Huntington disease (HD) is a hereditary neurodegenerative disorder characterized by a combination of motor disturbances, psychiatric symptoms, and cognitive decline. The cognitive impairment seen in HD gradually progresses to dementia, significantly affecting a person’s ability to think, reason, and function independently. Huntington disease dementia typically emerges in the middle to late stages of the illness and is associated with changes in attention, executive function, memory, and behavior. The condition is inherited in an autosomal dominant pattern and affects individuals across diverse geographic and ethnic populations.
Epidemiology
Huntington disease is found across diverse geographic regions and ethnic populations around the world. Globally, its prevalence is estimated to range between 5 and 10 cases per 100,000 people. In regions such as North America and Europe, reported prevalence rates vary from approximately 0.5 to 9.95 cases per 100,000 individuals.
Juvenile Huntington’s disease, which begins before the age of 20, is often marked by symptoms such as muscle rigidity, problems with coordination (ataxia), cognitive impairment, and a faster rate of disease progression. The average course of the illness is around 8 years, and seizures tend to occur more frequently in this early-onset form compared to adult-onset Huntington’s disease.
Anatomy
Pathophysiology
Huntington disease dementia results from widespread neurodegeneration caused by a mutation in the HTT gene, which involves an abnormal expansion of CAG trinucleotide repeats. This mutation leads to the production of a defective huntingtin protein that accumulates in neurons, disrupting normal cellular functions such as protein transport, synaptic transmission, and mitochondrial activity. The earliest and most severe damage occurs in the striatum, particularly the caudate nucleus and putamen, which are essential for motor and cognitive functions. Over time, neurodegeneration extends to the cerebral cortex, especially the frontal and temporal lobes, regions responsible for higher-order thinking, decision-making, and memory. The progressive loss of neurons and synaptic connections in these areas leads to the characteristic cognitive decline and behavioral disturbances seen in Huntington disease dementia.
Etiology
Huntington disease dementia is caused by a genetic mutation in the HTT gene on chromosome 4. This mutation involves an abnormal expansion of a CAG trinucleotide repeat, which leads to the production of a mutant form of the huntingtin protein. The number of CAG repeats determines disease expression: individuals with 36 or more repeats are at risk of developing the condition, with larger expansions generally associated with earlier onset and faster progression. The inheritance pattern is autosomal dominant, meaning a child has a 50% chance of inheriting the mutated gene if one parent is affected. The accumulation of the toxic protein disrupts neuronal function and survival, particularly in brain areas responsible for movement, cognition, and behavior, ultimately leading to the development of dementia.
Genetics
Prognostic Factors
CAG Repeat Length: A greater number of CAG trinucleotide repeats in the HTT gene is associated with earlier onset and more rapid progression of cognitive and motor decline.
Age at Onset: Younger onset, especially in juvenile cases, tends to correlate with a more aggressive disease course and earlier development of dementia.
Rate of Symptom Progression: The speed at which motor, cognitive, and psychiatric symptoms worsen can vary widely among individuals, influencing functional decline and life expectancy.
Presence of Psychiatric Symptoms: Severe psychiatric manifestations such as depression, psychosis, or aggression may complicate care and contribute to earlier institutionalization or reduced quality of life.
Level of Social and Medical Support: Access to multidisciplinary care, caregiver support, and early intervention can help slow functional decline and improve overall outcomes.
Nutritional Status and Comorbidities: Weight loss, poor nutrition, and coexisting conditions (e.g., cardiovascular disease, infections) can negatively impact prognosis.
Clinical History
Huntington disease typically presents between the ages of 30 and 50, and cognitive decline leading to dementia usually develops gradually as the disease progresses. While dementia can emerge at varying points in the disease course, it is more commonly seen in the mid to late stages. Juvenile-onset Huntington disease, which begins before age 20, may also involve cognitive impairment, but the pattern often differs from adult-onset forms. Overall, Huntington disease dementia most frequently affects adults in their 40s and 50s, with progression continuing over the following 10 to 20 years.
Physical Examination
The physical examination of a patient with Huntington disease dementia typically reveals a combination of motor, cognitive, and psychiatric features. Motor signs often include chorea (involuntary, dance-like movements), muscle rigidity, bradykinesia (slowness of movement), and impaired coordination. Gait abnormalities, such as unsteadiness and difficulty initiating walking, are also common. As the disease advances, motor symptoms may shift from chorea to more rigid and parkinsonian features.
