277
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
Volume-5, Issue-2, April-2015
International Journal of Engineering and Management Research
Page Number: 277-285
Risk Level Classification Dementia or Determination of Dementia via
Chaos Technique
Jagrati Srivastava1, Pradeep Tomar2
1,2
Department of Computer Science & Engineering, School of Information and Communication Technology, Gautam Buddha University, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, INDIA
ABSTRACT
This paper aim to classify and determine Dementia which is a collective term used to describe the problems that people with various underlying brain disorders or damage can have with their memory, language
and thinking.is the best known and
most common disorder under the umbrella of dementia. It measure brain function in the hope of determining and differentiating certain functional conditions of the brain. It is used in patients with cognitive dysfunction involving either a general decline of overall brain function or a
localized or lateralized deficit. The raw EEG signals are
sampled and parameter like energy, variance, peaks, sharp and spikes waves, duration, events and covariance are detected. In this classification it provides a better way to diagnosis dementia patients. It also aims to safeguard the
patient’s life during the critical situations.The aim of this
work is to investigate possible metabolic impairment as dementia results from brain damage. The causes include the following; Alzheimer’s Disease, Stroke, Pick’s disease, Huntington’s, Down’s Syndrome, Creutzfeldt-Jacob, AIDS, alcoholism, Parkinson’s disease and other neurodegenerations using Chaos-Voxel.
I.
INTRODUCTION
Histories of dementia commence with Alzheimer's description in 1906 of the first case of Alzheimer's disease, yet the history of dementia before 1906 is quite rich, dating back to the ancient Greek and Roman philosophers and physicians. Over the 2500 years since ancient times, the concept of dementia has evolved from a rather vague notion that mental decline occurred inevitably in old age, to become defined today by a distinct set of clinical and pathological features with the potential for treatment and prevention within grasp. Throughout history, many elderly individuals with unpredictable, and the line between mental disorders and dementia were hazy at best. The identification of Alzheimer's disease at the onset of the 20th century was a turning point for the understanding of dementia, and the concepts and Voxel.
Histological findings presented by the early researchers of Alzheimer's disease remain relevant still
today. Indeed, these early findings are proving to be a continuing source of insight, as many of the issues debated at the turn of the century remain unresolved still today. This paper thus traces the history of the evolution of our current conceptualization of dementia. Alzheimer's disease (AD), also known as Alzheimer disease, or just Alzheimer's, accounts for 60% to 70% of cases of
The uncovering of dementia which includes visual scan of EEG recordings for the spikes and seizures. These seizures are generated due to some drugs side-effects. This sometimes happens due to ageing due to hereditary irregularities, development anomalies’ and febrile convulsion. In some patients these seizures happens more than 100 times a day. Autopsy and craniotomy are no longer to demonstrate the useful correlates of useful deficits. In 20
disease that usually starts slowly and gets worse over time. The most common early symptom is difficulty in remembering recent events
Electroencephalogram (EEG) contains set of potential differences developed as a result of volume of currents from active tissue (neural) throughout the conductive media of the brain. The measurements can be either by placing special intracranial electrodes or using sensors. Due to large number of patients, it is impossibly lengthy task to treat every patient. So there is need of new technology which should be sensitive and generate every false alarm so neurologist can easily discard them. The purpose of the proposed system does not mean to replace neurologist but it is to lessen the burden and remove the time consumption. This can help us to lessen the percentage of population highly and rapidly. This false alarm feature can lessen the burden on neurologist and can handle the right seizure and can do treatment by either giving drug or through neuro-stimulation. The neuro-stimulation and drug delivery are better than antiepileptic drugs as in seizure patient cannot push the alarm by own.
th
278
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
mechanisms causing ischaemia or haemorrhage secondary to cerebrovasculardisease (multiple infarcts, single strategic infarct or small vessel disease.) Increasingly the term vascular cognitive impairment (VCI) is used to encompass the spectrum of deficit, in which VaD is the most severe form of disease. VaD is the second most common form of dementia in the West after Alzheimer’s disease. It is the most common form in some parts of Asia. Incidence increases with age. VaD is thought to account for around 17% of dementia in UK. Prevalence of dementia following first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia.
