ReviewOrphanet journal of rare diseases2008
Hereditary sensory neuropathy type I.
Review in Orphanet journal of rare diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 76 citations in OpenAlex.
- Neurotoxic 1-deoxysphingolipids and paclitaxel-induced peripheral neuropathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Trial
- Inherited Peripheral Neuropathies.Neurologic clinics · 2025Review
- Rab7a is an enhancer of TPC2 activity regulating melanoma progression through modulation of the GSK3β/β-Catenin/MITF-axis.Nature communications · 2024Article
- Spectrum of SPTLC1-related disorders: a novel case of 'Ser331 syndrome' that expand the phenotype of hereditary sensory and autonomic neuropathy type 1A and motor neuron diseases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Genetic pain loss disorders.Nature reviews. Disease primers · 2022Review
- Novel Gross Deletion Mutations inFrontiers in pediatrics · 2021Article
- Biosynthesis of long chain base in sphingolipids in animals, plants and fungi.Future science OA · 2019Review
- Cytotoxicity of 1-deoxysphingolipid unraveled by genome-wide genetic screens and lipidomics inMolecular biology of the cell · 2019Article
- Hereditary Sensory and Autonomic Neuropathies: Adding More to the Classification.Current neurology and neuroscience reports · 2019Review
- Canine neuropathies: powerful spontaneous models for human hereditary sensory neuropathies.Human genetics · 2019Review
- Structure of the human TRiC/CCT Subunit 5 associated with hereditary sensory neuropathy.Scientific reports · 2017Article
- Acro-osteolysis.Clinical rheumatology · 2017Review
- A Point Mutation in a lincRNA Upstream of GDNF Is Associated to a Canine Insensitivity to Pain: A Spontaneous Model for Human Sensory Neuropathies.PLoS genetics · 2016Article
- Trafficking and Functions of Bioactive Sphingolipids: Lessons from Cells and Model Membranes.Lipid insights · 2015Review
- Altered sphingoid base profiles in type 1 compared to type 2 diabetes.Lipids in health and disease · 2014Article
- Biochemical characterization of mutants in chaperonin proteins CCT4 and CCT5 associated with hereditary sensory neuropathy.The Journal of biological chemistry · 2014Article
- Neuroprotective effect of erythropoietin against pressure ulcer in a mouse model of small fiber neuropathy.PloS one · 2014Article
- Disorders of phospholipids, sphingolipids and fatty acids biosynthesis: toward a new category of inherited metabolic diseases.Journal of inherited metabolic disease · 2013Review
- Cardiac-locked bursts of muscle sympathetic nerve activity are absent in familial dysautonomia.The Journal of physiology · 2013Article
- [Genetics of neuropathies].Der Nervenarzt · 2013Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary sensory neuropathy type I (HSN I) is a slowly progressive neurological disorder characterised by prominent predominantly distal sensory loss, autonomic disturbances, autosomal dominant inheritance, and juvenile or adulthood disease onset. The exact prevalence is unknown, but is estimated as very low. Disease onset varies between the 2nd and 5th decade of life. The main clinical feature of HSN I is the reduction of sensation sense mainly distributed to the distal parts of the upper and lower limbs. Variable distal muscle weakness and wasting, and chronic skin ulcers are characteristic. Autonomic features (usually sweating disturbances) are invariably observed. Serious and common complications are spontaneous fractures, osteomyelitis and necrosis, as well as neuropathic arthropathy which may even necessitate amputations. Some patients suffer from severe pain attacks. Hypacusis or deafness, or cough and gastrooesophageal reflux have been observed in rare cases. HSN I is a genetically heterogenous condition with three loci and mutations in two genes (SPTLC1 and RAB7) identified so far. Diagnosis is based on the clinical observation and is supported by a family history. Nerve conduction studies confirm a sensory and motor neuropathy predominantly affecting the lower limbs. Radiological studies, including magnetic resonance imaging, are useful when bone infections or necrosis are suspected. Definitive diagnosis is based on the detection of mutations by direct sequencing of the SPTLC1 and RAB7 genes. Correct clinical assessment and genetic confirmation of the diagnosis are important for appropriate genetic counselling and prognosis. Differential diagnosis includes the other hereditary sensory and autonomic neuropathies (HSAN), especially HSAN II, as well as diabetic foot syndrome, alcoholic neuropathy, neuropathies caused by other neurotoxins/drugs, immune mediated neuropathy, amyloidosis, spinal cord diseases, tabes dorsalis, lepra neuropathy, or decaying skin tumours like amelanotic melanoma. Management of HSN I follows the guidelines given for diabetic foot care (removal of pressure to the ulcer and eradication of infection, followed by the use of specific protective footwear) and starts with early and accurate counselling of patients about risk factors for developing foot ulcerations. The disorder is slowly progressive and does not influence life expectancy but is often severely disabling after a long duration of the disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.