Related Experiment Video
Updated: May 13, 2026

05:02
Establishment of Acute Pontine Infarction in Rats by Electrical Stimulation
Published on: August 27, 2020
Thalamic infarction following a Russell's viper bite.
Abraham M Ittyachen1, Mohan B Jose
1Department of Medicine, Malankara Orthodox Syrian Church Medical College, Kolenchery, Kerala State, India. abyliz@rediffmial.com
The Southeast Asian Journal of Tropical Medicine and Public Health
|February 26, 2013
Summary
Russell's viper bites can cause brain damage. This case highlights a rare instance of bilateral thalamic infarction following a Russell's viper (Daboia russelii) envenomation, a complication not previously reported.
Area of Science:
- Neuroscience
- Toxicology
- Vascular Neurology
Background:
- Russell's viper (Daboia russelii) envenomation is a significant cause of morbidity and mortality, particularly in South Asia.
- Coagulopathy is a common complication of Daboia russelii bites, often leading to hemorrhagic or thrombotic events.
- Cerebral infarction following snakebites has been documented, but specific patterns of brain involvement are not fully characterized.
Observation:
- A 55-year-old male presented with a Russell's viper bite.
- Initial presentation included prolonged clotting times, raising concerns for intracranial hemorrhage.
- Despite coagulopathy control within 24 hours, the patient exhibited restlessness and disorientation.
Findings:
- Magnetic resonance imaging (MRI) revealed bilateral thalamic infarcts.
- These infarcts occurred despite the successful management of coagulopathy.
- This represents the first reported case of bilateral thalamic infarction secondary to Daboia russelii envenomation.
Implications:
- This case expands the spectrum of neurological complications associated with Russell's viper bites.
- It underscores the potential for ischemic cerebrovascular events, even after coagulopathy correction.
- Further research is needed to understand the pathophysiology and risk factors for thalamic infarction in snake envenomation.
Related Concept Videos
Transient Ischemic Attack l: Introduction
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
Hemorrhagic Stroke ll: Pathophysiology
A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Secondary Spinal Cord Injury llI: Pathophysiology
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