Presence of dementia-cognitive decline from higher level of functioning. This can be demonstrated as memory loss plus impairment in two or more different cognitive domains. It is established by clinical examination and neuropsychological testing using EEG signals. Deficits should be severe enough to interfere with activities of daily living-not secondary effects of the cerebrovascular event alone. Cerebrovascular disease, defined by the presence of signs on neurological examination and/or by brain imaging.
A. General Technique
During the final stages, the patient is completely dependent upon caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy an symptoms. People with Alzheimer's disease, Alzheimer disease or just Alzheimer's, accounts for 60% to 70% of cases of even the simplest tasks independently; mobility deteriorate to the point where they are bedridden and unable to feed themselves. The cause of death is usually an external factor, such as infection of
pressure or. Many
algorithms are designed to detect these stages using EEG signals. McSharry et.al introduced an algorithm using multidimensional probability but it provides less false alarms compared to variance. Many time-frequency analysis techniques have been devising such as smoothed pseudo- Winger- Ville and reduced interference are used in conjunction with an artificial neural network. This method has great accuracy in finding the seizure. However, Chaos is tricky thing to define.
B. Development of EEG Biomarkers for Alzheimer’s disease
A growing body of evidence suggests that EEG analyses, including both resting state and event-related stimulation protocols, may be useful in early detection of neural signatures of dementia. Moreover, EEG-based analysis shows potential for discriminating across dementia sub-types, including Alzheimer’s (AD), Mild
Cognitive Impairment (MCI), Vascular dementias, and the Lewy Body Dementias (LBD) – including Parkinson’s disease with Dementia (PDD) [1-6]. Although these approaches have been largely confined to university research investigations, if proven accurate, reliable, and scalable, the widespread use of EEG as a neuro imaging modality could provide an inexpensive, easy to implement alternative for early diagnosis and treatment outcome studies of the dementias.
Promising EEG biomarkers include: 1) increased power in the low frequency bands (i.e., theta, delta) with reductions in higher frequency bands (i.e., beta, gamma) [7, 8]; 2) changes in the amplitude and latency of evoked potentials for both cognitive (i.e., attention, memory, learning) and sensory stimuli (i.e., visual, auditory, somatosensory) [9-13]; 3) reduction in the complexity of the EEG dynamics assessed with non-linear analyses (e.g., entropy, Grainger causality) [14]; and 4) abnormal functional connectivity as assessed by coherence, phase, and source localization (e.g., LORETA) analyses.
C. Single Voxel Technique
This technique uses fixed amount of tissues as unified signal to gain single spectrum. The volume of Voxel ranges between 2-8 ml in proton in proton MRS. For prolix process 8cm3 Voxel is used. Voxel must be positioned from basis of susceptibility, relics and lipids. The limitation of this technique is anatomic coverage and assessment of single area only during acquisition. So positioning of Voxel is must. The fundamental single Voxel localisation is to use three orthogonal slice selective pulses equally and enterprise the pulse sequence to collect only the echo signal from the Voxel in space where all three shares intersect. The two sequences generally used are called Stimulated Echo Acquisition Mode (STEAM) and Point Resolved Spectroscopy (PRESS). Three 90 degree pulsations are used and stirred echo is serene in STEAM. All other signals should be dephrased by the large implement gradient applied during the so called mixing time. While in PRESS, second and third are changed by 180 degree and crusher gradient is applied across the pulses to select the desired spin echo sign arising from all three frequencies.
1) Main Characteristics of STEAM
It is cooler to produce a 900 pulse with a shrill slice profile than a 1800 pulse. There is incomplete recapture of signal.
A precise volume Voxel is formed. It can be formed with very short echo times
2) Main Characteristics of PRESS
Rather better signal to noise ratio because the motivated echo is formed from only half the available equilibrium magnetization.
279
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
II.
CARE FOR PATIENTS WITH
ADVANCED DEMENTIA AND EATING
PROBLEM
Problem with eating, swallowing, and poor caloric intake are common in patients with advanced dementia and often develop during an acute medical event when the immediate prognosis is unclear. For health care professionals, managing the patient with advanced dementia and swallowing problems and guiding caregivers through a process of decision making present enormous clinical challenges and require an interdisciplinary approach in order to provide an optimal care. Careful observation of patient at bedside is required to evaluate level of consciousness, position in bed, level of comfort, presence of muscle entropy and contractions, presence of an oxygen mask or nasal cannula, and presence of mouth breathing. Attention to the state of dentition and oral hygiene is paramount, as pain from dental carries, poor oral hygiene and xerostomia can contribute to problem with eating. Assessing the patient’s level of consciousness is critical for detecting delirium, a common and reversibly cause of eating problems. When delirium is present, a workup is aimed in diagnosing and treating modifiable factor is indicated.
