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Clinical Assessment of Neurotoxicity. Occupational and Environmental Medical Association of Canada 29th Annual Scientific Conference. Chris Martin, MD, MSc, FRCPC [email protected] Director, Institute of Occupational and Environmental Health.

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clinical assessment of neurotoxicity

Clinical Assessment of Neurotoxicity

Occupational and Environmental Medical Association of Canada

29th Annual Scientific Conference

Chris Martin, MD, MSc, FRCPC

[email protected]

Director, Institute of Occupational and Environmental Health

slide3

“Many complain of their Memory, few of their Judgment”.

- Benjamin Franklin

“Tout le monde se plaint de sa mémoire, et personne ne se plaint de son jugement”.

- François de la Rochefoucauld

overview
Overview
  • Review neuroanatomy
    • Vulnerability
    • Targets of neurotoxicity
  • Clinical approach
  • Case discussion
what makes the nervous system more vulnerable
What makes the Nervous System MORE vulnerable?
  • High aerobic energy requirements
    • Most sensitive tissue to loss of oxygen supply
  • Presence of long, complex cell structures
    • Axons are most sensitive to damage
targets of neurotoxicity
Targets of Neurotoxicity

Damage to:

  • Cell body
    • neuronopathy
  • Axon
    • axonopathy
  • Myelin
    • myelinopathy
  • Synapse or neuromuscular junction
    • “transmissionopathy”
neuronopathy
Neuronopathy
  • Damage is irreversible
neuronopathy1
Neuronopathy
  • Damage is irreversible

Examples:

  • methyl mercury
  • MPTP
axonopathy
Axonopathy
  • Damage is reversible in PNS

irreversible in CNS

  • Sensorimotor neuropathies
  • “Stocking and glove” distribution
axonopathy1
Axonopathy
  • Damage is reversible in PNS

irreversible in CNS

  • Sensorimotor neuropathies
  • “Stocking and glove”distribution

Examples:

  • carbon disulfide
  • n-hexane
  • acrylamide monomer
  • arsenic
  • trichloroethylene
transmissionopathy
“Transmissionopathy”
  • Organophosphate pesticides
what is the typical case before you
What is the typical case before you?
  • CNS: Chronic encephalopathy
  • PNS: Sensorimotor peripheral neuropathy
history
History
  • Take a detailed exposure history
    • Strong dose-response relationship
history1
History
  • Take a detailed exposure history
  • Ask about symptoms of acute intoxication for any body system when actively exposed
history2
History
  • Take a detailed exposure history
  • Ask about symptoms of acute intoxication for any body system when actively exposed

Example: For solvents, dermatitis? Headache? Nausea? Felt drunk? Syncope?

history3
History
  • Obtain detailed information about symptoms
    • Ask for examples of symptom manifestations
    • Functional status, activities of daily living
history4
History
  • Obtain detailed information about symptoms
  • Determine chronology of symptoms in relation to exposure
    • Symptoms occur at the time of or shortly after exposure
    • Course of symptoms after cessation of exposure important
history5
History
  • Obtain detailed information about symptoms
  • Determine chronology of symptoms in relation to exposure
  • Complete medical history to ascertain other possible causes
    • Alcohol, cardiovascular disease, psychiatric disease, family history
physical examination
Physical Examination
  • Folstein Mini-Mental Status Exam
physical examination1
Physical Examination
  • Folstein Mini-Mental Status Exam
  • Detailed neurological examination
  • Particular attention to nature and distribution of any abnormalities
investigations
Investigations

Peripheral Nervous System:

  • Nerve conduction studies / electromyography
  • Quantitative sensory testing
  • Nerve biopsy if n-hexane peripheral neuropathy
peripheral nervous system
Peripheral Nervous System
  • Key points in formulating diagnosis:
    • Most toxic neuropathies are symmetric with greater distal involvement
    • Recovery following cessation of exposure
    • In general, for about 25-40% of peripheral neuropathies, diagnosis is unknown
investigations1
Investigations

Central Nervous System:

  • Imaging studies usually normal unless very advanced disease
  • Other investigations (lumbar puncture, EEG, labs) to rule out other causes
  • Most sensitive investigation is neuropsychiatric testing
    • Testing is user dependent
    • Report should provide numerical scores on test
    • Read the entire report
  • Include investigations for effects of exposure on other systems (Example LFT’s for solvents)
central nervous system
Central Nervous System
  • Key points in formulating diagnosis:
    • Most toxic CNS disorders are diffuse without focal pathology
    • Onset when exposed
    • Stable following cessation of exposure for chronic solvent encephalopathy1
    • Must rule out other causes
    • May need longitudinal information
    • Consider the impact of a diagnosis of “brain damage” from “chemical poisoning”

1. van Valen E, Wekking E, van der Laan G, Sprangers M, van Dijk F. The course of chronic solvent induced encephalopathy: A systematic review. Neurotoxicology. 2009 Nov;30(6):1172-86.

case discussion
Case Discussion
  • 39-year old female clerk at prison facility
  • Exposed to sewer gases as well as agents applied to unclog commodes
  • At 1:30 PM upper airway irritation, headache, nausea with vomiting
  • Left work at 2:50 PM
case discussion1
Case Discussion

3 days later:

  • difficulty with concentration, poor memory, photophobia, difficulty speaking, reduced smell and taste, difficulty writing
  • Very poor level of functioning since exposure
  • Presents to ER one week after exposure
case discussion2
Case Discussion

Physical exam:

  • Mental status - poor recall, serial 7’s, good judgement, general knowledge
  • Performs tasks after approximately 3 second delay
  • Reduced olfaction, otherwise cranial nerves intact
  • Photophobia
case discussion3
Case Discussion

Physical exam:

  • Difficulty with alternating movements, finger-nose, tandem gait
  • Romberg’s sign negative
  • Power, tone, reflexes, sensation intact
  • Aphasia: rhythmic quality, selective omission of articles
case discussion4
Case Discussion

Do you think her presentation is due to the exposure?

case discussion5
Case Discussion

Do you think her presentation is due to the exposure?

  • Not a high level exposure, not likely to have been exposed to compatible neurotoxic agent
case discussion6
Case Discussion

Do you think her presentation is due to the exposure?

  • Not a high level exposure, not likely to have been exposed to compatible neurotoxic agent
  • Delay in symptoms
ad