Vascular disease

Vascular disease is the second leading cause of dementia, after Alzheimer's disease. Vascular disease can be prevented and treated, with increased vigilance and control of vascular factors, so that the incidence of dementia can be derived.

New little is known about the underlying cause of this vascular disease. Several studies in the U.S. reported a picture of the incidence of specific for vascular disease, and have been able to identify risk factors that berhubungan2.


At the end of the 19th century, Otto Biswanger and Alois Alzheimer studied the relationship between vascular pathology and reduced cognitive ability. Seventy years later, Tomlisson and equip Blessed with more systematic studies showing the relationship between vascular pathology with dementia.
In 1974, Hachinski introduce the term multi-infarct dementia (MID) to emphasize that unlicensed infarct dementia is associated with cerebral blood vessels both large and small vessels. Then the researchers use the term vascular dementia (VAD), which helps the doctors to consider a variety of vascular pathologies, including hemorrhage, which can cause dementia.

Recently, the researchers introduced isitlah vascular cognitive impairment (VCI) in order to expand the concept further. Intended that vascular disease can cause a cognitive deficit on the scale of mild to severe, and early recognition of these deficits to help clinicians to intervene before demesia terjadi1.

Incidence and reported VAD prevalence varies by study population, the detection method, the diagnosis criteria used and the period of observation time. Vascular dementia estimated to contribute 10% - 20% of all cases of dementia.

Data from European countries reported prevalence of 1.6% in the age group over 65 years with incidence of 3.4 per 1000 people per year. Research in Lundby in Sweden disclose the lifetime risk of developing VAD 34.5% in men and 19.4% in women when all levels of cognition disorders included in the calculation.

It has long been known that cognitive deficits can occur after a stroke. Recent research has shown that dementia occurs at an average of a quarter to a third of stroke cases.

The prevalence of all forms of dementia including vascular demesia, increased with age. In Europe, prevalence of vascular dementia is estimated around 1.5-4.8% in individuals aged between 70 and 80 years.

Recent research has also shown a link between a genetic factor € apolipoprotein E4 with vascular damage and cerebrovascular disease. DeCarli et. ApoE4 al found that the increase in cardiovascular patients and also in stroke patients. ApoE4 will cause changes in serum cholesterol, and LDL levels.

ApoE4 also played a part in forming arterosklerosis7. ApoE4 will assist hemostasis of cholesterol, and is a component of chylomicrons, VLDL, and their degradation products. Some receptors in liver recognize apoE, including receptor LDL, LDL receptor-bound protein, and receptor VLDL8. Research conducted by DeLeewu et. al concluded that patients with the ApoE4 are at high risk for lesions in substansia alba when he also suffered from hypertension.

In a recent study conducted Kokobu et al, reported an association between ApoE4 with subarachnoid hemorrhage. This makes the allegation that the ApoE4 play a role in response to the trauma of the central nervous system 10.

The purpose of this paper is to provide a deep understanding of the study of vascular dementia in a comprehensive manner. Expected to not give knowledge of pathology and pathophysiology, risk factors, diagnosis criteria, examination and prevention of disease will help the clinician in making the diagnosis of vascular dementia patients, so management will be more focused and measurable.

DISCUSSION

DefinisiDemensia syndrome is a progressive decline in intellectual ability that causes cognitive and functional decline, causing disruption of social function of work, and activities harian.Demensia vascular (VAD) is a heterogeneous group that includes all of the dementia syndrome due to ischemia, hemorrhage, anoxic or hypoxic brain with cognitive impairment ranging from mild to the most severe and include all domains, not necessarily with memory disorders menonjol4. Broadly speaking VAD consists of three subtypes, namely:
1. VAD post-stroke, which includes strategic infarct dementia, multi-infarct dementia, stroke and bleeding. Usually has a clear time correlation between the occurrence of stroke with dementia.
2. Subcortical VAD which includes myocardial lakuner and Binswanger disease with the incidence of TIA or stroke is often not detected but have vascular risk factors.
3. Mixed type dementia, ie with the pathology of vascular dementia in combination with Alzheimer's dementia (AD).
While the division of clinical VAD is as follows:
1. Post-stroke VAD
Strategic infarct dementia: lesions in girus angularis, thalamus, basal forebrain, the posterior cerebral artery territory, and the anterior cerebral artery.
Multiple infarction dementia (MID)
Intracerebral hemorrhage
2. Subcortical VAD
Ischemic lesions substansia Alb
Lakuner subcortical infarction
Non-lakuner subcortical infarction
3. VAD type mixture of Alzheimer Disease and Cerebrovascular Disease.

