The name senile dementia is an expression used quite often within popular culture. It’s a cognitive behavioral problem in the elderly. If we refer to a more technical definition, we can say that senile dementia corresponds to serious cognitive impairments which makes older people dysfunctional, which means that the patient cannot lead a normal life without the help of others. Lifestyle is a determining factor for the occurrence of senile dementia. An active life and a healthy diet can prevent the onset of this disorder.
“The term dementia (from Latin demens, meaning ‘without mind’), was incorporated into the European vernaculars in the 17th and 18th centuries. By the early 18thcentury, it had acquired a medical connotation, and it was included in Blancard’s Physical Dictionary in 1726. Since then, the term has had an interesting history with many vicissitudes in its meanings and usage. By the late 19thcentury, the primacy of cognitive impairment as the defining feature of dementia was generally accepted. The major debate of this time was between the vascular and parenchymal mechanisms of etiology, on which opinion has also shown many fluctuations over the last century. By early 20th century, the association with old age had become firmly established and the descriptor ‘senile dementia’ was widely applied.
When Alois Alzheimer described the neuropathology of dementia in a 51-year-old woman in 1906, the presence of neurofibrils5 and plaques in the brains of senile dementia patients had already been described. Alzheimer did not regard his description as that of a new disease, but rather of an atypical early presentation of senile dementia. Kraepelin probably did consider it to be a new disease when he called it ‘Alzheimer’s disease’ in the 8th edition of his Handbook. Senile and presenile dementia continued to be regarded as distinct disorders until the 1960s and ’70s, when comprehensive neuropathological studies demonstrated that the brain changes described by Alzheimer were a common cause of cognitive decline in the elderly. Although the heterogeneity of the concept of dementia was not in doubt, other developments in the later 19th and early 20th century highlighted this fact further.”1
Senile dementia is not a disease, but a condition. It originates in a multitude of diseases, the most common are Alzheimer’s, Parkinson’s, Huntington’s, the presence of Lewy body and frontotemporal degeneration. There are more than 100 diseases that can give rise to senile dementia, usually affecting people over 60 years of age and is irreversible.
“Although Alzheimer’s disease (AD) and Huntington’s disease (HD) are both neurodegenerative disorders that cause global dementia syndromes, there is considerable evidence that distinct neurobehavioral and neurocognitive deficits are associated with the two diseases. AD is characterized by a prominent amnesia with secondary deficits in language, abstract reasoning, and visuospatial functioning. These deficits are consistent with extensive damage to the medial temporal lobe structures important for memory (e.g., hippocampus, entorhinal cortex) and to the association cortices of the frontal, temporal, and parietal lobes. HD, in contrast, is characterized by marked motor disturbance (i.e., choreiform movements), bradyphrenia, prominent executive dysfunction, moderate concentration and memory deficits, and visuospatial impairments. The cognitive and motor deficits of HD are mediated by the extensive basal ganglia damage, particularly to the caudate nucleus and putamen, that occurs in the disease and the attendant interruption of several anatomically and functionally distinct circuits that link these subcortical structures with the frontal cortex.
Although differences and similarities in the memory, language, and executive function deficits associated with AD and HD have been well documented, the nature of the visuospatial dysfunction that occurs in the two disorders has received relatively little attention. Understanding the visuospatial deficits that result from these diseases is important, as visuospatial abilities are associated with functional competence in both normally 3 aging and demented older adults. Evidence also suggests that performance on visuospatial measures may be useful in the early detection of the dementia associated with HD and may differentiate mild from moderate dementia in AD.”2
The main risk factors for developing senile dementia are: age, a sedentary lifestyle, depression, low intellectual activity, diets rich in saturated fats and diabetes. These are the main illnesses that cause it:
Senile dementia due to Alzheimer’s disease
It is the most common type. It includes progressive loss of memory, difficulties in expressing oneself, disorientation and an increase in dependence to perform basic activities.
“Alzheimer disease (AD) is a neurodegenerative disorder featuring gradually progressive cognitive and functional deficits as well as behavioral changes and is associated with accumulation of amyloid and tau depositions in the brain. Cognitive symptoms of AD most commonly include deficits in short-term memory, executive and visuospatial dysfunction, and praxis. Several rarer variants of AD with relative preservation of memory have been recognized. Clinical assessment, including cognitive testing, remains critical for the diagnosis and staging of AD, although recent advances in amyloid imaging and genetics show great promise for facilitating early and presymptomatic diagnosis of AD and its discrimination from other neurodegenerative disorders.”3
Dementia of vascular origin
It originates during some type of vascular event, mainly a stroke. The symptoms depend on the area of the brain that has been affected.