III.
CAUSES OF DEMENTIA
Dementia involves damage of nerve cells in the brain, which may occur in several areas of the brain. Dementia may affect people differently, depending on the area of the brain affected. Dementias can be classified in a variety of ways and are often grouped by what they have in common, such as what part of the brain is affected, or whether they worsen over time (progressive dementias). Some dementias, such as those caused by a reaction to medications or an infection, are reversible with treatment.
Progressive dementias, Types of dementias that are not reversible and worsen over time include:
• Alzheimer's disease. In people age 65 and older, Alzheimer's disease is the most common cause of dementia. People generally may develop symptoms after age 60, but some people may have early-onset forms of the disease, often as the result of a defective gene. Although in most cases the exact cause of Alzheimer's disease isn't known, plaques and tangles are often found in the brains of people with Alzheimer's. Plaques are clumps of a protein called beta-amyloidal, and tangles are fibrous tangles made up of tau protein. Certain genetic factors also may make it more likely that people will develop Alzheimer's. Alzheimer's disease usually progresses slowly over about eight to 10 years. Your cognitive abilities slowly decline. Eventually, the affected areas of your brain don't work properly, including parts of your brain that control memory, language, judgment and spatial abilities.
• Vascular dementia. Vascular dementia, the second most common type of dementia, occurs as a result of brain damage due to reduced or blocked blood flow in blood vessels leading to your brain. Blood vessel problems may be caused by stroke, infection of a heart valve (endocarditic) or other blood vessel (vascular) conditions. Symptoms usually start suddenly and often occur in people with high blood pressure or people who have had strokes or heart attacks in the past. Several different types of vascular dementia exist, and the types have different causes and symptoms. Alzheimer's disease and other dementias also may be present at the same time as this dementia.
• Lewy body dementia. Lewy body dementia affects approximately 10 percent of people with dementia, making it one of the most common types of dementia. Lewy body dementia becomes more common with age. Lewy bodies are abnormal clumps of protein that have been found in the brains of people with Lewy body dementia, Alzheimer's disease and Parkinson's disease. Lewy body dementia symptoms are similar to symptoms of Alzheimer's disease. Its unique features include fluctuations between confusion and clear thinking (lucidity), visual hallucinations, and tremor and rigidity (parkinsonism).People with Lewy body dementia often have a condition called rapid eye movement (REM) sleep behavior disorder that involves acting out dreams.
• Front temporal dementia. This type of dementia tends to occur at a younger age than does Alzheimer's disease, generally between the ages of 50 and 70. This is a group of diseases characterized by the breakdown (degeneration) of nerve cells in the frontal and temporal lobes of the brain, the areas generally associated with personality, behaviour and language. Signs and symptoms of front temporal dementia can include inappropriate behaviours, language problems, difficulty with thinking and concentration, and movement problems. As with other dementias, the cause isn't known, although in some cases this dementia is related to certain genetic mutations.
IV.
