Last updated date: 07-May-2023
Originally Written in English
Memory is a reconstructive process that is divided into explicit and implicit memory based on the amount of awareness. Explicit memory refers to the conscious recall of either episodic or semantic memory. Episodic memory is based on personal experience and is context-specific, whereas semantic memory is based on generic information. Priming, procedure memory, and skills all contribute to implicit memory.
Working memory is the brain's online message storage. Prospective memory is concerned with something that will be done in the future. Overreliance on gist memory introduces false memory. Emotional upheaval has an impact on encoding and consolidation. The medial temporal and prefrontal lobes are involved in explicit memory.
Priming has a direct impact on the cerebral cortex. Basal ganglia are linked to procedure memory and motor abilities. The cerebellum is crucial in classical conditioning and complex motor learning. The age effect on memory is primarily caused by a decline in the speed and capacity of the central executive function.
Types of memory disorders
Normal aging might cause age-related memory deterioration, whereas moderate cognitive impairment could indicate preclinical dementia. Alzheimer's disease first affects episodic memory, whereas frontotemporal dementia impairs semantic memory and Lewy's body dementia impairs working memory.
Dementia is a condition marked by cognitive impairment in memory as well as at least one other area, such as personality, praxis, abstract thinking, language, executive functioning, complex attention, social, and visuospatial abilities. Aside from the observed decrease, the severity must be severe enough to interfere with everyday functioning. It is frequently a gradual condition, and sufferers frequently lack awareness of their impairments.
There is currently no cure for any of the causes of dementia. With better results from illnesses like cancer and a longer lifetime, the incidence and prevalence of dementia are predicted to rise further. Dementia affects 47 million people worldwide now, and the figure is anticipated to quadruple by 2050.
Dementia is a severe public health burden that dramatically raises healthcare expenses for both individuals and society. Individual lifetime care costs for a person with dementia were about $200,000 more than for a person without dementia. The cost of treating dementia in the United States was estimated to be about $200 billion in 2010.
Alzheimer's disease (AD) is the most frequent cause of dementia, accounting for 70 to 80 percent of all dementia cases. It might happen on its own or as a result of a family history.
Vascular dementia (VD) accounts for between 5% and 10% of all dementia cases. Its prevalence rises with age and doubles every five years. Hypercholesterolemia, diabetes, hypertension, and smoking are all risk factors for vascular dementia. Lewy body dementia (LBD) accounts for 5% to 10% of all dementia cases. Because the diagnosis of Lewy boy dementia is frequently overlooked, the epidemiological statistics may not be totally reliable.
Frontotemporal dementia (FTD) is the second most prevalent form of dementia in those under the age of 65. Frontotemporal dementia accounts for 25% of all dementia cases in adults over the age of 65. However, there are several limitations in frontotemporal dementia epidemiological research.
Creutzfeldt-Jakob disease (CJD) is extremely uncommon, affecting around one in a million people. Mixed dementia occurs when a patient has more than one kind of dementia. The most prevalent coexisting dementias in this scenario are AD with LBD or vascular dementia.
Dementia is caused by several illnesses. Alzheimer's disease (AD) is the most prevalent cause of dementia, accounting for over 70% of cases. Other prevalent causes of dementia include vascular dementia, Lewy body dementia (DLB), frontotemporal dementia (FTD), and Parkinson disease dementia (PDD). Huntington disease (HD), cortical basal degeneration (CBD), progressive supranuclear palsy (PBP), multisystem atrophy (MSA), and Creutzfeldt-Jakob disease are among the disorders that cause less incidences of dementia (CJD).
Alzheimer's disease is caused by the buildup of neurofibrillary tangles and senile plaques in the brain. Vascular dementia develops as a result of ischemic brain damage. Frontotemporal dementia is a condition caused by different mutations that result in the accumulation of tau protein and other proteins in the brain's grey and white matter. The aberrant aggregation of the synaptic protein lpha-synuclein in the brain causes Lewy body dementia.
The pathogenesis of dementia is not well understood. Except for vascular dementia, the majority of dementias are caused by a buildup of endogenous proteins in the brain.
Memory disorders can be caused by one or more factors, including:
- substance abuse
- heredity (inheriting genes associated with Alzheimer’s or Huntington’s disease)
- narrowing of the arteries that provide blood flow to the brain
- cardiovascular disease
- untreated infectious or metabolic disease
- brain tumors
- vitamin deficiencies.
