In this situation the hypercapnia can also be accompanied by respiratory acidosis. [11] Acute hypercapnic respiratory failure may occur in acute illness caused by chronic obstructive pulmonary disease (COPD), chest wall deformity, some forms of neuromuscular disease (such as myasthenia gravis , and obesity hypoventilation syndrome . [12] AHRF may also develop in any form of respiratory failure where the breathing muscles become exhausted, such as severe pneumonia and acute severe asthma . ... A failure of this reflex can be fatal, for example as a contributory factor in sudden infant death syndrome . [20] Hypercapnia can induce increased cardiac output, an elevation in arterial blood pressure (higher levels of carbon dioxide stimulate aortic and carotid chemoreceptors with afferents -CN IX and X- to medulla oblongata with following chrono- and ino-tropic effects), and a propensity toward cardiac arrhythmias . ... Retrieved 2009-05-16 . ^ Kinney, Hannah C; Thach, Bradley T (2009). "The sudden infant death syndrome" . The New England Journal of Medicine . 361 (8): 795–805. doi : 10.1056/NEJMra0803836 . ... External links [ edit ] Classification D ICD - 10 : R06.8 ICD - 9-CM : 786.09 MeSH : D006935 DiseasesDB : 95 v t e Symptoms and signs relating to the respiratory system Auscultation Stethoscope Respiratory sounds Stridor Wheeze Crackles Rhonchi Stertor Squawk Pleural friction rub Fremitus Bronchophony Terminal secretions Elicited findings Percussion Pectoriloquy Whispered pectoriloquy Egophony Breathing Rate Apnea Prematurity Dyspnea Hyperventilation Hypoventilation Hyperpnea Tachypnea Hypopnea Bradypnea Pattern Agonal respiration Biot's respiration Cheyne–Stokes respiration Kussmaul breathing Ataxic respiration Other Respiratory distress Respiratory arrest Orthopnea / Platypnea Trepopnea Aerophagia Asphyxia Breath holding Mouth breathing Snoring Other Chest pain In children Precordial catch syndrome Pleurisy Nail clubbing Cyanosis Cough Sputum Hemoptysis Epistaxis Silhouette sign Post-nasal drip Hiccup COPD Hoover's sign asthma Curschmann's spirals Charcot–Leyden crystals chronic bronchitis Reid index sarcoidosis Kveim test pulmonary embolism Hampton hump Westermark sign pulmonary edema Kerley lines Hamman's sign Golden S sign v t e Underwater diving Diving modes Atmospheric pressure diving Freediving Saturation diving Scuba diving Snorkeling Surface oriented diving Surface-supplied diving Unmanned diving Diving equipment Cleaning and disinfection of personal diving equipment Human factors in diving equipment design Basic equipment Diving mask Snorkel Swimfin Breathing gas Bailout gas Bottom gas Breathing air Decompression gas Emergency gas supply Heliox Nitrox Oxygen Travel gas Trimix Buoyancy and trim equipment Buoyancy compensator Power inflator Dump valve Diving weighting system Ankle weights Integrated weights Trim weights Weight belt Decompression equipment Decompression buoy Decompression cylinder Decompression trapeze Dive computer Diving shot Jersey upline Jonline Diving suit Atmospheric diving suit Dry suit Sladen suit Standard diving suit Rash vest 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Deep-water blackout Shallow-water blackout Hypercapnia Hypothermia Historical Ama Octopus wrestling Swimming at the 1900 Summer Olympics – Men's underwater swimming Organisations AIDA International Scuba Schools International Australian Underwater Federation British Freediving Association Confédération Mondiale des Activités Subaquatiques Fédération Française d'Études et de Sports Sous-Marins Performance Freediving International Professional diving Occupations Ama Commercial diver Commercial offshore diver Hazmat diver Divemaster Diving instructor Diving safety officer Diving superintendent Diving supervisor Haenyeo Media diver Police diver Public safety diver Scientific diver Underwater archaeologist Military diving Army engineer diver Clearance diver Frogman List of military diving units Royal Navy ships diver Special Boat Service United States military divers U.S. ... 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surveillance Safety culture Code of practice Diving safety officer Diving superintendent Health and safety representative Operations manual Safety meeting Standard operating procedure Diving medicine Diving disorders List of signs and symptoms of diving disorders Cramp Motion sickness Surfer's ear Pressure related Alternobaric vertigo Barostriction Barotrauma Air embolism Aerosinusitis Barodontalgia Dental barotrauma Pulmonary barotrauma Compression arthralgia Decompression illness Dysbarism Oxygen Freediving blackout Hyperoxia Hypoxia Oxygen toxicity Inert gases Avascular necrosis Decompression sickness Isobaric counterdiffusion Taravana Dysbaric osteonecrosis High-pressure nervous syndrome Hydrogen narcosis Nitrogen narcosis Carbon dioxide Hypercapnia Hypocapnia Breathing gas contaminants Carbon monoxide poisoning Immersion related Asphyxia Drowning Hypothermia Immersion diuresis Instinctive drowning response Laryngospasm Salt water aspiration syndrome Swimming-induced pulmonary edema Treatment Demand valve oxygen therapy First aid Hyperbaric medicine Hyperbaric treatment schedules In-water recompression Oxygen therapy Therapeutic recompression Personnel Diving Medical Examiner Diving Medical Practitioner Diving Medical Technician Hyperbaric nursing Screening Atrial septal defect Effects of drugs on fitness to dive Fitness to dive Psychological fitness to dive Research Researchers in diving physiology and medicine Arthur J.
