Cognitive Effects of Brain Injury and Disease 2012).
The care of patients with brain injury and diseases has improved substantially over the last thirty years. Nonetheless, the acute cognitive effects caused by brain injury are still a problem for the survivors. Such impairments are substantial contributors to functional disability after brain injury and reduce quality of life for affected persons and their families (Schultza, Cifub, McNameea, Nicholsb; Carneb, 2011). Accordingly, it is important for clinicians providing care to persons with brain injury to be familiar with the cognitive squeal of such injuries, their neuropathophysiologic bases, the treatment options that may alleviate such problems, and their effects on functional ability and quality of life.
Literature Review: Cognitive Effects
The anatomy, pathophysiology, and cognitive sequel of brain injury and diseases vary as a function of cause of brain injury. Accordingly, identification of the specific cause of injury and other relevant factors (e.g., age, injury severity, comorbid conditions, etc.) is needed to understand the cognitive sequel of brain injury. For the survivors of severe brain injury, 30 -- 60% will develop persistent cognitive, behavioral, and/or other neurological problems (Howard, Holmes, Koutroumanidis, 2011).
These problems may be functionally debilitating and severely affect quality of life for patients and their families. Common elementary neurological impairments include parkinsonism, dystonia, chorea, tremor, tics, athetosis, seizures, and myoclonic syndromes (Schultza, Cifub, McNameea, Nicholsb; Carneb, 2011). Cognitive impairments include disturbances of arousal (e.g., coma, vegetative states), awareness and attention (e.g., minimally conscious state, delirium), and higher-level cognitive functions, most commonly including disturbances of processing speed, memory, and executive function. Additionally, as many as 35% of these individuals experience depression within the first 3 months following brain injury and more than 30% are depressed at 12 months post-injury (Howard, Holmes, Koutroumanidis, 2011).Cognitive impairment is among the more fully characterized neurobehavioral sequel of brain injury, and one that neurologists and neuro-rehabilitation specialists are often asked to evaluate, to make recommendations regarding their management, and to opine on prognosis for recovery both in the early post-resuscitation period and thereafter. In the service of providing information that may be of use to clinicians performing these and related tasks, the present work reviews and summarizes the literature describing cognitive impairments due to brain injury. Studies published and indexed in Medline/PubMed were identified (Schultza, Cifub, McNameea, Nicholsb; Carneb, 2011).
Post-Brain Injury And Brain Disease Cognitive Impairments
Among patients whose severities of injury permit recovery to a level above MCS, a variety of other cognitive impairments may develop and produce substantial interference with functional independence and quality of life (Aaro, Smedler, Leis, Emanuelson, 2009). The cognitive effects of brain injury like attention, speed of processing, memory, and executive function are discussed below:
Attention and Processing Speed Impairments
Although the word 'attention' is often used as if it referred to a unitary cognitive function, attention actually denotes a collection of interrelated processes that detect, select, and sustain focus on one or more external or internal stimuli. Included in this set of processes are: cortical orientation, the process by which primary sensory cortices detect novel stimuli; selective attention, which refers to the selection from among the many sensory events processed simultaneously in the brain the one that will be admitted into consciousness for further processing; sustained attention (also referred to as concentration or vigilance), which refers to the maintenance of attention on a selected target; and divided attention, which refers to the selection and sustained processing of two or more stimuli simultaneously (Aaro, Smedler, Leis, Emanuelson, 2009
Working memory is closely related to attentional processes, and involves the temporary maintenance and manipulation of information 'off-line' (i.e., keeping one or a small set of words, numbers, images, sounds, etc. 'in mind' briefly after they are presented) . Closely related to attention is processing speed, which refers to the rate at which information is processed in the brain; this process is manifested clinically as reaction time or response latency. Attention and processing speed are supported by several large-scale selective distributed networks. These networks include: primary and secondary sensory cortical areas; tertiary (heteromodal parietal) cortical areas cross-linking information between primary and secondary sensory cortices; quaternary (heteromodal frontal) cortical areas that elaborate, organize, modulate, and permit interpretation of information processed elsewhere; the frontal-subcortical circuits required for higher-level attentional processing and ...
