By Joseph Quinn
This booklet seems at dementia and considers subject matters together with: prognosis and differential analysis of dementia; speedily revolutionary dementia and its imitators; younger onset dementia; melancholy and if it is a reason or hardship of cognitive decline; prodromal dementia; utilizing psychotropic medicinal drugs to regulate challenge behaviors in dementia; palliative care in complicated dementias; legal/economic/social matters in dementia; and assessing results in dementia care. crucial studying for neurologists, psychiatrists, and gerontologists.
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Leukodystrophies: classification, diagnosis, and treatment. Neurologist 2009; 15: 319–28. Dalmau J, Gleichman AJ, Hughes EG, et al. AntiNMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol 2008; 7: 1091–8. Flanagan EP, McKeon A, Lennon VA, et al. Autoimmune dementia: clinical course and predictors of immunotherapy response. Mayo Clinic Proc 2010; 85: 881–97. Gaig C, Valldeoriola F, Gelpi E, et al. Rapidly progressive DLBD. Mov Disord 2011; 26: 1316–23.
Epidemiology The term young onset dementia (YOD) has traditionally been used to describe a heterogeneous group of dementing disorders that affect individuals younger than 65 years of age. Few data exist on the true incidence and prevalence of all-cause dementia among persons in this age group in the United States. 9 cases per 100,000 person-years in age groups 40–69 years, 50–59 years, and 60–64 years, respectively. Epidemiological studies of various international populations have estimated prevalence rates of 54–81 cases per 100,000 person-years.
Other rapidly progressive neurodegenerative dementias At autopsy of patients with RPD, pathological evidence of neurodegenerative disorders other than prion disease is frequently detected. 6% of all patients referred for suspected CJD and represented 39% of the non-prion cases. The Mayo Clinic series of 22 patients diagnosed with RPD showed that 23% of the cases consisted of frontotemporal dementia with motor neuron disease, 18% had either CBD or PSP, 14% had DLBD, and 9% had AD. In the Case Western Reserve autopsy cohort, AD accounted for over half of patients with a rapidly progressive incurable dementia diagnosed in life as CJD; other diagnoses in the non-prion neurodegenerative group were (in order of commonality) neurodegenerative disorder not otherwise specified, FTLD, DLBD, tauopathy not otherwise specified, PSP, CBD, and Huntington’s disease (HD).