Familial Adenomatous Polyposis Coli
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  Familial Adenomatous Polyposis Coli



Familial Adenomatous Polyposis Coli

   An autosomal dominant polyposis syndrome in which the colon contains few to thousands of adenomatous polyps, often occurring by age 15 to 25.

RELATED TERMS
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Autosomal
"Pertaining to a chromosome that is not a sex chromosome; relating to any one of the chromosomes save the sex chromosomes. People normally have 22 pairs of autosomes (44 autosomes) in each cell together with two sex chromosomes (X and Y in the male and XX in the female). "

Dominant
A genetic trait is considered dominant if it is expressed in a person who has only one copy of that gene. (In genetic terms, a dominant trait is one that is phenotypically expressed in heterozygotes). A dominant trait is opposed to a recessive trait which is expressed only when two copies of the gene are present. (In genetic terms, a recessive trait is one that is phenotypically expressed only in homozygotes).

Polyposis
The presence of many polyps.

Syndrome
A grouping of signs and symptoms, based on their frequent co-occurrence, that may suggest a common underlying pathogenesis, course, familial pattern, or treatment selection.

Colon
Another name for the large intestine. The section of the large intestine extending from the cecum to the rectum. An adult colon is approximately five to six feet in length and is responsible for absorbing water and forming, storing and expelling waste.

Polyps
An abnormal growth of a mucous membrane, often in the nasal passages, bladder, rectum, or uterus. Polyps, though often benign, have been associated with cancers and can be surgically removed.



SIMILAR TERMS
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Familial
A condition that is tends to occur more often in family members than expected by chance alone. A familial disease may be genetic (such as cystic fibrosis) or environmental (such as tuberculosis).

Familial Acoustic Neuroma
An autosomal dominant disorder characterized by a high incidence of bilateral acoustic neuromas as well as schwannomas (NEURILEMMOMA) of other cranial and peripheral nerves, and other benign intracranial tumors including meningiomas, ependymomas, spinal neurofibromas, and gliomas. The disease has been linked to mutations of the NF2 gene (GENES, NEUROFIBROMATOSIS 2) on chromosome 22 (22q12) and usually presents clinically in the first or second decade of life.

Familial Acoustic Neuromas
An autosomal dominant disorder characterized by a high incidence of bilateral acoustic neuromas as well as schwannomas (NEURILEMMOMA) of other cranial and peripheral nerves, and other benign intracranial tumors including meningiomas, ependymomas, spinal neurofibromas, and gliomas. The disease has been linked to mutations of the NF2 gene (GENES, NEUROFIBROMATOSIS 2) on chromosome 22 (22q12) and usually presents clinically in the first or second decade of life.

Familial adenomatous polyposis
Abbreviated FAP. A syndrome characterized by the formation of thousands of polyps in the colon and rectum with colorectal cancer the inevitable consequence. Polyps can also occur in the stomach, duodenum and the terminal ileum. The polyps most often begin to form at puberty. And colon cancer usually occurs 10 to 15 years thereafter. The average age of diagnosis of familial polyposis is 25 years of age, with cancers developing at age 20 to 30. However, cancers may arise anywhere from late childhood to the sixties.

Familial alpha Lipoprotein Deficiency Disease
A rare autosomal recessive familial disorder of cholesterol metabolism, characterized by extremely low HDL-cholesterol, reduced total cholesterol, and increased triglyceride levels in serum. Clinical features include the onset before age 20 years of HEPATOMEGALY; SPLENOMEGALY; the deposition of cholesterol in each TONSIL (creating a yellow-orange appearance); and RETINITIS PIGMENTOSA. A sensorimotor or distal sensory POLYNEUROPATHY occurs in approximately 50% of affected individuals. The condition is associated with decreased synthesis and increased catabolism of APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II, and a defect in cellular signaling and mobilization of lipids. (From Nat Genet 1998 Sep;20(1):96-8; Adams et al., Principles of Neurology, 6th ed, pp1347-8; Menkes, Textbook of Child Neurology, 5th ed, p118)

Familial alpha-Lipoprotein Deficiency Disease
A rare autosomal recessive familial disorder of cholesterol metabolism, characterized by extremely low HDL-cholesterol, reduced total cholesterol, and increased triglyceride levels in serum. Clinical features include the onset before age 20 years of HEPATOMEGALY; SPLENOMEGALY; the deposition of cholesterol in each TONSIL (creating a yellow-orange appearance); and RETINITIS PIGMENTOSA. A sensorimotor or distal sensory POLYNEUROPATHY occurs in approximately 50% of affected individuals. The condition is associated with decreased synthesis and increased catabolism of APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II, and a defect in cellular signaling and mobilization of lipids. (From Nat Genet 1998 Sep;20(1):96-8; Adams et al., Principles of Neurology, 6th ed, pp1347-8; Menkes, Textbook of Child Neurology, 5th ed, p118)

Familial ALS
ALS (amyotrophic lateral sclerosis) in which there a family history of the disease. Familial ALS constitutes 5 to 10% of all cases of ALS. There are a number of different types of familial ALS. They are known as ALS1, ALS2, and so on. ALS1 -- caused by mutation in the superoxide dismutase-1 gene (SOD1) on chromosome 21q22.1. About 15 to 20% of familial ALS is type 1 (ALS1). Sporadic cases of ALS are sometimes due to new mutation in the SOD1 gene; ALS2 -- juvenile-onset ALS caused by mutation in the gene encoding alsin on chromosome 2q33; ALS3 -- adult-onset ALS due to mutation in a gene on chromosome 18q21; ALS4 -- juvenile-onset disease with no bulbar involvement due to mutations in a gene on chromosome 9q34; ALS5 -- due to mutations in a gene on chromosome 15q15.1-q21.1; ALS6 -- due to mutations in a gene on chromosome 16q12; ALS7 -- due to mutations in a gene on chromosome 20ptel; ALS8 -- due to mutations in a gene on chromosome 20q13.33. ALS1, ALS3, ALS4, ALS6, ALS7, and ALS8 are inherited in an autosomal dominant manner while ALS2 and ALS5 are inherited in an autosomal recessive manner.

Familial Amyloid Neuropathies
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Neuropathy
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Neuropathy, Andrade Type
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Neuropathy, Finnish Type
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Neuropathy, Portuguese Type
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathies
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Appalachian Type
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Jewish Type
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Type I
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Type II
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Type III
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Type IV
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Type V
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloid Polyneuropathy, Type VI
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Amyloidoses
Diseases in which there is a familial pattern of AMYLOIDOSIS.

Familial Amyloidosis
Diseases in which there is a familial pattern of AMYLOIDOSIS.

Familial amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) in which there a family history of the disease. Familial ALS constitutes 5 to 10% of all cases of ALS. There are a number of different types of familial ALS. They are known as ALS1, ALS2, and so on. ALS1 -- caused by mutation in the superoxide dismutase-1 gene (SOD1) on chromosome 21q22.1. About 15 to 20% of familial ALS is type 1 (ALS1). Sporadic cases of ALS are sometimes due to new mutation in the SOD1 gene; ALS2 -- juvenile-onset ALS caused by mutation in the gene encoding alsin on chromosome 2q33; ALS3 -- adult-onset ALS due to mutation in a gene on chromosome 18q21; ALS4 -- juvenile-onset disease with no bulbar involvement due to mutations in a gene on chromosome 9q34; ALS5 -- due to mutations in a gene on chromosome 15q15.1-q21.1; ALS6 -- due to mutations in a gene on chromosome 16q12; ALS7 -- due to mutations in a gene on chromosome 20ptel; ALS8 -- due to mutations in a gene on chromosome 20q13.33. ALS1, ALS3, ALS4, ALS6, ALS7, and ALS8 are inherited in an autosomal dominant manner while ALS2 and ALS5 are inherited in an autosomal recessive manner.

Familial Ataxia, Friedreich
An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts. Clinical manifestations include GAIT ATAXIA, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. Most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin. (From Adams et al., Principles of Neurology, 6th ed, p1081; N Engl J Med 1996 Oct 17;335(16):1169-75) The severity of Friedreich ataxia associated with expansion of GAA repeats in the first intron of the frataxin gene correlates with the number of trinucleotide repeats. (From Durr et al, N Engl J Med 1996 Oct 17;335(16):1169-75)

Familial Atypical Multiple Mole Melanoma
Clinically atypical nevi (usually exceeding 5 mm in diameter and having variable pigmentation and ill defined borders) with an increased risk for development of non-familial cutaneous malignant melanoma. Biopsies show melanocytic dysplasia. Nevi are clinically and histologically identical to the precursor lesions for melanoma in the B-K mole syndrome. (Stedman, 25th ed)

Familial Atypical Multiple Mole-Melanoma
Clinically atypical nevi (usually exceeding 5 mm in diameter and having variable pigmentation and ill defined borders) with an increased risk for development of non-familial cutaneous malignant melanoma. Biopsies show melanocytic dysplasia. Nevi are clinically and histologically identical to the precursor lesions for melanoma in the B-K mole syndrome. (Stedman, 25th ed)

Familial Benign Chronic Pemphigus
Rare hereditary disease characterized by recurrent eruptions of vesicles and bullae mainly on the neck, axillae, and groin. It exhibits autosomal dominant inheritance and is unrelated to pemphigus vulgaris though it closely resembles that disease.

