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PubMed1987

[Neuropathies and almitrine. 14 cases].

Previously reported cases of peripheral neuropathies occurring during almitrine therapy had only a few weeks follow-up after having stopped the drug. We have studied clinical and electrophysiological data 6 to 12 months after almitrine had been given up in 9 patients from a group of 14 whose epidemiologic, clinical, electrophysiological and pathological data had been registered. In 7 of them, without any chronic respiratory deficiency, almitrine was administered as almitrine bismésilate and raubasine, and in 7 others (6 with chronic respiratory deficiency) as almitrine bismesilate alone. In patients who had another possible cause of neuropathy, clinical disorders appeared after a lesser total quantity of almitrine (p less than 0.05). Clinical data were suggestive of sensory peripheral neuropathies of feet and lower third of legs. Electrophysiological data suggested distal axonopathy in spite of the absence of denervation: amplitudes of sensory potentials were reduced and nerve conduction velocities were moderately decreased. Biopsies revealed mild neurogenic atrophy of muscles and distal axonopathy. Clinical improvement was very slow and 6 to 12 months later, most of the patients still presented decreased vibration sense and ankle reflexes loss, but all of them were still improving. Amplitudes of sensory potentials and sensory nerve conduction velocities were significantly improved (p less than 0.05) but motor nerve conduction velocities were not (p greater than 0.05). Our study shows: 1) clinical, electrophysiological and pathological data similar to those previously reported; 2) subclinical disturbances of motor functions in lower limbs and sensory functions in upper limbs; 3) some patients presented with unusual signs: posture tremor (3 cases), painful legs and moving toes (1 case); 4) peripheral neuropathies may occur during almitrine therapy even in patients without any chronic respiratory insufficiency; 5) peripheral neuropathies occurred with lower doses in patients with other factors predisposing to neuropathies; 6) patients' improvement was very slow; 7) in 9 cases the imputability of these peripheral neuropathies to almitrine is plausible. We suggest not to prescribe almitrine without caution, especially in patients with other factors of neuropathy. Treatment should be regularly interrupted.

Aged↗
PubMed1985

Ulnar neuropathy at the wrist: case report and review of literature.

We present a case of pure motor ulnar neuropathy with sparing of the hypothenar muscles and a review of 55 published cases of ulnar neuropathy at the wrist in which the clinicoanatomic correlation was clearly delineated. We propose a classification of ulnar neuropathies at the wrist divided into five types based on clinical findings, electrophysiologic studies, and clinicoanatomic correlations. Type I: a mixed motor and sensory neuropathy, occurring just outside or within the proximal end of Guyon's canal. II: a pure sensory neuropathy, where the lesion involves the superficial branch of the ulnar nerve (UN) at the wrist but distal to the branch to the m. palmaris brevis. III: a pure motor neuropathy due to a lesion of the deep branch of the UN just distal to the superficial branch but proximal to the branch to the hypothenars. IV: a pure motor ulnar neuropathy with sparing of hypothenars; this lesion occurs on the deep branch of the UN distal to the origin of the superficial branch and distal to the branch going to the hypothenars. V: a distal motor neuropathy in which the lesion occurs just proximal to the branches going to the first dorsal interosseus and adductor pollicis muscles.

Adult↗
PubMed1981

Electrophysiologic and histologic studies in leprosy and some acrodystrophic neuropathies.

In vitro electrophysiologic and light microscopic studies were carried out on the sural nerve in six patients with non-leprous neuropathy with plantar ulceration and in six patients with various types of leprous neuropathy. In the non-leprous group (with congenital and acquired neuropathy) the abnormalities in the compound action potentials of the myelinated (large and small) fibers were usually more striking than those in the unmyelinated fibers potentials. In the leprous neuropathies, on the other hand, the three major fiber groups tended to be involved indiscriminately, the unmyelinated fiber potential being as liable to abnormality as the myelinated fiber potentials. Histologically the nerve fiber damage in the congenital neuropathies appeared to be moderate to gross involvement of the myelinated fibers without the prominent demyelination and degeneration/regeneration seen in leprosy and the other acquired neuropathies. Leprous neuropathy showed, besides fiber abnormalities, the simultaneous deleterious effects of inflammation and fibrosis. It is a matter for speculation whether disturbed conduction in the large myelinated touch-pressure mediating fibers contributes significantly to impaired pain perception (mediated by small fibers) and plantar ulceration in leprosy and other acrodystrophic neuropathies.

