POSTENCEPHALITIC PARKINSON DISEASE
\pˌə͡ʊstənsˌɛfɐlˈɪtɪk pˈɑːkɪnsən dɪzˈiːz], \pˌəʊstənsˌɛfɐlˈɪtɪk pˈɑːkɪnsən dɪzˈiːz], \p_ˌəʊ_s_t_ə_n_s_ˌɛ_f_ɐ_l_ˈɪ_t_ɪ_k p_ˈɑː_k_ɪ_n_s_ə_n d_ɪ_z_ˈiː_z]\
Sort: Oldest first
-
Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS, MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)
By DataStellar Co., Ltd
Word of the day
Proto Oncogene Proteins c erbB 2
- cell surface protein-tyrosine kinase that is found to be overexpressed in significant number adenocarcinomas. It has extensive homology can heterodimerize EGF EPIDERMAL GROWTH FACTOR), 3 receptor (RECEPTOR, 3) and the 4 receptor. Activation of erbB-2 receptor occurs during heterodimer formation with a ligand-bound erbB family members. EC 2.7.11.-.