Familial Benign Neonatal Convulsions
A condition marked by recurrent seizures that occur during the first 4-6 weeks of life despite an otherwise benign neonatal course. Autosomal dominant familial and sporadic forms have been identified. Seizures generally consist of brief episodes of tonic posturing and other movements, apnea, eye deviations, and blood pressure fluctuations. These tend to remit after the 6th week of life. The risk of developing epilepsy at an older age is moderately increased in the familial form of this disorder. (Neurologia 1996 Feb;11(2):51-5)

Familial Benign Neonatal Epilepsy
A condition marked by recurrent seizures that occur during the first 4-6 weeks of life despite an otherwise benign neonatal course. Autosomal dominant familial and sporadic forms have been identified. Seizures generally consist of brief episodes of tonic posturing and other movements, apnea, eye deviations, and blood pressure fluctuations. These tend to remit after the 6th week of life. The risk of developing epilepsy at an older age is moderately increased in the familial form of this disorder. (Neurologia 1996 Feb;11(2):51-5)

Familial breast cancer
A number of factors have been identified that increase the risk of breast cancer. One of the strongest of these risk factors is the history of breast cancer in a relative. About15-20% of women with breast cancer have such a family history of the disease, clearly reflecting the participation of inherited (genetic) components in the development of some breast cancers. Dominant breast cancer susceptibility genes, including BRCA1 and BRCA2, appear responsible for about 5% of all breast cancer. See related entries to: Breast cancer susceptibility genes; BRCA1; BRCA2.

Familial cancer
Cancer or a predisposition (tendency) to it that runs in families.

Familial Cerebello Retinal Angiomatosis
An autosomal dominant disorder associated with various neoplasms including central nervous system (most often cerebellar) and retinal HEMANGIOBLASTOMA, endolymphatic sac tumors, renal cell carcinoma (see CARCINOMA, RENAL CELL), renal and pancreatic cysts, HEMANGIOMA of the spinal cord, and PHEOCHROMOCYTOMA. The most common presenting manifestations are neurologic deficits associated with intracranial hemangioblastomas which may hemorrhage, causing ataxia, INTRACRANIAL HYPERTENSION, and other signs of neurologic dysfunction. (From Neurochirurgie 1998 Nov;44(4):258-66)

Familial Cerebello-Retinal Angiomatoses
An autosomal dominant disorder associated with various neoplasms including central nervous system (most often cerebellar) and retinal HEMANGIOBLASTOMA, endolymphatic sac tumors, renal cell carcinoma (see CARCINOMA, RENAL CELL), renal and pancreatic cysts, HEMANGIOMA of the spinal cord, and PHEOCHROMOCYTOMA. The most common presenting manifestations are neurologic deficits associated with intracranial hemangioblastomas which may hemorrhage, causing ataxia, INTRACRANIAL HYPERTENSION, and other signs of neurologic dysfunction. (From Neurochirurgie 1998 Nov;44(4):258-66)

Familial Cerebello-Retinal Angiomatosis
An autosomal dominant disorder associated with various neoplasms including central nervous system (most often cerebellar) and retinal HEMANGIOBLASTOMA, endolymphatic sac tumors, renal cell carcinoma (see CARCINOMA, RENAL CELL), renal and pancreatic cysts, HEMANGIOMA of the spinal cord, and PHEOCHROMOCYTOMA. The most common presenting manifestations are neurologic deficits associated with intracranial hemangioblastomas which may hemorrhage, causing ataxia, INTRACRANIAL HYPERTENSION, and other signs of neurologic dysfunction. (From Neurochirurgie 1998 Nov;44(4):258-66)

Familial Cerebelloretinal Angiomatoses
An autosomal dominant disorder associated with various neoplasms including central nervous system (most often cerebellar) and retinal HEMANGIOBLASTOMA, endolymphatic sac tumors, renal cell carcinoma (see CARCINOMA, RENAL CELL), renal and pancreatic cysts, HEMANGIOMA of the spinal cord, and PHEOCHROMOCYTOMA. The most common presenting manifestations are neurologic deficits associated with intracranial hemangioblastomas which may hemorrhage, causing ataxia, INTRACRANIAL HYPERTENSION, and other signs of neurologic dysfunction. (From Neurochirurgie 1998 Nov;44(4):258-66)

Familial Cerebelloretinal Angiomatosis
An autosomal dominant disorder associated with various neoplasms including central nervous system (most often cerebellar) and retinal HEMANGIOBLASTOMA, endolymphatic sac tumors, renal cell carcinoma (see CARCINOMA, RENAL CELL), renal and pancreatic cysts, HEMANGIOMA of the spinal cord, and PHEOCHROMOCYTOMA. The most common presenting manifestations are neurologic deficits associated with intracranial hemangioblastomas which may hemorrhage, causing ataxia, INTRACRANIAL HYPERTENSION, and other signs of neurologic dysfunction. (From Neurochirurgie 1998 Nov;44(4):258-66)

Familial Cerebral Amyloid Angiopathy
A familial condition marked by the deposition of AMYLOID in the walls of small blood vessels in the cerebral cortex and meninges and characterized clinically by cerebral ischemia (see BRAIN ISCHEMIA), CEREBRAL INFARCTION, and CEREBRAL HEMORRHAGE..

Familial cholesterolemia
An inherited disorder causing abnormally high levels of cholesterol in the blood.

Familial colorectal cancer
A label applied to families that contain an unusual aggregation of members with cancer of the colon or rectum but that do not appear to have a known inherited colorectal cancer syndrome. Familial colorectal cancer (FCC) is essentially a descriptive term and does not point to a particular underlying cause.

Familial Combined Hyperlipidemia
A disorder genetically distinct from the other inherited hyperlipidemias characterized by the type II or type IV lipoprotein pattern (the pattern may change from time to time and the lipid level may be normal at one time and abnormal at another time).

Familial Combined Hyperlipidemias
A disorder genetically distinct from the other inherited hyperlipidemias characterized by the type II or type IV lipoprotein pattern (the pattern may change from time to time and the lipid level may be normal at one time and abnormal at another time).

Familial Creutzfeldt Jakob Disease
A rare transmissible encephalopathy most prevalent between the ages of 50 and 70 years. Affected individuals may present with sleep disturbances, personality changes, ATAXIA; APHASIA, visual loss, weakness, muscle atrophy, MYOCLONUS, progressive dementia, and death within one year of disease onset. A familial form exhibiting autosomal dominant inheritance and a new variant CJD (potentially associated with ENCEPHALOPATHY, BOVINE SPONGIFORM) have been described. Pathological features include prominent cerebellar and cerebral cortical spongiform degeneration and the presence of PRIONS. (From N Engl J Med, 1998 Dec 31;339(27))

Familial Creutzfeldt-Jakob Disease
A rare transmissible encephalopathy most prevalent between the ages of 50 and 70 years. Affected individuals may present with sleep disturbances, personality changes, ATAXIA; APHASIA, visual loss, weakness, muscle atrophy, MYOCLONUS, progressive dementia, and death within one year of disease onset. A familial form exhibiting autosomal dominant inheritance and a new variant CJD (potentially associated with ENCEPHALOPATHY, BOVINE SPONGIFORM) have been described. Pathological features include prominent cerebellar and cerebral cortical spongiform degeneration and the presence of PRIONS. (From N Engl J Med, 1998 Dec 31;339(27))

Familial Creutzfeldt-Jakob Diseases
A rare transmissible encephalopathy most prevalent between the ages of 50 and 70 years. Affected individuals may present with sleep disturbances, personality changes, ATAXIA; APHASIA, visual loss, weakness, muscle atrophy, MYOCLONUS, progressive dementia, and death within one year of disease onset. A familial form exhibiting autosomal dominant inheritance and a new variant CJD (potentially associated with ENCEPHALOPATHY, BOVINE SPONGIFORM) have been described. Pathological features include prominent cerebellar and cerebral cortical spongiform degeneration and the presence of PRIONS. (From N Engl J Med, 1998 Dec 31;339(27))

Familial cylindromatosis
A genetic syndrome in which numerous benign tumors of skin adnexa (such as the sweat glands) develop, principally on the head and neck. This disorder is inherited in an autosomal manner and is caused by mutation of the CYLD gene on chromosome 16q12-q13. Mutation of CYLD has been likened to having faulty brakes on a car. Instead of a pileup of cars, a pileup of cells results. Topical application of aspirin, another type of brake on cell proliferation, may possibly be useful. Also called the turban tumor syndrome.

Familial Dandy-Walker Syndrome
A congenital abnormality of the central nervous system marked by failure of the midline structures of the cerebellum to develop, dilation of the fourth ventricle, and upward displacement of the transverse sinuses, tentorium, and torcula. Clinical features include occipital bossing, progressive head enlargement, bulging of anterior fontanelle, papilledema, ataxia, gait disturbances, nystagmus, and intellectual compromise. (From Menkes, Textbook of Child Neurology, 5th ed, pp294-5)

Familial Dementia
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.

Familial Dementias
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.

