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Creutzfeldt-Jakob Disease

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Creutzfeldt-Jakob Disease International Journal of Clinical Psychiatry 2016, 4(1): 1-7 DOI: 10.5923/j.ijcp.20160401.01 Neuropsychiatric Symptoms among the Major Categories of Creutzfeldt-Jakob Disease Richard P. Conti1,*, Jacqueline M. Arnone2 1Department of Psychology, Kean University, Union, USA 2Department of Nursing, Kean University, Union, USA Abstract Creutzfeldt-Jakob disease (CJD) is a progressive terminal neurodegenerative disease classified within the human prion disorders. There are four distinct categories of the disorder: variant, iatrogenic, sporadic and familial. Onset is typically precipitous with death occurring within a year of symptom commencement. Worldwide incidence is approximately one case per million per population each year. In the United States this translates to roughly 300 new cases a year. Presentation typically occurs between 50 and 70 years of age with median age onset of 60 and is without gender bias. Currently, no cure exists and treatment is only palliative for symptoms. Classic features of CJD include rapidly progressive dementia, myoclonus and ataxia, yet most case reports have demonstrated initial presentation in the form of nonspecific psychiatric and neurological symptoms. Since wide-ranging psychiatric symptoms are frequently the first indices of the disease, this paper reviews the symptoms across the four categories of CJD. Misdiagnosis early in the course of the disease is problematic and occurs most frequently from symptom heterogeneity. The preponderance of evidence suggests that since initial symptoms can occur with or without the hallmark signs of the disease, utilization of a global approach for early detection and diagnosis is warranted that is inclusive of repeated, supportive diagnostic tests performed at various points in time. Consideration of the patient and family and the benefits of obtaining an early diagnosis as it relates to the provision of care, treatment, and support are discussed in light of these findings. Keywords Creutzfeldt-Jakob disease (CJD), Prion, Mad cow disease, Spongiform encephalopathy variant or new-variant CJD (vCJD or nvCJD) – which is 1. Introduction transmissible from animal to human through bovine spongiform encephalopathy (BSE or “mad-cow” disease) Alfons Jakob first defined what is known today as contamination; iatrogenic CJD – which is transmissible from Creutzfeldt-Jakob disease (CJD) in 1921 with reference to human to human through medical procedures; and sporadic Hans-Gerhard Creutzfeldt’s similar work in 1913 [1]. (sCJD) – which does not have any of the previous described Although a rare disease, CJD is unique in that it is a prion causes and accounts for 85% of all CJD cases [4, 6]. (proteinaceous infectious particle) disease. Prion diseases are According to Chao and Han [7], since initial clinical a set of communicable, progressive, and ultimately fatal manifestations of CJD patients are often non-specific and neurodegenerative disorders where an aberrant folding of a diverse, the diagnosis of the disease can be problematic. host-encoded prion protein (PrP) occurs in abundance [2]. Additionally, the potential exists for physicians from Prion diseases occur in both humans and animals [3]. The numerous disciplines to have initial contact in caring for disease affects the central nervous system (CNS) and is these patients, as the clinical presentation may be exhibited classified as a transmissible spongiform encephalopathy through behavior, sensory, motor, or cognitive dysfunctions, (TSE) [4, 5]. This group of diseases became a household which therefore increases the probability for misdiagnosis name in the 1980s when “mad cow disease” or bovine [7]. Since wide-ranging psychiatric symptoms are frequently spongiform encephalopathy epidemic ensued in the United the first indications of the disease, it is important to know Kingdom from contaminated cattle feed that infected cattle what they are and if they vary across the different categories stock and then ultimately infected consumers [3]. of CJD [6, 8]. The purpose of this paper is to define the There are four main categories of CJD: familial CJD symptoms across the different classifications of CJD. (fCJD) – which is inherited and occurs in 15% of CJD cases; In addition to preventing further spread of the disease iatrogenically, early recognition and diagnosis can provide * Corresponding author: [email protected] (Richard P. Conti) more successful symptom treatments that can ease the stress Published online at http://journal.sapub.org/ijcp of the disease on the patient and caregiver. Furthermore, Copyright © 2016 Scientific & Academic Publishing. All Rights Reserved because to date there is no cure or treatment to prolong 2 Richard P. Conti et al.: