Acquired Brain Injury (Stroke and TBI) in Later Life
Summary and Keywords
The term “acquired brain injury” refers to any type of brain damage that occurs after birth. Two main types of acquired brain injury are stroke and traumatic brain injury (TBI). A stroke occurs when there is a blockage or bleed in the vascular system of the brain, while a TBI results from an external force to the head. Older adults are at a higher risk of both stroke and TBI; thus, overall incidence is increasing as the proportion of older adults in the population is growing. Stroke and TBI result in immediate and long-term cognitive changes. Impairments in the domains of language, attention, memory, executive functions, perception, and social cognition have been documented following stroke and TBI. However, strokes tend to cause focal or selective cognitive disorders, while cognitive deficits following TBI are widespread and can be generalized. Individuals who have suffered a stroke or TBI may also experience psychosocial changes; for example, symptoms of depression and anxiety are common. Functional outcomes, including independence in activities, are varied and are associated with a range of factors including age, injury severity, cognitive disorders, and psychosocial factors. To achieve optimal outcomes for individuals following stroke and TBI, and to reduce the impact of the injury on everyday functioning, a multidisciplinary rehabilitation process is recommended.
Acquired brain injury broadly encompasses any type of brain damage that occurs after birth. Acquired brain injury includes traumatic brain injury (TBI), which is caused by an external force to the head, and non-traumatic brain injury, which occurs as a result of internal factors. Non-traumatic brain injuries can result from a stroke caused by a blockage or bleed, a brain tumor, anoxia caused by a lack of oxygen to the brain, viral infections (e.g., encephalitis), poisoning or exposure to toxins, or a fluid build up in the brain (Zillmer, Spiers, & Culbertson, 2008). Acquired brain injury is one of the leading causes of death and disability worldwide, and comes with an array of physical, cognitive, functional, and psychosocial consequences. Older adults are at an increased risk of experiencing an acquired brain injury including a stroke or TBI (Chan, Zagorski, Parsons, & Colantonio, 2013). This is particularly pertinent as developed countries across the world are seeing an increase in the proportion of older adults that make up the population (Kinsella, 2011). This article details two main types of acquired brain injury, stroke and TBI, and the outcomes of each in the context of aging.
Definitions and Etiology
Stroke, otherwise known as a cerebrovascular accident (CVA), is the most common neurological disorder in the developed world (Geyer & Gomez, 2009). It occurs when the blood supply to the brain is disrupted. Stroke is defined by the World Health Organization (Hatano, 1976) as “rapidly developing clinical signs of focal (or global) disturbance of cerebral function lasting more than 24 hours or leading to death with no apparent cause other than of vascular origin”; it is a leading cause of disability and mortality worldwide (see Table 1) (Warlow, Sudlow, Dennis, Wardlaw, & Sandercock, 2003). The WHO estimates that 15 million people globally experience stroke every year, and this number is rising due to the aging population (Rothwell et al., 2004; Warlow et al., 2003). Age is a significant risk factor for stroke, with the risk doubling each decade after the age of 60 (Michael & Shaughnessy, 2006). The majority of stroke fatalities occur within the first 30 days; approximately one in eight strokes will be fatal during this time (Bray et al., 2016). However, overall stroke mortality is on the decline, which indicates an improvement in medical management (Feigin et al., 2015; Rothwell et al., 2004).
Table 1. Types and Causes of Stroke
Blockage interrupts blood flow to the brain.
Necrosis (neuronal cell death) occurs as oxygen and glucose cannot be delivered.
Accounts for >80% of all strokes.
Thrombotic stroke (a type of ischemic stroke) accounts for ~50% of all strokes.
Atherosclerosis: Thickening/hardening of the artery wall due to plaque accumulation in the brain’s vascular system. Plaques rupture and dislodge to cause clots.
Cerebral embolism: Thrombus (blood clot) travels from a distal artery to the brain (e.g., atherosclerotic plaque from the heart).
Cerebral vasculitis: Inflammation of arterial walls block blood supply to the brain.
Spontaneous bleeding in brain due to weakened blood vessel rupturing.
Intracerebral hemorrhage (bleeding within the brain) and subarachnoid hemorrhage (bleeding in the subarachnoid space).
Abrupt and severe symptom onset.
Accounts for <20% of all strokes but approximately half of all stroke deaths.
Ruptured cerebral aneurysm: Aneurysm forms when a section of artery wall becomes weak. Weakened spot balloons outwards as blood passes through vessel. Blood pools and the wall ruptures.
Weakened arteries: Chronic hypertension and aging can weaken arteries. Weakened arteries may rupture or leak.
Congenital blood vessel defects: For example, arteriovenous malformations are abnormal connections between arteries and veins. Can cause ruptures.
Head trauma: May cause bleeding in the brain or aneurysm to rupture.
Transient Ischemic Attack (TIA)
Blood supply is interrupted for a brief period of time.
Symptoms remit in <24 hours (often <60 minutes).
Not officially a type of stroke. Often referred to as a “mini stroke.”
Same symptoms and causes as ischemic stroke, but blockages are temporary.
Occlusion of multiple small arterial branches.
Usually in small, deep perforating arteries around subcortical structures (e.g., basal ganglia, thalamus, pons).
Microbleeds are associated with lacunar infarcts. Often occur in the context of small vessel disease.
Etiology and Risk Factors
There exists an array of risk factors for stroke. A number of these are non-modifiable, such as age and ethnicity, while others are related to lifestyle (O’Donnell et al., 2016). However, the most significant risk factor is having suffered a previous TIA or stroke. Indeed, approximately 15% to 20% of people who suffer a TIA will have a stroke in the following three months, with 5% of TIA patients suffering a stroke in the days following (Edlow, 2008; Johnston, Gress, Browner, & Sidney, 2000). Apart from TIA, hypertension is the most important and well-established risk factor for ischemic stroke, but can also increase the risk of hemorrhagic stroke. Hypertension places strain on blood vessels, causing a weakening (Zillmer et al., 2008). Weakened blood vessels are more likely to block or rupture. Other risk factors include:
• Age: Stroke risk increases exponentially with age (Michael & Shaughnessy, 2006).
• Sex: Men are at higher risk of stroke than women (Poorthuis, Algra, Algra, Kappelle, & Klijn, 2017).
• Ethnicity: Certain ethnic groups (e.g., African Americans) are at higher risk (Gutierrez & Williams, 2014).
• Familial history of stroke or cardiovascular disease.
• Heart conditions: The most common cardiac condition leading to embolism is atrial fibrillation, which is an irregular heart rhythm, although bloods clots can also be caused by cardiomyopathy, endocarditis, or congestive heart failure, or formed following a heart attack (Edlow, 2008).
• Diabetes (O’Donnell et al., 2016).
• High cholesterol (O’Donnell et al., 2016).
• Poor diet (O’Donnell et al., 2016).
• Excessive alcohol consumption (Reynolds et al., 2003).
• Smoking (Shinton & Beevers, 1989).
• Drug use (e.g., cocaine; Cheng et al., 2016).
Stroke remains a clinical diagnosis, as opposed to infarct, which is a term related to tissue death and can be diagnosed from imaging (Eckerle & Southerland, 2013). Initially, the priority for all stroke patients is medical stabilization (Zillmer et al., 2008), and the most critical factor is time. Tissue plasminogen activator (tPA) is a medication that dissolves blood clots (i.e., anticoagulant). TPA is currently regarded as the most effective treatment for ischemic stroke when administered within three hours of stroke onset (Wardlaw et al., 2012). However, to be eligible to receive tPA, it is critical to establish that there is no presence of hemorrhage, as anticoagulants can exacerbate bleeds and cause fatality. This can be done via neuroimaging (Table 2). Noncontrast computed tomography (CT) scans are the most common method of neuroimaging in hyperacute stroke; images are produced quickly (i.e., within seconds) and intracranial hemorrhages can be accurately identified. This allows for a quick decision regarding a patient’s eligibility to receive tPA. However, there are several other neuroimaging techniques that may be considered if available and appropriate (Arcot, Johnson, Lev, & Yoo, 2013; see Table 2). Furthermore, blood pressure and blood sugar levels must be obtained as early as possible, as very high levels of either may be considered contraindications to treatment (Eckerle & Southerland, 2013).
