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PubMed1990

[Ischemic neuropathy].

Ischemia plays an important role in the development of neuropathies associated with various disorders, such as peripheral vascular occlusive diseases, necrotizing vasculitides, diabetes mellitus and nerve compression or trauma. Although a multiple mononeuropathy or an asymmetrical polyneuropathy is the usual clinical presentation of ischemic neuropathy, some patients present with a neuropathy that is mainly distal and symmetrical. Pathologically, nerve ischemia results in focal or multifocal central fascicular or sector fiber degeneration. These ischemic lesions tend to begin at mid-upper arm or midthigh level, which is the watershed zone of poor perfusion, and become more diffuse distally. Nerve ischemia at the level of distal small fascicles often induces sub-perineurial crescent lesion rather than central fascicular fiber degeneration. Physiologically, reduced nerve blood flow with endoneurial hypoxia has been demonstrated in experimental diabetic and galactose neuropathies. Endoneurial ischemia/hypoxia in galactose neuropathy appears to be due to increased intercapillary distances and constriction of trans-perineurial vessels resulting from endoneurial edema. Although acute ischemic neuropathy has been well investigated, little is known about functional or structural responses of peripheral nerve to chronic ischemia.

Diabetic Neuropathies↗
PubMed1985

Somatostatin and counterregulatory hormone responses to hypoglycaemia in diabetics with and without autonomic neuropathy.

Blood glucose, somatostatin and counterregulatory hormone responses to an i.v. bolus of insulin were studied in insulin-dependent diabetics with different degrees of autonomic neuropathy, after 24 hours of optimised control with an artificial pancreas. There was no plasma catecholamine response in patients with a sympathetic autonomic neuropathy. A normal somatostatin response to hypoglycemia was absent in patients with autonomic neuropathy. Glucagon did not respond in diabetics, independently of the degree of neuropathy. In all diabetics, cortisol and GH were stimulated. Absence of warning symptoms was observed in patients with catecholamine deficiency. Despite different hormone behaviour, blood glucose fall and recovery were similar in all diabetic groups. It is concluded that the glucagon response to insulin hypoglycaemia is reduced in all type 1 longstanding diabetics, whereas catecholamine and somatostatin responses are only abolished in those with autonomic neuropathy. Patients with sympathetic neuropathy would be considered at increased risk severe hypoglycaemia.

Adult↗
PubMed1995

Reassessment of circadian profile of blood pressure and heart rate in diabetic patients with autonomic neuropathy.

Previous studies have shown that the normal circadian blood pressure fall is absent in patients with diabetic autonomic neuropathy, while the reported rise in blood pressure during the night in the same patients is controversial. This study analyzed the circadian profile in 19 diabetic patients with established autonomic neuropathy. Twenty-four hour ambulatory systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate were recorded every 20 minutes during the day and every 60 minutes at night in 29 patients, 19 with diabetic autonomic neuropathy and 10 nondiabetic hypertensive patients as controls. Twelve diabetic patients with autonomic neuropathy with unknown hypertension were found to have hypertension based on 24 hour ambulatory blood pressure monitoring. Repeated measured analysis of variance (ANOVA) and trend analysis indicated that the linear systolic blood pressure increased from night to morning to afternoon while mean arterial pressure and diastolic blood pressure increased from night to morning but decreased from morning to afternoon. In practice, the early morning rise in systolic blood pressure in diabetic neuropathy is not different from that in normal or hypertensive patients and requires appropriate treatment. The absence of the nocturnal rise in the blood pressure revealed a subgroup of patients with diabetic neuropathy which demonstrated no fatal cardiovascular or renal events over 18 to 24 months of follow-up.

Aged↗
PubMed1993

[Autonomic neuropathies in diabetes mellitus: diagnosis--therapy--risks].

Autonomic neuropathy is a complication of diabetes which is observed in about 20% of all patients. This complication is often not adequately diagnosed. Neuropathy is a syndrome of various diseases that is classified according to the organs involved in the clinical picture. For the diagnosis of autonomic neuropathy besides the careful examination of the patient (metabolic and neurologic status, diabetic complications) a number of specific tests are available i.e. cardiovascular reflex tests and some other organ-specific tests. The review attempts to give an update of the presently used diagnostic approaches. As far as the therapy of all forms of neuropathy is concerned the careful control of blood glucose of the diabetic patient is still the only therapy which counteracts specifically the pathogenesis of autonomic neuropathy. There is however a number of drugs available which are useful for symptomatic therapy. Their effectiveness is discussed in this review. There is no doubt that diabetic autonomic neuropathies will have consequences for long-term prognosis and quality of life.

