Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, September 22, 2022

Apathy after stroke: Diagnosis, mechanisms, consequences, and treatment

Apathy wouldn't exist post stroke if you had 100% recovery protocols. Solve the correct problem, 100% recovery instead of wasting time and money on apathy. Don't you people ever use your two functioning brain cells? 

Apathy after stroke: Diagnosis, mechanisms, consequences, and treatment


Abstract

Apathy is a reduction in goal-directed activity in the cognitive, behavioral, emotional, or social domains of a patient’s life and occurs in one out of three patients after stroke. Despite this, apathy is clinically under-recognized and poorly understood. This overview provides a contemporary introduction to apathy in stroke for researchers and practitioners, covering topics including diagnosis, neurobiological mechanisms, associated consequences, and potential treatments for apathy. Apathy is often misdiagnosed as other post-stroke conditions such as depression. Accurate differential diagnosis of apathy, which manifests as reductions in initiative, and depression, which manifests as negative emotionality, is important as it informs prognosis. Research on the neurobiology of apathy suggests that there are few consistent associations between stroke lesion location and the development of apathy. These may be resolved by adopting a network neuroscience approach, which models apathy as a pathology arising from structural or functional damage to brain networks underlying motivated behavior. Importantly, networks can be affected by physiological changes related to stroke, including the acute infarct but also diaschisis and neurodegeneration. Aside from neurobiological changes, apathy is also associated with other negative outcome measures such as functional disability, cognitive impairment, and emotional distress, suggesting that apathy is indicative of a worse prognosis following stroke. Unfortunately, high-quality trials aimed at treating apathy are scarce. Antidepressants may have limited effects on apathy. Acetylcholine and dopamine pharmacotherapy, behavioral interventions, and transcranial magnetic stimulation may be more promising avenues for treatment.

Introduction

Apathy is a behavioral syndrome characterized by a loss of motivation that occurs in one-third of patients after stroke.1,2 Post-stroke patients with apathy suffer from greater functional impairment and demonstrate slower recovery times to normal functioning.3,4 Furthermore, apathy is a risk factor for incident vascular disease, dementia, and mortality.5,6 Despite high prevalence and an impact on outcomes after stroke, apathy remains poorly understood. It is also under-recognized, although the extent of this is unknown. This leads to a dearth of treatment approaches. This overview provides a contemporary introduction to apathy in stroke for researchers and practitioners, covering topics including diagnosis, neurobiological mechanisms, associated consequences, and potential treatments for apathy. The search strategy and selection criteria for papers referenced in this overview can be found after the “Discussion” section.

Diagnostic criteria for apathy

Apathy can be defined as a quantitative reduction in goal-directed behaviors (GDB) occurring in the cognitive/behavioral, emotional, or social domains of an individual’s life (Box 1).7 Reductions are relative to an individual’s previous level of functioning and can be reported by the individual or others. A previous version of these diagnostic guidelines has been validated in patients with a range of neurological disorders, including those with cerebrovascular damage, showing good inter-rater reliability.8
Box 1. Diagnostic criteria for apathy.
CRITERION A: A quantitative reduction of goal-directed activity either in behavioral, cognitive, emotional or social dimensions in comparison to the patient’s previous level of functioning in these areas. These changes may be reported by the patient themselves or by observation of others.
CRITERION B: The presence of at least two of the three following dimensions for a period of at least four weeks and present most of the time:
B1. BEHAVIOR AND COGNITION
Loss of, or diminished, goal-directed behavior or cognitive activity as evidenced by at least one of the following:
General level of activity: The patient has a reduced level of activity either at home or work, makes less effort to initiate or accomplish tasks spontaneously or needs to be prompted to perform them.
Persistence of activity: They are less persistent in maintaining an activity or conversation, finding solutions to problems or thinking of alternative ways to accomplish them if they become difficult.
Making choices: They have less interest or take longer to make choices when different alternatives exist.
Interest in external issue: They have less interest in or reacts less to news, either good or bad, or has less interest in doing new things.
Personal wellbeing: They are less interested in their own health and wellbeing or personal image.
B2. EMOTION
Loss of, or diminished, emotion as evidenced by at least one of the following:
Spontaneous emotions: The patient shows less spontaneous (self-generated) emotions regarding their own affairs or appears less interested in events that should matter to them or to people that they know well.
Emotional reactions to environment: They express less emotional reaction in response to positive or negative events in their environment that affect them or people they know well.
Impact on others: They are less concerned about the impact of their actions or feelings on the people around them.
Empathy: They show less empathy to the emotions or feelings of others.
Verbal or physical expressions: They show less verbal or physical reactions that reveal their emotional states.
B3. SOCIAL INTERACTION
Loss of or diminished engagement in social interaction as evidenced by at least one of the following:
Spontaneous social initiative: The patient takes less initiative in spontaneously proposing social or leisure activities to family or others.
Environmentally stimulated social interaction: They participate less or are less comfortable or more indifferent to social or leisure activities suggested by people around them.
Relationship with family members: They show less interest in family members.
Verbal interaction: They are less likely to initiate a conversation or withdraw soon from it.
Homebound: They prefer to stay at home more frequently or longer than usual and show less interest in getting out to meet people.
CRITERION C: These symptoms (A–B) cause clinically significant impairment in personal, social, occupational, or other important areas of functioning.
CRITERION D: The symptoms (A–B) are not exclusively explained or due to physical disabilities, to motor disabilities, to a diminished level of consciousness, to the direct physiological effects of a substance, or to major changes in the patient’s environment.
Adapted with permission.7

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