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PubMed1996

[A 63 year-old man with progressive gait disturbance and dysarthria].

We report a 63-year-old man with progressive gait disturbance and dysarthria. The patient was apparently well until the age of 62 (February, 1990) when he noted unsteadiness of gait. Two months later, dysarthria appeared. He was admitted to Juntendo Izunagaoka Hospital on April 23, 1990. Neurologic examination revealed a mentally sound man with normal higher cerebral functions. Cranial nerves were unremarkable except for scanning speech. His gait was ataxic with positive Romberg sign. No motor weakness was noted, however, he had hypotonia and cerebellar ataxia. Deep tendon reflexes were retained and the plantar response was flexor. Pain, touch and vibration senses were diminished in the distal parts of the lower extremities. Laboratory examination revealed a 2.5 cm mass in the left lung field. Cranial MRI revealed a small T1-low and T2-high signal intensity lesion in the left temporal lobe. Abdominal CT scan revealed multiple low density lesions in the liver. His subsequent course was complicated by progressive deterioration in his gait and loss of deep tendon reflexes. He expired on November 24, 1990. The patient was discussed in the neurological CPC and the chief discussant arrived at the conclusion that the patient had anti-Hu associated paraneoplastic encephalomyelitis and sensory neuropathy. Some other participants thought that the patient had carcinomatous cerebellar degeneration. Postmortem examination revealed a 4x4 cm mass lesion involving the left S4-S5 segments. Histologic examination of the tumor was small cell carcinoma. Many metastatic foci were found in the liver. The cerebral hemispheres were unremarkable except for a small wedge-shaped tissue defect in the left temporal lobe which appeared to have been caused by old head trauma which the patient had received. The cerebellar vermis showed slight enlargement of cortical sulci, however, the cerebellar hemispheres appeared unremarkable. Upon histologic examination, marked loss of Purkinje cells was noted, particularly in the cerebellar anterior lobe. The dentate nucleus showed slight cell loss with increase in fat granule cells. The inferior olive was normal. The histologic characteristics were consistent with the pathologic diagnosis of carcinomatous cerebellar degeneration. No evidence of limbic encephalitis was seen. The peripheral nerve was not examined.

Carcinoma, Small Cell↗
PubMed1997

Congenital hypomyelinating neuropathy: a reversible case.

A boy was born at 39 weeks gestation with severe weakness and hypotonia, fractured femurs, poor suck and swallow, and absent deep tendon reflexes. Electrodiagnostic studies revealed marked slowing of motor nerve conduction velocities and normal muscle electrical activity with no evidence of acute denervation. Muscle biopsy showed mild type 2 fiber predominance, and sural nerve biopsy revealed large axons without myelin, and axons with insufficient amount of myelin for their diameter. There was no evidence of inflammation or demyelination. Gradual clinical improvement in tone and strength occurred in a cephalocaudal direction. By 4 months, motor nerve conduction velocities and clinical examination were normal apart from absent deep tendon reflexes. On review at 19 months, motor development and neurological examination were completely normal. Pathogenesis of this reversible pathologically documented case of congenital hypomyelinating neuropathy is unclear. No evidence was found for an inflammatory, toxic, metabolic, or demyelinating cause. Abnormal expression of a developmental gene, as in reversible cytochrome oxidase deficiency, may be a cause of this neuropathy.

Axons↗
PubMed1992

Mechanisms of baclofen action on spasticity.

This investigation estimated the mechanisms of baclofen action on spasticity using a battery of electromyographic methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with baclofen-mean daily dose 54.3 alpha 11.6 mg for a mean of 26.3 alpha 4.9 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of electromyographic methods was used to analyse different mechanisms of spasticity: for alpha motoneurone activity--the F wave parameters; for gamma motoneurone activity--the T/H reflex amplitude ratio; for presynaptic inhibition--the ratio of H reflex amplitudes before and after vibration on the achilles tendon (Hvibr./Hmax); for common interneurone activity--the flexor reflex parameters. Our results revealed that baclofen reduces spastically increased muscle tone and Babinski sign. It has no influence on muscle force, tendon reflexes and ankle clonus. Baclofen acts by normalizing the altered interneurone activity and decreasing of alpha motoneurone activity. When spasticity has altered interneurone activity and increased motoneurone activity, it is better to treat with baclofen.

