Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5221_Библиотеки_им_академика_М_И_Перельмана.pdf

Infectious Disease and Neurocognition
OTAKE, N., TSURUKIRI, J., NUMATA, J., MORIYA, M., KANEMARU, T., NAGURA, T. & SANO, H.
2023. Herpes simplex virus- induced acute necrotizing encephalopathy in an adult. Acute Med Surg,
10, e818.
POOJARI, V. S., SHAH, I. & SHETTY, N. S. 2021. Acute necrotising encephalopathy of childhood sec-
ondary to rotaviral diarrhoea. Indian Pediatr, 58, 491.
RADMANESH, F., RODRIGUEZ- PLA, A., PINCUS, M. D. & BURNS, J. D. 2020. Severe cerebral in-
volvement in adult- onset hemophagocytic lymphohistiocytosis. J Clin Neurosci, 76, 236– 237.
SARIGECILI, E., UCAR, H. K., HAVALI, C., CANSU, A. & AYDIN, K. 2023. Acute necrotizing en-
cephalopathy associated with RANBP2 mutation: Value of MRI ndings for diagnosis and interven-
tion. Acta Neurol Belg, 123, 571– 582.
SHINOHARA, M., SAITOH, M., TAKANASHI, J., YAMANOUCHI, H., KUBOTA, M., GOTO, T.,
KIKUCHI, M., SHIIHARA, T., YAMANAKA, G. & MIZUGUCHI, M. 2011. Carnitine palmitoyl
transferase II polymorphism is associated with multiple syndromes of acute encephalopathy with
various infectious diseases. Brain Dev, 33, 512– 517.
SONG, Y., LI, S., XIAO, W., SHEN, J., MA, W., WANG, Q., YANG, H., LIU, G., HONG, Y., LI, P. &
YANG, S. 2021. Inuenza- associated encephalopathy and acute necrotizing encephalopathy in chil-
dren: A retrospective single- center study. Med Sci Monit, 27, e928374.
STEVANOVIC, V., BARUSIC, Z., VISKOVIC, K., RODE, O. D. & TESOVIC, G. 2019. Acute necro-
tizing encephalopathy of childhood associated with human herpes virus 6 in Croatia. Neurol Sci, 40,
639– 641.
SUN, W., FU, C. & ZHU, X. 2022. Acute necrotizing encephalopathy associated with lymphoma-
associated hemophagocytic lymphohistiocytosis: A case report and literature review. Front Oncol,
12, 986957.
TABARKI, B., THABET, F., AL SHAFI, S., AL ADWANI, N., CHEHAB, M. & AL SHAHWAN, S. 2013.
Acute necrotizing encephalopathy associated with enterovirus infection. Brain Dev, 35, 454– 457.
TAKANASHI, J. 2009. Two newly proposed infectious encephalitis/ encephalopathy syndromes. Brain
De v, 31, 521– 528.
VIRHAMMAR, J., KUMLIEN, E., FALLMAR, D., FRITHIOF, R., JACKMANN, S., SKOLD, M.
K., KADIR, M., FRICK, J., LINDEBERG, J., OLIVERO- REINIUS, H., RYTTLEFORS, M.,
CUNNINGHAM, J. L., WIKSTROM, J., GRABOWSKA, A., BONDESON, K., BERGQUIST, J.,
ZETTERBERG, H. & ROSTAMI, E. 2020. Acute necrotizing encephalopathy with SARS- CoV- 2
RNA conrmed in cerebrospinal uid. Neurology, 95, 445– 449.
WANG, Y., YOUNCE, J. R., PERLMUTTER, J. S. & MAR, S. S. 2021. Excellent outcome of acute nec-
rotizing encephalopathy in an adult with bacterial infections, case report. Neurohospitalist, 11,
351– 355.
WILLIAMS, T. A., BRUNSDON, R. K., BURTON, K. L. O., DREVENSEK, S., BRADY, C., DALE, R. C.
& MOHAMMAD, S. S. 2019. Neuropsychological outcomes of childhood acute necrotizing enceph-
alopathy. Brain Dev, 41, 894– 900.
WONG, A. M., SIMON, E. M., ZIMMERMAN, R. A., WANG, H. S., TOH, C. H. & NG, S. H. 2006.
Acute necrotizing encephalopathy of childhood: Correlation of MR ndings and clinical outcome.
AJNR Am J Neuroradiol, 27, 1919– 1923.
