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Binswanger's disease

 
Neurological Disorder:

Binswanger disease

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Definition

Binswanger disease is a rare form of progressive dementia that develops after age 60 and involves degeneration of the brain's white matter.

Description

Also known as subcortical arteriosclerotic encephalopathy, Binswanger disease is a form of subcortical dementia. Dementia is a general term used to describe a generalized deterioration of thinking and reasoning skills. In the case of Binswanger disease, the deterioration is due to physiological problems (i.e., organic factors). While many dementias result from damage to cortical areas of the brain, some diseases, including Binswanger disease, Alzheimer's disease, Parkinson's disease, Huntington disease, and dementia associated with AIDS, result from damage to subcortical areas of the brain (specifically, to subcortical connections).

Alternate names for Binswanger disease include Binswanger-type multi-infarct dementia, Binswanger encephalopathy, and Binswanger-type vascular dementia.

As with other individuals suffering subcortical dementia, people with Binswanger experience difficulties in maintaining attention to tasks and show depressed levels of motivation often accompanied by mood swings or apathy.

Demographics

Although Binswanger disease may occur in younger groups, the symptoms usually become pronounced in patients over 60 years of age.

Causes and symptoms

The exact cause of Binswanger disease is unknown, however, lesions in cerebrovascular tissue located in the inner white matter of the brain cause most of the symptoms. Prominent symptoms include rapid mood changes, loss of the ability to focus on tasks, a deterioration in thought processes (e.g., loss of memory and cognition), and mood changes.

Individuals with Binswanger disease may also have elevated blood pressure or suffer from stroke. Binswanger disease is found to be associated with blood (hematological) abnormalities with regard to the types and numbers of cells present, diseases of large blood vessels (especially in the upper chest and neck regions), and diseases of the heart. Abnormal electrical disturbances in the brain may cause seizures.

Binswanger's symptoms may be elusive in both appearance and degree. Not all people experience all the symptoms normally associated with the disease, and patients may experience symptoms for a period of time, followed by brief periods in which they are relatively symptom free.

As with other dementias, patients often present evidence of forgetfulness, memory loss, confusion and/or confabulation of events in terms of time and space (e.g., having a memory of two events that occur on different days as a combined memory of one event).

People with Binswanger disease often suffer depression and withdraw from family, friends, and co-workers (social withdrawal). Although clinical depression is a psychiatric term and requires a separate diagnosis, Binswanger patients suffering depression show a marked loss of interest in activities they once found pleasurable.

As the dementia progresses, people with Binswanger disease may initially lose the ability to perform tasks involving fine motor coordination, such as tying shoes or writing by hand, followed by a loss of broader function. Loss of bladder control (urinary incontinence) may develop, as well as generalized clumsiness or difficulty in walking. Later, patients often develop a blank-like stare and may have difficulty speaking or swallowing.

Diagnosis

Binswanger disease is identified by detection and characterization of lesions in the cerebrovascular tissue located in the inner white matter of the brain, which are usually visible on computed tomography (CT) scan or magnetic resonance imaging (MRI).

A tentative diagnosis of Binswanger disease is made upon an evaluation of patient history and symptoms. A definitive diagnosis is made upon autopsy that reveals lesions in cerebrovascular tissue lying in the subcortical regions of the brain. Lesions are not always confined to subcortical areas and additional lesions also may extend into cortical areas.

Treatment team

The treatment team for patients suffering from dementia, either cortical or subcortical, usually includes physicians, nurses, and physical, speech, and occupational therapists.

The diagnosis of Binswanger disease is often made by a neurologist. Physical therapists evaluate deficits in strength, movement, and gait, and supervise exercises to improve these deficits. Speech-language pathologists evaluate deficits in the ability to eat and speak, and provide adaptive strategies to minimize their effects. Occupational therapists evaluate a person's ability to maintain posture and focus while executing normal activities of daily living (such as reaching for and using a toothbrush) and devise strategic movements and equipment to adapt to deficits.

An expanded network of professionals, including mental health counselors and social service workers, may be beneficial. Caregivers are often required for personal care during the late stages of the disease.

Treatment

There is no known cure or specific treatment for Binswanger disease. Patients are treated symptomatically, i.e., treated for the symptoms such as high blood pressure, seizures, or heart disease often associated with Binswanger disease.

In most cases, specialized treatment plans include medications to control mood swings and depression, blood pressure (both elevated and low), seizures, and rhythm irregularities in the heart. Treatment is designed to reduce the adverse effects of these associated conditions.