In pregnant women , especially in the third trimester, the disease is more often severe and is associated with a clinical syndrome called fulminant liver failure , with death rates around 20%. [8] [12] [13] Whereas pregnant women may have a rapid and severe course, organ transplant recipients who receive medications to weaken the immune system and prevent organ rejection can develop a slower and more persistent form called chronic hepatitis E, [14] which is so diagnosed after 3 months of continuous viremia. [15] HEV can be clustered genetically into 8 genotypes, and genotypes 3 and 4 tend to be the ones that cause chronic hepatitis in the immunosuppressed. [16] [17] In 2017, hepatitis E was estimated to affect more than 19 million people. [3] Those most commonly at risk of HEV are men aged 15 to 35 years of age. [11] A preventive vaccine (HEV 239) is approved for use in China . [18] Contents 1 Signs and symptoms 1.1 Acute infection 1.2 Chronic infection 1.3 Other organs 1.4 Infection in pregnancy 2 Virology 2.1 Classification 2.1.1 Distribution 2.2 Transmission 2.3 Animal reservoir 2.4 Genomics 2.5 Virus lifecycle 3 Diagnosis 3.1 Virological markers 4 Prevention 4.1 Sanitation 4.2 Blood products 4.3 Vaccines 5 Treatment 6 Epidemiology 6.1 Recent outbreaks 7 Evolution 8 References 9 Further reading 10 External links Signs and symptoms [ edit ] Acute infection [ edit ] The average incubation period of hepatitis E is 40 days, ranging from 2 to 8 weeks. ... For some of these reported conditions such as musculoskeletal or immune-mediated manifestations the relationship is not entirely clear, but for several neurological and blood conditions the relationship appears more consistent: [26] [27] [28] [29] Acute pancreatitis (HEV genotype 1 [5] ) Neurological complications (though the mechanism of neurological damage is unknown at this point. [11] ) include: Guillain-Barré syndrome (acute limb weakness due to nerve involvement), neuralgic amyotrophy (arm and shoulder weakness, also known as Parsonage-Turner syndrome), acute transverse myelitis and acute meningoencephalitis . Glomerulonephritis with nephrotic syndrome and/or cryoglobulinemia Mixed cryoglobulinemia , where antibodies in the bloodstream react inappropriately at low temperatures Severe thrombocytopenia (low platelet count in the blood) which confers an increased risk of dangerous bleeding Infection in pregnancy [ edit ] Pregnant women show a more severe course of infection than other populations. ... 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Tumorspheres with radial glial characteristics form tumors in orthotopic mouse xenografts , suggesting radial glial as cell of origin for ependymomas . [1] [2] Inheritance [ edit ] A number of genetic syndromes are associated with the development of ependymoma , including neurofibromatosis type II (NF2), Turcot syndrome B, and MEN1 syndrome. However, gene mutations linked to the familial syndromes are rarely found in sporadic cases of ependymoma . [3] For example, NF2 mutations have rarely been observed in ependymomas and MEN1 mutations have only been found in a small number of cases of ependymoma recurrences. [4] [5] [6] [7] Oncogenic lesions [ edit ] ERBB2 , ERBB4 , and human telomerase reverse transcriptase ( TERT ) gene expression promote tumor cell proliferation, contributing to aggressive tumor behavior. [8] [9] [10] High expression of epidermal growth factor receptor ( EGFR ) correlates with unfavorable outcome. [9] Over-expression of kinetochore proteins and down-regulation of metallothioneins are associated with recurrence in ependymomas . [11] KIT receptor tyrosine kinase and phospho - KIT were found to be present in pediatric ependymomas and may be involved in angiogenesis associated with those tumors. [12] Chromosomal changes [ edit ] Comparative genomic hybridization (CGH) experiments have shown pediatric ependymomas possess a number of genomic anomalies not seen in adult ependymomas . [13] In