Autonomic Nervous System↗
PubMed1995

[Dynamic scintigraphy of gastric emptying in non-insulin dependent diabetics with autonomic neuropathy].

To ascertain whether gastric emptying of solids is affected by visceral autonomic neuropathy, 30 noninsulin-dependent diabetics (10 with autonomic neuropathy, 10 with peripheral and 10 without neuropathy) and 10 control subjects were studied. Subjects were screened by clonidine test and two parasympathetic tests of cardiovascular reflexes to identify the presence of autonomic neuropathy. The peripheral neuropathy was diagnosed by classic neurological examination and EMG. Delayed gastric emptying was assessed by dynamic scintigraphy, using 99mTc labeled ham and eggs. The gastric emptying of solids was markedly delayed in diabetics, particularly in diabetics with poor metabolic control (p < 0.01) and those with autonomic and peripheral diabetic neuropathy (p < 0.05). The results of our study suggest that dynamic scintigraphy may be a more sensitive method than other tests for autonomic dysfunction of the gut in diabetics with the early manifestation of diabetic gastroparesis.

Autonomic Nervous System Diseases↗
PubMed1995

Acoustic nerve in peripheral neuropathy: a BAEP study. Brainstem Auditory Evoked Potentials.

We performed BAEP study to evaluate acoustic nerve involvement in 102 patients affected by peripheral neuropathies of different etiology, predominantly hereditary and inflammatory acquired neuropathies. Prolonged latency of early waves, indicative of slowing in VIII nerve conduction, was found in a high percentage of cases. Abnormalities were far more frequent (44% vs 14%) and severe in patients with demyelinating rather than axonal neuropathy. Among demyelinating neuropathy, the most severe latency delay was found in Hereditary Motor and Sensory Neuropathy type III. The pattern of acoustic nerve involvement differed slightly between Hereditary Motor and Sensory Neuropathy type I and acquired inflammatory demyelinating polyradiculoneuropathy, perhaps reflecting different pathogenetic mechanisms and different sites of VIII nerve demyelination.

Adolescent↗
PubMed1995

[Corrected QT interval and diabetic neuropathy of the cardiovascular system].

UNLABELLED: Our objective was the analysis of the utility of the corrected QT interval (QTc) for the assessment of severity of cardiac autonomic neuropathy. Fourty nine patients with insulin-dependent diabetes mellitus/IDDM/were enrolled in the study. Their ages ranged between 16 and 58 years, and the duration of IDDM ranged between 1 and 38 years. Patients were tested for cardiac autonomic neuropathy using ProSciCard system. We carried out four tests: resting pulse deep breathing pulse Ewing test Valsalva maneuver Our results showed the relationship between the QTc interval lengthening and the occurance of cardiac autonomic neuropathy. No correlation was found between the QTc interval and the extend of cardiac autonomic neuropathy. CONCLUSIONS: The QTc interval measurement is a good routine test for the diagnosis of cardiac autonomic neuropathy. The corrected QT interval is not a reliable indicator of the extend of cardiac autonomic neuropathy.

Adolescent↗
PubMed1997

[24-hour arterial pressure study and diabetic neuropathy and angiopathy of the lower limbs].