Baclofen↗
PubMed2003

Acute motor conduction block neuropathy Another Guillain-Barré syndrome variant.

OBJECTIVE: To report two patients with an acute exclusively motor neuropathy with conduction blocks. METHODS: Serial electrophysiologic studies were carried out. RESULTS: Two patients developed symmetric proximal and distal weakness without sensory abnormalities after enteritis. Tendon reflexes were normal in one patient and brisk in the other. One patient had high titer immunoglobulin G to GD1a and GM1, and the other to GD1b, GD1a, and GM1 and a recent Campylobacter jejuni infection. Electrophysiology showed early partial motor conduction block in intermediate and distal nerve segments, normal sensory conductions even across the sites of conduction block, and normal somatosensory evoked potentials. Conduction blocks resolved in 2 to 5 weeks without excessive temporal dispersion of proximal motor responses. CONCLUSIONS: Acute motor neuropathy with normal or brisk tendon reflexes, conduction block, and fast recovery appears to be a variant of Guillain-Barré syndrome. Conduction block may result from immune-mediated conduction failure at the nodes of Ranvier without demyelination.

Action Potentials↗
PubMed1997

Developmental adaptation of rat nociceptive withdrawal reflexes after neonatal tendon transfer.

Nociceptive withdrawal reflexes (NWRs) were studied in adult rats in which the movement patterns produced by single muscles had been altered by neonatal tendon transfer. NWRs evoked by cutaneous noxious mechanical and thermal (CO2-laser) stimulation were recorded using electromyography in a decerebrate spinal preparation. The sensitivity distribution within the receptive fields of the NWRs of the extensor digitorum longus and the peronei muscles exhibited changes corresponding to the altered movement patterns. No detectable change of NWRs was found in normal muscles whose receptive fields overlapped that of the modified muscle. Furthermore, NWRs of muscles that regained an essentially normal function after neonatal tendon transfer did not differ from normal. It is proposed that a developmental experience-dependent mechanism, which takes into account the hindlimb movement pattern caused by contraction of single muscles, underlies the functionally adapted organization of adult NWRs.

Adaptation, Physiological↗
PubMed1983

Chronic asymmetrical spinal muscular atrophy.

The clinical and neurophysiological features of 18 cases of chronic asymmetrical spinal muscular atrophy are described. These were patients presenting with asymmetrical neurogenic atrophy involving one or more limbs who had no evidence of pyramidal tract dysfunction after 3 or more years of symptoms. There were twice as many males as females and the mean age of onset of the disorder was about 32 years. None of the patients had bulbar involvement. The tendon reflexes tended to be depressed. The distribution of muscle weakness in the limbs was very variable, and only slowly progressive. In 5 cases symptoms and signs were confined to the hands and forearms. Motor nerve conduction velocities to wasted muscles were slightly reduced but there was no evidence of generalised neuropathy. A diagnosis of chronic asymmetrical spinal muscular atrophy, as opposed to that of classical motor neurone disease, is favoured by an age of onset under 40 years, an absence of pyramidal signs or bulbar involvement after 3 years or more of symptoms, and depressed or absent tendon reflexes. The 2 conditions appear to be clinically distinct and prognosis is considerably better in chronic asymmetrical spinal muscular atrophy. The aetiology of this condition in unknown; it may be of relevance that 2 patients in this series had close relatives with Werdnig-Hoffmann disease.

Adult↗
PubMed2003

Acute changes in neuromuscular excitability after exhaustive whole body vibration exercise as compared to exhaustion by squatting exercise.