Recovery and rehabilitation

Although currently no cure exists for dementias such as the Binswanger type, the goal of therapy is to maintain the highest state of physical health by managing the symptoms, along with maintaining the highest possible state of functional activity and well being. In addition to physical and occupational therapy, treatment for mood swings or depression helps the person with Binswanger disease to remain active, socially engaged, and mobile for as long as possible.

When the disease progresses and mobility, along with mental ability, decreases, the person with Binswanger or other dementias will likely require a nurturing environment that provides for medical care and safety. Whether at home or in a care facility, personal care assistance may be necessary for many or all hours of the day.

Many communities have adult daycare centers with targeted, stimulating activities for persons with dementia in the early stages. Long-term care facilities that specialize in dementia can provide an environment that fosters mobility in a soothing environment, where staff provides cues to orient the person with dementia to memories and surroundings.

Clinical trials

Research on a wide range of neurological diseases, including dementias, is conducted by agencies of the National Institutes of Health such as the National Institute of Neurological Disorders and Stroke (NINDS), and other institutes and research organizations such as the National Institute on Aging and the National Institute of Mental Health. As of November 2003, scientists at the National Institute of Neurological Disorders and Stroke are reevaluating the definitions for many forms of dementia, including Binswanger disease.

Prognosis

Because there is no known specific cure for Binswanger disease, in most cases the disease follows a slowly progressing course during which a patient may suffer progressive strokes interspersed with periods of partial recovery. Once symptoms become visible (manifest), persons with Binswanger disease often die within five years of the onset of the disease.

Resources

OTHER

BBC News: Health and Medical Notes. "Binswanger's Disease." April 12, 1999. (November 13, 2003 [June 1, [2004].) http://news.bbc.co.uk/1/hi/health/medical_notes/317488.stm.

National Institute of Neurological Disorders and Stroke (NINDS)/National Institutes of Health. "Binswanger's Disease." November 8, 2002. (November 13, 2003 [June 1, 2004].) http://www.ninds.nih.gov/health_and_medical/disorders/binswang_doc.htm.

ORGANIZATIONS

Alzheimer's Association. 919 North Michigan Avenue, Suite 1100, Chicago, IL 60611-1676. (312) 335-8700 or (800) 272-3900; Fax: (312) 335-1110. info@alz.org. http://www.alz.org.

Alzheimer's Disease Education and Referral Center (ADEAR). P.O. Box 8250, Silver Spring, MD 20907-8250. (301) 495-3311 or (800) 438-4380; Fax: (301) 495-3334. adear@alzheimers.org. http://www.alzheimers.org.

Family Caregiver Alliance. 690 Market Street / Suite 600, San Francisco, CA 94104. (415) 434-3388 or (800) 445-8106; Fax: (415) 434-3508. info@caregiver.org. http://www.caregiver.org.

National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health. P.O. Box 5801, Bethesda, MD 20824; (301) 496-5751 or (800) 352-9424; TTY (301) 468-5981. braininfo@ninds.nih.gov. http://www.ninds.nih.gov/.

National Organization for Rare Disorders (NORD). 55 Kenosia Avenue, Danbury, CT 06813-1968. (203) 744-0100 or (800) 999-NORD; Fax: (203) 798-2291. orphan@rarediseases.org. http://www.rarediseases.org.


Paul Arthur


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Medical Dictionary: Bins·wang·er's disease
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Home > Library > Health > Medical Dictionary
(bĭn'swăng'ərz, bĭns'väng'ərz)
n.

Organically caused dementia that is associated with chronic high blood pressure and that is characterized by recurrent edema of cerebral white matter with secondary demyelination. Also called Binswanger's encephalopathy.

