Acquired Brain Damage: Causes, Consequences And Treatment

The acquired brain injury ( DCA ) is an injury that occurs in a brain that had hitherto presented normal development or expected. It can be the result of different causes: head injuries (TBI), cerebrovascular accidents (CVA), brain tumors, anoxia, hypoxia, encephalitis, etc. (De Noreña et al., 2010). In some cases, the scientific literature uses the term supervening brain damage (DCS) to refer to this same clinical concept.

When an accident that involves acquired brain damage occurs, different neurological processes will be affected and acute injuries to the individual’s nervous system will in many cases lead to a situation of significant deterioration of health and functional independence (Castellanos-Pinedo et al., 2012).

acquired brain damage

It is one of the most important health problems in developed countries. This is due to the magnitude of its incidence and the physical, cognitive and social impact it causes on people who suffer this type of injury (García-Molína et al., 2015).


Normally, acquired brain damage is associated with head trauma, in fact, in the English-speaking medical literature, the term brain injury is frequently used as a synonym for traumatic brain injury (Castellanos- Pinedo et al., 2012).

But in addition, acquired brain damage can have its origin in stroke, brain tumors or infectious diseases (De Noreña et al., 2010).

Castellanos-Pinedo et al. (2012) show a wide list of possible causes of acquired brain damage depending on the agent that causes them:

Injuries caused by external agents

  • Head trauma
  • Toxic encephalopathy: drugs, drugs, and other chemicals
  • Encephalopathy due to physical agents: ionizing radiation, electrocution, hyperthermia or hypothermia.
  • Infectious diseases: meningoencephalitis

Injuries caused by endogenous causes

  • Hemorrhagic or ischemic stroke
  • Anoxic encephalopathy: due to various causes such as cardiorespiratory arrest.
  • Primary or secondary neoplasms
  • Autoimmune inflammatory diseases (connective tissue diseases-systemic lupus erythematosus, Behçet’s disease, systemic vasculitis and demyelinating diseases-multiple sclerosis or acute disseminated encephalomyelitis).

Depending on their incidence, an order of importance of these causes can be established, the most frequent being creneoencephalic injuries and strokes / cerebrovascular accidents. Third, anoxic encephalopathy would be placed. Less frequent would be causes of the infectious type or derived from brain tumors (Castellanos-Pinedo et al., 2012).

Head trauma

Ardila & Otroski (2012) propose that head trauma occurs as a consequence of the impact of a blow on the skull. Generally, the impact on the skull is transmitted both to the meningeal layers and to the cortical structures.

In addition, different external agents can cause the impact: use of forceps at birth, gunshot wound, blow against blow effect, extension of a mandibular blow, among many others.

Therefore, we can find open trauma (TCA) in which there is a bill of the skull and penetration or exposure of brain tissue, and closed head trauma, in which a skull fracture does not occur, but can take place serious lesions of brain tissue due to the development of edema, hypoxia, increased intracranial pressure or ischemic processes.


The term cerebrovascular accident (CVA) refers to an alteration of the blood supply of the brain . Within the cerebrovascular accidents we can find two groups: due to the obstruction of blood flow (obstructive or ischemic accidents) and hemorrhages (hemorrhagic accidents) (Ropper & Samuels, 2009; Ardila & Otroski, 2012).

In the group of strokes caused by an obstruction of blood flow, we can find the following causes described by Ardila & Otroski (2012):

  • Thrombotic accidents : the cause of obstruction is an arteriosclerotic plaque that is located in an arterial wall. This can impede blood flow, causing an ischemic area (which does not receive blood supply) and a heart attack in the area that the blocked artery supplies.
  • Cerebral embolism / embolic accidents : the cause of the obstruction is an embolus (blood clot, fat or gas type) that obstructs the blood circulation of a brain vessel, causing an ischemic zone and a heart attack in the area that the blocked artery supplies.
  • Transient ischemic attack : occurs when the obstruction resolves in less than a 24-hour period. They usually occur as a result of an arterioslerotic plaque or thrombotic embolus.

On the other hand, hemorrhagic accidents are usually the consequence of the rupture of a cerebral aneurysm (malformation of a blood vessel) that may be generating hemorrhagic blood flows at the intracerebral, subarachnoid, subdural or epidural level (Ardila & Otroski, 2012).

Anoxic encephalopathy

Anoxic or hypoxic encephalopathy occurs when there is an insufficient supply of oxygen to the central nervous system , due to respiratory, cardiac or circulatory causes (Serrano et al., 2001).

There are different mechanisms through which the oxygen supply can be interrupted: decreased cerebral blood flow (cardiac arrest, cardiac arrhythmia, severe hypotension, etc); due to a decrease in the amount of oxygen in the blood (guda polyradiculoneuritis, myasthenia gravis, pulmonary diseases, chest trauma, drowning or inhalation of toxins); reduced ability to carry oxygen (carbon monoxide poisoning); or due to the inability of the brain tissue to use the oxygen supply (cyanide poisoning) (Serrano et al., 2001).