The effects of hard squatting exercise with (VbX+) and without (VbX-) vibration on neuromuscular function were tested in 19 healthy young volunteers. Before and after the exercise, three different tests were performed: maximum serial jumping for 30 s, electromyography during isometric knee extension at 70% of the maximum voluntary torque, and the quantitative analysis of the patellar tendon reflex. Between VbX+ and VbX- values, there was no difference found under baseline conditions. Time to exhaustion was significantly shorter in VbX+ than in VbX- (349 +/- 338 s versus 515 +/- 338 s), but blood lactate (5.49 +/- 2.73 mmol l-1 versus 5.00 +/- 2.26 mmol l-1) and subjectively perceived exertion (rate of perceived exertion values 18.1 +/- 1.2 versus 18.6 +/- 1.6) at the termination of exercise indicate comparable levels of fatigue. After the exercise, comparable effects were observed on jump height, ground contact time, and isometric torque. The vastus lateralis mean frequency during isometric torque, however, was higher after VbX+ than after VbX-. Likewise, the tendon reflex amplitude was significantly greater after VbX+ than after VbX- (4.34 +/- 3.63 Nm versus 1.68 +/- 1.32 Nm). It is followed that in exercise unto comparable degrees of exhaustion and muscular fatigue, superimposed 26 Hz vibration appears to elicit an alteration in neuromuscular recruitment patterns, which apparently enhance neuromuscular excitability. Possibly, this effect may be exploited for the design of future training regimes.

Adult↗
PubMed1991

[Two brother cases of late-onset familial amyloidotic polyneuropathy in Kyoto].

Measurement of variant Met30 transthyretin is diagnostic for a patients with familial amyloidotic polyneuropathy (FAP) type I. The elder brother first noticed numbness of the feet at 64 years of age, and developed weakness of the legs. A few years later, he noticed numbness of the hands, and he was admitted to the hospital at 67 years of age. He was emaciated and had hoarseness and macroglossia. He had moderate muscle atrophy and weakness of all extremities with distal predominance. Deep tendon reflexes were hypoactive in the upper limbs and absent in the lower limbs. There was marked sensory loss of pain and temperature in all 4 limbs distally, and position sense was also impaired. He had mild orthostatic hypotension, severe cardiomegaly and arrhythmia. The younger brother noticed cold sensation of the feet and sexual impotence at 59 years of age. Two years later, he had numbness of the feet and developed weakness of the legs. At 65 years of age, he was admitted to the hospital because of the micturition syncope. He was emaciated and had macroglossia. He had moderate muscle atrophy and weakness of all extremities with distal predominance. Deep tendon reflexes were absent. There was marked sensory loss in the extremities which was predominant in pain and temperature. He had severe orthostatic hypotension (112/70 mmHg in supine position, 50/30 mmHg on standing). Plasma NE value was low and showed poor response to standing. He had neither cardiomegaly nor arrhythmia. Their parents were supposed to have no neurological symptom and were not related with any other Japanese foci of FAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2003

[Neurological disturbances in heroin addicts in acute withdrawal and early post-abstinence periods].

Neurological examination was performed in 79 heroin addicts (mean age 24.4 +/- 6.3 years; heroin abusing duration 16.6 +/- 12.4 months; heroin dose per day 0.48 +/- 0.42 grams). During the first week after withdrawal, "physical dependency" symptoms, mild hypomimia and hypokinesia, low muscle tone, low tendon reflexes and facilitated nociceptive reflexes were observed in more than 70% of the patients. Non-specific microneurological signs as nystagm, limited convergence, tremor and dynamic ataxia etc, were found in more than 35% of the cases. Previously reported meningeal irritation or polyneuropathy symptoms were not determined in the patients population. Most of the symptoms disappeared after 10 days of abstinence as the follow-up examination of the 34 patients revealed. Mild hypomimia and hypokinesia persisted along with characteristic psychopathological changes. The most abundant neurological disturbances were observed in patients abusing heroin for more than 6 months in dosages more than 0.4 grams per day. Heroin withdrawal symptoms include reversible decrease in muscle tone and tendon reflexes as well as facilitation of nociceptive reflexes and reversible non-specific neurological microsigns. Heroin encephalopathy is characterized by ventral striatum insufficiency signs.

