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PubMedDate not supplied

Peripheral neuropathy in Nigerian subjects with chronic renal failure.

BACKGROUND: Chronic Renal Failure (CRF) is common in Nigeria and has a high prevalence in the young age groups. While peripheral neuropathy is reported to be the commonest neurological complication in patients with CRF, its frequency and nature have not been documented in Nigerian subjects. The unavailable or expensive intervention measures in Nigeria make it imperative to consider all presenting features of CRF in order to improve its morbidity. METHODS: Twenty-one subjects with chronic renal failure at the University College Hospital, Ibadan, were studied. Chronic renal failure was confirmed by ultrasound scan, urea and creatinine values, 24 hour urinary creatinine values and clinical features of uraemia of more than 6 months. Excluded were subjects with diabetes mellitus, alcoholism, etc. All subjects had full neurological examination done and peripheral neuropathy was taken as the presence of two or more abnormal findings on peripheral nervous system examination. RESULTS: Peripheral neuropathy was documented in 6 (28.5%) of the subjects. The finding of peripheral neuropathy was associated with older age of subjects and longer duration of illness. It was not related to the serum levels of urea or creatinine. CONCLUSIONS: Peripheral neuropathy occurs in Nigerian CRF patients and is related to longer duration of illness, but not to prevailing serum urea or creatinine levels. Morbidity could be improved in these patients irrespective of severity of renal function if the symptoms of peripheral neuropathy are detected and treated.

Adult↗
PubMedDate not supplied

Sural nerve bioptic findings in essential cryoglobulinemic patients with and without peripheral neuropathy.

Peripheral neuropathy often occurs in cryoglobulinemia but the pathogenesis of the peripheral nerve involvement is not completely understood, so that the relation between the reported endoneural changes and neuropathy is not clear. In this study we compared the sural nerve biopsies of 6 cryoglobulinemic patients with or without signs of peripheral neuropathy and all affected by the essential mixed type II form (ECII) and, moreover, of 8 age-matched controls. We found that in all the patients with neuropathy, axonopathy occurred and it was invariably associated with endoneural vessel damage. Moreover, the fiber losses were patchily distributed within the nerve fascicles. On the contrary both nerve fibers and vessels were normal in the patients without clinical and neurophysiological evidence of neuropathy and in controls. Our results support the hypothesis that the endoneural damage observed during ECII is not simply coincidental, but is relevant in the pathogenesis of cryoglobulinemic neuropathy. They also favor the assumption that ischemic damage of the nerve fibers occurs during ECII.

Aged↗
PubMed1992

Peripheral neuropathy in mixed cryoglobulinemia: clinical and electrophysiologic investigations.

Peripheral neuropathy has been described in different rheumatic diseases such as rheumatoid arthritis, systemic lupus erythematosus and systemic vasculitis, but usually in limited numbers of patients. Nerve injury is more frequently reported in mixed cryoglobulinemia. In earlier studies generally performed in small series of patients, prevalence of peripheral neuropathy varied widely. We evaluated prevalence of peripheral neuropathy in 33 unselected patients with mixed cryoglobulinemia (25 women, 8 men, aged from 45-71 years). Neurologic involvement was detected using a complete clinical and electrophysiologic assessment, including sensory motor conduction velocities, F wave and H reflex. Neurologic examination revealed a neuropathy in 48% of subjects, while electrophysiologic variables were altered in 82%; a percentage similar to that of subjective symptoms (91%). Among electrophysiologic investigations, F wave was altered in 22/33 subjects (67%); therefore, this variable seems to be the most reliable for the detection of neurologic involvement. Cryocrit levels were significantly higher in patients with peripheral neuropathy: abnormal examination (p less than 0.01), sensory motor conduction (p less than 0.04), and F wave alterations (p less than 0.008). In addition, hemorheological abnormalities seem to contribute to the pathogenesis of nerve injury. Our results indicate that peripheral neuropathy, to a variable degree, is present in the majority of patients with mixed cryoglobulinemia, and a complete clinical and electrophysiologic investigation can be useful for an early and correct diagnosis.

Aged↗
PubMed1992

A study of neuropathy in HIV infection.

