cause. One of three factors must also be present: .... Subtracting serial threes from 20 is also included. A .... to rule out treatable causes of dementia include the ...
Russell J. Sawa
Senile Dementia and Family MediCine SUMMARY
SOMMAIRE
Senile dementia is an increasingly important disease in family medicine, because our population is growing old. Dementia can have many causes, some of which are reversible. Its definition varies with time, discipline, and country. Correctly diagnosing reversible dementing processes as early as possible may lead to reversal of an otherwise devastating process. This article discusses definition and diagnosis of senile dementia. (Can Fam Physician 1981; 27:137-142).
La demence senile est une maladie de plus en plus importante en medecine familiale parce que la population devient plus agee. La demence peut avoir plusieurs causes dont certaines sont irreversibles. Sa definition vane selon le temps, la discipline et le pays. Le diagnostic precoce et exact d'un processus de demence reversible peut justement prevenir l'evolution de ce processus. Cet article donne la definition de la demence senile et son diagnostic.
I
Dr. Sawa is assistant professor of family practice at the University of Calgary. Reprint requests to: Family Medicine Teaching Centre, Calgary General Hospital, 841 Centre Ave. E., Calgary, AB. T2E OA1. S ENILE DEMENTIA is an important clinical entity in family medicine because its incidence is rising as the North American population ages. In Canada eight percent (in the U.S.A., 9.8%) of the population is 65 or over. These figures are expected to double in Canada in the next 25 years.' Wang estimates that the median prevalence rate for dementia in the United States is five percent, or one million people.2 This is projected to rise by 43% by the year 2000. According to Schwenger,3 9.2% of our over ten million senior citizens are institutionalized. With this general aging of the population, careful consideration should be given to our management and understanding of senile dementia.
conditions which can be corrected in 15% of cases.5 He has also found that 35-40% of demented patients have conditions in which some form of therapeutic intervention other than symptom relief is important. While the above figures appear unrealistically high, it is nonetheless clear that a consistent effort in trying to uncover and treat underlying factors will help alleviate a tremendous amont of human suffering. One condition which can be treated before the symptoms of dementia arise is multi-infarct dementia. Hypertension is an important predisposing factor in this condition. Since normal autoregulation may be lost in individuals with severe hypertensive arteriosclerotic vascular disease, abrupt lowering of blood pressure may lead to infarct. In multi-infarct dementia, a moderate reduction is called for, not normal restoration.4 Prevention of multi-infarct dementia requires adequate control of diastolic and systolic hypertension.
Prevention
Definition
Recent surveys have shown that 20% of patients having dementia have underlying treatable disorders. Wells has found that a thorough evaluation of demented patients will produce
Because the incidence of senile dementia is steadily increasing, it becomes an important area for clinical research. Unfortunately, work in this area has been somewhat neglected
CAN. FAM. PHYSICIAN Vol. 27: JANUARY 1981
until recently. Comparative studies can be confusing due to confusion of the various meanings that the word dementia has had during the past. A major problem in any discussion of 'senile dementia' is the fact that the term can and does mean different things, depending on whether a psychiatrist or a neurologist, and/or an American or European is speaking. The word dementia itself has had dis-
tinctly different meanings throughout the ages. Pinel (17th century) used it to mean 'out of one's mind'. In the 19th century it meant 'madness from all mental causes'. In 1907 Kraeplin10 defined it as a diagnostic term meaning a specific form of involutional psychosis. In the 1950s the American Psychiatric Association tried to clarify this by introducing a new term, 'organic brain syndrome'. 20 The British meanwhile have suggested we abandon the term dementia entirely in favor of 'brain failure'.6 Last year the American Psychiatric Association introduced a new definition.7 While retaining the concept of organic brain syndrome, it has abandoned the distinction between psychotic and non-
psychotic organic brain syndromes. It also allows dementia to be condisered as reversible, maintaining that dementia is global cerebral impairment which is classified with five other entities as an organic brain syndrome. 137
