Publications, Lectures,
& Presentations
(Available upon request) (*manuscript in preparation)
- Rutchik, J and Wittman, R. Solvent Neurotoxity. In Philips,
S and Krieger, G, eds. Industrial Solvents and Human Health, Part
II. Clinics in Occupational and Environmental Medicine. WB Saunders.
November 2004..
- Rutchik, J. Neurological symptoms and chemical exposure; occupational,
environmental or product; a challenge for the expert and attorney
to share. BNA Legal Magazine, The Reporter, 2004.
- Rutchik, J. Heavy Metals and Industrial Dementia. In Medlink.
Internet Neurology Text. www.medlink.com.
2004.
- Rutchik, J. The evaluation of a patient with mold exposure and
neurologic complaints. JSR. Claims Magazine. February 2003.
- Rutchik, J. Heavy Metals and Industrial Dementia. In Medlink.
Internet Neurology Text. www.medlink.com.
2001. In press
- MCCullough JE, Dick R, Rutchik J. Chronic Mercury Exposure Examined
with a Computer Based TremorSystem. JOEM. (2001), 43, 3
- Rutchik J. Organic Solvents. In Emedicine, Neurology (An internet
medical textbook). www.emedicine.com,
2001
- Rutchik J. Toxic Neuropathy. In Emedicine, Neurology (An internet
medical textbook). www.emedicine.com,
2001
- Rutchik, JS and Feldman, RG. Tetrachloroethylene. In Feldman
RG. Occupational & Environmental Neurotoxicology. Philadelphia,
PA: Lippincott Raven. 1999
- Rutchik, JS and Feldman, RG. Carbon Disufide. In Feldman RG.
Occupational & Environmental Neurotoxicology. Philadelphia,
PA: Lippincott Raven. 1999
- Rutchik, JS and Feldman, RG. Xylene. In Feldman RG. Occupational
& Environmental Neurotoxicology. Philadelphia, PA: Lippincott
Raven. 1999
- Rutchik, JS and Feldman, RG. Ethylene Oxide. In Feldman RG.
Occupational & Environmental Neurotoxicology. Philadelphia,
PA: Lippincott Raven. 1999
- Rutchik, JS and Feldman, RG. Exposure to Hazardous Chemicals.
In Feldman RG. Occupational & Environmental Neurotoxicology.
Philadelphia, PA: Lippincott Raven. 1999
- Rutchik JS. Occupational Slow Virus Disease. In
Couturier A, ed. Occupational Infectious Diseases.
Boston: OEM Health. Massachusetts: OEM Press. 1999.
- Rutchik JS. Hazards of Anatomical Pathology. In:
McCunney RJ, ed. Medical Center Occupational Health and
Safety. Philadelphia: Lipincott, Williams and Wilkins.
1999.
- Rutchik JS. Occupational and Environmental Neurology.
In: Bowler R, ed. Occupational and Environmental Medicine
Secrets. Philadelphia: Hanley and Belfus. 1999.
- Rutchik JS, Rutkove S. Effect of Temperature on Motor Responses
in Organophosphate Intoxication. Muscle and Nerve (1998), 21,
958-960.
Go to Abstract Go
to Full Text
-
Rutchik JS, Barbanel
C. and Boskiewicz B. Addressing Dioxins in the Workplace. Occupational
and Environmental Medicine Report (1998);
12, 2. Go
to Abstract Go to Full
Text
- Rutchik JS. An Environmental and Occupational Neurology Subspecialty. Neurology (1998),
50, 4, S4, A54 Go to Abstract
- Rutchik JS. Neurological
Sequellae from Occupational and Environmental Exposure to Chlorinated Ethylenes.Neurotoxicology.
(1998); 19,3,473. Go to Abstract Go
to Table
-
Rutchik JS.
Neurological Sequellae from Chlorinated Ethylenes. Clinical Care
Update. NAOHP. 10/27/97.
-
Rutchik JS. Toxicology
of the Visual System. Journal of Occupational Medicine (1997), 39,4, 356a.
Go to Abstract
-
Rutchik JS. Chronic
Neurological Sequellae From An Acute Occupational Exposure to Lithium Salt:
Case Report and Review of the Literature. (Manuscript submitted to Archives
of Environmental Health Summer 1999) Go
to Abstract
-
Rutchik JS.