Hemorrhagic stroke demands a different course of action; in this case, the priority is to control the bleeding and to reduce the intracranial pressure (Zillmer et al., 2008). No effective targeted treatment yet exists for hemorrhagic stroke. Small hemorrhages may be controlled through blood pressure medications, but larger bleeds may require surgical intervention (e.g., surgical draining; Zillmer et al., 2008). In the case of aneurysms, inserting a “clip” or coil are possible methods of surgical treatment to reduce the risk of bleeding.
Table 2. Summary of Neuroimaging Techniques and Their Benefits
Computed Tomography (CT) is widely available but involves exposure to ionizing radiation and contrast agents.
Images produced quickly within seconds
Accurate method for identifying intracranial hemorrhages
Allows the evaluation of the blood vessels
Sensitive and specific for diagnosing vessel occlusions
Provides an estimate of the extent of the hypoperfusion and hypometabolism in the infarcted and ischemic tissue
Magnetic Resonance Imaging (MRI) is more expensive and less available than CT, but provides scans with far superior anatomical detail. There is no exposure to ionizing radiation with MRI. MRI cannot be performed on people with pacemakers or other ferromagnetic implants.
Diffusion-weighted imaging (DWI)
Most accurate method for detecting infarction
May also provide distinct embolic, lacunar and watershed patterns
Gradient echo T2-weighted imaging
Allows for accurate identification of bleeding
Provide similar information to their CT counterparts, without the exposure to radiation
MR perfusion-weighted imaging
It is estimated that each year over 10 million people globally sustain a TBI that results in hospitalization or death (Langlois, Rutland-Brown, & Wald, 2006). The highest rates of TBI occur in children and adolescents, and in older adults over age 65; however, older adults are at an increased risk of sustaining a TBI due to falls (Chan et al., 2013; Fu, Fu, Jing, McFaull, & Cusimano, 2017; Harvey & Close, 2012; Iverson & Lange, 2011; Kinsella, 2011). The prevalence of TBIs in older adults is relatively equal for males and females as a whole; however, a higher proportion of men sustain TBIs between the ages of 65 and 75 years, while the proportion of women increases with age, particularly >85 years (de Guise et al., 2015; Fu et al., 2017; Harvey & Close, 2012; Kinsella, Olver, Ong, Price, & Parsons, 2010). This may be due to the longer life expectancy of women, and that women often suffer from chronic conditions or disability in older age, increasing TBI risk (de Guise et al., 2015).
According to the National Institute of Neurological Disorders and Stroke (NINDS), a traumatic brain injury ( TBI) is defined by any alteration in brain function that has been caused by an external force (detailed in Table 3).
Table 3. Clinical Indications of Functional Alteration
Loss of Consciousness (LOC)
LOC refers to a “lack of awareness of the self or the environment.” Can be decreased (disorientation), or complete (i.e., individual appearing to be in a “sleep-like-state”; Iverson & Lange, 2011; Jennett, 1996).
Memory Disturbances (Post-Traumatic Amnesia: PTA)
Loss or disturbance in memory for events prior to injury (retrograde amnesia) or following the injury (anterograde amnesia). The length of the PTA period can be minutes, hours, days, weeks, or months (Iverson & Lange, 2011).
Disturbances in muscle tone, balance, vision, or speech and language, and others.
Alteration in Mental State
Alteration in mental state at time of injury (e.g., disorientation, confusion, slowed processing).
TBIs can be classified as either closed or open head injuries, and the “external force” or mechanisms of injury include:
• Being struck by an object or striking an object.
• An object penetrating the skull.
• An explosion (i.e., positive pressure wave followed by a negative pressure wave).
• An acceleration/deceleration movement.
A TBI can be classified as Mild, Moderate, or Severe. The most universal means of evaluating injury severity in TBI is via a combination of the Glasgow Coma Scale (GCS; Teasdale & Jennett, 1974), the duration of loss of consciousness (LOC), and length of post-traumatic amnesia (PTA) (Iverson & Lange, 2011). The GCS (Teasdale & Jennett, 1974; see Table 4) is the most widely used assessment of neurological functioning and state of arousal at time of injury. The ratings indicate the level of stimulus required to induce the responses, with overall scores ranging from 3 to 15, where lower scores equate to more severe injuries.
Table 4. The Glasgow Coma Scale
Responds to pain
Produces sound (incomprehensible)
Responds to speech
Produces words (inappropriate to context)
Confused & some disorientation
Flexion withdrawal from pain
Oriented to time, place and person
Moves to localized pain
Responds and obeys commands
Source: Teasdale and Jennett (1974).
Note: Table adapted from Basso, Previgliano, and Servadei (2006).
However, inconsistencies in the use and administration of the GCS (Zuercher, Ummenhofer, Baltussen, & Walder, 2009) have led to additional severity markers. Table 5 displays the combined severity indicators for TBI classification as Mild, Moderate, or Severe.
Table 5. Severity Indicators of Traumatic Brain Injury
Glasgow Coma Scale
Loss of Consciousness
Note: Table adapted from McCrea et al. (2014).
The majority of TBIs in both the general population and older adults are Mild injuries; these account for 70%–80% of cases (de Guise et al., 2015; Kinsella, 2011). One concern is that the incidence of Mild TBIs is likely to be underreported in healthcare settings, with estimates that 30%–40% are unreported (Faul & Coronado, 2015). A Mild TBI, often referred to as a “concussion,” can be classified as complicated (lesion or hematoma shown on computed tomography [CT] brain imaging) or uncomplicated (no abnormal findings on CT brain imaging). Older adults are more likely to have a complicated TBI with a greater prevalence of secondary injuries relative to the general adult population (Thompson, McCormick, & Kagan, 2006). However, overall, complicated TBIs are less common than uncomplicated TBIs. Approximately a third of Mild TBIs in older adults are classified as complicated (Kinsella, Olver, Ong, Gruen, & Hammersley, 2014; Rapoport et al., 2006). Notably, repeated Mild TBIs or “repetitive concussions” are considered different from a single Mild TBI as long-term outcomes differ significantly.
Moderate and Severe TBIs have been associated with poorer outcomes in older adults, in terms of both disability and mortality (Kinsella, 2011). For instance, an Australian study indicated that just under a third of older adults who sustained a TBI died in hospital (Utomo, Gabbe, Simpson, & Cameron, 2009), with most mortalities occurring within the first 48 hours (McIntyre, Janzen, & Teasell, 2014). For older adults (>60 years) up to one year post-TBI, >50% of Severe TBIs result in death, while the mortality rate is approximately 33% for Moderate TBIs and just over 10% for Mild TBIs (McIntyre, Mehta, Aubut, Dijkers, & Teasell, 2013). Higher mortality rates in older relative to younger adults may be due to greater complications and secondary injuries (e.g., hypoxia or post-traumatic seizures; Kinsella, 2011; Thompson et al., 2006), as well as pre-existing chronic diseases impacting on recovery such as hypertension, diabetes, and cancer (McIntyre et al., 2014).
Types of TBIs
TBIs can be classified as primary or secondary, as well as focal or diffuse. Primary focal injuries refer to damage to specific regions of the brain, and are usually caused by striking or being struck by an external force (Table 6). The anterior frontal and temporal regions of the brain are the most vulnerable to trauma (Iverson & Lange, 2011). Primary non-focal injuries are widespread injuries that affect a greater number of areas of the brain, where axons are stretched due to translational forces. These injuries are usually caused via acceleration and deceleration motions, such as during a motor vehicle accident (Iverson & Lange, 2011; McCrea, Janecek, Powell, & Hammeke, 2014). The severity of the injury is proportionate to the degree of “stretch” to the axon. For Mild to Moderate TBIs, the degree of stretch is typically <10% of the axon’s length and, with time, the axon is usually able to recover its function. However, for more severe injuries, stretching can lead to permanent damage if the axon is stretched >15% of its length, which may result in disruption to the membrane and can lead to axonal shearing (McCrea et al., 2014).