addition, ependymomas from different locations within the central nervous system (spinal, supratentorial , and infratentorial ) can be distinguished by their chromosomal , immunohistochemical , and gene expression differences. [13] Amplification of chromosome 1q and loss of 6q , 17p and 22q are the most common numerical chromosomal changes in pediatric ependymomas. [14] [15] [16] Gain of chromosome 1q (1q21.1-32.1) is more common in the pediatric population and is associated with tumor recurrence in intracranial ependymomas. ... "Neuropsychological consequences of cerebellar tumour resection in children: Cerebellar cognitive affective syndrome in a paediatric population" . Brain . 123 (5): 1041–50. doi : 10.1093/brain/123.5.1041 .
Extragonadal teratoma is an extremely rare, benign or malignant germ cell tumor characterized, clinically, by a teratoma presenting in an extragonadal location (e.g. retroperitoneum, mediastinum, craniofacial or sacrococcygeal region, intraosseous, solid organs) and, histologically, by displaying well-differentiated structures, as well as immature elements. Presenting symptoms are variable depending on size and location of tumor.
A teratoma with malignant transformation (TMT) is a tumor that develops from germ cells when they grow and divide abnormally, forming a mass . Approximately 6% of teratomas develop into TMTs by a process called malignant transformation , when some of the cells in the teratoma become cancerous. TMTs can occur anywhere in the body, but most are located in the testes in men or ovaries in women. The cause of TMT is unknown. Treatment may include surgery and chemotherapy.
Food protein-induced enterocolitis syndrome (FPIES) A food allergen can also cause what's sometimes called a delayed food allergy. ... Unlike some food allergies, food protein-induced enterocolitis syndrome (FPIES) usually resolves over time.
When these symptoms occur, the allergic reaction is called anaphylaxis . [19] Anaphylaxis occurs when IgE antibodies are involved, and areas of the body that are not in direct contact with the food become affected and show severe symptoms. [19] [20] Untreated, this can proceed to vasodilation , a low blood pressure situation called anaphylactic shock , and very rarely, death. [6] [20] For milk allergy, non-IgE-mediated responses are more common than IgE-mediated. [21] The presence of certain symptoms, such as angioedema or atopic eczema , is more likely related to IgE-mediated allergies, whereas non-IgE-mediated reactions manifest as gastrointestinal symptoms, without skin or respiratory symptoms. [18] [22] Within non-IgE cow's milk allergy, clinicians distinguish among food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP) and food protein-induced enteropathy (FPE). ... "International consensus guidelines for the diagnosis and management of food protein-induced enterocolitis syndrome: Executive summary-Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology" . ... "Food Protein-Induced Enterocolitis Syndrome, Allergic Proctocolitis, and Enteropathy".
Brain AVM s are seen in some people who have hereditary hemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu syndrome. HHT affects the way blood vessels form in several areas of the body, including the brain. ... For example, high blood pressure within the AVM and hereditary syndromes associated with neurological issues may play a role.
Vora et al. (1980) speculated that the heterogeneous group of hemolytic syndromes associated with partial red cell PFK deficiency without myopathy (Boulard et al., 1974; Kahn et al., 1975) may represent total absence of PFKL subunits or qualitative defects of M or L subunits. Vora et al. (1983) suggested that GSD VII could be classified clinically into 5 phenotypic subtypes: type I is the classic syndrome characterized by exertional myopathy and hemolysis; type II by isolated myopathy; type III by isolated hemolysis; and type IV by asymptomatic partial deficiency of red cell PFK.
