Advanced Edition
Leo J. Borrell, M.D.
President & Senior Medical Consultant

Our Mission
It is our pledge to provide compassionate service, care, and treatment for the emotional,  social and physical well-being of the elderly, their family and caregivers.

Our Goal
Our goal is to allow seniors to retain the highest possible level of comfort and cognitive  ability while maintaining their quality of life.

Because 50-90% of patients are undiagnosed with dementia and other brain or psychiatric problems that lead to behavior problems they are under treated or over treated. This often results in difficulties with Medicare surveyors with the consequences of F501, F329, F330 and F429 tags. Senior PsychCare, in cooperation with nursing staff, has developed a progress to conduct initial screening s on all patients. We utilize objective tests to evaluate the neurocognitive status of patients and cover a range of mental processes, such as motor performance, attention, and memory if there is suspicion of a problem. We ten have professionals so neurobehavioral evaluations and if indicated a more comprehensive computer assessment called BCNI (Borrell Cognitive Neuropsychiatric Inventory) is conducted. This assessment allows to:

• Establish and document current status and use in later treatment decisions
• This distinguishes early mild or subtle behavioral problems in patients through comparison to other individuals his/her age
• This leads to decision making on the course of action to take. Counseling, medications, and social treatments to maintain quality of life are provided.
• It helps families understand the problem that effect emotion and behavior. Also it allows making a
prediction of the future functions, emotional, and social needs to improve the quality of life.

Senior PsychCare will make best efforts to use the evaluation to direct treatment in collaboration with the family, facility, staff and primary care physician.

More information about the screening process is available by contacting Tammy Simon, FIR Director at SPC, at 713 850 0049. Based on the fact that we are committed to providing the best and available care, we are providing there services under the professional staff of your long-term health care center. Thus we comply and are compliant with all HIPAA regulations.

Thank you for your time and patience.

The Utility of Mandatory Depression Screening of Dementia Patients in Nursing Homes

Carl I. Cohen, M.D.
Kathryn Hyland, Ph.D.
David Kimhy, M.D.

Depression in Assisted Living is Common and Related to Physical Burden

Lea C. Watson, M.D., M.P.H., Susan Lehmann, M.D.,
Lawrence Mayer, M.D., PhD., Quincy Samus, M.S.,
Alva Baker, M.D., Jason Brandt, Ph.D.,
Cynthia Steele; R.N.,M.P.H., Peter Rabins,
Adam Rosenblatt, M.D., Constantine Lyketsos, M.D., M.H.S.

In the first clinical study implemented by geriatric psychiatry professionals in AL, depression was found to be common, under treated and related to physical burden. AK is a rapidly growing segment of long-term care and represents an important setting in which to find and treat serious depression. (Am J Geriatric Psychiatry 2006; 14:876-883)

Why Screening is Indicated on all Ltc. Residents for Depression and Dementia
Neuropsychological testing in Skilled Nursing Facilities: The Failure to Confirm Diagnoses of Dementia

Irwin J. Mansdorf, Ph.D., Mary Harrington, LCSW, Jacqueline Lund, LCSW, and Nancy Wohl, LCSW

Dementia diagnoses may be inaccurate for 90% nursing home residents. Using objective measurement of cognitive functioning provided by neuropsychological testing could result in greater diagnostic accuracy and help provide for more accurate and appropriate treatment planning (J Am Med. Dir. Assoc. 2008; 9: 271-274).

Why Do We Do Screening

This tool was developed to aid primary care clinicians in caring for their patients who suffer primarily from Dementia and Alzheimer’s. However , many of the tools will also be useful for managing chronic depression and minor depression, secondary to Dementia and Alzheimer’s. The care management process recommended here builds on the earlier guidelines from the Agency for Health Care Policy and research (AHCPR)- now known as the Agency for Healthcare Research and Quality (AHRQ)- which have been updated and adopted from other evidence based sources including recently published multi-site trials and current studies.

Quick Facts About Psychological Counseling
• In psychological counseling, patients with depression work with a qualified health care professional who listens to them, talks and helps them correct overly negative thinking (which reinforces depressed mood) and improve their relationships with others
• Psychological counseling for depression is not talking about your childhood, but rather focused on current concerns and ways to address them.

Treating Depression with Psychological Counseling
Psychological counseling has been shown to be effective as antidepressants in treating many people with depression. Psychological counseling can be done individually (only you and a mental health professional). in a group (a mental health professional, you and others with similar problems) or it can be family or marriage counseling where a mental health professional, you and your spouse or family members participate: -More than half of the people-with mild to moderate depression respond well to psychological counseling. While the length of time that persons are involved in counseling differs, people with depression can typically expect to attend a weekly hour-long counseling session for 6- 20 weeks. If your depression is not noticeably improved after 6-12 weeks of counseling, this usually means that you need to try different treatment for your depression. Psychological counseling by itself is not recommended as the only treatment for persons whose depression is recurrent, more chronic or severe. Medication is needed for those types of depression and it can be taken in combination with psychological counseling.