Age group
Associated comorbidity
Individuals with Huntington disease dementia often experience a range of comorbid conditions that can complicate management. Common psychiatric comorbidities include depression, anxiety, irritability, and psychosis. These symptoms may precede or accompany cognitive decline. Motor impairments such as chorea, dystonia, and gait disturbances further impact daily functioning and increase the risk of falls and injury. Sleep disturbances, weight loss, and metabolic abnormalities are also frequently observed. Social isolation, reduced physical activity, and impaired occupational or academic performance are common as the disease progresses. These comorbidities collectively contribute to a decline in quality of life and require a multidisciplinary approach to care.
Associated activity
Acuity of presentation
The onset of dementia in Huntington disease is typically gradual and insidious rather than acute. Cognitive symptoms often begin subtly, with early signs including difficulties in attention, planning, problem-solving, and impulse control. These changes may be mistaken for stress, aging, or psychiatric illness in the early stages. Over time, the decline becomes more pronounced, affecting memory, language, and judgment. Behavioral and personality changes, such as apathy, irritability, and social withdrawal, may also emerge early and progress alongside cognitive deficits. The slow and progressive nature of symptom development reflects the underlying neurodegenerative process characteristic of Huntington disease.
Differential Diagnoses
Parkinson’s disease with dementia
Alzheimer’s disease
Frontotemporal dementia (FTD)
Wilson’s disease
Spinocerebellar ataxias
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Pharmacologic Treatment: Medications may be used to address specific symptoms. Antipsychotics (e.g., olanzapine, risperidone) are commonly used for chorea and behavioral disturbances. Antidepressants, such as SSRIs or SNRIs, may help manage mood disorders. Cognitive enhancers, including acetylcholinesterase inhibitors and memantine, have shown limited benefit but may be considered in some cases.
Non-Pharmacologic Support: Cognitive rehabilitation, structured routines, and behavioral therapy may help support daily functioning. Physical therapy can address motor symptoms, while speech and occupational therapy support communication and adaptive skills.
Multidisciplinary Care: Regular involvement of neurology, psychiatry, social work, and palliative care is essential. Family education and genetic counseling are also key components of long-term management.
Advanced Planning: As the disease progresses, discussions around advance directives, long-term care, and supportive services become increasingly important.
Safety Enhancements: Remove tripping hazards, install grab bars, use non-slip mats, and ensure adequate lighting to reduce fall risk. Lock up potentially harmful items (e.g., sharp tools, medications).
Simplified Layout: Reduce clutter and create a predictable, organized space to minimize confusion and anxiety. Clearly label drawers, rooms, and items to support memory and orientation.
Assistive Devices: Use mobility aids, communication boards, and adaptive utensils to support physical limitations and maintain independence in daily tasks.
Calm and Structured Setting: Limit noise and visual distractions to help with concentration. Establish consistent routines and schedules to reduce agitation and disorientation.
Supervision and Support: As cognitive and motor skills decline, increased supervision may be required to ensure safety, especially in tasks involving cooking, driving, or medication management.
Effectiveness of Acetylcholinesterase inhibitors in treating Huntington Disease Dementia
Rivastigmine and memantine
Acetylcholinesterase inhibitors, such as rivastigmine and memantine, may offer modest cognitive benefits in some individuals; however, they do not alter the course of the disease. A recent review of available studies examining the use of these medications found limited evidence supporting their overall effectiveness in treating cognitive symptoms in Huntington disease.
Phases of Management:
The care of individuals with Huntington disease dementia is best approached in progressive phases, reflecting the evolving nature of symptoms over time. Each phase requires a tailored strategy to address the changing clinical, cognitive, and functional needs of the patient.
Early Phase:
Begin genetic counseling and support services; monitor for early cognitive, psychiatric, and motor signs. Introduce lifestyle modifications and safety planning. Initiate treatment for depression, anxiety, or chorea if present.
Middle Phase:
Implement structured routines and environmental adaptations. Use medications to manage motor and psychiatric symptoms. Cognitive rehabilitation, speech, physical, and occupational therapies become more important. Family and caregiver support intensifies, and discussions about advance care planning should begin.