DIAGNOSIS
280
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
different dementias can overlap. In some cases, a doctor may diagnose "dementia" and not specify a type. If this occurs it may be necessary to see a specialist such as a neurologist or gero-psychologist Alzheimer's disease accounts for up to 80 percent of all dementia cases. Diagnosis may be complicated by other forms of dementia that have symptoms and pathologies similar to Alzheimer's disease. Knowing the key features and pathology of each type of dementia can help in the
accurate diagnosis of patients, so they will receive the treatment and support services appropriate for their condition and maintain the highest possible quality of life. The following table identifies some of the clinical differences between the major dementias:
Diseas e
First Symptom Mental Status Neuropsychi
atry
Neurolog y
Imaging
AD Memory loss Episodic memory loss Initially
normal Initially normal Entorhinal cortex and hippocam pus atrophy
FTD Apathy: poor
judgement/insight/speech/language;hy perorality Frontal/executive,language ;spares drawing Apathy, disinhibition, hyperorality, euphoria, depression May have vertical gaze palsy, axial rigidity, dystonia, alien hand, or MND Frontal, insular, and/or temporal atrophy; spares posterior parietal lobe DLB Visual hallucinations, REM sleep
disorder,
Drawing and frontal/ executive; delirium, Capgras' syndrome,
parkinsonism
Visual hallucinations
, depression, spares memory; delirium
prone Parkinsoni sm sleep disorder, delusions Posterior parietal atrophy; hippocam pus larger than in AD
CJD Dementia, Variable,
frontal/ executive, mood, anxiety, movement disorders
Depression, anxiety
focal cortical, memory
Myoclonu s, rigidity, parkinsoni sm Cortical rib boning and basal ganglia or thalamus hyper intensity on diffusion/ FLAIR MRI Vascul ar
Often but not always sudden; variable; apathy, falls, focal weakness
Frontal/ executive, cognitive
Apathy,
slowing; can spare memory
delusions, Usually motor slowing, spasticity; can be Norma anxiety Cortical /or sub cortical infarctions .
V.
TREATMENT AND CARE
Dementia is not a specific disease. It's an overall term that describes a wide range of symptoms associated with a decline in memory or other thinking skills severe enough to reduce a person's ability to
perform everyday activities.
281
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
Treatment of dementia depends on its cause. In the case of most progressive dementias, including Alzheimer's disease, there is no cure and no treatment that slows or stops its progression. But there are drug treatments that may temporarily improve symptoms. The same the drugs sometimes prescribed to help with symptoms alleviate some symptoms of dementia. Ultimately, the path to effective new treatments for dementia is through increased research funding and increased participation in clinical studies. Right now, volunteers are urgently needed to participate in more than 180
Some risk factors for dementia, such as
about Alzheimer's and related dementias.
VI.
DEMENTIA RISK AND
PREVENTION
explore the impact of other risk factors on brain health and prevention of dementia. Some of the most active areas of research in risk reduction and prevention include cardiovascular factors, physical fitness, and diet.
Cardiovascular risk factors: Your brain is nourished by one of your body's richest networks of blood vessels. Anything that damages blood vessels anywhere in your body can damage blood vessels in your brain, depriving brain cells of vital food and oxygen. Blood vessel changes in the brain are linked to vascular dementia. They often are present along with changes caused by other types of dementia, including Alzheimer's disease and dementia with Lewy bodies. These changes may interact to cause faster decline or make impairments more severe. You can help protect your brain with some of the same strategies that protect your heart – don't smoke; take steps to keep your blood pressure, cholesterol and blood sugar within recommended limits; and maintain a healthy weight.
Physical exercise: Regular physical exercise may help lower the risk of some types of dementia. Evidence suggests exercise may directly benefit brain cells by increasing blood and oxygen flow to the brain.
Diet:
Data Acquisition and Pre-processing
The importance of EEG biomarkers in dementia clinical trials is increasingly recognized. As stated by the EMA guidelines:
What you eat may have its greatest impact on brain health through its effect on heart health. The best current evidence suggests that heart-healthy eating patterns, such as the Mediterranean diet, also may help protect the brain. A Mediterranean diet includes relatively little red meat and emphasizes whole grains, fruits and vegetables, fish and shellfish, and nuts, olive oil and other healthy fats.
VII. PROPOSED WORK
The EEG records of 347 patients data set has been taken from hospital Aligarh Muslim University, Aligarh, India who had been under treatment of Neurology.
- Energy in each epoch is given by the sum of all sample signals denoted by:𝐸𝐸=∑𝑛𝑛𝑖𝑖=1xi and total
is divided by 1024
"Ideally proof of a disease modifying effect would require demonstration of clinically relevant changes in key symptoms of the dementia syndrome and in addition supportive evidence for change in the underlying disease process based on biological markers, e.g. neuro imaging marker as serial EEG of the hippocampus region or whole brain, which are under validation." EEG data contain valuable information that can be used for patient selection and quantification of drug efficacy. By adding EEG biomarkers as an endpoint in the clinical trial, a claim for disease modification could be considered rather than just a limited claim, such as delay of disability. In this context, the use of advanced software is necessary, in order to obtain reliable and reproducible measurements of the brain.