Revising a Medical Surveillance Plan For A Hazardous Waste Company.
(Submitted to OEM Press)
-
Rutchik JS, Richards
KR. Toxicology of the Visual System: Industries and Populations.
(Submitted to Archives of Environmental Health, Summer 1999)
-
Rutchik JS.
Clinical Experiences of an Environmental and Occupational Neurology Program.*
-
Rutchik JS.
Perchloroethylene Induced Dementia; Case Report and Review of the Literature.*
-
Rutchik JS.
The Neurotoxicology of Ethylene Oxide.*
-
Rutchik JS. Drug
Use Rises in 1995 Among Youth. Medical Review Officer (MRO) Update (1996)
.
-
Rutchik JS. Neurology
data collection from ICD-9-CM codes to encourage departmental statistical
record keeping and analysis. Neurology (1995) 45 (Supp 4), 59P.
-
Simpson DM, Tagliati
M, Rutchik JS, Reichler B, and Lorch G. Brainstem syndrome associated with
CMV encephalitis in AIDS. Annals of Neurology (1995), 38, 2, T243.
-
Brandt PW, Diamond
MS, Rutchik JS, Schachat FH. Cooperative interactions between troponin
and tropomyosin units extend the length of the thin filament in skeletal
muscle. Journal of Molecular Biology (1987) 95, 885-896.
-
Brandt PW, Diamond
MS, Rutchik JS, Schachat FH. Cooperative Interactions between troponin-tropomyosin
units extend the length of the thin filament in skeletal muscle. Biophysical
Journal (1987) 51, 28a.
-
Diamond MS, Brandt
PW, Rutchik JS, Schachat FH. The thin filament of skeletal muscle acts
as a unit. Biophysical Journal (1985) 49, 46a.
Lectures and Presentations Evaluating a patient with Neurotoxic
Illness, State Of The Art Conference, SOTAC, American College of
Occupational and Environmental Medicine Conference, San Antonio,
TX, November 2004.
Current Controversies in Neurological Illness and Environmental
and Occupational Medicine, Fellowship Forum, UCSF, Division of Occupational
Medicine, August 2004.
Neurology in Occupational Medicine, North Bay Applicant Attorney
Conference, August 2004
"Electromyography Primer." Kaiser Permanente Occupational
Medicine Grand Rounds. San Francisco, CA. August 2003
"Elecromyography/ Nerve conduction velocity and Occupational
Neurology Case Studies." Center for Occupational and Environmental
Health, University of Calfornia at Berkeley Summer Lecture Series.
Emeryville, CA. August 2003
"Controversies in Neurotoxicology." UCSF Advances in
Occupational and Environmental Medicine, May 2003
"Occupational and Environmental Neurology." Occupational
Health Conference. Atlanta, GA. May 2003
"Common neurological disorders in the Workplace." Center
for Occupational and Environmental Health, University of Calfornia
at Berkeley Summer Lecture Series. Concord, CA. August 2002
"Electromyography and Evoked Potential Primer." Traveler's
Insurance Educational Seminar. Walnut Creek, CA. June 2002
"Neurology in Occupational Medicine." Lunch educational
series. Laughlin, Falbo LLP. June 2002
"Controversies in Neurotoxicology." American Occupational
Health Conference. Chicago, IL. March 2002
"Alternative Neurophysiological Methods of Assessing Neuropathy:
Clinical and Epidemiological Implications," Organizer, Chairperson
and Panel Moderator. American Occupational HEalth Conference. San
FRancisco, CA. April 2001
"Neurological Aspects of Occupational and Environmental Medicine." American
Occupational Health Conference. San Francisco, CA. April 2001
"PRactical Occupational and Environmental Neurology." North Bay Disability
Seminar. April 2001.
"The evaluation of a patient with neurotoxic illness" UCSF Occupational
Medicine Resident Lecture Series. July 2001.
"Practical
Occupational and Environmental Neurology." Northern California Occupational
Medicine Chiefs Meeting. Kaiser Permanente. Oakland, CA November 2000.
"Clinical Experiences
of an Occupational and Environmental Neurologist." Poster presentation.
AOHC 2000. Philadelphia, PA. May 2000.