What Can You Do To Help SPC and Senior Psychological Most Effectively Treat Your Depression With Psychological Counseling?

• Be honest and open and ask questions
• Work cooperatively by completing tasks assigned to you as part of the psychological counseling
• Be available and tell your mental health care professional how well the psychological counseling is working (e.g., whether your depression is getting better or worse).

Information for Clinicians, Administrators, and Primary Care Physicians about Screening

We believe that our integrated Model of Care (psychotropic management and therapy) and protocols developed over the years can provide your families with a distinct advantage in day-to-day operations resulting in a higher quality of care for your residents.

The integrated Model of care stresses regulatory compliance for long-term care facility by addressing medical management (F-329, F-4290), assessment, and administrative tag (F-501). Reduction in medications result in reduced falls and engage residents in more activities of daily living. This results in better participation in psychotherapy modules and behavior modification provided by higher training psychologists and therapists adhering to our protocols to further the quality of life of your clients. When residents respond to mediation and therapy, hospitalization is therefore reduced resulting in higher occupancy for the facility.

As you are aware, the more engaged the residents, the less prone to agitation they become. This reduces stress on your caregivers and turn over. You are bale to attract an retain happier staff and other clinical members of your facility. With stable occupancy and staff it is easier to plan for staffing, and scheduling, Educating physicians , family and the general public are also part of our responsibility.

If we can be of any assistance to you, please do not hesitate to contact any of us. We look forward to working with you.

Sincerely,
Leo J. Borrell

Reducing Psychotropic Drug use is Easy

67.7% of assisted living residents have dementia and 26.3% have an active non-cognitive psychiatric disorder. Screening has been found to be helpful in assisted living facilities and nursing homes.

Research shows that in nursing homes with treatment:
• 51% of participants with dementia and depression did improve their quality of life.
• 58% of those with depression alone, receiving counseling and medication recovered six months later and had a better quality of life.
• Only 25% of those receiving medication alone improved, but did not have a significantly better quality of life.
• Patients need to be seen 1-4 times per month in order to monitor-the constant fluctuation of behavioral and psychiatric symptoms and medical problems.
• Post stoke depression usually resolves in 6 months but can last two years.

In conclusion, patients who received psychotherapy (counseling) did 100% better than those that received medication alone. They also had a significant decrease in behavioral problems sooner and a better quality of life for longer.

Without psychotherapy, individuals with depression or dementia or both:
• 20% continued to-exhibit behavioral symptoms.
• 40% exhibited physically and/or verbally aggressive behavior

Because of these residents at nursing homes and assisted living facilities:
• Need to be routinely screened for depression
• All patients with behavioral problems need to be evaluated by a team of psychiatrist and mental health professionals.
• Most patients with many medical illnesses are not depressed.
• Staff needs to realize that many demented people will not spontaneously engage in activities because of depression or Alzheimer’s.
• Residents with dementia are taking several medications for problems such as insomnia or anxiety, the resident’s physician needs to review and possibly reduce the number of medications.

In conclusion, early evaluation and accurate comprehensive diagnosis is necessary. Medications alone are not enough. A comprehensive plan of 6-24 months with counseling is necessary to maximize results, prevent relapse and improve lie quality of life.

Screening is Important on Admissions to Nursing Homes

Psychiatric and Behavioral Symptoms in Dementia

• 80% of Nursing Home residents have psychiatric symptoms that progress unless properly treated.
• The elderly account for 20% of all suicides and have the greatest amount of depression, delirium, and dementia.
• Improving social skills, social involvement, the ability to participate in psychotherapy, coping skills, and avoid adjustment problems.
• Proper Diagnosis Important – Pseudo Dementia, Psychosis, and Cooperation.
• Psychotherapy minimizes the use of psychiatric medications and improves communicational development of the families.

Initiation of Services for Psychotherapy & Psychiatry
For All Primary Care Physicians and Charge Nurses

Please give completed form to the Director of Social Work.

Please refer to the list below as a guideline for determining which patients could benefit from psychiatric and/or psychotherapy treatment. If you have a question about whether or not a patient would benefit, please go ahead and refer that patient and an evaluation will be done to determine the course of treatment, if any.
Appropriate Mental Health Referrals include:
1. Residents who are newly admitted and dealing with adjusting to the loss of their previous residence and the nursing home setting.
2. Residents who are not new, but still struggling with adjusting to the nursing home setting and loss of their prior life.
3. Residents who are not complying with their medical or rehabilitation treatment needs.
4. Residents who are depressed about family or personal issues.
5. Residents who are nervous, anxious, or agitated.
6. Residents who have a history of depression, anxiety, or “nervous breakdown”.
7. Residents who have behavioral difficulties such as aggression, attempts at elopement, and resistance to A.DLS.
8. Residents who express a wish, intent or plan to die.
9. Residents who are dealing with chronic illness or disability (such as an amputation or gait disturbance with forced use of walker or wheelchair, etc).
10. Residents who are experiencing chronic pain and/or somatic symptoms that fail to remit with treatment.
11. Residents who are having difficulty resolving conflicts especially with their roommates.
12. Residents who are facing family conflicts.
13. Residents who are not responding to psychotropic medications.
14. Residents with previous psychiatric problems such as insomnia, depression, anxiety or previous psychiatric medications or hospitalizations.
15. Residents who are referred for Psychotherapy should also be seen by the Psychiatrist for medication review.