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Dementia is then a deterioration of previously acquired intellectual abilities, with memory impairment, and evidence of an underlying organic cause. One of three factors must also be present: impairment of abstract thinking as manifested by reduced capacity for generalizing, differentiating, concept formation, or logical reasoning; impairment of judgement, and impairment of impulse control, or personality changes. Dementia is excluded when intoxication or delirium are present. Delirium is defined as a disturbance of attention by either impaired ability to sustain attention or impaired goal directed thinking or behavior. Also, at least two of the following must be present in delirium: reduced wakefulness or insomnia, perceptual disturbance (illusions or hallucinations); or an increase or decrease in psychomotor activity. Delirium also develops over a short period of time and fluctuates rapidly. Again, an organic factor must be de138
tected by history, physical or laboratory tests. Whereas psychiatry tends to formulate its concepts in terms of affectual, intellectual and symbolic functions, neurologists conceptualize motor, sensory, reflex and symbol manipulative functions. Thus Wells, a neurologist, defines dementia as "a spectrum of mental states resulting from disease states of the cerebral hemispheres in adult life."5 He thus considers it a broad continuum of dysfunction rather than a diagnostic entity. According to Wells, dementia is most often, but not always (as with Korsakoff's disease) global in nature. The severity of the pathology seen at autopsy does not always correspond to the severity of the clinical symptoms. Delirium is conceptualized as being abrupt in onset, with variability as its hallmark. Alterations in consciousness and physiological functions with resulting signs such as restlessness, tremor, slurred speech, insomnia, nausea and vomit-
ing, sweating, pallor, flushing, tachycardia, and constipation, may be found in delirium. Alteration in consciousness occurs late in dementia. Many different pathological processes can lead to a final common picture. Since many studies describe symptomatology while not accurately documenting pathology (by autopsy) it is often difficult to know which specific diagnostic entity is being discussed or whether a host of entities share a common 'senile dementia' symptom complex. Alzheimer's disease is a specific entity histopathologically. Some authors'0 have assumed it to be the underlying process in a symptom complex when no other underlying or degenerative processes can be found. At autopsy the brain tissue of those described as being 'senile demented' in behavior is found to have an increase in the normal byproducts of the aging brain cell. These changes are seen as neurofibrillary tangles and senile plaques. Their CAN. FAM. PHYSICIAN Vol. 27: JANUARY 1981
numbers increase in all humans with increasing age. These entities are less prominent in mentally healthy people.8 The changes are normally in the hippocampus. Migration to the cerebral cortex may be responsible for the mental changes described as dementia.4 Katzman4 clearly distinguishes this entity by calling it senile (presenile if under 65) dementia of the Alzheimer's type. Autopsy findings consistent with hypertension and arteriosclerosis are found in patients who also have the symptom complex described as dementia.8 Whether or not patients who become demented from underlying pathology, such as infection, ultimately undergo the same histological degenerative changes as those who have Alzheimer' s disease is not clearly expressed in the literature. It has also been found that patients with senile dementia of the Alzheimer's type have a decrease in acetylocholine transferase.4 This might provide a key to the prevention or treatment of this condition.
'Functional' Differential Diagnosis Depression Depression must be considered in the differential diagnosis of senile dementia, and may be present concurrently with dementia. The dominant change is in mood, varying from mild despondency to abject despair. The mood is relatively fixed and lasts from days to years. Rather than frank depression, there may be depressive equivalents in the elderly, just as there are in children. Thus multiple somatic complaints, sleep disturbance, consti-
mentation, decreased interest or perplexity may be confused with a dementing process. Paraphrenia A British term which means 'schizophrenia with onset in old age', paraphrenia is characterized by paranoid delusions (particularly persecution) and hallucinations, auditory, visual or olfactory. Bizarre behavior and severely altered or inappropriate affect are present. The first two features may also occur with a psychosis related to organic brain syndrome as well.10 Differentiation between this and senile dementia rests on the mental status examination. The EEG is also very useful. It should be noted that any preexisting psychopathology will complicate any particular case.
