Clinical assessment of neurotoxicity
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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

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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


These are among the most challenging cases in Occupational Medicine


“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

  • Review neuroanatomy

    • Vulnerability

    • Targets of neurotoxicity

  • Clinical approach

  • Case discussion


1. Review of Neuroanatomy


What makes the nervous system LESS vulnerable?

  • Blood brain barrier for CNS


What makes the nervous system LESS vulnerable?

  • Excess neuronal capacity


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


Structure of the Neuron


Targets of Neurotoxicity

Damage to:

  • Cell body

    • neuronopathy

  • Axon

    • axonopathy

  • Myelin

    • myelinopathy

  • Synapse or neuromuscular junction

    • “transmissionopathy”


Neuronopathy

  • Damage is irreversible


Neuronopathy

  • Damage is irreversible

    Examples:

  • methyl mercury

  • MPTP


Axonopathy

  • Damage isreversible in PNS

    irreversible in CNS

  • Sensorimotor neuropathies

  • “Stocking and glove” distribution


Axonopathy

  • Damage isreversible in PNS

    irreversible in CNS

  • Sensorimotor neuropathies

  • “Stocking and glove”distribution

    Examples:

  • carbon disulfide

  • n-hexane

  • acrylamide monomer

  • arsenic

  • trichloroethylene


Myelinopathy

  • lead


“Transmissionopathy”

  • Organophosphate pesticides


2. Clinical Approach


What is the typical case before you?

  • CNS: Chronic encephalopathy

  • PNS: Sensorimotor peripheral neuropathy


History

  • Take a detailed exposure history

    • Strong dose-response relationship


History

  • Take a detailed exposure history

  • Ask about symptoms of acute intoxication for any body system when actively exposed


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?


History

  • Obtain detailed information about symptoms

    • Ask for examples of symptom manifestations

    • Functional status, activities of daily living


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


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

  • Folstein Mini-Mental Status Exam


Physical Examination

  • Folstein Mini-Mental Status Exam

  • Detailed neurological examination

  • Particular attention to nature and distribution of any abnormalities


Investigations

Peripheral Nervous System:

  • Nerve conduction studies / electromyography

  • Quantitative sensory testing

  • Nerve biopsy if n-hexane peripheral neuropathy


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


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

  • 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.


3. 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 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 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 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 Discussion

Do you think her presentation is due to the exposure?


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 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


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