Muscle phosphofructokinase (PFK) deficiency (Tarui's disease), or glycogen storage disease type 7 (GSD7), is a rare form of glycogen storage disease characterized by exertional fatigue and muscular exercise intolerance. It occurs in childhood. Epidemiology About 100 cases have been reported worldwide. Clinical description Clinical signs are muscular exercise intolerance (more severe than in type 5; see this term). Compensated hemolysis (increased bilirubin and reticulocytes) and hyperuricemia are associated. A rapidly fatal infant form has also been observed in 6 families. Etiology The condition is caused by mutations in the PFKM gene (12q13) encoding the muscular isoenzyme of PFK, a key enzyme in the regulation of anaerobic glycolysis which has 3 isoenzymes (for the muscle, liver, and platelets).
Glycogen storage disease type VII (GSDVII) is an inherited disorder caused by an inability to break down a complex sugar called glycogen in muscle cells. A lack of glycogen breakdown interferes with the function of muscle cells. There are four types of GSDVII. They are differentiated by their signs and symptoms and the age at which symptoms first appear. The classical form of GSDVII is the most common form. Its features usually appear in childhood. This form is characterized by muscle pain and cramps, often following moderate exercise; strenuous exercise can lead to nausea and vomiting.
Glycogen storage disease type 7 (GSD7) is an inherited condition in which the body is unable to break down glycogen (a complex sugar) in the muscle cells. Because glycogen is an important source of energy, this can interfere with the normal functioning of muscle cells. The severity of the condition and the associated signs and symptoms vary, but may include muscle weakness and stiffness; painful muscle cramps; nausea and vomiting; and/or myoglobinuria (the presence of myoglobin in the urine) following moderate to strenuous exercise. Symptoms typically resolve with rest. GSD7 is most commonly diagnosed during childhood; however, some affected people may rarely develop symptoms during infancy or later in adulthood. Those who develop the condition during infancy may experience additional symptoms such as hypotonia (poor muscle tone), cardiomyopathy and breathing difficulties that often lead to a shortened lifespan (less than 1 year).
These findings were consistent with a rare occurrence of autosomal dominant Bernard-Soulier syndrome (153670). However, the remaining 6 Italian families reported by Savoia et al. (2001) did not have GP1BA mutations, suggesting genetic heterogeneity. ... These studies showed that the hematologic syndrome of Mediterranean stomatocytosis can result from an excess of plasma phytosterols, perhaps due to abnormal lipid content in red cell and platelet membranes.
., nicotine-replacement therapies for long-term maintenance against tobacco dependence and for treatment of other syndromes such as Alzheimer disease (104300), and Tourette syndrome (137580).
Clinical Variability Reyniers et al. (1999) described a 'new' neurologic syndrome in 5 male patients from a 4-generation Luxembourg family. ... Mapping Reyniers et al. (1999) mapped the mental retardation and choreoathetosis syndrome in the 4-generation family described by them to chromosome Xp11 by linkage analysis, confirming X-linked inheritance.
HSD10 disease (also known as 2-methyl-3-hydroxybutyric aciduria) is an inherited disorder in which the body cannot effectively process the amino acid isoleucine. Signs and symptoms of this condition usually develop in infancy or early childhood and include metabolic acidosis , hypoglycemia, hypotonia, seizures, movement problems, retinal degeneration, and hearing loss. Affected males have severe neurodegeneration with loss of developmental milestones, whereas females have mild to moderate developmental delay. HSD10 disease is caused by mutations in the HSD17B10 gene; it has an X-linked dominant pattern of inheritance.
HSD10 disease is a disorder that affects the nervous system, vision, and heart. It is typically more severe in males than in females. Most affected males have a form of HSD10 disease in which early development seems normal, followed by a stage in which affected individuals rapidly lose skills they have acquired. This developmental regression often occurs between the ages of 1 and 2 and results in severe intellectual disability and loss of communication skills and motor skills such as sitting, standing, and walking. This form of the disorder is referred to as the infantile type. Less commonly, affected males have severe neurological problems from birth and never develop motor skills. This form is called the neonatal type. Males with the infantile or neonatal type frequently have weak muscle tone (hypotonia), recurrent seizures (epilepsy), and vision loss that gradually gets worse.