A common type of TBI sustained by a higher proportion of older than younger adults is traumatic subdural hemorrhages a (43%; Harvey & Close, 2012; Rathlev et al., 2006). Of these subdural hemorrhages, about a quarter (24%) are concussive injuries and a sixth (13%) are traumatic subarachnoid hemorrhages (Harvey & Close, 2012). Traumatic axonal injuries and other unclassified focal brain injuries each account for approximately 7% of injuries, with intracranial injuries, epidural hemorrhages, and cerebral edemas accounting for the remainder (Harvey & Close, 2012).
Table 6. Classifications of TBIs
Primary Focal Injuries
Primary Non-Focal Injuries
Primary TBIs can be complicated by secondary injuries. Secondary injuries refer to injury-associated changes that can occur hours to days following a TBI (Kinsella, 2011). Older adults are at increased risk of developing secondary brain injuries, which is one factor that increases the risk of poorer outcomes (Kinsella, 2011; Thompson et al., 2006). This increased risk may be in part due to greater use of anticoagulant medication (Franko, Kish, O’Connell, Subramanian, & Yuschak, 2006), or age-related changes in the brain (Kinsella, 2011).
Etiology and Risk Factors
The majority of TBIs in older adults aged over 65 years are attributed to falls, accounting for 60% to 85% of cases (de Guise et al., 2015; Fu et al., 2017; Harvey & Close, 2012; Kinsella et al., 2010; McIntyre et al., 2014). The proportion of falls resulting in a TBI steadily increases with age, accounting for >90% of TBIs after the age of 96 years (de Guise et al., 2015). The increased fall risk in older age can be attributed to reduced muscle tone, visual problems, poorer balance and gait, and side effects from medications (de Guise et al., 2015; Fu et al., 2017). Falls may result from:
• Slipping, tripping, or stumbling on the same level.
• Falling down stairs.
• Incidents involving furniture (e.g., falling from a bed or chair).
Falling or slipping on the same level increases with age, and falling down stairs decreases with age (Chan et al., 2013).
Motor vehicle accidents are the second most common mechanism of injury, accounting for 8% to 20% of TBIs (de Guise et al., 2015; Harvey & Close, 2012). This is more common in men than women (Thomas, Stevens, Sarmiento, & Wald, 2008). Other causes include being struck by/or against something (e.g., work related accidents), cycling accidents, or assault (de Guise et al., 2015; Harvey & Close, 2012; McIntyre et al., 2014).
The most prominent neuroimaging technique used in acute settings for TBI is CT scanning, as the initial priority is to identify whether intracranial hemorrhages are present. This may be deemed unnecessary for Mild TBIs: however, in this case, information is typically provided about signs to monitor that could indicate further complications, and the usual timeframe these are expected to remit, as well as advice on resuming daily activities (Basso, Previgliano, & Servadei, 2006). A small number of individuals who have sustained a Mild TBI require further monitoring, a CT scan, and possibly hospital admission. Indicators for further monitoring include decreasing LOC, neurological deficits, seizures, older age, and evidence of alcohol abuse (Basso et al., 2006).
Admission is standard for cases of Moderate to Severe TBI. Acute treatment may involve treating airway obstructions or lowered blood pressure, and management of other life threatening conditions including secondary brain injuries. Once the patient is stabilized, MRI in addition to CT is indicated to assess any structural abnormalities that may have resulted from the injury (McCrea et al., 2014).
Neurological and Neuropsychological Outcomes
Broadly, the neurological and physical consequences of stroke and TBI are similar. Both can result in:
• Motor functioning disturbances, such as paresis (weakness) or plegia (paralysis) or tremors.
• Difficulties with coordination, balance, or fine motor skills.
• Sensory function changes (e.g., problems with vision, hearing, facial movement, and swallowing).
• Speech/language difficulties (speaking or comprehending).
Problems with olfaction are more common following TBI, due to the placement of the associated cranial nerve and the nature of the injury (i.e., axonal shearing). In stroke, the most common hyperacute symptoms are hemiparesis (weakness on one side of the body) of the arm or face, and speaking difficulties. Headaches, fatigue, and sleep disturbances are also common complaints.
Both stroke and TBI can result in a range of cognitive or neuropsychological changes. Depending on the extent of the brain injury, these changes can be long-term, which can impact on daily functioning. Cognitive changes following TBI tend to be generalized and diffuse, whereas strokes are usually associated with more specific or focal cognitive disorders.
Cognitive disorders in the acute phase of stroke are robust predictors of long-term cognitive impairment, depressive symptoms, and ability to complete activities of daily living (Nys et al., 2005a, 2005b, 2006). More than half of all stroke patients, and up to 74% of those with a cortical stroke, have cognitive impairments in the acute phase (Nys et al., 2007), and about a third will continue to show cognitive impairments after six months (Nys et al., 2005a). The greatest recovery of cognitive function generally occurs within the first three months, although different cognitive skills tend to recover at different rates (Hurford, Charidimou, Fox, Cipolotti, & Werring, 2013). Deficits will differ, depending on where the stroke has occurred. Specific arteries supply different territories of the brain, and therefore, some cognitive disorders are more common than others. For example, the middle cerebral artery (MCA) is a common site of stroke. If a blockage occurs in the left MCA, an individual will likely experience weakness or paralysis on their right side of their body and language problems. This is because the left MCA supplies blood to the brain areas necessary for these functions.
Table 7 provides a summary of specific cognitive disorders and domains of cognition that may be affected following stroke. Aphasia, a disorder of verbal language, is considered the hallmark of a left hemisphere stroke. Right hemisphere damage can leave core language functions relatively intact, but is often associated with deficits in spatial attention; for example, spatial neglect occurs in up to 75% of right hemisphere strokes acutely (Nys et al., 2007). Broad reductions in attention and processing speed are particularly common following stroke (Zillmer et al., 2008), possibly because attentional processes involve diverse frontal, temporal, and parietal regions. One of the most common cognitive impairments following stroke is executive dysfunction, occurring in almost 40% of acute stroke patients (Nys et al., 2007). Executive dysfunction may underpin commonly reported behavioral changes in stroke patients. For example, disinhibition, which is an executive deficit, may result in impulsive or socially inappropriate behavior, or poor judgment (Zillmer et al., 2008). Executive dysfunction is reported to occur more commonly following left hemisphere strokes, but this may be due to the language demands of executive function tasks (Nys et al., 2007).
Table 7. Cognitive Disorders and Domains Affected Following Stroke
Aphasia: a disorder of verbal language
Spatial neglect (visual neglect, unilateral neglect, hemineglect, hemiagnosia): a disorder of spatial attention
Amnesia: a disorder of memory
Dyslexia: a disorder of reading
Dysgraphia: a central spelling disorder
Acalculia: a disorder of calculation
Agnosia: a disorder of recognition
Apraxia: a disorder of motor planning
One domain that has not traditionally been considered in cognitive assessments, but has recently gained traction, is social cognition. Social cognition involves theory of mind, empathy, and emotion recognition, which are necessary for successful interpersonal relationships. Impairments in social cognition have been documented following stroke, particularly following right hemisphere damage (e.g., Hamilton, Radlak, Morris, & Phillips, 2017; Siegal, Carrington, & Radel, 1996).