Wikipedia: Binswanger's disease
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Home > Library > Miscellaneous > Wikipedia
Binswanger's disease
Classification and external resources
ICD-10 I67.3
ICD-9 290.12
DiseasesDB 1405
MeSH D015140

Binswanger's disease is a form of multi-infarct dementia caused by damage to the white brain matter.[1] White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age.[2]. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. [3] It usually presents itself in 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.[4]

It was described by Otto Binswanger in 1894, and [5] Alois Alzheimer first used the phrase "Binswanger's disease" in 1902.[6] However, Olszewski is credited with much of the modern-day investigation of this disease which began in 1962.[4][7]

Contents

History

Binswanger in 1894 was the first to claim that white matter atrophy caused by 'vascular insufficiency' can result in dementia. He described a patient who had slow progression of dementia as well as subcortical white matter atrophy, ventricle enlargement, aphasia, hemianopsia, and hemiparesis. [8] He named this disease 'encenphailitis subcorticalis chronica progressive.' Binswanger did not conduct any microscopic investigations so many did not believe his findings an attributed the neural damage to neural syphilis. [2]Alzheimer in 1902 studied Binswanger's work with pathological evidence that concluded and supported Binswanger's ideas and hypotheses. Alzheimer renamed this disease Binswanger's disease. [3]

In the late 19th century vascular dementia was heavily studied, however by 1910 scientists were lumping Binswanger's disease with all other subcortical and cortical dementia and labeling everything senile dementia despite all previous research and efforts to distinguish this disease from the rest. In 1962 J. Olszewski published an extensive review of all literature about Binswanger's disease so far. He discovered that some of the information in the original reports was incorrect and that at least some of the patients studied in these cases probably had neurosyphilis or other types of dementia. Even with these errors, Olszewski concluded that Binswanger disease did exist as a subset of cerebral arteriosclerosis. [9] Yet again, in 1974 the term multi-infarct dementia was coined and all vascular dementia was grouped into one category. Because of this, the specific names of these types of this dementia, including Binswanger's disease were lost. [3] This was until 1992 when Alzheimer's diagnostic centers create specific criteria known as the Hachinski's Ischemic Scale which became the standard for diagnosing MID or vascular dementia. [10]

Because of the complicated history of Binswanger’s disease and the fact that it was overlooked as a disease at all for so many years, leads us to believe that many patients have been misdiagnosed as Alzheimer’s for years. This leads us to believe that Binswanger’s is more prominent in the population than once thought. [8]

Neural Presentation

Binswanger's disease is a type of subcortical vascular dementia caused by white matter atrophy to the brain. However, white matter atrophy alone is not sufficient for this disease; evidence of subcortical dementia is also necessary.[8]


The histologic findings are diffuse, irregular loss of axons and myelin accompanied by widespread gliosis, tissue death due to an infarction or loss of blood supply to the brain, and changes in the plasticity of the arteries. The pathologic mechanism may be damage caused by severe atherosclerosis. The onset of this disease is typically between 54 and 66 and the first symptoms are usually mental deterioration or stroke. [3]

The vessels that supply the subcortical white matter come from the vessels that support basal ganglia, internal capsule, and thalamus. It is described as its own zone by and susceptible to injury. Chronic hypertension is known to cause because it changes the tension of the smooth walls vessels and caused changes in the vessel diameter. Arterioles can become permeable resulting in compromise of the blood brain barrier. [3] [11] It has been shown that Binswanger’s disease targets the vessels in this zone of the subcortex, but spares the microvessel and capillaries which may be attributed to a difference between Alzheimer’s and Binswanger’s disease. [12] Chronic hypertension is known to cause because it changes the tension of the smooth walls vessels and caused changes in the vessel diameter. [2]

Mental Presentation

There is a difference between cortical and subcortical dementia. Cortical dementia is atrophy of the cortex which affects ‘higher’ functions such as memory, language, and semantic knowledge whereas subcortical dementia affects mental manipulation, forgetfulness, and personality/emotional changes. Binswanger’s Disease has shown correlations with impairment in executive functions, but have normal episodic or declarative memory. Executive functions are brain processes that are responsible for planning, cognitive flexibility, abstract thinking, rule acquisition, initiation appropriate actions and inhibiting inappropriate actions, and selecting relevant sensory information. There have been many studies done comparing the mental deterioration of Binswanger patients and Alzheimer patients. It has been found in the Graphical Sequence Test that Binswanger patients have hyperkinetic perseveration errors which cause the patients to repeat motion even when not asked whereas Alzheimer patients have semantic preservation because when asked to write a word they will instead draw the object of the word. [13]

Symptoms

Symptoms include mental deterioration, language disorder, transient ischemic attack, muscle ataxia, and impaired movements including change of walk, slowness of movements, and change in posture. These symptoms usually coincide with multiple falls, epilepsy, fainting, and uncontrollable bladder. [4]

Because Binswanger’s disease affects flow processing speed and causes impaired concentration, the ability to do everyday tasks such as manage finances, checkbook, preparing a meal, and driving may become very difficult. [2]

Diagnosis

Binswanger's disease can usually be diagnosed through a CT scan, MRI, and a proton MR spectrography. Indications include infarctions, lesions, or loss of intensity of central white matter and enlargement of ventricles, and leukoaraiosis or white matter atrophy.