HSD10 disease is a rare, life-threatening neurometabolic disease characterized by a progressive neurodegenerative course, epilepsy, retinopathy and progressive cardiomyopathy. Epidemiology Prevalence is unknown. So far, fewer than 40 cases have been reported worldwide. Clinical description HSD10 disease is heterogeneous, including several clinical subtypes, and manifests by severe manifestations in males only; females are either asymptomatic or show non-progressive cognitive impairment ranging from learning difficulties to intellectual disability, as well as variable neurological abnormalities. HSD10 disease, infantile form is the classical presentation. Affected boys may show lethargy, poor feeding and evidence of mitochondrial dysfunction in the newborn period, with subsequent mild developmental delay and abnormal muscle tone. Hallmark of the disease is progressive neurodegeneration and cardiomyopathy, which usually manifests between ages 6 months and 2 years with loss of cognitive and motor skills, epilepsy, progressive visual impairment leading to blindness, and/or hearing loss.
HSD10 disease, infantile type is a clinical subtype of HSD10 disease, a rare neurometabolic disorder. Affected boys may show lethargy, poor feeding and evidence of mitochondrial dysfunction in the newborn period, with subsequent mild developmental delay and abnormal muscle tone. Hallmark of the disease is progressive neurodegeneration and cardiomyopathy, which usually manifests between ages 6 months and 2 years with developmental regression, progressive visual and hearing loss, epilepsy and other neurological symptoms, and severe cardiomyopathy. Laboratory investigations show signs of mitochondrial dysfunction, and increased urinary excretion of specific isoleucine metabolites. The disease is often fatal around 2-4 years of age.
HSD10 disease, neonatal type is the most severe form of HSD10 disease, a rare neurometabolic disorder. It is characterized by severe metabolic/lactic acidosis in the neonatal period, little psychomotor development, seizures and severe progressive hypertrophic cardiomyopathy. Hepatic involvement and coagulopathy are rare. The disease is fatal within the first months of life.
Zambia in 10–20% band Human immunodeficiency virus infection and acquired immune deficiency syndrome (HIV/AIDS) is a set of conditions caused by infection with the human immunodeficiency virus (HIV). [2] [3] HIV is transmitted by three main ways: sexual contact , significant exposure to infected body fluids or tissues, and from mother to child during pregnancy, delivery, or breastfeeding (known as vertical transmission ). ... Further reading [ edit ] Children as Caregivers: The Global Fight Against Tuberculosis and HIV in Zambia by Jean Hunleth, 2017, Rutgers University Press v t e HIV/AIDS in Africa Sovereign states Algeria Angola Benin Botswana Burkina Faso Burundi Cameroon Cape Verde (Cabo Verde) Central African Republic Chad Comoros Democratic Republic of the Congo Republic of the Congo Djibouti Egypt Equatorial Guinea Eritrea Eswatini (Swaziland) Ethiopia Gabon The Gambia Ghana Guinea Guinea-Bissau Ivory Coast (Côte d'Ivoire) Kenya Lesotho Liberia Libya Madagascar Malawi Mali Mauritania Mauritius Morocco Mozambique Namibia Niger Nigeria Rwanda São Tomé and Príncipe Senegal Seychelles Sierra Leone Somalia South Africa South Sudan Sudan Tanzania Togo Tunisia Uganda Zambia Zimbabwe States with limited recognition Sahrawi Arab Democratic Republic Somaliland Dependencies and other territories Canary Islands / Ceuta / Melilla (Spain) Madeira (Portugal) Mayotte / Réunion (France) Saint Helena / Ascension Island / Tristan da Cunha (United Kingdom) v t e HIV / AIDS topics HIV/AIDS HIV HIV Lentivirus structure and genome subtypes CDC classification disease progression rates HIV/AIDS diagnosis management pathophysiology prevention research vaccination PrEP WHO disease staging system for HIV infection and disease Children Teens / Adults Countries by AIDS prevalence rate Conditions Signs and symptoms AIDS-defining clinical condition Diffuse infiltrative lymphocytosis syndrome Lipodystrophy Nephropathy Neurocognitive disorders Pruritus Superinfection Tuberculosis co-infection HIV Drug Resistance Database Innate resistance to HIV Serostatus HIV-positive people Nutrition Pregnancy History History