WU, L., PENG, H., JIANG, Y., HE, L., JIANG, L. & HU, Y. 2022. Clinical features and imaging manifest-
ations of acute necrotizing encephalopathy in children. Int J Dev Neurosci, 82, 447– 457.
YAMAMOTO, H., OKUMURA, A., NATSUME, J., KOJIMA, S. & MIZUGUCHI, M. 2015. A severity
score for acute necrotizing encephalopathy. Brain Dev, 37, 322– 327.
YEA, C., BARTON, M., BITNUN, A., MORRIS, S. K., EL TAL, T., ULLOA- GUTIERREZ, R., BRENES-
CHACON, H., YOCK- CORRALES, A., IVANKOVICH- ESCOTO, G., SORIANO- FALLAS, A.,
HERNANDEZ- DE MEZERVILLE, M., GILL, P., NATEGHIAN, A., ASKI, B. H., MANAFI, A. A.,
DWILOW, R., BULLARD, J., PAPENBURG, J., SCUCCIMARRI, R., LEFEBVRE, M. A., COOKE,
S., DEWAN, T., RESTIVO, L., LOPEZ, A., SADARANGANI, M., ROBERTS, A., WONG, J., SAUX,
N. L., BOWES, J., PUREWAL, R., LAUTERMILCH, J., FOO, C., MERCKX, J., ROBINSON, J., YEH,
E. A. & PEDIATRIC INVESTIGATORS COLLABORATIVE NETWORK ON INFECTIONS IN
CANADA (PICNIC). 2023. Neurological involvement in hospitalized children with SARS- CoV- 2
infection: A multinational study. Can J Neurol Sci, 51, 40– 49.

Acute Necrotizing Encephalopathy of Childhood 299
YOSHIDA, T., TAMURA, T., NAGAI, Y., UEDA, H., AWAYA, T., SHIBATA, M., KATO, T. & HEIKE,
T. 2013. MRI gadolinium enhancement precedes neuroradiological ndings in acute necrotizing encephalopathy. Brain Dev, 35, 921– 924.
ZHU, H. M., ZHANG, S. M., YAO, C., LUO, M. Q., MA, H. J., LEI, T., YUAN, C. H., WU, G. F., HU, J. S.,
CAI, C. Q. & LIU, Z. S. 2021. e clinical and imaging characteristics associated with neurological
sequelae of pediatric patients with acute necrotizing encephalopathy. Front Pediatr, 9, 655074.

19
Dementia Risk Associated
with Infectious Disease
Thomas J. Farrer
Introduction
As with other systems of the body, multiple infectious diseases can negatively affect the integrity of the central nervous system (CNS), including bacterial infections,
viral infections, parasitic infections, fungal infections, and prion diseases. While a
comprehensive discussion of all infectious diseases potentially aecting the CNS
is beyond the scope of this chapter, multiple infectious diseases frequently impact
CNS function and increase the risk of brain- related disorders, such as delirium, dementia, and stroke. is chapter focuses on common CNS infections and how such
infections increase the risk of dementia. It also discusses relevant epidemiology and
mechanisms of action.
Epidemiology of infection in older adults
Infectious disease among older adults is a signicant public health concern because
it accounts for higher rates of hospitalization, more days in the hospital, more healthcare utilization, and increased mortality (De Cock et al., 2022; Nelson et al., 2022).
Infectious diseases account for one- third of all deaths among individuals who are age
65 years and older (Yoshikawa, 2000), and 50 percent of older adults with infection
manifest some degree of delirium (Mouton et al., 2001). More recently, data from the
United States Centers for Disease Control and Prevention demonstrate that infection
with the severe acute respiratory syndrome coronavirus 2 (SARS- CoV- 2), which causes
coronavirus disease 2019 (Covid- 19), was the fourth leading cause of death in 2020 for
those age 65 years and older (Centers for Disease Control and Prevention, 2020).
Aging and immunosenescence
Individuals over the age of 65 years are uniquely susceptible to infectious diseases. is increased risk is associated with a decline in immune system function
Thomas J. Farrer, Dementia Risk Associated with Infectious Disease In: Medicine
DOI: 10.1093/ oso/ 9780192870414.003.0020

Dementia Risk Associated Infectious Disease 301
(immunosenescence) and an increase in comorbid conditions with age. Older adults
have an increased risk of chronic disorders that attenuates host resistance to infection. ere is also an increased risk of nutritional decits among elderly individuals.