AIMS: To study the circadian variation of BP in diabetics with chronic late complications (autonomic neuropathy, peripheral neuropathy and macroangiopathy of the lower limbs). PATIENTS AND METHODS: We studied 35 NIDDM patients, 22 male and 13 female, with a mean age of 62.17 +/- 8.66 years, all with hypertension (HBP) or with BP levels close to normal, many of them under anti-hypertensive therapy (mean BP in clinical measurements: 164 +/- 23.16 mmHg systolic and 92.14 +/- 11.06 mmHg diastolic). Twenty-four suffer from autonomic neuropathy, 23 from peripheral neuropathy and 11 from macroangiopathy of the lower limbs. The control group is composed of 10 patients with essential HBP without other observable pathology, with a mean age of 68.5 +/- 3.63 years and BP in clinical measurements: systolic 192 +/- 15.49 mmHg and diastolic 88 +/- 4.21 mmHg (without any previous therapy). The record of the BP circadian profile was made, with the use of a Spacelab monitor, model 90207, 5 days after anti-hypertensive therapy was suspended. RESULTS: The mean BPs in 24 hours were: control group-systolic BP 152.6 +/- 13 mmHg and diastolic 79.8 +/- 13 mmHg; diabetics-systolic BP 136.82 +/- 15 mmHg and diastolic 77.4 +/- 8 mmHg. The daily and nocturnal mean BPs were 158.5 +/- 8.5 and 146 +/- 8.4 mmHg (systolic) and 82.8 +/- 5.7 and 70.9 +/- 5.1 mmHg (diastolic) in the control group, while they were, in diabetics, 141.3 +/- 15.7 and 135.6 +/- 16.6 mmHg (systolic) and 79.6 +/- 7.1 and 72 +/- 8.2 mmHg (diastolic). In diabetic patients, considering the groups with and without autonomic neuropathy, the difference between daily and nocturnal mean BP was 1.6 vs 9.4 mmHg systolic and 4.9 vs 9.4 mmHg, diastolic. CONCLUSIONS: In both groups, the mean BP levels in 24 hours were notoriously lower than those obtained from the clinical measurements: the differences were 40 mmHg (control group) and 27.2 mmHg (diabetics) for systolic BP and 8.2 mmHg (control group) and 14.7 mmHg (diabetics) for diastolic. The BP circadian profiles show a lower variability, with absence of the nocturnal reduction, specially evident in diabetic patients with autonomic neuropathy versus other groups.

Aged↗
PubMed1997

[The effect of hyperbaric oxygen on ophthalmic artery blood velocity in patients with diabetic neuropathy].

We investigated changes in the blood velocity of the ophthalmic artery to observe its relationship to the complication of diabetes mellitus before and after hyperbaric oxygen therapy (HBO). Color Doppler imaging (Toshiba, SSA-260A) was used. In this study, there were 7 diabetic neuropathy patients, 3 diabetes patients without neuropathy, and 7 normal subjects for control. These patients were examined before and after HBO. The patients were made to breathe 100% oxygen at 2.0 atmosphere absolute (ATA) for one hour. HBO is sometimes used for treatment of diabetic neuropathy. HBO produced an average decrease in blood velocity of 15.0 +/- 9.0 (mean +/- standard deviation) % in normal subjects, 10.7 +/- 8.6% in diabetes patients without neuropathy, and returned to the baseline level 4 hours after the conclusion of HBO. On the other hand, the blood velocity increased by about 20.6 +/- 9.5% in diabetic neuropathy patients regardless the degree of severity of diabetic retinopathy. These results suggest that the increase in the blood velocity of the ophthalmic artery after HBO in diabetic neuropathy patients could be attributed to an imbalance in autonomic nervous function.

Blood Flow Velocity↗
PubMed1997

Early detection of diabetic neuropathy: a neurophysiological study on 100 patients.

As a long-term complication of diabetes mellitus, autonomic neuropathy has received considerable attention in the last few years since a tripled 5-year-mortality of patients with diabetic neuropathy including autonomic disturbances has been observed. In a total of 100 diabetics with clinical manifest neuropathy of different stages (N0 = 8, N1 = 15, N2a = 24, N2b = 28, N3 = 25), 26 of whom were insulin-dependent and 74 non-insulin-dependent, the validity of different neurophysiologic and autonomic function test procedures proposed in literature was assessed. Apart from clinical examination, nerve conduction velocity measurement of five nerves as well as amplitude measurement of evoked sensory and motor actin potentials, electromyography of at least four muscles of the lower limbs, and measurement of sympathetic skin response on hands and feet were performed. Furthermore, heart rate variation at deep periodical breathing (E/I-ratio), during Valsalva's manoeuver and after standing up (30/15-ratio) was determined. In addition, the drop in systolic blood pressure to standing up was measured. The further developed the clinical picture of neuropathy, the more pathological were the results obtained in different tests. The results suggest that most changes leading to pathological values of nerve conduction velocity and heart rate variation measurement take place in a clinical stage, in which no or only very slight clinical signs give evidence of diabetic neuropathy (N0-N1). Therefore, especially these examinations should be performed on diabetics with no or only slight clinical signs of neuropathy in order to reveal those with beginning neuropathic disturbances. EMG examination is preferable in later stages of the disease.

