Acute Painful Neuropathy Research Articles

Acute painful neuropathy and pseudo-phaeochromocytoma following severe weight loss in two young women with Type 1 diabetes

Acute painful neuropathy and pseudo-phaeochromocytoma following severe weight loss in two young women with Type 1 diabetes

Treatment-Induced Diabetic Neuropathy

In sporadic case reports — some published more than 50 years ago — clinicians have described acute severe painful neuropathy that can occur during

Treatment‐induced diabetic neuropathy: A reversible painful autonomic neuropathy

To describe the natural history, clinical, neurophysiological, and histological features, and outcomes of diabetic patients presenting with acute painful neuropathy associated with glycemic control, also referred to as insulin neuritis. Sixteen subjects presenting with acute painful neuropathy had neurological and retinal examinations, laboratory studies, autonomic testing, and pain assessments over 18 months. Eight subjects had skin biopsies for evaluation of intraepidermal nerve fiber density. All subjects developed severe pain within 8 weeks of intensive glucose control. There was a high prevalence of autonomic cardiovascular, gastrointestinal, genitourinary, and sudomotor symptoms in all subjects. Orthostatic hypotension and parasympathetic dysfunction were seen in 69% of subjects. Retinopathy worsened in all subjects. Reduced intraepidermal nerve fiber density (IENFD) was seen in all tested subjects. After 18 months of glycemic control, there were substantial improvements in pain, autonomic symptoms, autonomic test results, and IENFD. Greater improvements were seen after 18 months in type 1 versus type 2 diabetic subjects in autonomic symptoms (cardiovascular p < 0.01; gastrointestinal p < 0.01; genitourinary p < 0.01) and autonomic function tests (p < 0.01, sympathetic and parasympathetic function tests). Treatment-induced neuropathy is characterized by acute, severe pain, peripheral nerve degeneration, and autonomic dysfunction after intensive glycemic control. The neuropathy occurred in parallel with worsening diabetic retinopathy, suggesting a common underlying pathophysiological mechanism. Clinical features and objective measures of small myelinated and unmyelinated nerve fibers can improve in these diabetic patients despite a prolonged history of poor glucose control, with greater improvement seen in patients with type 1 diabetes.

Acute painful neuropathy of the perineum and scrotum following rapid improvement of glycemic control in type 1 diabetes

International Journal of UrologyVolume 16, Issue 11 p. 922-922 Acute painful neuropathy of the perineum and scrotum following rapid improvement of glycemic control in type 1 diabetes Katsumi Kadekawa md , Katsumi Kadekawa md Division of Urology, University of the RyukyusSearch for more papers by this authorKimio Sugaya md phd, Kimio Sugaya md phd Southern Knights' LaboratorySearch for more papers by this authorSaori Nishijima phd, Saori Nishijima phd Okinawa Institute of Science and TechnologyOkinawa, Japan[email protected]Search for more papers by this author Katsumi Kadekawa md , Katsumi Kadekawa md Division of Urology, University of the RyukyusSearch for more papers by this authorKimio Sugaya md phd, Kimio Sugaya md phd Southern Knights' LaboratorySearch for more papers by this authorSaori Nishijima phd, Saori Nishijima phd Okinawa Institute of Science and TechnologyOkinawa, Japan[email protected]Search for more papers by this author First published: 21 October 2009 https://doi.org/10.1111/j.1442-2042.2009.02381.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume16, Issue11November 2009Pages 922-922 RelatedInformation

A case of insulin neuritis that developed in a patient under regular insulin treatment on increasing the insulin dose

JO N 2 95 2 insulin therapy. Although the precise role of insulin is not well understood, all relevant studies have reported the development of acute painful neuropathy associated with rapid glycaemic control following the initiation of insulin therapy. Here, we report a case of acute painful neuropathy that developed in a patient under regular insulin treatment on increasing the insulin dose. A 30-year-old male presented with a burning sensation in his feet, which had persisted for 3 weeks. He had been diagnosed with type 1 diabetes mellitus 15 years earlier. Until 4 weeks prior to presentation, he had been receiving intermediate-acting (Lente) insulin at a dosage of 24 units/day and the short-acting insulin (Lispro) 6–14 units/time, 3 times/day; however, his HbA1c level was determined to be more than 11 %, and the fasting glucose level was up to 300 mg/dl. The intermediate-acting insulin dosage was increased up to 30 units/day during the last 4 weeks prior to presentation. His HbA1c level decreased to 8.8 % and the fasting glucose decreased to 127 mg/dl. Subsequently, he developed dizziness and sweating, and his blood sugar level frequently dropped below 45 mg/dl. One week after the dose was increased; he experienced a severe burning sensation in the soles and a tingling sensation in the dorsum of the feet. Physical and neurological examinations did not reveal any specific findings. An electrophysiological test revealed a mild reduction in the motor and sensory nerve conduction velocity but normal sensory and compound nerve action potentials. Amitryptine was used for pain control, and the pain subsided after a month. Insulin therapy itself has been reported to cause arteriovenous (A-V) shunting and to increase the epineurial blood flow [5]. This reKi-Bong Song Soo-Jin Cho Yang-Ki Minn Ki-Han Kwon Min-Keun Park