Malnutrition increases the risk of infection because poor nutrition decreases immune function. Additionally, infection increases metabolic demand, putting individuals at risk of nutritional decits, malnutrition, and further infection. e aging
process is also associated with anatomical and physiological modications that increase the risk of infectious disease. ese include changes in mucociliary clearance
in the lungs, decreased urinary clearance from the bladder, decreased gastric acid in
the gastrointestinal tract, decreased intestinal motility, and reduced integrity of the
blood– brain barrier (Erickson & Banks, 2019; Gavazzi & Krause, 2002). All these
age- associated changes make it more dicult for people to ght infection. Certain
infectious diseases are also more likely to occur among older adults, including urinary tract infections, respiratory tract infections, intra- abdominal infections, infective endocarditis, bacterial meningitis, herpes zoster, and skin infections (Gavazzi
& Krause, 2002; Yoshikawa, 2000). Less clear from the research literature is whether
there is the possibility that infection in earlier adult years sets the stage for a subsequent cascade of inammatory processes that impact cognitive function only later in
life. In fact, infection in childhood may be protective in nature, with one study suggesting that earlier illnesses somehow buer an individual from late- life dementia
(Rotstein & Levine, 2021). Nevertheless, as enumerated in the following section,
there is evidence of dementia risk following infection.
Infectious disease and dementia risk
A 2019 meta- analysis (Warren- Gash et al., 2019) examined the risk of mild cognitive
impairment and dementia among individuals with human herpesvirus infection,
herpes simplex virus (HSV), varicella zoster virus, Epstein– Barr virus, and cytomegalovirus. Overall, this meta- analysis suggested that past infection alone was not associated with an increased risk of dementia or mild cognitive impairment. However,
viral reinfection or recent infection seems to lead to systemic inammation, glial activation, and neuroinammation that may serve as mechanisms of action for cognitive decline and dementia in older adults. is meta- analysis acknowledges that the
included studies have variable methodological quality and heterogeneity. However,
the authors suggest the most robust nding was from an ophthalmic variant of varicella zoster virus, which results in vasculopathy and replication in cerebral arteries,
increasing the risk of vascular injury and subsequent cognitive symptoms (WarrenGash et al., 2019).
Ou et al. (2020) demonstrated in a recent meta- analysis that several infectious agents are associated with an increased risk of Alzheimer’s disease, including Chlamydia pneumoniae (odds ratio: 4.39), human herpesvirus 6 (odds

Infectious Disease and Neurocognition
ratio: 3.97) Epstein– Barr virus (odds ratio: 1.45), HSV- 1 (odds ratio: 1.34), and the
Herpesviridae viruses (odds ratio: 1.41).
A recent study of 1000 individuals with herpes was conducted with baseline cognitive testing and brain imaging. e average follow- up time was 3.4 years (Duggan
et al., 2022). Imaging markers included gray matter and white matter volume. e
study showed no signicant dierences in baseline brain volumes between those
with herpes and without. However, over the study period, the virus was associated with accelerated longitudinal declines in white matter volume, with the most
prominent atrophy in temporal lobe regions. e study also examined ve cognitive
domains among 2160 individuals across 8.6 years. is longitudinal analysis of cognitive function demonstrated that those individuals with herpes displayed greater
declines in areas of attention but no other aspect of cognition (Duggan et al., 2022).
In summary, multiple studies appear to demonstrate a relationship between infectious disease and neurodegenerative disorders, although a 2022 umbrella review (X.
Wang et al., 2022) questioned the study quality of previously published systematic
reviews and meta- analyses. ere are other lines of evidence supporting the role of
infection in dementia, including large population- based designs.
Evidence from large population- based designs
Increased risk of dementia has been associated with viral infections in multiple
studies, including postmortem studies, epidemiologic studies (Lovheim et al.,
2015a, 2015b), and genome- wide association studies (Burt et al., 2008; Kuo et al.,
2020). Robust evidence of a connection between dementia and infectious diseases
is provided by large cross- sectional cohorts. Dunn et al. (2005) studied 9000 older
adults with dementia and 9000 without, examining infection odds ratios in dierent
age groups over the preceding 4 years. When collapsed across all age groups of older
adults aged 60 years and older, the odds ratio of having an infection in the previous
4 years before dementia diagnosis was 1.3. ose aged 84 years and older had the
highest chance of infection (odds ratio: 1.4) in the 4 years before dementia diagnosis.