A prospective study of possible aetiological factors for neuropathy associated with HIV infection was performed in 80 patients and 28 homosexual controls. At entry to the study twelve patients (15 per cent) had evidence of a generalized neuropathy not due to any other cause and a further three patients developed symptomatic neuropathy during a mean (SD) follow-up of 20 (7.5) months. All but two of these neuropathies were of the distal symmetrical sensory type. Electrophysiology was consistent with an axonal pathology and nerve biopsy confirmed this as the major pathological change. Warming threshold was the diagnostic test most frequently abnormal, sometimes in the absence of other electrophysiological abnormalities. No association was seen with opportunistic infection (cytomegalovirus, herpes simplex, Pneumocystis pneumonia, toxoplasmosis, Cryptococcus infection or tuberculosis). HIV proviral DNA could not be detected in paraffin sections of peripheral nerve in six patients with neuropathy. The presence of the neuropathy did not show significant correlation with depression of the number of CD4+ T cells in the blood, impaired T cell function tests, or IgG, IgM, or IgA levels. Immune complexes containing C1q, but not those containing IgG, IgM, IgA or C3c, were significantly more common among neuropathic patients (p = 0.01).

AIDS-Related Opportunistic Infections↗
PubMed2003

[Two distinct types of neuropathy associated with Sjögren's syndrome developed in one patient. The importance of the selection of an appropriate therapeutic regimen].

A 62-year-old woman was admitted to our hospital because of muscle weakness and sensory disturbance in extremities. She showed weakness, muscle atrophy and sensory abnormality in four limbs with patchy distribution, suggesting involvement of multiple peripheral nerve trunks. Serum titers of anti-SS-A, SS-B, and antinuclear antibody were elevated. Sural nerve biopsy showed recanalization and lymphocytic infiltration in the epineural small vessels, suggesting the presence of vasculitis. She was diagnosed as having vasculitic neuropathy complicated with Sjögren's syndrome. Methylprednisolone pulse therapy followed by oral prednisolone was started and these symptoms gradually improved in one month. At age 63, she felt dysesthesia in the right lower limb and this sensory abnormality spreaded to upper limbs. Two years later, she was admitted again due to clumsiness of hands and gait disturbance. Neurological examination showed decreased vibration and position sense of lower limbs and limb ataxia in addition to dysesthesia. Electrophysiological studies demonstrated significant decrease in amplitude of sensory nerve action potentials and delayed somatosensory evoked potentials after N13, indicating impairment of dorsal root ganglions. She was treated with intravenous immunoglobulin (400 mg/kg, total 15 g/day) for 5 days. One week later, sensory ataxia was improved. It has been known that Sjögren's syndrome is often complicate with various types of neuropathies including vasculitic neuropathy and sensory neuropathy. Our patient developed these two different types of neuropathies which were dramatically improved after two different therapeutic regimens; indicating the importance to select a suitable treatment regimen in accordance with the mechanism of neuropathy associated with Sjögren's syndrome.

Adrenal Cortex Hormones↗
PubMed2004

Clinical and electrophysiological studies of a family with probable X-linked dominant Charcot-Marie-Tooth neuropathy and ptosis.

BACKGROUND: The X-linked dominant Charcot-Marie-Tooth neuropathy (CMTX) is a hereditary motor and sensory neuropathy linked to a variety of mutations in the connexin32 (Cx32) gene. Clinical and genetic features of CMTX have not previously been reported in Taiwanese. METHODS: Clinical evaluations and electrophysiological studies were carried out on 25 family members of a Taiwanese family group. Molecular genetic analysis of the Cx32 gene was performed. A sural nerve biopsy was obtained from 1 patient. RESULTS: Nine patients had clinical features of X-linked dominant inheritance and a moderate Charcot-Marie-Tooth (CMT) neuropathy phenotype. Molecular genetic analysis showed no mutation of the Cx32 coding region, but revealed a G-to-A transition at position -215 of the nerve-specific promoter P2 of the Cx32 gene. Ptosis is 1 clinical manifestation of neuropathy in this probable CMTX family. Familial hyperthyroidism is an additional independent feature of the family. Electrophysiological and histological studies showed features of axonal neuropathy. Multimodality evoked potential studies revealed normal central motor and sensory conduction velocities. CONCLUSIONS: The presence of ptosis in this family illustrates the existence of clinical heterogeneity among related family members with CMTX similar to that in CMT of autosomal inheritance. Electrophysiological and histological findings revealed normal central conduction and axonal neuropathy.

