This article outlines the clinical patterns, diagnostic strategies, and treatment principles for patients with inflammatory and autoimmune axonal neuropathies.

Parsonage-Turner syndrome, also called neuralgic amyotrophy, typically affects the brachial plexus, while involvement of the phrenic nerve is far less commonly documented. When present, it can compromise diaphragmatic function, producing breathlessness with activity, orthopnea, or, in more advanced presentations, respiratory failure. These features are easily mistaken for other cardiac or pulmonary conditions, which often delays correct diagnosis. A 51-year-old woman presented with a five-month course of worsening breathlessness on exertion and inability to breathe comfortably while supine. Cardiac work-up did not identify an underlying cause. Radiological assessment of the chest showed abnormal elevation of the right side of the diaphragm, with no associated pleural or lung tissue findings. Her history, obtained retrospectively, included an earlier episode of severe pain affecting the neck and left shoulder region, linked temporally to a stressful period. Ultrasound examination showed reduced diaphragmatic movement on both sides. Lung function testing showed a restrictive defect, and vital capacity fell markedly upon lying down compared with sitting. Electrophysiological testing identified a bilateral brachial plexopathy pattern, with phrenic nerve dysfunction predominating on the left side and additional denervation changes affecting other nerve territories, in keeping with neuralgic amyotrophy. She responded well to a combined respiratory rehabilitation approach incorporating ventilatory assistance, with subsequent improvement in her symptoms and lung volumes. While diaphragmatic involvement occurs infrequently in neuralgic amyotrophy, it carries meaningful clinical implications and merits consideration whenever dyspnea or orthopnea cannot be explained, especially after cardiac disease is excluded and imaging identifies a raised hemidiaphragm on either or both sides. The combination of a significant postural fall in vital capacity, suggestive diaphragmatic ultrasound findings, and electrophysiological data (nerve conduction studies/electromyography) supports the diagnosis. Prompt clinical suspicion of this etiology, when relevant, allows for faster initiation of respiratory rehabilitation and ventilatory support, if required.

Background/Objectives: Iatrogenic brachial plexus injuries (BPI) are known to occur following a host of surgeries, most often during procedures at the shoulder and cardiac procedures with a median sternotomy. The primary mechanisms include overstretching of the brachial plexus, direct trauma, or compression by hematoma or seroma. Our objective was to determine the pattern of iatrogenic BPI in patients referred to us for electrodiagnostic (EDX) evaluation. Methods: This is a review of 52 patients who were referred to our Neurodiagnostic Center for an iatrogenic BPI over a 16-year (9 July 2010-17 June 2026) period. All patients underwent a clinical examination and EDX studies. Results: The most frequent etiologies of the iatrogenic BPI were shoulder surgery in 28 [53.8%] patients and coronary artery bypass graft procedures with a median sternotomy in 13 [25.0%] patients. The topography of brachial plexus involvement was trunks in 22 (42.3%) and cords in 12 (23.1%). Ten (19.2%) patients had a pan-plexopathy, and the remaining eight (15.4%) patients had multiple sites involving the trunks, cords, and branches. The majority (48 [92.3%]) of patients sustained a stretch injury of the brachial plexus, and four (7.7%) sustained a direct injury. A total of 48 (92.3%) patients had reduced motor unit potential recruitment and/or increased polyphasic motor units on needle EMG, and a similar number had an absence of or low amplitude sensory nerve action potentials. Conclusions: Surgeons should take appropriate precautions to avoid BPI during many surgical procedures especially those of the shoulder and cardiac procedures with a median sternotomy. EDX studies are valuable in detecting and localizing an iatrogenic BPI as well as assessing reinnervation. Preoperative positioning limiting excessive shoulder abduction as well as intraoperative neuromonitoring are measures that may reduce the likelihood of an iatrogenic BPI.

Venous malformations (VMs) involving the brachial plexus are rare clinical entities that can mimic traumatic brachial plexus injuries. A 27-year-old male presented with progressive right upper limb weakness and numbness following an occupational fall with overhanging limb suggesting a traumatic tractional brachial plexus injury. However, magnetic resonance imaging (MRI) revealed an intramuscular VM in the subscapularis muscle which was compressing the cords of the brachial plexus. In view of difficult surgical access for removal associated with high risks of iatrogenic neurological injury, fluoroscopy-guided percutaneous bleomycin sclerotherapy was performed. Significant neurological recovery was observed post-intervention in conjunction with intensive rehabilitation. This case report outlines the diagnostic clues, management challenges, and functional outcomes of a right subscapularis intramuscular VM causing secondary compressive brachial plexopathy.