While these are small odds ratios, a large sample size suggests that there is an increased risk of dementia associated with infectious disease. However, the study did
not dierentiate the etiology of infection. ese authors postulated that the mechanism of action is associated with the inammatory response to infection and that
this mechanism may promote the onset of dementia (Dunn et al., 2005).
Similarly, a recent large population- based cohort study examined the association between hospitalizations with infections and the incidence of dementia diagnosis. e baseline cohort of individuals without dementia was 15,688 individuals.
Hospitalization due to infection occurred in 5999 participants. is study showed
that dementia rates were higher among individuals with exposure to an infection relative to individuals without exposure. Patients hospitalized with infection were two
times more likely to experience incident dementia. A post hoc analysis from these

Dementia Risk Associated Infectious Disease 303
data that excluded individuals who developed dementia less than 3 years or more
than 20 years from baseline showed an adjusted hazard ratio of 5.77. In addition,
the rates of dementia were higher among individuals hospitalized for urinary tract
infections, respiratory infections, hospital- acquired infections, skin infections, and
blood and circulatory system infections (Bohn et al., 2023), all of which are common
infections in older adults.
A large population- based study (Chen et al., 2017) examined the link between
herpes zoster and dementia diagnosis at a follow- up of 6.2 years. Comparing 39,000
individuals with herpes zoster to a control group of 39,000 individuals without the
virus, the researchers found an average 12- percent increased risk of dementia among
those with the virus. e study also examined interactions with other health factors
and the impact of antiviral treatment. is study demonstrated that with antiviral
treatment, the risk of developing dementia resulted in a hazard ratio of 0.47, suggesting a reduced risk of dementia in the context of antiviral agents. Interactions of
comorbid factors that increase the risk of dementia included the presence of herpes
zoster and depression (hazard ratio: 1.29) and herpes zoster with alcohol- use disorder (hazard ratio: 5.57) (Chen et al., 2017). In another study, researchers examined the risk of Alzheimer’s disease with a large population cohort of over 4 million
individuals over 10 years. e study demonstrated that in over 40,000 cases of
Alzheimer’s disease matched against 1.6 million controls, the burden of infectious
disease was associated with an increased risk of Alzheimer’s disease, with an odds
ratio of 1.05 (95 percent condence interval: 1.02– 1.08) (Douros et al., 2021).
A large population- based study of dementia risk showed that HSV infections had
a hazard ratio of 2.56, indicating a higher risk of dementia. e study showed that
among those with HSV infection who then subsequently received anti- herpetic
medication, there was a reduced risk of dementia, with a hazard ratio of 0.092 (Tzeng
et al., 2018).
Levine et al. (2023) conducted a major archival study using two databases to
investigate the connection between neurodegenerative and infectious diseases.
Specically, using medical billing codes, the study initially examined the association between six neurodegenerative diseases (NDDs) and infection in a longitudinal cohort of over 300,000 individuals. is initial analysis identied 45 separate
NDD × infection associations. e authors then veried 22 of these associations in
a separate large cross- sectional database of over 500,000 individuals in the United
Kingdom. is study also included a control cohort of healthy individuals matched
for age and ethnicity, which included over 96,000 individuals with no NDD. e
six NDDs examined in the study included Alzheimer’s disease, amyotrophic lateral sclerosis, multiple sclerosis, Parkinson’s disease, vascular dementia, and general dementia with no specic etiology. Aer replicating the 22 NDD × infection
associations, the authors provide detailed odds ratios or hazard ratios of each
NDD across multiple infection types and stratify these by the time of infection,
ranging from 1 to 15 years before NDD diagnosis. e largest hazard ratio was
30.72 (95 percent condence interval: 11.8– 79.6), which strongly demonstrated

Infectious Disease and Neurocognition
an association between viral encephalitis and Alzheimer’s disease. Additionally,
individuals with inuenza and pneumonia were more likely to develop ve of
the six studied NDDs. Another important nding from the study is that the increased risk of NDD persists years aer the initial virus infection. For example,
the authors demonstrated that even 15 years before Alzheimer’s diagnosis, inuenza with pneumonia resulted in a hazard ratio of 1.91. Infection within the last
5 years resulted in a hazard ratio of 6.76, and infection within the last year resulted
in a hazard ratio of 23. Similar risks were identied in other NDDs, suggesting
that more recent infections increase the risk of dementia. For example, inuenza
within the last 5 years resulted in a hazard ratio of 8.2, suggesting an increased risk
of general all- cause dementia, but this hazard ratio increased to 25 if inuenza
occurred in the last year (Levine et al., 2023). In summary, these large populationbased studies demonstrate a robust association between infectious disease and
dementia. ere are, of course, some contradictory research ndings, and not all
infectious diseases are associated with dementia. For example, dementia seems
to be rarely associated with the parasitic infection known as neurocysticercosis,
with one cross- sectional study of 592 individuals suggesting the prevalence of dementia around 1.3 percent (Varma & Gaur, 2002). e prevalence may be higher
in a hospitalized sample, with one study from India suggesting that 8 percent of
hospitalized dementia cases were associated with neurocysticercosis (Jha & Patel,
2004). Additionally, while the literature on Lyme disease is mixed, some ndings
suggest an association between Lyme disease and decreased cognitive function,
but there is little to no evidence that Lyme disease increases the risk of dementia
(Almeida & Lautenschlager, 2005). Additionally, in a cross- sectional study of a
community- dwelling population, Helicobacter pylori was not associated with general dementia (Fani et al., 2018). However, it may increase the risk of Parkinson’s
disease (X. Wang et al., 2022), and there may be interaction eects with various
periodontal pathogens by which the presence of both H. pylori and periodontal
pathogens uniquely increases the risk of dementia (Beydoun et al., 2021). Lastly,
there are viral infections that do not have enough research literature to this point.
