Post on 20-Apr-2015
Penyebab yang pasti belum diketahui. Beberapa alternatif penyebabyang telah dihipotesa adalah 1 intoksikasi logam, 2 gangguan fungsi imunitas, 3 infeksi virus, 4 polusi udara/industri, 5 trauma, 6 neurotransmiter, 7 defisit formasi sel-sel filament, 8 presdiposisi heriditer. 9 Dasar kelainan patologi penyakit alzheimer terdiridari degenerasi neuronal, kematian daerah spesifik jaringan otak yangmengakibatkan gangguan fungsi kognitif dengan penurunan daya ingat secaraprogresif.10 Adanya defisiensi faktor pertumbuhan atau asam amino dapatberperan dalam kematian selektif neuron. Kemungkinan sel-sel tersebutmengalami degenerasi yang diakibatkan oleh adanya peningkatan calsiumintraseluler, kegagalan metabolisme energi, adanya formasi radikal bebas atauterdapatnya produksi protein abnormal yang non spesifik.11Penyakit alzheimer adalah penyakit genetika, tetapi beberapapenelitian telah membuktikan bahwa peran faktor genetika, tetapi beberapapenelitian telah membuktikan bahwa peran faktor non-genetika (lingkungan)juga ikut terlibat, dimana faktor lingkungan hanya sebagai pencetus faktorgenetika.
1. Faktor genetik2. Faktor infeksi
Ada hipotesa menunjukkan penyebab infeksi virus pada keluarga penderita alzheimer yang dilakukan secara immuno blot analisis, ternyata diketemukan adanya antibodi reaktif. Infeksi virus tersebut menyebabkan infeksi pada susunan saraf pusat yang bersipat lambat, kronik dan remisi. Beberapa penyakit infeksi seperti Creutzfeldt-Jacob disease dan kuru, diduga berhubungan dengan penyakit alzheimer.
3. Faktor lingkunganEkmann (1988), mengatakan bahwa faktor lingkungan juga dapat berperan dalam patogenesa penyakit alzheimer. Faktor lingkungan antaralain, aluminium, silicon, mercury, zinc. Aluminium merupakan neurotoksik potensial pada susunan saraf pusat yang ditemukan neurofibrillary tangles (NFT) dan senile plaque (SPINALIS). Hal tersebut diatas belum dapat dijelaskan secara pasti, apakah keberadaan aluminum adalah penyebab degenerasi neurosal primer atau sesuatu hal yang tumpang tindih. Pada penderita alzheimer, juga ditemukan keadan ketidak seimbangan merkuri, nitrogen, fosfor, sodium, dengan patogenesa yang belum jelas.
4.Faktor imunologisBehan dan Felman (1970) melaporkan 60% pasien yang menderita alzheimer didapatkan kelainan serum protein seperti penurunan albumin dan peningkatan alpha protein, anti trypsin alphamarcoglobuli dan haptoglobuli. Heyman (1984), melaporkan terdapat hubungan bermakna dan meningkat dari penderita alzheimer dengan penderita tiroid. Tiroid Hashimoto merupakan penyakit inflamasi kronik yang sering didapatkan pada wanita muda karena peranan faktor immunitas.
5. Faktor traumaBeberapa penelitian menunjukkan adanya hubungan penyakit alzheimer dengan trauma kepala. Hal ini dihubungkan dengan petinju yang menderita demensia pugilistik, dimana pada otopsinya ditemukan banyak neurofibrillary tangles.
6. Faktor neurotransmiter
Alzheimer's disease is a chronic, progressive, and is a degenerative disorder of the brain and are
known to affect memory, cognition and ability to care for themselves.
(Suddart, & Brunner, 2002).
Alzheimer's is a degenerative disease characterized by memory loss, intellectual, and
personality. Not curable, treatment is aimed at stopping the progression of disease and
improving patient independence.
(Dr. Sofi Kumala Dewi, et al, 2008)
Alzheimer's is a devastating disease and cause paralysis, which occurs mainly in people aged 65
years and older (patofiologi: clinical concepts of disease processes, is also a disease with
degenerative disorders of the brain cells and causes disruption of intellectual functioning, these
diseases occur in men and women and according to documents occur at a specific person at the
age of 40 years.