Presentation

Leukoaraiosis (LA) are white matter changes that are common in Binswanger’s Disease. However, LA can be found in many different diseases and even in the general population, especially in people older than 65 years of age. [4]

There is controversy whether LA and mental deterioration actually have a cause and effect relationship. Recent research is showing that different types of LA can affect the brain differently, and that proton MR spectroscopy would be able to distinguish the different types more effectively and better diagnosis and treat the issue. [8] Because of this information, white matter changes indicated by a MRI or CT cannot alone diagnose Binswanger's disease, but can aid to a bigger picture in the diagnosis process. There are many diseases similar to Binswanger's disease including CADASIL syndrome and Alzheimer's disease which makes this specific type of white matter damage hard to diagnose. [4] Binswanger’s disease is best when diagnosed of a team by experts including a neurologist and psychiatrist to rule out other psychological or neurological problems. [2] Because doctors must successfully detect enough white matter alterations to accompany dementia as well as an appropriate level of dementia, two separate technological systems are needed in the diagnosing process.

Technology

Much of the major research today is done on finding better and more efficient ways to diagnose this disease. Many researchers have divided the MRIs of the brain into different sections or quadrants. A score is given to each section depending on how severe the white matter atrophy or leukoaraiosis is. Research has shown that the higher these scores, the more of a decrease in processing speed, executive functions, and motor learning tasks. [14] [15] Other researchers have begun using computeres to calculate the percentage of white matter atrophy by counting the hyper-intense pixels of the MRI. These reports have shown similar reports of have a correlation between the amount of white matter alterations and the decline of psychomotor functions, and reduced performance on attention and executive control. [16] [17] One recent type of technology is called susceptibility weighted imaging (SWI) which is a magnetic resonance technique which has an unusually high degree of sensitivity and can better detect white matter alternations. [18]

Recently a Mini Mental Test (MMT) has been created to accurately and quickly assess cognitive impairment due to vascular dementia across different cultures. Binswanger’s disease has been shown to be the most severe impairment of all of the vascular dementia. [19]

Prognosis

Binswanger's disease has no cure. The best way to manage the vascular risk factors that contribute to poor profusion in the brain is to treat whatever is causing it, such as chronic hypertension or diabetes. It has been shown that current Alzheimer’s medication, Aricept, may help Binswanger’s Disease patients as well. Aricept increases the acetocholine in the brain through a choline esterase inhibitor which deactivates the enzyme that breaks down acetocholine. [2] Alzheimer as well as Binswanger patients have low levels of acetocholine and this helps to restore the normal levels of neurotransmitters in the brain. [2] This drug may improve memory, awareness, and the ability to function. [20] If no medical interception of the disease is performed then the disease will continue to worsen as the patient ages due to the continuing atrophy of the white matter from whatever was its original cause. [2]