"Introduction
to Neurotoxicology." Spring Semester. Industrial Toxicology
Course. Columbia University School of Public Health. New York,
NY. March 2000.
"Chlorinated
Ethylenes: Neurological Sequellae." Environmental Health Grand Rounds.
School of Public Health. Columbia University. New York, NY.
November 1999.
"Occupational
and Environmental Neurology: Case Presentations." Occupational and
Environmental Medicine Grand Rounds. Environmental and Occupational
Health Sciences Institute. Rutgers Unversity. Piscataway, NJ.
October 1999.
"Neurological
Sequellae in Ammunitions Workers." Symposium Presentation.
American Psychological Association. Annual Meeting. Boston,
MA. August 1999.
"Neurology
in Occupational Health." Invited Lecturer. HIP Worker's Compensation
Division. New York City Adjusters and Nurse Case Managers. New York,
NY. May 1999.
"Practical
Occupational and Environmental Neurology." Postgraduate Seminar.
American Occupational Health Conference. New Orleans, LA., April
1999.
"Practical
Occupational and Environmental Neurology." Invited Lecturer.
Arbella Insurance. Massachusetts Insurance Adjusters and Case Managers.
Foxborough, MA. November 1998.
"Clinical Experiences
from a University Occupational and Environmental Neurology Program."
Poster Presentation. State of the Art Conference in Occupational
and Environmental Medicine. Phoenix, Arizona. October 1998.
"Neurology
in Occupational Health." Invited Lecturer. Chubb Insurance.
Eastern Massachusetts Adjusters and Nurse Case Managers. Westboro,
MA. August 1988.
Invited Participant.
Planning Committee Meeting for Persian Gulf War Syndrome Conference.
Center for Disease Control and Prevention. Washington, DC.
July 1998.
"Musician Injuries."
Invited Speaker. Berklee School of Music, Boston, MA. Summer
Program. June 1998.
"Choosing Neurology
as a Career." Lecture. National Youth Leadership Forum.
Boston, MA. Julys 1996, 1997 and 1998.
"An Occupational
and Environmental Neurology Subspecialist." Poster presentation.
American Academy of Neurology Annual Meeting. April 1998.
"Practical
Occupational and Environmental Neurology." Lecture. Grand Rounds.
Occupational Medicine Program. Harvard School of Public Health.
April 1998.
"Introduction
to Neurotoxicology." Guest Lecture. Toxicology Course.
BU School of Public Health. April 1998.
"Neurological
Sequellae to Chlorinated Ethylene." Poster Presentation. International
Neurotoxicology Conference. Little Rock, Arkansas. October
1997.
"Toxicology
of the Visual System." Poster presentation. American Occupational
Health Conference. American College of Occupational and Environmental
Medicine Annual Meeting. Orlando, Florida. May 1997.
"Neurotoxicological
Sequellae to Chlorinated Ethylene." Lecture. Seminar on Chlorinated
Ethylenes. Boston University School of Public Health. April
1997.
"Utilization
of Electromyography and Nerve Conduction Velocity to Evaluation of the
Peripheral Nervous System Dysfunction of Viscose Rayon Workers."
Lecture. Environmental Epidemiology Course. Boston School of
Public Health. October 1997.
"Toluene and
Manganese Neurotoxicity." Lecture. Health Standards Division.
Department of Labor. Occupational Safety and Health. February
1997.
"Neuropathy
and Carbon Disulfide." Lecture. Health Standards Division.
Department of Labor. Occupational Safety and Health. August
1996.
"Toxicology
of the Visual System." Lecture. Grand Rounds. Department
of Ophthalmology. Boston Medical Center. May 1996.
"Neurology
Data Collection From ICD-9-CM Codes to Encourage Departmental Statistical
Record Keeping and Analysis." Poster presentation. American
Academy of Neurology Annual Meeting, May 1995.
"Axonal Neuropathy
and Carpel Tunnel Syndrome." Lecture. Division of Neuromuscular
Diseases. Department of Neurology, Mount Sinai Medical Center, Spring
1995.
"Case studies in Occ. and Env Neurology. Occupational Medicine Grand Rounds. UCSF. January 2001."
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CLINICAL EXPERIENCES FROM A UNIVERSITY ENVIRONMENTAL AND OCCUPATIONAL (E/O)
NEUROLOGY PROGRAM.
