Normal ageing of the nervous system is the most common cognitive changes after the age of 40 years. Particularly vulnerable is the retention of memory, capacity of executive skills and divergent thinking such as short term memory use, retention/recall of information after 30 minutes and multitasking.
Alzheimer’s Dementia is the leading cause of dementia, especially in the population of 70 years and older. It has an insidious onset, prominently memory impairment with progressive degenerative disorder that leads to rapid forgetfulness, diminished executive skills, impaired semantic fluency and naming of people, things and objects it also impairs the visual perceptual analysis.
Lewy Body Dementia, although rare, varies from Alzheimer’s by the presentation of mental illness symptoms like visual hallucinations, may not demonstrate excessive memory impairment in the beginning; signs of Parkinsonism like symptoms may lead to falls resulting from orthostatic hypotension. This type of dementia is distinguished by its unique set of presenting symptoms of not only mental illness and cognitive defects but the neurological examination identifies rigidity, bradykinesia, strange postural changes and possible persistent grunting.
Pick’s Dementia is even rarer as it is often only diagnosed at post-mortem with the variable difference due to the site of change/damage within the frontal lobe. The first signs may have nothing to do with the loss of memory, but the loss of executive functions, change in personality, may have the ability to follow instructions but unable to motivate or work out for themselves what needs to be done.
Vascular Dementia profiles differ in many respects from other types of dementia due to, in some cases, an absence of profound memory impairment. The presentation varies according to the extent of the vascular damage in either physical or psychological function i.e. direct trauma, multi infarction, stroke, TIA, micro-vascular disease, cerebral hypo-perfusion, haemorrhage or any combination. In this type of dementia the individual does not always display major loss of memory, and in time it can dramatically improve depending on the damage and the recovery programme engaged. This suggests that the primary difficulty is in the retrieval rather than in the storage or consolidation of new information.
Other diseases that develop dementia are; Parkinson’s, Huntington’s Progressive Supranuclear gaze palsy, Hydrocephalus, and Creutzfeldt-Jakob Diseases. All of the examples have cognitive syndromes and characteristics that provide a neuropsychological profile that defines each diseases and type of dementia.
One of the predominant symptoms in the early onset of dementia is a level of depression, but at the same time it could be the depression symptoms which may appear as a dementia. Depression could in its self be the predominate driver or at the same time mask other symptoms that could be progressing dementia characteristics of memory loss, anxiety, panic and behaviours associated with dementia. The role that depression might play needs to be clearly evaluated as it can result in serious mood changes with disabling cognitive impairment or what has become known as the ‘dementia of depression’ or “pseudo-dementia”. Depression also frequently co-occurs in the context of arrange of medical disorders and often complicates the diagnosis and can exacerbate the functional loss associated with each disorder on its own or in combination especially in the older person. Previous drug abuse, alcohol or illicit or a combination of each could have dramatic affect on cognitive ability in prolonged use into older adults, the other area of concern is in some people the loss of memory after a general anaesthetics.
Many treatments for depression are successful in improving cognitive impairments, but not all. Those who respond poorly to oral medication, who are treatment intolerant, or the concerns of the interaction with concurrent treatments may benefit from Electroconvulsive Therapy (ECT). Improvements in anaesthetics and the ability to titrate levels of the current, in some cases the frail elderly can achieve better outcomes than younger service users.
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Korsakoff syndrome; Alcohol Related Dementia
Heavy alcohol use (is indicated when the liver does not have time to remove the alcohol from body before the next period of drinking) can interfere with the breakdown of thiamine (B1) even if an individual maintains a well-balanced diet, as most of the thiamine is not absorbed. When the deficiency reduces to a certain level the individual may well develop Wernicke encephalopathy and when memory is affected can develop Korsakoff syndrome. The age of onset for developing Wernicke-Korsakoff syndrome can be at any age following many years of alcohol abuse could be as young as young 25 – 30 years of age this is unusual, but it is common in people in their early 40’s. Wernicke-Korsakoff syndrome is seen in about 4 to 1 males to females.
Thiamine deficiency (vitamin B1): Thiamine deficiency can be found within two neurological disorders, beriberi and Wernicke-Korsakoff syndrome. Beriberi is caused by lack of dietary thiamine and can cause myocardial failure where Wernicke-Korsakoff syndrome is defined by an acute encephalopathy manly due to alcohol abuse, which causes cognitive impairment effecting impairment of short-term memory being stored into long term memory. Wernicke-Korsakoff syndrome is most commonly observed in people with chronic alcohol abuse suggesting that it affect the systems of absorption of nutrients from the digestive system. This has also been seen in people with eating disorders who are malnourished with dietary deficiencies also brain trauma or stroke causing neurological damage from a lack of oxygen to the brain, prolonged vomiting, starvation, uraemia that builds up toxins from the waste in the urine, prolonged kidney dialysis, prolonged intravenous therapy, gastric bypass or stapling, and has been reported by sufferers of tuberculosis, other drug abuse and side-effects of chemotherapy medications have also been indicated.
Thiamine is used in the production of connections necessary for neurons function, poor levels of thiamine can lead to damage or death of neurons in different regions of the brain, particularly the thalamus and the mammillary bodies, this disrupts the formation and storage of memories. Damage to the nervous system in the brain and spinal cord and the peripheral (external) systems throughout the body may be caused by alcohol withdrawal.
