Medial plantar and dorsal sural nerve conduction studies increase the sensitivity in the detection of neuropathy in diabetic patients.

OBJECTIVE: Clinical utility of nerve conduction studies (NCS) of the medial plantar and dorsal sural nerves in the early detection of polyneuropathy have already been shown separately. However, at present, there is no data about the combined assessment of these two nerves in distal sensory neuropathy. In the present study, we aimed to evaluate the medial plantar and dorsal sural NCS in a group of diabetic patients with distal sensory neuropathy (DSN) and in healthy controls. METHODS: Thirty healthy and 30 diabetic adult patients were included. In all subjects, peripheral motor and sensory NCS were performed bilaterally with surface electrodes on the lower limbs including medial plantar and dorsal sural nerves. In addition, motor and sensory nerves were studied unilaterally on the upper limb. RESULTS: In all patients, nerve action potential (NAP) amplitudes of sural and superficial peroneal nerves were within normal ranges, but in the patient group mean value was significantly lower than in the controls. Among clinically defined 30 DSN patients, medial plantar NAP amplitude was abnormal in 18 (60%) and dorsal sural nerve amplitude was abnormal in 13 (40%) of the patients bilaterally. Additionally, the onset NCV of the dorsal sural nerve was significantly slower in patients than controls (P=0.038). Evaluation of both of these nerves increased the sensitivity up to 70% in the detection of neuropathy. CONCLUSIONS: Bilateral NCS assessment of both of the medial plantar and dorsal sural nerves together increases the rate of diagnosis of diabetic distal sensory neuropathy compared to assessment of either of these nerves. SIGNIFICANCE: Assessment of medial plantar in addition to dorsal sural NCS together increases the sensitivity in the detection of neuropathy and allows earlier diagnosis, especially when routine NCS are normal.     

Mononeuropathy multiplex associated with acute parvovirus B19 infection: characteristics, treatment and outcome

To describe the characteristics of peripheral neuropathy related to acute parvovirus B19 (B19V) infection. We reviewed clinical, electrophysiological and histological data of three patients with peripheral neuropathy and positive B19V detection (IgG, IgM and PCR) compatible with acute infection. The neuropathy fulfilled criteria for mononeuropathy multiplex (MM). It could be preceded by or concurrent with a limited purpuric eruption, but systemic manifestations were absent. The first neurological symptoms were always sensory and localized in a hand. Neuropathy was initially limited to a restricted sensory part of a nerve trunk territory. The course was subacute with successive and asymmetric injury of the limb and cranial nerves. Electromyographic study confirmed the diagnosis of MM with multifocal asymmetric sensory and motor axonal loss in two patients, whereas the neuropathy was purely sensory and limited to two nerves in the other patient. Nerve biopsies showed no evidence of necrotizing vasculitis but, in one patient, revealed a lymphocytic perivascular infiltrate evocative of hypersensitivity vasculitis secondary to an infectious agent. Intravenous immunoglobulin (IVIg) was systematically administered. Long-term outcome was good but with incomplete sensory recovery and, for one patient, persistence of a functional disability. B19?V infection should be considered in the etiological assessment of MM, especially in the event of a progressive sensory disorder in the hands and a concomitant history of rash. IVIg may be an effective treatment for this inflammatory disorder.     

A case report of the compression syndrome due to hypertrophic neuropathy

We reported a case of hypertrophic neuropathy of adult onset. The pathological change in the sural nerve was decreased axonal population with onion-bulb formation. On examination, there were enlarged nerve on palpation and she was found to have distal muscle atrophy, weakness and sensory loss. The deep tendon reflexes of extremities were weak. The first clinical feature of this patient was mainly polyneuropathy. The lower limbs were slightly spastic and plantar responses were extensor bilaterally. There was also sensory level at C6 level. After 1.5 years from first examination, she had shown myelopathy. Magnetic resonance imaging (MRI) of the spine showed marked thickening of the nerve roots and it revealed the compression of the spinal cord by enlarged nerve roots from C2 to C6 level. The compression syndrome of the patients with hypertrophic neuropathy was unclear at the onset in this case. MRI study of the spinal cord would be very beneficial to disclose subclinical myelopathy associated with hypertrophic neuropathy, as indicated in this report.     