Action Potentials↗
PubMed1993

[3 cases of rare peripheral neuropathies associated with primary Gougerot-Sjögren syndrome].

Several forms of peripheral neuropathy occur in Sjögren's syndrome (dryness of eyes, mouth and other mucous membranes). Symmetrical sensorimotor polyneuropathy occurs most frequently followed by sensory neuropathy. Pure sensory neuronopathy, trigeminal sensory neuropathy and autonomic neuropathy are also common. We report three rare forms of peripheral neuropathy related to Sjögren's syndrome and analyze their clinical course and response to therapy. There were a case of mononeuropathy multiplex (MM), a case of recurrent cranial polyneuropathy (RCP) and a case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). The patients were females, 70, 63 and 81 years old respectively. All of them fulfilled the criteria of Sjögren's syndrome, without clinical or serological abnormalities of systemic disease. Only one patient presented with positive antinuclear antibodies. In two patients the onset of neuropathy occurred before the sicca syndrome long. The sural biopsy of the patient with MM exhibited vasculitis of the small vessels and a mild sensory polyneuropathy was superimposed. The patient with RCP had 8 episodes of isolated third nerve palsy and 5 episodes of multiple cranial neuropathy. The patient with CIDP responded poorly to treatment while in the patients with MM and CRP the response to corticotherapy was good. In conclusion, Sjögren's syndrome must be considered in neuropathies of unknown cause not only when they are sensory, autonomic or trigeminal but also when they are recurrent suggesting an ischemic mechanism. Even a CIDP requires a search for Sjögren's syndrome before being considered idiopathic.

Aged↗
PubMed1994

Thalidomide neuropathy incidence and clinico-electrophysiologic findings in 42 patients.

BACKGROUND AND DESIGN: Thalidomide therapy was shown to be effective in numerous dermatologic diseases. As reliable methods of contraception are now available, neurotoxicity has become the most important side effect limiting the use of thalidomide. The incidence of this neuropathy and its relationship to thalidomide doses are still matters of debate. In a retrospective study, we reviewed the files of 42 patients who had received thalidomide between 1987 and 1992 for various dermatologic diseases. The incidence and the conditions of occurrence of the neuropathy were analyzed. RESULTS: Evidence of a thalidomide-induced neuropathy was present in nine patients (21%), who had both clinical and electrophysiologic typical abnormalities. Twelve other patients (28%), however, presented with isolated clinical or electrophysiologic signs. Thus, the diagnosis of thalidomide neuropathy could not be affirmed. The occurrence of the neuropathy did not appear to be related to the daily dose nor to the duration of treatment. The highest risk of developing a thalidomide neuropathy was found in female and elderly patients. Two monozygotic twin sisters, who received thalidomide for Behçet's disease, both developed a neuropathy. CONCLUSIONS: These data suggest that the incidence of thalidomide neuropathy may be between 21% and 50%. Individual susceptibilities with possible genetic predisposition seem to be more important than daily dose and duration of thalidomide therapy.

Adult↗
PubMedDate not supplied

[Approach to the diagnosis and therapy of vascular neuropathy].

Peripheral neuropathy is a very common clinical manifestation of vasculitis syndromes which may present as an early sign of such neuropathy or else may be the only such sign as in the case of non-systemic vascular neuropathy. The clinical affectation of the neuropathy depends on the extent and course of the ischaemic changes brought on by vasculitis, with multineuritis being the most usual presenting form of vascular neuropathy. Neurophysiological studies show the extent and severity of the neuropathy and often identify subclinical affectation representing a mixed pattern of affectation with axomal predominance. Nerve biopsy is a prerequisite for diagnosis, noting any infiltration by inflammatory cells and/or necrosis at perivascular and transmural levels together with vessel thrombosis or rechanneling. Using immunofluorescent techniques, immune deposits of IgG, IgM and components may be noted. Vasculitis neuropathy treatment is fundamentally carried out at the expense of corticosteroids and immunosuppressive which may be administered individually or in combination. In vasculitis neuropathy bad prognostic factors would include old age, the presence of kidney disease and delayed diagnosis and treatment.

Adrenal Cortex Hormones↗
PubMed2004

Genetic evaluation of inherited motor/sensory neuropathy.