(Medical Surgical Nursing: Volume 1 p. 1003)
So that Alzheimer's is a chronic disease, degenerative characterized by memory loss,
intellectual, personality which can result in reduced ability to care for themselves. The disease
attacks people aged 65 years and older.
2.1.1 Alzheimer's Dementia
Diagnosis is made according to the completeness of clinical information, pathology and
similarities syndrome
of dementia. Diagnosis of Alzheimer's divided into a definite diagnosis, probable and possible.1
2.2 Classification
Dementia can be divided into reversible and irreversible dementia that is: 1.2
reversible:
- Alcoholism
- Disturbance pasikiatri
- Normal Pressure Hydrocephalus
- Vascular Dementia
irreversible:
Alzheimer-Dementia
-Pick's Disease
-Parkinson 's Disease Dementia
2.3 Etiology
Alzheimer's disease is a common type of dementia of unknown cause.
Autopsy studies reveal that more than half the patients who died
because of dementia Alzheimer type senil experiencing this disease.
2.4 Pathophysiology
Some of the theories underlying the pathophysiology of Alzheimer's dementia include: 1,3,4
1. Neurotransmitter abnormalities. Neurotransmitter abnormalities that were most responsible
pathophysiologic are acetylcholine and norepinephrine, both hypothesized to be
hipoaktif in diseases with cytoskeletal elements, especially protein berfosforilasi,
although other cytoskeletal proteins were also found. Creasing neurofibriler is
not unique to Alzheimer's disease, because the situation is also found in
Down syndrome, dementia pugilistic (punch-drunk syndrome) dementia complex
Parkinson from Guam, Hallervorden-Spatz disease, and brain and the elderly
to normal. Neurofibriler clutter usually found in the cortex, hippocampus, substantia
nigra, and locus sereleus.
2. Amyloid precursor protein. The gene for amyloid precursor protein is in the arm
length of chromosome 21. Through the process of differential splicing, in fact there
four forms of amyloid precursor protein. Beta/A4 protein, which is the content
of the senile plaques, is a peptide with 42 amino acids which are
destruction of the amyloid precursor protein products. In Down syndrome (trisomy 21),
There are three prints of amyloid precursor protein, and in diseases where the mutations occur
at codon 717 in the amyloid precursor protein gene, a pathological process
result in excessive deposition of protein beta/A4. The question of whether the process on
abnormal amyloid precursor protein is an important primary cause of the
Alzheimer's disease remain unanswered. However, many research groups are actively
studying the normal metabolic process of the amyloid precursor protein and the process on
patients with Alzheimer type dementia in an attempt to answer the question
them. Senile plaques are also known as amyloid plaques, is far more indicative for
Alzheimer's disease, although the situation is also found in Down syndrome
and to some extent, in normal aging.
3. Other potential causes. Other causative theories have been proposed to explain
the development of Alzheimer's disease. One theory is that the abnormalities in the regulation
membrane phospholipid metabolism causing a shortage of liquid membrane is
more rigid than normal. Some researchers have used imaging
molecular resonance spectroscopic (molecular resonance spectroscopic: MRS) to examine the
hypothesis that in patients with Alzheimer type dementia. Toxicity
Aluminium has also been hypothesized as a causative factor, because the levels of aluminum
high have been found in the brains of some patients with Alzheimer's disease.
A gene (E4) have been associated in the etiology of Alzheimer's disease. People with a
copy of the gene suffer from Alzheimer's disease three times more often than people without
the gene
E4. People with two E4 gene had eight times as likely to suffer from the disease
more often than those without E4 gene.
2.5 Clinical Manifestation
Clinical manifestations in patients with demesia include: 2,4,5
1. Amnesia / memory, especially short-term memory. In normal parents, he
can not remember the name of his neighbor, but he knew this man was his neighbor. In
patients
Alzheimer's, he not only forgot the name of his neighbors but also forget that the person is
its neighbors.