In order to obtain reliable EEG biomarkers, it is of paramount importance that all steps in the process, from data acquisition and multi-centre EEG protocols until image analysis and reporting, are standardized. At ico Metrix, we have the experience in setting-up multi-centre EEG trials, harmonizing EEG protocols across scanner vendors, performing robust quality checks on all incoming images, and using reliable and validated software pipelines to obtain the biomarkers.
In this we have to take threshold value and plot the recurrence plot and also find following parameters
- The total number of positive and negative peaks are calculated which exceeds our threshold value. Threshold value is calculated as: r=0.5 - Spikes are detected when duration of very high
amplitude peaks in the EEG waveform between 5-10ms and sharp waves are between 15-20 ms. - Total number of spikes and sharp waves are
counted and stored as event
- Variance is computed as σ2
- The average duration is calculated as D=∑ 𝑡𝑡𝑖𝑖 𝑑𝑑 𝑖𝑖=1
𝑑𝑑 where d is number of duration and t
=∑ (𝑥𝑥𝑖𝑖−µ)2 𝑛𝑛 𝑛𝑛
𝑖𝑖=1 where
µ is average amplitude.
i is peak
282
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
C. Risk Level EstimationThe output of the chaos technique provides two risk levels i.e. risk level 1 and risk level 2. Since we are dealing with dementia patients so exact risk level cannot be found. So this can be done by automated system which can classify the risk level of patient being examined. The performance of this method is being given by: PI=𝑝𝑝−𝑚𝑚−𝑓𝑓
𝑝𝑝 𝑋𝑋 100%. Where p is perfect
classification and is given when physician and method both agrees; m is missed classification and is true negative of the machine to the physician. (I.e. complement values) and f is false alarm and is false positive of the machine in reference with the neurologist. Since the machine has to be sensitive. So its sensitivity can be calculated as S= 𝑝𝑝
𝑝𝑝+𝑓𝑓𝑥𝑥 100.
Based on anatomical EEG data sets, we are able to measure:
• Cortical thickness in the medial temporal lobe, frontal lobe, etc.
• Total brain volume,
• Total cerebrospinal fluid volume in the brain. • Hippocampal volume.
VIII. RESULT AND DISCUSSION
The output of three epochs for each patient is optimized at single level. The study of the performance is given by performance index and quality value. These are calculated for each set of patients and are to be compared. The performance index obtained by Common
Energy Level (determining and measuring accuracy) was 28% and for Chaos-Voxel it is 49%. EEG-based biomarkers show promise for utility in early detection of Alzheimer’s disease, notably:
• Frequency Bandwidths – significant decreases
in parietal/temporal alpha, and global sigma, beta
• Frequency Bandwidth Ratios – excessive
slowing in parietal and temporal regions
• Wavelet Analysis – significant increases in
slow wave activity over the sensor motor region. These findings support potential for EEG as an inexpensive, easily-implementable biomarker for AD.
A. Quality Value
Goal of this research was to get perfect classification of dementia patients and get fewer false alarms. This can be done by the calculating following parameters as follows
• Classification rate • Classification delay • False alarm rate
Quality value can be computed as follows
Fa is the false alarm rate; td is the delayed time; ppc is the
percentage of perfect classification and pms is the
percentage of missed classification. The value of constant C is set to be 10 for convenience. The higher the value of Qv better the method is.
283
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
As shown in table, The Risk Level is higher in this optimization technique also weighted delay is very less. Number or false alarm rate are also reduced by this technique. The quality value is highly increased. Hence it is more reliable than the previous technique.
IX.
CONCLUSION
This Chaos Voxel technique is very successful in determining and classifying the risk level. Almost negligible false alarm/set is calculated which leads neurologist’s burden much lower. This also has high performance index. The future research can be done on this chaos Voxel technique can rely this system accurately.
REFERENCES
[1] Rullier L, Lagarde A, Bouisson J, Bergua V, Torres M, Barberger-Gateau P. Psychosocial correlates of nutritional status of family caregivers of persons with dementia. Int Psychogeriatr 2014; 26: 105–113.
[2] Tsakos G, Herrick K, Sheiham A, Watt RG. Edentulism and fruit and vegetable intake in low-income adults. J Dent Res 2010; 89: 462–467.