Inherited disorders of peripheral nerves represent a common group of neurologic diseases. Charcot-Marie-Tooth neuropathy type 1 (CMT1) is a genetically heterogeneous group of chronic demyelinating polyneuropathies with loci mapping to chromosome 17 (CMT1A), chromosome 1 (CMT1B), chromosome 16 (CMT1C) and chromosome 10 (CMT1D). CMT1A is most often associated with a tandem 1.5-megabase (Mb) duplication in chromosome 17p11.2-p12. In rare patients it may result from a point mutation in the peripheral myelin protein-22 (PMP22) gene. CMT1B is associated with point mutations in the myelin protein zero (Po or MPZ) gene. Mutations in the SIMPLE gene cause CMT1C, and CMT1D is the result of mutations in the early response 2 (ERG2 or Krox-20) gene. An X-linked form of CMT1 (CMT1X) maps to Xq13 and is associated with mutations in the connexin32 (Cx32) gene. Charcot-Marie-Tooth neuropathy type 2 (CMT2) is an axonal neuropathy that maps to chromosome 1p35-p36 (CMT2A), chromosome 3q13-q22 (CMT2B), chromosome 7p14 (CMT2D), chromosome 8p21 (CMT2E), chromosome 1q22-q23 (CMT2F) or chromosome 3q13 (CMT2G). Two X-linked forms of CMT2 have been reported (CMT2XA and CMT2XB), but the genes remain unidentified. An area that has recently expanded is the identification of autosomal recessive forms of CMT type 1 and 2. Of the eight recessive forms of CMT1 that have been identified to date, only two have been fully characterized at the molecular level (CMT1 AR B 1 and CMT1 AR D). Point mutations were found in the myotubularin-related protein-2 (MTM2) gene for CMT1 AR B1. CMT1 AR D is the result of point mutations in the N-myc downstream-regulated gene 1 (NDRG1). Dejerine-Sottas disease (DSD), also called hereditary motor and sensory neuropathy type III (HMSNIII), is a severe, infantile-onset demyelinating polyneuropathy syndrome that may be associated with point mutations in either the PMP22 gene, PO gene, EGR2 gene or the PRX gene (for the recessive form). It shares considerable clinical and pathological features with CMT1. Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder that results in a recurrent, episodic demyelinating neuropathy. HNPP is associated with a 1.5-Mb deletion in chromosome 17p11.2-p12 that results in reduced expression of the PMP22 gene. CMT1A and HNPP are reciprocal duplication/deletion syndromes that originate from unequal crossover during germ cell meiosis. Other rare forms of demyelinating peripheral neuropathies map to chromosome 8q, 10q and 11q.

Animals↗
PubMed2004

Prognostic ability of Tinel sign in determining outcome for decompression surgery in diabetic and nondiabetic neuropathy.

During the past 12 years, 6 studies reported restoration of sensation and relief of pain in the foot by decompression of the tibial nerve and its distal branches in diabetic neuropathy. Although a positive Tinel sign related to favorable outcomes in some of the reports, this relationship was not evaluated specifically. In this study, the presence of the Tinel sign, positive or negative, over the tibial nerve was recorded in 46 patients with diabetic neuropathy and in 40 patients with idiopathic neuropathy. Outcomes were dichotomized into either a good/excellent or failure/poor category. Postoperative data were analyzed at 1 year. In diabetic neuropathy, the presence of a positive Tinel sign had a sensitivity of 88%, a specificity of 50%, and a positive predictive value of 88% in identifying patients who would have a good/excellent outcome. In idiopathic neuropathy, the presence of a positive Tinel sign had a sensitivity of 95%, a specificity of 56%, and a positive predictive value of 93% in identifying patients who would have a good/excellent outcome. It is concluded that a positive Tinel sign is a reliable indicator of successful outcome from decompression of the tibial nerve in patients with diabetes with symptomatic neuropathy, and in patients with symptomatic idiopathic neuropathy.

Decompression, Surgical↗
PubMed1994

Nerve biopsy findings in different patterns of proximal diabetic neuropathy.

Besides distal symmetrical sensory polyneuropathy (DSSP), middle-aged diabetic patients may present with focal or multifocal neuropathies, including proximal neuropathy of the lower limbs, the pathophysiological features of which are uncertain. We studied 10 non-insulin-dependent diabetic patients, 45 to 72 years of age, who developed a painful proximal neuropathy of the lower limbs for which other causes of neuropathy were carefully excluded. The proximal neuropathy was asymmetrical in all patients, sensory in 4, motor and sensory in the others. Signs of DSSP were present in all. A sample of the intermediate cutaneous nerve of the thigh, a sensory branch of the femoral nerve, was taken by biopsy and examined by light and electron microscopy. Examination of the nerve specimens revealed ischemic nerve lesions in 3 patients. Nerve ischemia was associated with vasculitis and inflammatory infiltration in 2 of them. In the other patients the lesions of the cutaneous nerve of the thigh included a varying incidence of axonal and demyelinative lesions similar to those observed in DSSP, with mild inflammatory infiltration in 4 of them. The density of myelinated and of unmyelinated was variably decreased. This study shows that axonal and demyelinative lesions similar to those found in diabetic DSSP are present in proximal nerves in mild forms of proximal diabetic neuropathy; while nerve ischemia, inflammatory infiltration, and vasculitis are encountered in the most severe forms of proximal diabetic neuropathy.