Acute painful neuropathy induced by rapid correction of serum glucose levels in diabetic patients

We report on acute painful neuropathy following reduction of high serum glucose levels in six diabetic patients, aged 27–52 (5 males). Initial glucose levels ranging between 270 and 600 mg/dL decreased to 60–160 mg/dL following insulin, pharmacologic or dietary treatment. Four patients had long-standing untreated diabetes (3–5 years). All six patients experienced severe excruciating neuropathic pain 2–4 weeks after initiation of treatment. Pain was generalized in all, starting in the feet in 4 cases. Pain intensity prompted the use of combination therapy with various anti-neuropathic pain agents. Symptoms gradually improved in all patients, allowing discontinuation of symptomatic therapy within 3–8 months. We conclude that acute painful neuropathy can complicate the correction of high glucose levels in diabetic patients. Therefore, careful correction of glucose levels should be considered in patients with long-standing uncontrolled diabetes.

Oxaliplatin Acts on IB4-Positive Nociceptors to Induce an Oxidative Stress-Dependent Acute Painful Peripheral Neuropathy

The toxicity profile of oxaliplatin, a platinum derivative currently used in the treatment of colorectal cancer, differs from those of the other platinum compounds, cisplatin and carboplatin. Oxaliplatin treatment induces an acute neurotoxicity characterized by a rapid onset of cold-induced distal dysesthesia and a chronic sensory peripheral neuropathy. A single intravenous dose of oxaliplatin produced a dose-dependent mechanical hyperalgesia and heat and cold allodynia; repeated administration intensified symptoms. A single intradermal dose of oxaliplatin produced a dose-dependent mechanical hyperalgesia. A single dose intravenous oxaliplatin also lowered thresholds and increased responses of C-fiber nociceptors to mechanical stimulation, confirming a peripheral site of action. Whereas peripheral administration of inhibitors of second messengers implicated in models of other painful peripheral neuropathies (PKA, PKC, NO, Ca(2+), and caspase) had no effect; both systemic and local administration of antioxidants (acetyl-L-carnitine, alpha-lipoic acid or vitamin C), all markedly inhibited oxaliplatin-induced hyperalgesia. Intrathecal administration of the neurotoxin for IB4-positive nociceptors, IB4-saporin, markedly attenuated IB4 staining in the dorsal horn of the spinal cord and completely prevented oxaliplatin-induced hyperalgesia. We suggest that oxaliplatin acts on IB4 (+)-nociceptors to induce oxidative stress-dependent acute peripheral sensory neuropathy. Many drugs used to treat cancer produce pain as their dose-limiting side effect. We used a model of this pain syndrome induced by oxaliplatin to demonstrate that pain is produced by action on a subset of nociceptors, the IB4-positive DRG neurons. This information could help define cellular targets against which protective therapies could be developed.

Biphasic insulin aspart 30 treatment improves glycaemic control in patients with type 2 diabetes in a clinical practice setting: experience from the PRESENT study

