Chronic solvent encephalopathy is a degenerative neurologic disorder caused by exposure to toxic substances like organic solvents. Exposure to toxic substances can lead to a variety of symptoms, characterized by an altered mental status, memory loss, visual problems,etc etc. Toxic encephalopathy can be caused by various chemicals, some of which are commonly used in everyday life. Toxic encephalopathy can permanently damage the brain and currently, treatment is mainly just for the symptoms.
Contents
- 1 Signs and symptoms
- 2 Causes
- 3 Treatment
- 4 Prognosis
- 5 Research
- 6 See also
- 7 Notes
- 8 References
- 9 External links
Signs and symptoms[edit]
"Encephalopathy" is a general term describing brain malfunctions and "toxic" asserts that the malfunction is caused by toxins on the brain. The most prominent characteristic of toxic encephalopathy is an altered mental status. Toxic encephalopathy has a wide variety of symptoms, which can include memory loss, small personality changes/increased irritability, insidious onset of concentration difficulties, involuntary movements, fatigue, seizures, arm strength problems, and depression. Neurobehavioural effects of occupational exposure to organic solvents among construction painters . The condition may also be referred to as substance-induced persistent dementia. Acute intoxication symptoms include lightheadedness, dizziness, headache and nausea, and regular cumulative exposure to these toxic solvents over a number of years puts the individual at high risk for developing toxic encephalopathy.
Magnetic Resonance Imaging (MRI) analyses have also demonstrated increased rates of dopamine synthesis in the putamen, reduced anterior and total corpus callosum volume, demyelination in the parietal white matter, basal ganglia, and thalamus, as well as atypical activation of frontal areas of the brain due to neural compensation. A thorough and standard diagnostic process is paramount with toxic encephalopathy, including a careful occupational history, medical history, and standardized imaging/neurobehavioral testing.
Causes[edit]
In addition, chemicals, such as lead, that could instigate toxic encephalopathy are sometimes found in everyday products such as cleaning products, building materials, pesticides, air fresheners, and even perfumes. These harmful chemicals can be inhaled (in the case of air fresheners) or applied (in the case of perfumes).[1][2] The substances diffuse into the brain rapidly, as they are lipophilic and readily transported across the blood–brain barrier. This is a result of increased membrane solubility and local blood flow, with central nervous system (CNS) solvent uptake being further increased with high levels of physical activity.[3] When they are not detoxified immediately, the symptoms of toxic encephalopathy begin to emerge.[2] However, in chronic situations, these effects may not become severe enough to be noticed until much later. Increased exposure time and increased concentration of the chemical solvents will worsen the effects of toxic encephalopathy, due to the associated structural CNS damage and direct functional impairment consequences.[3]
Treatment[edit]
Treatment is mainly for the symptoms that toxic encephalopathy brings upon victims, varying depending on how severe the case is. Diet changes and nutritional supplements may help some patients. To reduce or halt seizures, anticonvulsants may be prescribed. Dialysis or organ replacement surgery may be needed in some severe cases.[4]
Management of affected individuals consists of immediate removal from exposure to the toxic substance(s), treatment of the common clinical manifestation of depression if present, and counselling for the provision of life strategies to help cope with the potentially debilitating condition.[3]
Prognosis[edit]
Toxic encephalopathy is often irreversible. If the source of the problem is treated by removing the toxic chemical from the system, further damage can be prevented, but prolonged exposure to toxic chemicals can quickly destroy the brain.[5] Long term studies have demonstrated residual cognitive impairment (primarily attention and information-processing impairment resulting in dysfunction in working memory) up to 10 years following cessation of exposure.[3] Severe cases of toxic encephalopathy can be life threatening.[6]
Research[edit]
Research is being done by organizations such as NINDS (National Institute of Neurological Disorders and Stroke) on what substances can cause encephalopathy, why they do this, and eventually how to protect, treat, and cure the brain from this condition.[7]
See also[edit]
- Brain damage
- Encephalopathy
- Neurology
Notes[edit]
- ^ "National Toxic Encephalopathy Foundation". Retrieved 2009-03-30.
- ^ a b Rogers, Sherry (1996). "Toxic Brain Encephalopathy". TOTAL WELLNESS Newsletter. Prestige Publishing. Retrieved 2009-04-21.
- ^ a b c d Baker, E. (2008). Chronic toxic encephalopathy caused by occupational solvent exposure. Annals of Neurology. 63(5): 545-547
- ^ "Is there any treatment?". Disorders A-Z. National Institute of Neurological Disorders and Stroke. 2007-02-12. Retrieved 2009-04-12.
- ^ "What is the prognosis?". Disorders A-Z. National Institute of Neurological Disorders and Stroke. 2007-02-12. Retrieved 2009-04-12.