Some memory impairments emerge quickly, while others may be present for years before symptoms manifest. A knowledgeable neurologist can assist in determining whether the evolution of a memory problem may be delayed or even reversed.
Alzheimer's disease is characterized by extensive cortical atrophy and the accumulation of amyloid plaques and tangles of hyperphosphorylated tau protein in neurons, which contribute to their destruction. The intracellular deposition of Lewy bodies (insoluble clumps of alpha-synuclein) in neurons, primarily in the cortex, characterizes Lewy body dementia.
The patient's and their family members' histories must be gathered. Patients may exhibit symptoms such as behavioral changes, getting lost in familiar neighborhoods, memory loss, mood changes, aggression, social withdrawal, self-neglect, cognitive difficulty, personality changes, difficulty performing tasks, forgetfulness, communication difficulties, vulnerability to infections, loss of independence, and so on. A thorough history should include previous medical, familial, drug, and alcohol histories.
In addition to symptoms of dementia, the following atypical symptoms may be seen in the following conditions:
- LBD patients may exhibit symptoms including as well-formed visual hallucinations, delusions, sleep difficulties, and difficulty processing visual information.
- Symptoms of CJD include muscular stiffness, twitches, muscle jerks, visual hallucinations, and double vision.
- Chorea, impatience, and obsessive-compulsive behavior are all characteristics of Huntington disease.
- Symptoms of instability, headache, sensory abnormalities, and speech problems may be present in people with vascular dementia.
- Patients with FTD may exhibit behavioral abnormalities, difficulty with spatial orientation, and communication impairments.
- Parkinsonism signs such as garbled speech, delayed movement, and tremors may be noticed in persons with PDD. Visual hallucinations and delusions may also be observed, particularly in the late stages.
Only at autopsy can a clear identification of the form of dementia be made. A patient's clinical history is a very crucial element of evaluating a dementia sufferer. Laboratory tests must be performed as part of the work-up to rule out treatable causes of cognitive impairment.
A thorough physical and neurological evaluation is required. All cognitive domains must be evaluated. The Mini-mental Status Examination (MMSE) can be used to assess attention, orientation, language, memory, and visuospatial abilities. The MMSE is not a dementia diagnostic test and cannot distinguish between dementia and other curable causes of dementia.
Complete blood count, urinalysis, metabolic panel, B12, folic acid, thyroid function tests, and serological testing for syphilis are all laboratory tests that should be considered in all dementia patients. Erythrocyte sedimentation rate, electroencephalography (EEG), magnetic resonance imaging (MRI) of the brain, lumbar puncture, heavy metal screen, ceruloplasmin levels, Lyme disease titer, human immunodeficiency virus (HIV) screening, serum protein electrophoresis, and other tests should be considered when symptoms are atypical for Alzheimer dementia.
Formal cognitive testing can aid in the diagnosis and social decision-making as the disease progresses. These have a high degree of sensitivity and specificity. They can aid in determining the level and severity of cognitive and behavioral deficits. They can assist in distinguishing normal aging from moderate cognitive impairment and determining the kind of dementia.
PET, SPECT, and fMRI functional brain imaging can aid in the early diagnosis and monitoring of individuals with dementia, particularly Alzheimer's disease. These can also aid in determining the origin of dementia. These are costly, and their frequent usage in clinical practice is not recommended.
Cholinesterase inhibitors and memantine are two FDA-approved medicines for improving cognitive function. Donepezil, galantamine, and rivastigmine are cholinesterase inhibitors. Cholinesterase inhibitors prevent the breakdown of acetylcholine and can slow or prevent symptoms from worsening.
Memantine is an NMDA antagonist that reduces glutamine activity. Donepezil is licensed for all stages of Alzheimer's disease, galantamine and rivastigmine for mild to moderate Alzheimer's disease, and memantine for moderate to severe Alzheimer's disease.
Irritability, anxiety, and sadness are examples of behavioral symptoms. These symptoms can be alleviated by antidepressants such as SSRIs, antipsychotics, and anxiolytics. Non-drug techniques to symptom treatment, including as supportive care, memory training, physical exercise programs, and mental and social stimulation, must also be used.
Treatment of sleep complaints in dementia patients must be a top priority. Amitriptyline, lorazepam, zolpidem, temazepam, quetiapine, and more medications are available. Non-drug therapies include regular exercise, light therapy, a consistent sleep schedule, avoiding coffee and alcohol, pain management, biofeedback, and multicomponent cognitive-behavioral therapy.