Depending on the specific site of the lesion, any of the cognitive disorders detailed in the previous section can occur following TBI. For this reason, assessment is necessary; however, cognitive impairments following TBI tend to be widespread rather than focal. Following Mild TBI, individuals frequently report a cluster of symptoms that have been termed “post-concussive syndrome” (see Table 8; Broshek et al., 2015; Dikmen et al., 2009; McCrea et al., 2014). Moderate and Severe TBIs experience post-concussive symptoms to a greater degree and are associated with poorer neurological and neuropsychological outcomes, which are typically proportionate to the severity of the injury (Dikmen et al., 2009). The neurological and neuropsychological consequences are variable and broad, and depend on the type of injury sustained.
Table 8. Symptoms of Post-Concussive Syndrome
Physical and somatic
Headaches, high levels of fatigue, sleep disturbances, feelings of nausea or dizziness, balance disturbances, and visual disturbances (e.g., double vision).
Emotional and Behavioral
Irritability, anxiety, low mood, and greater emotional lability.
Difficulties with attention and concentration, speed of information processing and memory.
In the acute stage of a single Mild TBI, individuals may exhibit reduced cognitive performance, with gradual improvement over the following days, weeks, and months. The greatest neuropsychological deficits at an acute stage are in verbal and visual memory, and verbal comprehension (Rohling et al., 2011). Mild TBIs are typically associated with quicker and better recovery, with typically minimal or no ongoing neurological or cognitive effects after three months (Dikmen et al., 2009; Kinsella et al., 2014; Rohling et al., 2011). However, long-term cognitive changes following Mild TBI (e.g., working memory) have been documented (e.g., Langlois et al., 2006), particularly in cases of repeated Mild TBIs (e.g., memory and executive functioning; Belanger, Spiegel, & Vanderploeg, 2010). In relation to older adults, cognitive outcomes may vary compared to the general adult population as age-related changes in the brain may exacerbate the impact of an injury. Furthermore, persisting cognitive difficulties following Mild TBI in older adults may be related to pre-existing declines or a generalized effect of multi-system trauma (Kinsella et al., 2014).
In contrast, Moderate and Severe TBIs are associated with long-term cognitive difficulties. While there is rapid recovery in the first six months post injury (Christensen et al., 2008), and continual, gradual recovery during the first 2 years (Schretlen & Shapiro, 2003), cognitive difficulties often persist beyond this time frame. Long-term difficulties in Moderate or Severe TBI have been documented in:
• General intellectual functioning (Marsh, Ludbrook, & Gaffaney, 2016).
• Attention (Marsh et al., 2016).
• Speed of information processing (Finnanger, Skandsen, Andersson, Lydersen, Vik, & Indredavik, 2013).
• Prospective memory (Shum, Levin, & Chan, 2011).
• Visuospatial skills (Marsh et al., 2016).
• Social cognition (Milders, Fuchs, & Crawford, 2003).
At 5 years after Severe TBI, the most frequent impairments are in attention (39%–62%), visual memory (23%–51%), verbal memory (16%–46%), and visual spatial skills (~38%), with impairments in overall general cognitive functioning and executive functions less frequent (Marsh et al., 2016).
Increasing severity of TBI is associated with greater and more persistent long-term cognitive difficulties (e.g., Dikmen et al., 2009; Finnanger et al., 2013). With regard to older adults following Moderate and Severe TBIs, cognitive impairments occur in verbal memory, attention, abstract reasoning, and word fluency (Aharon-Peretz et al., 1997; Breed et al., 2008; Rapoport et al., 2006; Senathi-Raja, Ponsford, & Schonberger, 2010).
Cognition and Aging
Numerous cognitive changes occur as part of healthy aging. With increasing age there is a loss of overall brain volume, including reductions in gray and white matter (Scahill et al., 2003) and neurochemical and vascular changes (e.g., reduced vascular elasticity; Kinsella, 2011). The frontal lobes, which are associated with higher-order complex thinking, are disproportionately vulnerable to age-related changes (Scahill et al., 2003), although other brain regions are also affected.
With regard to the long-term impacts of TBI in older age, sustaining a TBI at any age increases the risk of cognitive decline in older age (Li, Risacher, McAllister, & Saykin, 2017) and of developing dementia (Fleminger, Oliver, Lovestone, Rabe-Hesketh, & Giora, 2003). Furthermore, having sustained a TBI is associated with an earlier age of onset for mild cognitive decline or dementia (Li et al., 2017). Similarly, vascular dementia (recently termed vascular cognitive impairment) occurs as a result of either multiple small infarctions or one major stroke incidence. Post-stroke vascular dementia affects up to a third of stroke survivors, particularly if there are recurrent strokes (Mijajlovic et al., 2017).
Individuals may experience a range of psychosocial changes following a stroke or TBI of any magnitude. Depression is the most common psychological presentation following TBI and stroke, although estimates vary widely due to discrepancies in definitions and assessment tools.
Between 20% and 50% of stroke survivors experience depression (Barker-Collo, 2007; Hackett, Yapa, Parag, & Anderson, 2005). Depressive symptoms are common during the acute phase, but often persist even past the first few months (Hackett et al., 2005). Depression has been associated with left hemisphere strokes in the acute phase, but not after the first three months post injury (e.g., Carson et al., 2000). There are no consistent gender differences in post-stroke depression (Barker-Collo, 2007). Importantly, depression following stroke is associated with poorer cognitive outcomes for memory, visual perception/construction, language (Nys et al., 2006), and attention (Hosking, Marsh, & Friedman, 2000). Post-stroke anxiety is less common; estimates range from 4% to 28% (Barker-Collo, 2007; Campbell et al., 2013).
Similar to stroke, 17%–61% of individuals who have suffered a TBI will experience depression (Rapoport, 2012). Depression following TBI is related to injury severity for older but not younger adults (Albrecht et al., 2016). Following Mild TBI, 12%–44% of people experience depression within 3 months post-injury, with lower rates for older than for younger adults (Iverson & Lange, 2011; Rapoport, McCullagh, Streiner, & Feinstein, 2003). However, 10%–42% of older adults experience depression following a Moderate to Severe TBI (Albrecht et al., 2016; McIntyre et al., 2014), with higher incidence in the acute post-injury stage (Albrecht et al., 2016). Risk factors for depression following TBI in older age include a longer period of hospitalization and discharge to a skilled nursing facility, which both indicate a greater injury severity (Albrecht et al., 2016). Other factors, like alcohol abuse or dependence, have been linked to depression following a TBI (Albrecht et al., 2016).
Anxiety is equally common following TBI for individuals of any age, even when other factors are considered: demographic: education, marital status; health: co-morbid medical conditions, psychological history; and lifestyle: stressful events, social support (Corrigan & Hammond, 2013; Osborn, Mathias, Fairweather-Schmidt, & Anstey, 2017). Milder manifestations of anxiety, including irritability, restlessness, and ongoing somatic concerns (e.g., sleep disturbances) also occur following TBI (Deb & Burns, 2007; McIntyre et al., 2014; Rapoport et al., 2006). Older adults who have sustained a TBI are at increased risk of developing anxiety relative to their peers. However, older adults are less likely than younger or middle-aged adults to develop anxiety following a TBI (Osborn et al., 2017).
Age is a primary factor that influences functional outcomes in both stroke and TBI. Although 50%–70% of stroke survivors eventually regain their functional independence (Belagaje & Butler, 2013), older stroke survivors are more likely to have problems completing activities of daily living, even when stroke severity is considered (e.g., Harvey, 2015; Nakayama, Jørgensen, Raaschou, & Olsen, 1994). Likewise, older age is associated with poorer recovery and functional outcomes following TBI. Older adults who have suffered a TBI have reduced independence when carrying out activities of daily living (Hukkelhoven et al., 2003; Leblanc, de Guise, Gosselin, & Feyz, 2006). Furthermore, older age is associated with a greater number of comorbidities and complications following TBI and stroke; this impacts independence levels.