“Vascular dementia is one of the most common causes of dementia after Alzheimer’s disease, causing around 15% of cases. However, unlike Alzheimer’s disease, there are no licensed treatments for vascular dementia. Progress in the specialty has been difficult because of uncertainties over disease classification and diagnostic criteria, controversy over the exact nature of the relation between cerebrovascular pathology and cognitive impairment, and the paucity of identifiable tractable treatment targets. Although there is an established relation between vascular and degenerative Alzheimer’s pathology, the mechanistic link between the two has not yet been identified.”4
“Unlike other common causes of dementia, vascular dementia is not easily identifiable by a specific neuropathological hallmark, such as neuritic plaques in AD or Lewy bodies in Parkinson’s disease. In addition, vascular changes are also found frequently in brains of cognitively normal elderly, making it difficult to establish a causal relationship between brain lesions and cognitive decline.
Moreover, vascular changes are likely to have a synergistic rather than an additive effect to primary neurodegenerative processes. Therefore, a pathological diagnosis of vascular dementia (VaD) is often reached by excluding other causes.
A drastic change in the way cerebrovascular lesions are defined is critical for the creation of a new set of pathological diagnostic criteria. Vascular dementia is not a single entity, but an umbrella term to describe cognitive decline due to a series of different vessel disorders, frequently seen in combination with other non-vascular changes. These vessel disorders can induce various types of cerebral tissue lesions such as hemorrhage, infarction, hippocampal sclerosis, and white matter lesions.
Currently, vascular lesions are classified based on their morphological characteristics rather than by their pathogenesis. The aims of this review article were to review characteristics of cerebrovascular lesions associated with cognitive decline, discuss overlapping nomenclature and propose strategies to harmonize the nomenclature adopted for vascular brain disorders.”5
Dementia with Lewy bodies (DLB)
Its main characteristic is the presence of visual hallucinations. It is common to present sudden changes in the mental state, postural instability, slow movements and muscular rigidity.
“DLB is typically associated with cognitive complaints rather than aphasia or other language disturbances early in the course of the disease. Cognitive impairment in DLB is related to severe memory impairment, attentional deficits, visuospatial dysfunction, prosopagnosia, color agnosia, constructional and ideomotor apraxia. Language disturbance in DLB is characterized by confabulation, incoherence, and perseveration during conversation, difficulty naming common objects, and a reduction in verbal fluency. Symptoms of the disease progress with deteriorating motor function, severe memory disturbance, neuroleptic reactions, disproportionate visuospatial deficits, and global functioning deterioration in late stages.”6
“DLB is a complex disease with many challenging treatment decisions. It is often under-recognized in the clinic, in part because the core clinical diagnostic features – fluctuations in cognition, visual hallucinations, and parkinsonism – are nonspecific and subject to varied interpretation. For example, how much parkinsonism is enough to qualify for this feature? Treatment options can improve quality of life, but do not alter the course of the disease. For many symptoms, the best treatments are nondrug treatments. Regular reviews aimed at rationalizing therapy can be beneficial. For example, anti-hypertensive medications that were erstwhile well tolerated may induce postural dizziness because alpha-synucleinopathy weakens neurovascular tone. The most difficult decision relates to the use of antipsychotic medications; these occasionally benefit patients with hallucinations and delusions, but severe reactions such as prolonged rigidity and decreased responsiveness are common in DLB. Recent trials of antipsychotics with novel mechanisms of action hold promise for this vulnerable population.”7
Dementia associated with Parkinson’s
Not all people with Parkinson’s disease develop senile dementia. If it happens, the first symptoms usually occur one year after having the disease. “Parkinson’s disease is a progressive disorder associated with acquired parkinsonism and the loss of substantia nigra neurons in the presence of Lewy bodies. Parkinsonism is defined by the presence of two cardinal signs among resting tremor, rigidity, bradykinesia and postural or gait impairment, and can be caused by disorders other than idiopathic PD. Lewy bodies are eosinophilic inclusions that stain with antibodies directed against alpha-synuclein, a ubiquitous synaptic protein evident in a number of neurodegenerative disorders. Clinical features that make a diagnosis of idiopathic PD more likely include asymmetrical onset, resting tremor, and a favorable response to levodopa. Good accuracy (approximately 90% positive predictive value) and sensitivity (90%) can now be achieved.9,10 Nevertheless in the general medical setting parkinsonism is often not diagnosed and specific diagnoses may be inaccurate.”8
“Together, Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB) represent the second most common cause of dementia worldwide. Both diseases are synucleinopathies and involve pathological accumulations of the protein alpha-synuclein. The cognitive deficits in PDD and DLB are distinct from Alzheimer’s dementia, with notable relative preservation of delayed memory, but severely impaired executive function, attention, and visuospatial skills. Parkinson’s disease is a disorder of motor symptoms, but approximately 30% of such patients have cognitive symptoms at initial diagnosis and as many as 80% will develop cognitive symptoms at some point in their disease. In DLB, cognitive symptoms appear before, or at the same time, as motor symptoms.
