Over 69 million people suffer a Traumatic Brain Injury (TBI) each year and lifelong disability is common in those who survive.¹  Animal models are being used to replicate various features of human traumatic brain injury to increase our understanding of the underlying pathophysiology and potential acute and chronic treatments. 

Intracranial Pressure

Traumatic brain injury (TBI) often results in increased intracranial pressure (ICP).  Secondary injuries, up to and including death, are a natural consequence as the brain swells within the rigid skull.^1,2   As a result, continuous ICP monitoring is seen as a vital aspect of clinical treatment for patients with TBI.^2,3  Current methods of monitoring ICP in animals are implantable telemetry, intraventricular catheters,
and epidural probes.

Google Scholar Indexes 500 Publications Citing DSI and Intracranial Pressure

Sleep and Seizure

Sleep disturbances occur in 30-70% of individuals following traumatic brain injury (TBI).¹ When chronic sleep disruption occurs it may exacerbate other symptoms, impair recovery and lead to cognitive decline.²  Researchers use electroencephalography (EEG) and electromyography (EMG) to monitor sleep in animal models. EEG is also used to monitor seizure activity post injury as 1 in 5 TBI patients develop epilepsy in the first week post-injury.¹ 

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Google Scholar Indexes 1,410 Publications Citing DSI and Sleep
Google Scholar Indexes 447 Publications Citing DSI and Seizure

Behavior

Traumatic brain injuries, especially repetitive damage, can lead to a range of acute and chronic effects including cognitive deficits, social abnormalities, anxiety, depression, pain, and motor dysfunction. Behavioral assessments help to determine these effects after injury, providing a greater understanding of underlying pathophysiology as well as relevant treatment options.

Google Scholar Indexes 531 Publications Citing Panlab and Traumatic Brain Injury
Google Scholar Indexes 269 Publications Citing Coulbourn Instruments and Traumatic Brain Injury

Respiratory

Immune-suppression is often associated with TBI and can lead to pulmonary complications including respiratory failure, pneumonia, pleural effusions, and empyema, acute lung injury and acute respiratory distress syndrome (ALI/ARDS), pulmonary edema, and pulmonary embolism (PE).^1,2 However, new research suggests TBI patients may actually be less susceptible to pneumonia as TBI activates vagus nerve signaling through neurokinin and cholinergic pathways.^1,3

Metabolism

Temperature monitoring has several applications in TBI research. A noninfectious increase in core body temperature, known as Posttraumatic Hyperthermia (PTH), often occurs post-injury and negatively impacts recovery.¹ There is significant research into the cause of PTH and its impact on the patient.¹ Core body temperature monitoring is also used in hypothermic treatment approaches. Mild therapeutic hypothermia is neuroprotective against multiple brain insults, and can reduce seizure incidence and severity in some cases.^2,3,4  To accurately measure core body temperature invasive measurements are required.

Google Scholar Indexes 146 Publications Citing DSI, Temperature and Traumatic Brain Injury

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