Chronic exertional compartment syndrome: diagnosis and management.Bull Hosp Jt Dis. 2005;62(3-4):77-84. ^ Locke S. Exercise related chronic lower leg pain.
Overview Popliteal artery entrapment syndrome (PAES) is an uncommon condition in which an abnormally positioned or enlarged calf muscle presses on the main artery behind the knee (popliteal artery). The artery becomes trapped, making it harder for blood to flow to the lower leg and foot. Popliteal artery entrapment syndrome is most common among athletes. Popliteal artery entrapment syndrome care at Mayo Clinic Symptoms The main symptom of popliteal artery entrapment syndrome (PAES) is pain or cramping in the back of the lower leg (the calf) that occurs during exercise and goes away with rest. Other signs and symptoms may include: Cold feet after exercise Tingling or burning in your calf (paresthesia) Numbness in the calf area If the nearby vein (popliteal vein) also becomes trapped by the calf muscle, you may have: Heavy feeling in the leg Lower leg cramping at night Swelling in the calf area Changes in skin color around the calf muscle Blood clots in the lower leg (deep vein thrombosis) Symptoms typically affect young, otherwise healthy people under age 40. When to see a doctor See your doctor if you have any type of leg pain, especially if you have calf or foot cramping during activity that gets better with rest.
Good syndrome, also known as thymoma-immunodeficiency, is a very rare acquired immunodeficiency syndrome characterized by the association of thymoma and combined B-cell and T-cell immunodeficiency of adult onset with increased susceptibility to infections.
Good syndrome is a rare, adult-onset primary immunodeficiency suspected in patients who exhibit hypogammaglobulinemia and low levels of B cells along with a benign thymic tumor (thymoma) on chest X-ray. Symptoms include frequent opportunistic infections involving the sinuses and lungs, including severe CMV disease , P. carinii pneumonia , and mucocutaneous candidiasis . While the cause of Good syndrome remains unknown, there is some evidence that a defect of the bone marrow is involved. Treatment includes removal of the thymic tumor and immunoglobulin replacement .
Kendra and Maliyah Herrin Born ( 2002-02-26 ) February 26, 2002 (age 18) Salt Lake City, Utah , US Nationality American Parent(s) Jake and Erin Herrin Relatives Courtney Reiley Herrin (Sister) Justin Erron Jeffrey Herrin (brother) Austin Jacob Lamar Herrin (brother) Website http://herrintwins.com/ Kendra Deene Herrin and Maliyah Mae Herrin (born February 26, 2002) are former conjoined twins .
A rare disorder of the anterior segment of the eye characterized by slowly progressive, bilateral, asymmetric, usually non-inflammatory degeneration of the peripheral cornea, resulting in stromal thinning, vascularization, lipid deposition, and against-the-rule astigmatism with decreased visual acuity. Degeneration typically involves the superior aspect of the cornea first and extends circumferentially, leading to circumferential ectasia of the peripheral cornea. Opacification of the central cornea may occur at a very advanced stage. In rare cases, the condition is complicated by perforation.
. ^ a b Clark C, McIntyre PG, Evans A, McInnes CJ, Lewis-Jones S (April 2005). "Human sealpox resulting from a seal bite: confirmation that sealpox virus is zoonotic".
Conversely, a lower motor neuron lesion affects nerve fibers traveling from the anterior horn of the spinal cord or the cranial motor nuclei to the relevant muscle(s). [1] Upper motor neuron lesions occur in the brain or the spinal cord as the result of stroke , multiple sclerosis , traumatic brain injury , cerebral palsy , atypical parkinsonisms , multiple system atrophy , and amyotrophic lateral sclerosis .
PMID 4792047 . Free Full Text . ^ Silver, S. M. (December 1995). "Cerebral edema after rapid dialysis is not caused by an increase in brain organic osmolytes" .
These masses are generally contained within a capsule, so surgical removal is often successful. [3] Schwannomas can be associated with neurofibromatosis type II , which may be due to a loss-of-function mutation in the protein merlin . [4] They are universally S-100 positive, which is a marker for cells of neural crest cell origin.
A schwannoma is a tumor of the peripheral nervous system or nerve root. A schwannoma develops from cells called Schwann cells , a type of cell that wraps itself around peripheral nerves and provides protection and support. Schwannomas are almost always benign (not cancerous), but rarely, may become cancerous (a malignant schwannoma ). Symptoms of a schwannoma may be vague and will vary depending on its location and size, but may include a lump or bump that can be seen or felt, pain, muscle weakness, tingling, numbness, hearing problems, and/or facial paralysis. Sometimes schwannomas do not cause any symptoms. Schwannomas usually develop in otherwise healthy people for unknown reasons.
See Wikipedia's guide to writing better articles for suggestions. ( November 2018 ) ( Learn how and when to remove this template message ) A group of Nauruans Participating to a walk against diabetes around Nauru International Airport Young Nauruans in 1914 Obesity in Nauru is a major issue for the Republic of Nauru . The World Health Organization 's (WHO) estimated that 94.5% of Nauruans were identified as overweight and obese , [1] with an obesity rate of 71.7%. [2] Nauru is known to have the highest rates of obese inhabitants worldwide. [3] The average body weight among Nauruans is approximately 100 kilograms (220 lb). [2] Nauru has an average BMI between 34 and 35. [4] Contents 1 Causes 2 Consequence 3 Efforts to treat obesity 4 See also 5 References Causes [ edit ] 14th president of Nauru Baron Waqa The causes of obesity in Nauru are due to multiple factors.
