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Impaired temperature sensation

MedGen UID:
Concept ID:
Synonym: Impaired thermal sensitivity
HPO: HP:0010829


A reduced ability to discriminate between different temperatures. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Impaired temperature sensation

Conditions with this feature

Congenital sensory neuropathy with selective loss of small myelinated fibers
MedGen UID:
Concept ID:
Disease or Syndrome
Hereditary sensory and autonomic neuropathy type V (HSAN5) is a condition that primarily affects the sensory nerve cells (sensory neurons), which transmit information about sensations such as pain, temperature, and touch. These sensations are impaired in people with HSAN5.\n\nThe signs and symptoms of HSAN5 appear early, usually at birth or during infancy. People with HSAN5 lose the ability to feel pain, heat, and cold. Deep pain perception, the feeling of pain from injuries to bones, ligaments, or muscles, is especially affected in people with HSAN5. Because of the inability to feel deep pain, affected individuals suffer repeated severe injuries such as bone fractures and joint injuries that go unnoticed. Repeated trauma can lead to a condition called Charcot joints, in which the bones and tissue surrounding joints are destroyed.
Sandhoff disease
MedGen UID:
Concept ID:
Disease or Syndrome
Sandhoff disease comprises a phenotypic continuum encompassing acute infantile, subacute juvenile, and late-onset disease. Although classification into these phenotypes is somewhat arbitrary, it is helpful in understanding the variation observed in the timing of disease onset, presenting manifestations, rate of progression, and life span. Acute infantile Sandhoff disease (onset age <6 months). Infants are generally normal at birth followed by progressive weakness and slowing of developmental progress, then developmental regression and severe neurologic impairment. Seizures are common. Death usually occurs between ages two and three years. Subacute juvenile Sandhoff disease (onset age 2-5 years). After attaining normal developmental milestones, developmental progress slows, followed by developmental regression and neurologic impairment (abnormal gait, dysarthria, and cognitive decline). Death (usually from aspiration) typically occurs in the early to late teens. Late-onset Sandhoff disease (onset older teen years or young adulthood). Nearly normal psychomotor development is followed by a range of neurologic findings (e.g., weakness, spasticity, dysarthria, and deficits in cerebellar function) and psychiatric findings (e.g., deficits in executive function and memory). Life expectancy is not necessarily decreased.
Tangier disease
MedGen UID:
Concept ID:
Disease or Syndrome
Tangier disease is characterized by severe deficiency or absence of high-density lipoprotein (HDL) in the circulation resulting in tissue accumulation of cholesteryl esters throughout the body, particularly in the reticuloendothelial system. The major clinical signs of Tangier disease include hyperplastic yellow-orange tonsils, hepatosplenomegaly, and peripheral neuropathy, which may be either relapsing-remitting or chronic progressive in nature. Rarer complications may include corneal opacities that typically do not affect vision, premature atherosclerotic coronary artery disease occurring in the sixth and seventh decades of life (not usually before age 40 years), and mild hematologic manifestations, such as mild thrombocytopenia, reticulocytosis, stomatocytosis, or hemolytic anemia. The clinical expression of Tangier disease is variable, with some affected individuals only showing biochemical perturbations.
Channelopathy-associated congenital insensitivity to pain, autosomal recessive
MedGen UID:
Concept ID:
Disease or Syndrome
Hereditary sensory and autonomic neuropathy type II (HSAN2) is characterized by progressively reduced sensation to pain, temperature, and touch. Onset can be at birth and is often before puberty. The sensory deficit is predominantly distal with the lower limbs more severely affected than the upper limbs. Over time sensory function becomes severely reduced. Unnoticed injuries and neuropathic skin promote ulcerations and infections that result in spontaneous amputation of digits or the need for surgical amputation. Osteomyelitis is common. Painless fractures can complicate the disease. Autonomic disturbances are variable and can include hyperhidrosis, tonic pupils, and urinary incontinence in those with more advanced disease.
Cerebellar ataxia, benign, with thermoanalgesia
MedGen UID:
Concept ID:
Disease or Syndrome
Congenital insensitivity to pain-hypohidrosis syndrome
MedGen UID:
Concept ID:
Disease or Syndrome
Hereditary sensory and autonomic neuropathy type VIII is an autosomal recessive neurologic disorder characterized by congenital insensitivity to pain resulting in ulceration to the fingers, tongue, lips, and other distal appendages. Affected individuals may also have decreased sweating and tear production (summary by Chen et al., 2015). For a discussion of genetic heterogeneity of hereditary sensory and autonomic neuropathy, see HSAN1A (162400).
Indifference to pain, congenital, autosomal dominant
MedGen UID:
Concept ID:
Disease or Syndrome
Marsili syndrome (MARSIS) is an autosomal dominant pain insensitivity disorder characterized by a lowered ability to sense pain, to experience temperature, and to sweat. Affected individuals do not perceive broken bones and burns as painful, and have lowered sensitivity to capsaicin. However, visceral pain (e.g., childbirth-related) and light touch are perceived (summary by Habib et al., 2018).
Charcot-Marie-Tooth disease, axonal, Type 2HH
MedGen UID:
Concept ID:
Disease or Syndrome
Axonal Charcot-Marie-Tooth disease type 2HH (CMT2HH) is an autosomal dominant peripheral neuropathy characterized predominantly by onset of vocal cord weakness resulting in stridor in infancy or early childhood. The vocal cord paresis remains throughout life and may be severe enough to require tracheostomy. Additional features of the disorder usually include pes cavus and scoliosis. Some patients have mild distal muscle weakness and atrophy primarily affecting the lower limbs, although the upper limbs may also be involved, and distal sensory impairment, often with hyporeflexia (Sullivan et al., 2020). For a discussion of genetic heterogeneity of axonal CMT, see CMT2A1 (118210).
Spastic paraplegia 85, autosomal recessive
MedGen UID:
Concept ID:
Disease or Syndrome
Autosomal recessive spastic paraplegia-85 (SPG85) is a neurologic disorder characterized by the onset of motor symptoms in the first few years of life. Affected individuals have spasticity and hyperreflexia of the lower limbs resulting in gait abnormalities. Older patients may have upper limb involvement and demonstrate axonal polyneuropathy. Additional features include optic atrophy, dysarthria, dysphagia, ataxia, and urinary incontinence. Brain imaging may show cerebellar atrophy (summary by Wagner et al., 2019). For a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see SPG5A (270800).

Professional guidelines

Recent clinical studies


Strobel AV, Tankisi H, Finnerup NB, Fuglsang-Frederiksen A, Jennum P, Svendsen KB, Kirov FI, Otto M
Sleep Med 2018 Feb;42:83-89. Epub 2017 Oct 28 doi: 10.1016/j.sleep.2017.09.035. PMID: 29458751


Hanada K, Yokoi K, Kashida N, Shimomura R, Murata D, Hirayama K
BMC Neurol 2022 Jul 19;22(1):268. doi: 10.1186/s12883-022-02796-x. PMID: 35854223Free PMC Article


Minde J, Svensson O, Holmberg M, Solders G, Toolanen G
Acta Orthop 2006 Apr;77(2):198-202. doi: 10.1080/17453670610045911. PMID: 16752279

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