Please Evaluate: ? Psychiatric Medication Management ? Psychotherapy ? Other
Facility Name: ______________________________________________________________
Date: __________________ Referred by: ________________________________________
Send to DON or the Social Worker who is the coordinator of Mental Health referrals and if it is an emergency then call (210) 438-1900 or fax form to (800) 605-2138.

Lists of Patients:
Patient Name Room Number
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
SCREENING FOR PSYCHIATRIC MEDICATIONS AND PSYCHOTHERAPY REFERRALS

This form is to assist staff of non professionals in identifying behavior and psychiatric problems that require evaluation and treatment. Please have the Director of Social Work complete the request for Psychiatry & Psychotherapy Family Evaluation and forward it to SPC by fax at the number listed above.

Staff Member who completed this form:

Name: ____________________________________________

Primary Care Physician: ______________________________

REASON FOR REFERRAL
MEDICAL PROBLEMS/MEDICATION PROBLEMS

1. Having hallucinations/delusions/disordered thinking
2. Crying and/or persistent feelings of sadness/depression
3. Suicidal ideation (talks about suicide)
4. Persistent verbal/physical aggression toward others
5. Not coping well with terminal illness
6. Sexually inappropriate behaviors
7. Appears anxious/fearful
8. Significant change in eating/sleeping habits
9. Significant decline in physical/cognitive functioning or loss of limb
10. Death of family member or friend
11. Persistently low self esteem
12. Family issues that adversely effect resident’s emotional state
13. Has a new/old mental illness diagnosis Dx: ________________
14. Agitation and/or depression related to unrealistic expectations for rehabilitation
15. Somatization (obsessive health complaints not consistent with current physical status)
16. Withdrawal from activities/isolation
17. Resistant, uncooperative to counsel
18. Behavioral or cognitive side effects of psychoactive medications
19. Diagnosis of alcohol, drugs or pain medication dependence/addiction
20. Having significant difficulty adjusting to nursing home environment
21. Recent or impending loss of limb, speech or hearing
22. New medical problem that may affect behavior
23. Family concerns or problems
24. Evaluate medication

Other/Comments: _______________________________________________________
______________________________________________________________________

SENIOR PSYCHCARE, INC. IN AFFILIATION WITH SENIOR PSYCHOLOGICAL CARE, INC.
4314 Yoakum Blvd. Houston, Texas 77006 Phone: 713-850-0049 Fax: 713-850-0036 Toll-Free Fax: 800-605-2138
Web:http://www.SeniorPsychiatry.com
Patient Name:
Nursing Home:
Room #
Date Consultant :
Age:

FACILITY REFERRAL REQUEST FOR PSYCHIATRIC MEDICATIONS/PSYCHOTHERAPY CONSULTATIONS
(Short Form – for more detail use the Long Form)

Consent Form/ Face Sheet appreciated at time of consult. PCP order and info required before patient can be seen.
*******************TO BE COMPLETED BY REFERRAL MANAGER/ NURSING HOME STAFF***************
(CIRCLE) 48HRS / Routine: 3 to 7 Days Requested by______________________ Primary Care Physician______________
Urgent: Call Dr. Borrell at 713-850-0049; if no response, call cell phone 832-265-2882_______________________________
Nature of Urgency: ___________________________  Resistant to Care ? Family Session  Other: _________________
Please Check One:
Psychiatric
Psychotherapy
Both
Medicare Part A
SNF
Guardian
Chief complaint or immediate reason for Referral (Please Check all that Apply):
Depression
Anxiety
Psychosis
Agitation
Aggression
Suicide
Confusion
Other: ___________________
Chief complaint or immediate reason for Referral (Please Check all that Apply):
Depression
Anxiety
Psychosis
Agitation
Aggression
Suicide
Confusion
Other: ___________________
Dementia
Yes
No
Other Diagnoses: _________________________________________________________
A. EMOTIONAL SIGNS & SYMPTOMS (*E1,a,b,c,d,e,f,g,l,m,h,I) A resident’s emotional status interferes or enhances his/her ability to adjust to the institutional environment or to achieve self-actualization. Description:
A1. Anger
A2. Anxiety
A3. High Risk Behavior
A4. Reduced Social Interaction
A5. Depression/Sadness
A6. Sleep Problems
Comments: ______________________________________________________________________________________________________
PSYCHOSIS:
Delusions
Hallucinations Description: _________________________________________________