Aged↗
PubMed1988

Clinical aspects of diabetic neuropathies.

Diabetic neuropathy is a common complication of diabetes that may be associated both with considerable morbidity (painful polyneuropathy, neuropathic ulceration) and mortality (autonomic neuropathy). The epidemiology and natural history of diabetic neuropathy is clouded with uncertainty, largely due to confusion in the definition and measurement of this disorder. We have reviewed a variety of the clinical manifestations associated with somatic and autonomic neuropathy and discussed current views related to the management of the different abnormalities. Although unproven, the best evidence suggests that near normal control of blood glucose in the early years following onset of diabetes may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose may also lead to reversibility of early diabetic neuropathy, but again this is unproven. Our ability to manage successfully the many different manifestations of diabetic neuropathy depends ultimately on our success in uncovering the pathogenic processes underlying this disorder. The recent resurgence of interest in the vascular hypothesis, for example, has opened up new avenues of investigation for therapeutic intervention. Paralleling our increased understanding of the pathogenesis of diabetic neuropathy, there must be refinements in our ability to measure quantitatively the different types of defects that occur in this disorder. These tests must be validated and standardized to allow comparability between studies and more meaningful interpretation of study results.

Diabetes Mellitus, Type 1↗
PubMed2002

The natural history of long thoracic and spinal accessory neuropathies.

A cohort of 106 patients with electrodiagnostically confirmed long thoracic neuropathy (50 patients) or spinal accessory neuropathy (56 patients) seen at the Mayo Clinic over a 22-year period were retrospectively studied to better understand the natural history of these disorders and to determine the role of electrodiagnostic testing in predicting prognosis. Mean follow-up was 48 and 50 months, respectively. Good functional recovery was generally observed regardless of the results of electrodiagnostic studies, but improvement in the amplitude of the spinal accessory compound muscle action potential on serial nerve conduction studies tended to predict a good outcome. No electrodiagnostic findings correlated with poor outcome. Traumatic neuropathies generally did worse than neuropathies of other causes. In spinal accessory neuropathies, involvement of the dominant limb, scapular winging, and impaired arm elevation were associated with a poor outcome. Our data suggest that, contrary to other focal neuropathies, the electrodiagnostic findings do not predict functional outcome in these neuropathies.

Accessory Nerve↗
PubMed2006

Dispersion of compound muscle action potential in hereditary neuropathies and chronic inflammatory demyelinating polyneuropathy.

Distal compound muscle action potential (DCMAP) dispersion, defined as a DCMAP duration > or = 9 ms, and proximal-distal (P-D) CMAP dispersion are considered useful in the electrodiagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP). Distal and P-D CMAP dispersion have not been fully studied in hereditary neuropathies, and it is not known whether these measures distinguish hereditary from acquired demyelination. We compared DCMAP duration and P-D CMAP dispersion in 91 genetically characterized hereditary neuropathies and 33 subjects with CIDP. DCMAP dispersion was more frequent in nerves affected by CIDP (41.5%) than in Charcot-Marie-Tooth disease (CMT)1A (24.4%), CMT1B (7.4%), hereditary neuropathy with liability to pressure palsies (HNPP) (10.5%), or CMTX (9.8%). P-D CMAP dispersion was more frequent in CIDP (27.7% of nerves) than in hereditary neuropathies (16.3%) when applying American Academy of Neurology (AAN) criteria; however, its frequency was similar in CIDP and the hereditary neuropathies using the more restrictive criteria of the American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM). Although dispersion is more common in CIDP than in the hereditary neuropathies, DCMAP and P-D dispersion occur in at least one motor nerve in a significant proportion of hereditary neuropathies, and cannot be used in isolation to distinguish acquired from hereditary demyelination.

Action Potentials↗
PubMedDate not supplied

A clinicopathologic study of acrodystrophic neuropathies.