Familial dysautonomia
A genetic disorder of the autonomic nervous system, affecting especially Ashkenazi Jewish children. Familial dysautonomia is inherited in an autosomal recessive manner and is due to mutation in the IKBKAP gene on chromosome 9q31. Dysautonomia refers to the dysfunction of the autonomic nervous system. Familial dysautonomia is symbolized DYS.

Familial Dysautonomia
An autosomal disorder of the peripheral and autonomic nervous systems limited to individuals of Ashkenazic Jewish descent. Clinical manifestations are present at birth and include diminished lacrimation, defective thermoregulation, orthostatic hypotension (HYPOTENSION, ORTHOSTATIC), fixed pupils, excessive SWEATING, loss of pain and temperature sensation, and absent reflexes. Pathologic features include reduced numbers of small diameter peripheral nerve fibers and autonomic ganglion neurons. (From Adams et al., Principles of Neurology, 6th ed, p1348; Nat Genet 1993;4(2):160-4)

Familial Endocrine Adenomatoses
A group of autosomal dominant, often overlapping diseases characterized by hyperplasia or neoplasia of more than one endocrine gland, many of which are made up of APUD cells. (From Segen, Dictionary of Modern Medicine, 1992)

Familial Endocrine Adenomatosis
A group of autosomal dominant, often overlapping diseases characterized by hyperplasia or neoplasia of more than one endocrine gland, many of which are made up of APUD cells. (From Segen, Dictionary of Modern Medicine, 1992)

Familial eosinophilia
An autosomal dominant condition characterized by an abnormally high level of eosinophils in the blood. Despite the prolonged eosinophilia, there may be no symptoms. The gene for familial eosinophilia, called EOS, has been mapped to chromosome region 5q31-33 containing the cytokine gene cluster which includes the genes for interleukin-3 (IL-3), interleukin-5 (IL-5), and granulocyte colony-stimulating factor (G-CSF), and all of which are thought play roles in the development, proliferation, and activation of eosinophils.

Familial Exostoses
Hereditary disorder transmitted by an autosomal dominant gene and characterized by multiple exostoses (multiple osteochondromas) near the ends of long bones. The genetic abnormality results in a defect in the osteoclastic activity at the metaphyseal ends of the bone during the remodeling process in childhood or early adolescence. The metaphyses develop benign, bony outgrowths often capped by cartilage. A small number undergo neoplastic transformation.

Familial Exostosis
Hereditary disorder transmitted by an autosomal dominant gene and characterized by multiple exostoses (multiple osteochondromas) near the ends of long bones. The genetic abnormality results in a defect in the osteoclastic activity at the metaphyseal ends of the bone during the remodeling process in childhood or early adolescence. The metaphyses develop benign, bony outgrowths often capped by cartilage. A small number undergo neoplastic transformation.

Familial Facial Neuropathies
Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation.

Familial Facial Neuropathy
Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation.

Familial Form of Canavan Disease
A rare neurodegenerative condition of infancy or childhood characterized by white matter vacuolization and demeylination that gives rise to a spongy appearance. Aspartoacylase deficiency leads to an accumulation of N-acetylaspartate in astrocytes. Inheritance may be autosomal recessive or the illness may occur sporadically. This illness occurs more frequently in individuals of Ashkenazic Jewish descent. The neonatal form features the onset of hypotonia and lethargy at birth, rapidly progressing to coma and death. The infantile form features developmental delay, DYSKINESIAS, hypotonia, spasticity, blindness, and megalencephaly. The juvenile form is characterized by ATAXIA; OPTIC ATROPHY; and DEMENTIA. (From Adams et al., Principles of Neurology, 6th ed, p944; Am J Med Genet 1988 Feb;29(2):463-71)

Familial Hemiplegic Migraine
A condition characterized by throbbing headaches which are preceded or accompanied by reversible symptoms that reflect cortical or brain stem dysfunction. The most common type of aura consists of a positive visual phenomenon, usually in the form of a scintillating scotoma. An aura may also take the form of other focal neurologic symptoms or signs, including loss of sensation or weakness in an extremity. In general, the aura precedes the headache by less than 60 minutes, develops over 4 minutes or longer, and has a duration of less than one hour. (From Adams et al., Principles of Neurology, 6th ed, p172; Cephalalgia 1988;8:Suppl 7:1-96)

Familial Hemiplegic Migraines
A condition characterized by throbbing headaches which are preceded or accompanied by reversible symptoms that reflect cortical or brain stem dysfunction. The most common type of aura consists of a positive visual phenomenon, usually in the form of a scintillating scotoma. An aura may also take the form of other focal neurologic symptoms or signs, including loss of sensation or weakness in an extremity. In general, the aura precedes the headache by less than 60 minutes, develops over 4 minutes or longer, and has a duration of less than one hour. (From Adams et al., Principles of Neurology, 6th ed, p172; Cephalalgia 1988;8:Suppl 7:1-96)

Familial High Density Lipoprotein Deficiency Disease
A rare autosomal recessive familial disorder of cholesterol metabolism, characterized by extremely low HDL-cholesterol, reduced total cholesterol, and increased triglyceride levels in serum. Clinical features include the onset before age 20 years of HEPATOMEGALY; SPLENOMEGALY; the deposition of cholesterol in each TONSIL (creating a yellow-orange appearance); and RETINITIS PIGMENTOSA. A sensorimotor or distal sensory POLYNEUROPATHY occurs in approximately 50% of affected individuals. The condition is associated with decreased synthesis and increased catabolism of APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II, and a defect in cellular signaling and mobilization of lipids. (From Nat Genet 1998 Sep;20(1):96-8; Adams et al., Principles of Neurology, 6th ed, pp1347-8; Menkes, Textbook of Child Neurology, 5th ed, p118)

Familial High-Density Lipoprotein Deficiency Disease
A rare autosomal recessive familial disorder of cholesterol metabolism, characterized by extremely low HDL-cholesterol, reduced total cholesterol, and increased triglyceride levels in serum. Clinical features include the onset before age 20 years of HEPATOMEGALY; SPLENOMEGALY; the deposition of cholesterol in each TONSIL (creating a yellow-orange appearance); and RETINITIS PIGMENTOSA. A sensorimotor or distal sensory POLYNEUROPATHY occurs in approximately 50% of affected individuals. The condition is associated with decreased synthesis and increased catabolism of APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II, and a defect in cellular signaling and mobilization of lipids. (From Nat Genet 1998 Sep;20(1):96-8; Adams et al., Principles of Neurology, 6th ed, pp1347-8; Menkes, Textbook of Child Neurology, 5th ed, p118)

Familial Hypercholesterolemia
A familial disorder characterized by increased plasma concentration of cholesterol carried in low density lipoproteins (LDL) and by a deficiency in a cell surface receptor which regulates LDL degradation and cholesterol synthesis.

Familial Hypercholesterolemias
A familial disorder characterized by increased plasma concentration of cholesterol carried in low density lipoproteins (LDL) and by a deficiency in a cell surface receptor which regulates LDL degradation and cholesterol synthesis.

Familial Hyperchylomicronemia
A rare familial condition characterized by massive chylomicronemia and decreased levels of other lipoproteins. It is due to deficiency of lipoprotein lipase, an alkaline triglyceride hydrolase which catalyzes an important step in the extrahepatic removal of triglyceride-rich lipoproteins from the blood.

Familial Hyperchylomicronemias
A rare familial condition characterized by massive chylomicronemia and decreased levels of other lipoproteins. It is due to deficiency of lipoprotein lipase, an alkaline triglyceride hydrolase which catalyzes an important step in the extrahepatic removal of triglyceride-rich lipoproteins from the blood.

Familial Hyperkalemic Periodic Paralysis
An autosomal dominant familial disorder which presents in infancy or childhood and is characterized by episodes of weakness associated with hyperkalemia. During attacks, muscles of the lower extremities are initially affected, followed by the lower trunk and arms. Episodes last from 15-60 minutes and typically occur after a period of rest following exercise. A defect in skeletal muscle sodium channels has been identified as the cause of this condition. Normokalemic periodic paralysis is a closely related disorder marked by a lack of alterations in potassium levels during attacks of weakness. (Adams et al., Principles of Neurology, 6th ed, p1481)

Familial Hyperlysinemia
A group of inherited metabolic disorders which have in common elevations of serum LYSINE levels. Enzyme deficiencies of alpha-aminoadipic semialdehyde dehydrogenase and the SACCHAROPINE DEHYDROGENASES have been associated with hyperlysinemia. Clinical manifestations include mental retardation, recurrent emesis, hypotonia, lethargy, diarrhea, and developmental delay. (From Menkes, Textbook of Child Neurology, 5th ed, p56)

Familial Hyperlysinemias
A group of inherited metabolic disorders which have in common elevations of serum LYSINE levels. Enzyme deficiencies of alpha-aminoadipic semialdehyde dehydrogenase and the SACCHAROPINE DEHYDROGENASES have been associated with hyperlysinemia. Clinical manifestations include mental retardation, recurrent emesis, hypotonia, lethargy, diarrhea, and developmental delay. (From Menkes, Textbook of Child Neurology, 5th ed, p56)

Familial Hypertriglyceridemia
A familial disorder characterized by an isolated elevation in the plasma level of endogenously synthesized triglyceride carried in VLDL. It is considered to be an autosomal dominant trait.