Late Phase:
Emphasis on comfort, dignity, and quality of life. Feeding assistance, mobility aids, and full-time care may be required. Treat infections, prevent pressure sores, and manage end-of-life decisions. Involve palliative care or hospice services as needed.
Huntington disease (HD) is a hereditary neurodegenerative disorder characterized by a combination of motor disturbances, psychiatric symptoms, and cognitive decline. The cognitive impairment seen in HD gradually progresses to dementia, significantly affecting a person’s ability to think, reason, and function independently. Huntington disease dementia typically emerges in the middle to late stages of the illness and is associated with changes in attention, executive function, memory, and behavior. The condition is inherited in an autosomal dominant pattern and affects individuals across diverse geographic and ethnic populations.
Huntington disease is found across diverse geographic regions and ethnic populations around the world. Globally, its prevalence is estimated to range between 5 and 10 cases per 100,000 people. In regions such as North America and Europe, reported prevalence rates vary from approximately 0.5 to 9.95 cases per 100,000 individuals.
Juvenile Huntington’s disease, which begins before the age of 20, is often marked by symptoms such as muscle rigidity, problems with coordination (ataxia), cognitive impairment, and a faster rate of disease progression. The average course of the illness is around 8 years, and seizures tend to occur more frequently in this early-onset form compared to adult-onset Huntington’s disease.
Huntington disease dementia results from widespread neurodegeneration caused by a mutation in the HTT gene, which involves an abnormal expansion of CAG trinucleotide repeats. This mutation leads to the production of a defective huntingtin protein that accumulates in neurons, disrupting normal cellular functions such as protein transport, synaptic transmission, and mitochondrial activity. The earliest and most severe damage occurs in the striatum, particularly the caudate nucleus and putamen, which are essential for motor and cognitive functions. Over time, neurodegeneration extends to the cerebral cortex, especially the frontal and temporal lobes, regions responsible for higher-order thinking, decision-making, and memory. The progressive loss of neurons and synaptic connections in these areas leads to the characteristic cognitive decline and behavioral disturbances seen in Huntington disease dementia.
Huntington disease dementia is caused by a genetic mutation in the HTT gene on chromosome 4. This mutation involves an abnormal expansion of a CAG trinucleotide repeat, which leads to the production of a mutant form of the huntingtin protein. The number of CAG repeats determines disease expression: individuals with 36 or more repeats are at risk of developing the condition, with larger expansions generally associated with earlier onset and faster progression. The inheritance pattern is autosomal dominant, meaning a child has a 50% chance of inheriting the mutated gene if one parent is affected. The accumulation of the toxic protein disrupts neuronal function and survival, particularly in brain areas responsible for movement, cognition, and behavior, ultimately leading to the development of dementia.
CAG Repeat Length: A greater number of CAG trinucleotide repeats in the HTT gene is associated with earlier onset and more rapid progression of cognitive and motor decline.
Age at Onset: Younger onset, especially in juvenile cases, tends to correlate with a more aggressive disease course and earlier development of dementia.
Rate of Symptom Progression: The speed at which motor, cognitive, and psychiatric symptoms worsen can vary widely among individuals, influencing functional decline and life expectancy.
Presence of Psychiatric Symptoms: Severe psychiatric manifestations such as depression, psychosis, or aggression may complicate care and contribute to earlier institutionalization or reduced quality of life.
Level of Social and Medical Support: Access to multidisciplinary care, caregiver support, and early intervention can help slow functional decline and improve overall outcomes.
Nutritional Status and Comorbidities: Weight loss, poor nutrition, and coexisting conditions (e.g., cardiovascular disease, infections) can negatively impact prognosis.
Huntington disease typically presents between the ages of 30 and 50, and cognitive decline leading to dementia usually develops gradually as the disease progresses. While dementia can emerge at varying points in the disease course, it is more commonly seen in the mid to late stages. Juvenile-onset Huntington disease, which begins before age 20, may also involve cognitive impairment, but the pattern often differs from adult-onset forms. Overall, Huntington disease dementia most frequently affects adults in their 40s and 50s, with progression continuing over the following 10 to 20 years.
The physical examination of a patient with Huntington disease dementia typically reveals a combination of motor, cognitive, and psychiatric features. Motor signs often include chorea (involuntary, dance-like movements), muscle rigidity, bradykinesia (slowness of movement), and impaired coordination. Gait abnormalities, such as unsteadiness and difficulty initiating walking, are also common. As the disease advances, motor symptoms may shift from chorea to more rigid and parkinsonian features.