Jonathan S.
Rutchik, MD, MPH
Clinical characteristics
of a series of patients from a University Environmental and Occupational
Neurology Program are reported. Evaluations were focused on whether chemical
exposure was associated with patient difficulties. 21 (9 females ) medical
records, including environmental and occupational (E/O) questionnaires
and neurodiagnositic testing were reviewed. 17 attributed their symptoms
to exposures at work. Occupations: office workers (4); laboratory workers
(4); nurses (2); dry cleaner, cutting machine cleaner, company physician,
aircraft engineer, plumber, roofer (1). Neurotoxicity associated with exposure
to lead, carbon disulphide, mercury, organic acids, tetrachloroethylene,
methane, methylmercaptan, toluene, styrene, polycyclic aromatic hydroocarbons
and methylene chloride was investigated. Concentration difficulties, insomnia,
headache, numbness and fatigue commonly lead to an inability to perform
work tasks. The most common finding was anxiousness. 17 had neuropsychological
testing, 15 had MRI, 13 had EMG/ NCV/ Blink testing and 8 had an EEG. Encephalopathy
was diagnosed in 11, depression in 7, toxic neuropathy in six and multiple
chemical sensitivity in four. The EON evaluation helped resolve many Worker's
Compensation, liability and/or return to work disputes. An E/O history,
literature search and complete neurological work up is essential to the
evaluation of a patient with possible neurological sequellae from O/E exposure.
CLINICAL EXPERIENCES
FROM A UNIVERSITY
ENVIRONMENTAL
AND OCCUPATIONAL NEUROLOGY (EON) PROGRAM.
Objective.
To review the presentation, neurological evaluation, and outcome for patients
who presented to a University Environmental and Occupational Neurology
(EON) Program over a one year period.
Background.
Clinical characteristics of a series of patients are reported. Evaluations
were focused on diagnosis, treatment and whether chemical exposure was
associated with a patient's chief complaint(s). Referral sources included
internists, occupational medicine physicians, neurologists, insurance companies
and attorneys.
Design / Methods.
Medical records, (EON) questionnaires and neurodiagnostic testing were
reviewed for 21 (9 females) patients. Exposure data was difficult to obtain.
Results. Exposures
at work were responsible for symptoms reported by 17 of the 21 patients.
Their occupations were as follows: office workers (4); laboratory workers
(4); nurses (2); dry cleaner (1), cutting machine cleaner (1), company
physician (1), aircraft engineer (1), plumber (1), roofer (1). Neurotoxicity
associated with exposure to lead, carbon disulfide, mercury, organic acids,
tetrachloroethylene, methane, methylmercaptan, toluene, styrene, polycyclic
aromatic hydroocarbons and methylene chloride was investigated. Chief complaints
included concentration difficulties, insomnia, headache, numbness and fatigue.
These commonly led to an inability to perform work tasks. The most common
finding on examination was anxiousness. Neuropsychological testing was
performed on 17 of the 21. 15 had an MRI of the brain, 13 had EMG/ NCV/
Blink testing and 8 had an EEG. Encephalopathy was diagnosed in 11, depression
in 7, toxic neuropathy in six and multiple chemical sensitivity in four.
Conclusions.
The EON evaluation, diagnosis and treatment plan was helpful to resolve
worker's compensation, liability and disability insurance, and return to
work disputes. The clinician should seek to obtain exposure data. A thorough
literature search is essential to this evaluation. In the medical legal
arena, a diagnosis requires a reasonable degree of medical certainty. A
biologically plausible hypothesis is best supported by statistically significant
results from reliable epidemiological studies.
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ADDRESSING DIOXINS IN THE WORKPLACE. Occupational and Environmental
Medicine Report (1998);
Rutchik, JS,
Barbanel C. and Boskiewicz B.
ABSTRACT
OBJECTIVE.
To perform a risk assessment of exposure to 2,3,7,8 tetrachlorodibenzodioxin
(TCDD) for laboratory researchers studying the effects of a group of chemicals
on cell death, and to assess the state of the art of biological monitoring
and medical surveillance for these researchers.
METHODS. Material
Safety Data Sheets were obtained and work-site evaluations were performed.