Core diagnostic features of DLB include parkinsonism, visual hallucinations, fluctuations, and rapid eye movement (REM) sleep behavior disorder. These features are also common in PDD, but for this diagnosis, patients need a prior diagnosis of Parkinson’s disease. Crucially, if a patient has parkinsonism, PDD vs. DLB can only be clinically distinguished by the relative temporal onset of cognitive vs. motor disease. According to criteria set forth by the consensus report of the Lewy Body Consortium, PDD is diagnosed when there is at least a 1-year interval between onset of parkinsonian motor symptoms and diagnosis of dementia. Many clinical studies use more stringent criteria of temporal onset of motor symptoms vs. dementia to separate DLB from PDD, thus the full spectrum of these diseases has rarely been studied. Accordingly, it is unclear if PDD and DLB are really two different diseases affecting distinct cortical circuits and thus separate neuropsychological profiles, or a spectrum of one disease.”9
General symptoms of senile dementia include: loss of social skills, progressive isolation, inappropriate and aggressive behaviors, difficulty in memorization, poor orientation and reduced reasoning. It is also common to suffer disruptive sleep patterns.
It is not easy to establish phases in senile dementia since they usually vary quite a bit, depending on the characteristics of the patient and the underlying disease that gives rise to dementia. Therefore, there is no unique classification. However, we can make general differentiations in the following way:
- Mild Phase: In this phase the patient is still fully functional. There are just a few short-term memory problems compared to minor issues. Patients show difficulty in finding words when communicating.
- Moderate Phase: It is the longest phase in which the family usually consults a doctor as the person is discouraged and progressively isolated. Their personality changes, they tend to wander and cannot perform daily activities.
- Advanced Phase: The patient no longer recognizes anyone. Motor skills are extremely deteriorated and need the help of others to survive.
There is no single test to diagnose senile dementia. The doctor performs a detailed clinical history and physical exam to determine the condition presented by the patient. The medical professional will also investigate the symptomatology. In particular, different tests are indicated to check the state of functioning of the nervous system. For example, CAT scans help to verify in what condition the brain is. Finally, tests are ordered to evaluate the psychological state of the patient in order to determine current cognitive and behavioral abilities.
(1) Sachdev, P. (2000). Is it time to retire the term “dementia”?. The Journal of neuropsychiatry and clinical neurosciences, 12(2), 276-279. Available online at https://neuro.psychiatryonline.org/doi/pdf/10.1176/jnp.12.2.276
(2) Apostolova, L. G. (2016). Alzheimer disease. Continuum: Lifelong Learning in Neurology, 22(2 Dementia), 419. Available online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390933/
(3) T O’Brien, J., & Thomas, A. (2015). Vascular dementia. The Lancet, 386(10004), 1698-1706. Available online at https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)00463-8/fulltext
(4) Grinberg, L. T. (2012). Vascular dementia: current concepts and nomenclature harmonization. Dementia & neuropsychologia, 6(3), 122-126. Available online at http://www.demneuropsy.com.br/imageBank/PDF/v6n3a02.pdf
(5) Macijauskiene, J., & Lesauskaite, V. (2012). Dementia with Lewy bodies: the principles of diagnostics, treatment, and management. Medicina, 48(1), 1. Available online at https://www.mdpi.com/1010-660X/48/1/1
(6) Boot, B. P. (2015). Comprehensive treatment of dementia with Lewy bodies. Alzheimer’s research & therapy, 7(1), 45. Available online at https://dash.harvard.edu/bitstream/handle/1/16121012/4448151.pdf?sequence=1
(7) Camicioli, R., & Fisher, N. (2004). Progress in clinical neurosciences: Parkinson’s disease with dementia and dementia with Lewy bodies. Canadian journal of neurological sciences, 31(1), 7-21. Available online at http://www.neurology-asia.org/articles/20052_079.pdf
(8) Aldridge, G. M., Birnschein, A., Denburg, N. L., & Narayanan, N. S. (2018). Parkinson’s disease dementia and dementia with Lewy bodies have similar neuropsychological profiles. Frontiers in neurology, 9, 123. Available online at https://www.frontiersin.org/articles/10.3389/fneur.2018.00123/full
(9) Lineweaver, T. T., Salmon, D. P., Bondi, M. W., & Corey-Bloom, J. (2005). Differential effects of Alzheimer’s disease and Huntington’s disease on the performance of mental rotation. Journal of the International Neuropsychological Society, 11(1), 30-39. Available online at https://pdfs.semanticscholar.org/4e4d/4fd632ab975eb663425c599d2daa7ee2044b.pdf