Individuals with Huntington disease dementia often experience a range of comorbid conditions that can complicate management. Common psychiatric comorbidities include depression, anxiety, irritability, and psychosis. These symptoms may precede or accompany cognitive decline. Motor impairments such as chorea, dystonia, and gait disturbances further impact daily functioning and increase the risk of falls and injury. Sleep disturbances, weight loss, and metabolic abnormalities are also frequently observed. Social isolation, reduced physical activity, and impaired occupational or academic performance are common as the disease progresses. These comorbidities collectively contribute to a decline in quality of life and require a multidisciplinary approach to care.
The onset of dementia in Huntington disease is typically gradual and insidious rather than acute. Cognitive symptoms often begin subtly, with early signs including difficulties in attention, planning, problem-solving, and impulse control. These changes may be mistaken for stress, aging, or psychiatric illness in the early stages. Over time, the decline becomes more pronounced, affecting memory, language, and judgment. Behavioral and personality changes, such as apathy, irritability, and social withdrawal, may also emerge early and progress alongside cognitive deficits. The slow and progressive nature of symptom development reflects the underlying neurodegenerative process characteristic of Huntington disease.
Parkinson’s disease with dementia
Alzheimer’s disease
Frontotemporal dementia (FTD)
Wilson’s disease
Spinocerebellar ataxias
Pharmacologic Treatment: Medications may be used to address specific symptoms. Antipsychotics (e.g., olanzapine, risperidone) are commonly used for chorea and behavioral disturbances. Antidepressants, such as SSRIs or SNRIs, may help manage mood disorders. Cognitive enhancers, including acetylcholinesterase inhibitors and memantine, have shown limited benefit but may be considered in some cases.
Non-Pharmacologic Support: Cognitive rehabilitation, structured routines, and behavioral therapy may help support daily functioning. Physical therapy can address motor symptoms, while speech and occupational therapy support communication and adaptive skills.
Multidisciplinary Care: Regular involvement of neurology, psychiatry, social work, and palliative care is essential. Family education and genetic counseling are also key components of long-term management.
Advanced Planning: As the disease progresses, discussions around advance directives, long-term care, and supportive services become increasingly important.
Psychiatry/Mental Health
Safety Enhancements: Remove tripping hazards, install grab bars, use non-slip mats, and ensure adequate lighting to reduce fall risk. Lock up potentially harmful items (e.g., sharp tools, medications).
Simplified Layout: Reduce clutter and create a predictable, organized space to minimize confusion and anxiety. Clearly label drawers, rooms, and items to support memory and orientation.
Assistive Devices: Use mobility aids, communication boards, and adaptive utensils to support physical limitations and maintain independence in daily tasks.
Calm and Structured Setting: Limit noise and visual distractions to help with concentration. Establish consistent routines and schedules to reduce agitation and disorientation.
Supervision and Support: As cognitive and motor skills decline, increased supervision may be required to ensure safety, especially in tasks involving cooking, driving, or medication management.
Psychiatry/Mental Health
Rivastigmine and memantine
Acetylcholinesterase inhibitors, such as rivastigmine and memantine, may offer modest cognitive benefits in some individuals; however, they do not alter the course of the disease. A recent review of available studies examining the use of these medications found limited evidence supporting their overall effectiveness in treating cognitive symptoms in Huntington disease.
Psychiatry/Mental Health
Phases of Management:
The care of individuals with Huntington disease dementia is best approached in progressive phases, reflecting the evolving nature of symptoms over time. Each phase requires a tailored strategy to address the changing clinical, cognitive, and functional needs of the patient.
Early Phase:
Begin genetic counseling and support services; monitor for early cognitive, psychiatric, and motor signs. Introduce lifestyle modifications and safety planning. Initiate treatment for depression, anxiety, or chorea if present.
Middle Phase:
Implement structured routines and environmental adaptations. Use medications to manage motor and psychiatric symptoms. Cognitive rehabilitation, speech, physical, and occupational therapies become more important. Family and caregiver support intensifies, and discussions about advance care planning should begin.
Late Phase:
Emphasis on comfort, dignity, and quality of life. Feeding assistance, mobility aids, and full-time care may be required. Treat infections, prevent pressure sores, and manage end-of-life decisions. Involve palliative care or hospice services as needed.