[3] Yu YH, Kuo HK. Association between cognitive function and periodontal disease in older adults. J Am Geriatr Soc 2008; 56: 1693–1697.
[4] Gil-Montoya JA, Ponce G, Sanchez Lara I, Barrios R, Llodra JC, Bravo M. Association of the oral health impact profile with malnutrition risk in Spanish elders. Arch Gerontol Geriatr 2013; 57: 398–402.
[5] Furuta M, Komiya-Nonaka M, Akifusa S, Shimazaki Y, Adachi M, Kinoshita T, Kikutani T, Yamashita Y. Interrelationship of oral health status, swallowing function, nutritional status, and cognitive ability with activities of daily living in Japanese elderly people receiving home care services due to physical disabilities. Community Dent Oral Epidemiol 2013; 41: 173–181.
[6] Dion N, Cotart JL, Rabilloud M. Correction of nutrition test errors for more accurate quantification of the link between dental health and malnutrition. Nutrition 2007; 23: 301–307
[7] Cabre M, Serra-Prat M, Palomera E, Almirall J, Pallares R, Clave P. Prevalence and prognostic implications of
dysphagia in elderly patients with pneumonia. Age Ageing 2010; 39: 39– 45.
[8] Van der Maarel-Wierink CD, Meijers JM, De Visschere LM, de Baat C, Halfens RJ, Schols JM. Subjective dysphagia in older care home residents: A cross-sectional, multi-centre point prevalence measurement. Int J Nurs Stud 2014; 51: 875–881.
[9] Alagiakrishnan K, Bhanji RA, Kurian M. Evaluation and management of oropharyngeal dysphagia in different types of dementia: a systematic review. Arch Gerontol Geriatr 2013; 56: 1–9
[10] Sura L, Madhavan A, Carnaby G, Crary MA. Dysphagia in the elderly: management and nutritional considerations. Clin Interv Aging 2012; 7: 287–298.
[11] Vanderwee K, Clays E, Bocquaert I, Gobert M, Folens B, Defloor T. Malnutrition and associated factors in elderly hospital patients: a Belgian cross-sectional, multi-centre study. Clin Nutr 2010; 29: 469–476.
[12] McCaddon A. Vitamin B12 in neurology and ageing; clinical and genetic aspects. Biochimie 2013; 95: 1066– 1076.
[13] Inada M, Toyoshima M, Kameyama M. Cobalamin contents of the brains in some clinical and pathologic states. Int J Vitam Nutr Res 1982; 52: 423–429.
[14] Karnaze DS, Carmel R. Low serum cobalamin levels in primary degenerative dementia. Do some patients harbor atypical cobalamin deficiency states? Arch Intern Med 1987; 147: 429–431
[15] Regland B, Gottfries CG, Oreland L, Svennerholm L. Low B12 levels related to high activity of platelet MAO in patients with dementia disorders. A retrospective study. Acta Psychiatr Scand 1988; 78: 451–457.
[16] Renvall MJ, Spindler AA, Ramsdell JW, Paskvan M. Nutritional status of free-living Alzheimer’s patients. Am J Med Sci 1989; 298: 20–27
[17] Ikeda T, Furukawa Y, Mashimoto S, Takahashi K, Yamada M. Vitamin B12 levels in serum and cerebrospinal fluid of people with Alzheimer’s disease. Acta Psychiatr Scand 1990; 82: 327– 329.
[18] Nijst TQ, Wevers RA, Schoonderwaldt HC, Hommes OR, de Haan AF. Vitamin B12 and folate concentrations in serum and cerebrospinal fluid of neurological patients with special reference to multiple sclerosis and dementia. J Neurol Neurosurg Psychiatry 1990; 53: 951–954.
[19] Bottiglieri T, Godfrey P, Flynn T, Carney MW, Toone BK, Reynolds EH. Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine. J Neurol Neurosurg Psychiatry 1990; 53: 1096–1098.
[20] Joosten E, Lesaffre E, Riezler R, Ghekiere V, Dereymaeker L, Pelemans W, Dejaeger E. Is metabolic evidence for vitamin B-12 and folate deficiency more frequent in elderly patients with Alzheimer’s disease? J Gerontol A Biol Sci Med Sci 1997; 52: M76–M79.