Pathology and PatofisologiPatologi of vascular disease and cognitive changes have been studied. Various macroscopic and microscopic changes were observed. Some studies have successfully demonstrated the location of the tendency of pathological lesions, that is bilateral and involves the large blood vessels (cerebral arteries anterior and posterior cerebral arteries).

Other studies demonstrate the existence of lakuna-lakuna in the brain such as in the anterolateral and medial thalamus, which is associated with severe neuropsychological deficits. Some strategic locations including substansia alba frontal or basal forebrain of, basal ganglia, internal capsule, genu of the hippocampus, mamillary bodies, midbrain and the pons. At microscopic analysis of change - change in Alzheimer's type (neurofibrillary tangles and senile plaques) was found as well so that will complicate the picture. The term dementia is used when a good mixture and degeneration of the vascular changes contribute to the decline kognisi1.

Patoisiologi mechanism whereby vascular pathology causing cognitive damage is unclear. This can be explained that in reality several different vascular pathologies can cause cognitive damage, including brain embolism thrombosis heart, and abnormalities substansia perdarahan.Peran of alba as a cause of cognitive dysfunction has been known. A recent study of pathology substansia alba in 40 cases with vascular dementia showed:
1. Pathology focal infarct area includes broad and narrow at substansia alba
2. Diffuse pathology substansia alba involving rarefaction surrounded perifokal infarction and substansia alba without infarction.

ResikoFaktor-factor risk factors have been studied by several scientists in 4 years.
They share that risk factors into 4 categories:
1. Demographic factors, including the old age, race and ethnicity (Asian, Africo-American), gender (male), low education, rural area.
2. Atherogenic factors, including the hypertension, cigaret smoking, cardiovascular disease, diabetes, hyperlipidemia, carotid noisy, menopause without estrogen replacement therapies, and the picture of the abnomal ECG.
3. Non-atherogenic factors, including the genetic, changes in hemostatis, high alcohol consumption, aspirin use, psychologic stress, exposure to job-related substances (pesticides, herbicides, plastics), socio-economics.
4. Factors related to stroke including the volume of brain tissue loss, and the number and location of infarction.

Sex is a factor that remains controversial, and some studies have found no difference in gender. Everything can be affected in the same comparison.

Genetics is also an influential factor. Arteriopati cerebral autosomal dominant with subcortical infarcts and leukoencepalopati (CADASIL) is a genetic disease involving a mutation Notch 3, causing subcortical infarcts and dementia in 90% of affected patients who ultimately died with this condition.

History of previous stroke is an important risk factor in vascular dementia. Not only associated with an area and the number of infarcts, but also location and even single strategic lesions can lead to demensia1.Katzman et.al have reported risk of vascular dementia are associated with a state of depression or psychological stress before.

Depression is a syndrome premonitori to VAD in patients with stroke, and also an important marker for damage to the otak.Hubungan between VAD and € 4 of the apoE alleles have been observed in several studies, and found that the presence of this allele is not only an specific marker for Alzheimer's Disease, but also connected with the repair process in the nervous system.

Frison et. al hypothesized that apoE plays a role in normal brain metabolism, and the presence of allele € 4 in a large amount of damage to the brain indicate the presence of either degenerative or vascular. However, since the diagnosis of VAD is set by using the NINDS-AIREN criteria, then the concurrency with Alzheimer's Disease is possible and explain the relationship with apoE.

Risks associated with exposure pepstisida and fertilizers have been confirmed in many previous studies, and explain the relationship with rural areas. The high incidence of VAD in rural areas also reported Liu et.al, and. relationship between this substance also present in Alzheimer's Disease and Parkinson's.

EtiologiBaru recently shown that vascular demesia not only due to the discret infarction (multi-infarct dementia), but also by a cerebrovascular condition. Several vascular disorders that can cause dementia, among others listed in the table on next page of this.

DiagnosisKriteria diagnostic criteria used today is the NINDS-AIREN (National Institute Neurological Disorders and of Stroke, and L'Association pour la Recherche et Internationale L'Enseignmement en Neurosciences), .1. Probable clinical diagnosis of VAD include all of the following: a) Demensiab) cerebrovascular disease (CVD) is characterized by focal neurologic deficit on physical examination such as hemiparese, lower facial muscle paralysis, Babinski reflex, sensory deficits, hemianopsia, disartria, etc..

Consistent with stroke (with or without a history of stroke), and relevant evidence of CVD by brain imaging studies (CT scan or MRI) involves multiple large blood vessels of stroke or myocardial single vantage point (girus angularis, thalamus, basal forebrain, territory posterio cerebral artery and anterior), or multiple lakuner infarction in the basal ganglia and substantia alba substantia alba periventrikuler or extensive lesions, or a combination of abnormalities in atas.c) There is a relationship between the two problems above by one or more of the following circumstances: - Awitan dementia were within 3 months post stroke cognitive functions .- Deterioration of sudden or fluctuating, progressive cognitive deficits and are the stepwise.