2. Difficulty doing the usual routine activities, such as do not know how to unlock
clothes or do not know the sequences of preparing food.
3. Difficulty speaking. Generally in the elderly find it difficult to get the word
the right, but people with Alzheimer's will forget simple words or substitute
a word with the word unusual.
4. Disorientation of time and place. We sometimes forget where we will go or what day
this, but people with Alzheimer's may get lost in places that are familiar to him, forgetting the
where he is today, do not know how he arrived at this place, including whether the current
This night or day.
5. The decrease in deciding something or executive functions, for example can not be
decided to use warm clothes for cold weather or otherwise.
6. One place the goods. A person can temporarily misplaced wallet
or keys. People with Alzheimer's may put things in unusual places, such as
watch on the box of sugar.
7. Changes in behavior. One can be happy or sad from time to time.
People with Alzheimer's can change the mood or emotion is not unusual for no reason that can
be
be accepted.
8. Changes in People with Alzheimer's behavior will look different than usual, it will be
suspicious, irritable, depressed, apathetic or easy rampage, especially when the problem
memory difficulties caused him to do something.
9. Loss of initiative. Sitting in front of the TV for hours, sleeping more than usual or not
show interest in this hobby for ditekuninya.
The characteristics of dementia in Alzheimer's
1. Predementia:
· Mild cognitive disorder (8 years before diagnosis)
· Memory Deficit
· Apathy
2. Early onset dementia
· Improved memory & learning disorders
· Disorders of language, vocabulary & word ↓, ↓ oral and written language skills
· Disturbance of perception (agnosia)
· Impaired movements (apraxia)
· Visible stupid
· Lack of initiation to perform activities
3. Dementia MODERA
· Progressive deterioration
· Not being able to read & write
· Impaired long-term memory
· Substitution use of the word (parafasia)
· Misidentification
· Labile
· Easily angry
· Delusions
· Incontinence urinary system
4. Dementia stage (advanced)
Unable to take care of themselves
· Loss of total verbal ability
· Aggressive
· Apathy extreme
· Deterioration of muscle mass & mobility
· Loss of ability to eat
Based on the stage:
Stage I (1-3 years old diseases)
· Memory: The new memory defects (Leaning), mild impairment of recall
· Visuospatial abilities: topographical disorientation, not able to form complex
· Language: difficult to form a new word, anomia
· Personality: indifference, sometimes irritable
· Psychiatric manifestations: sadness or some delusional
· Motor system: normal
· EEG: normal
· CT / MRI: normal
· PET / SPECT: bilateral posterior hypometabolism / hyperfusion
Stage II (3-10 years old diseases)
· Memory: The new memory (Leaning) & severe impairment of recall
· Visuospatial abilities: spatial disorientation, poor contructions
Languages: fluent
· Aphasia calculation: akalkulation
· Personality: Indifference & irritability
· Manifestation of psychiatry: delusions
· Motor system: restlessness, pacing
· EEG: slow background rhythm
· CT / MRI: normal or ventricular and sulcal enlargement
· PET / SPECT: bilateral parietal and frontal hypometabolism / hyperfusion
Stage III (disease 8-12 years old)
· Intellectual function: severely deteriorated
· Motor system: limb rigidity and flexion poeture
· Sphincter control: urinary and fecal
· EEG: diffusely slow
· CT / MRI: ventricular and sulcal enlargement
· PET / SPECT: bilateral parietal and frontal hypometabolism / hyperfusion
2.6 History and Physical Examination 1.6
A. The medical history includes:
1. General medical history: an interview covering medical disorder that can cause
dementia such as coronary heart disease, heart valve disorders, heart disease collagen,
hypertension, hyperlipidemia, diabetes, peripheral arteriosclerosis, hypothyroidism.,
neoplasms,
infeksikronik (syphilis, AIDS)
2. General Neurology History: Interview neurological history as a history of stroke, TIA,
trauma capitis, central nervous system infections, a history of epilepsy and brain surgery
because of tumor or
hydrocephalus. Accompanying symptoms of dementia such as sensory motor disorders,
impaired
running, coordination and balance disturbances are suddenly in the early phase indicates
focal neurologic deficits that lead to vascular dementia
3. Neurobehaviour History: Information from a family of penurunanfuingsi cognition,
intellectual ability dalama daily activities danperubahan behavior is very
important in the diagnosis of dementia.