Acute Disease↗
PubMed2004

The clinical spectrum of amiodarone-associated optic neuropathy.

PURPOSE: To describe the clinical spectrum of amiodarone-associated optic neuropathy. METHODS: Observational cases series and review. RESULTS: Of 55 cases, the median interval for onset of optic neuropathy was four months after initiating amiodarone; 88% occurred within 12 months. Seven (13%) patients were asymptomatic. Twenty-two (40%) patients presented with sudden visual loss, while 26 (47%) had insidious loss of vision. Visual acuity ranged from 20/15 to light perception; 10 (18%) patients had legal blindness with visual acuity of 20/200 or worse. Visual field loss was present in 91% of cases. Color vision loss was present in eight (40%) of 20 cases. Optic disc edema was present in 85% of cases, while eight (15%) patients had retrobulbar optic neuropathy, without evidence of disc edema. Optic disc edema resolved over a median time of three months. Five patients had raised intracranial pressure on lumbar puncture. CONCLUSION: We were able to classify amiodarone-associated optic neuropathy into five clinical categories with respect to temporal characteristics and optic nerve appearance: insidious-onset (43%), acute-onset (28%), retrobulbar (13%), increased intracranial pressure (8%), and delayed-progressive onset (8%). Most cases of optic neuropathy commenced within 12 months of initiating amiodarone, with the median onset being four months. Over 10% of patients will have no visual symptoms at the onset. Ophthalmologic examinations within the first 12 months--and particularly within four months of initiating amiodarone--should improve early detection of amiodarone-associated optic neuropathy.

Aged↗
PubMed2004

[Physiological approach to peripheral neuropathy. Conventional nerve conduction studies and magnetic motor root stimulation].

In this communication, I first show some points we should mind in the conventional peripheral nerve conduction studies and later present clinical usefulness of motor root stimulation for peripheral neuropathy. CONVENTIONAL NERVE CONDUCTION STUDIES (NCS): The most important point revealed by the conventional NCSs is whether neuropathy is due to axonal degeneration or demyelinating process. Precise clinical examination with this neurophysiological information leads us to a diagnosis and treatment. Poor clinical examination makes these findings useless. Long standing axonal degeneration sometimes induces secondary demyelination at the most distal part of involved nerves. On the other hand, severe segmental demyelination often provokes secondary axonal degeneration at distal parts to the site of demyelination. These secondary changes show the same abnormal neurophysiological findings as those of the primary involvement. We should be careful of this possibility when interpreting the results of NCS. NCS of sensory nerves is not good at revealing demyelinating process. Mild temporal dispersion of potentials often reduces an amplitude of SNAP or loss of responses, which usually suggests axonal degeneration, because of short duration of sensory nerve potentials. MOTOR ROOT STIMULATION IN PERIPHERAL NEUROPATHY: Magnetic stimulation with a coil placed over the spine activates motor roots and evokes EMG responses from upper and lower limb muscles. The site of activation with this method was determined to be where the motor roots exit from the spinal canal (intervertebral foramina) (J Neurol Neurosurg Psychiatry 52 (9): 1025-1032, 1989) because induced currents are very dense at such a foramen made by electric resistant bones. In several kinds of peripheral neuropathy, this method has been used to detect a lesion at a proximal part of the peripheral nerves which can not be detected by the conventional NCSs. I present a few cases in whom motor root stimulation had a clinical merit. In a patient with neuralgic amyotrophy, motor root stimulation disclosed a conduction block between the cervical intervertebral foramen and brachial plexus which was not detected by conventional NCSs. Motor root stimulation clearly revealed demyelination in a patient with CIDP in whom sural nerve biopsy findings suggested axonal degeneration, that must be secondary to demyelination. In a patient with tomacular neuropathy, magnetic stimulation revealed conduction delay in the spinal nerve within the spinal canal (Clin Neurol (Jap), 28: 447-452, 1988). Based on the above results, combination of NCSs and magnetic motor root stimulation must brush up the neurophysiological approach to peripheral neuropathy.

Electric Stimulation↗
PubMed2005

[Some properties of mixed saliva in diabetic autonomic neuropathy].

