Women with a history of preeclampsia have preserved sensory nerve‐mediated dilation in the cutaneous microvasculature

2021 ◽  
Author(s):  
Michael Pyevich ◽  
Lacy M Alexander ◽  
Anna E. Stanhewicz
Keyword(s):  
2017 ◽  
Vol 89 (2) ◽  
pp. 231-248 ◽  
Author(s):  
Christopher Green ◽  
Farrha B. Hopkins ◽  
Christopher D. Lindsay ◽  
James R. Riches ◽  
Christopher M. Timperley

AbstractPain! Most humans feel it throughout their lives. The molecular mechanisms underlying the phenomenon are still poorly understood. This is especially true of pain triggered in response to molecules of a certain shape and reactivity present in the environment. Such molecules can interact with the sensory nerve endings of the eyes, nose, throat and lungs to cause irritation that can range from mild to severe. The ability to alert to the presence of such potentially harmful substances has been termed the ‘common chemical sense’ and is thought to be distinct from the senses of smell or taste, which are presumed to have evolved later. Barbecue a burger excessively and you self-experiment. Fatty acids present in the meat break off their glycerol anchor under the thermal stress. The glycerol loses two molecules of water and forms acrolein, whose assault on the eyes is partly responsible for the tears elicited by smoke. Yet the smell and taste of the burger are different experiences. It was this eye-watering character of acrolein that prompted its use as a warfare agent during World War I. It was one of several ‘lachrymators’ deployed to harass, and the forerunner of safer chemicals, such as ‘tear gas’ CS, developed for riot control. The history of development and mechanism of action of some sensory irritants is discussed here in relation to recent advice from the Scientific Advisory Board (SAB) of the Organisation for the Prohibition of Chemical Weapons (OPCW) on chemicals that conform to the definition of a riot control agent (RCA) under the Chemical Weapons Convention.


1997 ◽  
Vol 22 (1) ◽  
pp. 34-37 ◽  
Author(s):  
L.-G. GUNNARSSON ◽  
A. AMILON ◽  
P. HELLSTRAND ◽  
P. LEISSNER ◽  
L. PHILIPSON

The study group consisted of 100 persons referred with suspected carpal tunnel syndrome. Clinical and neurophysiological examinations were performed blinded from each other. The gold standard for the carpal tunnel syndrome (CTS) diagnosis was based on the results of these examinations but relief of CTS symptoms after surgery was also required. The sensitivity and specificity for the combined results of the clinical examinations were 94% and 80% respectively, and for the neurophysiological examinations, 85% and 87%. Of the neurophysiological methods used, the quotient of sensory nerve conduction velocity between palm to wrist and wrist to elbow was best and the cut-off for this test was studied by means of an ROC-curve. According to our results clinical examination by an experienced doctor seems to be sufficient if there are typical symptoms of carpal tunnel syndrome, but if there is a history of pain, atypical symptoms or earlier fractures in the arm, wrist or hand, it is important to add a neurophysiological examination.


2021 ◽  
pp. 194187442098705
Author(s):  
Jonathan Morena ◽  
Bakri Elsheikh ◽  
J. Chad Hoyle

MFS has been reported to recur in 10-12% of patients. There may be a genetic component related to HLA-DR2. Anti-GAD antibodies can be present in MFS along with anti-GQ1b. Common EMG/NCS associations consist of a predominantly axonal, sensory polyneuropathy and absent H reflexes. A 32-year-old female with a history of hypothyroidism presented to our institution twice with symptoms of diplopia, lower extremity weakness and distal paresthesias occurring a year apart. She had ophthalmoplegia, reduced reflexes, and ataxia on exam. CSF showed a borderline elevated protein of 47 and white blood cells <3. She was positive for anti-GQ1b both times. Her anti-GAD65 antibody was elevated during both admissions. EMG/NCS on her first admission revealed comparatively reduced sensory nerve action potentials (SNAPs) and a normal blink reflex. Her SNAPs improved on the second admission, however, the EMG was performed only 2 days after the onset of her symptoms, limiting some early findings that may have not matured electrophysiologically. She was treated with IVIG on both occasions with rapid recovery within 5 days. This case highlights the fact that MFS can be recurrent. It also provides further evidence that anti-GAD antibodies may be associated with MFS. Reported findings of the blink reflex in MFS are diverse and further data is needed to determine if certain findings are more predominant than others. Treatment typically consists of IVIG, though steroids may also be considered for recurrence. Prognosis is generally favorable, regardless of treatment.