Chemical supply companies were interviewed regarding their own medical
surveillance programs and a literature search for these chemicals was conducted
using Medline from the last decade. The Duke Occupational and Environmental
Medicine e-mail server was used to query others in industry, laboratory
medicine and toxicology throughout the world in regards to their experience
with these chemicals.
RESULTS. Dioxin
(TCDD) exposure may occur by inhalation, ingestion and skin contact. Chemical
supply companies do not routinely include biological monitoring in their
medical surveillance plans for their employees. These laboratory researchers
were potentially exposed when opening the disposal drum containing airborne
particulate materials from previously discarded pipettes and culture bottles.
Proper protective gloves, masks and a functional ventilation hood is important
to reduce exposure. Since dioxin is ubiquitous, serum is rarely specific
or sensitive to occupational exposures. Air monitoring for TCDD is mainly
qualitative.
CONCLUSIONS.
Worker exposure to TCDD should include strict engineering controls. Routine
history and physical examinations can be performed but are not likely to
detect early adverse effects. Biological monitoring is expensive, a large
amount of serum is required, and is not specific for occupational exposures.
Occupational and Environmental work and health questionnaires may be helpful.
Go
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NEUROLOGICAL SEQUELLAE FROM OCCUPATIONAL AND ENVIRONMENTAL (O/E) EXPOSURE
TO CHLORINATED ETHYLENES (CEs)
Jonathan S.
Rutchik, MD, MPH
Medical Director,
Division of Occupational and Environmental Neurology Occupational Health
and Rehabilitation, Inc., Boston, MA.
CEs are a family
of five double bonded carbon molecules with one to four substituted chlorines:
vinyl chloride (VC); 1,1 dichloroethene (1,1 DCE:) and 1,2 dichloroethene
(1,2 DCE), trichloroethylene (TRI) and tetrachloroethylene (TET). VC is
used widely to manufacture polyvinyl chloride; DCEs for manufacturing packaging
materials; TRI as a metal degreaser and TET as a dry cleaning solvent.
CEs are widely produced and contamination of ground water is feared. High
lipid solubility allows them to be absorbed by inhalation, ingestion and
skin contact. Biological monitoring may be helpful to document exposure.
Government regulations aim to prevent excessive O/E exposure to workers
and citizens. A literature search for human neurological sequellae secondary
to CE exposure revealed more than 70 case reports, case series and case
control studies. Acute and chronic occupational exposure to VC, and O/E
exposure to both TRI and PER separately, together or in mixtures with other
chemicals may lead to neurological impairment. Neurophysiological testing,
such as electromyography, nerve conduction studies and blink latencies
as well as neuropsychological testing aimed at testing memory, visuospatial
and attention/ executive functions have been most helpful in these evaluations.
Awareness, research and more strict government regulation is important
to reduce public health risks.
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AN OCCUPATIONAL AND ENVIRONMENTAL NEUROLOGY SUBSPECIALIST
Jonathan S.
Rutchik, MD, MPH
Medical Director,
Division of Occupational and Environmental Neurology
Occupational
Health and Rehabilitation, Inc., Boston, MA.
OBJECTIVE:
To describe the post graduate medical curriculum of an occupational and
environmental neurology (O/E) subspecialist.
BACKGROUND:
O/E Neurology is the subspecialty that focuses on workplace injury and
chemical exposure. Musculoskeletal disorders, entrapment and overuse syndromes
as well as the identification of a neurotoxic syndrome are common clinical
challenges. Strong clinical skills and an ability to focus on worker fitness,
disability status or medical legal issues are required and offer a distinct
advantage in industrial health settings. A familiarity with established
neurotoxins and their associated health effects, biological monitoring,
governmental regulations, and common sources of exposure is mandatory for
the clinician. A background in epidemiology is useful to evaluate populations
for dysfunction.
DESIGN/METHODS:
A two year post graduate curriculum was sponsored by a University Neurology
Department that included a fellowship in O/E Neurology, a Master's Degree
in Public Health and a residency in O/E medicine following a three year
neurology residency. In year one, a case study format was utilized to concentrate
on the clinical presentation, diagnosis and treatment of neurotoxic syndromes.
The relationships between O/E exposures (heavy metals, organic solvents
and organophosphates) and primary neurological diagnoses (neurodegenerative
and autoimmune disorders, neuropathies and dementing illnesses) were dissected.
