Stroke Recovery: Can Intelligence Rebound?

A stroke can cause a range of cognitive impairments, including aphasia, memory problems, and trouble speaking. These issues can affect a stroke survivor's ability to perform daily tasks and can also impact their emotional state, potentially leading to depression and impulsivity. The first three months after a stroke are critical for recovery, with most improvements occurring during this period. Rehabilitation plays a crucial role in helping stroke survivors regain function and develop compensation strategies for any remaining impairments. While improvements may continue beyond the initial three months, they tend to slow down significantly, and most stroke patients reach a relatively steady state by the six-month mark.

The impact of early-life intelligence quotient on post-stroke cognitive impairment

Stroke can interfere with any or all of the functions that define who we are and how we relate to one another. Cognitive impairment can complicate minor strokes, but there is limited information on risk factors, including peak cognitive ability earlier in life. This study aims to determine the risk of cognitive impairment after lacunar and minor non-lacunar ischaemic stroke and assess the effect of pre-morbid (best-ever) intelligence quotient (IQ) versus educational attainment.

Methods

This study recruited 157 patients (87 lacunar, 64 non-lacunar ischaemic strokes) with a median age of 66 years. Cognitive testing was performed at 1-3 and 12 months post-stroke, assessing educational attainment, current cognition, pre-morbid intelligence, and dependency.

Results

The results showed that 23% of patients had cognitive impairment at 1-3 months, and 19% at one year. Lower pre-morbid IQ and older age were significant predictors of one-year cognitive impairment, more so than stroke severity or vascular risk factors. Additionally, cognitive impairment was associated with more white matter hyper-intensities.

Discussion

This observational study provides evidence that pre-morbid IQ and education are significant predictors of cognition after a stroke. It also confirms the association between cognitive impairment and small vessel disease. These findings suggest that pre-morbid IQ should be considered in future studies of post-stroke cognition.

Cognitive impairment and dementia

Neuroimaging markers of brain lesions that are associated with dementia after stroke include silent brain infarcts, white matter changes, lacunar infarcts, and medial temporal lobe atrophy. The most common type of dementia after stroke is vascular dementia, which involves multiple substrates. Microinfarction, microvascular changes related to blood-brain barrier damage, focal neuronal atrophy, and low burden of co-existing neurodegenerative pathology appear to be key substrates of dementia after stroke.

Cognitive rehabilitation focuses on several areas of cognition such as attention, concentration, perception, memory, comprehension, communication, reasoning, problem-solving, judgment, initiation, planning, self-monitoring, and awareness.

Aphasia: an acquired language disorder

Aphasia is an acquired language disorder that affects a person’s ability to comprehend and produce language. It is a common effect of stroke, impacting around one-third of stroke survivors, with roughly 40% continuing to experience significant language impairment a year and a half after their stroke. The left cerebral hemisphere is dominant for language in 99% of right-handed people (93% of the population), and so aphasia usually occurs due to damage to this area of the brain. However, in around 30% of left-handed people with post-stroke aphasia, the damage occurs in the right hemisphere.

Specific linguistic impairments, such as phonological, lexical semantic, and syntactic impairments, can show substantial recovery in the first few months following a stroke. Recovery of language function after a stroke is thought to occur in three phases: the acute phase, lasting around two weeks after the stroke; the subacute phase, lasting up to six months after the stroke; and the chronic phase, which begins months or years after the stroke and may continue for the rest of the person's life.

The therapeutic management of aphasia is a long-term process that often does not end with a complete recovery of language and communication functions. For many patients, progress toward functional communication is steady but slow, while others need to be assisted to learn compensatory strategies for effective communication.

Visual-perceptual disorders

Unilateral spatial neglect is a visual-perceptual disorder caused by damage to the parietal lobe, where a person is unaware of the contralateral side of the body, including half of the visual field. It causes a disruption of a person's body schema and spatial orientation and adversely affects their balance and safety awareness. Those suffering from neglect may deny that anything is wrong.

The presence of neglect has been associated with both the severity of the stroke and the age of the individual. Limb apraxia is more common in those with left hemisphere involvement but can also be seen in right hemisphere damage. Severity of apraxia is associated with changes in functional performance.

Rehabilitation and Treatment

People with stroke should be screened for visual, visual motor and visual perceptual deficits as a routine part of the broader rehabilitation assessment process. Patients with suspected perceptual impairments should be assessed using validated tools. Patients, families and caregivers should receive education on visual-spatial neglect and treatment recommendations.

Visual scanning techniques should be used to improve perceptual impairments caused by neglect. Virtual reality or computer-based interventions for neglect should be used to improve visual perception and alleviate right-hemisphere bias. Prism glasses and eye-patches may be used to improve neglect, but there is conflicting evidence on their effectiveness.

Patients with suspected limb apraxia should be treated using errorless learning, gesture training and graded strategy training. Mirror therapy may be used to improve neglect and may be combined with limb activation to improve outcomes.

Factors affecting intelligence rebound after a stroke

Several factors influence the rebound of intelligence after a stroke. Here are some of the key factors:

• Pre-morbid intelligence quotient (IQ): The "best-ever" IQ, typically measured in young adulthood, is a strong predictor of post-stroke cognition. Lower pre-morbid IQ is associated with poorer cognitive outcomes after a stroke.
• Education: Higher levels of education are linked to better cognitive outcomes after a stroke. Education may influence cognitive recovery through its association with pre-morbid IQ.
• Age: Older age is a risk factor for cognitive impairment after a stroke and can negatively impact cognitive recovery.
• Stroke severity: The severity of a stroke can affect cognitive function. More severe strokes are associated with a higher risk of cognitive impairment.
• Vascular risk factors: Factors such as hypertension and diabetes can increase the risk of cognitive impairment after a stroke.
• White matter hyperintensities: The presence of white matter hyperintensities, as seen on brain imaging, is associated with an increased risk of cognitive impairment after a stroke.
• Lesion location: The location of the stroke lesion can impact specific cognitive functions. For example, left hemisphere strokes are associated with difficulties in spelling and writing, while right hemisphere strokes can lead to a loss of empathy.
• Time since stroke: Cognitive recovery can occur up to a year after a stroke, with most improvement happening in the first three months.
• Rehabilitation and intervention: Cognitive rehabilitation can help improve cognitive function after a stroke. Interventions such as language therapy and physical activity programs can enhance recovery.
• Genetic factors: Genetic variations, such as the ApoE ε4 allele, may influence the risk of vascular cognitive impairment and dementia after a stroke.
• Inflammation: Inflammatory markers, such as C-reactive protein and interleukin-6, have been linked to post-stroke cognitive impairment and depression.
• Psychosocial factors: Factors like social support and coping strategies can influence the development of post-stroke depression, which is associated with cognitive impairment.

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