remarks: Not long ago neuropathic pain was rarely diagnosed, and treatment often included invasive procedure with low yield and short lasting effects such as nerve blocks. The introduction of new more effective drugs has improved the management and also contributed to a better, although still far from optimal, understanding of pain mechanisms.

In many of the described peripheral nerve diseases pain is the most distressing symptom for the patient. Often it is the cause of seeking for medical help. Pain therapists should be aware of the most common neurological presentation of peripheral neuropathic pains to guarantee timely treatment of neuropathies in which pain is the heralding symptom. Peripheral nerve experts should take advantage of the improved understanding of pain mechanisms and the new available treatments to avoid needless suffering in patients with peripheral neuropathies.

The differential diagnosis between nociceptive and neuropathic components of the pain and a timely and fearless use of opioids might make the difference for controlling the most disabling pains of acute ganglionopathy and plexopathy.

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Many patients with small fibres neuropathy have dysautonomia with orthostatic hypotension and intestinal paresis. For lumbosacral plexopathy caused by compression such as eg, retroperitoneal hematomas , outcomes can be excellent but patients may have lingering symptoms. Similarly, for diabetic lumbosacral plexopathy, significant improvement with time occurs through some non-progressive deficits may remain.

In radiation-induced plexopathies, unfortunately, a slow but progressive loss of function is expected. Patients of plexopathy may be left with decreased function and an abnormal gait related to muscle weakness including foot drop. There could be sensory deficits [ insensate skin]. Chronic pain may also be present. Neoplastic plexopathy generally has a very poor prognosis when they are not resectable and resistant to radiotherapy. Needle electromyography may be used to monitor the progress.

Common Lumbosacral Plexopathies Retroperitoneal hemorrhage is most commonly seen in Complication of anticoagulation Hemophilia Aortic aneurysm rupture. Such hemorrhages usually are located within the psoas muscle itself, where they can compress the lumbar plexus. The presentation is of acute severe pain where the hip is flexed and slightly externally rotated.

The major neurologic deficit usually is in the femoral nerve territory, with the weakness of hip flexion and knee extension and a reduced or absent knee-jerk. However, the examination would reveal some dysfunction in the obturator or lateral femoral cutaneous nerve or both.

The treatment would depend on the cause but a decompression is almost always required. Mass Lesions Tumors from the bladder, cervix, uterus, ovary, prostate, colon, or rectum may compress the lumbosacral plexus leading to lumbosacral plexopathy. Lymphoma and leukemia can directly infiltrate nerves, even in the absence of a mass lesion on imaging studies. Aneurysms or pseudoaneurysms of the internal iliac or common iliac artery have been reported to compress the lumbosacral plexus.

In women, endometriosis can cause implantation of abnormal tissue on the plexus and cause compression. These lesions more often affect the lower lumbosacral plexus.

Endometriosis may result in intermittent symptoms but other lesions are usually slowly progressive. Idiopathic Lumbosacral Plexitis Idiopathic plexitis pathology is not completely known.

It is thought to be inflammatory, often occurring within a few weeks of a possible inciting immunologic event, such as a cold, flu, or immunization. There is a severe deep pain in the pelvis or in the upper leg.

It characteristically persists for 1 to 2 weeks but may last many months. Because both the upper and lower plexus may be involved leading to different patterns of weakness and sensory loss.A comprehensive epidemiology of painful peripheral neuropathies is not yet available [ 56 ], although, as a whole, pain is a relevant problem in peripheral nerve diseases and injury, because of its frequency and resistance to treatment.

Although many diseases have been reported as a cause of myoclonus 8 , only one recently reported a case of spinal myoclonus has been attributed to cervical herniated intervertebral disc HIVD. As the fibers that eventually form the peroneal division of the sciatic nerve lie posteriorly, closest to the bone, and are more vulnerable. The natural history of acute painful neuropathy in diabetes mellitus. Anesth Analg. At the time of death, 3 out of 4 HIV patients have a peripheral neuropathy, although clinical findings of polyneuropathy might be detected in about half to a third of the patients.

A recent study has reported that pain is a significant medical issue with a moderate-to-substantial impact on quality of life in some patients with diabetic neuropathy [ 19 ]. At times nociceptive nerve pain and neuropathic pain coexist and last together for a long time.