The Glasgow Outcome Scale (GOS; Jennett & Bond, 1975) is widely used to classify level of disability (see Table 9). The annual incidence of disability following a moderate-to-severe TBI is approximately 100 per 100,000 (Thornhill et al., 2000). However, older adults have a slower rate of functional recovery, longer stays in rehabilitation units, and greater levels of disability (Basso et al., 2006).
Table 9. Glasgow Outcome Scale
Persistent vegetative state
Completely dependent due to physical or cognitive disability
Independent but disabled (i.e., requires supported environment)
Able to resume normal life, with only minor neurological or psychological problems
Source: Jennett and Bond (1975).
Note: Table adapted from Basso et al. (2006).
Cognitive dysfunction predicts functional outcomes for both stroke and TBI patients. In stroke, acute cognitive disorders in attention and perception (Barker-Collo & Feigin, 2006; Nys et al., 2005a), executive functioning (Lesniak, Bak, Czepiel, Seniow, & Czlonkowska, 2008), and language and memory (Barker-Collo & Feigin, 2006) predict poorer functional outcomes. In TBI, cognitive dysfunction, particularly in executive functions, is linked with decreased independent living, impaired social relationships, and lower rates of return to employment and leisure activities (Finnanger et al., 2013).
Finally, depression and apathy (or “indifference”) are associated with poorer functional outcomes for stroke and TBI patients, and older adults are at a higher risk of apathy (Gray, Shepherd, & McKinley, 1994; Hama, Yamashita, Yamawaki, & Kurisu, 2011; Herrmann et al., 1998; Mayo, Fellows, Scott, Cameron, & Wood-Dauphinee, 2009; Mikami Jorge, Moser, Jang, & Robinson, 2013; Rapoport, Kiss, & Feinstein, 2006).
The goals of rehabilitation following stroke and TBI are broadly similar. Guidelines suggest that stroke patients should be transferred to a rehabilitation unit as soon as possible (Michael & Shaughnessy, 2006). With regard to uncomplicated TBI, many older adults are discharged home and approximately a quarter to rehabilitation (Kinsella, 2011). However, the majority are discharged to a rehabilitation facility following a complicated or more severe TBI (Kinsella, 2011).
The goal of rehabilitation is to attain skills that reduce the impact of the brain injury on everyday functioning and achieve an optimum level of wellbeing. Outcomes are generally better when there is a multidisciplinary team, including speech, physical, and occupational therapists, and neuropsychologists (Guy et al., 2004; Wilson & Gracey, 2009). Physiotherapists assist with improving motor control (e.g., strength, co-ordination, sitting, walking), and occupational therapists focus on assisting the patient to regain functional independence (e.g., driving, cooking, shopping) and determine if home modifications are required (Zillmer et al., 2008). Speech therapists assist with mechanical speech difficulties (e.g., dysarthria) as well as broader language problems (e.g., spoken language, reading, understanding speech). Clinical neuropsychologists administer assessments of cognitive ability, which help determine the individual’s capacity to engage in rehabilitation and may inform rehabilitation goals (Zillmer et al., 2008). Neuropsychologists also advise on cognitive training programs, provide strategies to compensate for impaired cognition, and assist with achieving daily activity goals, for example, return to work or capacity to perform instrumental activities (e.g., paying bills).
The rehabilitation process typically involves a goal-setting approach, whereby patients, families, and staff agree upon a set of appropriate goals (Wilson & Gracey, 2009). These goals consider that cognitive, behavioral, physical, social, and emotional consequences of brain injury are intrinsically linked (see the biopsychosocial model depicted in Figure 1). Generally, rehabilitation is holistic and broad, and involves the domains of cognitive functioning, emotion, social interaction, behavior, and learning (Wilson & Gracey, 2009). Interventions for psychosocial or emotional concerns are also instrumental in the rehabilitation process, with emphasis on supporting community integration (i.e., social integration and participation in leisure activities). This approach maximizes the individual’s quality of life and, consequently, functional outcomes (Ritchie, Wright-St Clair, Keogh, & Gray, 2014). Rehabilitation also addresses psychosocial risk factors by encouraging positive lifestyle changes, such as increasing physical activity and reducing alcohol consumption.
Although older adults who have suffered a stroke or TBI generally benefit less from rehabilitation than younger individuals, rehabilitation remains valuable. Following a TBI, the majority of older adults are able to return home after a period of rehabilitation, which suggests that recovery may simply be slower for older adults (Frankel et al., 2006). Although older age is associated with lower functional status overall, it is not associated with change in functional status following rehabilitation (Bagg, Pombo, & Hopman, 2002). Furthermore, even small improvements gained from rehabilitation can affect independence and quality of life (Michael & Shaughnessy, 2006). Importantly, pre-existing conditions, comorbidities, and cognitive changes common in older adults should be considered during rehabilitation, as these factors can greatly impact cognitive and functional outcomes (Chan et al., 2013).
Conclusions and Future Directions
The developed world is seeing a rapid increase in its aging population. With older age comes an increased risk of acquired brain injury, including stroke and TBI. Even mild strokes and TBIs can have significant effects on physical functioning, cognition, psychosocial factors, and quality of life. This will inevitably place a greater demand on healthcare and rehabilitation services. As such, key directions for the future are in the prevention and management of acquired brain injury. Falls are the major contributor to TBIs in older adults, and identifying the causes of falls can inform prevention strategies (Chan et al., 2013; Ritchie et al., 2014). With regard to stroke, medical management is a key area with a vast evidence base relating to the risk factors for stroke. For instance, a recent international case-control study of approximately 27,000 adults across 32 countries concluded that over 90% of strokes can be explained by just ten risk factors (O’Donnell et al., 2016). It is now pertinent for efforts to be directed at the implementation of preventative strategies (Feigin & Krishnamurthi, 2016), as this will play a role in maintaining a healthy aging population.
