Response to treatment with chelating agents of anaemia, chronic encephalopathy, and myelopathy due to lead poisoning

Simpson, J. A.; Seaton, D. A.; Adams, J. F.

doi:10.1136/jnnp.27.6.536

Cited by 57 publications

(23 citation statements)

References 12 publications

(6 reference statements)

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“…Chronic encephalopathy is characterized by similar symptoms, such as lethargy and defective memory (3). Memorizing and abstract reasoning are poor in lead poisoned patients, but the language function is not as affected (4,25). The development of psychological defects may not occur suddenly but appears rather to be a result of a continuous deterioration.…”

Section: Discussionmentioning

confidence: 99%

Psychological dysfunctions in lead-exposed workers. Relation to biological parameters of exposure.

Grandjean¹,

Arnvig²,

Beckmann³

1978

Scand J Work Environ Health

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Psychological dysfunctions in lead-exposed workers: Relation to biological parameters of exposure. Scand. j. work environ. & health 4 (1978) 295-303. Insidious neurotoxic effects of lead have been studied in a popoulation of 42 lead-exposed workers and a reference group of 22 comparable workers with no lead exposure. The age of the individuals ranged from 18 to 50 years. The complete Wechler Adult Intelligence Scale, as well as psychomotor and memory tests, was included in the test battery. The exposure was assessed by means of the lead concentration in blood and hair and the ratio between zinc protoporphyrin and hemoglobin in the blood. Significant differences were found between the two groups of workers, especially concerning long-term memory, verbal and visuos:gatia1 abstraction, and psychomotor speed. Decreased performance in these tests was in most cases associated with indices of increased lead exposure, not only in the total population studied, but also within the lead-exposed group alone. Blood lead and zinc protoporphyrin appeared to correlate better with the intellectual impairment than did hair lead, and thus these analyses are probably better predictors for neurotoxic effects of lead. Age and exposure time were not found to be significant confounding factors in this study.

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Section: Discussionmentioning

confidence: 99%

Psychological dysfunctions in lead-exposed workers. Relation to biological parameters of exposure.

Grandjean¹,

Arnvig²,

Beckmann³

1978

Scand J Work Environ Health

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“…Cullen et al 11 described one patient with wrist extensor weakness and normal sensation who had normal motor nerve conduction studies, denervation on needle EMG, and prolonged sensory latencies. Simpson et al 39 studied a patient with severe upper-limb weakness and atrophy and normal sensation. Needle EMG examination revealed small numbers of fibrillation potentials and reduced recruitment of motor units.…”

Section: Electrodiagnostic Evaluation In Patients With Subacutementioning

confidence: 99%

Neuropathies associated with excessive exposure to lead

2006

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Exposure to lead is a ubiquitous problem of the modern era. The majority of cases of all forms of lead intoxication, especially lead neuropathy, result from industrial exposure. In the Western world meticulous monitoring in industry has reduced the risk of overt lead neuropathy. The classic form of lead neuropathy consists of weakness that primarily involves the wrist and finger extensors but which later spreads to other muscles. There is only minimal sensory involvement. Less commonly, there is a more typical toxic neuropathy with distally accentuated sensory and motor involvement. The motor neuropathy is more likely to develop following relatively short-term exposure to high lead concentrations and evolves in a subacute fashion. Prognosis for recovery is good as long as exposure is terminated promptly. The distal sensory and motor neuropathy develops after many years of exposure, evolves more slowly, and recovery is less certain. There is a generally weak relationship between the development of lead neuropathy and blood lead levels, at least for the subacute motor neuropathy, leading to speculation that the metabolic basis for the neuropathy is interference with porphyrin metabolism. Lead intoxication in humans causes axonal degeneration, but in some other species it causes a primarily demyelinating neuropathy. It should be possible to prevent lead neuropathy by good industrial hygiene. Close monitoring should identify excessive lead exposure before it causes overt neuropathy. If evidence of excessive exposure is found or if overt neuropathy develops, exposure must be terminated immediately. The role of chelation therapy in the treatment of lead neuropathy is controversial.

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“…Although the peripheral manifestations of lead toxicity are exceedingly rare, descriptions exist of asymmetric proximal arm or intrinsic hand muscle involvement resembling a progressive muscular atrophy.' ', 15 It is unclear whether the abnormal SNAPs should have excluded the diagnosis of lead neuropathy, because few reports exist using modern electrodiagnostic techniques. The patient presented by Oh" had absent SNAPs at various times, but also reported heavy illicit alcohol use.…”

Section: Discussionmentioning

confidence: 99%

X‐linked bulbospinomuscular atrophy (Kennedy's disease) masquerading as lead neuropathy

Albers

Bromberg

1994

Muscle and Nerve

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A 43-year-old male was referred by a veterinarian who evaluated his dog for a seizure and suspected a toxic lead exposure for both. He refurbished houses, removing old paint, and complained of decreased cognition, fatigue, and muscle cramps. He had a depressed affect, postural tremor, right arm weakness with partial denervation on EMG, and borderline-low sensory nerve action potential (SNAP) amplitudes. A mild anemia and elevated serum and urine lead levels supported a diagnosis of lead neuropathy. Chelation therapy increased urine lead excretion without symptomatic improvement. His brother worked part-time with him and developed similar findings, but also had difficulty chewing, dysphagia, perioral twitching, gynecomastia, and multifocal denervation of extremity and facial muscles. His lead levels were not elevated, but an androgen receptor mutation identified on the X chromosome for both brothers confirmed the diagnosis of X-linked bulbospinomuscular atrophy (Kennedy's disease).

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Response to treatment with chelating agents of anaemia, chronic encephalopathy, and myelopathy due to lead poisoning

Cited by 57 publications

References 12 publications

Psychological dysfunctions in lead-exposed workers. Relation to biological parameters of exposure.

Psychological dysfunctions in lead-exposed workers. Relation to biological parameters of exposure.

Neuropathies associated with excessive exposure to lead

X‐linked bulbospinomuscular atrophy (Kennedy's disease) masquerading as lead neuropathy

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