INTRODUCTION: The purpose of this work was to determine the influence of diabetic autonomic neuropathy on some basic properties of saliva such as volume of stimulated mixed saliva, concentration and secretion rates of sodium, potassium and calcium ions, and of glucose. MATERIAL AND METHODS: The study was carried out in 55 patients (25 females and 30 males). The study group consisted of 19 patients with type 2 diabetes mellitus and autonomic neuropathy affecting the cardiovascular system--DM-N(+). Two control groups were formed. One of them included 18 diabetic patients without any autonomic neuropathy--DM-N(-), the other (K) comprised 18 patients without diabetes. In the latter group there were nine patients on atropine (K-A) due to bradycardia and nine patients on propranolol (K-P) due to tachycardia. In the latter group, saliva samples were collected before and after administration of atropine or propranolol. RESULTS: A significantly lower (p < 0.001) mean volume of stimulated mixed saliva was found in diabetic patients with autonomic neuropathy (1.91 +/- 0.34 mL) and control patients on atropine (K-A) (2.24 +/- 0.68 mL) as compared to DM-N(-) (5.37 +/- 0.78 mL) and K-P patients (5.51 +/- 1.05 mL). The volume of saliva did not correlate with glycosylated haemoglobin in either DM-N(-) or DM-N(+) groups. Secretion of glucose, as well as sodium, potassium and calcium ions to saliva was significantly lower in diabetics with autonomic neuropathy DM-N(+) and in non-diabetics after administration of atropine. CONCLUSION: Based on these results it was concluded that secretion of stimulated mixed saliva, glucose, as well as sodium, potassium and calcium ions is significantly reduced in autonomic neuropathy. These findings may be associated with lesions to parasympathetic nerve fibers caused by long-lasting diabetes.

Aged↗
PubMed1991

Peripheral neuropathy of mitochondrial myopathies.

Peripheral neuropathy has attracted relatively little attention in mitochondrial myopathy. However, mitochondrial myopathies are clinically heterogeneous disorders that can affect multiple systems including peripheral nerves other than the skeletal muscle. In addition to the survey of the literature, we studied 6 cases of mitochondrial myopathy with peripheral neuropathy; 3 cases of oligo-systemic involvement confined mainly to skeletal muscles and peripheral nerves, and 3 cases of multi-systemic involvement diagnosed as myoclonus epilepsy with ragged-red fibers (MERRF) or mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). This study suggests that peripheral neuropathy may be relatively common and has similar clinical and laboratory features in a broad spectrum of mitochondrial myopathies. The clinical manifestation is usually of mild sensorimotor neuropathy with frequent subclinical involvement. Sensory disturbances are more evident than manifestations of motor neuropathy which is usually subclinical. It is also noteworthy that there exist some cases of oligo-systemic involvement, which present with peripheral neuropathy as main clinical manifestations. Electrophysiological findings include decreased nerve conduction velocities and neuropathic electromyograms. Peripheral nerves show loss of myelinated fibers, particularly of large ones, and the remaining fibers have disproportionately thin myelin sheaths with or without onion-bulb formation. Thus the pathological process is axonal degeneration with demyelination resulting from involvement of both neurons (axons) and Schwann cells.

Acidosis, Lactic↗
PubMed1991

[Peripheral neuropathies in dysglobulinemia].

Peripheral neuropathies are frequently associated with different types of dysglobulinemia. These neuropathies may have different chemical features depending on the nature of the dysglobulinemia. Most frequently it is a picture of predominantly sensory polyneuropathy. The autoimmune origin of the neuropathies with demyelination, observed in "benign" monoclonal gammopathies or some Waldenström diseases, is strongly suggested by immunohistochemical studies. Neuropathies associated with multiple myeloma or amyloidosis, are generally due to compressions, infiltrations or hemorragic destructions. The neuropathy frequently reveals and preceeds the dysglobulinemia, which should be looked for in all neuropathy without any obvious cause.

Amyloidosis↗
PubMed2006

[Nerve excitability studies in the assessment of dysimmune neuropathies].