Quantitative pathology of cutaneous nerve terminal degeneration in the human skin

Pathological diagnosis of neuropathy has traditionally depended on ultrastructural examinations of nerve biopsy specimens, particularly for sensory neuropathies affecting unmyelinated and small-myelinated nociceptive nerves. These sensory nerves terminate in the epidermis of the skin, and the pathology of neuropathy usually begins from nerve terminals. We investigated the feasibility of diagnosing small-fiber sensory neuropathy by evaluating cutaneous innervation. Skin biopsy specimens of 3-mm in diameter were obtained from the distal leg and the distal forearm of 55 healthy controls and 35 patients with sensory neuropathy. In the healthy controls, conventional intraepidermal nerve fiber densities (IENF densities) as measured using the image analysis system in the distal forearm and in the distal leg were correlated (r=0.55, P<0.0001), with significantly higher values in the distal forearm than in the distal leg (17.07+/-6.51 vs 12.92+/-5.33 fibers/mm, P<0.001). Compared to IENF densities of healthy controls, these values of neuropathic patients were significantly reduced in the distal forearm (5.82+/-6.50 fibers/mm, P<0.01) and in the distal leg (2.40+/-2.30, P<0.001). We further explored the possibility of quantifying skin innervation by counting "ocular intraepidermal nerve fiber density" (ocular nerve fiber density) with no aid of an image analysis system. This was based on the fact that the epidermal length on specifically defined sections was very close to the predicted epidermal length of 3 mm, the diameter of skin punches (P=0.14). Ocular nerve fiber densities were significantly correlated with IENF densities as measured by the image analysis system (r=0.99, P<0.0001). Dermal nerve fibers of neuropathic patients either disappeared or became degenerated. These findings were consistent with the notion of early terminal degeneration in neuropathy, and will facilitate quantitative interpretation of epidermal innervation in human neuropathy.     

Electrophysiological studies in diabetic neuropathy

In 30 patients with diabetic neuropathy sensory potentials in the median nerve, motor conduction in the lateral popliteal and median nerves, and electromyographic findings in distal and proximal muscles were compared with the severity of symptoms and signs. All patients had abnormalities in at least one of the electrophysiological parameters. The sensory potentials were the most sensitive indicator of subclinical involvement; abnormalities were found in 24 patients, 12 of whom had no sensory symptoms or signs and five of whom had no other clinical or electrophysiological evidence of neuropathy in the upper extremities. This indicates that sensory nerve fibres may be affected before motor. The next most sensitive parameter was the presence of fibrillation potentials, found in more than half the distal muscles examined. Slowing in motor conduction in the lateral popliteal nerve was the only electrophysiological change correlated to the severity of the neuropathy, and no other electrophysiological parameter was correlated to the duration or the severity of the neuropathy or the diabetes. An onset of neuropathy before or simultaneously with the manifestations of the diabetes, as well as the frequent occurrence of asymptomatic changes in sensory conduction, support the evidence at hand that the neuropathy develops concomitantly with and as an integral part of the metabolic disturbance rather than as a consequence of the vascular complications of diabetes. Of three patients with clinical signs or symptoms of a diabetic amyotrophy, two had asymptomatic electrophysiological abnormalities in distal nerves and muscles, consistent with widespread involvement of the peripheral nerves. The third patient had electromyographic changes in the medial vastus muscles suggestive of a myopathy. Motor and sensory conduction in distal and proximal nerves were normal.     