Radiation-induced lumbosacral plexopathy (RILSP) is an uncommon but potentially devastating complication of pelvic radiotherapy. Most published series involve gynecologic or colorectal malignancies, and limited data exist regarding plexus dosimetry and clinical presentation following contemporary prostate radiotherapy. We report two cases of suspected RILSP following prostate radiotherapy with detailed clinical, radiographic, and dosimetric correlation. Case 1 involved a 75-year-old man who underwent salvage pelvic radiotherapy with focal boost for recurrent prostate cancer. Four weeks after treatment completion, he developed progressive unilateral pain and weakness that evolved into bilateral neurologic decline and eventual wheelchair dependence despite lumbar decompression, vitamin B12 repletion, and empiric immunotherapy. Retrospective contouring of the lumbosacral plexus demonstrated focal high-dose exposure with a maximum dose (Dmax) of 72.3 Gy and direct overlap between the ≥70 Gy isodose line and the symptomatic plexus segment. Re-optimization reduced but did not eliminate hotspot overlap because of anatomic constraints. Case 2 involved a 65-year-old man treated with definitive pelvic radiotherapy and intensified androgen deprivation therapy for node-positive prostate cancer. He developed subacute bilateral proximal weakness and neuropathic pain one month after treatment completion. Electromyography raised concern for plexopathy, but no compressive lesion was identified. Retrospective plexus contouring demonstrated substantially lower exposure (Dmax 58.6 Gy) without measurable dose above 65 Gy or focal boost convergence. Following rehabilitation and discontinuation of enzalutamide, the patient experienced substantial neurologic recovery. These contrasting cases suggest that focal high-dose geometry to the lumbosacral plexus, particularly maximum point dose, may contribute to clinically significant neurologic toxicity beyond prescription dose alone. They also highlight the importance of trajectory-based multidisciplinary reassessment when clinical progression diverges from expected imaging findings. As prostate-specific membrane antigen positron emission tomography increasingly guides target expansion and focal dose escalation in prostate radiotherapy, routine plexus contouring and attention to maximum dose may become increasingly important to reduce the risk of severe neural morbidity.

Neurolymphomatosis, resulting from direct infiltration of the peripheral nervous system by lymphoma, is a rare presentation of aggressive B-cell lymphoma and an uncommon cause of brachial plexopathy. We report a 32-year-old man who presented with a painful swelling around the right shoulder followed by rapidly progressive weakness, complete sensory loss, and marked muscle wasting confined to the right upper limb, associated with a 10-kg unintentional weight loss over five months. Neurological examination localized the lesion to the right brachial plexus. Radiographs and computed tomography demonstrated an infiltrative soft-tissue lesion with cortical destruction of the proximal humerus. Magnetic resonance imaging of the shoulder and brachial plexus revealed diffuse thickening and T2/STIR hyperintensity of the distal divisions, cords, and branches of the brachial plexus, with contiguous infiltration of the humeral marrow, surrounding musculature, and adjacent soft tissues, strongly suggesting lymphomatous infiltration. Subsequent bone marrow biopsy confirmed Stage IV high-grade B-cell lymphoma with a high proliferative index. The patient was treated with R-CHOP chemoimmunotherapy and demonstrated significant clinical and neurological improvement on follow-up, with marked reduction in shoulder swelling and substantial recovery of motor and sensory function. This case highlights the importance of considering neurolymphomatosis in patients presenting with rapidly progressive painful brachial plexopathy, particularly when associated with shoulder swelling, constitutional symptoms, and infiltrative imaging findings. Early clinicoradiological recognition and prompt tissue diagnosis are essential for timely initiation of lymphoma-directed therapy and favorable neurological outcomes.

Foot drop, characterized by weakness of ankle and toe dorsiflexion, is a clinical sign rather than a diagnosis and requires accurate neuroanatomic localization. Potential sites of injury include the L5 nerve root, lumbosacral plexus, sciatic nerve, and common fibular (peroneal) nerve. Because lesions at different levels can produce overlapping motor and sensory findings, incorrect localization may lead to inappropriate diagnostic testing or treatment. This narrative review presents an anatomical, clinical, and electrodiagnostic framework for localizing neurogenic foot drop, with particular emphasis on distinguishing L5 radiculopathy, common fibular neuropathy at the fibular head, fibular-division predominant sciatic neuropathy, and lumbosacral plexopathy. High yield examination findings include ankle inversion and hip abduction strength, while electrodiagnostic localization relies on strategically selected sensory and motor nerve conduction studies and needle electromyography of muscles representing competing anatomic levels. The short head of the biceps femoris is particularly useful for distinguishing a proximal fibular division sciatic lesion from a typical common fibular neuropathy at the fibular head. Ultrasound and magnetic resonance imaging provide complementary structural information when focal nerve pathology is suspected. Integrating examination, electrodiagnostic testing, and targeted imaging provides a systematic approach to localization and guides subsequent etiologic evaluation and management.

