Shy children, phobic adults: Nature and treatment of social anxiety disorders (2nd ed.) (pp. 11–46). Washington, DC US: American Psychological Association. doi:10.1037/11533-001
Berent, Jonathan, with Amy Lemley (1993). Beyond Shyness: How to Conquer Social Anxieties. New York: Simon & Schuster. ISBN 0-671-74137-3. Boyle, L.E. (2018) "The (un)habitual geographies of Social Anxiety Disorder", Social Science and Medicine, DsocOI:10.1016/j.socscimed.2018.03.002
Bruch M. A. (1989). "Familial and developmental antecedents of social phobia: Issues and findings". Clinical Psychology Review. 9: 37–47. doi:10.1016/0272-7358(89)90045-7. Burns, D. D. (1999). Feeling Good: the new mood therapy (Rev. ed.). New York: Avon. ISBN 0-380-81033-6. Crozier, W. R., & Alden, L. E. (2001). International Handbook of Social Anxiety: Concepts, Research, and Interventions Relating to the Self and Shyness. New York: John Wiley & Sons, Ltd. ISBN 0-471-49129-2. Hales, R. E., & Yudofsky, S. C. (Eds.). (2003). Social phobia. In Textbook of Clinical Psychiatry (4th ed., pp. 572–580). Washington, D.C.: American Psychiatric Publishing. Marteinsdottir I.; Svensson A.; Svedberg M.; Anderberg U.; von Knorring L. (2007). "The role of life events in social phobia". Nordic Journal of Psychiatry. 61 (3): 207–212. doi:10.1080/08039480701352546. PMID 17523033. S2CID 11620169. External links

Social Anxiety (including self-help links) at Curlie
Support Group Providers for  Social anxiety disorder at Curlie
The symptoms are progressive, and individuals with MEAK often need to use a wheelchair by their late teenage years because of movement difficulties and myoclonus. Many individuals with MEAK report temporary improvement of symptoms when they have a high fever. Seizures may become less frequent in adulthood, but other neurological complications, including myoclonus, ataxia and tremor, may worsen. Myoclonic epilepsy and ataxia due to potassium (K+) channel mutation (MEAK) is caused by a specific pathogenic variant ("mutation") in KCNC1 (c. 959G>A; p.Arg320His). KCNC1-related developmental and epileptic encephalopathy is associated with other pathogenic variants in KCNC1. In most individuals with KCNC1-related disorders, the pathogenic KCNC1 variant occurred spontaneously (de novo) and was not inherited from either parent. Epidemiology
PME accounts for less than 1% of epilepsy cases at specialist centres. The incidence and prevalence of PME is unknown, but there are considerable geography and ethnic variations amongst the specific genetic disorders. One cause, Unverricht Lundborg Disease, has an incidence of at least 1:20,000 in Finland. See also
Juvenile myoclonic epilepsy
Spinal muscular atrophy with progressive myoclonic epilepsy

References
External links

GeneReview/NCBI/NIH/UW entry on Progressive Myoclonus Epilepsy with Ataxia