2. Criteria for diagnosis of probable subcortical VAD:
A. Syndrome cognition that include both:
• disexecution syndrome: disturbance formulation purposes, initiation, planning, organizing, sequential, execution, set-shifting, maintain activity and abstraction.
Deterioration of memory function • cause occupational and social dysfunction are not caused by a physical disturbance due to a stroke.
B. CVD that include both:
CVD • which is evidenced by neuroimaging
• A history of neurological deficits as part of a CVD: hemiparese, parese facial muscle, a positive Babinski reflex, sensory disturbances, disartri, walking disturbances, extrapyramidal disorder associated with subcortical brain lesions.

Preview KlinisSesuai with NINDS-AIREN clinical picture of VAD are obtained as follows: A. The clinical features consistent with a diagnosis of probable VAD:
1. Walking disturbance (small steps, or marche a petit-fitting, magnetic, apraxic-ataxic gait or Parkinson's)
2. History miksi early and urinary complaints that were not caused by abnormalities urologi3. Changes in personality and mood, abulia and depression. Emotional incontinence, the symptoms of subcortical deficits include psychomotor retardation and impaired function of execution.

B. Clinical features which do not contribute to diagnosis of VAD
: 1. Memory deficits in early stages, deterioration of memory function and other cognitive disorders such as language (transkortikal sensory ataxia), motor skills (apraksia) and perception (agnosia) without any corresponding lesion on brain imaging.
2. No finding of focal neurologic deficit other than cognition disorders. Not found lesions on CT-scan or MRI of the head.

C. Clinical features which contribute to diagnose subcortical VAD:
1. Episodes of upper motor neuron lesion disorders (UMN) light as a mild paralysis, reflex asymmetry, and inkoordinasi.
2. Impaired walking at an early stage of dementia.
3. History of balance disorder, frequent falls, without cause
4. The urgency of early miksi not caused by urologic abnormalities
5. Disartri, disfagi and extrapyramidal symptoms
6. Behavior and psychological disorders such as depression, personality changes, emotional instability, and psychomotor retardation.

D. The picture does not support the diagnosis of subcortical VAD
1. Early Awitan progressive worsening of memory disorders and cognitive disturbances such as disfasia, dispraksi, and agnosia.
2. Nothing found related focal lesions on imaging
3. No finding of relevance to the cerebral lesion in the CT-scan or MRI1.7.

PemeriksaanPemeriksaan VAD generally include:
A. Medical history included
1. UmumWawancara medical history includes medical disorders can cause dementia, such as coronary heart disease, disorders of the heart valves, collagen of heart disease, hypertension, hyperlipidemia, diabetes, peripheral arteriosclerosis, hypothyroidism., Neoplasms, chronic infections (syphilis, AIDS)
2. History umumWawancara Neurology neurology history as a history of stroke, TIA, head injury, central nervous system infection, history of epilepsy and brain surgery because of tumor or hydrocephalus. Accompanying symptoms of dementia such as sensory motor disturbances, impaired walking, coordination and balance disturbances are sudden in the early phase of focal neurologic deficit suggests that lead to VAD.
3. NeurobehaviourInformasi history of the family about the decline in cognition fuingsi, glittering intellectual abilities of daily activities and behavior change is very important in the diagnosis of dementia.
4. History of psychiatric psikiatrikRiwayat important to determine whether patients experienced depression, psychosis, personality changes, aggressive behavior, delusions, hallucinations, paranoid thoughts, and whether this disorder occurs before or after awitan dementia.
5. History poisoning, nutrition, drug-obatan.Keracunan heavy metals, pesticides, glue, and fertilizer, nutritional deficiencies, chronic alcohol consumption can lead to dementia, although not specific to VAD. The use of drugs antidepressants, anticholinergics and herb also may interfere with cognition.
6. History keluargaPemeriksa must explore all the incidence of dementia in the family.

B. Objective examination include:
1. Physical examination appearance umumMeliputi observation, vital signs, arteriosclerosis, vascular risk factors.
2. Examination neurologisGangguuan walking, impaired strength, tone or motor control, sensory disturbance and visual field of the brain nerve disorders, balance disorders and impaired reflexes.
3. MentalPemeriksaan cognitive status examination mental status include memory, orientation, language, cortical function, associated with arithmetic, writing, the praxis, gnosis, visuospasial, and visuopersepsi.

4. Inspection activities fungsionalAdalah real performance examination persons in everyday life activities as premorbid or current.
5. This psikiatrikPemeriksaan examination to determine the mental condition of persons with dementia, whether he is suffering from depression, delirium., Anxiety or psychotic symptoms.