Many additional medications, including as anti-tau protein agents, are still being researched. So yet, these have not yielded encouraging outcomes. Patients and their families should get information about the condition and its effects. They should be given all of the essential information about what to expect and how to react to it. Patients and their families should also be encouraged to seek social service consultations and to join support organizations such as the Alzheimer's Association. Driving restrictions may be necessary.
- Drug use
- Normal age-associated memory changes
- Mild cognitive impairment
- Structural brain abnormalities like subdural hematoma, brain tumor, and normal pressure hydrocephalus
- Infections like HIV, neurosyphilis
- Thiamine deficiency
- Vitamin B12 deficiency
- Folic acid deficiency
- Thyroid disorders
- Metabolic abnormalities and derangements
- Vitamin E deficiency
Dementia has a terrible prognosis. Dementia is frequently a progressive disease with no cure or therapy. The 1-year death rate was 30-40%, whereas the 5-year mortality rate was 60-65%. Men were more at danger than women. The mortality rate among hospitalized dementia patients was greater than that of those with cardiovascular disorders.
Dementia can affect many body systems and can lead to the following complications:
- Inadequate nutrition
- Inability to perform self-care tasks
- Personal safety challenges
- Fractures due to falls
- Hallucinations and delusions
- Personality changes
Alzheimer's disease is a kind of dementia that impairs memory, thinking, and behavior. Eventually, the symptoms become severe enough to interfere with daily activities.
Alzheimer's disease is not a natural component of the aging process. The most significant known risk factor is growing age, and the majority of Alzheimer's patients are 65 and older. Alzheimer's disease is called younger-onset Alzheimer's if it strikes someone under the age of 65. Younger-onset Alzheimer's disease is also known as early-onset Alzheimer's disease. People who get Alzheimer's disease at a younger age might be in the early, medium, or late stages of the disease.
Alzheimer's disease symptoms vary depending on the stage of the disease. Alzheimer's disease is categorized into three stages based on the degree of cognitive impairment: preclinical or presymptomatic, mild, and dementia-stage. These phases do not correspond to the DSM-5 categorization of Alzheimer's disease. The earliest and most frequent presenting symptom is episodic short-term memory loss with relative sparing of long-term memory, which may be evoked in the majority of patients even if it is not the presenting symptom.
Impaired short-term memory is followed by impaired problem-solving, judgment, executive functioning, lack of motivation, and disorganization, resulting in difficulties with multitasking and abstract thinking. Executive functioning impairment ranges from modest to substantial in the early stages. This is followed by a language dysfunction and a loss of visuospatial abilities. In the mid to late stages, neuropsychiatric symptoms such as apathy, social isolation, disinhibition, agitation, psychosis, and wandering are also prevalent.
Late in the disease, difficulty executing learned motor tasks (dyspraxia), olfactory dysfunction, sleep difficulties, and extrapyramidal motor indications such as dystonia, akathisia, and parkinsonian symptoms appear. Following this come rudimentary reflexes, incontinence, and absolute reliance on caretakers.
Diagnosis of Alzheimer's disease
Routine laboratory testing reveal no abnormalities. To rule out other reasons, a complete blood count (CBC), complete metabolic panel (CMP), thyroid-stimulating hormone (TSH), and B12 are routinely performed.
The third ventricle has expanded and cerebral atrophy is visible on a CT scan of the brain. It is suggestive, but it is not specific because similar anomalies are also found in other disorders and in persons who are experiencing typical aging changes. The measurement of cerebrospinal fluid (CSF) for low beta-amyloid 42 and increased tau is useful in determining the preclinical stage.
The EEG often demonstrates a broad slowing with no specific characteristics. It is diagnostically useful but not specific. Neuropsychological testing is the most accurate tool for detecting moderate cognitive impairment in early illness.
Volumetric MRI has recently been utilized to precisely assess volumetric changes in the brain. Volumetric MRI reveals shrinkage in the medial temporal lobe in Alzheimer's disease. However, because hippocampal shrinkage is also associated with normal age-related memory impairment, the efficacy of volumetric MRI for early diagnosis of Alzheimer's disease is dubious. Volumetric MRI has yet to be shown as a useful tool in the diagnosis of Alzheimer's disease.
PET, fMRI, and SPECT functional brain imaging methods are being utilized to identify patterns of dysfunction in smaller brain regions in the medial temporal and parietal lobes. These investigations may be useful in early identification and monitoring clinical courses; nevertheless, their relevance in Alzheimer's disease diagnosis is not entirely proven.