Acute Disease↗
PubMed1989

[Two patients with cervical diastematomyelia].

Two patients with cervical diastematomyelia are reported here. A nineteen year-old-man (patient 1) admitted to our hospital because of muscular weakness of right upper limb. He noted muscular atrophy of right upper limb at 16 years old, and then paresthesia was gradually aggravated in the ulnar side of the right hand. Physical examination showed muscular atrophy of right upper limb and hypesthesia in the right eight cervical and first thoracic dermatomes. The deep tendon reflexes were decreased in the right upper limb and were increased in the lower limb without pathological reflexes. In electromyographic examination, neurogenic motor units were observed in the upper right limb, dominantly in 1st interosseous muscle (between the fourth cervical and the first thoracic dermatome). Metrizamide computed tomographic (CT) myelography revealed sagittal splitting of the spinal cord from the third to the sixth cervical vertebra, producing two asymmetrical hemicords. A osseous or fibrous septum were not seen. The right hemicord was smaller than the left one. Patient 2 was a twenty-four-year-old woman. She visited our hospital because of muscular weakness of the right upper limb. In physical examination, there were the muscular atrophy of right hand and hypesthesia in the right eighth and first thoracic dermatomes. The deep tendon reflexes were decreased in the right upper limb and were increased in the right lower limb without pathological reflexes. The EMG studies revealed the neurogenic NMU in the right upper limb (between the fourth cervical and the first thoracic dermatome). Magnetic resonance imaging showed marked narrowing of the dural sac in flexion of the neck.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Dumbbell cervical neurinomas with subcutaneous extension: report of two cases].

Two cases of dumbbell cervical neurinomas with massive subcutaneous extension were reported. The first case was A 30-year-old woman who was admitted to our hospital because she had been aware of a left lateral cervical subcutaneous mass and was suffering from shoulder dullness. On admission, neurological examination revealed hypesthesia to touch and pain in the segmental area of C4, and hyperreflexia in the left biceps and patellar tendon reflexes. Plain X-ray showed enlargement of the left C3/4 intervertebral foramen. CT scan, post-myelogram CT and MRI demonstrated a dumbbell shaped tumor at the level of C3-4. Angiogram showed an anterior shift of the left vertebral artery (VA) and tumor stain. Temporary occlusion of the left VA by a balloon catheter was performed leaving no neurological deficits. The second case was a 36-year-old woman who had been aware of a left lateral cervical subcutaneous mass. She complained of shoulder pain and finger clumsiness. On admission, neurological examination revealed weakness of the left deltoid muscle, hypesthesia in the segmental area of C3-4 and exaggeration of all deep tendon reflexes in the left-side extremities. Plain X-ray showed enlargement of the C2/3, C3/4 and C4/5 intervertebral foramina. CT scan, post myelogram CT and MRI demonstrated a dumbbell shaped tumor at the level of C2-5. Angiogram showed an anteromedial shift of the left VA and tumor stain. Temporary occlusion test of the left VA by a balloon catheter was performed with negative results. In each case two-stage operations were undertaken with excellent results.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

[Two cases of neuralgic amyotrophy].