Familial Hypertriglyceridemias
A familial disorder characterized by an isolated elevation in the plasma level of endogenously synthesized triglyceride carried in VLDL. It is considered to be an autosomal dominant trait.

Familial Hypertrophic Cardiomyopathies
An inherited form of hypertrophic cardiomyopathy. It is associated with mutations of genes coding for heart muscle proteins.

Familial hypertrophic cardiomyopathy
A genetic disorder of the heart characterized by increased growth (hypertrophy) in thickness of the wall of the left ventricle, the largest of the four chambers of the heart. Familial hypertrophic cardiomyopathy (FHCM) can surface any time in life. It may, in a worst-case scenario, lead to death. One in about 500 people have FHCM. Five to 10%of people with FHCM suffer fatal cardiac arrest. It is the leading cause of sudden death in athletes and young people.

Familial Hypertrophic Cardiomyopathy
An inherited form of hypertrophic cardiomyopathy. It is associated with mutations of genes coding for heart muscle proteins.

Familial Hypoalphalipoproteinemia
A rare autosomal recessive familial disorder of cholesterol metabolism, characterized by extremely low HDL-cholesterol, reduced total cholesterol, and increased triglyceride levels in serum. Clinical features include the onset before age 20 years of HEPATOMEGALY; SPLENOMEGALY; the deposition of cholesterol in each TONSIL (creating a yellow-orange appearance); and RETINITIS PIGMENTOSA. A sensorimotor or distal sensory POLYNEUROPATHY occurs in approximately 50% of affected individuals. The condition is associated with decreased synthesis and increased catabolism of APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II, and a defect in cellular signaling and mobilization of lipids. (From Nat Genet 1998 Sep;20(1):96-8; Adams et al., Principles of Neurology, 6th ed, pp1347-8; Menkes, Textbook of Child Neurology, 5th ed, p118)

Familial Hypoalphalipoproteinemias
A rare autosomal recessive familial disorder of cholesterol metabolism, characterized by extremely low HDL-cholesterol, reduced total cholesterol, and increased triglyceride levels in serum. Clinical features include the onset before age 20 years of HEPATOMEGALY; SPLENOMEGALY; the deposition of cholesterol in each TONSIL (creating a yellow-orange appearance); and RETINITIS PIGMENTOSA. A sensorimotor or distal sensory POLYNEUROPATHY occurs in approximately 50% of affected individuals. The condition is associated with decreased synthesis and increased catabolism of APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II, and a defect in cellular signaling and mobilization of lipids. (From Nat Genet 1998 Sep;20(1):96-8; Adams et al., Principles of Neurology, 6th ed, pp1347-8; Menkes, Textbook of Child Neurology, 5th ed, p118)

Familial Hypokalemic Periodic Paralysis
An autosomal dominant familial disorder characterized by recurrent episodes of skeletal muscle weakness associated with falls in serum potassium levels. The condition usually presents in the first or second decade of life with attacks of trunk and leg paresis during sleep or shortly after awakening. Symptoms may persist for hours to days and generally are precipitated by exercise or a meal high in carbohydrates. (Adams et al., Principles of Neurology, 6th ed, p1483)

Familial Hypophosphatemia
Familial disorder characterized by hypophosphatemia associated with decreased renal tubular reabsorption of inorganic phosphorus. It is sometimes associated with osteomalacia or rickets which do not respond to the usual doses of vitamin D.

Familial Hypophosphatemias
Familial disorder characterized by hypophosphatemia associated with decreased renal tubular reabsorption of inorganic phosphorus. It is sometimes associated with osteomalacia or rickets which do not respond to the usual doses of vitamin D.

Familial Idiocies, Amaurotic
A disturbance of lipid metabolism with abnormal deposit of lipids in the cells. (Dorland, 27th ed)

Familial Idiocy, Amaurotic
A disturbance of lipid metabolism with abnormal deposit of lipids in the cells. (Dorland, 27th ed)

Familial Insomnia, Fatal
A group of genetic, infectious, or sporadic degenerative human and animal nervous system disorders associated with abnormal PRIONS. These diseases are characterized by conversion of the normal prion protein to an abnormal configuration via a post-translational process. In humans, these conditions generally feature DEMENTIA, ataxia, and a fatal outcome. Diseases in this category include CREUTZFELDT-JAKOB SYNDROME; GERSTMANN-STRAUSSLER-SCHEINKER SYNDROME; KURU; SCRAPIE; fatal familial insomnia; bovine spongiform encephalopathy (see ENCEPHALOPATHY, BOVINE SPONGIFORM); transmissible mink encephalopathy; and chronic wasting disease of mule deer and elk. Pathologic features include a spongiform encephalopathy without evidence of inflammation. The literature occasionally refers to these as unconventional SLOW VIRUS DISEASES. (From Proc Natl Acad Sci USA 1998 Nov 10;95(23):13363-83)

Familial Insomnias, Fatal
A group of genetic, infectious, or sporadic degenerative human and animal nervous system disorders associated with abnormal PRIONS. These diseases are characterized by conversion of the normal prion protein to an abnormal configuration via a post-translational process. In humans, these conditions generally feature DEMENTIA, ataxia, and a fatal outcome. Diseases in this category include CREUTZFELDT-JAKOB SYNDROME; GERSTMANN-STRAUSSLER-SCHEINKER SYNDROME; KURU; SCRAPIE; fatal familial insomnia; bovine spongiform encephalopathy (see ENCEPHALOPATHY, BOVINE SPONGIFORM); transmissible mink encephalopathy; and chronic wasting disease of mule deer and elk. Pathologic features include a spongiform encephalopathy without evidence of inflammation. The literature occasionally refers to these as unconventional SLOW VIRUS DISEASES. (From Proc Natl Acad Sci USA 1998 Nov 10;95(23):13363-83)

Familial juvenile nephronophthisis (FJN)
A childhood genetic kidney disease in which there is progressive symmetrical destruction of the kidneys involving both the tubules and glomeruli, characteristically resulting in anemia, polyuria, polydipsia, isosthenuria (decreased ability to concentrate the urine), progressive renal failure and death in uremia. Hypertension and proteinuria are conspicuous by their absence. The chronic kidney failure affects growth and leads to short stature. The age at death ranges from around 4 to 15 years.

Familial Juvenile Parkinsonism
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.

Familial Lipoprotein Lipase Deficiency
A rare familial condition characterized by massive chylomicronemia and decreased levels of other lipoproteins. It is due to deficiency of lipoprotein lipase, an alkaline triglyceride hydrolase which catalyzes an important step in the extrahepatic removal of triglyceride-rich lipoproteins from the blood.

Familial lung cancer
Lung cancer that recurs in families. Lung cancer can occur sporadically in people with no known family history of lung cancer or it can recur in two or more members of the same family and constitute familial lung cancer. A gene for familial lung cancer is on the long (q) arm of chromosome 6 in a region that runs from chromosome band 6q23 through band 6q25. People carrying this gene for familial lung cancer appear unusually sensitive to tobacco smoke. Even a small amount of smoking may be enough to cause lung cancer. By contrast, the risk of lung cancer rises with the amount of smoking in people who do not carry this gene.

Familial Mediterranean Fever
FMF. Autosomal recessive inheritance. Causes attacks of abdominal pain, fever and arthritis. Amyloidosis occurs. Predominantly affects Mediterranean races - e.g. Sephardic Jews.

Familial Mediterranean fever (FMF)
An inherited disorder featuring short recurring crises of severe abdominal pain and bouts of fever. Other symptoms include arthritis, chest pain from inflammation of the lung cavity, and skin rashes. Between attacks, the patient seems healthy. Amyloidosis (the abnormal deposition of a particular protein, called amyloid, in various tissues of the body) is a potentially serious complication and can develop without overt attacks of FMF. The kidney is a prime target for the amyloid.

Familial Metabolic Brain Diseases
Errors of brain metabolism resulting from inborn, primarily enzymatic, deficiency states. The majority of these conditions are familial, however spontaneous mutation may also occur. Deficient enzyme activity may cause brain dysfunction by leading to the accumulation of substrate, reduced product formation, or by causing metabolism to occur through alternate pathways.

Familial Metabolic Disorders, Brain
Errors of brain metabolism resulting from inborn, primarily enzymatic, deficiency states. The majority of these conditions are familial, however spontaneous mutation may also occur. Deficient enzyme activity may cause brain dysfunction by leading to the accumulation of substrate, reduced product formation, or by causing metabolism to occur through alternate pathways.

Familial Motor Neuron Disease
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvment of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)

Familial Nephritides
Hereditary disease characterized initially by hematuria and slowly progressing to renal insufficiency. It is sometimes associated with perceptual deafness and/or congenital ocular defects.

Familial Nephritis
Hereditary disease characterized initially by hematuria and slowly progressing to renal insufficiency. It is sometimes associated with perceptual deafness and/or congenital ocular defects.