B. INTERACTIVE SIGNS & SYMPTOMS (*C-1, 2, 3, 4, 5) Communication problems may interfere with an individual’s ability to interact in positive ways, putting them at risk for isolation and sensory deprivation. The following are indicators.
B1. Aphasia
B2. Hearing
B3. Rarely understands others
B4. Rarely understood by others
B5. Sight Impairment
B6. Speech
Comments: ______________________________________________________________________________________________________

C. BEHAVIORAL SIGNS AND SYMPTOMS (*E4) Behavior associated with cognitive, emotional or diagnostic symptom logy may interfere with the efficient and safe operation of a facility. Such behaviors include:
C1. Disruptive Behaviors (also consider C3)
C2. Resistance to Care or ADL/Medications
C3. Inappropriate Behaviors (also consider C1)
C4. Aggressive Behaviors (Verbal/Physical)
C5. Wandering (also consider C2b, C2c, F3-Elopement)
C6. Weight Loss
Comments: ______________________________________________________________________________________________________

D. COGNITIVE SIGNS & SYMPTOMS: Many factors contribute to changes or decline. If addressed, symptoms may be minimized to improve quality of life.

____________________________________________________
D1. Confusion (also consider B3 and B4)
D2. Delusions
D3. Disorganized Speech
D4. MR/Developmental Disorder with Organic Condition
D5. Restlessness
D6. Short/Long-term memory problems
Comments: ______________________________________________________________________________________________________

E. SOCIAL SIGNS & SYMPTOMS Difficulties in social relationships may lead to emotional and/or behavioral problems.
E1. Adjustment Difficulty
E2. Conflict/Anger with family and/or friends
E3. Constantly Critical
E4. Loss of Close Family Member or Friend
E5. Sadness/Anger/Emptiness over Loss of Status
E6. Unhappy with Others
Comments: ______________________________________________________________________________________________________

F. OTHER CONCERNS
F1. Substance Abuse
F2. Discharging
F3. Elopement (also consider C5-Wandering)
F4. End Stage
F5. Wants and Needs
????F6. Pain ????F7. Evaluations
Comments: ______________________________________________________________________________________________________

Alzheimer’s disease is a relentlessly progressing dementing disorder. Major pathological earmarks include extracellular sediments of amyloid protein and intraneuronal neurofibrillary alterations. No remittances take place in the path of the disease. Prototypical amylaceous deposits originate in poorly myelinated regions of the basal neocortex. From there, they spread into bordering areas and the hippocampus. Deposits eventually infiltrate all cortical areas, including thickly myelinated primary fields of the neocortex (stages A-C).

Intraneuronal lesions arise initially in the transentorhinal region, then spread in a predictable fashion across other areas (stages I-VI). At stages I-II, neurofibrillary alterations develop preferentially in the absence of amyloid deposits. A balance of cases shows early development of amyloid deposits and/or intraneuronal changes. Advanced age is therefore not a requirement for the development of the lesions. Alzheimer’s disease is an age-related, not an age-dependent disease. The level of brain destruction at stages III-IV frequently results to the appearance of prototypical clinical symptoms. The stages V-VI representing fully developed Alzheimer’s disease are increasingly prevailing with increasing age. The arithmetical mean values of the stages of both the amyloid-depositing and the neurofibrillary pathology increase with age. Age is a risk element for Alzheimer’s disease.

INTRODUCTION — Alzheimer disease (AD) is a neurodegenerative disorder of uncertain cause and pathogenesis that mainly impacts senior adults. The fundamental clinical manifestations of AD are selective retentiveness deterioration and dementia. AD is the most frequent cause of dementia. While treatments are accessible that can modulate the course of the disease and/or improve many symptoms, there is no remedy, and the disease inevitably progresses in all patients.

This topic recaps the clinical manifestations and diagnosis of AD. Other topics review the risk factors and treatment of AD and the clinical manifestations of other causes of dementia and cognitive impairment.

DEMOGRAPHIC FEATURES — Alzheimer disease (AD) is characteristically a disease of senior years [1]. It is exceptional for AD to occur before age 60. The incidence and preponderance of AD increment exponentially with age.

AD is slightly more common in women than men, with a comparative risk of 1.5. This does not seem to be explicated by the greater longevity in women.

There are genetic grades of AD, all autosomal dominant, that routinely present before age 65, and frequently in the fifth decade or before. These account for less than 5 percent of all types of AD. Patients with Down syndrome acquire AD at an earlier age, 10 to 20 years younger than the broad population with AD.

Other risk categories for AD are discoursed on an individual basis.

CLINICAL FEATURES

Retentiveness impairment — Memory impairment is an essential feature of AD and is oftentimes its earliest manifestation. Even when not the primary complaint, retention shortfalls can be elicited in most patients with AD at the time of introduction.