Aharon-Peretz, J., Kliot, D., Amyel-Zvi, E., Tomer, R., Rakier, A., & Feinsod, M. (1997). Neurobehavioral consequences of closed head injury in the elderly. Brain Injury, 11, 871–875.Find this resource:
Aho, K., Harmsen, P., Hatano, S., Marquardsen, J., Smirnov, V. E., & Strasser, T. (1980). Cerebrovascular disease in the community: Results of a WHO collaborative study. Bulletin of the World Health Organization, 58(1), 113.Find this resource:
Albrecht, J. S., Kiptanui, Z., Tsang, Y., Khokhar, B., Liu, X., Simoni-Wastila, L., & Zuckerman, I. H. (2016). Depression among older adults after traumatic brain injury: A national analysis. American Journal of Geriatric Psychiatry, 23, 607–614.Find this resource:
Arcot, K., Johnson, J. M., Lev, M. H., & Yoo, A. J. (2013). Neurovascular imaging of the acute stroke patient. In K. Barrett & J. Meschia (Eds.), Stroke (pp. 16–36). Chinchester, West Sussex, UK: Wiley-Blackwell.Find this resource:
Bagg, S., Pombo, A. P., & Hopman, W. (2002). Effect of age on functional outcomes after stroke rehabilitation. Stroke, 33(1), 179–185.Find this resource:
Barker-Collo, S., & Feigin, V. (2006). The impact of neuropsychological deficits on functional stroke outcomes. Neuropsychology Review, 16(2), 53–64.Find this resource:
Barker-Collo, S. L. (2007). Depression and anxiety 3 months post stroke: Prevalence and correlates. Archives of Clinical Neuropsychology, 22(4), 519–531.Find this resource:
Basso, A., Previgliano, I., & Servadei, F. (2006). Neurological disorders: Public health challenges. Geneva, Switzerland: World Health Organization.Find this resource:
Belagaje, S. R., & Butler, A. J. (2013). Poststroke recovery. In K. Barrett & J. Meschia (Eds.), Stroke (pp. 1–15). Chinchester, West Sussex, UK: Wiley-Blackwell.Find this resource:
Belanger, H. G., Spiegel, E., & Vanderploeg, R. D. (2010). Neuropsychological performance following a history of multiple self-reported concussions: A meta-analysis. Journal of International Neuropsychological Society, 16(2), 262–267.Find this resource:
Bray, B. D., Cloud, G. C., James, M. A., Hemingway, H., Paley, L., Stewart, K., . . . & SSNAP collaboration. (2016). Weekly variation in health-care quality by day and time of admission: A nationwide, registry-based, prospective cohort study of acute stroke care. The Lancet, 388(10040), 170–177.Find this resource:
Breed, S., Sacks, A., Ashman, T. A., Gordon, W. A., Dahlman, K., & Spielman, L. (2008). Cognitive functioning among individuals with traumatic brain injury, Alzheimer’s disease, and no cognitive impairments. Journal of Head Trauma Rehabilitation, 23(3), 149–157.Find this resource:
Broshek, D. K., De Marco, A. P., & Freeman, J. R. (2015). A review of post-concussion syndrome and psychological factors associated with concussion. Brain Injury, 2(2), 228–237.Find this resource:
Campbell Burton, C., Murray, J., Holmes, J., Astin, F., Greenwood, D., & Knapp, P. (2013). Frequency of anxiety after stroke: A systematic review and meta-analysis of observational studies. International Journal of Stroke, 8(7), 545–559.Find this resource:
Carson, A. J., MacHale, S., Allen, K., Lawrie, S. M., Dennis, M., House, A., & Sharpe, M. (2000). Depression after stroke and lesion location: A systematic review. The Lancet, 356(9224), 122–126.Find this resource:
Chan, V., Zagorski, B., Parsons, D., & Colantonio, A. (2013). Older adults with acquired brain injury: A population based study. BMC Geriatrics, 13(1), 97.Find this resource:
Cheng, Y. C., Ryan, K. A., Qadwai, S. A., Shah, J., Sparks, M. J., Wozniak, M. A., . . . Cole, J. W. (2016). Cocaine use and risk of ischemic stroke in young adults. Stroke, 47, 918–922.Find this resource:
Christensen, B. K., Colella, B., Inness, E., Hebert, D., Monette, G., Bayley, M., & Green, R. E. (2008). Recovery of cognitive function after traumatic brain injury: A multilevel modeling analysis of Canadian outcomes. Archives of Physical Medicine & Rehabilitation, 89(12), S3–15.Find this resource:
Corrigan, J. D., & Hammond, F. M. (2013). Traumatic brain injury as a chronic health condition. Archives of Physical Medicine and Rehabilitation, 94(6), 1199–1201.Find this resource:
Deb, S., & Burns, J. (2007). Neuropsychiatric consequences of traumatic brain injury: A comparison between two age groups. Brain Injury, 21, 301–307.Find this resource:
Dikmen, S. S., Corrigan, J. D., Levin, H. S., Machamer, J., Stiers, W., & Weisskopf, M. G. (2009). Cognitive outcome following traumatic brain injury. Journal of Head Trauma Rehabilitation, 24(6), 430–438.Find this resource:
Eckerle, B. J., & Southerland, A. M. (2013). Bedside evaluation of the acute stroke patient. In K. Barrett & J. Meschia (Eds.), Stroke (pp. 1–15). Chinchester, West Sussex, UK: Wiley-Blackwell.Find this resource:
Edlow, J. (2008). Stroke. Westport, CT: Greenwood.Find this resource:
Evans, J. (2006). Theoretical influences on brain injury rehabilitation. Presented at the Oliver Zangwill Centre 10th Anniversary Conference.
Faul, M., & Coronado, V. (2015). Epidemiology of traumatic brain injury. Handbook of Clinical Neurolology, 127, 3–13.Find this resource:
Feigin, V. L., & Krishnamurthi, R. (2016). Stroke is largely preventable across the globe: Where to next?The Lancet, 388(10046), 733.Find this resource:
Feigin, V. L., Krishnamurthi, R. V., Parmar, P., Norrving, B., Mensah, G. A., Bennett, D. A., . . . Davis, S. (2015). Update on the global burden of ischemic and hemorrhagic stroke in 1990–2013: The GBD 2013 study. Neuroepidemiology, 45(3), 161–176.Find this resource:
Finnanger, T. G., Skandsen, T., Andersson, S., Lydersen, S., Vik, A., & Indredavik, M. (2013). Differentiated patterns of cognitive impairment 12 months after severe and moderate traumatic brain injury. Brain Injury, 27(13–14), 1606–1616.Find this resource:
Fleminger, S., Oliver, D. L., Lovestone, S., Rabe-Hesketh, S., & Giora, A. (2003). Head injury as a risk factor for Alzheimer’s disease: The evidence 10 years on: A partial replication. Journal of Neurology, Neurosurgery, & Psychiatry, 74, 857–862.Find this resource:
Frankel, J. E., Marwitz, J. H., Cifu, D. X., Kreutzer, J. S., Englander, J., & Rosenthal, M. (2006). A follow-up study of older adults with traumatic brain injury: taking into account decreasing length of stay. Archives of Physical Medicine and Rehabilitation, 87, 57–62.Find this resource:
Franko, J., Kish, K. J., O’Connell, B. G., Subramanian, S., & Yuschak, J. V. (2006). Advanced age and preinjury warfarin anticoagulation increase the risk of mortality after head trauma. Journal of Trauma and Acute Care Surgery, 61(1), 107–110.Find this resource:
Fu, W. W., Fu, T. S., Jing, R., McFaull, S. R., & Cusimano, M. D. (2017). Predictors of falls and mortality among elderly adults with traumatic brain injury: A nationwide, population-based study. PLoS ONE, 12(4), e0175868.Find this resource:
Geyer, J. D., & Gomez, C. R. (2009). Stroke: A practical approach. Philadelphia: Lippincott Williams & Wilkins.Find this resource:
Gray, J. M., Shepherd, M., & McKinley, W. W. (1994). Negative symptoms in the traumatically brain-injured during the first year post-discharge, and their effect on rehabilitation status, work status, and family burden. Clinical Rehabilitation, 8, 188–197.Find this resource:
de Guise, E., LeBlanc, J., Dagher, J., Tinawi, S., Lamoureux, J., Marcoux, J., . . . Feyz, M. (2015). Traumatic brain injury in the elderly: A level 1 trauma centre study. Brain Injury, 29(5), 558–564.Find this resource:
Gutierrez, J., & Williams, O. A. (2014). A decade of racial and ethnic stroke disparities in the United States. Neurology, 82(12), 1080–1082.Find this resource:
Guy, S., Clarke, L., Bryant, H., Robinson, G., Stewart, T., Segaran, E., & Ross, M. (2004). An interdisciplinary team approach to acute stroke rehabilitation. In N. A. Losseff (Ed.), Neurological Rehabilitation of Stroke (pp. 26–56). London: Taylor & Francis.Find this resource:
Hackett, M. L., Yapa, C., Parag, V., & Anderson, C. S. (2005). Frequency of depression after stroke. Stroke, 36(6), 1330–1340.Find this resource:
Hama, S., Yamashita, H., Yamawaki, S., & Kurisu, K. (2011). Post‐stroke depression and apathy: Interactions between functional recovery, lesion location, and emotional response. Psychogeriatrics, 11(1), 68–76.Find this resource:
Hama, S., Yamashita, H., Yamawaki, S., Yamawaki, S., & Kurisu, K. (2011). Post-stroke depression and apathy: Interactions between functional recovery, lesion location, and emotional response. Psychogeriatrics, 11, 68–76.Find this resource:
Hamilton, J., Radlak, B., Morris, P. G., & Phillips, L. H. (2017). Theory of mind and executive functioning following stroke. Archives of Clinical Neuropsychology, 32(5), 507–518.Find this resource:
Harvey, L. A., & Close, J. C. T (2012). Traumatic brain injury in older adults: Characteristics, causes, and consequences. Injury, 43(11), 1821–1826.Find this resource:
Harvey, R. L. (2015). Predictors of functional outcome following stroke. Physical Medicine and Rehabilitation Clinics of North America, 26(4), 583–598.Find this resource:
Hatano, S. (1976). Experience from a multicentre stroke register: a preliminary report. Bulletin of the World Health Organization, 54(5), 541–553.Find this resource:
Herrmann, N., Black, S. E., Lawrence, J., Szekely, C., & Szalai, J. P. (1998). The Sunnybrook Stroke Study. Stroke, 29(3), 618–624.Find this resource:
Hosking, S., Marsh, N., & Friedman, P. (2000). Depression at 3-months poststroke in the elderly: Predictors and indicators of prevalence. Aging Neuropsychology & Cognition, 7(4), 205–216.Find this resource:
Hukkelhoven, C. W., Steyerberg, E. W., Rampen A. J., Farace, E., Habbema, J. D., Marshall, L. F., . . . Maas, A. I. (2003). Patient age and outcome following severe traumatic brain injury: An analysis of 5,600 patients. Journal of Neurosurgery, 99, 666–673.Find this resource:
Hurford, R., Charidimou, A., Fox, Z., Cipolotti, L., & Werring, D. J. (2013). Domain-specific trends in cognitive impairment after acute ischaemic stroke. Journal of Neurology, 260(1), 237–241.Find this resource:
Iverson, G. L., & Lange, R. T. (2011). Moderate and severe traumatic brain injury. In M. R. Schoenberg & J. G. Scott (Eds.), The little black book of neuropsychology: A syndrome-based approach (pp. 663–696). New York, NY: Springer.Find this resource:
Johnston, S. C., Gress, D. R., Browner, W. S., & Sidney, S. (2000). Short-term prognosis after emergency department diagnosis of TIA. JAMA, 284, 2901–2906.Find this resource:
Jennett, B. (1996). Clinical and pathological features of vegetative survival. In H. S. Levin, A. L. Benton, J. P. Muizelaar, & H. M. Eisenberg (Eds.), Catastrophic brain injury (pp. 3–14). New York: Oxford University Press.Find this resource:
Jennett, B., & Bond, M. (1975). Assessment of outcome after severe brain damage. Lancet, 1(7905), 480–484.Find this resource:
Kinsella, G. J. (2011). What are the characteristics of traumatic brain injury in older adults? Brain Impairment, 12(1), 71–75.Find this resource:
Kinsella, G. J., Olver, J., Ong, B., Gruen, R., & Hammersley, E. (2014). Mild traumatic brain injury in older adults: Early cognitive outcome. Journal of the International Neuropsychological Society, 29, 663–671.Find this resource:
Kinsella, G. J., Olver, J., Ong, B., Price, S., & Parsons, S. (2010). Traumatic brain injury in older adults: Preliminary findings (Report to the Victorian Neurotrauma Initiative).
Langlois, J. A., Rutland-Brown, W., & Wald, M. W. (2006). The epidemiology and impact of traumatic brain injury. Journal of Head Trauma Rehabilitation, 21(5), 375–378.Find this resource:
Leblanc, J., de Guise, E., Gosselin, N., & Feyz, M. (2006). Comparison of functional outcome following acute care in young, middle-aged, and elderly patients with traumatic brain injury. Brain Injury, 20, 779–790.Find this resource:
Lesniak, M., Bak, T., Czepiel, W., Seniow, J., & Czlonkowska, A. (2008). Frequency and prognostic value of cognitive disorders in stroke patients. Dementia and Geriatric Cognitive Disorders, 26(4), 356–363.Find this resource:
Li, W., Risacher, S. L., McAllister, T. W., & Saykin, A. J. (2017). Age at injury is associated with the long-term cognitive outcome of traumatic brain injuries. Alzheimers Dementia, 6, 196–200.Find this resource:
Marsh, N. V., Ludbrook, M. R., & Gaffaney, L. C. (2016). Cognitive functioning following traumatic brain injury: A five-year follow-up. Neurorehabilitation, 38, 71–78.Find this resource:
Mayo, N. E., Fellows, L. K., Scott, S. C., Cameron, J., & Wood-Dauphinee, S. (2009). A longitudinal view of apathy and its impact after stroke. Stroke, 40(10), 3299–3307.Find this resource:
McCrea, M., Janecek, J. K., Powell, M. R., & Hammeke, T. A. (2014). Traumatic Brain Injury and the postconcussion syndrome. In M. W. Parsons & T. A. Hammeke (Eds.), Clinical neuropsychology: A pocket handbook for assessment (3rd ed., pp. 208–236). Washington, DC: American Psychological Association.Find this resource:
McIntyre, A., Janzen, S., & Teasell, R. (2014). Traumatic brain injury in older adults: A review. Topics in Geriatric Rehabilitation, 30(3), 230–236.Find this resource:
McIntyre, A., Mehta, S., Aubut, J., Dijkers, M., & Teasell, R. W. (2013). Mortality among older adults after a traumatic brain injury: A metaanalysis. Brain Injury, 27, 31–40.Find this resource:
Michael, K. M., & Shaughnessy, M. (2006). Stroke prevention and management in older adults. Journal of Cardiovascular Nursing, 21(5), S21–S26.Find this resource:
Mijajlović, M. D., Pavlović, A., Brainin, M., Heiss, W. D., Quinn, T. J., Ihle-Hansen, H. B., . . . & Kliper, E. (2017). Post-stroke dementia–a comprehensive review. BMC medicine, 15(1), 11.Find this resource:
Mikami, K., Jorge, R. E., Moser, D. J., Jang, M., & Robinson, R. G. (2013). Incident apathy during the first year after stroke and its effect on physical and cognitive recovery. The American Journal of Geriatric Psychiatry, 21(9), 848–854.Find this resource:
Milders, M., Fuchs, S., & Crawford, J. R. (2003). Neuropsychological impairments and changes in emotional and social behaviour following severe traumatic brain injury. Journal of Clinical and Experimental Neuropsychology, 25(2), 157–172.Find this resource:
Mitchell, A. B., Cole, J. W., McArdle, P. F., Cheng, Y. C., Ryan, K. A., Sparks, M. J., . . . Kittner, S. J. (2015). Obesity increases risk of ischaemic stroke in young adults. Stroke, 46(6), 1690–1692.Find this resource:
Nakayama, H., Jørgensen, H. S., Raaschou, H. O., & Olsen, T. S. (1994). The influence of age on stroke outcome. The Copenhagen Stroke Study. Stroke, 25(4), 808–813.Find this resource:
National Institute of Neurological Disorders and Stroke (NINDS). Traumatic Brain Injury Information Page. National Institutes of Health.