Epidemiology Multiple sex partners Timeline AIDS Museum Timothy Ray Brown Women and HIV/AIDS Social AIDS orphan Catholic Church and HIV/AIDS Circumcision and HIV Criminal transmission Discrimination against people Economic impact Cost of treatment HIV-affected community HIV/AIDS activism HIV/AIDS denialism Red ribbon Safe sex Sex education List of HIV-positive people People With AIDS Self-Empowerment Movement HIV/AIDS in the porn industry Culture Discredited HIV/AIDS origins theories International AIDS Conference International AIDS Society Joint United Nations Programme on HIV/AIDS (UNAIDS) Media portrayal of HIV/AIDS Misconceptions about HIV/AIDS President's Emergency Plan for AIDS Relief (PEPFAR) The SING Campaign Solidays Treatment Action Campaign World AIDS Day YAA/Youthforce "Free Me" Larry Kramer Gay Men's Health Crisis ACT UP Silence=Death Project HIV/AIDS pandemic by region / country Africa Angola Benin Botswana Democratic Republic of the Congo Egypt Eswatini Ethiopia Ghana Guinea Côte d'Ivoire (Ivory Coast) Kenya Lesotho Madagascar Malawi Mali Mozambique Namibia Niger Nigeria Rwanda Senegal Tanzania South Africa Uganda Zambia Zimbabwe North America Canada Mexico El Salvador Guatemala Honduras Nicaragua United States New York City Caribbean Haiti Jamaica Dominican Republic South America Bolivia Brazil Colombia Guyana Peru Asia Afghanistan Armenia Azerbaijan Bahrain Bangladesh Bhutan Cambodia China (PRC) ( Yunnan ) East Timor India Indonesia Iran Iraq Japan Jordan North Korea Laos Malaysia Myanmar (Burma) Nepal Pakistan Philippines Saudi Arabia Sri Lanka Taiwan (ROC) Thailand United Arab Emirates Turkey Vietnam Europe United Kingdom Russia Ukraine Oceania Australia New Zealand Papua New Guinea List of countries by HIV/AIDS adult prevalence rate List of HIV/AIDS cases and deaths registered by region
A person can have reactive lymph nodes throughout multiple areas of the body which can cause swelling, pain, warmth and tenderness. [5] Causes [ edit ] The following are examples of potential causes for reactive lymphadenopathies , all of which have predominantly follicular patterns: [1] Rheumatoid arthritis Sjögren syndrome IgG4-related disease (IgG4-related lymphadenopathy ) [6] Kimura disease Toxoplasmosis Syphilis Castleman disease Progressive transformation of germinal centers (PTGC) Microorganisms can infect lymph nodes by causing pain and inflammation including redness and tenderness. Bacterial, fungal and viral infections including Bartonella , Staphylococcal , Granulomatous , Adenoviral and Lyme disease are all associated with follicular hyperplasia. [7] Other autoimmune related diseases that are associated are rheumatoid arthritis , systemic lupus , dermatomyositis and Sjögren syndrome . Immunoglobulin G - related diseases are immune-mediated fibroinflammatory conditions that affect many organs in the body.
External links [ edit ] Classification D ICD - 10 : H81.2 , H83.0 ICD - 9-CM : 386.3 , 386.12 MeSH : D007762 DiseasesDB : 29290 SNOMED CT : 23919004 External resources MedlinePlus : 001054 Patient UK : Labyrinthitis Labyrinthitis at Curlie v t e Disorders of hearing and balance Hearing Symptoms Hearing loss Excessive response Tinnitus Hyperacusis Phonophobia Disease Loss Conductive hearing loss Otosclerosis Superior canal dehiscence Sensorineural hearing loss Presbycusis Cortical deafness Nonsyndromic deafness Other Deafblindness Wolfram syndrome Usher syndrome Auditory processing disorder Spatial hearing loss Tests Hearing test Rinne test Tone decay test Weber test Audiometry pure tone visual reinforcement Balance Symptoms Vertigo nystagmus Disease Balance disorder Peripheral Ménière's disease Benign paroxysmal positional vertigo Labyrinthitis Labyrinthine fistula Tests Dix–Hallpike test Unterberger test Romberg's test Vestibulo–ocular reflex
Initially, researchers tried to isolate the cause to left hemisphere lesions in the parietal lobe because of its similarities to Gerstmann syndrome ; however, lesions in the dorsal stream also result in visual agnosia and a piecemeal drawing. [1] Although constructional apraxia can result from lesions in any part of the brain, it is most commonly associated with lesions in the parietal-occipital lobes. ... "Understanding the parietal lobe syndrome from a neurophysiological and evolutionary perspective" .