When acquired brain damage occurs, most patients have serious consequences that affect multiple components: from the development of a vegetative or minimally conscious state to significant deficits in sensorimotor, cognitive or affective components.

Frequently, the appearance of aphasias , apraxia , motor limitations, visuospatial alterations or heminegligence has been described (Huertas-hoyas et al., 2015). On the other hand, cognitive deficits tend to appear, such as problems with attention, memory and executive functions (García-Molina et al., 2015).

Together, all these deficits will have an important functional impact and will be an important source of dependency, making social relationships and labor reintegration difficult (García-Molina et al., 2015).

In addition, not only will consequences be given to the patient. At the family level, suffering from acquired brain damage in one of its members will be the cause of a strong moral blow.

Generally, a single person, the main caregiver, will assume most of the work, that is, he / she assumes most of the care for the dependent patient. Only in 20% of cases, care is assumed by more relatives (Mar et al., 2011)

Different authors highlight that caring for a person in a serious situation of dependency involves an effort that can be compared to a working day. Thus, the main caregiver endures an overload of work that negatively affects their quality of life in the form of stress or inability to cope with tasks.

It is estimated that the presence of psychiatric disorders in caregivers is 50%, among them are anxiety ,  depression , somatizations and insomnia (Mar et al., 2011).


Due to the wide variety of causes and consequences of acquired brain damage, both the involvement of brain systems and the magnitude of this can vary considerably between individuals.

Despite this, the working group headed by Castellanos-Pinedo (2012) proposes the following definition of acquired brain damage: 

“Injury of any origin that occurs acutely in the brain , causing permanent neurological deterioration in the individual, which conditions a deterioration of their functional capacity and their previous quality of life.”

In addition, they extract five criteria that must be present for a case to be defined as acquired brain damage:

  1. Injury affecting part or all of the brain (brain, brainstem, and cerebellum).
  2. The onset is acute (occurs within a few seconds to days).
  3. A deficiency occurs as a result of the injury.
  4. There is a deterioration in the functioning and quality of life of the person.
  5. Hereditary and degenerative diseases and injuries that occur in the prenatal stage are excluded.


In the acute phase, the therapeutic measures will be directed fundamentally to the physical sphere. At this stage, individuals are hospitalized and the objective will be to achieve control of vital signs and the consequences of acquired brain damage, such as bleeding, intracranial pressure, etc. At this stage, treatment is developed from surgical and pharmacological approaches.

In the post-acute phase, intervention will be made from a physiotherapeutic level to treat possible motor sequelae, as well as at a neuropsychological level to address cognitive sequelae: orientation deficit, amnesia , language deficit, attention deficit, etc.

In addition, in many cases psychological care will be necessary, since the event and its consequences can become a traumatic event for the individual and their environment.


Acquired brain damage has a strong personal and social impact. Depending on different factors such as the location and severity of the injuries, a series of physical and cognitive consequences will occur that can have a devastating impact on the individual’s social sphere.

Therefore, the development of post-acute intervention protocols that attempt to restore the functional level of the patient to a point close to the premorbid level are essential.


  1. Ardila, Alfredo; Othersky, Feggy ;. (2012). Guide for neuropsychological diagnosis.
  2. Castellanos-Pinedo, F., Cid-Gala, M., Duque, P., Ramírez-Moreno, J., & Zurdo-Hernández, J. (2012). Occurring brain damage: definition proposal, diagnostic criteria and classification. Rev Neurol, 54 (6), 357-366.
  3. De Noreña, D., Ríos-Lago, M., Bombín-González, I., Sánchez-Cubillo, I., García-Molina, A., & Triapu-Ustárroz, J. (2010). Effectiveness of neuropsychological rehabilitation in acquired brain damage (I): attention, processing speed, memory and language. Rev Neurol, 51 (11), 687-698.
  4. FEDACE. (2013). People with Acquired Brain Injury in Spain.
  5. García-Molina, A., López-Blázquez, R., García-Rudolph, A., Sánchez-Carrión, R., Enseñat-Cantallops, A., Tormos, J., & Roig-Rovira, T. (2015) . Cognitive rehabilitation in acquired brain damage: variables that mediate the response to treatment. Rehabilitation, 49 (3), 144-149.
  6. Huertas-Hoyas, E., Pedrero-Pérez, E., Águila Maturana, A., García López-Alberca, S., & González-Alted, C. (2015). Functionality predictors in acquired brain damage. Neurology, 30 (6), 339-346.
  7. Mar, J., Arrospide, A., Begiristain, J., Larrañaga, I., Sanz-Guinea, A., & Quemada, I. (2011). Quality of life and burden of caregivers of patients with acquired brain damage. Rev Esp Geriatr Gerontol., 46 (4), 200-205.
  8. Serrano, M., Ara, J., Fayed, N., Alarcia, R., & Latorre, A. (2001). Hypoxic encephalopathy and cortical laminar necrosis. Rev Neurol, 32 (9), 843-847.

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