4. Psychiatric History: History is important to determine whether psychiatric patients
experiencing depression, psychosis, personality changes, aggressive behavior, delusions,
hallucinations,
paranoid thoughts, and whether this interference occurs before or after the onset of dementia.
5. A history of poisoning, nutrition, drugs: Toxicity of heavy metals, pesticides, glues and
fertilizer, nutritional deficiencies, chronic alcohol consumption can lead to dementia, although
not specific to VAD. The use of antidepressants, anticholinergics and herbs
can disrupt the function of cognition.
6. Family history: The examiner must explore all of the incidence of dementia in the family.
B. Objective examination include:
1. A general physical examination: Includes observation of appearance, the sign-tandavital,
arteriosclerosis,
vascular risk factors.
2. Neurological examination: Impaired walking, impaired strength, tone or motor control,
sensory disturbances and visual field of brain nerve disorders, impaired balance and
reflex disturbances.
3. Mental status examination: Mental status examination meliputimemori cognition,
orientation,
language, cortical function, is associated with math, writing, praxis, gnosis, visuospasial and
visuopersepsi.
4. Examination of the functional activity: An examination of the patient performanyata
activities of daily life during this atausaat premorbid.
5. Psychiatric examination: This examination is to determine the physically kondisimental
dementia, whether he suffered from mental depression, delirium, anxiety, or experiencing
symptoms
psychotic.
2.6 Examination of Alzheimer's Dementia
To determine this disease can do some investigation, namely: 6,8,10
A. Neuropathology
Definitive diagnosis can not be enforced without the confirmation of neuropathology. In general
found atrophy of the bilateral, symmetrical, often the brain weight was 1000 g (850 -
1250gr).
Some studies reveal atrophy more prominent in temporoparietal lobes, anterior
frontal, whereas the occipital cortex, primary motor cortex, somatosensory system remains
intact
(Jerins 1937). Abnormalities in Alzheimer's disease neuropathology consists of:
a. Neurofibrillary tangles (NFT)
Neuronal cytoplasm is made of abnormal filaments containing the proteins
neurofilament, ubiquine, epitoque. NFT are also found in the neocortex, hippocampus,
amygdala,
substantia alba, locus ceruleus, dorsal raphe nucleus of the brain stem. NFT than obtained in
Alzheimer's disease, also found in the brains of elderly, Down syndrome, Parkinson's, SSPE,
ektrapiramidal syndrome, supranuklear palsy. NFT density correlated with the severity
of dementia.
b. Senile plaque (SP)
Is a complex structure that occurs due to degeneration of nerve endings containing
filamenfilamen
abnormal, ektraseluler amyloid fibers, astrocytes, microglia. Amloid precursor protein
contained in the SP is associated with chromosome 21. Senile plaque is mainly contained
the neocortex, amygdala, hippocampus, cortex piriformis, and little was found in the cortex
primary motor, somatosensory cortex, visual cortex, and auditory. Senile plaque is also
present in peripheral tissues.
Perry (1987) said that the density of senile plaques associated with decreased cholinergic.
The second picture of histopathology (NFT and senile plaque) are characteristic features for
Alzheimer's disease patients.
c. Degeneration of neurons
On microscopic examination of change and death of neurons in Alzheimer's disease is very
selectively. Death of neurons in the neocortex mainly found in pyramidal neurons lobe
temporal and frontal. Also found in the hippocampus, amygdala, brain stem nuclei
including the locus serulues, raphe nucleus and substanasia nigra.