Nys, G. M. S., Van Zandvoort, M. J. E., De Kort, P. L. M., Jansen, B. P. W., De Haan, E. H. F., & Kappelle, L. J. (2007). Cognitive disorders in acute stroke: Prevalence and clinical determinants. Cerebrovascular Diseases, 23(5–6), 408–416.Find this resource:
Nys, G. M. S., van Zandvoort, M. J. E., de Kort, P. L. M., Jansen, B. P. W., van der Worp, H. B., Kappelle, L. J., & de Haan, E. H. F. (2005b). Domain-specific cognitive recovery after first-ever stroke: A follow-up study of 111 cases. Journal of the International Neuropsychological Society, 11, 795–806.Find this resource:
Nys, G. M. S., van Zandvoort, M. J. E., de Kort, P. L. M., van der Worp, H. B., Jansen, B. P. W., Algra, A., . . . Kappelle, L. J. (2005a). The prognostic value of domain-specific cognitive abilities in acute first-ever stroke. Neurology. 64, 821–827.Find this resource:
Nys, G. M. S., van Zandvoort, M. J. E., van der Worp, H. B., de Haan, E. H. F., de Kort, P. L. M., Jansen, B. P. W., & Kappelle, L. J. (2006). Early cognitive impairment predicts long-term depressive symptoms and quality of life after stroke. Journal of the Neurological Sciences, 247, 149–156.Find this resource:
O’Donnell M. J., Chin, S. L., Rangarajan, S., Xavier, D., Liu, L., Zhang, H., . . . Yusuf, S. (2016). Global and regional effects of potentially modifiable risk factors associated with acute stroke in 32 countries (INTERSTROKE): A case-control study. The Lancet, 388(10046), 761–775.Find this resource:
Osborn, A. J., Mathias, J. L., Fairweather-Schmidt, A. K., & Anstey, K. J. (2017). Anxiety and comorbid depression following traumatic brain injury in a community-based sample of young, middle-aged and older adults. Journal of Affective Disorders, 213, 214–221.Find this resource:
Poorthuis, M. H., Algra, A. M., Algra, A., Kappelle, L. J., & Klijn, C. J. (2017). Female-and male-specific risk factors for stroke: A systematic review and meta-analysis. JAMA Neurology, 74(1), 75–81.Find this resource:
Rapoport, M. J. (2012). Depression following traumatic brain injury: Epidemiology, risk factors, and management. CNS Drugs, 26(2), 111–121.Find this resource:
Rapoport, M. J., Herrmann, N., Shammi, P., Kiss, A., Phillips, A., & Feinstein, A. (2006). Outcome after traumatic brain injury sustained in older adulthood: A one-year longitudinal study. American Journal Geriatric Psychiatry, 14, 456–465.Find this resource:
Rapoport, M. J., Kiss, A., & Feinstein, A. (2006). The impact of depression on outcome following mild-to-moderate traumatic brain injury in older adults. Journal of Affective Disorders, 92, 273–276.Find this resource:
Rapoport, M. J., McCullagh, S., Streiner, D., & Feinstein, A. (2003). Age and major depression after mild traumatic brain injury. American Journal of Geriatric Psychiatry, 11(3), 365–369.Find this resource:
Rathlev, N. K., Medzon, R., Lowery, D., Pollack, C., Bracken, M., Barest, G., & Mower, W. R. (2006). Intracranial pathology in elders with blunt head trauma. Academic Emergency Medicine, 13, 302–307.Find this resource:
Reynolds, K., Lewis, B., Nolen, J. D. L., Kinney, G. L., Sathya, B., & He, J. (2003). Alcohol consumption and risk of stroke: A meta-analysis. JAMA, 289(5), 579–588.Find this resource:
Ritchie, L., Wright-St Clair, V. A., Keogh, J., & Gray, M. (2014). Community integration after traumatic brain injury: A systematic review of the clinical implications of measurement and service provision for older adults. Archives of Physical Medicine and Rehabilitation, 95, 163–174.Find this resource:
Rohling, M. L., Binder, L. M., Demakis, G. J., Larrabee, G. J., Ploetz, D. M., & Langhinrichsen-Rohling, J. (2011). A meta-analysis of neuropsychological outcome after mild traumatic brain injury: Re-analyses and reconsiderations of Binder et al. (1997), Frencham et al. (2005), and Pertab et al. (2009). The Clinical Neuropsychologist, 25(4), 608–623.Find this resource:
Rothwell, P. M., Coull, A. J., Giles, M. F., Howard, S. C., Silver, L. E., Bull, L. M., . . . Farmer, A. (2004). Change in stroke incidence, mortality, case-fatality, severity, and risk factors in Oxfordshire, UK from 1981 to 2004 (Oxford Vascular Study). The Lancet, 363(9425), 1925–1933.Find this resource:
Scahill, R., Frost, C., Jenkins, R., Whitwell, J. L., Rossor, M. N., & Fox, N. C. (2003). A longitudinal study of brain volume changes in normal ageing using serial registered magnetic resonance imaging. Archives of Neurology, 60, 989–994.Find this resource:
Schretlen, D., & Shapiro, A. M. (2003). A quantitative review of the effects of traumatic brain injury on cognitive functioning. International Review of Psychiatry, 15(4), 341–349.Find this resource:
Senathi-Raja, D., Ponsford, J., & Schonberger, M. (2010). Impact of age on long-term cognitive function after traumatic brain injury. Neuropsychology, 24(3), 336–344.Find this resource:
Shinton, R., & Beevers, G. (1989). Meta-analysis of relation between cigarette smoking and stroke. British Medical Journal, 298(6676), 789–794.Find this resource:
Shum, D., Levin, H., & Chan, R. C. K. (2011). Prospective memory in patients with closed head injury: A review. Neuropsychologia, 49, 2156–2165.Find this resource:
Siegal, M., Carrington, J., & Radel, M. (1996). Theory of mind and pragmatic understanding following right hemisphere damage. Brain and Language, 53(1), 40–50.Find this resource:
Suk, S. H., Sacco, R. L., Boden-Albala, B., Cheun, J. F., Pittman, J. G., Elkind, M. S., & Paik, M. C. (2003). Abdominal obesity and risk of ischaemic stroke. Stroke, 34(7), 1586–1592.Find this resource:
Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: A practical scale. The Lancet, 2, 81–84.Find this resource:
Thomas, K. E., Stevens, J. A., Sarmiento, K., & Wald, M. M. (2008). Fall-related traumatic brain injury deaths and hospitalizations among older adults-United States, 2005. Journal of Safety Research, 39(3), 269–272.Find this resource:
Thompson, H. J., McCormick, W. C., & Kagan, S. H. (2006). Traumatic brain injury in older adults: Epidemiology, outcomes, and future implications. Journal of American Geriatric Society, 54, 1590–1595.Find this resource:
Thornhill, S., Teasdale, G. M., Murray, G. D., McEwen, J., Roy, C. W., & Penny, K. (2000). Disability in young people and adults one year after head injury: Prospective cohort study. British Medical Journal, 320, 1631–1635.Find this resource:
Utomo, W. K., Gabbe, B. J., Simpson, P. M., & Cameron, P. A. (2009). Predictors of in hospital mortality and 6-month functional outcomes in older adults after moderate to severe traumatic brain injury. Injury, 40, 973–977.Find this resource:
Wardlaw, J. M., Murray, V., Berge, E., Del Zoppo, G., Sandercock, P., Lindley, R. L., & Cohen, G. (2012). Recombinant tissue plasminogen activator for acute ischaemic stroke: An updated systematic review and meta-analysis. The Lancet, 379(9834), 2364–2372.Find this resource:
Warlow, C., Sudlow, C., Dennis, M., Wardlaw, J., & Sandercock, P. (2003). Stroke. Lancet, 362, 1211–1224.Find this resource:
Werring, D. (2007). Cerebral microbleeds in stroke. Advances in Clinical Neuroscience & Rehabilitation, 7(1), 6–8.Find this resource:
Wilson, B. A., & Gracey, F. (2009). Background and theory: Towards and comprehensive model of neuropsychological rehabilitation. In B. A Wilson, F. Gracey, J. J. Evans, & A. Bateman (Eds.), Neuropsychological rehabilitation: Theory, models, therapy, and outcome (pp. 1–21). Cambridge, UK: Cambridge University Press.Find this resource:
Wilson, B. A., Gracey, F., Evans, J. J., & Bateman, A. (Eds.). (2009). Neuropsychological rehabilitation: Theory, models, therapy, and outcome. Cambridge, UK: Cambridge University Press.Find this resource:
Zillmer, E. A., Spiers, M. V., & Culbertson, W. (2008). Principles of Neuropsychology (2nd ed.). Belmont, CA: Thompson Wadsworth.Find this resource:
Zuercher, M., Ummenhofer, W., Baltussen, A., & Walder, B. (2009). The use of Glasgow Coma Scale in injury assessment: A critical review. Brain Injury, 23(5), 371–384.Find this resource: