Traumatic brain injury is defined as brain damage after external head trauma. The annual incidence is approximately 2 million cases, and traumatic brain injury is the leading cause of mortality in people under 45 years of age. Survival rates have recently improved due to advances in trauma medicine, and this casts greater light on their morbidity, with specific focus on psychiatric complications. Head injury increases the risk of subsequently developing dementia. This is true as an immediate consequence of the injury, as a consequence of multiple head traumas (as in dementia pugilistica), or even as an independent risk factor for the development of AD.
Deficits result from cortical brain damage, with the anterior temporal and orbitofrontal regions most susceptible. Cognitive impairment is very common following head trauma, although the severity and duration of the deficits are related to the extent and location of damage. Other variables that significantly affect the course and nature of cognitive impairment are duration of posttraumatic amnesia, brain stem dysfunction, and degree of axonal injury.
In the acute post-concussion state, amnesia and confusion are the most common symptoms. If brain damage is extensive, memory impairment frequently persists, and disturbances of attention, language, and executive function may also develop. Patients typically complain of short-term memory deficits such as misplacing things and difficulty recalling recent events. Episodic memory has been found to be impaired, with relative preservation of procedural memory. Disturbances in attention include concentration difficulty, impaired focus, and easy distractibility. Language disturbances vary greatly according to extent and location of damage. Deficits may range from lack of spontaneous speech to severe forms of expressive and receptive aphasia. Language impairment is typically characterized by word-finding problems, difficulty with expression, dysarthria, and dysprosody. Patients with a history of traumatic brain injury may be impulsive, with decreased motivation, poor judgment, and lack of insight. They may also exhibit concrete thinking with poor concept formation and difficulty shifting cognitive tasks.
Dementia Pugilistica or boxer’s dementia, affects approximately 17% of retired professional boxers and is characterized by motor, cognitive and behavioral changes. The motor abnormalities may begin with dysarthria and balance difficulties and progress to incoordination, ataxia, and parkinsonism. Cognitive changes usually affect memory, attention and executive functioning. The behavioral changes, which are more poorly documented, include disinhibition, irritability, paranoia and violent outbursts. The etiology is thought to be related to multiple petechial hemorrhages in the cerebrum and cerebellum, which progress over time to gliosis or progressive cell loss. Microscopically, diffuse plaques and tangles may be seen, as is depigmentation and gliosis in the substantia nigra.
The treatment of cognitive impairment secondary to traumatic brain injury has been attempted with dopamine agonists, psychostimulants, and cholinesterase inhibitors. Some cognitive deficits have been hypothesized to occur as a result of acetylcholine deficiency and randomized controlled trials with physostigmine have demonstrated moderate efficacy. Additional studies are needed to fully evaluate the potential role of cholinesterase inhibitors. Controlled trials with dopamine agonists have shown benefit for executive dysfunction associated with traumatic brain injury, and psychostimulants are effective for symptoms of inattention and distractibility.