Peripheral neuropathy in multiple sclerosis: a clinical and electrophysiologic study

Peripheral nerve abnormalities are uncommon in multiple sclerosis (MS). When present, they are usually attributed to factors associated with advanced disease, such as malnutrition or cytotoxic drugs. We prospectively evaluated 22 mildly disabled MS patients with sensory complaints for evidence of neuropathy using the Neuropathy Symptom Score (NSS), clinical examination, and electrophysiologic studies of peripheral nerves. Distal latency, F-wave response, and nerve conduction velocity (NCV) and amplitude in the ulnar, median, tibial, peroneal and sural nerves were examined. Neuropathy was recorded if electrophysiologic abnormalities were detected in at least two peripheral nerves in the same patient. The most frequent electrophysiologic abnormalities noted were prolonged F-wave response and low motor amplitude in the peroneal nerve, slow sensory conduction velocities of the ulnar and sural nerves, and prolonged distal latencies in the sensory ulnar and sural nerves. Electrophysiologic abnormalities were found in 33 of 244 nerves examined (14.7%) and occurred in 10 patients (45.5%). Neuropathic symptoms were mild and did not correlate with electrophysiologic abnormalities. Age, disease duration, disease course and neurologic disability as evaluated by the Kurtzke Expanded Disability Status Scale, were not associated with the presence of neuropathy. Our findings indicate a high frequency of sensory-motor neuropathy in a selected group of MS patients.     

Chronic ischemic monomelic neuropathy from critical limb ischemia

OBJECTIVE: To describe the peripheral neuropathy resulting from chronic and critical arterial leg ischemia. METHODS: The authors evaluated 19 patients on entry to a gene therapy treatment trial for chronic and critical leg ischemia. Measurements included medical history, examination, neurologic symptom (NSS) and neurologic examination (NES) scores, motor and sensory nerve conduction studies, and quantitative sensory testing. The critically ischemic leg was compared with the less affected contralateral limb. RESULTS: All patients experienced pain from skin ulceration or vascular claudication, but many also had rest pain (58%), numbness (58%), burning (42%), and paresthesias (37%) in the ischemic foot that were consistent with peripheral nerve ischemia. Only three patients (16%) were free of neuropathic symptoms. The most common asymmetric neurologic signs included hypalgesia (74%), toe weakness (64%), hyperesthesia (63%), and pallanesthesia (53%) in the distal leg. NSS and NES were more abnormal in the critically ischemic leg, as were distal motor, total motor, and sensory examination subscores (p < 0.01 for each). Sural sensory potentials were reduced or absent, frequently on both sides. The symptomatic limb had reduced tibial motor amplitudes and increased thermal (cold) sensory thresholds (p < 0.01 for both) whereas the distal latencies, conduction velocities, and vibration thresholds were similar in the two legs. CONCLUSIONS: There is a predominantly sensory neuropathy associated with chronic and critical limb ischemia. Neuropathic symptoms are often obscured by the effects of ischemia on other tissues. The neurophysiologic changes suggest that the underlying pathophysiology is a distal axonopathy affecting nerve fibers of all sizes. Measures of blood flow in the leg correlate with neurologic symptom scores, examination scores, and electrophysiologic testing.     

Neurophysiologic parameters and symptoms in chronic renal failure

We studied: (1) the sensitivity of various neurophysiologic parameters in the diagnosis of uremic polyneuropathy, (2) the relationship between subjective symptoms and neurophysiologic parameters, and (3) the effect of a single hemodialysis on the neurophysiologic parameters in 21 patients undergoing hemodialysis. The following parameters were studied: sensory and motor nerve conduction, including F-wave parameters; vibration detection thresholds; and thermal thresholds. The clinical findings and subjective symptoms were studied using a standardized questionnaire. The most sensitive parameters in the diagnosis of uremic neuropathy were F-wave parameters from lower limbs, vibration detection thresholds from the feet, and the sural nerve sensory action potential amplitude. The nerves from the upper extremities on the side of the fistula should not be used in the diagnosis of uremic polyneuropathy due to numerous mild local nerve lesions. The positive neuropathic symptoms correlated with quantitative vibratory detection thresholds and sensory nerve conduction studies, especially the amplitude of the sensory nerve action potential in the sural nerve. We found no significant change in any of the neurophysiologic parameters following a single hemodialysis session.     