Sixteen patients presenting with trophic changes associated with a peripheral neuropathy were investigated. Muscle power was normal in all patients, but neurogenic muscle atrophy was demonstrated in 4 of the 7 patients who had a muscle biopsy. Alcoholism was responsible for the neuropathy in 11 patients. In the other patients, one had primary hemochromatosis without diabetes and another a dominantly inherited primary hypertrophic neuropathy. Qualitative and quantitative light and electron microscopic studies, including teased nerve fiber preparations, showed axonal loss as the most salient feature. In the alcoholic patients, the large myelinated fibers were primarily involved, followed by small myelinated and unmyelinated fibers. The lesions were predominant distally as shown in patients who had a sural nerve biopsy at both calf and ankle levels. A mechanism of dying-back degeneration of the longest sensory fibers is the most plausible explanation for neurological and pathological abnormalities. In alcoholic neuropathy with trophic changes, loss of sensory fibers is more important than in alcoholic neuropathy without trophic changes. In familial and sporadic cases, axonal loss is more severe and unmyelinated fibers are more severely affected than in alcoholic acrodystrophic neuropathy. Patients with peripheral neuropathies who present with loss of pain sensation but have preserved muscle power are especially exposed to the development of trophic changes induced by usual trauma in insensitive tissues.

Adult↗
PubMed1984

Genetic and metabolic studies in diabetic neuropathy.

Forty-one diabetic patients with symptomatic diabetic neuropathy were studied together with an equal number of matched diabetic subjects without neuropathy. The acetylator status was determined and HLA-A, B, C and DR antigens were investigated. Metabolic control was assessed by measurement of glycosylated haemoglobin and by the mean of multiple random clinic blood glucose values. No significant difference was observed between the two groups in the proportion of fast and slow acetylators. The distribution of HLA frequencies was similar in subjects with and without neuropathy for both Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients. When compared with diabetic subjects without neuropathy, the neuropathy group had higher levels of both glycosylated haemoglobin (mean +/- SEM: 50.1 +/- 1.4 versus 57.5 +/- 1.8 mmol hydroxymethylfurfural/mol haemoglobin (10.5 +/- 0.3 versus 12.0 +/- 0.4% haemoglobin A1, p less than 0.01) mean blood glucose (9.3 +/- 0.4 versus 11.3 +/- 0.5 mmol/l, p less than 0.005). This study provides no evidence that genetic factors increase the susceptibility of diabetic patients to develop neuropathy. In contrast, the elevated glycosylated haemoglobin and blood glucose levels strengthen the association between hyperglycaemia and diabetic neuropathy.

Adult↗
PubMed1984

Augmented gastrin responses in diabetic patients with vagal neuropathy.

We evaluated serum gastrin responses to a test meal in normal subjects and diabetic patients with or without vagal neuropathy. Vagal neuropathy was defined as a heart rate variation during deep breathing of less than 9 beats/min. Forty-three percent (54 out of 124) of the diabetic patients had abnormal heart rate variation, compared with 5% (3 out of 53) of the normal subjects. Serum gastrin responses to a test meal were examined in 17 normal subjects, 20 out of 70 diabetic patients without vagal neuropathy and 17 out of 54 diabetic patients with vagal neuropathy. Meal-stimulated gastrin levels were significantly higher in the diabetic patients with vagal neuropathy than in the normal subjects, while the findings in the diabetic patients without vagal neuropathy were similar to those in normal subjects. These data suggest that augmented gastrin responses are due to vagal denervation induced by autonomic neuropathy.

Diabetic Neuropathies↗
PubMed1989

Plasma adrenaline kinetics in type 1 (insulin-dependent) diabetic patients with and without autonomic neuropathy.

