Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...

Depolarizing Blockers: Mechanism of Action

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...

Depolarizing Blockers: Pharmocokinetics

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

Directly acting muscle relaxants like dantrolene and botulinum toxin (BoNT) have distinct mechanisms and applications. Dantrolene, a hydantoin derivative, acts on the ryanodine receptor (RYR1) in skeletal muscle cells. RYR1 are calcium channels present at the sarcoplasmic reticulum membrane. In response to excitation, they release calcium ions from the sarcoplasmic reticulum to the cytosol. Calcium promotes actin-myosin-mediated contraction of muscles.
The binding of dantrolene to the RYR1...

Toxidromes: Clinical Features

Toxidromes: Clinical Features

Toxidromes are specific patterns of symptoms resulting from toxic substance exposure. They help in the identification and treatment of poisoning. The symptoms of each toxidrome group indicate poisoning by a certain class of chemicals or drugs.1. Sympathomimetic: Stimulates the sympathetic nervous system. Symptoms include agitation, increased heart rate (HR), blood pressure (BP), respiratory rate (RR), temperature, and pupil size. Drugs like cocaine and amphetamines, along with tremors and...

Diphtheria

Diphtheria

Diphtheria is an acute, toxin-mediated infectious disease that primarily affects the upper respiratory tract. It is caused by Corynebacterium diphtheriae, a Gram-positive, pleomorphic rod that lacks spore-forming capability and exhibits a characteristic club-shaped morphology under microscopic examination. While C. diphtheriae can asymptomatically colonize mucosal surfaces, clinical disease manifests only when the bacterial strain is lysogenized by a specific β-corynephage. This phage...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Haemodynamic effects of pan masala in healthy volunteers.

The Journal of the Association of Physicians of India·2001

Same author

A randomized comparison of classical mode of administration of amphotericin B with its newer modes of administration in kala-azar.

The Journal of the Association of Physicians of India·2001

Same author

Relaxin decreases renal interstitial fibrosis and slows progression of renal disease.

Kidney international·2001

Same author

A polystyrene based membrane electrode for cadmium(II) ions.

Fresenius' journal of analytical chemistry·2001

Same author

The circadian pattern of ischaemic heart disease events in Indian population.

The Journal of the Association of Physicians of India·2001

Same author

Amberlite XAD-7 impregnated with Xylenol Orange: a chelating collector for preconcentration of Cd(II), Co(II), Cu(II), Ni(II), Zn(II) and Fe(III) ions prior to their determination by flame AAS.

Fresenius' journal of analytical chemistry·2001

Search research articles

Related Experiment Video

Updated: May 13, 2026

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Published on: September 12, 2020

Delayed onset generalised dystonia after cyanide poisoning

R Borgohain¹, A K Singh, H Radhakrishna

¹Department of Neurology, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, India.

Clinical Neurology and Neurosurgery

|August 1, 1995

Summary

A patient developed persistent dystonia after a potassium cyanide suicide attempt. Imaging revealed putaminal damage, but levodopa treatment showed improvement, suggesting a potential therapeutic avenue for cyanide-induced neurological damage.

More Related Videos

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease

Published on: October 14, 2021

Related Experiment Videos

Last Updated: May 13, 2026

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Published on: September 12, 2020

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease

Published on: October 14, 2021

Area of Science:

Neurotoxicology
Neurology
Neuroimaging

Background:

Cyanide poisoning is a severe medical emergency with potential for delayed neurological sequelae.
Dystonia is a movement disorder characterized by involuntary muscle contractions.
The neurotoxic effects of cyanide on the basal ganglia, particularly the putamen, are not fully elucidated.

Observation:

A 27-year-old female presented with delayed-onset, persistent generalized dystonia after a potassium cyanide suicidal attempt.
Cranial CT revealed bilateral putaminal hypodensities.
MRI confirmed these lesions as hypointense on T1 and hyperintense on T2 weighted images, indicative of cytotoxic edema or necrosis.

Findings:

Multimodality evoked potentials were within normal limits, despite significant clinical and radiological findings.
The patient showed notable clinical improvement following treatment with levodopa.
Putaminal hypodensities on CT and MRI correlated with the development of dystonia.

Implications:

This case highlights the potential for delayed-onset dystonia as a neurological consequence of cyanide poisoning.
The putamen appears to be a vulnerable target for cyanide neurotoxicity.
Levodopa may be a beneficial therapeutic agent for managing cyanide-induced dystonia, warranting further investigation.