Hereditary motor and sensory neuropathy-russe: new autosomal recessive neuropathy in Balkan Gypsies

A novel peripheral neuropathy of autosomal recessive inheritance has been identified in Balkan Gypsies and termed hereditary motor and sensory neuropathy-Russe (HMSN-R). We investigated 21 affected individuals from 10 families. Distal lower limb weakness began between the ages of 8 and 16 years, upper limb involvement beginning between 10 and 43 years, with an average of 22 years. This progressive disorder led to severe weakness of the lower limbs, generalized in the oldest subject (aged 57 years), and marked distal upper limb weakness. Prominent distal sensory loss involved all modalities, resulting in neuropathic joint degeneration in two instances. All patients showed foot deformity, and most showed hand deformity. Motor nerve conduction velocity was moderately reduced in the upper limbs but unobtainable in the legs. Sensory nerve action potentials were absent. There was loss of larger myelinated nerve fibers and profuse regenerative activity in the sural nerve. HMSN-R is a new form of autosomal recessive inherited HMSN caused by a single founder mutation in a 1 Mb interval on chromosome 10q.     

Chronic Progressive Inflammatory Demyelinating Polyneuropathy In Childhood: Clinical And Electrophysiological Features

Chronic inflammatory demyelinating neuropathy (CIDP) occurring in childhood is rare and the diagnosis in indolently progressive cases may be difficult. We report 7 children (age 8–12 years) with insidiously progressive weakness and atrophy (in 3 cases) predominantly involving the lower limbs and mimicking a genetically determined neuropathy. Family history was negative in all cases. Numbness and paresthesias were present in 1/7 and mild sensory signs in 3/7 patients. Motor conductions were slowed in at least two nerves in 6/7, distal motor latencies prolonged in 4/7 and F waves delayed in 6/7 children, but these findings, although characteristic of a demyelinating neuropathy, did not help in the differential diagnosis with an inherited disorder. The following features documenting focal and non-uniform nerve conduction abnormalities indicated an acquired demyelinating disorder: 1) abnormal terminal latency index in at least one nerve in 5/7 children, 2) conduction block (reduction of proximal CMAP area> 50%) in at least one nerve in 5/7 children, 3)> 10 m/s conduction velocity difference among nerves of upper limbs or nerves of lower limbs in 4/7 children, 4) abnormal median sensory in presence of normal sural sensory conduction in 3/7 children. CSF protein concentration was increased in 5/7 (59–120 mg/dl). One patient had a self-limited course and recovered spontaneously in 10 months. Three children had a monophasic course, improved with steroids and had little or no residual disability. The remaining three with the longest disease duration before diagnosis (>2 years) improved with steroids but showed some residual distal weakness and atrophy and two developed foot deformities. Three children had at least one relapse at steroid tapering or discontinuation. Because of therapeutic implication the possibility of a CIDP occurring in childhood should always be kept in mind. An extensive electrophysiological study searching for indicators of non-uniform nerve conduction abnormalities may suggest the diagnosis in most cases. When the diagnosis is doubtful and genetic studies are negative we recommend a therapeutic trial of steroids for at least four weeks.     

多灶性运动神经病的临床特征及治疗

目的:分析多灶性运动神经病(MMN)的临床特征及治疗方法。方法:回顾性分析24例多灶性运动神经病患者的临床资料。结果:24例MMN表现为进行性、非对称性肢体运动无力,以远端为重,伴或不伴感觉障碍。部分患者抗-GM1抗体滴度升高。10例应用激素治疗,8例无效;20例应用免疫球蛋白(IVIg)治疗,15例有效。结论:MMN是一种以运动神经受累为主的不对称性周围神经病,临床症状和体征是诊断MMN的基础,免疫学检查发现抗-GM1抗体滴度升高支持诊断,但与临床症状和体征并非完全相关,免疫球蛋白(IVIg)治疗有效。     