Recently, advances in brain imaging methods have been made to identify the fundamental histological hallmarks of Alzheimer's disease, which are amyloid plaques and neurofibrillary tangles. The usefulness of these strategies is currently being researched. In most cases, genetic testing is not suggested for Alzheimer's disease. It is occasionally used in families with rare early-onset Alzheimer's disease.
It is critical to recognize that, despite a strong clinical history, physical examination, and appropriate tests, identifying the kind of dementia with absolute confidence may not be achievable. Some individuals will complain of cognitive impairment that can be objectively validated, but is not severe enough to limit daily activities and so does not fulfill dementia criteria, and is commonly classed as moderate cognitive impairment. However, in 5 to 7 years, a considerable proportion of persons with moderate cognitive impairment will acquire dementia of some kind.
Alzheimer's disease has no known cure. There is just symptomatic therapy available. For the treatment of Alzheimer's disease, two types of medications have been approved: cholinesterase inhibitors and partial N-methyl D-aspartate (NMDA) antagonists.
- Cholinesterase Inhibitors
Cholinesterase inhibitors work by raising the amount of acetylcholine in the body, which is a neurotransmitter utilized by nerve cells to communicate with one another and is essential for learning, memory, and cognitive functioning. Three medications in this category are FDA-approved for the treatment of Alzheimer's disease: donepezil, rivastigmine, and galantamine.
Donepezil is effective at all stages of Alzheimer's disease. Galantamine and rivastigmine are licensed for use in the treatment of MCI and dementia. Donepezil and galantamine are acetylcholinesterase inhibitors that act quickly and are reversible. Rivastigmine is a slow, reversible acetylcholinesterase and butyrylcholinesterase inhibitor. Because of its once-daily dose, donepezil is frequently favored above the others.
Galantamine comes in the form of a twice-daily pill or a once-daily extended-release capsule. It is not appropriate for patients with end-stage renal disease or severe liver impairment. Rivastigmine comes in both oral and transdermal forms. Cholinesterase inhibitors' most frequent adverse effects are gastrointestinal-like nausea, vomiting, and diarrhea. With donepezil, sleep problems are more prevalent. Bradycardia, cardiac conduction problems, and syncope can develop as a result of elevated vagal tone, and these drugs are contraindicated in individuals with severe cardiac conduction abnormalities.
- Partial N-Methyl D-Aspartate (NMDA) Memantine
Memantine, a partial NMDA receptor antagonist, inhibits NMDA receptors and decreases intracellular calcium buildup. The FDA has authorized it for the treatment of moderate to severe Alzheimer's disease. Common adverse effects include dizziness, body pains, headaches, and constipation. It can be used with cholinesterase inhibitors.
It is also critical to treat anxiety, sadness, and psychosis, all of which are common in the middle to late stages of Alzheimer's disease. Because of their anticholinergic action, tricyclic antidepressants should be avoided. Antipsychotics are only used for acute agitation if the patient or caregiver has exhausted all other options. Their limited advantages, however, should be balanced against the slight risk of stroke and mortality.
Environmental and behavioral techniques are extremely useful in dealing with behavioral issues. Maintaining a familiar setting, checking personal comfort, giving security items, redirecting attention, eliminating doorknobs, and avoiding confrontation are all simple measures that may be extremely useful in controlling behavioral disorders.
Mild sleep disruptions can be alleviated to lessen caregiver strain by offering exposure to sunshine and daytime activity.
The treatment's projected advantages are limited. If there are no meaningful benefits or if the adverse effects are unacceptable, treatment should be discontinued or changed. Aerobic exercise on a regular basis has been shown to slow the progression of Alzheimer's disease.
Memory problems arise when injury to certain regions of the brain impairs or limits the capacity to store, maintain, or recall memories. Memory impairments also have an influence on cognitive abilities and social behaviors, impacting language, problem-solving skills, and the capacity to do simple activities. They might be moderate to severe, gradual to instantaneous.
Dementia is a broad word that refers to a decrease in cognitive abilities severe enough to impede with daily activities. Alzheimer's disease (AD) is the most prevalent kind of dementia, accounting for at least two-thirds of dementia cases in persons aged 65 and over. Alzheimer's disease is a neurological illness that causes gradual decline in behavioral and cognitive capabilities such as memory, understanding, language, attention, reasoning, and judgment.