pation, dyspnea, weight loss, appetite disturbance, weakness and fatigue may be the chief complaints, and depression the diagnosis.9 Poor concentration, lack of interest, lack of ambition or motivation, indecisiveness and poor memory may be present. There may be a slowing down of movement, or agitation. Suicide threats must be Underlying Physical Causes Common causes of the senile detaken seriously in the elderly. The early signs of depression, which in- mentia syndrome which is referred to clude memory complaints, slowed as 'brain failure' in Britain, are: II
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1. Acute infections, especially of chest and urine. 2. Chronic medical conditions, such as hypothyroidism, anemias of any cause, chronic renal failure, syphilis, malabsorption and vitamin deficiencies, such as B 1 and B2. 3. External agents, as in chronic alcoholism, the use of psychotropic, hypertensive or other drugs. 4. Depression, which mimics brain failure. 5. Space-occupying lesions of the brain, especially tumors secondary to lung or breast cancer. Other potentially reversible underlying causes should be added: 1. Trauma: with subdural fat embolism from fractures and burns. 2. Infarction: cerebral, cardiac or pulmonary. 3. Other toxins, such as in brominism, steroid drugs, uremia, hepatic failure and carbon monoxide poisoning. 4. Deficiencies, as in hypoxia, hypoglycemia, hemorrhage, hypothermia and water or salt depletion. 5. Other general diseases, such as arteritis and diabetes. 6. Normal pressure hydrocephalus. When there is no obvious underlying organic symptomatology, 'silent' physical disorders should be considered. A list of such conditions includes: 1. Dehydration, a common cause in nursing homes. 2. Silent myocardial infarction. 3. Bronchopneumonia (in the elderly the temperature may be normal or subnormal.) 4. Urinary tract infection. 5. Mild uremia due to prostatic obstruction. 6. Myxedema. 7. Pernicious anemia. 8. Diabetes mellitus. 9. Pain and discomfort due to bladder distention, fecal impaction or other factors. In the case of those patients with cerebrovascular disease, factors which generally predispose to cerebral degeneration and senile dementia include premorbid personality traits, previous mental disorders, longstanding tendency to be unsociable, bereavement, retirement and poverty. Acute physical illness may precipitate cerebral decompensation: 1. Fever, which leads to increased metabolic needs. 140
2. Diabetes, with hyper- or hypoglycemia. 3. Respiratory insufficiency, which leads to hypoxia. 4. Blood loss or anemia. 5. Cardiac arrhythmias, leading to hypotension or microemboli. 6. Induced and spontaneous hypotension, especially due to use of phenothiazines. 7. Polycythemia, leading to increased blood viscosity and possible intravascular thrombosis. 8. Hyperlipemia, leading to intravascular thrombosis. 9. Cervical spondylosis with extrinsic artery narrowing and possible vessel occlusion. A relatively frequent emergency situation, the alcoholic in coma, should be mentioned. Because of the high incidence of head injuries, a chronic subdural (with early symptoms of irritability, headache, somnolence, lethargy and personality changes) should be ruled out. Chronic subdural may present a picture of psychosis with the symptoms of a brain tumor.12
Diagnosis Early signs of dementia5 include multiple physical complaints which fit no discernible pattern of physical disease, delirium occurring upon apparently slight provocation, or when the story remains vague and unclear to the examiner after a long and sympathetic hearing. The appearance of a variety of psychiatric symptoms, such as depression, anxiety and irritability (especially when no specific functional diagnosis or previous history of emotional difficulties exist), may also be early clues to the presence of dementia. Often a relative, friend or employer first becomes aware of a certain lack of initiative, irritability, loss of interest, and inability to perform up to the usual standards. Later distractibility, inability to think with accustomed clarity, reduced general comprehension, perseveration in speech, action, and thought, and defective memory, especially for recent events, may be noticed. There are a number of validated reliable brief mental status examinations now available. In 1975 Pfieffer published the 'Short Portable Mental Status Questionnaire,'13 in which the date, day of the week, name of this place, patient's telephone and address,