Cholinergic neuronal cell death mainly in the nucleus basalis of meynert, and cell
especially the noradrenergic locus ceruleus and raphe nuclei of cells in the dorsal serotogenik,
nucleus of the dorsal tegmentum. It has been found of nerve growth factor on cholinergic
neurons
which degenerates on the lesions of experimental animals and it is an expectation in
treatment of Alzheimer's disease.
d. Changes vakuoler
It is an oval shaped neuronal cytoplasm and nucleus can shift.
The amount of this vakuoler significantly associated with the number of NFT and SP, this change
often obtained at temporomedial cortex, amygdala and insula. Was never found
in the frontal cortex, parietal, occipital, hippocampus, cerebellum and brain stem.
e. Lewy body
Intraneuronal cytoplasmic part that is widely available on enterhinal, gyrus
cingulate cortex, insula, and amygdala. A small number in the frontal cortex, temporal,
parietal, occipital. Cortical Lewy body is the same as immunoreaktivitas that occur in the brain
stem Lewy body in Parkinson's disease histopathology images. Hansen et al
states Lewy body variant of Alzheimer's disease is.
2. Examination NeuropsikologikAlways cause symptoms of Alzheimer's disease dementia. The function checks neuropsikologikis to determine the presence or absence of general cognitive dysfunction and find outin detail the pattern of deficit. Psychological test also aims to assess the function of theshown by some sections of different brain such as memory impairment, loss ofexpression, calculation, attention and understanding language. Neuropsychological evaluationSystematic has important diagnostic function because:1. The existence of cognitive deficits associated with early dementia that can be known whenminor changes that occur due to normal aging.2. Neuropsikologik comprehensive examination allows to distinguishglobal cognitive disorders in dementia with selective deficits caused byFocal dysfunction, metabolic factors, and psychiatric disorders3. Identify picture neuropsikologik abnormalities caused by dementia
due to various causes. The Consortium to Establish a Registry for Alzheimer's Disease(CERALD) present a neuropsychological assessment procedures withbatrey use tool that manifests impaired cognitive function, whichexamination consists of:· Verbal Fluency animal category· Modified Boston naming test· Mini-mental state· Word list memory· Constructional praxis· Word list recall· Word list recognitionThis test takes 30-40 minutes and <20-30 minutes in control.3. CT Scan and MRIIs a non-invasive method of high resolution to see the quantification of changesvolume of brain tissue in Alzheimer's patients antemortem. These checks are instrumental in getting rid of the possible causes of dementia other than Alzheimer's asmultiinfark and cerebral tumors. Overall cortical atrophy and ventricular enlargement are bothis the dominant image of a highly specific marker in this disease. But the pictureIt is also found in other dementias such as multiinfark, Parkinson's disease, Binswanger soit is hard to distinguish from Alzheimer's disease.Thinning of the cerebral substantia alba and ventricular enlargement correlated with the severity of symptomsclinics and mini-mental status examination. On MRI found an increase in intensityin cortical regions and periventrikuler (Capping the anterior horn in the lateral ventricles). CappingThis is a predilection for early dementia. In addition to abnormalities found in cortical, pictureatrophy was also seen in subcortical areas such as the atrophy of the hippocampus, amygdala, andsisterna basal enlargement and fissures sylvii.Seab et all, states are more sensitive MRI to distinguish dementia from Alzheimer's diseasewith other causes, taking into account the size (atrophy) of the hippocampus.4. EEGUseful to identify activities that suklinis resurrection. Being on the diseaseAlzheimer changes in slow-wave obtained in a non-specific frontal lobe5. PET (Positron Emission Tomography)In people with Alzheimer's, PET results found decreased blood flow, O2 metabolism, andcerebral glucose area. Up take I.123 greatly decreased in the parietal region, these results are verycorrelated with cognitive dysfunction and always and in accordance with observationsneuropathology studies.6. SPECT (Single Photon Emission Computed Tomography)Activity I. 123 ratio was lowest in patients with Alzheimer's parieral. These abnormalities correlated withextent of damage and functional deficits kogitif. Both of these checks (SPECT and PET) are notused routinely.7. Laboratory bloodNo specific laboratory tests in patients with Alzheimer's. Examination
this laboratory only to rule out other causes of dementia such asroutine blood tests, B12, calcium, phosphorous bombs, BSE, renal and hepatic function, thyroid, folic acid,syphilis serology, skreening antibody selectively performed.2.7Kriteria Diagnosis
Diagnostics criteria for dementia in Alzheimer's disease emphasize the presence of interference
memory and with the presence of at least one other symptom of cognitive impairment
(Aphasia, apraxia, agnosia, or executive function is abnormal). Criteria for diagnosis as well
penururnan which requires a continuous and gradual in the function, impaired function
social or work, and get rid penyebaba other dementia. 1,8,10,13
There are several criteria for clinical diagnosis of Alzheimer's disease are:
1. Criteria for diagnosis of suspected Alzheimer's disease consists of:
· Dementia established by clinical examination and mini mental status examination
or some similar examination and confirmed with a test neuropsikologik
· Obtained impaired cognitive function deficits> 2
• No disturbance of consciousness level
· Onset between the ages of 40-90 years, or often> 65 years
· There is no systematic abnormalities or other brain diseases.
