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From the international Amalgam Mailing list :
15 - 08 - 1999
I found something very interesting:

this is the text:




Peripheral neuropathies are of three types: First, is that of a rapid
onset, usually sensory, sometimes caused by mercury or adriamycin. The
second type is rapid onset, primarily motor. Can be caused by buckthorn
poisoning. The third type is gradual onset, stocking glove with a mixed
motor and sensory component, and this comprises a majority of the
chemicals. This classification is probably the most helpful from a
clinical perspective (Schaumburg and Spencer, 1979).

In sensory peripheral neuropathy there may be a decreased sensation to
pain with a sharp object such as a pin. DeGowin suggests running the
stroke from the non-sensitive to the sensitive skin, having the patient
indicate a change. Temperature discrimination may be lost when tactile
sense is still present. Proprioceptive sense, specifically vibratory
sense, may be lost with sensory peripheral neuropathy.

Motor peripheral neuropathy may be focal and in a nerve root

If there is disease of the pyramidal track, there may be hyperactive
reflexes. In its extreme clonus, and a positive babinski reflex (DeGowin
and DeGowin, 1969).

Differential diagnosis of peripheral neuropathy include the following:
chronic arsenic exposure; benzene; carbon monoxide; chlorine; phenocoll;
dinitrophenols; ethambutol; ethanol; goldsalts; herbicides; hexane;
hydrogen sulfide; isoniazid; lead; mercury; methanol; methaqualone;
narcotics; nicotine; paralytic shellfish; thallium (Noji and Kelen,
1989). Additionally, thalidomide monomers, carbon disulfide, hexane,
methyl- and butyl-ketone, organophosphates (tocp, leptophos,
poly-chlorinated byphenals, pcb's) (Schaumburg and Spencer, 1979).

Lead can cause a peripheral neuropathy and a sensory neuropathy when the
lead levels reach up to 60 g% (Araki and Honma, 1976; Ashby, 1980;
Seppalainen et al, 1975).

N-hexane and methyl n-butyl-ketone have been reported to cause
peripheral neuropathy (Billmaier et al, 1974; Herskowitz et al, 1971;
Iida et al, 1969). These peripheral neuropathies are usually symmetric
and sensory motor.

In electromyography (EMG) and nerve conduction studies (NCS), the
majority of toxic neuropathies are normal, therefore a normal does not
rule out a toxic neuropathy (Sullivan and Krieger, 1993). However, if
there is a myopathy that develops, the electromyography may be abnormal.
Fibrillation and high frequency potentials in organophosphate induced
neuropathy may have EMG and NCS abnormalities (Sullivan and Krieger,

Serum lead levels may be obtained when there is a question of such
exposure. Twenty-four hour urine arsenic levels may be helpful. Sural
nerve biopsy may be helpful in diagnosing toxic neuropathy.

Araki S, Honma T: Relationships between lead absorption and peripheral
nerve conduction velocities in lead workers. Scand J Work Environ Health
4:225, 1976.

Ashby J: A neurological and biochemical study of early lead poisoning.
Br J Ind Med 37:133, 1980.

Billmaier D, Yee H, Allen H, et al: Peripheral neuropathy in a coated
fabrics plant. J Occup Med 16:665, 1974.

DeGowin E, DeGowin R: Bedside Diagnostic Examination. The MacMillan
Company, 1969.

Herskowitz A, Ishii N, Schaumburg H: n-Hexane neuropathy. A syndrome
occurring as a result of industrial exposure. N Engl J Med 285:82, 1971.

Iida M, Yamamura Y, Sobue I: Electromyographic findings and conduction
velocity on n-hexane polyneuropathy. Electromyography 9:247, 1969.

Noji E, Kelen G: Manual of Toxicologic Emergencies. Year Book Medical
Publishers, Inc., 1989; page 209.

Schaumburg H, Spencer P: Toxic Neuropathies. Neurology 29:431, 1979.

Seppalainen A, Tola S, Hernberg S, et al: Subclinical neuropathy at
"safe" levels of lead exposure. Arch Environ Health 30:180, 1975.

Sullivan J, Krieger G: Hazardous Materials Toxicology. Williams &
Watkins, Baltimore, Maryland; 1992.

Sullivan J, Krieger G: Hazardous Materials Toxicology. Williams &
Watkins, Baltimore, Maryland; 1993.