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Traumatic Brain Injury l: Introduction

Traumatic Brain Injury l: Introduction

DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...

Cerebral Edema ll: Pathophysiology

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

Increased Intracranial Pressure ll: Pathophysiology

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...

Hemorrhagic Stroke ll: Pathophysiology

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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...

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Updated: Jul 13, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

Substance P in traumatic brain injury.

James J Donkin¹, Renee J Turner, Islam Hassan

¹Discipline of Pathology, University of Adelaide, Adelaide, South Australia, Australia.

Progress in Brain Research

|July 10, 2007

Summary

Substance P (SP) contributes to brain damage after injury. Inhibiting SP reduces swelling and improves outcomes in traumatic brain injury and stroke.

Area of Science:

Neuroscience
Neuroinflammation
Neuropeptide signaling

Background:

Neuropeptides, particularly substance P (SP), are implicated in acute brain injury.
The role of SP and neurogenic inflammation in traumatic brain injury (TBI) and stroke is under-investigated.
SP release post-CNS injury may increase blood-brain barrier permeability, leading to edema and cell death.

Purpose of the Study:

To review the role of substance P in acute brain injury.
To examine SP's function as a neurotransmitter in the context of brain insults.
To discuss the potential negative impact of SP on recovery after brain injury.

Main Methods:

Literature review of studies investigating substance P in acute brain injury.
Analysis of evidence on SP release and its effects on the central nervous system (CNS).

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Examination of therapeutic strategies targeting SP activity.

Main Results:

SP is released following CNS injury, exacerbating blood-brain barrier permeability and vasogenic edema.
Inhibition of SP release or antagonism of its receptor significantly reduces edema.
Intervention against SP activity leads to marked improvements in functional outcomes post-injury.

Conclusions:

Substance P plays a significant role in the pathophysiology of acute brain injury, including TBI and stroke.
Targeting SP offers a promising therapeutic avenue for mitigating brain damage and improving recovery.
Further research into SP's neurotransmitter functions is crucial for developing effective treatments.