Familial Olivopontocerebellar Atrophies
A group of inherited and sporadic disorders which share progressive ataxia in combination with atrophy of the CEREBELLUM; PONS; and inferior olivary nuclei. Additional clinical features may include MUSCLE RIGIDITY; NYSTAGMUS; RETINAL DEGENERATION; MUSCLE SPASTICITY; DEMENTIA; URINARY INCONTINENCE; and OPHTHALMOPLEGIA. The familial form has an earlier onset (second decade) and may feature spinal cord atrophy. The sporadic form tends to present in the fifth or sixth decade, and is considered a clinical subtype of MULTIPLE SYSTEM ATROPHY. (From Adams et al., Principles of Neurology, 6th ed, p1085)

Familial Olivopontocerebellar Atrophy
A group of inherited and sporadic disorders which share progressive ataxia in combination with atrophy of the CEREBELLUM; PONS; and inferior olivary nuclei. Additional clinical features may include MUSCLE RIGIDITY; NYSTAGMUS; RETINAL DEGENERATION; MUSCLE SPASTICITY; DEMENTIA; URINARY INCONTINENCE; and OPHTHALMOPLEGIA. The familial form has an earlier onset (second decade) and may feature spinal cord atrophy. The sporadic form tends to present in the fifth or sixth decade, and is considered a clinical subtype of MULTIPLE SYSTEM ATROPHY. (From Adams et al., Principles of Neurology, 6th ed, p1085)

Familial Parkinson disease type 1
A familial form of Parkinson disease inherited in an autosomal dominant manner due to mutation in the alpha-synuclein gene (SNCA) on chromosome 4q21. Also known as PARK1.

Familial Parkinson disease type 10
A familial form of Parkinson disease inherited in an autosomal dominant manner due to a gene on chromosome 1p. Also known as PARK10.

Familial Parkinson disease type 11
A familial form of Parkinson disease inherited in an autosomal dominant manner due to a gene on chromosome 2q. Also known as PARK11.

Familial Parkinson disease type 2
A familial form of Parkinson disease inherited in an autosomal recessive manner due to mutation in the gene encoding parkin on chromosome 6q25.2-q27. Also known as PARK2.

Familial Parkinson disease type 3
A familial form of Parkinson disease inherited in an autosomal dominant manner due to a gene on chromosome 2p13. Also known as PARK3.

Familial Parkinson disease type 4
A familial form of Parkinson disease inherited in an autosomal dominant manner due to a gene on chromosome 4p15. Also known as PARK4.

Familial Parkinson disease type 5
A familial form of Parkinson disease inherited in an autosomal dominant manner due to mutation in the UCHL1 gene on chromosome 4p14. Also known as PARK5.

Familial Parkinson disease type 6
A familial form of Parkinson disease inherited in an autosomal recessive manner due to mutation in a gene on chromosome 1p distinct from DJ1. Also known as PARK6.

Familial Parkinson disease type 7
A familial form of Parkinson disease inherited in an autosomal recessive manner due to mutation in the DJ1 gene on 1p36. Also known as PARK7.

Familial Parkinson disease type 8
A familial form of Parkinson disease inherited in an autosomal dominant manner due to a gene on chromosome 12p11.2-q13.1. Also known as PARK8.

Familial Parkinson disease type 9
A familial form of Parkinson disease inherited in an autosomal recessive manner due to a gene on chromosome 1p36. Also known as PARK9.

Familial Parkinson Disease, Autosomal Recessive
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.

Familial Pemphigus, Benign
Rare hereditary disease characterized by recurrent eruptions of vesicles and bullae mainly on the neck, axillae, and groin. It exhibits autosomal dominant inheritance and is unrelated to pemphigus vulgaris though it closely resembles that disease.

Familial Periodic Paralyse
A heterogenous group of inherited disorders characterized by recurring attacks of rapidly progressive flaccid paralysis or myotonia. These conditions have in common a mutation of the gene encoding the alpha subunit of the sodium channel in skeletal muscle. They are frequently associated with fluctuations in serum potassium levels. Periodic paralysis may also occur as a non-familial process secondary to THYROTOXICOSIS and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1481)

Familial Periodic Paralyses
A heterogenous group of inherited disorders characterized by recurring attacks of rapidly progressive flaccid paralysis or myotonia. These conditions have in common a mutation of the gene encoding the alpha subunit of the sodium channel in skeletal muscle. They are frequently associated with fluctuations in serum potassium levels. Periodic paralysis may also occur as a non-familial process secondary to THYROTOXICOSIS and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1481)

Familial Periodic Paralysis
A heterogenous group of inherited disorders characterized by recurring attacks of rapidly progressive flaccid paralysis or myotonia. These conditions have in common a mutation of the gene encoding the alpha subunit of the sodium channel in skeletal muscle. They are frequently associated with fluctuations in serum potassium levels. Periodic paralysis may also occur as a non-familial process secondary to THYROTOXICOSIS and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1481)

Familial Polyneuropathies
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.

Familial Polyneuropathy
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.

Familial polyposis
An inherited condition in which several hundred polyps develop in the colon and rectum.

Familial Polyposis Coli
An autosomal dominant polyposis syndrome in which the colon contains few to thousands of adenomatous polyps, often occurring by age 15 to 25.

Familial Polyposis Syndrome
An autosomal dominant polyposis syndrome in which the colon contains few to thousands of adenomatous polyps, often occurring by age 15 to 25.

Familial Polyposis Syndromes
An autosomal dominant polyposis syndrome in which the colon contains few to thousands of adenomatous polyps, often occurring by age 15 to 25.

Familial Progressive Myoclonic Epilepsy
A heterogeneous group of primarily familial disorders characterized by myoclonic seizures, tonic-clonic seizures, ataxia, progressive intellectual deterioration, and neuronal degeneration. These include LAFORA DISEASE; MERRF SYNDROME; NEURONAL CEROID-LIPOFUSCINOSIS; sialidosis (see MUCOLIPIDOSES), and UNVERRICHT-LUNDBORG SYNDROME.

Familial Retinoblastoma
A malignant tumor arising from the nuclear layer of the retina that is the most common primary tumor of the eye in children. The tumor tends to occur in early childhood or infancy and may be present at birth. The majority are sporadic, but the condition may be transmitted as an autosomal dominant trait. Histologic features include dense cellularity, small round polygonal cells, and areas of calcification and necrosis. An abnormal pupil reflex (leukokoria); NYSTAGMUS; STRABISMUS; and visual loss represent common clinical characteristics of this condition. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2104)

Familial Retinoblastomas
A malignant tumor arising from the nuclear layer of the retina that is the most common primary tumor of the eye in children. The tumor tends to occur in early childhood or infancy and may be present at birth. The majority are sporadic, but the condition may be transmitted as an autosomal dominant trait. Histologic features include dense cellularity, small round polygonal cells, and areas of calcification and necrosis. An abnormal pupil reflex (leukokoria); NYSTAGMUS; STRABISMUS; and visual loss represent common clinical characteristics of this condition. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2104)

Familial Spinocerebellar Degeneration
A heterogenous group of degenerative syndromes marked by progressive cerebellar dysfunction either in isolation or combined with other neurologic manifestations. Sporadic and inherited subtypes occur. Inheritance patterns include autosomal dominant, autosomal recessive, and X-linked.

Familial Spinocerebellar Degenerations
A heterogenous group of degenerative syndromes marked by progressive cerebellar dysfunction either in isolation or combined with other neurologic manifestations. Sporadic and inherited subtypes occur. Inheritance patterns include autosomal dominant, autosomal recessive, and X-linked.

Familial Tonic Clonic Epilepsy
A generalized seizure disorder characterized by recurrent major motor seizures. The initial brief tonic phase is marked by trunk flexion followed by diffuse extension of the trunk and extremities. The clonic phase features rhythmic flexor contractions of the trunk and limbs, pupillary dilation, elevations of blood pressure and pulse, urinary incontinence, and tongue biting. This is followed by a profound state of depressed consciousness (post-ictal state) which gradually improves over minutes to hours. The disorder may be cryptogenic, familial, or symptomatic (caused by an identified disease process). (From Adams et al., Principles of Neurology, 6th ed, p329)

Familial Tonic-Clonic Epilepsies
A generalized seizure disorder characterized by recurrent major motor seizures. The initial brief tonic phase is marked by trunk flexion followed by diffuse extension of the trunk and extremities. The clonic phase features rhythmic flexor contractions of the trunk and limbs, pupillary dilation, elevations of blood pressure and pulse, urinary incontinence, and tongue biting. This is followed by a profound state of depressed consciousness (post-ictal state) which gradually improves over minutes to hours. The disorder may be cryptogenic, familial, or symptomatic (caused by an identified disease process). (From Adams et al., Principles of Neurology, 6th ed, p329)

Familial Tonic-Clonic Epilepsy
A generalized seizure disorder characterized by recurrent major motor seizures. The initial brief tonic phase is marked by trunk flexion followed by diffuse extension of the trunk and extremities. The clonic phase features rhythmic flexor contractions of the trunk and limbs, pupillary dilation, elevations of blood pressure and pulse, urinary incontinence, and tongue biting. This is followed by a profound state of depressed consciousness (post-ictal state) which gradually improves over minutes to hours. The disorder may be cryptogenic, familial, or symptomatic (caused by an identified disease process). (From Adams et al., Principles of Neurology, 6th ed, p329)

Familial Tremor
A relatively common disorder characterized by a fairly specific pattern of tremors which are most prominent in the upper extremities and neck, inducing titubations of the head. The tremor is usually mild, but when severe may be disabling. An autosomal dominant pattern of inheritance may occur in some families (i.e., familial tremor). (Mov Disord 1988;13(1):5-10)

Familial Tremors
A relatively common disorder characterized by a fairly specific pattern of tremors which are most prominent in the upper extremities and neck, inducing titubations of the head. The tremor is usually mild, but when severe may be disabling. An autosomal dominant pattern of inheritance may occur in some families (i.e., familial tremor). (Mov Disord 1988;13(1):5-10)

Familiarity
The knowledge or perception that someone or something present has been previously encountered.