The design of memory impairment in AD is also peculiar. Declarative memory for facts and outcomes, which reckon on mesial temporal and neocortical structures are profoundly impacted in AD, while subcortical systems supporting procedural memory and motor learning are relatively spared until rather late in the disease. A subset of declarative memory, that of particular events and contexts (episodic memory) is more profoundly impaired in early AD, compared with retentiveness for facts such as vocabulary and constructs (semantic memory), which oftentimes becomes impaired somewhat later. Semantic memory is encoded in neocortical (nonmesial) temporal areas.

Within episodic memory, there is a differentiation between immediate recall (eg, mental rehearsal of a telephone number), memory for recent events (which comes into play once material that has departed from cognisance must be recalled), and memory of more removed events. Memory for recent events, assisted by the hippocampus, entorhinal cortex, and related structures in the mesial temporal lobe, is prominently impaired in early AD. In direct contrast, immediate memory (encoded in the sensory association and prefrontal cortices) is spared early on, as are memories that are integrated for long periods of time (years), which can be retrieved without hippocampal function.

The early retentiveness deficit in AD is most precisely discovered as anterograde long-term episodic amnesia. Because the absolute time interval over which long-term memory can fail can actually be brief (eg, inability to recall a few words after a couple minutes of distraction), patients and primary care providers typically refer to “short-term memory” problems. For this reason, we try to avoid the confusion afforded by the technical terms of long-term and short-term memory and use the term “recent memory impairment” to refer to the characteristic impairment.

Memory deficits develop insidiously and build up slowly over time, evolving to include deficits of semantic memory and immediate recall. Deteriorations of procedural memory appear only in late phases of AD.

Memory is ordinarily tested by asking patients to recall three objects immediately and then at a delay of 5 to 10 minutes. Queries about orientation and recent current events are likewise useful memory tests. Clinicians should not rely on a patient’s report of memory impairment, as many older individuals are unreliable reporters of their own retention impairment and can both over and under approximate their deficits.

Amnestic mild cognitive impairment — A state of circumscribed anterograde long-term retentiveness impairment, with preserved general cognitive, sociable functioning is identified as amnestic mild cognitive impairment (MCI). Amnestic MCI is more and more recognized as an early point of AD, with a transition rate to dementia at about 10 to 15 percent per year.

Other facets of cognitive decline — Deficits in other cognitive fields may appear with or after the evolution of memory impairment. Speech function and visuospatial skills incline to be impacted comparatively early, while deficits in executive function and behavioural symptoms frequently manifest afterward in the disease course. These deficits appear and advance insidiously.

Language — Verbal dysfluency and anomia are often early characteristics of AD and are sometimes the exhibiting characteristic. The first manifestations of language disfunction usually include word-finding troubles, ambage, and decreased lexicon in instinctive language and with anomia on confrontational naming tests. This advances to include agrammatism, paraphasic errors, broken speech content, and impaired comprehension. Patients can usually repeat phrases word for word until the disease is quite advanced.

Language disfunction and departure of semantic memory are interconnected in AD. Some investigators have discovered that loss of semantic eloquence is an early determination in AD. When asked to give word lists in one minute’s time, patients with AD perform significantly worse on a category fluency test (eg, lists of animals) than on a letter fluency test (eg, lists of words starting with F). Typical execution is age associated, with at least 15 items expected at age 65.

Visuospatial skills — Loss of visuospatial skills is an early characteristic of AD that is sometimes very prominent at presentation. Visuospatial impairments manifest as malposition of details and difficulty navigating in first unfamiliar then common terrain. Ocular agnosia (inability to recognize objects) and prosopagnosia (inability to recognize faces) are more advanced characteristics. Numerous clinicians have noted hemispatial visual neglect in their patients with AD.

Visuospatial skills may be screened by asking patients to re-create simple figures (eg, crossed pentagons) and to make a clock face. The latter, when compounded with a request to fill in the time at “ten after eleven,” is a deceptively trying test and measures semantic cognition as well as executive and spacial operation.

Insight — Reduced perceptivity into his or her deficits (anosognosia) is a characteristic feature of AD and has been connected to frontal lobe pathology. It is commonplace for patients to underestimate their deficits and offer alibis or explanations for them when they are pointed out. Questioning a collateral historian, ordinarily a family member, who has known the patient over time, is helpful, and oftentimes it is the family member, not the patient, who takes the complaint of cognitive impairment to medical attention.

Loss of perceptivity increases over time along with overall disease severity. Comparative loss of insight is affiliated with behavioral disturbances; those with comparatively preserved insight are more liable to be depressed, while those with more impaired insight are likely to be agitated, disinhibited, and present psychotic features.

Apraxia — Dyspraxia, or trouble executing learned motor tasks, commonly comes about later in the disease after deficits in memory and language are apparent. Before it is clinically apparent, dyspraxia can be elicited by asking the patient to execute ideomotor tasks, ie, pantomime the use of tools (eg, “show me how you would use a comb”). Clinical dyspraxia leads to progressive difficulty first with involved, multi-step motor actions, then with getting dressed, eating, and other self-care tasks and is a primary contributor to dependence in mid to late phases of AD.