Persian Gulf War syndrome, multiple chemical sensitivity and visual system
toxicology as well as neuropsychological testing were also important focuses.
Coursework included epidemiology, biostatistics, toxicology and risk assessment.
Year two included outpatient care in a university O/E medical clinic and
electives in corporate medicine settings, government agencies (OSHA and
NIOSH), a hazardous waste company and electromyography.
RESULTS: This
clinician will focus his career on clinical neurology: industry, government
and medical legal consulting; and research associated with preventive medicine,
worker and musicians injuries, O/E toxicology, ergonomics and regulations.
CONCLUSION:
An O/E neurologist is an important resource to help identify and treat
occupational and environmental neurologic syndromes efficiently and to
resolve insurance, worker compensation and medical legal disputes. Assisting
a patient with these issues is a vital aspect of medical care. A neurologist
with this secondary specialty training can make unique contributions to
industry, government, medical legal policy and neurological science.
Supported by
the Agency of Toxic Substance and Disease Registry of the Center for Disease
Control and Prevention.
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EFFECT OF TEMPERATURE ON MOTOR RESPONSES IN ORGANOPHOSPHATE INTOXICATION
Jonathan S.
Rutchik, MD, MPH and Seward B. Rutkove, MD
Department
of Neurology, Beth Israel Deaconess Medical Center Harvard Medical School,
Boston, Massachusetts
ABSTRACT
We studied
the effect of temperature on median motor responses in a 41 year old man
with organophosphate intoxication. At 32C, a normal amplitude compound
motor action potential (CMAP) and a smaller spontaneous repetitive discharge
(SRMAP) were present. When the hand was warmed to 39C, the CMAP amplitude
decreased 20% while the SRMAP amplitude decreased 33%. With cooling to
14C, the CMAP amplitude decreased 9% from baseline while the SRMAP became
unobtainable. The SRMAP returned when the hand was re-warmed to 32C. Although
the CMAP amplitude changes with temperature are similar to that of normal
subjects, the interaction of temperature with the SRMAP has not been previously
described. The excess reduction in SRMAP amplitude at high temperature
may be secondary to enhanced dysfunction of neuromuscular transmission.
Prolongation of the absolute refractory period of nerve and muscle may
explain the disappearance of the SRMAP at cold temperature.
Key Words:
Organophosphates, temperature, compound motor action
potential,
neuromuscular junction, refractory period
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TOXICOLOGY OF THE VISUAL SYSTEM. Journal of Occupational Medicine (1997),
39,4, 356a.
Jonathan S.
Rutchik, MD, MPH
ABSTRACT
Case reports,
cases series and epidemiological studies involving subjects in occupational
and environmental settings have led to associations between many industries
and chemical agents with neuro- ophthalmological dysfunction.
Often subclinical,
these abnormalities may herald more significant health effects from exposure.
Organic solvent exposure is associated with dyschromatopsia, visual field
(VF) abnormalities, and oculomotor impairments. Heavy metals, particularly
lead and mercury, have been linked to VF deficiencies, retinopathy, and
oculomotor impairment. Exposure to carbon disulfide is associated with
vascular retinopathies, such as microaneurysms and hemorrhages. A variety
of diagnostic methods, including visual evoked potential, critical flicker
fusion, and contrast sensitivity analysis, have been employed to measure
neuro-visual function and have found abnormalities in the neuro-visual
system. This review helps identify the industries, populations, and particular
agents that are associated with neuro-visual impairment. Clinicians should
utilize this information to focus evaluations of their patients both for
prevention and treatment.