age, date of birth, mother's maiden name, name of the present and past presidents are asked. Subtracting serial threes from 20 is also included. A score is devised according to the number of correct answers. The mini-mental status14 is an excellent brief examination documented for validity and reliability, and also can be scored for degree of organicity. It tests orientation by naming the year, date, day, month, province, town, and hospital. Registration is tested by asking the patient to learn the names of three objects (i.e. red, table, 23 Broadway). Attention and calculation is tested by five serial sevens or spelling 'world' backwards. Recall is tested by asking the patient to recall the above names of the three objects learned, several minutes after learning them. Language is assessed by asking them to name a pencil and a watch, to repeat "no ifs, ands, or buts" and to follow a three stage command: "Take a paper in your right hand, fold it in half, and put it on the floor." The patient is also asked to read and obey the command "Close your eyes", and to write a sentence and copy a design (intersecting pentagons). The performance is assessed by a point system for the number of correct responses. Jenkyn'5 statistically analyzed the validity and reliability of 13 questions from typical mental status examinations and 32 signs of neurological dysfunction. He found that 13 of these could be useful predictors of diffuse cerebral dysfunction in brief bedside screening. Some of the helpful items include the days of the week in reverse, recall of past presidents in order (normal is three presidents if 20 years old, five if 40 years old, and seven if 60), serial sevens and spelling 'world' backwards. The three items with distraction (red, table, 23 Broadway) should be recalled immediately and at the end of the examination with a maximum of three promptings. Simple reflexes which can be tested at the bedside include the nuchocephalic reflex, the glabellar blink, the suck reflex, visual tracking, paratonia of both arms and legs, and limb placement. Abnormal responses indicate diffuse cerebral dysfunction. The nuchocephalic reflex is assessed by turning the shoulders of the standing subject (whose eyes are closed) briskly to the left and right. Normally the head turns actively after a pause of half a CAN. FAM. PHYSICIAN Vol. 27: JANUARY 1981
second. The abnormal response is when the head remains in the original position relative to the shoulders. The glabellar blink is assessed by asking the subject to fix his gaze on a point across the room. The index finger is then introduced from above the forehead (outside the visual field) and the glabella is tapped eight to ten times. Normally the patient blinks two or three times and then the eyes remain open. The suck reflex is tested by putting the flexed index finger between the subject's lips. There should be no response. In visual tracking, the subject is instructed to hold his head still and follow the examiner's index finger as it is moved between both extremes of horizontal gaze. Trregular, hesitant or jerking eye movements are abnormal. Paratonia (geigenhalten) is assessed by testing passive flexion and extension of the limbs. An irregular opposition to the examiner's movements after instructions to relax may result in a 'catching sensation' which is abnormal. Limb placement is assessed by holding the subject's arms up and telling him to relax and let the examiner do all the work. The examiner then drops his hands and the subject's arms should drop immediately. Any delay is abnormal, once Parkinsonian rigidity and spasticity have been excluded. If patients feel it is implied that their minds are 'slipping' they may become resistant, even hostile. Thus it may be helpful if the questions can be adapted to individual circumstances and worked into the history in an unobtrusive manner where indicated. Clearly explaining what you are doing and why may also help in some cases. When following delirium, it is helpful to use the same questions and tests each day so that fluctuations can be noted.
cles are larger than the intellectual impairment would suggest, and other clinical features are compatible, then investigation for obstructive or normal pressure hydrocephalus is indicated; if they are smaller than expected, metabolic or psychogenic factors in the illness must be diligently pursued.17 The EEG is useful in evaluating patients displaying confusion, dementia, peculiar behavior, obtundation or coma. A depressed elderly patient may appear organically demented, but the EEG will most likely be normal or contain much low-voltage beta activity instead of diffuse slowing as is found in dementia.'8 The EEG is more likely to show a definite abnormality early in the course of a treatable rather than an irreversible dementia. The EEG is especially useful when the physician seeks to distinguish organic vs. functional disorders, diffuse vs. focal disorders, and to determine if the process is stable or evolving (by. serial EEGs).'9 A normal EEG never rules out organic disease. It may be normal in a variety of dementing processes, especially in their early phases or when the dementia is mild. An abnormal EEG suggests organicity and the need for further studies. Laboratory investigations necessary to rule out treatable causes of dementia include the following: 1. Complete blood count, sedimentation rate, blood sugar. 2. Serum protein, blood urea nitrogen, electrolytes. 3. Urinalysis. 4. Thyroid function tests, serum B. 12 and VDRL. 5. EEG and CT scan where appropriate and available. The services of a psychometrist may be required for more sophisticated tests of psychomotor function.