Families
A social group consisting of parents or parent substitutes and children.

Families, Alu
The Alu sequence family (named for the restriction endonuclease cleavage enzyme Alu I) is the most highly repeated interspersed repeat element in humans (over a million copies). It is derived from the 7SL RNA component of the SIGNAL RECOGNITION PARTICLE and contains an RNA polymerase III promoter. Transposition of this element into coding and regulatory regions of genes is responsible for many heritable diseases.

Families, Dual Income
The science of utilization, distribution, and consumption of services and materials.

Families, Extended
A social group consisting of parents or parent substitutes and children.

Families, Multigene
A set of genes descended by duplication and variation from some ancestral gene. Such genes may be clustered together on the same chromosome or dispersed on different chromosomes. Examples of multigene families include those that encode the hemoglobins, immunoglobulins, histocompatibility antigens, actins, tubulins, keratins, collagens, heat shock proteins, salivary glue proteins, chorion proteins, cuticle proteins, yolk proteins, and phaseolins, as well as histones, ribosomal RNA, and transfer RNA genes. The latter three are examples of reiterated genes, where hundreds of identical genes are present in a tandem array. (King & Stanfield, A Dictionary of Genetics, 4th ed)

Families, Nuclear
A family composed of spouses and their children.

Families, One Parent
A household that includes children and is headed by one adult.

Families, One-Parent
A household that includes children and is headed by one adult.

Families, Reconstituted
A social group consisting of parents or parent substitutes and children.

Families, Single Parent
A household that includes children and is headed by one adult.

Families, Single-Parent
A household that includes children and is headed by one adult.

Family
1. A group of individuals related by blood or marriage or by a feeling of closeness. 2. A biological classification of related plants or animals that is a division below the order and above the genus. 3. A group of genes related in structure and in function that descended from an ancestral gene. 4. A group of gene products similarly related in structure and function and of shared genetic descent. 5. Parents and their children. The most fundamental social group in humans.

Family Allowance
Financial assistance provided by the government to indigent families with dependent children who meet certain requirements as defined by the Social Security Act, Title IV, in the U.S.

Family Allowances
Financial assistance provided by the government to indigent families with dependent children who meet certain requirements as defined by the Social Security Act, Title IV, in the U.S.

Family and Household
Size and composition of the family.

Family and Medical Leave Act
Passed in 1993, the U.S. Family and Medical Leave Act mandates up to 12 weeks of unpaid medical leave for employees of companies with more than 50 employees. Under this act, people can also take leave to care for a sick child, parent, or spouse

Family Caregiver
Persons who provide care to those who need supervision or assistance in illness or disability. They may provide the care in the home, in a hospital, or in an institution. Although caregivers include trained medical, nursing, and other health personnel, the concept also refers to parents, spouses, or other family members, friends, members of the clergy, teachers, social workers, fellow patients, etc.

Family Caregivers
Persons who provide care to those who need supervision or assistance in illness or disability. They may provide the care in the home, in a hospital, or in an institution. Although caregivers include trained medical, nursing, and other health personnel, the concept also refers to parents, spouses, or other family members, friends, members of the clergy, teachers, social workers, fellow patients, etc.

Family Centered Maternity Care
Family Centered Maternity Care is a hospital in Dallas, Texas (USA).

Family Centered Nursing
The provision of care involving the nursing process, to families and family members in health and illness situations. From Lippincott Manual of Nursing Practice. 6th ed.

Family Characteristic
Size and composition of the family.

Family Characteristics
Size and composition of the family.

Family Demographies
Size and composition of the family.

Family Demography
Size and composition of the family.

Family doctor
A general practitioner (GP) or family physician (FP) is a physician who provides primary care. A GP/FP treats acute and chronic illnesses, provides preventive care and health education for all ages and both sexes. Some also care for hospitalized patients, do minor surgery and/or obstetrics.

Family Enhancement Center
The Family Enhancement Center is a hospital in Wilkes Barre, Pennsylvania, United States.

Family Health
The health status of the family as a unit including the impact of the health of one member of the family on the family as a unit and on individual family members; also, the impact of family organization or disorganization on the health status of its members.

Family history
The family structure and relationships within the family, including information about diseases in family members. The family history is often recorded in a family pedigree (family tree), which uses conventional symbols. The pedigree provides a ready view of problems or illnesses within the family and facilitates analysis of inheritance patterns. Study of a trait or disease begins with the affected person (the index case). The pedigree is drawn as the relatives are described. One begins with the siblings of the proband and proceeds to the parents; relatives of the parents, including brothers, sisters, nephews, and nieces; grandparents; and so on. At least 3 generations are usually included. Illnesses, hospitalizations, causes of death, miscarriages, abortions, congenital anomalies, and any other unusual features are recorded.

Family Hospital
The Family Hospital is a hospital in Lahore, Punjab, Pakistan.

Family Hospital Corporation
Family Hospital Corporation is a hospital in Lewiston, Idaho (USA).

Family Leave
The authorized absence from work of a family member to attend the illness or participate in the care of a parent, a sibling, or other family member. For the care of a parent for a child or for pre- or postnatal leave of a parent, PARENTAL LEAVE is available.

Family Life Cycle
A social group consisting of parents or parent substitutes and children.

Family Life Cycles
A social group consisting of parents or parent substitutes and children.

Family Life Survey
Size and composition of the family.

Family Life Surveys
Size and composition of the family.

Family medicine
Also called family practice. The medical specialty which provides continuing and comprehensive health care for the individual and family. It is the specialty in breadth which integrates the biological, clinical, and behavioral sciences. The scope of family practice encompasses all ages, both sexes, each organ system, and every disease entity.

Family Member
A social group consisting of parents or parent substitutes and children.

Family Members
A social group consisting of parents or parent substitutes and children.

Family Nursing
The provision of care involving the nursing process, to families and family members in health and illness situations. From Lippincott Manual of Nursing Practice. 6th ed.

Family Nursings
The provision of care involving the nursing process, to families and family members in health and illness situations. From Lippincott Manual of Nursing Practice. 6th ed.

Family Patient Lodging
Living facilities for humans.

Family physician
A physician who is educated and trained in family practice.

Family Physician
Those physicians who have completed the education requirements specified by the American Academy of Family Physicians.

Family Physicians
Those physicians who have completed the education requirements specified by the American Academy of Family Physicians.

Family Planning
Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility.

Family Planning Center
Those facilities which administer health services to individuals who do not require hospitalization or institutionalization.

Family Planning Centers
Those facilities which administer health services to individuals who do not require hospitalization or institutionalization.

Family Planning Clinic Attendance
Voluntary cooperation of the patient in following a prescribed regimen.

Family Planning Education
Education which increases the knowledge of the functional, structural, and behavioral aspects of human reproduction.

Family Planning Information Centers
Facilities for collecting and organizing information. They may be specialized by subject field, type of source material, persons served, location, or type of services.

Family Planning Instructor
Education which increases the knowledge of the functional, structural, and behavioral aspects of human reproduction.

Family Planning Instructors
Education which increases the knowledge of the functional, structural, and behavioral aspects of human reproduction.

Family Planning Personnel
Persons trained to assist professional health personnel in communicating with residents in the community concerning needs and availability of health services.

Family Planning Personnel Characteristics
Persons trained to assist professional health personnel in communicating with residents in the community concerning needs and availability of health services.

Family Planning Personnel Evaluation
The assessment of the functioning of an employee in relation to work.

Family Planning Policies
A course or method of action selected, usually by a government, to guide and determine present and future decisions on population control by limiting the number of children or controlling fertility, notably through family planning and contraception within the nuclear family.

Family Planning Policy
A course or method of action selected, usually by a government, to guide and determine present and future decisions on population control by limiting the number of children or controlling fertility, notably through family planning and contraception within the nuclear family.

Family Planning Program
Planning for needed health and/or welfare services and facilities.

Family Planning Program Administration
The planning and managing of programs, services, and resources.

Family Planning Program Evaluation
Studies designed to assess the efficacy of programs. They may include the evaluation of cost-effectiveness, the extent to which objectives are met, or impact.

Family Planning Programs
Planning for needed health and/or welfare services and facilities.

Family Planning Survey
Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility.

Family Planning Surveys
Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility.

Family Planning Training
Education which increases the knowledge of the functional, structural, and behavioral aspects of human reproduction.

Family Planning, Behavioral Methods
Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility.

Family Planning, Environment
Physical surroundings or conditions of a hospital or other health facility and influence of these factors on patients and staff.

Family Planning, Natural
Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility.

Family Planning, Traditional Methods
Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility.

Family Policies
A course or method of action selected, usually by a government, to guide and determine present and future decisions on population control by limiting the number of children or controlling fertility, notably through family planning and contraception within the nuclear family.