Coexistence of Charcot‐Marie‐Tooth disease type 1A and anti‐MAG neuropathy

At age 35, a man with a genetic diagnosis of Charcot‐Marie‐Tooth disease type 1A (CMT1A) but no family history of neuropathy and no clinical symptoms developed rapidly progressive loss of balance, distal limb numbness, loss of manual dexterity, and hand tremor. Five years later, he walked with support and had mild pes cavus, marked sensory ataxia, severe leg and hand weakness, absent deep tendon reflexes (DTRs), severe sensory loss, and hand tremor. He had dramatically reduced motor nerve conduction velocity (MNCV), strikingly prolonged motor distal latencies, absent sensory action potentials and lower limb compound muscle action potentials. CMT1A duplication was reconfirmed but the dramatic change in his clinical course suggested a superimposed acquired neuropathy. An IgM‐kappa monoclonal gammopathy of uncertain significance (MGUS) with high titer anti‐myelin associated glycoprotein (anti‐MAG) activity was found. Nerve biopsy showed severe loss of myelinated fibers with onion bulbs, no evidence of uncompacted myelin, and few IgM deposits. Rituximab was given and he improved. It is very likely that this is a chance association of two rare and slowly progressive neuropathies; rapidly worsening course may have been due to a “double hit”. Interestingly, there are reports of possible superimposition of dysimmune neuropathies on hereditary ones, and the influence of the immune system on inherited neuropathies is matter for debate.     

Clinical,electrophysiological and magnetic resonance findings in a family with hereditary neuropathy with liability to pressure palsies caused by a novel PMP22 mutation

Hereditary neuropathy with liability to pressure palsies (HNPP) is a disorder mainly caused by a 1.5-Mb deletion at 17p11.2-12 (and in some rare cases by point mutations) and clinically associated with recurrent painless palsies. Here, we performed electrophysiological (motor, sensory and terminal latency index), MRI and genetic studies in a family referred for ulnar neuropathy with pain.Surprisingly, we found typical neurophysiological features of HNPP (prolongation of distal motor latencies and diffuse SNCV slowing with significant slowing of motor nerve conduction velocities). Besides, the proband presented conduction block in left ulnar, left median and both peroneal nerves. MRI findings were consistent with an underlying neuropathy. Molecular studies identified a novel frameshift mutation in PMP22 confirming the diagnosis of HNPP.Our data suggest that neurophysiological studies are essential to characterize underdiagnosed HNPP patients referred for peripheral neuropathy. Our experience shows that MRI could be a complementary tool for the diagnosis of these patients.     

Multifocal acquired demyelinating sensory and motor neuropathy: report of a case and review of the literature

Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is characterized by an asymmetric multifocal pattern of motor and sensory loss, and conduction block and other features of demyelination in nerve conduction studies. MADSAM neuropathy needs to be differentiated from chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). In classic CIDP, there are symmetric proximal and distal weakness, sensory deficit in both upper and lower extremities and reduced deep tendon reflex. In MMN, limb weakness without sensory loss is asymmetric in the distribution of individual peripheral nerves and the weakness typically begins in the distal upper extremities. We report one patient with chronic progression of asymmetric numbness and weakness in four extremities. MADSAM neuropathy was diagnosed after extensive clinical and laboratory evaluations. It is very important to distinguish between CIDP, MADSAM neuropathy, and MMN by clinical, laboratory, and histological features because of different effective therapeutic strategies.     

Electrophysiological findings in immune checkpoint inhibitor-related peripheral neuropathy