Investigations
Conclusion
Senile dementia is increasing in inComputerized tomography (CAT or CT scan), has revolutionized neurol- cidence as the average age of North ogy. It is of particular value in assess- Americans increases. A clear undering dementia because it identifies potentially treatable causes. Brain tumor, normal pressure hydrocephalus, as well as metabolic causes may be differentiated. 16 Relatively little sulcal atrophy on CT scan suggests metabolic causes. Patients with little atrophy also have a better prognosis than those with moderate or severe atrophy. If the ventri142
standing of how to assess it and treat underlying processes that can lead to a demented existence thus must assume increasing importance in family medicine. As family physicians will spend more time with the elderly in future, efficient methods of screening and evaluating patients with senile dementia will become increasingly important tools. i
References 1. Bayne JR, Caygill J: Identifying needs and services for the aged. J Am Geriatr Soc 1977 June; 25:264-268. 2. Wang HS: Dementia in old age, in Wells CE: Dementia, ed 2. (Continuing Neurological Series). Philadelphia, F. A. Davis, 1977, vol 15, pp 15-27. 3. Schwenger CW: Health and care for aging Canadians. Canadian Welfare 1977; 52:9-12. 4. Katzman R: Dementias. Postgrad Med 1978 Aug; 64:119-125. 5. Wells CE (ed): Dementia. (Continuing Neurological Series, no 9). Philadelphia, F. A. Davis, 1971, p 250. 6. Isaacs B, Caird FI: Brain failure: A contribution to the terminology of mental abnormality in old age. Age Ageing 1976 Nov; 5:241-244. 7. American Psychiatric Association, Task Force on Nomenclature and Statistics: Diagnostic and Statistical Manual of Mental Disorders, ed 3. Washington, DC, American Psychiatric Association, 1978. 8. Morimatsu M, et al: Senile degenerative brain lesions and dementia. J Am Geriatr Soc 1975; 23:390406. 9. McNab BR, Powell GW: Depression in the geriatric patient. Can Fam Physician 1978; 24:882-886. 10. Wang HS: Dementia of old age. In: Smith W, Lynn K (eds.): Aging and Dementia. New York, Spectrum Publications, 1977. 11. Brain Failure, editorial. J R Coll Gen Pract 1977; 27:451-453. 12. Freedman AM, Kaplan HI (eds): Comprensive Textbook of Psychiatry, Baltimore, Williams and Wilkins, 1967. 13. Pfeiffer E: A short portable mental status questionnaire for the assessment of organic brain deficit in elderly patients. J Am Geriatr Soc 1975; 23:433-441. 14. Folstein MF, Folstein SE, McHugh PR: Mini-mental state. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975 Nov; 12.189-198. 15 Jenkyn LR, et al: Clinical signs in diffuse cerebral dysfunction. J Neurol Neurosurg Psychiatry 1977 Oct; 40:956-966. 16. Fox JH, Huckman MS: Computerized tomography: A recent advance in evaluating senile dementia. Geriatrics 1975 Nov; 30:97-100. 17. Caird Fl: Computerized tomography (emiscan) in brain failure in old age. Age Ageing 1977; 6 (suppl):50-51. 18. Androila MR: Role of the EEG in evaluating central nervous system dysfunction. Geriatrics 1978 Feb; 33:59-65. 19. Wilson WP, Musella L, Short MJ: The encephalogram in dementia, in Wells CE: Dementia, ed 2: (Continuing Neurological Series). Philadelphia, F. A. Davis, 1977, vol 15. -20. American Psychiatric Association, Tasle Force on Nomenclature and Statistics: Diagnostic and Statistical Manual of Mental Disorders, ed. 1. Washington, DC, American Psychiatric Association, 1950. 21. Conomy JP: Impact of arterial hypertension on the brain. Postgrad Med 1980; 68:86-97. CAN. FAM. PHYSICIAN Vol. 27: JANUARY 1981
