The condition is observed on the left side of the face about as often as on the right side. History
The disease was first described in 1825 by Caleb Hillier Parry (1755–1822), in a collection of his medical writings which were published posthumously by his son Charles Henry Parry (1779–1860). It was described a second time in 1846 by Moritz Heinrich Romberg (1795–1873) and Eduard Heinrich Henoch (1820–1910). German neurologist Albert Eulenburg (1840–1917) was the first to use the descriptive title "progressive hemifacial atrophy" in 1871. See also
Hemifacial microsomia
List of cutaneous conditions
Trigeminal trophic lesion

References
Further reading
Karim A, Laghmari M, Ibrahimy W, Essakali HN, Mohcine Z (October 2005). "[Neuroretinitis, Parry-Romberg syndrome, and scleroderma]". Journal Français dOphtalmologie (in French). 28 (8): 866–70. doi:10.1016/S0181-5512(05)81008-3. PMID 16249769. Lakhani PK, David TJ (February 1984). "Progressive hemifacial atrophy with scleroderma and ipsilateral limb wasting (Parry-Romberg syndrome)". Journal of the Royal Society of Medicine. 77 (2): 138–9. doi:10.1177/014107688407700215. PMC 1439690. PMID 6737396. Larner AJ, Bennison DP (September 1993). "Some observations on the aetiology of progressive hemifacial atrophy ("Parry-Romberg syndrome")". Journal of Neurology, Neurosurgery, and Psychiatry. 56 (9): 1035–6. doi:10.1136/jnnp.56.9.1035-a. PMC 489747. PMID 8410030. Miller MT, Spencer MA (1995). "Progressive hemifacial atrophy. A natural history study". Transactions of the American Ophthalmological Society. 93: 203–15, discussion 215–7. PMC 1312058. PMID 8719679. Pinheiro TP, Silva CC, Silveira CS, Botelho PC, Pinheiro MD, Pinheiro JJ (March 2006). "Progressive Hemifacial Atrophy--case report". Medicina Oral, Patologia Oral y Cirugia Bucal. 11 (2): E112-4. PMID 16505785. Zafarulla MY (July 1985). "Progressive hemifacial atrophy: a case report". The British Journal of Ophthalmology.
Lactic acidosis is a medical condition characterized by a build-up of lactate (especially L-lactate) in the body, with formation of an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the bodys oxidative metabolism. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, Kussmaul breathing (laboured and deep), and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification
The Cohen–Woods classification categorizes causes of lactic acidosis as:
Type A: Decreased tissue oxygenation (e.g., from decreased blood flow)
Type B
B1: Underlying diseases (sometimes causing type A)
B2: Medication or intoxication
B3: Inborn error of metabolism

Signs and symptoms
Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.