ObjectiveTo report the electrodiagnostic features of immune checkpoint inhibitor (ICI)-related neuropathy.MethodsWe retrospectively reviewed clinical presentations and electrodiagnostic features of 23 patients studied after receiving immune checkpoint inhibitors (ICIs). The presentations for electrodiagnostic evaluation included an acute neuropathy or neuromuscular junction disorder. We applied established electrodiagnostic criteria for polyneuropathy and acute demyelinating neuropathy.ResultsWe identified acute demyelinating neuropathy (13 cases), axonal sensory motor neuropathy (5), pure sensory neuropathy (4) and mononeuropathy (1). 13 patients had acute demyelinating neuropathy confirmed by demonstrating demyelination in 2 or more nerves; 3 additional patients had demyelination in only one nerve. Analysis of motor nerve conduction parameters revealed demyelination involving median and ulnar nerve distal motor latencies as well as median, ulnar and peroneal nerve conduction velocities. Conduction block was found in median, ulnar and peroneal nerves. The remaining one-third patients without demyelination had acute painful axonal neuropathy. Coexisting myopathic changes (6) and neuromuscular junction dysfunction (4) were also identified.ConclusionsOur findings suggest that, while immune-mediated motor nerve demyelination is the primary underlying mechanism of ICI-related neuropathy, axonal painful neuropathy can also be an important presentation. Early recognition and effective intervention may reduce morbidity and permanent disability.SignificanceElectrophysiological studies might be useful in the evaluation of ICI-related neuropathy.     

Skin denervation in vasculitic neuropathy

BACKGROUND: Skin denervation in vasculitic neuropathy has rarely been documented despite frequent manifestations of small-fiber neuropathy including reduced sensitivity and neuropathic pain. Recently, skin biopsy has been established as a new approach to diagnose small-fiber sensory neuropathy. OBJECTIVES: To investigate the pathologic features of cutaneous nerves and to evaluate inflammatory vasculopathy in the skin of patients with vasculitis. DESIGN: Case series. SETTING: National Taiwan University Hospital, Taipei.Patients Six patients with vasculitic neuropathy. INTERVENTIONS: Patients had 3-mm punch biopsy specimens taken from the distal part of the leg (without active vasculitic lesions) and a sural nerve biopsy specimen was taken in addition to detailed neurologic examinations, laboratory investigations, and nerve conduction studies. MAIN OUTCOME MEASURES: Results of nerve conduction studies, epidermal nerve fiber density studies, and immunohistochemistry. RESULTS: All 6 patients had combined large- and small-nerve-fiber involvement on the neurologic examinations. Nerve conduction studies showed a pattern of axonal neuropathy or mononeuropathy multiplex. Epidermal nerve fiber densities were significantly reduced in the skin of all patients, consistent with concomitant small-fiber neuropathies. Perivascular infiltration by T cells and macrophages was demonstrated by immunohistochemistry. All patients experienced neurologic improvement in muscle strength and alleviation of sensory symptoms after immunotherapy with corticosteroids, plasma exchange, or cyclophosphamide. CONCLUSIONS: Small-diameter sensory nerves are affected in vasculitis in addition to the well-known effect of vasculitis on large-diameter nerves. Significant inflammatory vasculopathy is present in the skin despite the absence of clinically active vasculitic lesions.     

Plasmapheresis in the treatment of ataxic sensory neuropathy associated with Sjögren's syndrome

Sj?gren's syndrome (SS) is an important but poorly recognized cause of peripheral neuropathy. Several forms of peripheral nerve dysfunction occur, including trigeminal sensory neuropathy, mononeuropathy multiplex, distal sensorimotor polyneuropathy and pure sensory neuronopathy. The pathological findings vary and the definite treatment is not known. Here we present 4 cases of acute ataxic sensory polyneuropathy with SS, and the experience of treatment with plasmapheresis (PP). The 4 patients were all females; ages ranged from 30 to 58 years. All had prominent loss of kinesthetic and proprioceptive sensation. The course ranged from acute to subacute onset. Patients were treated with 5-9 sessions of PP. Two patients with initiation of treatment within 2 weeks of onset showed dramatic and sustained responses after PP, while the other 2 had no detectable effects. Our experience showed that PP should be considered in patients who present with sensory neuropathy associated with SS, and the treatment should be given as early as possible.     