For example, a case study of chronic dengue virus suggested the virus may persist in the CNS and can contribute to progressive dementia (Johnson et al., 2019).
However, it would be prudent to avoid generalization from a single case study.
Mechanisms of action and the viral infection theory
Two main pathways exist for dementia following infection disease: direct or indirect. A direct mechanism suggests that infection enters the brain directly and causes
inammation and cell death. Primary CNS infections are an example of a direct
mechanism. Conversely, an indirect mechanism is associated with systemic infection and inammation elsewhere in the body. Peripheral or systemic infection increases inammation systemwide, and prior studies suggest that a general increase

Dementia Risk Associated Infectious Disease 305
in inammation acts on vascular health and increases the risk of cognitive decline
(De Vlieger et al., 2022).
Direct pathway
e proposed mechanistic pathway for the viral infection theory suggests that the
virus enters the CNS via the blood– brain barrier or the blood– cerebrospinal uid
barrier through transcellular or pericellular migration. Once the virus is within the
CNS, it replicates resulting in an immune response, with the release of cytokines,
chemokines, antimicrobial peptides, and reactive oxygen species. ere is secondary activation of microglia and astrocytes and subsequent cell death. While the
host may be able to recover from infection, the viral infection theory proposes that
the latent virus may result in reinfection multiple times across the lifespan and ultimately increase the risk of dementia over time (De Vlieger et al., 2022). Additionally,
neurodegeneration is induced in infection when a virus disrupts homeostatic processes at the cellular level. is includes an increased expression of quinolinic acid
in the brain, which is excitotoxic. is results in increased calcium in the cytosol,
depletion of adenosine triphosphate, and increased free radicals. Cell death is the ultimate consequence of this cascade, and biomarkers of this process have been found
in individuals with Alzheimer’s disease and mild cognitive impairment (De Vlieger
et al., 2022).
Indirect pathway
e proposed mechanism for the indirect pathway suggests that infections in the
peripheral system result in similar proinammatory markers. ese biomarkers
can then be transported to the CNS, particularly when the blood– brain barrier or
blood– cerebrospinal uid barrier is compromised. ese biomarkers then transfer
a proinammatory signal to tissue in the CNS. As such, a similar cascade of events
occurs in CNS tissue even if the virus was not initially present there (De Vlieger
et al., 2022).
Other mechanisms
While the direct and indirect mechanisms for NDD aer infection have been studied
extensively, an additional hypothesis has examined the role of extracellular vesicles.
roughout the body, and particularly in the CNS, extracellular vesicles play a role
in transporting multiple important molecules needed for metabolism, protein synthesis, and cellular maintenance, including proteins, lipids, and nucleic acids. Recent
studies have suggested that infectious diseases can interfere with extracellular vesicle

Infectious Disease and Neurocognition
pathways. Further, cellular vesicles can transport viral deoxyribonucleic acid. As viruses interfere with extracellular vesicle transport, the metabolic and homeostatic
function of cells is reduced, and cellular function fails. e disruption of extracellular vesicles increases the occurrence of misfolded proteins, both within neurons
and in the extracellular space, and has been associated with the prototypical plaques
and tangles observed in Alzheimer’s disease (De Vlieger et al., 2022).
