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Neurotoxicology & Nutritional Deficiencies

Neurotoxicology & Nutritional Deficiencies

What You'll Learn

Overview of Neurotoxic Heavy Metals

Metal	Source / Exposure	Neurologic Features	Other Key Findings	Treatment
Lead	Old paint, contaminated water, batteries, occupational	Children: encephalopathy (irritability, seizures, cerebral edema). Adults: wrist drop (radial nerve), foot drop (peroneal nerve), peripheral neuropathy	Basophilic stippling on blood smear; lead lines on gums (Burton lines); abdominal colic; microcytic anemia; impaired heme synthesis	Succimer (oral, mild); EDTA (moderate-severe); dimercaprol + EDTA (encephalopathy)
Arsenic	Pesticides, contaminated groundwater, homicide attempts	Painful sensorimotor neuropathy (axonal, length-dependent); encephalopathy in acute poisoning	Mees lines (transverse white lines on nails); "rain drop" skin pigmentation; GI symptoms (watery diarrhea, garlic breath); QT prolongation	Dimercaprol (acute); succimer (chronic)
Mercury (organic)	Contaminated fish (methylmercury), Minamata Bay	Minamata disease: visual field constriction (calcarine cortex), cerebellar ataxia, sensory neuropathy, paresthesias, hearing loss	Constriction of visual fields is characteristic; affects calcarine cortex and granule cell layer of cerebellum; teratogenic	Succimer; selenium supplementation
Mercury (inorganic)	Industrial exposure, thermometers, dental amalgam (minimal)	Intention tremor; erethism (psychiatric — irritability, shyness, insomnia); peripheral neuropathy	"Mad Hatter" syndrome (hat-making industry); gingivitis, salivation	Succimer; penicillamine
Manganese	Miners, welders, smelters; chronic liver disease (impaired hepatic clearance)	Parkinsonism — affects globus pallidus preferentially (spares caudate/putamen); "cock-walk" gait (strutting on toes); psychiatric symptoms early	T1 hyperintensity in basal ganglia (especially globus pallidus) on MRI; poor response to levodopa (unlike idiopathic PD)	Remove exposure; chelation with EDTA (limited evidence)
Thallium	Rodenticides, homicidal poisoning	Painful sensorimotor neuropathy (ascending); encephalopathy	Alopecia (hallmark; 2–3 weeks after exposure); Mees lines (like arsenic); GI symptoms	Prussian blue (potassium ferric hexacyanoferrate); activated charcoal
Aluminum	Dialysis patients (contaminated dialysate), antacids	Dialysis dementia: progressive speech difficulty (stuttering/dysarthria), myoclonus, seizures, cognitive decline	Osteomalacia; microcytic anemia; EEG shows generalized slowing with bursts	Deferoxamine; remove aluminum source
Bismuth	Pepto-Bismol (bismuth subsalicylate), other bismuth compounds	Myoclonus (prominent); encephalopathy; ataxia; seizures	Reversible with discontinuation; dark discoloration of tongue/stool	Discontinue bismuth-containing products
Cadmium	Battery/electroplating/welding factories; cigarette smoke (major source); contaminated rice/seafood	Length-dependent sensorimotor polyneuropathy; anosmia (olfactory nerve direct injury); parkinsonism and progressive cognitive decline with chronic exposure	Long half-life (10–30 years); itai-itai disease (osteomalacia + renal tubulopathy); BBB permeability increased; no reliable chelator	Remove exposure; supportive care

Key Organic and Environmental Neurotoxins

Toxin	Source / Exposure	Neurologic Features	Key Findings	Treatment
Carbon monoxide	Fires, car exhaust, gas heaters, charcoal burning	Acute: headache, confusion, coma, seizures. Delayed neuropsychiatric syndrome (days–weeks later): cognitive decline, parkinsonism, personality changes	Cherry-red skin (classic but unreliable); bilateral globus pallidus necrosis on MRI; carboxyhemoglobin level elevated	100% normobaric O₂ for ALL suspected CO poisoning; hyperbaric oxygen for SELECTED severe/high-risk cases (loss of consciousness, neurologic deficits, cardiac ischemia, severe acidosis, very high COHb, or pregnancy per local protocol)
Organophosphates	Pesticides, nerve agents (sarin, VX)	Cholinergic crisis (DUMBELS: Diarrhea, Urination, Miosis, Bradycardia, Emesis, Lacrimation, Salivation). Intermediate syndrome: proximal weakness, respiratory failure (days 1–4). OPIDN: delayed distal neuropathy (weeks later)	Acetylcholinesterase inhibition (irreversible); depressed RBC cholinesterase; fasciculations, muscle cramps	Atropine (muscarinic blockade) + pralidoxime (reactivates AChE if given within 24–48 hours, before "aging")
n-Hexane	Glue sniffing, solvents, shoe manufacturing	Sensorimotor peripheral neuropathy (distal → proximal)	Giant axonal swellings on nerve biopsy (accumulation of neurofilaments); metabolite 2,5-hexanedione is the toxic agent	Remove exposure; slow recovery
Toluene	Paint thinners, spray paint huffing	Cerebellar ataxia, cognitive decline, dementia, anosmia, hearing loss	White matter changes on MRI; renal tubular acidosis; hypokalemia	Remove exposure; supportive care
Methanol	Moonshine, windshield wiper fluid, industrial solvent	Visual loss (optic nerve and retinal toxicity); blindness may be permanent; headache, confusion	Putaminal necrosis (bilateral) on MRI; high-anion-gap metabolic acidosis; formate is the toxic metabolite	Fomepizole (preferred) or ethanol (competitive alcohol dehydrogenase inhibition); dialysis for severe cases
Ethylene glycol	Antifreeze	Altered mental status, seizures, cranial neuropathies (especially CN VII)	Calcium oxalate crystals in urine; renal failure; high-anion-gap metabolic acidosis; osmolar gap	Fomepizole or ethanol; dialysis

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