[21] McCaddon A, Davies G, Hudson P, Tandy S, Cattell H. Total serum homocysteine in senile dementia of Alzheimer type. Int J Geriatr Psychiatry 1998; 13: 235–239.
284
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
homocysteine levels in confirmed Alzheimer disease. Arch Neurol 1998; 55: 1449– 1455
[23] Farkas M, Keskitalo S, Smith DE, Bain N, Semmler A, Ineichen B, Smulders Y, Blom H, Kulic L, Linnebank M. Hyperhomocysteinemia in Alzheimer’s disease: the hen and the egg? J Alzheimers Dis 2013; 33: 1097–1104.
[24] Hinterberger M, Fischer P. Folate and Alzheimer: when time matters. J Neural Transm 2013; 120: 211–224.
[25] Morris MS. The role of B vitamins in preventing and treating cognitive impairment and decline. Adv Nutr 2012; 3: 801–812
[26] Boucher BJ. The problems of vitamin D insufficiency in older people. Aging Dis 2012; 3: 313–329.
[27] Zhao Y, Sun Y, Ji HF, Shen L. Vitamin D levels in Alzheimer’s and Parkinson’s diseases: a meta-analysis. Nutrition 2013; 29: 828–832.
[28] Lu’o’ng KV, Nguyen LT. The role of vitamin D in Alzheimer’s disease: possible genetic and cell signaling mechanisms. Am J Alzheimers Dis Other Demen 2013; 28: 126–136.
[29] Lu’o’ng KV, Nguyen LT. The beneficial role of vitamin D in Alzheimer’s disease. Am J Alzheimers Dis Other Demen 2011; 26: 511–520
[30] Annweiler C, Fantino B, Schott AM, Krolak-Salmon P, Allali G, Beauchet O. Vitamin D insufficiency mild cognitive impairment: cross-sectional association. Eur J Neurol 2012; 19: 1023–1029.
[31] Peterson A, Mattek N, Clemons A, Bowman GL, Buracchio T, Kaye J, Quinn J. Serum vitamin D concentrations are associated with falling and cognitive function in older adults. J Nutr Health Aging 2012; 16: 898– 901.
[32] Troesch B, Eggersdorfer M, Weber P. The role of vitamins in aging societies. Int J Vitam Nutr Res 2012; 82: 355–359.
[33] Lopes da Silva S, Vellas B, Elemans S, Luchsinger J, Kamphuis P, Yaffe K, Sijben J, Groenendijk M, Stijnen T. Plasma nutrient status of patients with Alzheimer’s disease: Systematic review and meta-analysis. Alzheimers Dement 2014; 10: 485–502
[34] Cardoso BR, Cominetti C, Cozzolino SM. Importance and management of micronutrient deficiencies in patients with Alzheimer’s disease. Clin Interv Aging 2013; 8: 531– 542
[35] Volkert D, Berner YN, Berry E, Cederholm T, Coti Bertrand P, Milne A, Palmblad J, Schneider S, Sobotka L, Stanga Z et al. ESPEN Guidelines on Enteral Nutrition: Geriatrics. Clin Nutr 2006; 25: 330–360.
[36] Allen VJ, Methven L, Gosney MA. Use of nutritional complete supplements in older adults with dementia: systematic review and meta-analysis of clinical outcomes. Clin Nutr 2013; 32: 950–957.
[37] Allen VJ, Methven L, Gosney M. Impact of serving method on the consumption of nutritional supplement drinks: randomized trial in older adults with cognitive impairment. J Adv Nurs 2014; 70: 1323–1333.
[38] Mendiratta P, Tilford JM, Prodhan P, Curseen K, Azhar G, Wei JY. Trends in percutaneous endoscopic gastrostomy
placement in the elderly from 1993 to 2003. Am J Alzheimers Dis Other Demen 2012; 27: 609–613
[39] Loser C, Aschl G, Hebuterne X, Mathus-Vliegen EM, Muscaritoli M, Niv Y, Rollins H, Singer P, Skelly RH. ESPEN guidelines on artificial enteral nutrition--percutaneous endoscopic gastrostomy (PEG). Clin Nutr 2005; 24: 848–861.
[40] Sobotka L, Schneider SM, Berner YN, Cederholm T, Krznaric Z, Shenkin A, Stanga Z, Toigo G, Vandewoude M, Volkert D et al. ESPEN Guidelines on Parenteral Nutrition: Geriatrics. Clin Nutr 2009; 28: 461–466.