2015 ◽  
Vol 10 (1) ◽  
pp. 99 ◽  
Author(s):  
Wen-tao Zhang ◽  
Lu Bai ◽  
Yan-ni Han ◽  
Wei Huang ◽  
Hong-lei Zhang

2021 ◽  
Vol 12 ◽  
pp. 507
Author(s):  
Rohin Singh ◽  
Yeonsoo Sara Lee ◽  
Pelagia E. Kouloumberis ◽  
Shelley S. Noland

Background: Radial tunnel syndrome arises due to compression of the radial nerve through the radial tunnel.[1,5] The radial nerve divides into superficial and deep branches in the forearm. The deep branch travels posteriorly through the heads of the supinator where compression commonly occurs.[3,9,7] This syndrome results in pain in the hand and forearm with no motor weakness.[8] This condition can be treated conservatively with splinting and anti-inflammatory medication.[2,4,6] For cases of refractory radial tunnel syndrome, surgical management can be considered. Herein, we have presented a step-by-step video guide on how to perform a radial nerve decompression with a review of the relevant anatomy and surgical considerations. Case Description: A 68-year-old right-handed woman presented to the Mayo Clinic (Scottsdale, AZ) with the right elbow pain which radiated to the forearm causing significant difficulties with daily tasks. She had been dealing with worsening symptoms for 4 months. The patient’s history of gardening and clinical presentation allowed for diagnosis of radial tunnel syndrome. After conservative measures failed and other differential diagnoses were excluded, surgical decompression was recommended to treat her symptoms. The patient’s right arm was marked preoperatively between the brachioradialis and extensor carpi radialis longus (ECRL) muscles. The posterior cutaneous nerve of the forearm was identified which allowed for the determination of the interval between the brachioradialis and ECRL. Separation of the two muscles allowed for the identification of the radial sensory nerve. A nerve stimulator was used to confirm the sensory nature of this nerve. The nerve to the extensor carpi radialis brevis (ECRB) was identified and retracted with a vessel loop. Dorsal to the nerve to the ECRB is the posterior interosseous nerve (PIN), which was identified and retracted with a vessel loop. The fascia of the ECRB was divided both longitudinally and transversely and the supinator below was identified. The supinator muscle was carefully divided to further decompress the PIN. Informed consent for publication of this material was obtained from the patient. Conclusion: The patient tolerated the procedure well and reported significantly reduced pain at 7-month follow-up. To the best of our knowledge, video tutorials on this procedure have not been published. This video can serve as an educational guide for peripheral nerve specialists dealing with similar lesions.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Jasmine Shimin Koh ◽  
James Wei Min Tung ◽  
Genevieve Lynn Yu Tan-Yu ◽  
Thirugnanam Umapathi

Chronic immune sensory polyradiculopathy (CISP) is an uncommon and treatable inflammatory disorder of the proximal sensory nerve roots. Patients typically present with severe sensory ataxia, normal motor examination, unsteady gait, and normal nerve conduction studies (NCS). We describe an elderly man who presented with a two-week history of progressive numbness of both legs and recurrent falls. He had hyporeflexia, normal strength, severe proprioceptive, and vibration sense loss in both lower limbs and was unable to stand or walk because of severe sensory ataxia. The NCS and MR scan of the spine were normal. Tibial somatosensory evoked potentials revealed proximal conduction defect and localized the pathology to the lumbar sensory nerve roots proximal to the dorsal root ganglion. Cerebrospinal fluid showed cytoalbuminergic dissociation suggestive of inflammation. CISP was diagnosed; he was given aggressive immunotherapy consisting sequentially of corticosteroids with mycophenolate mofetil and three cycles of intravenous immunoglobulin after which he regained independent mobility. Unlike previous reports where patients presented months-years after symptom onset and improved after single-line immunotherapy, our patient presented fairly acutely and made dramatic improvement only after aggressive combination therapy. We urge physicians to recognize this uncommon neurologic cause of sensory ataxia where early aggressive treatment is crucial for better functional outcomes.


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