OBJECTIVE: To analyze and compare the characteristics and causes of F wave changes in patients with Charcot-Marie-Tooth1A (CMT1A) and chronic inflammatory demyelinating polyneuropathy (CIDP). METHODS: Thirty patients with CMT1A and 30 patients with CIDP were enrolled in Peking University Third Hospital from January 2012 to December 2018. Their clinical data, electrophysiological data(nerve conduction velocity, F wave and H reflex) and neurological function scores were recorded. Some patients underwent magnetic resonance imaging of brachial plexus and lumbar plexus, and the results were analyzed and compared. RESULTS: The average motor conduction velocity (MCV) of median nerve was (21.10±10.60) m/s in CMT1A and (31.52±12.46) m/s in CIDP. There was a significant difference between the two groups (t=-6.75, P < 0.001). About 43.3% (13/30) of the patients with CMT1A did not elicit F wave in ulnar nerve, which was significantly higher than that of the patients with CIDP (4/30, 13.3%), χ²=6.65, P=0.010. Among the patients who could elicit F wave, the latency of F wave in CMT1A group was (52.40±17.56) ms and that in CIDP group was (42.20±12.73) ms. There was a significant difference between the two groups (t=2.96, P=0.006). The occurrence rate of F wave in CMT1A group was 34.6%±39%, and that in CIDP group was 70.7%±15.2%. There was a significant difference between the two groups (t=-5.13, P < 0.001). The MCV of median nerve in a patient with anti neurofascin 155 (NF155) was 23.22 m/s, the latency of F wave was 62.9-70.7 ms, and the occurrence rate was 85%-95%. The proportion of brachial plexus and lumbar plexus thickening in CMT1A was 83.3% (5/6) and 85.7% (6/7), respectively. The proportion of brachial plexus and lumbar plexus thickening in the CIDP patients was only 25.0% (1/4, 2/8). The nerve roots of brachial plexus and lumbar plexus were significantly thickened in a patient with anti NF155 antibody. CONCLUSION The prolonged latency of F wave in patients with CMT1A reflects the homogenous changes in both proximal and distal peripheral nerves, which can be used as a method to differentiate the CIDP patients characterized by focal demyelinating pathology. Moreover, attention should be paid to differentiate it from the peripheral neuropathy caused by anti NF155 CIDP. Although F wave is often used as an indicator of proximal nerve injury, motor neuron excitability, anterior horn cells, and motor nerve myelin sheath lesions can affect its latency and occurrence rate. F wave abnormalities need to be comprehensively analyzed in combination with the etiology, other electrophysiological results, and MRI imaging.
Humans ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/pathology* ; Median Nerve/pathology* ; Ulnar Nerve/pathology* ; Brachial Plexus/pathology* ; Magnetic Resonance Imaging/methods*

Brachial plexus avulsion (BPA) is a combined injury involving the central and peripheral nervous systems. Patients with BPA often experience severe neuropathic pain (NP) in the affected limb. NP is insensitive to the existing treatments, which makes it a challenge to researchers and clinicians. Accumulated evidence shows that a BPA-induced pain state is often accompanied by sympathetic nervous dysfunction, which suggests that the excitation state of the sympathetic nervous system is correlated with the existence of NP. However, the mechanism of how somatosensory neural crosstalk with the sympathetic nerve at the peripheral level remains unclear. In this study, through using a novel BPA C7 root avulsion mouse model, we found that the expression of BDNF and its receptor TrκB in the DRGs of the BPA mice increased, and the markers of sympathetic nervous system activity including α1 and α2 adrenergic receptors (α1-AR and α2-AR) also increased after BPA. The phenomenon of superexcitation of the sympathetic nervous system, including hypothermia and edema of the affected extremity, was also observed in BPA mice by using CatWalk gait analysis, an infrared thermometer, and an edema evaluation. Genetic knockdown of BDNF in DRGs not only reversed the mechanical allodynia but also alleviated the hypothermia and edema of the affected extremity in BPA mice. Further, intraperitoneal injection of adrenergic receptor inhibitors decreased neuronal excitability in patch clamp recording and reversed the mechanical allodynia of BPA mice. In another branch experiment, we also found the elevated expression of BDNF, TrκB, TH, α1-AR, and α2-AR in DRG tissues from BPA patients compared with normal human DRGs through western blot and immunohistochemistry. Our results revealed that peripheral BDNF is a key molecule in the regulation of somatosensory-sympathetic coupling in BPA-induced NP. This study also opens a novel analgesic target (BDNF) in the treatment of this pain with fewer complications, which has great potential for clinical transformation.
Humans ; Mice ; Animals ; Hyperalgesia/metabolism* ; Brain-Derived Neurotrophic Factor/metabolism* ; Hypothermia/metabolism* ; Neuralgia ; Brachial Plexus/injuries* ; Edema/metabolism*

The mass vaccination against COVID-19 has saved millions of lives globally. The majority of people experience short-term mild side effects; however, in rare cases, some develop long-term severe adverse events. This case report illustrates the case of a middle-aged man with Parsonage–Turner syndrome, a rare adverse event following COVID-19 immunisation. The patient presented with pain and weakness of the right upper arm for 2 months, which developed 5 days after he received his mRNA COVID-19 booster vaccine. He sought medical attention after 9 weeks of experiencing weakness with obvious muscle wasting. He reported his condition only via a phone application, as he thought that his condition was self-limiting and will improve with time. Herein, we discuss the syndrome and highlight the importance of patient education and early recognition of serious adverse events related to vaccinations in the primary care setting.
COVID-19 Vaccines ; Brachial Plexus Neuritis ; Primary Health Care