Huntington disease (HD) is a hereditary neurodegenerative disorder characterized by a combination of motor disturbances, psychiatric symptoms, and cognitive decline. The cognitive impairment seen in HD gradually progresses to dementia, significantly affecting a person’s ability to think, reason, and function independently. Huntington disease dementia typically emerges in the middle to late stages of the illness and is associated with changes in attention, executive function, memory, and behavior. The condition is inherited in an autosomal dominant pattern and affects individuals across diverse geographic and ethnic populations.
Huntington disease is found across diverse geographic regions and ethnic populations around the world. Globally, its prevalence is estimated to range between 5 and 10 cases per 100,000 people. In regions such as North America and Europe, reported prevalence rates vary from approximately 0.5 to 9.95 cases per 100,000 individuals.
Juvenile Huntington’s disease, which begins before the age of 20, is often marked by symptoms such as muscle rigidity, problems with coordination (ataxia), cognitive impairment, and a faster rate of disease progression. The average course of the illness is around 8 years, and seizures tend to occur more frequently in this early-onset form compared to adult-onset Huntington’s disease.
Huntington disease dementia results from widespread neurodegeneration caused by a mutation in the HTT gene, which involves an abnormal expansion of CAG trinucleotide repeats. This mutation leads to the production of a defective huntingtin protein that accumulates in neurons, disrupting normal cellular functions such as protein transport, synaptic transmission, and mitochondrial activity. The earliest and most severe damage occurs in the striatum, particularly the caudate nucleus and putamen, which are essential for motor and cognitive functions. Over time, neurodegeneration extends to the cerebral cortex, especially the frontal and temporal lobes, regions responsible for higher-order thinking, decision-making, and memory. The progressive loss of neurons and synaptic connections in these areas leads to the characteristic cognitive decline and behavioral disturbances seen in Huntington disease dementia.
Huntington disease dementia is caused by a genetic mutation in the HTT gene on chromosome 4. This mutation involves an abnormal expansion of a CAG trinucleotide repeat, which leads to the production of a mutant form of the huntingtin protein. The number of CAG repeats determines disease expression: individuals with 36 or more repeats are at risk of developing the condition, with larger expansions generally associated with earlier onset and faster progression. The inheritance pattern is autosomal dominant, meaning a child has a 50% chance of inheriting the mutated gene if one parent is affected. The accumulation of the toxic protein disrupts neuronal function and survival, particularly in brain areas responsible for movement, cognition, and behavior, ultimately leading to the development of dementia.
CAG Repeat Length: A greater number of CAG trinucleotide repeats in the HTT gene is associated with earlier onset and more rapid progression of cognitive and motor decline.
Age at Onset: Younger onset, especially in juvenile cases, tends to correlate with a more aggressive disease course and earlier development of dementia.
Rate of Symptom Progression: The speed at which motor, cognitive, and psychiatric symptoms worsen can vary widely among individuals, influencing functional decline and life expectancy.
Presence of Psychiatric Symptoms: Severe psychiatric manifestations such as depression, psychosis, or aggression may complicate care and contribute to earlier institutionalization or reduced quality of life.
Level of Social and Medical Support: Access to multidisciplinary care, caregiver support, and early intervention can help slow functional decline and improve overall outcomes.
Nutritional Status and Comorbidities: Weight loss, poor nutrition, and coexisting conditions (e.g., cardiovascular disease, infections) can negatively impact prognosis.
Huntington disease typically presents between the ages of 30 and 50, and cognitive decline leading to dementia usually develops gradually as the disease progresses. While dementia can emerge at varying points in the disease course, it is more commonly seen in the mid to late stages. Juvenile-onset Huntington disease, which begins before age 20, may also involve cognitive impairment, but the pattern often differs from adult-onset forms. Overall, Huntington disease dementia most frequently affects adults in their 40s and 50s, with progression continuing over the following 10 to 20 years.
The physical examination of a patient with Huntington disease dementia typically reveals a combination of motor, cognitive, and psychiatric features. Motor signs often include chorea (involuntary, dance-like movements), muscle rigidity, bradykinesia (slowness of movement), and impaired coordination. Gait abnormalities, such as unsteadiness and difficulty initiating walking, are also common. As the disease advances, motor symptoms may shift from chorea to more rigid and parkinsonian features.
