Diaschisis (from Greek διάσχισις meaning "shocked throughout") is a sudden loss (or change) of function in a portion of the brain connected to a distant, but damaged, brain area. The site of the originally damaged area and of the diaschisis are connected to each other by neurons. The loss of the damaged structure disrupts the function of the remaining intact systems and causes a physiological imbalance. The injury is produced by an acute focal disturbance in an area of the brain, from traumatic brain injury or stroke, for example. Some function may be restored with gradual readjustment of the intact but suppressed areas through intervention and the brain's natural neuroplasticity.

The term "diaschisis" was coined by Constantin von Monakow in 1914. Currently the term "diaschisis" is used to describe a depression of regional neuronal metabolism and cerebral blood flow caused by in an anatomically separate but functionally related neuronal region.

Von Monakow's concept of neurophysical changes in distant brain tissue to the focal lesion led to a widespread clinical interest. Doctors were interested in how diaschisis could describe the signs and symptoms of brain lesions that could not be explained.

The areas of the brain are connected by vast organized neuronal pathways that allow one area of the brain to influence other areas more distal to it. Understanding these dense pathways helps to link a lesion causing brain damage in one area of the brain to degeneration in a more distal brain area. A focal lesion causes damage that also disturbs the structural and functional connectivity to the brain areas distal to the lesion.

The primary mechanism of diaschisis is functional deafferentation, which is the loss of the input of information from the part of the brain that is now damaged. The decrease in information and neural firing to the distal brain area causes those synaptic connections to weaken and initiates a change in the structural and functional connectivity around that area. This leads to diaschisis. Diaschisis is also influenced by many other factors, including stoke, brain swelling, and neuroanatomical disconnection. The severity of these factors is manifested in altered neuronal excitability, hypo-metabolism, and hypo perfusion.

There are two types of diaschisis. The first is focal diaschisis, which refers to the remote neurophysiological changes that are caused by a focal lesion based on von Monakow's definition. The second type of diaschisis is non-focal diaschisis and it focuses on the changes in the strength and direction of neural pathways and connectivity between brain areas. This type of diaschisis has only been a topic in recent study as a result of the advancement of brain imaging tools and technology. These new tools allow for better understanding of the organization of the brain connectivity and further investigation into new types of diaschisis, like non-focal or connectional diascisis. This new type of diaschisis relates much more closely to clinical findings.

Transneuronal degeneration can be grouped into two general categories: anterograde and retrograde.

Transneuronal degeneration is the death of neurons resulting from the disruption of input from or output to other nearby neurons. It is an active excitotoxic process when a neuron is overstimulated by a neurotransmitter (most commonly glutamate) causing the dysfunction of that neuron (either damaging it or killing it) which drives neighboring neurons into metabolic deficit, resulting in rapid, widespread loss of neurons. This can be either anterograde or retrograde, indicating the direction of the degeneration relative to the original site of damage (see types). There are varying causes for transneuronal degeneration such as brain lesions, disconnection syndromes, respiratory chain deficient neuron interaction, and lobectomies. Although there are different causes, transneuronal degeneration generally results in the same effects (whether they be cellular, dendritic, or axonal) to varying degrees. Transneuronal degeneration is thought to be linked to a number of diseases, most notably Huntington's disease and Alzheimer's disease, and researchers recently have been performing experiments with monkeys and rats, monitoring lesions in different parts of the body to study more closely how exactly the process works.

The most prominent symptom of post-traumatic amnesia (PTA) is a loss of memory of the present time. As a result, patients are often unaware of their condition and may behave as if they are going about their regular lives. This can cause complications if patients are confined to a hospital and may lead to agitation, distress and/or anxiety. Many patients report feeling as though they were being "held prisoner" and being prevented from carrying on with their daily lives. Other symptoms include agitation, confusion, disorientation, and restlessness.

Patients also often display behavioral disturbances. Patients may shout, swear and behave in a disinhibited fashion. There have been cases in which patients who do not recognize anyone will ask for family members or acquaintances that they have not seen in years. Some patients exhibit childlike behavior. Other patients show uncharacteristically quiet, friendly and loving behavior. Although this behavior may seem less threatening because of its lack of aggressiveness, it may be equally worrisome.

PTA patients are often unaware of their surroundings and will ask questions repeatedly. Patients may also have a tendency to wander off, which can be a major concern in those who have suffered additional injuries at the time of trauma, such as injured limbs, as it may lead to the worsening of these secondary injuries.

The severity of post-traumatic amnesia (PTA) is directly related to its duration, although a longer duration does not necessarily indicate more severe symptoms. The duration of PTA in brain-injured patients is a useful predictor of the expected long-term effects of the injury, along with the duration of loss of consciousness(LOC), and scores on the Glasgow Coma Scale (GCS), which measures degrees of consciousness, with higher scores indicating higher levels of functioning. A score of 3 indicates complete unconsciousness, and a score of 15 indicates normal functioning.

In patients experiencing PTA for the duration of:

Up to 1 hour – The injury is very mild in severity and full recovery is expected. The patient may experience a few minor post-concussive symptoms (e.g. headaches, dizziness).

1 – 24 hours – The injury is moderate in severity and full recovery is expected. The patient may experience some minor post-concussive symptoms (e.g. headaches, dizziness).

1 – 7 days – The injury is severe, and recovery may take weeks to months. The patient may be able to return to work, but may be less capable than before the injury.

1 – 2 weeks – The injury is very severe, and recovery is likely to take many months. The patient is likely to experience long-lasting cognitive effects such as decreased verbal and non-verbal intelligence as well as decreased performance on visual tests. Patients should, however, still be able to return to work.

2 – 12 weeks – The injury is very severe, and recovery is likely to take a year or more. The patient is likely to exhibit permanent deficits in memory and cognitive function, and the patient is unlikely to be able to return to work.

12+ weeks – injury is very severe and accompanied by significant disabilities that will require long-term rehabilitation and management. The patient is unlikely to be able to return to work.

Note: return to work is meant to indicate a return to a reasonable level of functionality, both in professional and personal arenas.

The long-term prognosis of PTA is generally positive. Many patients do recover a great deal of cognitive function, although they may not return to their pre-injury state.