Subcortical Dementia Syndrome-Binswanger's Disease
Subcortical Dementia Syndrome (Binswanger's Disease) is a type of dementia that affects the subcortical areas of the brain, causing symptoms such as tremors, memory difficulties, and emotional instability.
Doctors see symptoms of subcortical dementia syndrome more often in patients with Huntington’s or Parkinson’s disease rather than Alzheimer’s Disease because of where damage occurs. The sub-cortical area of the brain contains structures controlling personality, movement, and mood–the cerebellum, the basal ganglia and the brain-stem nuclei.
Sometimes called the “little brain”, the cerebellum is primarily concerned with human motor control. When damage occurs to this portion of the brain, coordination, balance and the ability to perform skilled, precise movements is impaired.
The cerebellum also assists cortical structures with fine-tuning attention and learning abilities, especially when learning something new involves assessing sensory input and planning motility actions.
Consisting of five different nuclei that includes the nucleus accumbens, substantia nigra, and caudate nucleus, the basal ganglia are responsible for receiving vast amounts of information from the cerebral cortex, processing this information and then transmitting it back to the cortex through the thalamus.
When subcortical dementia syndrome symptoms affect an individual with Parkinson’s or Alzheimer’s, it is this cortico-basal ganglia-cortical loop that is disrupted enough to cause symptoms such as:
- Tremors and muscle spasms
- Memory difficulties
- Inability to recall everyday words
- Slowed or involuntary movements
- Emotional instability
The brainstem nuclei, or simply the brainstem, is the evolutionarily oldest part of the brain and connects the spinal cord to the cerebrum. Sensory and motor neurons pass through the brainstem up into the brain where information is received and processed by various parts of the brain.
Without the brainstem, humans would not be able to perform automatic functions such as breathing, regulation of blood pressure and heart rate and food digestion. In regards to subcortical dementia symptoms, an affected brain stem will produce deficits in alertness and arousal, speech and visual problems and muscle weakness.
Personality and Mood Changes
Apathy, depression, disinhibition (socially inappropriate behavior), and irritability represent the primary changes in mood and personality caused by this type of dementia. Alternately, individuals with specific, cortical-type dementia will suffer more severe issues with language, memory and problem-solving than with mood. However, these dementias sometimes co-exist, especially in advanced stages of Alzheimer’s or vascular dementia and eventually present other classic symptoms associated with Alzheimer’s disease.
Medical conditions causing the onset and development of subcortical dementia include:
- Chronic alcoholism
- Vascular dementia
- Late-stage Parkinson’s disease
- AIDS dementia complex
- Lyme disease
- Brain tumors
- Huntington’s and Wilson’s disease
- Multiple sclerosis
- Severe head traumas
Diagnosis, Tests and Treatment
Obtaining an accurate diagnosis regarding the cause of subcortical dementia symptoms is vital to receiving appropriate and effective treatment. Complete physical, neurological and neuropsychological testing is necessary before medications can be prescribed. Cognitive abilities are usually assessed by giving patients the Mini-Mental State Examination. Brain imaging scans will also provide information about the condition of the brain and reveal areas that are experiencing signs of degeneration.
Individuals suffering from moderate to severe AD exhibit abnormal electroencephalo-grams when subjected to EEG tests. Patients with Parkinson’s or Huntington’s reveal contrasting electrical brain wave patterns from those with AD, enabling physicians to give a more accurate diagnosis when confronted with a dementia patient.
Lab tests used to rule out other medical conditions and contribute to a precise diagnosis of dementia include blood glucose, complete blood count, thyroid, urinalysis, and cerebrospinal fluid screening.
Patients suspected of suffering from Parkinson’s rather than Alzheimer’s are given a drug called levodopa, or L-dopa. Because Parkinson’s disease results from reduced dopamine levels in the brain, L-dopa (a precursor to dopamine) is provided to see if motor impairment is alleviated. If the jerkiness, tremors, stiffness and involuntary movements associated with Parkinson’s is not relieved, then doctors may rule out Parkinson’s and continue treatment plans beneficial to a diagnosis of vascular dementia or Alzheimer’s disease upon completion of further testing.
Unless dementia is caused by a reversible condition such as operable tumors, metabolic syndromes, or nutritional deficiencies, it remains incurable. Attempting to control symptoms and keep patients as comfortable as possible is currently the best treatment method.
Patients suffering subcortical as well as cortical dementias will need pervasive, if not 24 hour care, in advanced stages of the disease. Drugs such as atypical neuroleptics (Risperdal or Depakote) and antidepressants (Paxil or Effexor) may help reduce the irritability, disinhibition, motor difficulties, and depression associated with this type of dementia.
Preventing Dementia
Although research has yet to discover why Parkinson’s and Huntington’s disease is triggered in certain individuals, belief that a genetic component may exist to explain the origin of the disease is a theory popular among neurologists.
However, it is possible to prevent or substantially delay the development and progression of subcortical dementia due to Alzheimer’s disease or vascular dementia by adopting a lifestyle that emphasizes regular exercise, a healthy diet, avoidance of smoking, excessive alcohol intake and chronic stress. In addition, engaging in intellectual stimulation promotes the ability of the brain to grow new connections among neurons, an action that has been proved in research to effectively avert the development of Alzheimer’s disease.
http://www.nlm.nih.gov/medlineplus/ency/article/001069.htm
http://www.biology.emory.edu/research/Jaeger/BasalGanglia/BG_page.html
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