Osteoid osteoma, a benign bone tumor, typically affects individuals under the age of 20. It is uncommon in children under five, with an incidence rate of 3%. It affects long bones and usually presents with nocturnal pain that can be treated with non-steroidal anti-inflammatory drugs. It is uncommon for osteoid osteoma to present with weakness. We present the case of a four-year-old boy exhibiting right arm weakness for a period of three months, along with floppiness and localized discomfort on the proximal arm. He was found to have proximal and distal muscle weakness in addition to widespread muscle atrophy involving the affected arm. A needle exam was inconclusive, but neurophysiological investigations revealed low compound muscle action potentials in several nerves on the affected arm. Brachial plexus and cervical spinal magnetic resonance imaging findings were normal. However, the child was found to have osteoid osteoma on the humerus of the affected side. All his symptoms, including muscle weakness, resolved after surgical treatment. Our case highlights the atypical presentation of this benign tumor.

Parsonage-Turner syndrome (PTS) is a rare neuromuscular disorder. Parvovirus B19 infection commonly causes a childhood exanthematous illness. Most previous case reports have documented unilateral parvovirus B19-associated PTS along with the systemic manifestations of parvovirus infection. This report highlights parvovirus B19-associated bilateral PTS without systemic manifestations. A 20-year-old gentleman was asymptomatic one and a half months ago when he developed an acute onset of excruciating right shoulder pain. After 7-10 days, he developed weakness and wasting in the right shoulder girdle. One month into the illness, he developed similar complaints in the left shoulder. At presentation, there was marked wasting of the bilateral deltoids, biceps, triceps, and the periscapular muscles. The motor power was Medical Research Council (MRC) grade 0/5 at the right shoulder, elbow, and wrist joints and grades 1/5 and 4/5 at the left shoulder and elbow joints, respectively. Bilateral hand grip was weak. The deep tendon reflexes were absent in both upper limbs. Touch, pain, and temperature sensation were lost by 50-60% over the right upper limb and by 30-40% over the left upper limb. Nerve conduction studies and electromyography (NCS-EMG) were suggestive of a bilateral pan-brachial plexopathy. The brachial plexus MRI showed short-tau inversion recovery (STIR) hyperintensity involving all the roots, divisions, and cords of the bilateral brachial plexus. Cerebrospinal fluid (CSF) revealed five cells and mildly elevated protein levels. Parvovirus B19 DNA was detected in both the CSF and serum. Serum parvovirus B19 IgG antibodies were positive, while IgM antibodies were negative. Thus, a diagnosis of parvovirus B19-associated bilateral PTS was made. He was given analgesics, gabapentin, nortriptyline, and duloxetine for pain. He received intravenous methylprednisolone (1000 mg) followed by oral steroids (1 mg/kg) along with intravenous immunoglobulin (IVIG) and physiotherapy. Clinicians must consider parvovirus B19-associated PTS as a possibility, especially when evaluating rapidly progressive bilateral brachial plexitis, even in the absence of typical viral prodromal symptoms such as fever, rash, and arthralgia.

Parsonage-Turner Syndrome (PTS) is a rare disorder of the brachial plexus typically characterized by acute shoulder and/or upper extremity pain, followed by muscle weakness. Though the specific etiology of PTS is unclear, numerous associations are cited in the literature, including after routine vaccinations. A previously healthy 22-year-old male developed subacute left upper extremity weakness and numbness < 24 hours following a routine Tdap (tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis) booster vaccination, later evolving into diffuse weakness and sharp shoulder pain. Electromyography (EMG) findings were suggestive of early PTS, and subsequent magnetic resonance imaging (MRI) of the brachial plexus confirmed mild inflammatory changes consistent with brachial plexitis. Over several months, the patient showed clinical improvement with conservative management. This case highlights a rare presentation of post-vaccination PTS, emphasizing the need for early recognition and supportive management. Although rare, clinicians should consider PTS in patients presenting with acute-onset upper extremity pain and weakness following vaccination.