Case 1: A 27-year-old man had a fever of 38 degrees C, followed by acute onset of bilateral upper arm pain. Two days later severe muscle weakness in bilateral upper arms appeared and he was admitted to our hospital. On admission, severe atrophy of the left deltoid and mild atrophy of the right deltoid were observed, with severe muscle weakness in bilateral deltoid and mild weakness in other parts of upper extremities. Tendon reflexes were decreased in the upper extremities. Sensation was intact. CSF showed mild pleocytosis. Nerve conduction velocity was normal and electromyography showed mild NMU decrease in upper extremities. Muscle biopsy of the right deltoid one month after the onset was normal. Muscle weakness began to improve 3 months after the onset, with only mild weakness at 10 months. Case 2: A 60-year-old man had acute onset of left shoulder and upper arm pain, followed by muscle atrophy and weakness of the left upper arm. He showed marked atrophy of the left deltoid, moderate atrophy of the left biceps and left scapular region, and severe muscle weakness in the left upper arm. Deep tendon reflexes were absent in the left upper extremity. Sensation was intact. Nerve conduction velocity was normal and electromyography showed marked NMU decrease in the left upper arm. Muscle biopsy of the left biceps 4 months after the onset showed grouped atrophies on HE staining, type 2 fiber atrophies on routine ATPase staining, and many targetoid atrophic fibers on NADH-TR staining. Muscle weakness began to improve slowly 6 months after the onset, but considerable weakness persisted at 10 months. Detailed muscle biopsy findings in neuralgic amyotrophy have not been documented. Muscle biopsy of Case 2 showed marked neurogenic changes compared to Case 1, which may be associated with the difference in clinical course between the two cases.

Adult↗
PubMed1991

Cognition-independent neurologic symptoms in normal aging and probable Alzheimer's disease.

Deep tendon reflexes, plantar responses, muscle tone, and release signs were studied as 14 individual clinical variables and as five summary variables in 135 aged subjects, including 27 control subjects, 20 subjects with mild cognitive impairment, and 88 subjects with successive stages of probable Alzheimer's disease. Changes in activity of elicited responses were rated on a seven-point scale. Results were analyzed both as prevalence and mean degree of change in activity. Rating on a variable combining all 14 individual variables was significantly higher in a group with mild cognitive impairment than in a control group. Subjects with an early stage of Alzheimer's disease had both higher prevalence of increased activity and increased mean scores of deep tendon reflexes and muscle tone. They had a higher prevalence of increased activity on a variable combining three release signs. Patients with a late stage of Alzheimer's disease had significantly increased prevalence and mean scores of muscle tone and grasping and sucking reflexes compared with control subjects and patients with the early stage of Alzheimer's disease.

Activities of Daily Living↗
PubMed1995

Chronic symmetric symptomatic polyneuropathy in the elderly: a field screening investigation in two Italian regions. I. Prevalence and general characteristics of the sample. Italian General Practitioner Study Group (IGPSG).

The prevalence and general characteristics of chronic symmetric symptomatic polyneuropathy were assessed in two elderly populations living in Varese, northern Italy, and San Giovanni Rotondo, southern Italy. We interviewed 4,191 subjects (3,027 in Varese and 1,164 in San Giovanni Rotondo), 55 years and older, seen in office consultations by 27 general practitioners. A neurologist examined 734 patients who had two or more symptoms of polyneuropathy. A diagnosis of possible polyneuropathy (screening neuropathic symptoms and one of the following findings: bilateral impairment of strength; bilateral impairment of sensation; bilateral impairment of deep tendon reflexes) was made in 213 patients (7.0%) in Varese and 94 (8.1%) in San Giovanni Rotondo. Probable polyneuropathy (screening symptoms and at least two of the physical findings) was present in 111 Varese patients (3.7%) and 40 San Giovanni Rotondo patients (3.4%). The age- and sex-adjusted prevalence rate of probable polyneuropathy was 3.6 per 100 in Varese and 3.3 per 100 in San Giovanni Rotondo. The disease was more prevalent in women in Varese and in men in San Giovanni Rotondo and was significantly correlated with age in Varese. Diabetes was found in association with probable polyneuropathy in 43.7% of patients. Muscle cramps and distal paresthesia were the main symptoms. In general, polyneuropathy was mild to moderate, impairment of deep tendon reflexes and sensation being the most common findings.

Aged↗
PubMed1999

Involvement of the spinal posterior horn in Gerstmann-Sträussler-Scheinker disease (PrP P102L).