Signs and Symptoms at the beginning of Thiamine deficiency the symptoms are nonspecific and are difficult to differentiate, they may include fatigue, irritability, poor memory, sleep disturbances, pericardial (heart) pain, anorexia, and a range of non-specific discomfort. Other defining symptoms of encephalopathy are mental confusion, eye twitching, poor balance and lack of coordination. Symptoms may resemble the effects of severe alcohol intoxication but on carrying out a blood alcohol test found to be negative. In the acute phase treatment with thiamine will help some individuals to recover without memory deficits, particularly if they are treated quickly. The untreated phase or chronic stage is called Korsakoff syndrome and is distinguished by no recovery and persistent anterograde amnesia where the individual cannot transfer new memories into long-term memories. Untreated individuals with Wernicke’s encephalopathy nearly always will develop this severe memory disorder, which affects all aspects of life and relationships especially those that need executive decisions. Symptoms of Korsakoff syndrome has been reported to spontaneously develop in persons who have not suffered Wernicke’s encephalopathy this thought to come about due to long term use of alcohol on a daily bases over many years (20 or more). Once patients develop Korsakoff amnesia, full recovery is unlikely, but when treated in a specialist unit a reasonable quality of life may be able to be reached. In some persons with Korsakoff syndrome suffer retrograde amnesia with memory loss of past events in addition to anterograde amnesia, with most being able to recall most long term memories of the distant past.
Short term memory up to a few minutes may not affected and can repeat a sequence of numbers or objects soon after hearing them, but will be forgotten 10 to 20 minutes later. Because immediate memory remains intact in individuals can interact with others, respond to questions, and function within small groups and follow simple instructions but often confabulate during discussions by making up stories to compensate for an inability to remember often confusing the past and present.
Individuals may also show signs of indifference with what is going on around them and have poor insight or emotional response. Self-harm, is unlikely although part of their delirium may injure them self. This sudden confusion due to changes in brain function can be associated with hallucinations and hyperactivity, which does not respond to normal interaction. Individuals going through detoxification will start with a varying degree of withdrawal, in long term abusers you may see delirium tremens (DTs) with very vivid hallucinations or epileptic fits, withdraws may include sweats, tremors, irritability, confusion, stupor, and depersonalised episodes.
Diagnosis Wernicke’s encephalopathy is suspected when individuals seeking medical attention present with signs of mental confusion, eye movement (nystagmus) disorders, and lack of coordination. It will have thought to become Korsakoff syndrome when there is loss of memory of present events, a history of long-term heavy drinking, or possibility of malnutrition could suggest a diagnosis of Korsakoff syndrome. When Korsakoff follows a previous diagnosis of Wernicke’s it would be appropriate to have the diagnosis of Wernicke-Korsakoff syndrome. The diagnosis can be confirmed by neuro-imaging (brain imaging) or an autopsy after death with findings that show degeneration of parts of the brain including the thalamus and mammillary bodies, along with loss of brain volume in the area surrounding the fourth ventricle (a fluid-filled cavity near the brainstem).
Mental status: Mental status changes are commonly present and appear in various forms from being withdrawn to presenting with major challenging behaviour. Memory impairment will significantly inhibit an individual’s ability to perform normal activities and functions and present as a decline from a previous level of testing and can affect executive functions where individuals capacity to make decisions for themselves, even at the simple level very difficult. It is not unusual once the memory has been affected for the individual to feel that everyone has gang up on him/her because of the loss of memory live in a world of the past capabilities which are now not possible especially around their ability to drink alcohol. Will often not understand why they end up in a mental health institution due to the individual’s behaviour while intoxicated by alcohol. This will/can end up with repeated challenging behaviour.
Physical Condition: Physical examination of the nervous/muscular systems may show decreased reflexes and impaired gait and coordination. Muscles may be weak and may show atrophy (loss of tissue mass). Examination of the eyes may show abnormalities of eye movement. Blood pressure and body temperature measurement may be low. Pulse (heart rate) may be rapid. Vertical and horizontal nystagmus that cause involuntary eye movements, ptosis causing drooping eyelids, weakness or paralysis of muscles in the eye, non-reacting miotic causing constricted pupils, or complete loss of ocular movements in degenerative cases.
Blood Tests: Blood tests used to check an individual’s nutrition status include serum B1 (thiamine) levels, along with liver function. Blood or urine alcohol levels and liver enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), are usually tested and may be high if the individual has a history of chronic (long-term) alcohol abuse. Blood tests may include electrolytes (including sodium, potassium, and chloride).
Blood tests may also be done to rule out other chronic conditions that may cause thiamine deficiency including acquired immunodeficiency syndrome (AIDS), hyperemesis gravidarum (continuous nausea and vomiting during pregnancy), thyrotoxicosis (very high thyroid hormone levels), cancers that have metastasized (spread), long-term dialysis in kidney problems, and congestive heart failure (CHF, or the inability of the heart to pump the blood) when treated with long-term diuretic therapy.
Neuro-Imaging: Computerized tomography (CT) scans may help in rapid assessment to rule out haemorrhaging, oedema (swelling), and sub-acute stroke (neurological damage due to lack of oxygen to the brain). A brain magnetic resonance imaging (MRI) study rarely shows changes in the tissue of the brain indicating Wernicke-Korsakoff syndrome. However, MRIs can detect acute lesions of Wernicke-Korsakoff syndrome in regions of the brain.
Poor Diet/Malnutrition: Eating processed foods (such as packaged meats and canned foods), food that contains too many refined carbohydrates (such as white breads, sweets, and other foods containing refined sugars), and white rice can cause thiamine deficiencies. Thiamine deficiency may result in the development of Wernicke-Korsakoff syndrome, although this is now rare and is caused mostly by alcohol abuse. Most developed nations add thiamine to some foods, such as flour and white rice.