Brachial Plexus Neuritis/etiology* ; COVID-19/prevention & control* ; Humans ; Vaccination/adverse effects*

INTRODUCTION: In patients with delayed presentation between 6 to 12 months, surgical treatment guidelines are not well defined in brachial plexus injury. Still, several authors have agreed that functional outcomes in patients treated within six months from the date of injury have the best results. Nerve transfers are still considered one of the treatment options in the said subset of patients even after six months. In contrast, a primary Steindler flexorplasty, or proximal advancement of the flexor-pronator group, is an ideal technique for elbow flexion with an elapsed time from injury >6 to 9 months. OBJECTIVE: The purpose of this investigation was to compare the clinical outcome s of nerve transfers versus modified Steindler flexorplasty for the restoration of elbow flexion in upper type brachial plexus injuries (BPI). METHODS: A retrospective review of 28 patients who underwent nerve transfers (NT) and 12 patients who underwent modified Steindler flexorplasty (MSF) was done to determine the outcome of treatments. The manual muscle testing using the Medical Research Council scaling system, Visual Analog Scale for pain, active range of motion, and Disabilities of the Arm, Shoulder and Hand form scores were taken as dependent variables. RESULTS: The NT group had a median age of 27.5 years, with 26 men, a median surgical delay of 5.6 months, and a median follow-up of 33 months. Twenty out of 28 patients (71%) had ≥M3 with a median range of 117.6° elbow flexion motion. Median postoperative DASH (n=16) and VAS scores were 29.2 and 3, respectively. For the MSF patients, the median age was 27 years, including ten men, the median surgical delay was 12 months, and the median follow-up was 18.4 months. All the 12 patients had ≥M3, with a median range of motion of 106°. The median postoperative DASH score (n=5) and VAS score were 28.3 and 0, respectively. In the NT group, 73.3% (11/15) achieved ≥M3 elbow flexion if the operation was done in <6 months. CONCLUSION: Nerve transfers and the modified Steindler procedure are still excellent options for successful elbow flexion reanimation in patients with brachial plexus injuries. Our results also showed that those with surgical delays of less than six months had the highest rate of achieving ≥M3 elbow flexion strength in the nerve transfer group.
Nerve Transfer ; Elbow ; Brachial Plexus ; Elbow Joint ; Range of Motion, Articular

Anesthetics, Local ; Brachial Plexus ; Injections

Our previous investigation suggested that faster seventh cervical nerve (C7) regeneration occurs in patients with cerebral injury undergoing contralateral C7 transfer. This finding needed further verification, and the mechanism remained largely unknown. Here, Tinel's test revealed faster C7 regeneration in patients with cerebral injury, which was further confirmed in mice by electrophysiological recordings and histological analysis. Furthermore, we identified an altered systemic inflammatory response that led to the transformation of macrophage polarization as a mechanism underlying the increased nerve regeneration in patients with cerebral injury. In mice, we showed that, as a contributing factor, serum amyloid protein A1 (SAA1) promoted C7 regeneration and interfered with macrophage polarization in vivo. Our results indicate that altered inflammation promotes the regenerative capacity of the C7 nerve by altering macrophage behavior. SAA1 may be a therapeutic target to improve the recovery of injured peripheral nerves.
Animals ; Brachial Plexus ; Brachial Plexus Neuropathies/surgery* ; Humans ; Mice ; Nerve Transfer ; Peripheral Nerves ; Spinal Nerves

Brachial Plexus/injuries* ; Disabled Persons ; Humans

We performed a revisionary open reduction and internal fixation for treating nonunion of the mid-shaft of the left clavicle with an autogenous cancellous bone graft. On postoperative day 4, the patient presented with neurologic deficits in the left upper extremity. We removed the implant and made a superior angulation to decompress the brachial plexus. At 6 months postoperatively, callus bridging and consolidation were visible and all hand and elbow functions were fully recovered. Our case suggests that brachial plexus neuropathy may be caused by stretching and compression after reduction and straightening of the nonunion site around adhesions or scar tissue. Therefore, care should be taken whether there are the risk factors that can cause brachial plexus neuropathy when revision surgery is performed for treating nonunion of a clavicle shaft fracture.
Bony Callus ; Brachial Plexus Neuropathies ; Brachial Plexus ; Cicatrix ; Clavicle ; Elbow ; Hand ; Humans ; Neurologic Manifestations ; Risk Factors ; Transplants ; Upper Extremity

A number of patients with thoracic outlet syndrome experience intractable pain unresponsive to pharmacologic treatment. In this case, a brachia! plexus neurolysis was performed to address the patient's pain secondary to an enlarging left supraclavicular node. Guided under CT scan, 3 ml of 95% alcohol was injected in between the anterior and middle scalene muscles onto the trunks of the left brachia! plexus, affording immediate pain relief. Particular concerns of motor blockade, phrenic nerve palsy, stellate ganglion blockade, and bleeding did not occur. Therefore, brachia! plexus neurolysis can be safely done at a lower volume, without the above debilitating complications. It can be an option in relieving intractable upper extremity pain.
Brachial Plexus ; Thoracic Outlet Syndrome