OBJECTIVE: The authors studied the pathomechanisms of the characteristics associated with Gerstmann-Sträussler-Scheinker disease (GSS). BACKGROUND: GSS, associated with a missense mutation at codon 102 of the prion protein (PrP) gene (GSS102), is a hereditary disorder that presents with progressive ataxia and dementia, and is characterized by the loss of deep tendon reflexes and painful dysesthesias of the legs in its early stage. METHODS: The authors conducted immunohistochemical studies of the spinal cord and peripheral nervous system in one of two patients from a Japanese family with GSS102 in comparison with patients with GSS105. RESULTS: The authors found intense PrP immunoreactivities mainly in the posterior horn of the spinal cord, but not in the dorsal root ganglia or peripheral nerves. In addition to PrP amyloid plaques, synaptic-type, fine granular PrP deposits were distributed in the spinal posterior horns. In contrast to the GSS102 patient, the spinal cords of the GSS105 patients showed no granular PrP deposits. CONCLUSIONS: The PrP abnormalities in synaptic structures of the spinal posterior horn may cause synaptic dysfunction that leads to loss of deep tendon reflexes and painful dysesthesias in patients with GSS102.

Adult↗
PubMed1991

[Analysis of hemiparesis with homolateral ataxia by single photon emission CT].

Case 1. A 46-year-old man suddenly developed mild gait disturbance and left hemiparesis. On examination, gross strength was slightly reduced in the left extremities. The finger-to-nose and heel-to-knee tests disclosed moderate dyssynergia and dysmetria on the left side that could not be explained by the muscular weakness. Deep tendon reflexes were more brisk in the left extremities. There was no Babinski sign. Magnetic resonance imaging showed a region of high signal intensity in the right posterior limb of internal capsule with extension into lateral thalamus. The lesion involved the cortico-ponto-cerebellar pathway and partly the dentato-rubro-thalamo-cortical pathway. No lesions were seen in the brainstem. Single photon emission CT with 123I-IMP showed left cerebellar hypoperfusion termed crossed cerebellar diaschisis by Baron et al. Case 2. A 65-year-old female developed weakness of the left extremities and gait disturbance. On examination, there was a horizontal nystagmus on lateral gaze to each side. She showed dysarthria, mild left hemiparesis and slight left hypesthesia. The finger-nose and heel-knees tests revealed moderate dysmetria and dyssynergia on the left side. Deep tendon reflexes were hyperactive in the left extremities with left Babinski sign. CT showed a low density area in the right basis pontis at about middle level. Intravenous digital subtraction angiography revealed a slight stenosis of right vertebral artery, but no other abnormality. The lesion involved the cortico-ponto-cerebellar pathway. Single photon emission CT with 123I-IMP showed left cerebellar hypoperfusion. The right cerebellar blood flow was normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2006

Spectrum of neurological diseases associated with antibodies to minor gangliosides GM1b and GalNAc-GD1a.

The authors reported the neurological disease spectrum associated with autoantibodies against minor gangliosides GM1b and GalNAc-GD1a. IgG and IgM antibody reactivity against gangliosides GM1, GM2, GM1b, GD1a, GalNAc-GD1a and GQ1b was investigated in sera from 7000 consecutive patients who had various neurological conditions. The clinical diagnoses for 456 anti-GM1b-positive patients were Guillain-Barré syndrome (GBS, 71%), atypical GBS with preserved deep tendon reflexes (12%), Fisher syndrome (10%), Bickerstaff's brainstem encephalitis (2%), ataxic GBS (2%) and acute ophthalmoparesis (1%). For 193 anti-GalNAc-GD1a-positive patients, the diagnoses were GBS (70%), atypical GBS (16%), Fisher syndrome (10%) and Bickerstaff's brainstem encephalitis (3%). Of the patients with GBS or atypical GBS, 28% of 381 anti-GM1b-positive and 31% of 166 anti-GalNAc-GD1a-positive patients had neither anti-GM1 nor anti-GD1a antibodies. Of those patients with Fisher syndrome, Bickerstaff's brainstem encephalitis, ataxic GBS or acute ophthalmoparesis, 33% of 67 anti-GM1b-positive, and 52% of 25 anti-GalNAc-GD1a-positive patients had no anti-GQ1b antibodies. Autoantibodies against GM1b and GalNAc-GD1a are associated with GBS, Fisher syndrome and related conditions. These antibodies should provide useful serological markers for identifying patients who have atypical GBS with preserved deep tendon reflexes, ataxic GBS, Bickerstaff's brainstem encephalitis or acute ophthalmoparesis, especially for those who have no antibodies to GM1, GD1a or GQ1b. A method to prepare GM1b was developed.

