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

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

These are among the most challenging cases in Occupational Medicine


Clinical assessment of neurotoxicity

“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


1 review of neuroanatomy

1. Review of Neuroanatomy


What makes the nervous system less vulnerable

What makes the nervous system LESS vulnerable?

  • Blood brain barrier for CNS


What makes the nervous system less vulnerable1

What makes the nervous system LESS vulnerable?

  • Excess neuronal capacity


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


Structure of the neuron

Structure of the Neuron


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 isreversible in PNS

    irreversible in CNS

  • Sensorimotor neuropathies

  • “Stocking and glove” distribution


Axonopathy1

Axonopathy

  • Damage isreversible in PNS

    irreversible in CNS

  • Sensorimotor neuropathies

  • “Stocking and glove”distribution

    Examples:

  • carbon disulfide

  • n-hexane

  • acrylamide monomer

  • arsenic

  • trichloroethylene


Myelinopathy

Myelinopathy

  • lead


Transmissionopathy

“Transmissionopathy”

  • Organophosphate pesticides


2 clinical approach

2. Clinical Approach


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.


3 case discussion

3. Case Discussion


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


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