Pathogenic and clinical aspects of polyneuropathies, with reference to the hand-arm vibration syndrome.

Juntunen, Juhani; Taskinen, Helena

doi:10.5271/sjweh.2043

Cited by 5 publications

(5 citation statements)

References 7 publications

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“…'7 There is also support for the contention that a raised vibrotactile threshold in the 100-128 Hz range, presumably reflecting injury to the FAII mechanoreceptor or pacinian corpuscle, is a particularly sensitive measure of injury in vibration exposed subjects, becoming abnormal before deficits are recognised on clinical or electrodiagnostic tests. '729 In the present group of highly symptomatic patients, 30 Hz tuning fork extinction, two point discrimination, and 120 Hz vibrotactile thresholds were significantly intercorrelated, and none was correlated significantly with nerve conduction velocities. Comparisons between the two symptom groups showed that vibrotactile thresholds at 120 Hz discriminated best, whereas 30 Hz tuning fork extinction times were less discriminatory and two point thresholds showed only non-significant trends toward differences.…”

Section: Discussionmentioning

confidence: 60%

“…These findings confirm other reports of raised vibrotactile threshold2 and diminished grip strength2"26 in vibration exposed workers. Three tests-two point discrimination, 30 Hz vibration recognition, and 120 Hz vibrotactile thresholdsdiscriminated between symptom groups and were significantly correlated with one another in this patient group. They should be considered as candidates for inclusion in studies of less severely affected groups because they are simple, can be quantified, and can be administered to a specific site of potential injury.…”

Section: Discussionmentioning

confidence: 74%

“…Anamnestic quantification of the latent period between initial exposure and initial symptoms is problematic, however, as reliability fades with longer tenure and persistence of symptoms. Table 1 also presents the results of clinical assessment of light touch, pinprick, 30 Hz tuning fork extinction time, and two point discrimination. A similar proportion of abnormality (25%-33%) was found among these tests.…”

Section: Symptoms and Clinical Abnormalitiesmentioning

confidence: 99%

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Detailed clinical assessment of neurological function in symptomatic shipyard workers.

Cherniack

Letz

Gerr

et al. 1990

Occupational and Environmental Medicine

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Forty eight patients with extensive occupational exposure to pneumatic grinding tools were evaluated at a university sponsored occupational health clinic. All patients were interviewed and examined by a physician and assessed neurologically with standard clinical, functional motor, quantitative vibrotactile, and electrodiagnostic tests. Sensorineural symptoms were nearly universal; 47 patients (98%) reported numbness and tingling of the hands and fingers. Among clinical tests, two point discrimination and 30 Hz vibration perception were most frequently abnormal. In order to evaluate associations between quantitative test results and sensorineural symptoms, patients were stratified into two groups of symptom severity according to a consensus sensorineural staging system. The tests that discriminated best between the groups ofmore and less symptomatic patients were hand strength dynamometry, and vibrotactile thresholds. Age standardised 120 Hz vibrotactile thresholds were significantly raised in digit II in 41% of hand measurements. Nerve conduction studies were neither significantly different between more and less symptomatic groups nor correlated with clinical and quantitative sensory tests. Twenty five per cent of the patients had slowing of sensory conduction velocities in the median nerve at the wrist ( < 48 m/s). Of this subset ofpatients only two showed abnormal slowing of the median nerve distal to the wrist, but half also showed ulnar nerve slowing (< 47 mis). This observation highlights the difficulty of differentiating median nerve entrapment from diffuse distal A Brammer neuropathy in workers exposed to vibration and points to the need for concomitant quantitative sensory and functional motor assessment.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 74%

Section: Symptoms and Clinical Abnormalitiesmentioning

confidence: 99%

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Detailed clinical assessment of neurological function in symptomatic shipyard workers.

Cherniack

Letz

Gerr

et al. 1990

Occupational and Environmental Medicine

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“…Although the late‐stage pathophysiology of HAVS is well characterized, the onset and progression of the disease to an irreversible condition is poorly understood at the cellular and molecular levels. It is unknown whether the neurological symptoms that include tingling, numbness, and loss of dexterity are primary or secondary to the vascular symptoms of vasospasm and ischemia 12. Also unknown are the initial cell types injured by vibration in either tissue.…”

mentioning

confidence: 99%

Vibration injury damages arterial endothelial cells

et al. 2002

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Prolonged exposure to hand-transmitted vibration can cause debilitating neural and vascular dysfunction in humans. It is unclear whether the pathophysiology involves simultaneous or sequential injury of arteries and nerves. The mechanism of vibration injury was investigated in a rat tail model, containing arteries and nerves structurally similar to those in the human hand. Tails were selectively vibrated for 1 or 9 days with the remainder of the animal at rest. One vibration bout of 4 h/day, 60 HZ, 5 g (49 m/s(2)) acceleration, injured endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor. Electron microscopy revealed that vibration for 9 days produced loss and thinning of endothelial cells, with activated platelets coating the exposed subendothelial tissue. Endothelial cells and arterial smooth muscle cells contained double membrane-limited, swollen processes indicative of vasoconstriction-induced damage. Laser doppler surface recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion. These findings indicate that early injury involves vasoconstriction and denuding of the arterial endothelium.

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“…One of the hallmarks of hand-arm vibration syndrome in humans and corresponding animal models is the demyelination and orthograde degeneration of axons that have been separated from the neuronal cell body in the DRG 31354254 , a process known as Wallerian degeneration 52 . Wallerian degeneration is accompanied by an inflammatory response during which injured axons release molecules that enhance vascular permeability and activate glial cells, which in turn produce and release molecules that ensure the survival of injured neurons and attract leukocytes to the site of injury 49 .…”

Section: Discussionmentioning

confidence: 99%

Role of Kv4.3 in Vibration-Induced Muscle Pain in the Rat

Conner

Álvarez

Bogen

et al. 2016

The Journal of Pain

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We hypothesized that changes in the expression of Kv4.3 contribute to the mechanical hyperalgesia induced by vibration injury, a rodent model for hand-arm vibration syndrome in humans. Here we show that the exposure of the gastrocnemius muscle to vibration injury induces muscle hyperalgesia that is accompanied by a significant down-regulation of Kv4.3 in affected sensory nerve fibers in dorsal root ganglia (DRG). We additionally demonstrate that the intrathecal administration of antisense oligonucleotides for Kv4.3 mRNA itself induces muscle hyperalgesia in the rat. Our results suggest that attenuation in the expression of Kv4.3 may contribute to neuropathic pain in people affected by hand-arm vibration syndrome.

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Pathogenic and clinical aspects of polyneuropathies, with reference to the hand-arm vibration syndrome.

Cited by 5 publications

References 7 publications

Detailed clinical assessment of neurological function in symptomatic shipyard workers.

Detailed clinical assessment of neurological function in symptomatic shipyard workers.

Vibration injury damages arterial endothelial cells

Role of Kv4.3 in Vibration-Induced Muscle Pain in the Rat

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