Degeneration of nociceptive nerve terminals in human peripheral neuropathy

Patients with peripheral neuropathy have symptoms involving small-diameter nociceptive nerves and elevated thermal thresholds. Nociceptive nerves terminate in the epidermis of the skin and are readily demonstrated with the neuronal marker, protein gene product 9.5 (PGP 9.5). To investigate the pathological characteristics of elevated thermal thresholds, we performed PGP 9.5 immunocytochemistry on 3 mm punch skin biopsies (the forearm and the leg) from 55 normal subjects and 35 neuropathic patients. Skin innervation was evaluated by quantifying epidermal nerve densities. Epidermal nerve densities were reduced in neuropathic patients compared to normal subjects. Epidermal nerve densities were variably correlated with thermal thresholds. The proportion of neuropathic patients with reduced epidermal nerve densities was larger than the proportion of neuropathic patients with elevated thermal thresholds. These results indicated that degeneration of epidermal nerve terminals preceded the elevation of thermal thresholds. Skin biopsy together with immunocytochemical demonstration of epidermal innervation offers a new approach to evaluate small-fiber sensory neuropathy.     

Interrelationship among nerve conduction velocity, amplitudes of compound muscle and compound nerve action potentials in diabetic neuropathy]

In order to clarify the relationship among amplitudes of compound nerve action potential (CNAP), compound muscle action potential (CMAP) and nerve conduction velocity parameters, data of nerve conduction studies were analyzed in 102 patients with diabetes mellitus. In motor conduction studies CMAP amplitudes after stimulations at the distal nerve trunk, and the polyneuropathy index (PNI), a mean percentage of normal for 12 indices from 4 nerves concerning to the velocity or long distance latency, were evaluated. CNAP was recorded in the median and ulnar nerves from an intrafascicularly inserted microelectrode at the elbow after wrist stimulation. CMAP amplitudes were high in the median and ulnar nerves, and were reduced in the tibial and peroneal nerves. A close relationship was found between PNI and CNAP amplitudes. Among CMAP amplitude parameters tibial nerve, not median or ulnar nerves, had a good correlation with PNI and CNAP amplitude. Along with the progression of diabetic neuropathy, neuropathic signs or symptoms become conspicuous, and nerve conduction velocity drops as is expressed by the PNI level, which reflects the change in nerve conduction velocity in the upper and lower limbs. At the same time CNAP amplitude or CMAP amplitude in the tibial nerve decreases, but in nerves of the upper limb CMAP amplitude doesn't always decrease. So, tibial nerve is best among CMAP amplitude parameters in evaluating the degree of diabetic neuropathy. It is necessary to judge the degree of diabetic neuropathy after due consideration of these facts.     

Electrophysiological findings of peripheral neuropathy in newly diagnosed type II diabetes mellitus

This study was aimed at assessing the electrophysiological signs of peripheral neuropathy in diabetes mellitus (DM) type II patients at diagnosis. Nerve conduction studies (NCS) of median, ulnar, peroneal, tibial and sural nerves were performed in 39 newly diagnosed DM subjects and compared to those of 40 healthy controls. Metabolic indices were also investigated. Electrophysiological alterations were found in 32 (82%) of the DM patients, and more than half of them (62.2%) showed multiple (two to five) abnormal parameters. Because most of the subjects (84.4%) had from two to five nerves involved, these alterations were widespread in the seven nerves evaluated. Forty-two percent of the patients had NCS alterations suggestive of distal median mononeuropathy, implying that metabolic factors in DM make the median nerve more susceptible to focal entrapment. A reduced sensory nerve action potential (SNAP) amplitude was observed in the median nerve in 70% of the patients, in the ulnar in 69% and in the sural nerve only in 22%. In the presence of a decrease in the SNAP amplitude of the ulnar or median nerve, the SNAP amplitude of the sural nerve was normal in 82 or 80% of the subjects, respectively. This finding may be in keeping with a distal involvement of the sensory fibres, as explored by routine median or ulnar NCS. No correlation was found between metabolic indices and NCS parameters. In conclusion, a high percentage of newly diagnosed DM patients show signs of neuropathy, and upper limb nerve sensory NCS seem to be more sensitive in detecting it than lower limb NCS.