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Does Personhood Begin During Pregnancy?
Published in Christopher Kaczor, The Ethics of Abortion, 2023
In considering whether human beings who do not feel pain should be accorded the rights of persons, we are actually not dealing with merely imaginary examples. Although there have been very few human beings, most of them children, ever diagnosed with the condition, Congenital Insensitivity to Pain renders human beings totally insensitive to pain, for they lack proper beta-endorphins which modulate pain sensations.
What's Causing My Gut Symptoms?
Published in Melissa G. Hunt, Aaron T. Beck, Reclaim Your Life From IBS, 2022
Melissa G. Hunt, Aaron T. Beck
Some people are born without the ability to sense pain (called congenital insensitivity to pain). This sounds like a blessing, but it’s actually a curse. Many of these people suffer horrible disabling or disfiguring accidents and very few survive past age 25. So, pain can be an important signal and can give us information that something is wrong that has to be fixed. Like a smoke detector, pain tells us there’s a fire to put out.
Diaphyseal fractures
Published in Amaka C Offiah, Christine M Hall, Radiological Atlas of Child Abuse, 2018
Amaka C Offiah, Christine M Hall
Abnormal stresses through normal bone occur in active children with congenital insensitivity to pain. Repeated trauma or normal activity in the presence of painless underlying fractures results in re-fracturing, bone fragmentation, exuberant callus and deformity.
Preclinical target validation for non-addictive therapeutics development for pain
Published in Expert Opinion on Therapeutic Targets, 2022
Richard Hargreaves, Karen Akinsanya, Seena K. Ajit, Neel T. Dhruv, Jamie Driscoll, Peter Farina, Narender Gavva, Marie Gill, Andrea Houghton, Smriti Iyengar, Carrie Jones, Annemieke Kavelaars, Ajamete Kaykas, Walter J. Koroshetz, Pascal Laeng, Jennifer M. Laird, Donald C. Lo, Johan Luthman, Gordon Munro, Michael L. Oshinsky, G. Sitta Sittampalam, Sarah A. Woller, Amir P. Tamiz
Numerous retrospective analyses indicate that targets supported by human genetics are more likely to succeed in the clinic than targets without such evidence [17]. Although most of the examples are from non-pain indications there are a few clear examples for pain targets through human genetic studies. Studies of families with either pain insensitivity or hypersensitivity revealed genes that have significant contribution to sensation of pain [18]. A large Swedish family with pain free joint destruction found to carry a mutation in the nerve growth factor beta (NGFB) gene causing insensitivity to deep pain without anhidrosis (hereditary sensory and autonomic neuropathy, type V; HSAN V) [19]. Biallelic loss of function in NGF has been found to be the underpinning cause of congenital insensitivity to pain and anhidrosis (CIPA) of consanguineous families. Furthermore, carriers of biallelic loss of function mutations in the NGF receptor TRKA have also been found to have CIPA [20]. Similarly, carriers of loss-of-function mutations within the sodium channel gene SCN9A have been found to have no pain sensation whereas gain-of-function mutations underlie Erythromelalgia [21].
Neuropathic pain: preclinical and early clinical progress with voltage-gated sodium channel blockers
Published in Expert Opinion on Investigational Drugs, 2020
Mikhail Kushnarev, Iulia Paula Pirvulescu, Kenneth D. Candido, Nebojsa Nick Knezevic
Currently available treatment options leave approximately 50% of patients without any improvement [1,5]. VGSCs are an attractive target for developing novel analgesics, as isoforms Nav1.3, Nav 1.6, Nav1.7, Nav1.8, and Nav1.9 have been demonstrated to play important roles in pain signaling [10,12]. In particular, genetic evidence points to Nav1.7 as a promising target. A known human disorder, congenital insensitivity to pain, is caused by homozygous loss-of-function mutations in Nav1.7, and presents as absence of nociception without cardiovascular or autonomic dysfunction [33,34]. We have provided the readers with updates on novel VGSC blockers, of which several are continuing in clinical trials, notably BIIB074, XEN402 (FX301), and DSP-3905. Finally, we shed light on a wide array of small molecules and toxins that are being studied in in vitro and in vivo models of pain. It is our hope that continuing research and pharmaceutic development will produce novel, potent, and safe analgesics that would be devoid of abuse potential.
A Child Presenting with Recurrent Corneal Ulcers: Hereditary Sensory and Autonomic Neuropathy IV (HSAN IV)
Published in Neuro-Ophthalmology, 2019
Beena Suresh, Vaishnavi Reddy, Ingo Kurth, Sujatha Jagadeesh
There was anhidrosis and serum uric acid levels were normal (2.7 mg/dl range 1.4–6.7), ruling out Lesch Nyhan syndrome. His nerve conduction studies revealed that the sensory responses were smaller in amplitude but otherwise normal. Hence the provisional diagnosis was HSAN IV or Congenital Insensitivity to Pain and Anhidrosis. In view of recurrent corneal ulcers he underwent a detailed ophthalmological evaluation and was noted to have neurotrophic keratitis with decreased corneal sensation. He was treated with 0.3% Tobramycin eye drops 3 hourly, atropine eye drops and carboxymethyl cellulose eye drops 0.5%w/v for a week and the ulcers healed with a resultant corneal opacity. Subsequently the child presented with recurrence of corneal ulcers and underwent bilateral lateral tarsorrhaphy which had reduced the frequency of his corneal ulcers.