2. Diagnosis of suspected Alzheimer's disease is supported by:
· Worsening progressive specific cognitive functions such as language, motor skills, and
perception
· ADL impaired and changes in behavior patterns
· A history of the family, especially if confirmed by neuropathology
· In the EEG provides a picture of a normal or nonspecific changes such as
increase in slow wave activity
· On CT scans obtained cerebral atrophy
3. Another picture of the suspect diagnosis of Alzheimer's disease after being expelled cause of
dementia
Other consists of:
· Symptoms associated with depression, insomnia, inkontinentia, delusions, hallucinations,
emotional, sexual disorders, weight loss
· Other neurological disorders in some patients, especially at an advanced stage of disease
and including motor signs such as increased muscle tone, myoclonus or
There is a rise of interference runs at an advanced stage
4. Picture of the suspect diagnosis of Alzheimer's disease is not clearly consist of:
· Onset of sudden
· Found focal neurologic symptoms such as hemiparese, hipestesia, roomy deficit
view and coordination problems
· There is a resurrection or walking at the time of onset disorders
5. Possible clinical diagnoses of Alzheimer's disease are:
· Dementia syndrome, there is no other neurologic symptoms, psychiatric symptoms or
disorders
systemic causes of dementia
· The existence of a secondary systemic disorders or abnormalities of the brain that causes
dementia,
severe cognitive deficits identified a gradual progressive
· There is no other cause
6. Criteria for definite diagnosis of Alzheimer's disease is a combination of clinical criteria for
suspect
Alzheimer's disease and histopathological images obtained from biopsy or autopsy.
2.9 Management
Treatment of Alzheimer's disease is still very limited because of the causes and
pathophysiological
remains unclear. Symptomatic and supportive treatment as if only to give a sense of satisfaction
in patients and families. Provision of stimulant medications, vitamins B, C, and E do not have
menguntungkan.10 effect, 11,12,14
1. Cholinesterase inhibitors
In recent years, many researchers use an inhibitor for the treatment
symptomatic Alzheimer's disease, where patients with Alzheimer's found decreased levels of
acetylcholine. To prevent a decline in acetylcholine levels can be used anti-cholinesterase
centrally acting like fisostigmin, THA (tetrahydroaminoacridine). Drug delivery
This is said to improve memory danapraksia during the last administration. Some
Researchers claim that the medicines will worsen the appearance of anti-cholinergic
intellectuals in normal people and patients with Alzheimer's. Drugs - drugs of this class that can
be
given, among others, 5-10 mg donepezil, rivastigmine and galantamine 6-12 mg 8-24 mg.
2. Thiamin
Research has shown that in people with Alzheimer's found a decrease thiamin
pyrophosphatase ketoglutarate dependent enzyme that is 2 (75%) and transketolase (45%), this
caused neuronal damage in the nucleus of thiamin basalis.Pemberian hydrochlorida with
dose of 3 g / day for 3 months peroral, showed significant improvement of function
cognition compared to placebo during the same period.