[41] Wu HS, Lin LC, Wu SC, Lin KN, Liu HC. The effectiveness of spaced retrieval combined with Montessori-based activities in improving the eating ability of residents with dementia. J Adv Nurs 2014; 70: 1891–1901.
[42] Alarcon G., Nashef L., Cross H., Nightingale J., Richardson S. (2009) Epilepsy (Oxford Specialist Handbooks in Neurology), Oxford: Oxford University Press. [43] Antelo R.E., Stanilla J.K., Martin-Llonch N. (1994) Myoclonic seizures and “leg folding” phenomena with clozapine therapy: Report of two cases. Biol Psychiatry 36: 759–762.
[44] Atkinson J.M., Douglas-Hall P., Fischetti C., Sparshatt A., Taylor D.M. (2007) Outcome following clozapine discontinuation: A retrospective analysis. J Clin Psychiatry 68: 1027–1030
[45] Baker R.W., Conley R.R. (1991) Seizures during clozapine therapy. Am J Psychiatry 148: 1265–1266.
[46] Begum M. (2005) Clozapine-induced stuttering, facial tics and myoclonic seizures: A case report. Aust NZ J Psychiatry 39: 202.
[47] Berman H., Zalma A., DuRand C.J., Green A.I. (1992) Clozapine-induced myoclonic jerks and drop attacks. J Clin Psychiatry 53: 329–330.
[48] Boachie A., McGinnity M.G.A. (1997) Use of clozapine in a mental handicap hospital-report of the first 17 patients. Ir J Psychol Med 14: 16–19.
Bowden C.L., Calabrese J.R., Sachs G., Yatham L.N., Asghar S.A., Hompland M., et al. (2003) A placebo-controlled 18-month trial of lamotrigine and lithium maintenance treatment in recently manic or hypomanic patients with bipolar I disorder. Arch Gen Psychiatry 60: 392–400.
[50] Chung S.J., Jeong S.H., Ahn Y.M., Kang U.G., Koo Y.J., Ha J.H., et al. (2002) A retrospective study of clozapine and electroencephalographic abnormalities in schizophrenic patients. Prog Neuropsychopharmacol Biol Psychiatry 26: 139–144.
[51] Conca A., Beraus W., Konig P., Waschgler R. (2000) A case of pharmacokinetic interference in comedication of clozapine and valproic acid. Pharmacopsychiatry 33: 234– 235.
[52] Cunnington M., Tennis P. (2005) Lamotrigine and the risk of malformations in pregnancy. Neurology 64: 955– 960.
285
Copyright © 2011-15. Vandana Publications. All Rights Reserved.
[54] Duggal H.S., Jagadheesan K., Nizamie S.H. (2002) Clozapine-induced stuttering and seizures. Am J Psychiatry 159: 315.
[55] DuMortier G., Mahe V., Pons D., Zerrouk A., Januel D., DeGrassat K. (2001) Clonic seizure associated with high clozapine plasma level. J Neuropsychiatry Clin Neurosci 13: 302–303.
[56] Dursun S.M., McIntosh D., Milliken H. (1999) Clozapine plus lamotrigine in treatment-resistant schizophrenia. Arch Gen Psychiatry 56: 950.
[57] Englisch S., Esser A., Enning F., Hohmann S., Schanz H., Zink M. (2010) Augmentation with pregabalin in schizophrenia. J Clin Psychopharmacol 30: 437–440.
[58] Facciola G., Avenoso A., Scordo M.G., Madia A.G., Ventimiglia A., Perucca E., et al. (1999) Small effects of valproic acid on the plasma concentrations of clozapine and its major metabolites in patients with schizophrenic or affective disorders. Ther Drug Monit 21: 341–345.
[59] Foster R., Olajide D. (2005) A case of clozapine-induced tonic-clonic seizures managed with valproate: Implications for clinical care. J Psychopharmacol 19: 93– 96.
[60] Freudenreich O., Weiner R.D., McEvoy J.P. (1997) Clozapine-induced electroencephalogram changes as a function of clozapine serum levels. Biol Psychiatry 42
[62] Funderburg L.G., Vertrees J.E., True J.E., Miller A.L. (1994)
: 132–137.