Plasma adrenaline kinetics (clearance, extraction across the forearm, initial plasma disappearance rate, mean sojourn time, volume of distribution) were studied in sixteen Type 1 (insulin-dependent) diabetic patients during constant i.v. infusion of tritium labelled adrenaline. In patients with (n = 8) and without (n = 8) neuropathy forearm venous plasma noradrenaline and adrenaline concentrations as well as plasma clearance of adrenaline based on arterial sampling (1.7 vs 2.1 l/min) were not significantly different. The initial disappearance time (T 1/2) after the infusion of the tritium labelled adrenaline had been stopped was significantly prolonged in Type 1 diabetic patients with neuropathy compared to those without (after 20 min infusion 2.7 vs 2.2 min, p less than 0.02, after 75 min infusion 3.7 vs 2.9 min, p less than 0.05). The corresponding values for the mean sojourn time of adrenaline in plasma were 6.5 vs 4.7 min (p less than 0.05) after 20 min infusion and 18 vs 10 min (p less than 0.05) after 75 min of infusion. The unchanged plasma clearance and the prolonged initial halftime and mean sojourn time of adrenaline in plasma suggest that adrenaline is distributed in a larger volume in Type 1 diabetic patients with neuropathy as compared to patients without neuropathy (estimated space of distribution 29 vs 20 l). Our results suggest that patients with diabetic neuropathy do not adjust the plasma adrenaline concentration to changes in adrenaline infusion rate as rapidly as those without neuropathy, i.e. the effect of an elevated adrenaline secretion rate may be prolonged in patients with diabetic autonomic neuropathy.

Adult↗
PubMed1996

Arterio-venous shunting and proliferating new vessels in acute painful neuropathy of rapid glycaemic control (insulin neuritis).

Insulin neuritis, or painful neuropathy following rapid improvement in glycaemic control, is well recognised but its aetiology is unclear. An understanding of the processes involved in the genesis of acute painful neuropathy of rapid glycaemic control may give an insight into the early pathogenetic factors leading to diabetic nerve damage in general. We have identified five subjects with insulin neuritis including one who developed severe autonomic neuropathy following treatment with insulin. Subjects underwent: 1) assessment of neuropathic symptom and deficit scores; 2) quantitative sensory and electrophysiological studies and 3) sural nerve epineurial vessel photography and fluorescein angiography in vivo. The sural nerve photographs were independently graded by an ophthalmologist. All subjects with insulin neuritis presented with severe sensory symptoms but clinical examination and electrophysiological tests were normal except in the subject with the severe autonomic neuropathy in whom all the tests were abnormal. On nerve photography, there was an abundance of epineurial nutrient vessels although these showed severe abnormalities including arteriolar attenuation, tortuosity and arterio-venous shunting in all subjects. Proliferating neural 'new vessels' which bear striking similarities to those found in the retina and that were more leaky to fluorescein than normal vessels, were observed in three subjects. Venous distension and/or tortuosity was also observed in three subjects and this was most marked in the subject with severe autonomic neuropathy. This study shows that epineurial nutrient vessel anatomy is abnormal in subjects with acute painful neuropathy of rapid glycaemic control, a condition previously thought to be purely metabolic in origin. The presence of epineurial arterio-venous shunting and a fine network of vessels resembling the new vessels of the retina, may lead to a 'steal' effect rendering the endoneurium ischaemic. This process may be important in the genesis of neuropathic pain, and further supports the importance of vascular factors in the pathogenesis of diabetic neuropathy.

Acute Disease↗
PubMed1996

Measurement of myocardial accumulation of 123I-metaiodobenzylguanidine for studying cardiac autonomic neuropathy in diabetes mellitus.

The association of myocardial 123I-metaiodobenzylguanidine (MIBG) accumulation and autonomic neuropathy, as well as factors known to affect autonomic nervous function, were studied in a group of 12 diabetic patients representing different degrees of autonomic failure. The early myocardial uptake phase of 123I-MIBG was measured by calculating the peak net influx rate for the first 30 min after the 123I-MIBG injection and by single photon emission computed tomography (SPECT) imaging 1 h after the injection. The retainment of 123I-MIBG in the myocardium was measured using SPECT imaging 6 h after the injection, and myocardial uptake and the myocardium/liver uptake ratio were calculated. The 6-h myocardium/liver uptake ratio of 123I-MIBG was significantly (p < 0.05) lower in the diabetic patients with clinically evident autonomic neuropathy compared with those without autonomic neuropathy. Greater body mass index was associated with lower peak net influx rate and 1-h myocardial uptake of 123I-MIBG, and greater diastolic blood pressure was associated with lower 1-h myocardial uptake of 123I-MIBG, whether or not the patients had diabetic autonomic neuropathy. In conclusion, reduction in the 6-h myocardium/liver uptake ratio of 123I-MIBG is related to diabetic autonomic neuropathy. Because the early 123I-MIBG accumulation in myocardium is reduced in diabetic patients with greater body mass index and diastolic blood pressure, irrespective of autonomic neuropathy, our results encourage the use of the late myocardial accumulation of 123I-MIBG for studying sympathetic neuropathy in the diabetic heart.

3-Iodobenzylguanidine↗