INTRODUCTION: Various changes in axonal membrane excitability might explain negative symptoms in dysimmune neuropathies, e.g., acute or chronic inflammatory demyelinating neuropathies or multifocal neuropathies with persistent conduction blocks. Several electrophysiological methods have recently been designed to specifically assess such axonal membrane excitability changes. STATE OF ART: Resting and action potentials are related to ionic movements through the axonal membrane, mainly involving various types of sodium and potassium channels, as well as the ATP-dependent Na+/K+ pump. The functional status of these channels and pumps can be assessed in man, by studying the excitability recovery cycle after a single impulse, the strength-duration and stimulus-response curves, and the effects of hyperpolarization and depolarization depending on activity (voluntary contraction), ischemia or application of prolonged subthreshold currents. Various features of altered axonal membrane excitability might characterize dysimmune neuropathies, according to the course of the disease and its treatment. PERSPECTIVES: This electrophysiological approach allowed changes in axonal membrane properties to be objectively determined. In particular, some results obtained with these methods could explain the rapid action of intravenous immunoglobulins, and various pathophysiological mechanisms of conduction block or axonal degeneration. CONCLUSIONS: Nerve excitability studies appeared to be useful for the diagnosis and the follow-up of dysimmune neuropathies. New therapeutical strategies for such neuropathies will be probably developed in the future intending to improve nerve function by acting on axonal membrane excitability.

Animals↗
PubMed2006

Approach to a case of autonomic peripheral neuropathy.

Autonomic neuropathy is the term used to describe autonomic disturbances resulting from diseases of the peripheral autonomic nervous system. This is a group of disorders in which the small, lightly myelinated and unmyelinated autonomic nerve fibers are selectively targeted. Most often, autonomic neuropathies occur in conjunction with a somatic neuropathy (i.e. with motor weakness and/or sensory loss), but they can occur in isolation. Causes of autonomic neuropathies are immune-mediated, paraneoplastic, infectious, toxic and drug-induced, hereditary, nutritional and idiopathic. Amongst all, diabetes mellitus is the most common cause. Autonomic features, which involve the cardiovascular, gastrointestinal, urogenital, sudomotor, and pupillomotor systems, occur in varying combination in these disorders. Orthostatic hypotension is often the first recognized and most disabling symptom. Noninvasive, well-validated clinical tests of autonomic functions along with a host of laboratory tests are of immense value to diagnose the presence and to demonstrate the distribution of autonomic failure. Treatment aims to treat specific cause of the autonomic neuropathy (if possible) and to control symptoms of autonomic dysfunction. Present review attempts to outline clinical approach to a case of autonomic peripheral neuropathy.

Arrhythmias, Cardiac↗
PubMed1991

[Recovery of visual field defects in ischemic optic neuropathy and idiopathic optic neuritis].

Fifty-four eyes of 41 patients with optic nerve disease demonstrating acute visual field defects without any traumatic, compressive, or other known etiology were classified into four categories. Those showing poor recovery of visual field defects were ischemic optic neuropathy which was subclassified into either anterior ischemic optic neuropathy (AION) or posterior ischemic optic neuropathy (PION) according to the ophthalmoscopic changes in the optic nerve head. Those showing good recovery of visual field defects were idiopathic optic neuritis which was subclassified into either papillitis or retrobulbar neuritis according to the ophthalmoscopic pathology of the optic disc. Patients with ischemic optic neuropathy were significantly older than those with optic neuritis. All eyes with optic neuritis showed good recovery of vision, whereas those with ischemic optic neuropathy showed varying outcomes of vision. With regard to the pattern of field defect, central or paracentral scotoma was predominant in all but eyes with AION in which altitude defect predominated. Pale swelling of the optic nerve head and angiographic evidence of circulatory disturbance in the optic disc or adjacent choroid were common findings in eyes with AION, whereas such findings were never observed in eyes with papillitis. The amplitude of pattern visual evoked potential was significantly lower in eyes with PION than in those with retrobulbar optic neuritis. Four patients classified as optic neuritis developed into multiple sclerosis in the follow-up study. It was concluded that poor recovery of visual field defect is one of the most convincing evidences for the diagnosis of ischemic optic neuropathy.

Adult↗
PubMed1990

[Humoral antibodies in immune mediated neuropathy].