Executive function — In early stages of AD, damage in executive function may be subtle rather than obvious; family members and coworkers may find them less motivated and engaged. In addition to poor insight, depressed ability for abstract reasoning may be elicited. As the disease builds, a more apparent modification of personality, bad judgment and planning, and an unfitness to finish tasks typically emerges.

Neuropsychiatric symptoms — Neuropsychiatric symptoms are commonplace in AD, particularly in the intermediate and late path of disease. These can start out with subtle personality changes including indifference, social detachment, and disinhibition. The former may be a materialization of overlying clinical depression, which can be difficult to diagnose in the setting of dementia.

More troublesome in patient management is the emergence of behavioral interferences, including excitement, aggressiveness, wandering, and psychosis (hallucinations, delusions, misidentification syndromes). A resultant medical illness, medication toxicity, and other causes of delirium should be considered whenever new behavioral disturbances develop. The behavioral disturbances affiliated with AD are talked about in detail separately.

Dementia can be caused by several different brain disorders. It is commonplace for older people to have more than one disorder contributing to dementia. These include:

Alzheimer disease — Alzheimer disease is affiliated with the death of nerve cells (neurons) in important sections of the brain. Scientists have not yet ascertained precisely why and how Alzheimer disease formulates, but they do acknowledge that the brains of patients with Alzheimer disease build up deposits of a protein called beta amyloid (these deposits are also known as plaques), and that individuals also develop disordered volumes of protein fibers within the brain cells known as neurofibrillary tangles.

Vascular dementia — People with vascular dementia have lost or damaged regions of brain because of decreased blood flow. This can take place when the blood vessels in the brain get congested with blood clots or fatty deposits. This form of dementia is more common among people who have had strokes or are at risk for strokes, especially those with long-term high blood pressure and diabetes. It can occur together with Alzheimer disease.

Dementia with Lewy bodies — Dementia with Lewy bodies is a kind of dementia caused by irregular protein structures called Lewy bodies forming within brain cells. It oftentimes happens with symptoms of Parkinson disease, such as trembling, stiffness, and slowness. This disorder often causes colorful and prolonged delusions.

Parkinson disease dementia — Dementia can also occur later in the course of Parkinson disease and has symptoms that are very analogous to dementia with Lewy bodies.

Frontotemporal dementia (formerly called Pick’s disease) — Like Alzheimer disease, frontotemporal dementia stimulates nerve cell loss in the brain, but frontotemporal dementia targets two specific components of the brain, called the frontal and temporal lobes.

Frontotemporal dementia ordinarily develops at an earlier age than Alzheimer disease. Three forms are more commonplace than others: One induces personality alterations and irregular societal demeanor; one impairs speech and eventually leaves the patient unable to talk; another causes trouble in understanding speech.

Other causes of dementia — Dementia can also be induced by cumulative harm to the brain, which can occur in individuals with long-term alcohol addiction or recurring head injuries (eg, among former professional boxers or football players).

Assessment and Care
A new technology has been created to enhance behavioral health care and allow providers to better serve patients. BCNI, an innovative software program, aims to provide the clinician a rapid in-office procedure that produces a quantitative view of their patient’s neurocognitive status that is valid, reliable, objective, and reimbursable. Just as you carefully monitor the vital signs (weight. blood pressure, cholesterol, etc.) of your loved ones, consider the value of having a baseline for neurocognitive functions for those same patients.
BCNI power the tests and the neurocognitive testing has been in use by clinicians and researchers around the world. All patients, age 50 and older, are recommended to have a baseline neurocognitive test performed.

This type of testing has been utilized at respected institutions such as John Hopkins, Duke, UNC, Chapel Hill, the VA and clinical research sites in over 30 countries.
The BCNI assessment process itself is simple. A patient’s test s completed in approximately 30 minutes and is covered by most insurance as well as Medicare. The patient responds to stimuli on the screen by tapping a few keys on the keyboard. The assessment then utilizes scientifically validated objective tests to evaluate the neurocognitive status of the patient and covers a range of mental processes such as motor performance, attention, memory, reaction time and executive function. Following the assessment, a report and interpretation of the patient’s test results will be forwarded.
Medical professionals and researchers know that good health has many dimensions, one of the most important and yet least measured is the health of a patient’s brain. Now with the advent of BCNI clinicians have an east-to-use clinical tool that ineasures neurocognitive functions, such as Memory, Reaction Time,Psychomotor Speed, Complex Attention, and Cognitive Flexibility. Proper neurocognitive function is a major factor in determining a person’s quality of life.