Adolescent↗
PubMed2000

[Diabetic somatic polyneuropathy. Pathogenesis, clinical manifestations and therapeutic concepts].

Diabetic polyneuropathy is the most frequent neuropathy in western countries. In Germany, there are 3.5 to 4 million diabetic patients. Diagnosis should rule out other polyneuropathies and assess two out of the five diagnostic criteria: neuropathic symptoms, neuropathic deficits, pathological nerve conduction studies, pathological quantitative sensory testing and pathological quantitative autonomic testing. So far, the pathophysiology of diabetic neuropathy remains to be fully understood. Among the various pathophysiological concepts are the Sorbitol-Myo-Inositol hypothesis attributing Myo-Inositol depletion to the accumulation of Sorbitol and Fructose, the concept of deficiency of essential fatty acids with reduced availability of gamma-linolenic-acid and prostanoids, the pseudohypoxia- and hypoxia-hypothesis attributing endothelial and axonal dysfunction and structural lesions to increased oxidative stress and free radical production. Obviously, the hyperglycemia induced generation of advanced glycation end products (AGEs) also contributes to structural dysfunctions and lesions. Elevated levels of circulating immune complexes and activated T-lymphocytes as well the identification of autoantibodies against vagus nerve or sympathetic ganglia support the concept of an immune mediated neuropathy. The reduction of neurotrophic factors such as nerve growth factor, neurotrophin-3 or insulin-like growth factors also seems to further diabetic neuropathy. The symmetrical, distally pronounced and predominantly sensory neuropathy is far more frequent than the symmetrical neuropathy with predominant motor weakness or the asymmetrical neuropathy. The painless neuropathy manifests with impaired light touch sensation, position sense, vibratory perception and diminished or absent ankle deep tendon reflexes. The painful sensory diabetic neuropathy primarily affects small nerve fibers and accounts for decreased temperature perception and paresthesias. The proximal, diabetic amyotrophy evolves subacutely or acutely, induces motor weakness of the proximal thigh and buttock muscles and is painful. Cranial nerve III-neuropathy is also painful and has an acute onset. Truncal radiculopathy follows the distribution of truncal roots and frequently causes intense pain. Autonomic neuropathy occurs with and without somatic neuropathy. The most important therapy is to attempt optimal blood glucose control, to reduce body weight and hyperlipidemia. Symptomatic therapy includes alpha-lipoic acid treatment, as the antioxidant seems to improve neuropathic symptoms. Aldose reductase inhibitors might reduce sorbitol and fructose production and normalize myo-inositol levels. However, there are no aldose reductase inhibitors available in Europe as yet. Evening primrose oil, containing gamma-linolenic acid, might improve nerve conduction velocities, temperature perception, muscle strength, tendon reflexes and sensory function. Substitution of nerve growth factor showed promising results in pilot studies but failed in a large-scale multicenter study. Symptomatic pain treatment can be achieved with tricyclic antidepressants, selective serotonin reuptake inhibitors, anticonvulsants such as carbamazepine, gabapentin or lamotrigine, or anti-arrhythmic drugs such as mexiletine. Topical capsaicin application should reduce neuropathic pain but also induces local discomfort in the beginning of therapy. Vasoactive substances, so far have not proven to be of major benefit in diabetic neuropathy. Physical therapy and thorough footcare are of primary importance and allow prevention of secondary complications such as foot amputations.

Diabetic Neuropathies↗