Primary central nervous infection: Classification
and specific infections
Infections aecting CNS function fall into multiple categories that are briey reviewed here.
Meningitis
Meningitis is infection and inammation of the meninges covering the brain and
spinal cord, which can result from bacterial, viral, or fungal infection. Meningitis,
regardless of etiology, is associated with several neurological and cognitive sequelae.
Infections from bacteria can lead to meningitis and brain abscesses. When a bacterial infection is the primary cause, the infection typically originates elsewhere in
the body. ese infections can have characteristic symptoms, including fever, neck
stiness and neck pain, headache, and sensitivity to sound and light (Blumenfeld,
2010). Viral infection can also iname the meninges and cause similar symptoms.
Viral meningitis is also termed aseptic meningitis. Treatment is challenging in
viral meningitis, which can be associated with several viruses, including herpesviruses, human immunodeciency virus (HIV), and enteroviruses. Viruses may
also enter the brain parenchyma and result in viral encephalitis. e most common
form of viral encephalitis is HSV. Viral encephalitis from herpes is a medical emergency because it can cause coma or death. is form of encephalitis has a predilection for limbic regions involving frontal and temporal lobes (Blumenfeld, 2010).
Severe meningitis can cause ischemic brain injury and infarction, vasculitis, cerebral abscesses, parenchymal bleeding, and increased risk of seizure, delirium,
and dementia (Farmen et al., 2021). Most meningitis cases are caused by one of
three agents: Haemophilus inuenza type b, Neisseria meningitides, or Streptococcus
pneumonia.
Encephalitis
An infection of the encephalon (i.e., brain tissue or parenchyma) results in encephalitis. Encephalitis can be caused by multiple bacteria, viral, parasitic, or fungal

Dementia Risk Associated Infectious Disease 307
pathogens, and a comprehensive discussion of all such pathogens is not included
here. In general, however, encephalitis is typically described as primary or secondary. Primary encephalitis refers to an infection directly to the brain. Secondary
encephalitis is a post- infection encephalitis in an immune response to a dormant
virus or immunization (i.e., attenuated virus). While several viruses have been implicated in encephalitis, the most common viral infections resulting in encephalitis
include herpes simplex, Epstein– Barr, varicella zoster, enteroviruses, and arboviruses. As with meningitis, encephalitis results in multiple psychiatric and neurological sequelae. Inammation results in edema, leading to tissue damage and
ischemic injury. ere is also an increased risk of stroke and seizure, and multiple
studies demonstrate an increased risk of dementia, even aer infection recovery
(Campos et al., 2021; Hokkanen & Launes, 1997). Individuals with measles can
have post- infectious encephalitis. is occurs when there is a delay in encephalitis,
sometimes days or weeks aer the initial infection, making it dicult to associate
the encephalitis with illness. Transverse myelitis occurs when infection results in
inammation of the spinal cord. is is frequently related to enteroviruses but can
occur in multiple viral infections. Common symptoms of transverse myelitis include pain, sensory changes, weakness, and bladder or bowel control diculties
when lower aspects of the spine are involved. HIV- associated cognitive change is
frequently identied in the literature, and numerous studies have demonstrated
that HIV can result in dementia and increase the risk of other conditions, such as
Alzheimer’s disease. e John Cunningham virus (commonly called the JC virus)
can result in demyelination throughout the CNS, resulting in progressive multifocal leukoencephalopathy. e JC virus is endemic in most populations, with
70– 90 percent of the population having this virus in a harmless dormant form.
However, the risk of progressive multifocal leukoencephalopathy from the JC virus
increases among individuals who are immunocompromised. For instance, this condition has been identied among individuals with AIDS and multiple sclerosis or
other immunocompromised states. Common symptoms include dementia, blindness, paralysis, and seizures. Progressive multifocal leukoencephalopathy is typically fatal (Blumenfeld, 2010).
Delirium
Although delirium is clinically distinct from dementia, it does warrant discussion
here given that infections oen result in delirium, which is oen misdiagnosed as
dementia. Delirium is a confusional state, with an acute onset that typically presents
with uctuation in mental status. ere are typically changes in arousal and disturbances in attention, and patients are oen illogical and have uctuations in alertness.
Patients may even have delusions, hallucinations, or psychomotor features. Delirium
is quite common, with almost 60 percent of patients in post- acute care or assistedliving facilities experiencing delirium at some point. Among older adults, the most
Соседние файлы в папке Библиотека им академика М.И. Перельмана