The brain and central nervous system (CNS) have “vital signs,” but they have never been easy to objectively measure. Until now…
BCNI is effective in detecting early signs of dementia, Alzheimer’s, and tracking recovery from neurological problems. This computerized testing platform has been used:
• When lengthier assessments are either impractical or inappropriate
• Measured repeatedly or in patients in whom the diagnosis is known (e.g. mild and severe head injury or early neurodegenerative disease — early dementia and Alzheimer’s)
• To provide a valuable secondary clinical endpoint that may be an indicator for compliance or quality of life (e.g. psychiatric symptoms , chemo fog, fibro fog, sleep disorders, medication effects)
• In lengthy clinical treatment programs where minimal disruptions for cognitive assessment may be beneficial (e.g. cardiac surgery)
When the monitoring and management of medications is necessary (e.g. Alzheimer’s, depression, behavioral problems).

The psychometric characteristics of the tests are very similar to the characteristics of the conventional neuropsychological tests upon which they are based.
To learn more about BCNI call Senior PsychCare at 713-850-0049

Statin treatment may bring down the chance of later dementia by more than 50%, a domestic Finnish report has ascertained.

“Perturbations in cholesterol metabolic process have previously been connected to dementia evolution,” Dr. Alina Solomon wrote in a poster introduced at the International Conference on Alzheimer’s Disease. All the same, Dr. Solomon, of the University of Kuopio, Finland, observed that not all studies have reasoned that statins bestow a preventive effect against dementia onset.

Doctor. Solomon and her fellows analyzed this question applying information elicited from the national FINRISK report, an extensive, population-based review of cardiovascular risk elements among Finnish citizens. The survey started in 1972 and is conducted every five years. MD. Solomon’s substudy of FINRISK included information about 17,257 citizens who were included in the 1997 and 2002 cohorts, and who were at least 60 years old in 1995, when statins became accessible in Finland.

By the study’s conclusion at 2007, 1,551 of the subjects had acquired dementia and 15,706 hadn’t. Just 18% of those who developed dementia had gotten at least 1 year of statin therapy, while 37% of those who were dementia-free had taken a statin – a substantial deviation.

No meaningful affiliations were ascertained between dementia and the consumption of other cholesterol-lowering medicines, doctor. Solomon stated, indicating that “the effect of statins in dementia is partially unaffiliated of their cholesterol-lowering effect.”

Subjects who acquired dementia likewise had significantly greater baseline total cholesterol and baseline systolic and diastolic blood pressure. But a variable regression framework that controlled for age, gender, education, cholesterol, weight, and blood pressure still ascertained that statins bestowed a 57% risk decrease for dementia across the run of the study.

The determination doesn’t establish that statins prevent dementia. But it does indicate that more reports should research the theme, centering on statin types, doses, and length of treatment, doctor. Solomon stated at the gathering, which was sponsored by the Alzheimer’s Association.

Neither she nor her coinvestigators announced any possible conflict of interest in relation to the report.

Circumstance: Pandemic influenza A(H1N1) egressed quickly in California in April 2009. Explorative comparabilities with seasonal flu indicate that pandemic 2009 influenza A(H1N1) disproportionately impacts younger ages and induces normally meek disease.

Objective: To distinguish the clinical and epidemiological characteristics of pandemic 2009 influenza A(H1N1) instances that resulted in hospitalization or death.

Conception, Setting, and Participants: Statewide increased public health surveillance of California residents who were hospitalized or passed away with research lab evidence of pandemic 2009 influenza A(H1N1) infection reported to the California Department of Public Health between April 23 and August 11, 2009.

Primary Result: Assess features of hospitalized and lethal cases.

Outcomes: During the study time period there were 1088 cases of hospitalization or death due to pandemic 2009 flu A(H1N1) infection reported in California. The average age was twenty-seven years (scope, <1-92 years) and 68% (741/1088) had risk components for seasonal influenza complications. 66 percent (547/833) of those with chest radiograms executed had infiltrates and 31% (340/1088) necessitated intensive care. Rapid antigen examinations were falsely negative in 34% (208/618) of cases assessed. Secondary bacterial contagion was discovered in 4% (46/1088). Twenty-one percent (183/884) received no antiviral drug treatment. Gross fatality was 11% (118/1088) and was greatest (18%-20%) in individuals aged fifty years or older. The primary causes of demise were viral pneumonia and acute respiratory distress syndrome.

Determinations: In the introductory 16 weeks of the present-day pandemic, the average age of hospitalized infected cases was younger than is common with seasonal flu. Babies had the steepest hospitalization rates and individuals aged fifty years or older had the greatest mortalities when hospitalized. Most cases had established risk components for complications of seasonal flu.

Description: Update of the 2002 U.S. Preventive Services Task Force (USPSTF) recommendation statement on testing for breast cancer in the overall population.

Processes: The USPSTF analyzed the evidence on the efficaciousness of five screening modalities in subduing fatality rate from breast cancer: film mammography, clinical breast exam, breast self-examination, digital mammography, and magnetic resonance imaging in order to update the 2002 recommendation. To achieve this update, the USPSTF authorised 2 reports: 1) a targeted orderly evidence reexamination of 6 chosen inquiries referring to benefits and damages of screening, and 2) a decision analysis that applied population modeling methods to equate the anticipated health results and resource demands of initiating and terminating mammography screening at various ages and employing yearly versus biyearly screening intervals.