- ^ Upledger, John (07 2004). "Toxic Brain Injury(Encephalopathy)". Massage Today. MPA. Retrieved 2009-04-12.
- ^ "What research is being done?". Disorders A-Z. National Institute of Neurological Disorders and Stroke. 2007-02-12. Retrieved 2009-04-12.
References[edit]
- Bradley, Walter (2004). Neurology in Clinical Practice (4 ed.). Taylor & Francis. ISBN [[Special:BookSources/9997625897|9997625897[[Category:Articles with invalid ISBNs]]]].
- Baker, E. (2008). Chronic toxic encephalopathy caused by occupational solvent exposure. Annals of Neurology. 63(5): 545-547
External links[edit]
- NINDS Encephalopathy Information Page
- FELA Law: Toxic Encephalopathy
- National Toxic Encephalopathy Foundation
- “Is It Safe?” (Video) from the Toxicology Education Foundation
- Encephalopathy Causes, Symptoms, Diagnosis and Treatment by MedicineNet
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Pathology of the nervous system, primarily CNS (G04–G47, 323–349)
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| Inflammation |
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Brain
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- Encephalitis
- Viral encephalitis
- Herpesviral encephalitis
- Cavernous sinus thrombosis
- Brain abscess
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Spinal cord
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- Myelitis: Poliomyelitis
- Demyelinating disease
- Tropical spastic paraparesis
- Epidural abscess
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Both/either
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- Encephalomyelitis
- Meningoencephalitis
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Brain/
encephalopathy |
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Degenerative
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Extrapyramidal and
movement disorders
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- Basal ganglia disease
- Parkinsonism
- PKAN
- Tauopathy
- Striatonigral degeneration
- Hemiballismus
- HD
- OA
- Dyskinesia
- Dystonia
- Status dystonicus
- Spasmodic torticollis
- Meige's
- Blepharospasm
- Athetosis
- Chorea
- Myoclonus
- Akathisia
- Tremor
- Essential tremor
- Intention tremor
- Restless legs
- Stiff person
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Dementia
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- Tauopathy
- Alzheimer's
- Primary progressive aphasia
- Frontotemporal dementia/Frontotemporal lobar degeneration
- Pick's
- Dementia with Lewy bodies
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Mitochondrial disease
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Demyelinating
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- autoimmune
- Multiple sclerosis
- Neuromyelitis optica
- Schilder's disease
- hereditary
- Adrenoleukodystrophy
- Alexander
- Canavan
- Krabbe
- ML
- PMD
- VWM
- MFC
- CAMFAK syndrome
- Central pontine myelinolysis
- Marchiafava-Bignami disease
- Alpers' disease
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Episodic/
paroxysmal
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Seizure/epilepsy
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- Focal
- Generalised
- Status epilepticus
- Myoclonic epilepsy
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Headache
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Cerebrovascular
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- TIA
- Amaurosis fugax
- Transient global amnesia
- Acute aphasia
- Stroke
- MCA
- ACA
- PCA
- Foville's
- Millard-Gubler
- Lateral medullary
- Weber's
- Lacunar stroke
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Sleep disorders
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- Insomnia
- Hypersomnia
- Sleep apnea
- Obstructive
- Ondine's curse
- Narcolepsy
- Cataplexy
- Kleine-Levin
- Circadian rhythm sleep disorder
- Advanced sleep phase disorder
- Delayed sleep phase disorder
- Non-24-hour sleep–wake disorder
- Jet lag
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CSF
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- Intracranial hypertension
- Hydrocephalus/NPH
- Choroid plexus papilloma
- Idiopathic intracranial hypertension
- Cerebral edema
- Intracranial hypotension
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Other
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- Brain herniation
- Reye's
- Hepatic encephalopathy
- Toxic encephalopathy
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Spinal cord/
myelopathy |
- Syringomyelia
- Syringobulbia
- Morvan's syndrome
- Vascular myelopathy
- Foix-Alajouanine syndrome
- Spinal cord compression
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| Both/either |
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Degenerative
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SA
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- Friedreich's ataxia
- Ataxia telangiectasia
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MND
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- UMN only:
- Primary lateral sclerosis
- Pseudobulbar palsy
- Hereditary spastic paraplegia
- LMN only:
- Distal hereditary motor neuropathies
- Spinal muscular atrophies
- SMA
- SMAX1
- SMAX2
- DSMA1
- Congenital DSMA
- SMA-PCH
- SMA-LED
- SMA-PME
- Progressive muscular atrophy
- Progressive bulbar palsy
- Fazio–Londe
- Infantile progressive bulbar palsy
- both:
- Amyotrophic lateral sclerosis
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anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp
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noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr
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proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
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