Hypertensive encephalopathy Specialty Emergency medicine , cardiology Symptoms Headache , vomiting, trouble with balance, confusion [1] Complications Seizures , bleeding in the back of the eye [1] Usual onset Sudden [1] Causes Kidney failure , rapidly stopping blood pressure medication , pheochromocytoma , taking monoamine oxidase inhibitor with foods containing tyramine, eclampsia [2] Diagnostic method Blood pressure > 200/130 mmHg and general brain dysfunction [1] Differential diagnosis Uremic encephalopathy , stroke (ischemic or bleeding ), hydrocephalus , cocaine toxicity [1] [2] Medication Labetalol , sodium nitroprusside [2] Frequency Uncommon [2] Hypertensive encephalopathy ( HE ) is general brain dysfunction due to significantly high blood pressure . [3] Symptoms may include headache, vomiting, trouble with balance, and confusion. [1] Onset is generally sudden. [1] Complications can include seizures , posterior reversible encephalopathy syndrome , and bleeding in the back of the eye . [1] [3] In hypertensive encephalopathy, generally the blood pressure is greater than 200/130 mmHg. [1] Occasionally it can occur at a BP as low as 160/100 mmHg. [4] This can occur in kidney failure , those who rapidly stop blood pressure medication , pheochromocytoma , and people on a monoamine oxidase inhibitor (MAOI) who eat foods with tyramine. [2] When it occurs in pregnancy it is known as eclampsia . [2] The diagnosis requires ruling out other possible causes. [1] The condition is generally treated with medications to relatively rapidly lower the blood pressure. [2] [3] This may be done with labetalol or sodium nitroprusside given by injection into a vein . [2] In those who are pregnant, magnesium sulfate may be used. [2] Other treatments may include anti-seizure medications . [2] Hypertensive encephalopathy is uncommon. [2] It is believed to occur more often in those without easy access to health care. [2] The term was first used by Oppenheimer and Fishberg in 1928. [5] [6] It is classified as a type of hypertensive emergency . [4] Contents 1 Signs and symptoms 2 Pathogenesis 3 Diagnosis 4 Treatment 5 Prognosis 6 History 7 References 8 External links Signs and symptoms [ edit ] Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who have hypertension. [7] [8] [9] Overall, the condition is rare even among people with hypertension. ... Additionally, hypertensive encephalopathy may occur in pheochromocytoma , Cushing's syndrome, renal artery thrombosis . The impairment of cerebral blood flow that underlies hypertensive encephalopathy is still controversial.
Behçet's disease [ edit ] Pregnancy does not have an adverse effect on the course of Behçet's disease and may possibly ameliorate its course. [17] [18] Still, there is a substantial variability in clinical course between patients and even for different pregnancies in the same patient. [17] Also, the other way around, Behçet's disease confers an increased risk of pregnancy complications , miscarriage and Cesarean section . [18] Multiple sclerosis [ edit ] Being pregnant decreases the risk of relapse in multiple sclerosis ; however, during the first months after delivery the risk increases. [19] Overall, pregnancy does not seem to influence long-term disability. [19] Multiple sclerosis does not increase the risk of congenital abnormality or miscarriage . [20] [21] Others [ edit ] The following conditions may also become worse or be a potential risk to the pregnancy: Cancer [MMHE 2] Chronic hypertension [MMHE 3] Cirrhosis [MMHE 4] Congenital disorders that may be passed on to offspring Heart defects , especially primary pulmonary hypertension and Eisenmenger's syndrome [MMHE 5] Kidney disorders [MMHE 6] Mental health . ... Journal of Acquired Immune Deficiency Syndromes . 23 (3): 246–254. doi : 10.1097/00042560-200003010-00006 .
Overview Epididymitis (ep-ih-did-uh-MY-tis) is an inflammation of the coiled tube, called the epididymis, at the back of the testicle. The epididymis stores and carries sperm. Males of any age can get epididymitis. Epididymitis is most often caused by a bacterial infection, including sexually transmitted infections (STIs), such as gonorrhea or chlamydia. Sometimes, a testicle also becomes inflamed — a condition called epididymo-orchitis. Epididymitis is usually treated with antibiotics and measures to relieve discomfort.