Family Policy
A course or method of action selected, usually by a government, to guide and determine present and future decisions on population control by limiting the number of children or controlling fertility, notably through family planning and contraception within the nuclear family.

Family practice
The medical specialty which provides continuing and comprehensive health care for the individual and family. It is the specialty in breadth which integrates the biological, clinical, and behavioral sciences. The scope of family practice encompasses all ages, both sexes, each organ system, and every disease entity.

Family Practice
A medical specialty concerned with the provision of continuing, comprehensive primary health care for the entire family.

Family Practices
A medical specialty concerned with the provision of continuing, comprehensive primary health care for the entire family.

Family practitioner
An updated version of the general practitioner who provided one-stop care for all ages and both sexes, the family practitioner has several years ofspecialty training in primary care, including obstetrics.

Family Reconstitution
Statistical interpretation and description of a population with reference to distribution, composition, or structure.

Family Reconstitutions
Statistical interpretation and description of a population with reference to distribution, composition, or structure.

Family Relation
Behavioral, psychological, and social relations among various members of the nuclear family and the extended family.

Family Relations
Behavioral, psychological, and social relations among various members of the nuclear family and the extended family.

Family Relationship
Behavioral, psychological, and social relations among various members of the nuclear family and the extended family.

Family Relationship, Professional
The interactions between the professional person and the family.

Family Relationships
Behavioral, psychological, and social relations among various members of the nuclear family and the extended family.

Family Relationships, Professional
The interactions between the professional person and the family.

Family Research
A social group consisting of parents or parent substitutes and children.

Family Size
Size and composition of the family.

Family Size, Average
Size and composition of the family.

Family Size, Completed
Size and composition of the family.

Family Size, Desired
Size and composition of the family.

Family Size, Expected
Size and composition of the family.

Family Size, Ideal
Size and composition of the family.

Family Sizes
Size and composition of the family.

Family Sizes, Average
Size and composition of the family.

Family Sizes, Completed
Size and composition of the family.

Family Sizes, Desired
Size and composition of the family.

Family Sizes, Expected
Size and composition of the family.

Family Sizes, Ideal
Size and composition of the family.

Family Therapies
A form of group psychotherapy. It involves treatment of more than one member of the family simultaneously in the same session.

Family therapy
A type of psychotherapy designed to identify family patterns that contribute to a behavior disorder or mental illness and help family members break those habits. Family therapy involves discussion and problem-solving sessions with the family. Some of these sessions may be as a group, in couples, or one on one. In family therapy, the web of interpersonal relationships is examined and, ideally, communication is strengthened within the family.

Family Therapy
A form of group psychotherapy. It involves treatment of more than one member of the family simultaneously in the same session.

Family Tree
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.

Family Trees
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.

Family Violence
Deliberate, often repetitive, physical abuse by one family member against another: marital partners, parents, children, siblings, or any other member of a household.

Family, Alu
The Alu sequence family (named for the restriction endonuclease cleavage enzyme Alu I) is the most highly repeated interspersed repeat element in humans (over a million copies). It is derived from the 7SL RNA component of the SIGNAL RECOGNITION PARTICLE and contains an RNA polymerase III promoter. Transposition of this element into coding and regulatory regions of genes is responsible for many heritable diseases.

Family, Chaperonin
A class of sequence-related MOLECULAR CHAPERONES found in bacteria, mitochondria, and plastids. Chaperonins are abundant constitutive proteins that increase in amount after stresses such as heat shock, bacterial infection of macrophages, and an increase in the cellular content of unfolded proteins. Bacterial chaperonins are major immunogens in human bacterial infections because of their accumulation during the stress of infection. Two members of this class of chaperones are CHAPERONIN 10 and CHAPERONIN 60.

Family, Dual Income
The science of utilization, distribution, and consumption of services and materials.

Family, Extended
A social group consisting of parents or parent substitutes and children.

Family, gene
A group of genes related in structure and often in function. The genes belonging to a gene family are descended from an ancestral gene. For example, the hemoglobin genes of critical importance to red blood cells belong to one gene family created by gene duplication (making extra copies of a gene) and divergence (divergent changes in the copies of the gene).

Family, hsp10
Members of the chaperonin heat-shock protein family. Chaperonin 10 purified from bacteria, plastids, or mitochondria occurs as an oligomer of seven identical subunits arranged in a single ring.

Family, hsp60
Members of the chaperonin heat-shock protein family. Chaperonin 60 purified from bacteria, plastids, or mitochondria is an oligomeric protein with a distinctive structure of fourteen subunits, arranged in two rings of seven subunits each.

Family, hsp70
A class of MOLECULAR CHAPERONES found in both prokaryotes and in several compartments of eukaryotic cells. There is evidence that these proteins can interact with polypeptides during a variety of assembly processes in such a way as to prevent the formation of nonfunctional structures.

Family, hsp90
A class of MOLECULAR CHAPERONES whose members act in the mechanism of signal transduction by steroid receptors.

Family, Leu-CAM Receptor
Family of proteins associated with the capacity of leukocytes, including lymphocytes, monocytes, and neutrophils, to adhere to each other and to certain substrata, e.g., the C3bi component of complement. Members of this family are the LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1; (LFA-1), the MACROPHAGE-1 ANTIGEN; (Mac-1), and the COMPLEMENT 4-BINDING PROTEIN or p150,95 leukocyte adhesion protein. They all share a common beta-subunit which is the CD18 antigen. All three of the above antigens are absent in inherited LEUKOCYTE-ADHESION DEFICIENCY SYNDROME, which is characterized by recurrent bacterial infections, impaired pus formation, and wound healing as well as abnormalities in a wide spectrum of adherence-dependent functions of granulocytes, monocytes, and lymphoid cells.

Family, Multigene
A set of genes descended by duplication and variation from some ancestral gene. Such genes may be clustered together on the same chromosome or dispersed on different chromosomes. Examples of multigene families include those that encode the hemoglobins, immunoglobulins, histocompatibility antigens, actins, tubulins, keratins, collagens, heat shock proteins, salivary glue proteins, chorion proteins, cuticle proteins, yolk proteins, and phaseolins, as well as histones, ribosomal RNA, and transfer RNA genes. The latter three are examples of reiterated genes, where hundreds of identical genes are present in a tandem array. (King & Stanfield, A Dictionary of Genetics, 4th ed)

Family, Nuclear
A family composed of spouses and their children.

Family, One Parent
A household that includes children and is headed by one adult.

Family, One-Parent
A household that includes children and is headed by one adult.

Family, Reconstituted
A social group consisting of parents or parent substitutes and children.

Family, Single Parent
A household that includes children and is headed by one adult.

Family, Single-Parent
A household that includes children and is headed by one adult.

Family-Centered Nursing
The provision of care involving the nursing process, to families and family members in health and illness situations. From Lippincott Manual of Nursing Practice. 6th ed.

Family-Centered Nursings
The provision of care involving the nursing process, to families and family members in health and illness situations. From Lippincott Manual of Nursing Practice. 6th ed.

Family-Patient Lodging
Living facilities for humans.

Family-Patient Lodgings
Living facilities for humans.

Famine
Lengthy and continuous deprivation of food. (Stedman, 25th ed)

Famines
Lengthy and continuous deprivation of food. (Stedman, 25th ed)



PREVIOUS AND NEXT TERMS
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False Aneurysm
An aneurysm in which the entire wall is injured and the blood is contained by the surrounding tissues, with eventual formation of a sac communicating with the artery or heart. (Dorland, 28th ed)

Fallout, Radioactive
The material that descends to the earth or water well beyond the site of a surface or subsurface nuclear explosion. (McGraw-Hill Dictionary of Chemical and Technical Terms, 4th ed)

Fallots Trilogy
Combination of pulmonary valve stenosis and atrial septal defect with right ventricular hypertrophy.

Familial Amyloid Polyneuropathies
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.

Familial Acoustic Neuroma
An autosomal dominant disorder characterized by a high incidence of bilateral acoustic neuromas as well as schwannomas (NEURILEMMOMA) of other cranial and peripheral nerves, and other benign intracranial tumors including meningiomas, ependymomas, spinal neurofibromas, and gliomas. The disease has been linked to mutations of the NF2 gene (GENES, NEUROFIBROMATOSIS 2) on chromosome 22 (22q12) and usually presents clinically in the first or second decade of life.

Familial Adenomatous Polyposis Coli

False Positive Reactions
Positive test results in subjects who do not possess the attribute for which the test is conducted. The labeling of healthy persons as diseased when screening in the detection of disease. (Last, A Dictionary of Epidemiology, 2d ed)

Familial Amyloidosis
Diseases in which there is a familial pattern of AMYLOIDOSIS.

Familial Combined Hyperlipidemia
A disorder genetically distinct from the other inherited hyperlipidemias characterized by the type II or type IV lipoprotein pattern (the pattern may change from time to time and the lipid level may be normal at one time and abnormal at another time).

Familial Benign Chronic Pemphigus
Rare hereditary disease characterized by recurrent eruptions of vesicles and bullae mainly on the neck, axillae, and groin. It exhibits autosomal dominant inheritance and is unrelated to pemphigus vulgaris though it closely resembles that disease.