Therapy Management
A. FarmakologikPenderita therapy with cerebrovascular disease risk factors such as hypertension, diabetes mellitus, heart disease, atherosclerosis, arteriosclerosis, dyslipidemia, and smoking, should control the disease well and improving lifestyles. Regular control of primary disease can improve the function of vascular dementia kognisinya.Terapi simptomatikPada the cholinergic neurotransmitter decline so that cholinesterase inhibitors can be given. Recent studies show this class of drugs may stabilize fiungsi improve cognition and daily activities in patients with mild and moderate vascular dementia. Cholinergic side effects that need attention are nausea, vomiting, diarrhea, bradycardia and supraventricular conduction disorders. B. Therapy of non-farmakologisBertujuan to maximize / maintain cognitive function is still there.

The program must be made on an individual basis include interventions to patients themselves, caregivers and the environment, according to the stages of the disease and resources available.

The intervention of the patient includes:
1. Healthy behavior
2. Rehabilitation therapy, is the reality orientation, cognitive stimulation, reminiscent, movement and train the brain and other sports, education, counseling, music therapy, speech therapy and occupational.
3. Environmental interventions, carried out through spatial facilitation activities, tarapi light, the provision of care facilities, day care center, nursing home, and respite center.

Mood and behavioral disorders found in patients with vascular dementia can vary according to location of the damaged brain function. Symptoms that often arises is depression, agitation, hallucinations, delusions, anxiety, violence, trouble sleeping and wandering (walking to and fro). Before starting pharmacological therapy, non-pharmacological therapy should be conducted first to control this disorder but in practice is often necessary a combination of both methods of therapy. It is important to carefully analyze every symptom that arises, is there any behavioral or psychiatric symptoms related to physical conditions (pain), situation (crowded, forced, etc.) or solely due penyakitnya3.DepresiPasien vascular dementia with depression showed severe functional impairment that labih compared with dementia of Alzheimer's patients without depression. Antidepressants can improve depressive symptoms, reduce disability but does not improve cognition disorders.

Handling of non-pharmacological;
1. Giving encouragement of inactivity.
2.Menghindari complex task.
3.Bersosialisasi to reduce depression.
4.Konseling with a psychiatrist.

Management pharmacologic therapy:
1.Semua antidepressants mampunyai the same effectiveness and onset of action within a specified period (about 2 weeks) in the treatment of depression.
2.Pemilihan appropriate medication based on a history of previous drug response, drug side effects and drug interactions.
3. Antidepressants that can be used in patients with vascular dementia, among others
a. Group Selective serotonin reuptake inhibitors (SSRIs). This group has a high tolerability in elderly patients larena without anticholinergic effects and cardiotoxic, orthostatic hypotension is minimal effect
b. Group Reversible MAO-A inhibitors (RIMA)
c. NASSA4 Group. Class of atypical antidepressants
d. Tricyclic class. Not recommended for the elderly because of the effects agitasi.Sebagian sampingnya.Ansietas and vascular dementia patients can be hypersensitive to the surrounding events.

Management of non-pharmacological therapy:
1.Usahakan home environment calm and stable.
2.Tanggapi patients with patience and loving
3.Buatlah constructive activities for the supply of restless.
Caffeinated beverages 4.Hindari unbtuk help reduce symptoms of anxiety and restlessness.

Management pharmacological therapy:
1. Ansiolitik bezodiazepin particularly useful, especially for short-term therapy is not too severe anxiety or agitation.
2. Neuroleptics is indicated in severe agitation, completely unable to sleep, great anxiety, hallucinations or delusions.
3. Antidepressants especially SSRIs and trazadone also effective in treating agitation.

Sleep disturbance
Sleep disorders in patients with vascular dementia often lead to caregiver often waking at night. Some useful practical guide for caregivers (caregiver) are:
1. Give activity during the day
2. Avoid naps if possible
3.Kurangi drink before bed
4. Try daytime exposure to sunlight

PencegahanManajemen of risk factors has a target at various levels, depending on the medical background of patients and where patients are in the course of disease. Chui et. al propose an integrated classification of vascular brain injury, based on the treatment strategy. For each case, clinicians should focus systematically on specific treatment strategies, aimed at primary prevention (risk factors), secondary prevention (the basic mechanisms of vascular brain damage) and tertiary prevention (in cases where there is functional impairment). This classification also emphasizes the need for early detection of patients with minimal cognitive disorders who are at risk of developing dementia uintuk. These patients will receive benefit from treatment agresif1.

CONCLUSIONS AND SUGGESTIONS
1. Vascular dementia is a form that can be reduced incidence of dementia by controlling risk factors, and also the underlying disease.
2. The need for a comprehensive treatment of vascular dementia patients.
3. Need further studies to explore risk factors that influenced the incidence of vascular dementia