Recommendations: The USPSTF advocates against regular screening mammography in women aged 40 to 49 years. The determination to begin orderly, biennial testing mammography prior to the age of 50 years should be a case-by-case one and take into account patient circumstance, including the patient’s values concerning particular benefits and harms. (Grade C recommendation)

The USPSTF recommends biennial screening mammography for women between the ages of 50 and 74 years. (Grade B recommendation)

The USPSTF resolves that the present-day evidence is inadequate to measure the supplementary benefits and harms of screening mammography in women 75 years or older. (I statement)

The USPSTF reasons that the prevailing evidence is inadequate to evaluate the extra benefits and damages of nonsubjective breast testing beyond testing mammography in women 40 years or older. (I statement)

The USPSTF advocates against clinicians instructing women how to execute breast self-examination. (Grade D recommendation)

The USPSTF concludes that the contemporary evidence is insufficient to evaluate further benefits and harms of either digital mammography or magnetic resonance imaging rather than film mammography as screening modes for breast cancer. (I statement)

The DIAD Study: A Randomized Regimented Trial

Context: Hardening of the arteries (CAD) is the leading cause of mortality and morbidity in patients with type 2 diabetes. But the usefulness of testing patients with type 2 diabetes for asymptomatic CAD is contentious.

Objective To evaluate whether regular screening for CAD identifies patients with type 2 diabetes as being at utmost cardiac peril and whether it impacts their cardiac issues.

Conception, Setting, and Patients: The detecting of ischaemia in Asymptomatic Diabetics (DIAD) report is a randomized controlled trial in which 1123 participants with type 2 diabetes and no symptoms of CAD were arbitrarily designated to be screened with adenosine-stress radionuclide myocardial perfusion imaging (MPI) or not to be screened. Participants were enrolled from diabetes clinics and practices and prospectively followed up from August 2000 to September 2007.

Primary Result: Appraise Cardiac demise or nonlethal myocardial infarction (myocardial infarct).

Outcomes: The cumulative cardiac event grade was 2.9% over a normal (SD) reexamination of 4.8 (0.9) years for an average of 0.6% each year. Seven nonfatal MIs and 8 cardiac deaths (2.7%) came about among the screened group and 10 nonfatal MIs and 7 cardiac deaths (3.0%) among the not-screened group (risk ratio [HR], 0.88; 95% confidence interval [CI], 0.44-1.88; P = .73). Of those in the screened group, 409 participants with standard outcomes and 50 with reduced MPI faults had more deficient event rates than the 33 with modest or sizable MPI defects; 0.4% per year vs 2.4% per year (HR, 6.3; 95% CI, 1.9-20.1; P = .001). All the same, the affirmative prognostic value of sustaining moderate or large MPI defects was merely 12%. The gross rate of coronary revascularization was depressed in both groups: 31 (5.5%) in the screened group and 44 (7.8%) in the unscreened group (HR, 0.71; 95% CI, 0.45-1.1; P = .14). During the course of study there was a considerable and tantamount growth in basic medical prevention in both groups.

Determination: In this contemporaneous study universe of patients with diabetes, the cardiac event rates were modest and weren’t significantly contracted by MPI screening for myocardial ischemia across 4.8 years.

Backdrop: Vertebroplasty is generally employed to address painful, osteoporotic vertebral compression fractures.

Processes: In this multicenter trial, we arbitrarily allotted 131 patients who had one to three painful osteoporotic vertebral compression fractures to receive either vertebroplasty or an imitative operation without cement (control group). The basic results were grades on the modified Roland–Morris Disability Questionnaire (RDQ) (on an ordered series of 0 to 23, with greater scores signaling higher disability) and patients’ valuations of ordinary pain saturation during the previous twenty-four hours at 1 month (on a scale of 0 to 10, with higher scores suggesting more intense infliction). Patients were permitted to cross over to the additional study grouping after 1 month.

Outcomes: All patients experienced the delegated intercession (sixty-eight vertebroplasties and sixty-three simulated processes). The baseline features were similar in the two groups. At 1 month, there was no substantial deviation between the vertebroplasty group and the control group in either the RDQ score (deviation, 0.7; 95% confidence interval [CI], –1.3 to 2.8; P=0.49) or the pain evaluation (difference, 0.7; 95% CI, –0.3 to 1.7; P=0.19). Both groups had prompt betterment in disability and pain scores after the intercession. Although the two groups didn’t differ significantly on any subordinate result measurement at 1 month, there was a tendency toward a greater value of clinically significant betterment in pain (a 30% reduction from baseline) in the vertebroplasty group (64% vs. 48%, P=0.06). At 3 months, there was a greater crossover rate in the control group than in the vertebroplasty group (43% vs. 12%, P<0.001). There was one critical untoward event in each group.

Determinations: Advances in pain and pain-related disability affiliated with osteoporotic compression fractures in patients cared for with vertebroplasty were akin to the improvements in a control group.