3. Nootropik
Nootropik is a psychotropic drug, has been proven to improve cognitive function and
learning process in experimental animals. But the provision of 4000 mg in patients with
Alzheimer's
did not show a clinically meaningful improvement.
4. Clonidine
Impaired intellectual function in patients with Alzheimer's can be caused by damage to
noradrenergic
cortical. Giving Clonidine (catapres) which is a noradrenergic alpha 2 receptor agonist
with a maximum dose of 1.2 mg orally for 4 weeks, showed a less
satisfactory to improve cognitive function
5. Haloperiodol
In people with Alzheimer's, psychosis disorder often occurs (delusions, hallucinations) and
behavior
behavior. Haloperiod oral administration of 1-5 mg / day for 4 weeks will improve the
symptoms
them. When Alzheimer's patients suffer from depression should be given tricyclic anti depresant
(Amitryptiline 25-100 mg / day)
6. Acetyl L-Carnitine (ALC)
Is an endogenous subtrate synthesized within the mitochondria with the aid of enzymes
ALC transferase. This study shows that ALC can increase the activity of acetyl
cholinesterase, choline acetyltransferase. In giving a dose of 1-2 g / day / orally for 1 year in
treatment, it was concluded that can improve or inhibit the progression
damage to cognitive function.
2:11 Prognosis
From examination of 42 patients with probable Alzheimer's clinical show that the prognostic
value
depends on three factors:
1. The degree of severity of illness
2. Variability of the clinical picture
3. Individual differences such as age, family dementia and sex
These three factors are tested statistically, was the first factor that most affects
prognostic patients with Alzheimer's. Patients with Alzheimer's disease have expectancy
The average life 4-10 years after diagnosis, and usually died of infection
secondary, such as pneumonia.
Measures Handling / Management
Treatment of Alzheimer's disease is still very limited because of the causes and pathophysiological still unclear. Symptomatic and supportive treatment as if only to give a sense of satisfaction in patients and families.
Symptomatic treatment:
1) cholinesterase inhibitors
Objective: To prevent a decline in anti-acetylcholine levels can be used centrally acting cholinesterase Example: fisostigmin, THA (tetrahydroaminoacridine), donepezil (Aricept), galantamin (Razadyne), & rivastigmin Drug administration is said to improve memory and apraxia during the last administration ESO: worsen the appearance of the intellectual in normal people and patients with Alzheimer's disease, nausea & vomiting, bradycardia, HCl ↑, and ↓ appetite.
2) Thiamin
In people with Alzheimer's found a decrease of thiamin pyrophosphatase ketoglutarate dependent enzyme that is 2 (75%) and transketolase (45%), this is due to neuronal damage in the nucleus basalis.
Example: thiamin hydrochloride
Dose of 3 g / day for 3 months peroral
Purpose: significant improvement of cognitive function compared to placebo during the same period.
3) Nootropik
Nootropik is a psychotropic drug. Objective: to improve the function of cognition and learning. But the provision of 4000 mg in patients with Alzheimer's disease showed no significant clinical improvement.
4) Clonidine
Impaired intellectual function in patients with Alzheimer's can be caused by damage to cortical noradrenergic.
Example: Clonidine (catapres) which is an alpha 2 noradrenergic receptor agonist
Dose: maximum 1.2 mg orally for 4 weeks The goal: less than satisfactory for improving the cognitive functions
5) Haloperiodol
In people with Alzheimer's, often occur:
Disorder psychosis (delusions, hallucinations) and behavior: Giving Oral Haloperiodol 1-5 mg / day for 4 weeks will improve the symptoms When Alzheimer's patients suffer from depression gave tricyclic anti depresant (amitryptiline 25-100 mg / day)
6) Acetyl L-Carnitine (ALC)
Is an endogenous substrate is synthesized within the mitochondria with the help of ALC transferase enzymes.
Objective: increase the activity of acetyl cholinesterase, choline acetyltransferase. Dose :1-2 g / day / orally for 1 year in treatment Effect: repairing damage or inhibit the progression of cognitive function (Yulfran, 2009)