Injury to any of these areas may affect attention and processing speed; in general, injury to or dysfunction of cortical areas disrupts one or more aspects of attention whereas injury to or dysfunction of their white matter or subcortical elements impairs processing speed. Impairments of attention (and particularly vigilance) and processing speed are observed commonly among survivors of brain injury in both the recent and remote post-injury periods.
These impairments most likely reflect a combination of several forms of neural damage, including laminar necrosis (ischemic injury to cortical layers 3, 4, and 5), damage to white matter at the zones between the major cerebral artery territories, and damage to white matter and subcortical structures supplied by the distal branches of deep and superficial penetrating vessels. Additionally, involvement of superior brainstem and cerebellar structures -- whether gray or white matter -- may also contribute to these impairments (Piros et al. 2012). Attention or processing speed impairments may be qualitatively apparent during patient interview and examination, particularly among persons with severe brain injury, but are not quantitatively assessed by many commonly used bedside cognitive screening tools, including the Mini-Mental State Examination. Since the anatomy of brain injury predicts attention and processing speed impairments, and since studies including metrics of these cognitive functions usually identify problems in this population, the evaluation of persons with brain injury requires the use vigilance or cancellation tasks, continuous performance tasks, or other tests of attention and processing speed (e.g., the Trail Making Test or the Test of Everyday Attention ) (Piros et al. 2012).
Disturbances of memory are common after brain injury. The term 'memory' encompasses a variety of processes that permit learning, storage, and retrieval of declarative (i.e., semantic, episodic, autobiographical) and procedural (i.e., sensorimotor, emotional) information. In other words, memory is not a unitary function but instead denotes a collection of cognitive processes (Kohl, Wylie, Genova, Hillary, Deluca, 2009). The dissociable psychological properties of memory are predicated on distinct, functionally independent but interactive neuroanatomical networks that allow for the acquisition of new information, online manipulation and retention, transfer to long-term storage, and then the timely declarative recall of salient memories or the performance of previously learned motor routines (Kohl, Wylie, Genova, Hillary, Deluca, 2009). The adverse effects of brain injury on declarative memory are understandable in light of the intersection between the neuro-anatomy of this cognitive function and the pathophysiology of this event.
Declarative memory encompasses information regarding facts about the world (i.e., semantic content), about events (i.e., episodic content), and personal information (i.e., autobiographical content). In addition to information type, declarative memory is also subdivided by time. As noted earlier in this article, working memory denotes temporary maintenance and manipulation of information 'off-line' (i.e., keeping one or a small set of words, numbers, images, sounds, etc. 'in mind' briefly after they are presented). Although the interval between information presentation and retrieval that defines short-term memory is highly variable (and sometimes applied in a manner that makes it synonymous with working memory), in medical parlance short-term memory is generally used to denote an interval between the storage and retrieval of information of several minutes or slightly longer (Kohl, Wylie, Genova, Hillary, Deluca, 2009). The point at which information is regarded as having passed from short-term and into long-term memory is unclear and a subject of controversy; practically speaking, however, long-term memory denotes information that has been encoded and is available for retrieval at a time relatively remote from that at which it was learned. Primary and association sensory cortices are the entry point all information processed within the networks sub-serving declarative memory (Tsaousides, Gordon, 2009).
The entry of information into working memory engages bi-hemispheric heteromodal cortices (i.e., areas of cortex that link, or associate, information between multiple sensory and/or motor areas, or 'modes' of neural function) in the frontal and parietal lobes. When information is held 'in mind' for several minutes or more, information is networked between the heteromodal parietal and frontal cortices and medial temporal areas (including the entorhinal-hippocampalcomplex) (Tsaousides, Gordon, 2009). Amygdalarhippocampal interactions imbue the information being processed with emotional/motivational/survival valences; these interactions drive the process of encoding of emotionally or functionally relevant information. Connections between these medial temporal areas, via the hippocampal-forniceal-mamillothalamic pathway, and the frontal, parietal, and medial temporal cortices in which information is being processed create large-scale representational networks; the stability of these newly-developed networks is predicated upon the process of long-term potentiation (LTP) (Tsaousides, Gordon, 2009).