Immune mediated neuropathy includes acute inflammatory demyelinating polyneuropathy (AIDP), chronic inflammatory demyelinating neuropathy (CIDN), paraproteinemic polyneuropathy (PPN) and Crow-Fukase syndrome (CFS). Serum antibodies as humoral immunity in patients with immune mediated neuropathy were measured by the method of immunoblots and ELISA. P0 protein, P2 protein, 170K-Mr glycoprotein and ganglioside (GGD) of human peripheral nerve myelin and MBP, myelin associated glycoprotein (MAG) of human central nerve myelin were used as antigens. In AIDP anti P2 antibodies were elevated significantly. However, anti MBP antibodies were also elevated in parallel. In PPN anti MAG antibodies were detected in 4 patients with IgM-M proteinemia and demyelinating neuropathy. High titers of anti MAG antibodies were also detected in the same 4 patients. Characteristic pathological findings of biopsied sural nerve were segmental demyelination with widening of the intraperiod line of the outer myelin lamella in all 4 patients. Positive rate of anti myelin antibodies were 23% in 23 cases with PPN. Anti 170K-Mr glycoprotein was detected only in one patient with IgM-M proteinemia, polyneuropathy and incurable dermatitis. Anti GGD antibodies were not detected in PPN or CFS. A few patients with GBS or CIDN have anti GGD antibodies in ELISA. It is well known that various antibodies to peripheral nerve myelin are detected in neuropathy, especially demyelinating state. The most important antigen established in this study in the pathogenesis of neuropathy is MAG. IgM monoclonal protein including anti MAG antibodies was absorbed by purified MAG completely. Anti 170K Mr glycoprotein was also absorbed by purified 170K-Mr glycoprotein. Role of humoral antibody to peripheral nerve myelin specific 170K-Mr glycoprotein remains to be solved.

Antibody Formation↗
PubMed1989

Disulfiram neuropathy: a review (1971-1988) and report of a case.

Neuropathy is one of the most severe side effects of disulfiram therapy. We report the case of a young man who developed a neuropathy following disulfiram administration, with a virtually complete recovery in 14 months. We then discuss 37 cases of disulfiram neuropathy reported since 1971. Evidence is given that: (1) there is no numerical sex prevalence, although the incidence of the disease in women is probably disproportionately high; (2) symptom onset latency is dose-dependent, being longer at 250 mg/day or less; (3) neurological deficits are also dose-dependent, being milder at 250 mg/day or less; (4) the two previous findings and single observations suggest that disulfiram neuropathy is a dose-dependent phenomenon; (5) recovery probably follows a course which depends primarily on the initial degree of impairment; (6) the genetic mechanism probably involves carbon disulfide and a hypothesis as to the possible biochemical mechanism is proposed; (7) chloral hydrate can bear a potentiation effect on neuropathy, and the association with disulfiram is best avoided. Further, we give guidelines for the differentiation between alcoholic and disulfiram neuropathy, advise prescribing the drug at 250 mg daily or less, if possible, and stress the utmost importance of an early diagnosis.

Adult↗
PubMed1989

[Peripheral neuropathy in HIV infection].

Neuropathy may complicate all stages of human immunodeficiency virus infection (HIV). Different types of peripheral neuropathy and myelopathy have been reported associated with HIV infection: sensory symmetrical polyneuropathy, acute inflammatory demyelinating polyneuropathy, chronic inflammatory demyelinating polyneuropathy, mononeuropathy multiplex, sensory ataxic neuropathy (ganglioneuronitis), cauda equina syndrome, amyotrophic lateral sclerosis, spastic paraparesia, and subclinical neuropathy diagnosed by electrophysiologic study. We describe the main clinical, electrophysiological and pathological features in these different types of neuropathy and comment their pathogenesis and treatment. Results in our series of twenty-two patients are also reported. In this series we want to underline three cases in which a chronic demyelinating polyneuropathy was the first manifestation of HIV infection. Thus, patients with predominantly motor demyelinating neuropathies and suspicious risk factors should be screened for silent HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1987

[Acquired metabolic neuropathies (2): Kidney failure, hypothyroidism and hypoglycemia].

This is the second part of a review article on metabolic neuropathies. The frequency and severity of neuropathy due to chronic renal failure have dramatically decreased during the last ten years, as a result of improvement in management of patients with renal failure, even though the mechanism leading to development of the neuropathy is not well understood. Measurement of nerve conduction velocity does not appear to be appropriate to the detection of axonal neuropathy and follow-up of patients with neuropathy associated with chronic renal failure. Peripheral neuropathy observed in association with hypoglycaemia and with hypothyroidism are briefly reviewed.

Humans↗