Neuropsychiatric Symptoms among the Major Categories of Creutzfeldt-Jakob Disease survival, and because of the rapidity and fatal trajectory of with longer duration than the sporadic form [3]. In fCJD, the disease, early detection and diagnosis can afford the there is oftentimes a younger age of onset than sCJD, with patient and their family to be able to make palliative care and occurrence resulting from either a stressor or sporadically as end of life decisions while the patient is still cogent. Last, in the other categories, but the course after onset is similar to early recognition of the disease and the point in time that the sCJD [15, 16]. disease is correctly diagnosed can have marked significance especially if treatment modalities do become available that can be rendered to the patient [9]. 4. Diagnosis The classic features of CJD consists of a triad of 2. Brief History of CJD symptoms that include dementia, myoclonus, and ataxia, yet initial clinical portraiture via case reports in the extant The first account of human spongiform encephalopathies literature have demonstrated initial presentation in the form commenced in the early 20th century. In 1920, Breslau of nonspecific psychiatric and neurological symptoms [7, 8, neurologist Hans Gerhard Creutzfeldt described a case of a 17-20]. Aside from a clinical assessment of the patient 22 year-old female with a clinical presentation of advanced (complete history and physical exam), supportive tests for terminal degenerative dementia accompanied by numerous probable diagnosis may be administered and include neurological anomalies that included both myoclonus and magnetic resonance imaging (MRI), electroencephalography spasticity [10]. Shortly thereafter, Hamburg (EEG) and lumbar puncture [3]. The cerebrospinal fluid neuropathologist Alfons Maria Jakob published a manuscript (CSF) obtained from the lumbar puncture is tested with an detailing the clinical presentation of two men and three immunoassay 14-3-3 test that looks for the presence of women between the ages of 34 and 51 who demonstrated 14-3-3 protein in the CSF [2, 3, 21]. This protein is released progressive motor function, alterations in speech, emotion, into the CSF indicating an extensive destruction of neurons personality, and memory loss [11]. More serious symptoms [3], one criterion of probable CJD [21]. However, it should rapidly ensued, such as the inability to stand, move or speak, be noted other brain disorders can yield a positive assay and all five patients succumbed within a year after the initial result and therefore probable diagnosis requires additional onset of symptoms [11, 12]. The name Creutzeldt-Jakob criteria that need to be met [21]. The World Health disease arose then, after Jakob concluded that Creutzfeldt’s Organization (WHO) [22] outlines these additional criteria. single case study paralleled his own cases in both The WHO criteria [22] for probable diagnosis of sCJD are presentation and outcome [12]. Later, the term subacute as follows: (1) exclusion of alternative diagnoses with spongiform encephalopathy was suggested, with spongiform routine investigations; (2) rapid progressive dementia; (3) at change in the CNS now recognized as the hallmark definitive least two of the following four clinical features-myoclonus, diagnostic criterion for the disease [13]. Interestingly, after a visual disturbance or cerebellar dysfunction, pyramidal, or retrospective review of the initial case reports years later, it extrapyramidal feature, and akinetic mutism; (4) a typical was discovered that the first cases documented by EEG pattern (periodic sharp-wave complex), and/or CSF Creutzfeldt in 1921, did not actually meet the required positive for 14-3-3 by immunoblot; and (5) a clinical histological benchmarks for the disease [13]. On the contrary, duration of less than 2 years before death. Interestingly, the two of Jakob’s cases did demonstrate the histological WHO does not include MRI as diagnostic criteria for spongiform change in the CNS. Yet to this day, probable sCJD, although the University of California, San Creutzfeldt-Jackob disease has remained the accepted Francisco has updated guidelines that support the utilization medical nomenclature for the disorder [14]. However, of the MRI as an adjunctive criterion for diagnosis of the Katscher [12] writes that to give “historical justice” to Jakob disorder [23]. Definitive diagnosis for CJD is only positively and to accredit him with first discovering the disease, the confirmed through pathological inspection of brain tissue name order is commonly reversed to Jakob-Creutzfeldt post-mortem [3]. disease within the German medical literature (p. 11). 4.1. Variant CJD (vCJD) 3. Incidence and Prevalence Spencer et al. [24] retrospectively examined the first 100 cases of vCJD recorded in the United
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