LTP is a glutamatergically- and cholinergically-dependent process that strengthens and modifies neuronal synaptic connections within the networks processing declarative information; when these networks becomes stable, information is described as encoded and consolidated (or 'stored')…
Aaro, Jonsson C., Smedler, AC., Leis, Ljungmark M., & Emanuelson, I (2009). Long-term cognitive outcome after neurosurgically treated childhood traumatic brain injury. Brain Injury: ISSN: 1362-301X, Vol. 23 (13-14), pp. 1008-16. doi:10.3109/02699050903379354
Cozzarelli, Tara A. (2010). Evaluation and Treatment of Persistent Cognitive Dysfunction Following Mild Traumatic Brain Injury. LCDR USPHS. Journal of Special Operations Medicine. Volume 10, Edition 1.pg 39-42. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed
Howard, RS., Holmes, PA & Koutroumanidis, MA. (2011). Hypoxic-ischaemic brain injury. Practical Neurology [Pract Neurol], ISSN: 1474-7766, Vol. 11 (1), pp. 4-18; PMID: 21239649. doi:10.1136/jnnp.2010.235218
Kinnunen, Kirsi Maria., Greenwood, Richard., Powell, Jane Hilary., Leech, Robert., Hawkins, Peter Charlie., Bonnelle, Valerie., Patel, Maneesh Chandrakan., Counsell, Serena Jane., and Sharp, David James (2011). White matter damage and cognitive impairment after traumatic brain injury. Brain A Journal Of Neurology. 134; 449 -- 463. doi:10.1093/brain/awq347
Piros, Elisaveta Ligia; Ciobanu, Gheorghe; Mustea, Anca; Deme, Sanda Maria; Grossmann, Harry; Podea & Delia Marina (2012). Analysis Of Type Of Brain Injury And Their Correlation. With Vascular Dementia Cognitive Decline Degree. Vol. 22, issue 1,. 47-51pp. Retrieved from http://connection.ebscohost.com/c/articles/74239972
patients diagnosed with TBI cope better with counseling and outreach programs when dealing with new or abnormal behaviors? Traumatic brain injury (TBI) may result in social and emotional defects (such as delayed word recall) that result in frustrating and embarrassing moments for the victim. Of all counseling and intervention programs, rehabilitation therapy (CRT) is the one that is commonly used and, therefore, this literature review will conduct a meta-analytic search
MTBI and Depression Traumatic brain injury (TBI) occurs as a result of force to the skull or brain. The probability of receiving a TBI is increased if one is participates in a number of sports such as professional football in the National Football League (NFL) and in a number of vocations such being in the military. The results of a TBI include a number of cognitive and emotional symptoms (McCrea, 2008).
condition known as Post-traumatic Amnesia. This condition occurs when an individual suffers an acute brain damaging injury. Automobile crashes are said to be the most common origin of such injuries, and thus, the fundamental source of this disorder, in young adults. The condition persists for a few minutes or hours after the accident, or may go on for as long as weeks, months or years. Post-traumatic amnesia is accompanied
The soldiers who informed that their injury didn't include any altered mental status or the loss of consciousness worked as the reference group for all of the analyses (2008). Mild TBI was significantly correlated with psychiatric symptoms -- especially PTSD, and the correlation maintained its significance after combat experiences had been controlled for (Hoge et al. 2008). Over 40% of soldiers with injuries linked with loss of consciousness met the
Traumatic Brain Injury Pathophysiology Traumatic brain injury, continues to remain an enigma and treatment is elusive, causing death and disability across the globe. Luckily, significant progress has been made in helping improve short-term outcome in victims facing a severe brain injury. Unfortunately, it is still not possible to get back the victims to their normative level of brain functioning. Injuries to the brains caused by forceful impact may cause tissue distortion. Clinically,
Alternatively, degeneration of the ascending cholinergic and catechola- minergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease. (Dubois & Pillon, 1996, pp.2-8) The development of a greater understanding, over time of the causal factors as well as the manifestations and possible interventions for cognitive function in Parkinson's disease has continued since this time. Greater functional understanding of neurotransmitters and