RadioGraphics . 20 : 829. doi : 10.1148/radiographics.20.3.g00ma20819 . PMID 10835130 . ^ Perry, CR; Rice S; Rao A; Burdge R. (Oct 1983). "Posterior fracture-dislocation of the distal part of the fibula.
See also [ edit ] Addiction Social aspects of television Television consumption Video game addiction References [ edit ] ^ Sussman S, Moran MB (2013). "Hidden addiction: Television" .
A number sign (#) is used with this entry because of evidence that mental retardation, enteropathy, deafness, peripheral neuropathy, ichthyosis, and keratoderma (MEDNIK) is caused by homozygous mutation in the AP1S1 gene (603531) on chromosome 7q22. Description MEDNIK is a severe multisystem disorder characterized by mental retardation, enteropathy, deafness, peripheral neuropathy, ichthyosis, and keratoderma. It shows phenotypic similarities to CEDNIK (609528) (summary by Montpetit et al., 2008). Clinical Features Erythrokeratodermia variabilis (EKV; 133200) is a congenital disorder of the skin that causes hyperkeratosis and red patches of variable sizes, shapes, and duration. In 5 children from 3 families originating from the Kamouraska region of the province of Quebec, Saba et al. (2005) described an atypical form of erythrokeratodermia variabilis, designated erythrokeratodermia variabilis-3 (Kamouraska type) and symbolized EKV3.
MEDNIK syndrome, previously known as Erythrokeratodermia Variabilis type 3 (EKV3), is characterized by intellectual deficit, enteropathy, sensorineural hearing loss, peripheral neuropathy, lamellar and erythrodermic ichthyosis, and keratodermia (MEDNIK stands for Mental retardation, Enteropathy, Deafness, peripheral Neuropathy, Ichtyosis, Keratodermia). Epidemiology The syndrome has been described in four families descending from limited number of ancestors in Quebec. Etiology The disease is due to a mutation in the AP1S1 gene encoding the small subunit sigma1A of the AP-1 complex. Genetic counseling Transmission is autosomal recessive.
INHERITANCE - Autosomal recessive HEAD & NECK Head - Microcephaly (in some patients) Face - Coarse facial features - Deep philtrum - Wrinkled forehead Ears - Hearing loss (in some patients) - Thick helices - Thick ears - Posteriorly rotated ears Eyes - Almond-shaped palpebral fissures - Arched eyebrows - Nystagmus - Cortical visual impairment (in some patients) - Inability to track or smile Nose - Long nose Mouth - Macroglossia - Gingival hypertrophy Teeth - Widely spaced teeth CHEST External Features - Pectus carinatum ABDOMEN External Features - Umbilical hernia Liver - Hepatomegaly Gastrointestinal - Feeding difficulties GENITOURINARY External Genitalia (Male) - Cryptorchidism SKELETAL - Arthrogryposis (family A) - Joint laxity Pelvis - Hip laxity Hands - Brachydactyly - Short fourth metacarpals - Hypoplastic distal phalanges - Fifth finger clinodactyly - Single transverse palmar crease Feet - Short fourth metatarsals - Bulbous toes MUSCLE, SOFT TISSUES - Hypotonia - Inguinal hernia NEUROLOGIC Central Nervous System - Global developmental delay, profound - Balance problems - Ataxia - Inability to walk - Poor or absent speech - Seizures, febrile and nonfebrile, intractable - Cerebellar atrophy - Diffuse cortical atrophy PRENATAL MANIFESTATIONS Movement - Decreased fetal movements MISCELLANEOUS - Onset in utero or early infancy - Variable severity - Three unrelated families have been reported (last curated October 2018) - Family A had 2 affected fetuses MOLECULAR BASIS - Caused by mutation in the phosphatidylinositol glycan anchor biosynthesis class S protein gene (PIGS, 610271.0001 ) ▲ Close
Description Cornea plana is clinically characterized by reduced corneal curvature leading in most cases to hyperopia, hazy corneal limbus, and arcus lipoides at an early age. CNA1, an autosomal dominant form of the disorder, is mild (summary by Tahvanainen et al., 1996). Genetic Heterogeneity of Cornea Plana Also see CNA2 (217300), an autosomal recessive form of the disorder, which is severe and frequently associated with additional ocular manifestations. Clinical Features Larsen and Eriksson (1949) described 13 patients in 3 generations of each of 2 families. Eriksson et al. (1973) described families. Waizenegger et al. (1995) described autosomal dominant cornea plana with conjunctival xerosis in an Albanian family.
A rare developmental defect of the eye characterized by usually bilateral absence of the normal protrusion of the cornea from the sclera, the corneal curvature being the same as that of the adjacent sclera. Most patients develop hyperopia, hazy corneal limbus, and arcus lipoides at an early age. The condition may present as an autosomal dominant or an autosomal recessive form, with the latter showing more severe signs and symptoms (such as a round and opaque thickening located centrally in the cornea) and more frequent association with other ocular anomalies.