The Physicians' Routine Evaluation of Safety and Efficacy of NovoMix 30 Therapy (PRESENT) study aims to assess the safety and efficacy of biphasic insulin aspart 30 (BIAsp 30) in patients with type 2 diabetes mellitus in routine clinical practice. This was a 6-month, prospective, multinational, multiethnic observational study involving 21 977 patients from 13 countries (India, Iraq, Jordan, Kuwait, Lebanon, Qatar, Romania, Russia, Saudi Arabia, South Africa, South Korea, Turkey and the United Arab Emirates). The patients were transferred to BIAsp 30 with or without oral antidiabetic drugs (OADs) from prior treatment with OAD (n = 8583), insulin (n = 5942), OAD + insulin (n = 4673) or diet (i.e. treatment naive) (n = 1707). One thousand and seventy-two patients had incomplete or no information on previous treatment. At 3 and 6 months, significant reductions from baseline were observed in the mean haemoglobin A(1c) (HbA(1c)) (-1.33 and -1.81%), fasting plasma glucose (-3.02 and -3.74 mmol/l) and postprandial plasma glucose (-4.76 and -5.82 mmol/l) (p < 0.001). A significantly greater proportion of patients achieved target HbA(1c) of less than 7% at 3 months (15.3%) and 6 months (27.7%) compared with baseline (4.8%) (p < 0.001). Overall, the mean HbA(1c) at 6 months was lowered in patients regardless of prior treatment: -2.15% (OAD), -1.45% (insulin), -1.47% (OAD + insulin) and -2.35% (treatment naive). In the overall cohort, the rate of total hypoglycaemia was reduced from 5.4 events per patient-year at baseline to 2.2 events per patient-year at study end (p < 0.001). Among prior treatment subgroups, the rates of total hypoglycaemia were reduced from 2.5 to 2.1 events per patient-year in the OAD group, from 9.6 to 2.2 events per patient-year in the insulin group and from 7.6 to 2.5 events per patient-year in the OAD + insulin group but were increased from 1.0 to 1.8 events per patient-year in the treatment-naive group (p < 0.001). There were 444 adverse drug reactions (ADRs), including 13 serious ADRs: lipodystrophy (three events), symptoms of generalized hypersensitivity (two events), acute painful neuropathy (one event), worsening of diabetic retinopathy (one event), oedema (one event) and unspecified ADRs (five events). The use of BIAsp 30 monotherapy or in combination with OADs in clinical practice was effective and safe in patients with poorly controlled type 2 diabetes mellitus.

Novel myelin protein zero mutation (Arg36Trp) in a patient with acute onset painful neuropathy

We present a patient with acute onset painful polyneuropathy found to have a novel MPZ mutation (Arg36Trp). The Arg36Trp mutation described in this report occurs at a putative adhesion interface. An alternative explanation for his polyneuropathy was not found and his mother was identified to have polyneuropathy and carry the same mutation. Two hundred normal controls were without this base alteration. The temporal profile of the index case may provide further indirect evidence suggesting an immune mechanism contributing to the pathogenesis of some cases of MPZ mutations. We predict that other rapid symptom onset polyneuropathies will be found to have direct genetic susceptibility.

Painful Neuropathy with Trigeminal Nerve Involvement in Type 2 Diabetes

After several years of treatment for type 2 diabetes mellitus, a 69-year-old Japanese man developed an acute painful neuropathy, characterized by bilateral causalgia and dysaesthesia in his cheeks and around his eyes, typically 30 min to 3 h after meals. As his glycaemic control deteriorated, his haemoglobin (Hb) A1c level gradually increased from 7 - 8% to 10.3% and his symptoms became more severe. The pain radiated out along the distribution of the ophthalmic and maxillary divisions of the trigeminal nerve. The patient was treated with insulin therapy and his HbA1c level decreased from 10.3% to 6.8% within 7 months. Five months after initiating insulin therapy, his symptoms showed a dramatic improvement. This was a very unusual case of bilateral acute painful neuropathy that involved the ophthalmic and maxillary divisions of the trigeminal nerve, and in which aggravation of the symptoms clearly related to poor glycaemic control.

Acute painful neuropathy in thallium poisoning

Dysesthesia, allodynia, distal muscle weakness, and sensory impairment were noted in two patients with acute thallium intoxication. Two months later, nerve conduction studies showed an axonal degeneration. Sural nerve biopsy disclosed a decreased fiber density in the large myelinated fibers. Quantitative sensory testing also revealed an impairment of pinprick, temperature, and touch sensations. Cutaneous nerve biopsy confirmed a loss of epidermal nerves indicating an involvement of the small sensory nerves.