Familial Cerebelloretinal Angiomatosis
An autosomal dominant disorder associated with various neoplasms including central nervous system (most often cerebellar) and retinal HEMANGIOBLASTOMA, endolymphatic sac tumors, renal cell carcinoma (see CARCINOMA, RENAL CELL), renal and pancreatic cysts, HEMANGIOMA of the spinal cord, and PHEOCHROMOCYTOMA. The most common presenting manifestations are neurologic deficits associated with intracranial hemangioblastomas which may hemorrhage, causing ataxia, INTRACRANIAL HYPERTENSION, and other signs of neurologic dysfunction. (From Neurochirurgie 1998 Nov;44(4):258-66)

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   familialadenomatouspolyposiscoli / amilial adenomatous polyposis coli / fmilial adenomatous polyposis coli / failial adenomatous polyposis coli / famlial adenomatous polyposis coli / famiial adenomatous polyposis coli / familal adenomatous polyposis coli / familil adenomatous polyposis coli / familia adenomatous polyposis coli / familialadenomatous polyposis coli / familial denomatous polyposis coli / familial aenomatous polyposis coli / familial adnomatous polyposis coli / familial adeomatous polyposis coli / familial adenmatous polyposis coli / familial adenoatous polyposis coli / familial adenomtous polyposis coli / familial adenomaous polyposis coli / familial adenomatus polyposis coli / familial adenomatos polyposis coli / familial adenomatou polyposis coli / familial adenomatouspolyposis coli / familial adenomatous olyposis coli / familial adenomatous plyposis coli / familial adenomatous poyposis coli / familial adenomatous polposis coli / familial adenomatous polyosis coli / 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familial adenomatoous polyposis coli / familial adenomatouus polyposis coli / familial adenomatouss polyposis coli / familial adenomatous polyposis coli / familial adenomatous ppolyposis coli / familial adenomatous poolyposis coli / familial adenomatous pollyposis coli / familial adenomatous polyyposis coli / familial adenomatous polypposis coli / familial adenomatous polypoosis coli / familial adenomatous polypossis coli / familial adenomatous polyposiis coli / familial adenomatous polyposiss coli / familial adenomatous polyposis coli / familial adenomatous polyposis ccoli / familial adenomatous polyposis cooli / familial adenomatous polyposis colli / familial adenomatous polyposis colii / ramilial adenomatous polyposis coli / tamilial adenomatous polyposis coli / gamilial adenomatous polyposis coli / bamilial adenomatous polyposis coli / vamilial adenomatous polyposis coli / camilial adenomatous polyposis coli / damilial adenomatous polyposis coli / eamilial adenomatous polyposis coli / fqmilial adenomatous polyposis coli / fwmilial adenomatous polyposis coli / fsmilial adenomatous polyposis coli / fxmilial adenomatous polyposis coli / fzmilial adenomatous polyposis coli / fanilial adenomatous polyposis coli / fajilial adenomatous polyposis coli / fakilial adenomatous polyposis coli / fa,ilial adenomatous polyposis coli / fa ilial adenomatous polyposis coli / famlial adenomatous polyposis coli / famioial adenomatous polyposis coli / famipial adenomatous polyposis coli / fami;ial adenomatous polyposis coli / fami.ial adenomatous polyposis coli / fami,ial adenomatous polyposis coli / famikial adenomatous polyposis coli / famiiial adenomatous polyposis coli / familal adenomatous polyposis coli / familiql adenomatous polyposis coli / familiwl adenomatous polyposis coli / familisl adenomatous polyposis coli / familixl adenomatous polyposis coli / familizl adenomatous polyposis coli / familiao adenomatous polyposis coli / familiap adenomatous polyposis coli / familia; adenomatous polyposis coli / familia. adenomatous polyposis coli / familia, adenomatous polyposis coli / familiak adenomatous polyposis coli / familiai adenomatous polyposis coli / familial qdenomatous polyposis coli / familial wdenomatous polyposis coli / familial sdenomatous polyposis coli / familial xdenomatous polyposis coli / familial zdenomatous polyposis coli / familial aeenomatous polyposis coli / familial arenomatous polyposis coli / familial afenomatous polyposis coli / familial avenomatous polyposis coli / familial acenomatous polyposis coli / familial axenomatous polyposis coli / familial asenomatous polyposis coli / familial awenomatous polyposis coli / familial ad3nomatous polyposis coli / familial ad4nomatous polyposis coli / familial adrnomatous polyposis coli / familial adfnomatous polyposis coli / familial addnomatous polyposis coli / familial adsnomatous polyposis coli / familial adwnomatous polyposis coli / familial adebomatous polyposis coli / familial adehomatous polyposis coli / familial adejomatous polyposis coli / familial ademomatous polyposis coli / familial ade omatous polyposis coli / familial aden9matous polyposis coli / familial aden0matous polyposis coli / familial adenpmatous polyposis coli / familial adenlmatous polyposis coli / familial adenkmatous polyposis coli / familial adenimatous polyposis coli / familial aden8matous polyposis coli / familial adenonatous polyposis coli / familial adenojatous polyposis coli / familial adenokatous polyposis coli / familial adeno,atous polyposis coli / familial adeno atous polyposis coli / familial adenomqtous polyposis coli / familial adenomwtous polyposis coli / familial adenomstous polyposis coli / familial adenomxtous polyposis coli / familial adenomztous polyposis coli / familial adenoma5ous polyposis coli / familial adenoma6ous polyposis coli / familial adenomayous polyposis coli / familial adenomahous polyposis coli / familial adenomagous polyposis coli / familial adenomafous polyposis coli / familial adenomarous polyposis coli / familial adenoma4ous polyposis coli / familial adenomat9us polyposis coli / familial adenomat0us polyposis coli / familial adenomatpus polyposis coli / familial adenomatlus polyposis coli / familial adenomatkus polyposis coli / familial adenomatius polyposis coli / familial adenomat8us polyposis coli / familial adenomato7s polyposis coli / familial adenomato8s polyposis coli / familial adenomatois polyposis coli / familial adenomatoks polyposis coli / familial adenomatojs polyposis coli / familial adenomatohs polyposis coli / familial adenomatoys polyposis coli / familial adenomato6s polyposis coli / familial adenomatouw polyposis coli / familial adenomatoue polyposis coli / familial adenomatoud polyposis coli / familial adenomatoux polyposis coli / familial adenomatouz polyposis coli / familial adenomatoua polyposis coli / familial adenomatouq polyposis coli / familial adenomatous 0olyposis coli / familial adenomatous -olyposis coli / familial adenomatous [olyposis coli / familial adenomatous ;olyposis coli / familial adenomatous lolyposis coli / familial adenomatous oolyposis coli / familial adenomatous 9olyposis coli / familial adenomatous p9lyposis coli / familial adenomatous p0lyposis coli / familial adenomatous pplyposis coli / familial adenomatous pllyposis coli / familial adenomatous pklyposis coli / familial adenomatous pilyposis coli / familial adenomatous p8lyposis coli / familial adenomatous pooyposis coli / familial adenomatous popyposis coli / familial adenomatous po;yposis coli / familial adenomatous po.yposis coli / familial adenomatous po,yposis coli / familial adenomatous pokyposis coli / familial adenomatous poiyposis coli / familial adenomatous pol6posis coli / familial adenomatous pol7posis coli / familial adenomatous poluposis coli / familial adenomatous poljposis coli / familial adenomatous polhposis coli / familial adenomatous polgposis coli / familial adenomatous poltposis coli / familial adenomatous pol5posis coli / familial adenomatous poly0osis coli / familial adenomatous poly-osis coli / familial adenomatous poly[osis coli / familial adenomatous poly;osis coli / familial adenomatous polylosis coli / familial adenomatous polyoosis coli / familial adenomatous poly9osis coli / familial adenomatous polyp9sis coli / familial adenomatous polyp0sis coli / familial adenomatous polyppsis coli / familial adenomatous polyplsis coli / familial adenomatous polypksis coli / familial adenomatous polypisis coli / familial adenomatous polyp8sis coli / familial adenomatous polypowis coli / familial adenomatous polypoeis coli / familial adenomatous polypodis coli / familial adenomatous polypoxis coli / familial adenomatous polypozis coli / familial adenomatous polypoais coli / familial adenomatous polypoqis coli / familial adenomatous polyposs coli / familial adenomatous polyposiw coli / familial adenomatous polyposie coli / familial adenomatous polyposid coli / familial adenomatous polyposix coli / familial adenomatous polyposiz coli / familial adenomatous polyposia coli / familial adenomatous polyposiq coli / familial adenomatous polyposis xoli / familial adenomatous polyposis soli / familial adenomatous polyposis doli / familial adenomatous polyposis foli / familial adenomatous polyposis voli / familial adenomatous polyposis oli / familial adenomatous polyposis c9li / familial adenomatous polyposis c0li / familial adenomatous polyposis cpli / familial adenomatous polyposis clli / familial adenomatous polyposis ckli / familial adenomatous polyposis cili / familial adenomatous polyposis c8li / familial adenomatous polyposis cooi / familial adenomatous polyposis copi / familial adenomatous polyposis co;i / familial adenomatous polyposis co.i / familial adenomatous polyposis co,i / familial adenomatous polyposis coki / familial adenomatous polyposis coii / familial adenomatous polyposis col /