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CHRONIC NEUROLOGICAL SEQUELLAE FROM AN ACUTE OCCUPATIONAL EXPOSURE TO LITHIUM
SALT: Case Report and Review of the Literature
Jonathan Silver
Rutchik, MD, MPH
Departments
of Neurology and Occupational and Environmental Medicine, Boston Medical
Center
ABSTRACT
An occupational
medicine physician was exposed to vapors from a lithium salt spill while
observing the processes of a diamond manufacturing company. He experienced
difficulty with taste, then developed trouble with hand writing, concentration
and fatigue that have medically disabled him. MRI revealed an abnormality
suggestive of a demyelinating lesion in his brainstem. Cerebrospinal fluid
changes consistent with multiple sclerosis. No biological monitoring, clinical
or neurophysiological evidence could clearly implicate lithium in the pathophysiology
of his medical problem. A review of the medical literature for occupational
exposure to lithium provided few results. One aimed at the neurological
sequella from lithium carbonate ingestion by prescribed medication, however,
revealed that the clinical history described was consistent with that of
lithium neurotoxicity. Furthermore, neuroimaging has revealed evidence
for dysfunction in the cerebellum, basal ganglia and brainstem structures
from lithium toxicity. The hypothesis that the pathophysiology of lithium
neurotoxicity involving the brainstem may be similar to that for central
pontine myelinolysis is introduced. Occupational exposure to lithium salt
may have resulted in a clinical syndrome resembling multiple sclerosis.
Key Words:
Toxicology, Neurotoxicology, Lithium, Occupational Exposure, Diamond Manufacturing
Industry, Brainstem Dysfunction, Multiple Sclerosis, Neurophysiological
Testing
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OCCUPATIONAL SLOW VIRUS INFECTION In Occupational Infectious Disease:
A Practical Guide. Beverly, MA: OEM Press. 1999.
Jonathan S.
Rutchik, MD, MPH
Medical Director,
Division of Occupational and Environmental Neurology
Boston, MA
December 1998
Introduction
The term slow
virus is a commonly used, though poorly descriptive term that describes
infectious diseases resulting from a transmissible prion protein, PrP.
Known as transmissible spongiform encephalopathies, TSE, this group of
diseases include scrapie of sheep, bovine spongiform encephalopathy, BSE,
of cattle as well as Creutzfeld- Jakob disease, CJD, Gerstman- Straussler-
Shenker syndrome, GSS, fatal familial insomnia and atypical prion disease
in humans. Prusiner and colleagues have demonstrated that PrP is a slowly
proteinaceous infectious particle that is devoid of nucleic acid, resists
the action of enzymes that destroy RNA and DNA and electron microscroscopically
does not have the structure of a virus.
CJD is the
most important of the TSEs in humans; GSS, FFI and atypical prion disease
are inheritable and extremely rare. CJD is a fatal dementing neurodegenerative
illness that presents most commonly in late middle age. Neurological and
psychological symptoms are common. Its incubation period varies from months
to decades. When symptoms develop, however, death ensures within one year.
CJD is predominantly sporadic, but prion disease have both infective and
genetic properties. 2 Researchers have demonstrated that the agent responsible
is transmissible from humans to primates by injecting brain tissue from
patients with this disorder. CJD does not appear to be spontaneously contagious
but iatrogenic transmission has been reported in many instances. Corneal
transplantation, implantation of cerebral depth encephalography electrodes,
implantation of dura mater grafts and human growth hormone therapy have
been suggested modes of transmission.2 Occupations where contact with human
or animal neural tissues is common risk exposure. These include histopathologists,
laboratory technicians, veterinarian neuroscientists, pathologists, anatomists,
neurosurgeons and other surgeons as well as morticians and others in the
health related profession. Since CJD has been reported in animal handlers
where exposure to neural tissues could have occurred, butchers and farmers
may also risk exposure. Proper preparations, precautions and handling techinques
will be discussed below.
Recently a
new variant (nv) of CJD has been discovered in younger patients predominantly
in the United Kingdom, UK. Ten years prior to this, the UK experienced
a epizootic of BSE, thought to be secondary to exposure of calves to contaminated
rendered cattle carcasses in the form of meat and bone meal nutritional
supplements. This has raised concerns over whether transmission may occur
from animal to man by means other than contact with neural tissues. A UK
government expert panel announced that the agent responsible for BSE might
have spread to humans, based on the recognition of ten persons with nvCJD.
The US has began active surveillance; CDC reported no nvCJD in the US in
1996. 7 Although no clear evidence has been demonstrated that supports
blood, bodily fluid or non central nervous system transmission, UK epidemiologists
in one study have reported an increased incidence of CJD in dairy farmers
in the UK and other countries. These authors underscore that mouse transmission
studies presently underway, will help reveal whether the causative agent
for BSE has infected humans. (BMJ 315 1997)
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