Acute painful peripheral neuropathy due to metronidazole

Acute painful peripheral neuropathy due to metronidazole

Itraconazole-Induced Painful Neuropathy in a Man With Type 1 Diabetes

The antifungal agent itraconazole is considered safe in patients with diabetes (1,2) but has been associated with acute painful neuropathy in patients taking vincristine (3–5). We describe a patient with diabetic neuropathy who developed acute painful neuropathy with itraconazole therapy. A 37-year-old man with poorly controlled type 1 diabetes of 19 years’ duration presented with an excematous rash affecting his lower abdomen. Skin scrapings grew C. albicans . Itraconazole (200 mg/day) was prescribed, but on the 4th day of treatment he developed acute bilateral leg weakness with stabbing pain in the hips and legs and difficulty walking. He …

Acute Painful Neuropathy Restricted to the Abdomen following Rapid Glycaemic Control in Type 2 Diabetes

A 46-year-old Japanese man with type 2 diabetes mellitus, whose only diabetic complication was simple retinopathy, developed acute painful neuropathy. This presented as paresthesia and hyperesthesia restricted to the abdomen. The patient's haemoglobin A(1c) had dropped from 12% to 7.5% within 5 months, following a rapid improvement in glycaemic control. On investigation, there were no indications of disease in the intraabdominal area. Nerve conduction studies were consistent with mild sensorimotor peripheral and autonomic neuropathy. The patient required medication (mexiletine, sulpiride and imipramine hydrochloride) to control the pain. Four months after presentation, the symptoms showed a dramatic improvement and the treatment for pain relief was discontinued without any recurrence of paresthesia or hyperesthesia in the patient's abdomen. This was a very unusual case of diabetic post-treatment painful neuropathy in which the prominent features were severe pain, paresthesia and hyperesthesia restricted to the abdomen.

腰部交感神経節ブロックが著効した急性有痛性糖尿病性神経障害

腰部交感神経節ブロックが著効した急性有痛性糖尿病性神経障害

Management of diabetic neuropathy

The only strategy shown to be consistently beneficial in the treatment of diabetic neuropathy is meticulous control of blood glucose. The largest study of the effects of glycemic control on progression of neuropathy was the Diabetes Control and Complications Trial, which enrolled 1,500 patients. Meticulous control of blood glucose by multiple injections or continuous subcutaneous infusion both delayed the onset of neuropathy and slowed its progression. A weakness of this and other studies of the effect of glycemic control is that they used surrogate measures of improvement (or slowing of progression) of neurologic function. Most used sensory and motor nerve conduction studies and some used vibration perception thresholds. Whether such measures correlate reliably with neuropathy symptom scores, neurologic examination, quality-of-life measures, neuropathic complications (foot ulcers and amputation), and mortality remains controversial. Also, most studies of tight glycemic control do not address the complications of more intensive therapy, among them severe hypoglycemia. Severe hypoglycemia can precipitate acute painful neuropathy, and it markedly increases axonal degeneration in experimental diabetic neuropathy. Finally, all studies have been confined to patients with mild neuropathy; some patients had no clinical evidence of neuropathy. Whether benefit can accrue to patients with more advanced neuropathy is not known. The most physiologic means of achieving glycemic control is through pancreas transplantation; this can result in significant improvement in clinical and electrophysiologic measures of motor and sensory function and slightly improve autonomic function. Strategies to reduce the metabolic consequences of hyperglycemia on nerves and to enhance axonal regeneration are needed to supplement careful glycemic control. Aldose reductase inhibitors hold promise for reducing metabolic nerve injury, but further study is needed.

DIABETIC NEUROPATHIC CACHEXIA: THE IMPORTANCE OF POSITIVE RECOGNITION AND EARLY NUTRITIONAL SUPPORT

SUMMARY We report on a patient with acute painful diabetic neuropathy in whom abdominal pain and severe weight loss mimicked neoplastic disease. Positive recognition of the diabetic neuropathic cachexia syndrome might have avoided extensive invasive investigation. Intensive enteral nutritional support was associated with prompt resolution.

Delayed somatosensory conduction in acute painful neuropathy of diabetes

We examined the peripheral-central sensory conduction by using somatosensory evoked potential (SEP) in a 48 year old diabetic patient with acute painful neuropathy. The sural, ulnar and median sensory nerve conduction and SEP elicited by wrist stimulation showed no abnormalities, nevertheless, the tibial nerve SEP revealed absent spinal N19 and a remarkable delay of the cortical arrival time. These findings suggest involvement of the dorsal roots or the dorsal column in the acute painful neuropathy of diabetes.

Acute painful diabetic neuropathy following severe weight loss

A 34-year-old man, recently diagnosed as diabetic, presented an acute painful neuropathy. He reported a profound weight loss during the months preceding onset. There were no motor symptoms, and only mild neurological signs were observed on examination. Improvement was related to a good glycemic control and weight gain. Acute painful diabetic neuropathy is a condition that may affect diabetic patients shortly after development of the disease. The pathogenetic roles played by different factors are reviewed.

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.