Concussion generally refers to the set of clinical symptoms that are secondary to the head injury and are characteristic by altered state of consciousness like instant onset of transient neurologic dysfunction, lack of consciousness or temporary respiratory arrest and loss of reflexes.
Since it's connected to the head trauma by definition, there is in principium no other cause of it.
The patophysiologic mechanism of concussion is not well understood yet, it's thought it results from two main sources:
- the acceleration of brain causes increase of pressure
- the impact of brain on the hard shell causes deformation and sheer stress in brain tissue (probably stronger cause of cytologic changes discussed later on)
These two mechanisms might lead to changes in the tissue structure and also trigger cytologic changes in the astrocytes and neurons such as:
Astrocytes respond to a focal mechanical stimulation by propagating intercellular waves through their network. Mechanically stimulated astrocyte networks show changes in the cytoskeleton, organelle function, and biochemical cascades over time.
The changes in neurons detected in vitro include microstructural changes, direct membrane permeability change and change in the receptor abundance, structure of subunits and
Early evidence showed that these physical insults can affect the properties of important synaptic glutamate receptors that can regulate neurotransmission and plasticity in networks. Moreover, inhibitory synaptic receptor functions can be altered with a physical force, showing that the balance of excitation/inhibition coupling is important to consider when assessing the effects of these physical forces. Perhaps equally important is the alteration in the receptor composition and intracellular signaling that occurs after a microinjury.
Microinjury is also linked to triggering of cell death pathways in brain cells.
The importance of these mechanisms are not yet clearly understood though and there probably are many more playing their role.
- Overview study
- Robbins and Cotran pathologic basis of disease