Individuals with Huntington disease dementia often experience a range of comorbid conditions that can complicate management. Common psychiatric comorbidities include depression, anxiety, irritability, and psychosis. These symptoms may precede or accompany cognitive decline. Motor impairments such as chorea, dystonia, and gait disturbances further impact daily functioning and increase the risk of falls and injury. Sleep disturbances, weight loss, and metabolic abnormalities are also frequently observed. Social isolation, reduced physical activity, and impaired occupational or academic performance are common as the disease progresses. These comorbidities collectively contribute to a decline in quality of life and require a multidisciplinary approach to care.
The onset of dementia in Huntington disease is typically gradual and insidious rather than acute. Cognitive symptoms often begin subtly, with early signs including difficulties in attention, planning, problem-solving, and impulse control. These changes may be mistaken for stress, aging, or psychiatric illness in the early stages. Over time, the decline becomes more pronounced, affecting memory, language, and judgment. Behavioral and personality changes, such as apathy, irritability, and social withdrawal, may also emerge early and progress alongside cognitive deficits. The slow and progressive nature of symptom development reflects the underlying neurodegenerative process characteristic of Huntington disease.
Parkinson’s disease with dementia
Alzheimer’s disease
Frontotemporal dementia (FTD)
Wilson’s disease
Spinocerebellar ataxias
Pharmacologic Treatment: Medications may be used to address specific symptoms. Antipsychotics (e.g., olanzapine, risperidone) are commonly used for chorea and behavioral disturbances. Antidepressants, such as SSRIs or SNRIs, may help manage mood disorders. Cognitive enhancers, including acetylcholinesterase inhibitors and memantine, have shown limited benefit but may be considered in some cases.
Non-Pharmacologic Support: Cognitive rehabilitation, structured routines, and behavioral therapy may help support daily functioning. Physical therapy can address motor symptoms, while speech and occupational therapy support communication and adaptive skills.
Multidisciplinary Care: Regular involvement of neurology, psychiatry, social work, and palliative care is essential. Family education and genetic counseling are also key components of long-term management.
Advanced Planning: As the disease progresses, discussions around advance directives, long-term care, and supportive services become increasingly important.
Psychiatry/Mental Health
Safety Enhancements: Remove tripping hazards, install grab bars, use non-slip mats, and ensure adequate lighting to reduce fall risk. Lock up potentially harmful items (e.g., sharp tools, medications).
Simplified Layout: Reduce clutter and create a predictable, organized space to minimize confusion and anxiety. Clearly label drawers, rooms, and items to support memory and orientation.
Assistive Devices: Use mobility aids, communication boards, and adaptive utensils to support physical limitations and maintain independence in daily tasks.
Calm and Structured Setting: Limit noise and visual distractions to help with concentration. Establish consistent routines and schedules to reduce agitation and disorientation.
Supervision and Support: As cognitive and motor skills decline, increased supervision may be required to ensure safety, especially in tasks involving cooking, driving, or medication management.
Psychiatry/Mental Health
Rivastigmine and memantine
Acetylcholinesterase inhibitors, such as rivastigmine and memantine, may offer modest cognitive benefits in some individuals; however, they do not alter the course of the disease. A recent review of available studies examining the use of these medications found limited evidence supporting their overall effectiveness in treating cognitive symptoms in Huntington disease.
Psychiatry/Mental Health
Phases of Management:
The care of individuals with Huntington disease dementia is best approached in progressive phases, reflecting the evolving nature of symptoms over time. Each phase requires a tailored strategy to address the changing clinical, cognitive, and functional needs of the patient.
Early Phase:
Begin genetic counseling and support services; monitor for early cognitive, psychiatric, and motor signs. Introduce lifestyle modifications and safety planning. Initiate treatment for depression, anxiety, or chorea if present.
Middle Phase:
Implement structured routines and environmental adaptations. Use medications to manage motor and psychiatric symptoms. Cognitive rehabilitation, speech, physical, and occupational therapies become more important. Family and caregiver support intensifies, and discussions about advance care planning should begin.
Late Phase:
Emphasis on comfort, dignity, and quality of life. Feeding assistance, mobility aids, and full-time care may be required. Treat infections, prevent pressure sores, and manage end-of-life decisions. Involve palliative care or hospice services as needed.
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