References

  1. ^ Akiguchi I, Tomimoto H, Suenaga T, Wakita H, Budka H (1997). "Alterations in glia and axons in the brains of Binswanger's disease patients". Stroke 28 (7): 1423–9. PMID 9227695. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=9227695. 
  2. ^ a b c d e f g h Giovannetti, T. Personal Interview. 16 October 2009
  3. ^ a b c d e Libon, David; Price, C., Davis Garrett, K., and T. Giovannetti (2004). "From Binswanger’s Disease to Leukoaraiosis: What We Have Learned About Subcortical Vascular Dementia". The Clinical Neuropsychologist 18 (1): 83-100. 
  4. ^ a b c d e Loeb C (2000). "Binswanger's disease is not a single entity". Neurol. Sci. 21 (6): 343–8. doi:10.1007/s100720070048. PMID 11441570. http://link.springer-ny.com/link/service/journals/10072/bibs/0021006/00210343.htm. 
  5. ^ Pantoni L, Moretti M, Inzitari D (1996). "The first Italian report on "Binswanger's disease"". Ital J Neurol Sci 17 (5): 367–70. doi:10.1007/BF01999900. PMID 8933231. 
  6. ^ "Review: Binswanger's disease, leukoaraiosis and dementia". http://findarticles.com/p/articles/mi_m2459/is_n1_v23/ai_14904670. Retrieved 2008-01-30. 
  7. ^ Olszewski J (1962). "Subcortical arteriosclerotic encephalopathy. Review of the literature on the so-called Binswanger's disease and presentation of two cases". World Neurol 3: 359–75. PMID 14481961. 
  8. ^ a b c d Libon, D., Scanlon, M., Swenson, R., and H. Branch Coslet(1990): "Binswanger's disease: some Neuropsychological Considerations", Journal of Geriatric Psychiatry and Neurology, 3(1):31-40.
  9. ^ Thajeb, Peterus; Thajeb, T., and D. Dai (March 2007). "Cross-cultural studies using a modified mini mental test for healthy subjects and patients with various forms of vascular dementia". Journal of Clinical Neuroscience 14 (3): 236-241. 
  10. ^ Hachinski, V.C., Iliff, L.D., Zilhka, E., Du Boulay, G.H., McAllister, V.L., Marshall, J., Russell, R.W.R., and Symon, L. (1975): “Cerebral blood flow in dementia”, Archives of Neurology, 32:632-7.
  11. ^ de Reuck, J. (1971). "The human periventricular arterial blood supply and anatomy of cerebral infarctions.". European Neurology 5: 321-334. 
  12. ^ Kitaguchi, Hiroshi; Ihara, M., Saiki, H., Takahashi, R., and H. Tomimoto (1 May 2007). "Capillary beds are decreased in Alzheimer's disease, but not in Binswanger's disease". Neuroscience Letters 417 (2): 128-131. 
  13. ^ Goldberg, E. (1986): “Varieties of perseveration: A comparison of two taxonomies.”, Journal of Clinical and Experimental Neuropsychology, 8:710-726.
  14. ^ Junque, C.; Pujol, J., Vendrell, P., Bruna, O., Jodar, M., Ribas, J.C., Vinas, J., Capevila, A., and Marti-Wilalta, J.L. (1990). "Leukoaraiosis on magnetic resonance imaging and speed of mental processing.". Archives of Neurology 47: 151-156. 
  15. ^ Libon, David; Bogdanoff, B., Cloud, B.S., Skalina, S., Carew, T.G., Gitlin, H.L., and Bonavita, J. (1998). "Motor Learning and quantitative measures of the hippocampus and subcortical white alterations in Alzheimer's disease and Ischaemic Vascular Dementia.". Journal of Clinical and Experimental Neuropsychology 20: 20-41. 
  16. ^ Davis-Garrett, K.L.; Cohen, R.A., Paul, R.H., Moser, D.J., Malloy, P.F., and Shah, P. (2004). "Computer-mediated measurement and subjective ratings of white matter hyperintensities in vascular dementia: Relationships to neuropsychological performance.". The Clinical Neuropsychologist. 18 (1). 
  17. ^ Moser, D.J.; Cohen, R.A., Paul, R.H., Paulsen, J.S., Ott, B.R., Gordon, N.M., Bell, S., and Stone, W.M. (2001). "Executive function and magnetic resonance imaging subcortical hyperintensities in Vascular dementia.". Neuropsychiatry, Neuropsychology, and Behavorial Neurology. 14: 89-92. 
  18. ^ Santhosh, K.; Kesavadas, C., Thomas, B., Gupta, A.K., Thamburaj, K,, and T. Raman Kapilamoorthy (January 2009). "Susceptibility weighted imaging: a new tool in magnet resonance imaging of stroke". Clinical Radiology 64 (1): 74-83. 
  19. ^ Thajeb, Peterus; Thajeb, T., and D. Dai (March 2007). "Cross-cultural studies using a modified mini mental test for healthy subjects and patients with various forms of vascular dementia". Journal of Clinical Neuroscience 14 (3): 236-241. 
  20. ^ "[www.webmd.com Aricept]". www.webmd.com. Retrieved 2009-11-30. 
v • d • e
CNS disease, Vascular disease: Cerebrovascular diseases (G45-G46 and I60-I69, 430-438)
Brain ischemia/
cerebral infarction
(ischemic stroke/TIA)
General
Intracranial hemorrhage
(hemorrhagic stroke)
Extra-axial
Aneurysm
Other/general
central nervous system navs: anat/physio/dev, noncongen/congen/neoplasia, symptoms+signs/eponymous, proc
vascular navs: anat/physio/dev, noncongen/systemic vasculitis/congen/neoplasia, symptoms+signs/eponymous, proc
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