Action Potentials↗
PubMed1998

[The examination of apoE phenotypes in diabetic patients with peripheral neuropathy].

Apolipoprotein E (apoE), which is reported to recognize the low density lipoprotein receptor and remnant receptor, mediates the delivery of cholesterol and other lipids to the cells all over the body. There are several phenotypes such as apoE2, apoE3 and apoE4. Recently, it is reported that apoE plays an important role in neurite outgrowth. To determine whether apoE phenotype is concerned in diabetic peripheral neuropathy, we investigated the incidence of apoE phenotypes in diabetic patients with peripheral neuropathy. The occurrence of retinopathy and nephropathy were not different in apoE2, apoE3 and apoE4. However, the frequency of diabetic neuropathy was higher in apoE4 than apoE2 and apoE3 (p < 0.05). Furthermore, as the stage of diabetic neuropathy advanced, the incidence of apoE4 increased. From these results we conclude that apoE phenotype influences the progress of diabetic peripheral neuropathy and that apoE4 contributes to the deterioration of diabetic peripheral neuropathy.

Aged↗
PubMed1998

[Assessment of diabetic cardiovascular autonomic neuropathy by heart rate variability and pulse wave velocity].

Neuropathy is a frequent complication in diabetes mellitus. Since the involvement of the autonomic nervous system indicates a poor prognosis, early detection and subsequent management are important. Analysis of heart rate variability (HRV) provides a quantitative measure of sympathovagal modulation activities on the heart and has been proven to be useful for the early assessment of the diabetic autonomic neuropathy. We recently developed a simple method of measuring pulse wave velocity (PWV) to evaluate sympathetic nervous activity in the vascular system. In this paper, we examined 33 diabetic patients with and without peripheral neuropathy (15 and 18 respectively) using these methods. In time domain analysis, the mean heart rate, standard deviation and coefficient of variation of HRVs significantly differed between these two groups, whereas the indices of PWVs did not show a significant difference. In frequency domain analysis of HRV, both low and high frequency components were decreased, and the low frequency component in normalized unit did not increase after standing in patients with peripheral neuropathy. We previously reported that the mean PWV decreased after standing in patients with diabetic neuropathy. This disagreement suggests that beta sympathetic dysfunction precedes alpha sympathetic dysfunction in diabetic neuropathy.

Adult↗
PubMed1995

Autonomic and peripheral neuropathies in patients with chronic alcoholism. A dose-related toxic effect of alcohol.

OBJECTIVE: To assess autonomic and peripheral nervous system function in patients with chronic alcoholism. DESIGN: A cross-sectional study. PATIENTS: A consecutive sample of 107 alcoholic patients and 61 controls. MAIN OUTCOME MEASURE: For autonomic assessment, heart rate variations during deep breathing and Valsalva maneuver and on standing were measured. Blood pressure response to standing up and to sustained handgrip were also evaluated. For assessment of the peripheral nervous system, an electrophysiologic examination was performed. RESULTS: Alcoholic patients exhibited reduced heart rate variability compared with controls (P < .01, on all parasympathetic tests), whereas no differences in the mean values of the blood pressure responses between both groups were found. Twenty-six patients (24.3%) had criteria of autonomic neuropathy, and 34 (32%) had electrophysiologic criteria of peripheral neuropathy. None of the controls exhibited criteria of autonomic neuropathy, and only one had criteria of peripheral neuropathy. The estimated total lifetime dose of alcohol correlated inversely with the parasympathetic indexes (r = -.48 to -.51; P < .001 on all parasympathetic tests) and the sensory potential amplitudes of upper and lower limbs (r = -.43; P < .001, both limbs). Finally, a significant correlation between autonomic and peripheral neuropathies was observed (P = .01). By contrast, these lesions were not related to age, nutritional status, or other alcohol-related diseases. CONCLUSIONS: Autonomic and peripheral neuropathies are common among hospitalized alcoholic patients. Alcohol appears to be toxic to autonomic and peripheral nerves in a dose-dependent manner.

Adolescent↗
PubMed2001

Hereditary neuropathy with liability to pressure palsies is not a major cause of idiopathic carpal tunnel syndrome.

BACKGROUND: Carpal tunnel syndrome is a debilitating neuropathy affecting millions of individuals. Although there are published reports of familial associations of carpal tunnel syndrome, the molecular mechanisms are unknown. OBJECTIVE: To determine the prevalence and potential role of the chromosome 17 microdeletion associated with hereditary neuropathy with liability to pressure palsies in patients diagnosed as having carpal tunnel syndrome. DESIGN: Prospective study. PATIENTS AND METHODS: Since hereditary neuropathy with liability to pressure palsies may present as carpal tunnel syndrome, we evaluated 50 patients with idiopathic carpal tunnel syndrome for hereditary neuropathy with liability to pressure palsies. RESULTS: No hereditary neuropathy with liability to pressure palsies deletions were detected. CONCLUSION: Molecular genetic testing for hereditary neuropathy with liability to pressure palsies in patients with idiopathic carpal tunnel syndrome is of limited value.

Adult↗
PubMed2005

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.

Adolescent↗
PubMed2006

Optic neuropathy in patients using amiodarone.

OBJECTIVE: To refine the criteria for the diagnosis of amiodarone-related optic neuropathy by including a broader spectrum of clinical features, thus helping to differentiate this entity from nonarteritic anterior ischemic optic neuropathy coincidentally affecting a patient taking amiodarone. METHODS: A retrospective case review of 22 patients who developed optic neuropathy while taking amiodarone, in whom other systemic causes were excluded. RESULTS: We identified 3 groups of patients: those in whom a diagnosis of amiodarone-induced optic neuropathy seems probable (n = 14), those in whom an association with amiodarone optic neuropathy is indeterminate (n = 5), and those in whom the occurrence of nonarteritic anterior ischemic optic neuropathy seems to be coincidental (ie, unrelated to amiodarone) (n = 3). We formulated specific diagnostic criteria for each of these categories. CONCLUSIONS: We recommend a systematic approach that includes assessment of bilaterality, mode of onset, degree of optic nerve dysfunction, structure of the uninvolved optic disc in unilateral cases, and systemic toxic effects. Such well-defined diagnostic criteria can help the clinician in the treatment of patients with this disorder.

Aged↗
PubMed1996

Severe vincristine neuropathy in Charcot-Marie-Tooth disease type 1A.

BACKGROUND: A general predisposition for vincristine-related neuropathy has been observed in persons with a family history of hereditary neuropathies. METHODS: In a retrospective case series, we investigated the possible association between the DNA rearrangement found in patients with Charcot-Marie-Tooth Disease Type 1A (CMT1A) and susceptibility to the neurotoxicity of vincristine. In selected patients and family members, we performed electrodiagnostic studies and analyzed DNA samples for 17p11.1-12 duplication associated with CMT1A. RESULTS: We describe three families with autosomal dominant CMT1, among whom a family member with a neoplastic disease suffered rapid onset, severe neuropathy after receiving initial doses of vincristine as a part of a routine chemotherapy protocol. All three families had at least one affected family member with 17p11.2-12 duplication. CONCLUSIONS: These cases show that 17p11.2-12 duplication predisposes patients to severe neurotoxicity from vincristine and that this drug should be avoided with patients with CMT1A. It is therefore essential to obtain a detailed family history for all oncology patients to screen for possible hereditary neuropathies. In patients with unexplained or preexisting familial neuropathy, testing for 17p11.2-12 duplication should be carried out prior to initiating vincristine therapy. Patients with other hereditary neuropathies may also be at risk for severe neurotoxic reactions.

Adolescent↗
PubMed1997

Motor nerve biopsy studies in motor neuropathy and motor neuron disease.

The clinical presentation of motor neuropathy often resembles that of motor neuron disease, sometimes leading to an erroneous diagnosis. Moreover, the underlying pathological process in motor neuropathy has been rarely investigated and there are no systematic studies of the affected motor nerves. We describe a new motor nerve biopsy procedure, performed in 15 patients: 6 with motor neuropathy and 9 with motor neuron disease. The motor branch from the anterior division of the obturator nerve to the gracilis muscle in the thigh was biopsied. In both groups of patients the motor nerves exhibited depletion of myelinated nerve fibers. In motor neuropathy there was a significantly higher density of regenerative clusters of small myelinated fibers in comparison to motor nerves from patients with motor neuron disease. In addition, in 3 patients with motor neuropathy there was evidence for demyelination with thinly myelinated axons and small onion bulb formations. These pathological studies of motor nerve biopsies can help to differentiate motor neuropathy from motor neuron disease.

Adult↗