Thrombocytosis is defined by guidelines as a platelet count of 450 × 103/μL or greater. It most often results from secondary causes and should resolve with treatment of the underlying condition. Primary thrombocytosis in adults is most commonly due to myeloproliferative neoplasms, including essential thrombocythemia. Thrombocytosis may be identified incidentally in asymptomatic patients or when performing blood tests to investigate symptoms or signs that could indicate microvascular conditions (eg, headaches, paresthesia, erythromelalgia), splenomegaly, thrombosis, and hemorrhage, which are presenting features of essential thrombocythemia. A repeat complete blood cell count with differential and peripheral blood smear should be performed to confirm persistent thrombocytosis and assess other blood cell lines for findings suggestive of myeloproliferative neoplasms. Additional testing, including C-reactive protein levels and iron studies with ferritin levels, should be performed based on history and examination findings. If essential thrombocythemia is suspected in patients with persistent thrombocytosis without an identified cause, testing for Janus kinase 2 gene sequence variations should be performed and, if negative, testing for calreticulin and myeloproliferative leukemia gene sequence variations; a bone marrow biopsy should also be performed. The revised International Prognostic Score of Thrombosis for Essential Thrombocythemia should be calculated to stratify thrombosis risk and guide management, including when to use low-dose aspirin and cytoreductive therapy. Cardiovascular risk factors should also be addressed. Hydroxyurea is the first-line agent in cytoreductive therapy. No treatments have been shown to increase survival or prevent progression to myelofibrosis or leukemia in patients with essential thrombocythemia.

Neurenteric cysts (NCs), also known as endodermal cysts, are rare congenital lesions of endodermal origin. They were thought to originate from a failure of dissolution of the neurenteric canal between the notochord and endoderm during the third week of embryogenesis. The primary clinical symptoms differ from focal pain to paresthesia and weakness based on the cyst's location. This study presents a case of intradural extramedullary NC of the spine at the cervical level. A 10-year-old boy was referred to the hospital, with neck pain and weakness in his left hand. Imaging studies revealed fusion of cervical vertebrae at the levels of C3-C4 and C5-C6. On MRI, a cystic lesion in the intradural extramedullary region compressing the cord was evident. As the preferred treatment option, surgical total resection was completed through the posterior approach, and the definitive diagnosis was made based on the histochemical analysis. NC is a rare lesion and should be kept in mind as a differential diagnosis. Surgical intervention, particularly total resection, frequently improves the sensory and motor deficits associated with NC and is the treatment of choice.

Beaded lizards (Heloderma spp) are venomous lizards capable of inflicting local and systemic envenoming. An exotic pet collector presented with a reportedly prolonged bite by a presumed Guatemalan beaded lizard (Heloderma charlesbogerti). He reported immediate symptoms of envenoming, including severe pain, paresthesia, local swelling, dizziness, and nausea. Follow-up assessments conducted over a period of up to 4 y revealed a persistent boutonnière deformity of the right middle finger. This case report describes envenomation caused by the uncommonly documented bite of a beaded lizard (Heloderma spp) that was presumed by the patient to be the rare Guatemalan beaded lizard (H charlesbogerti). It illustrates the risks of long-term sequelae that may result from noncompliance with treatment after a helodermatid bite and also reemphasizes concerns about the underground sale of rare, endangered wildlife. Beaded lizard bites can inflict severe local envenomation and potentially cause permanent hand deformities. Proper referral and follow-up are essential to prevent long-term sequelae.

Meralgia paresthetica is a sensory mononeuropathy of the lateral femoral cutaneous nerve that remains frequently underdiagnosed despite its characteristic clinical presentation. Burning pain, paresthesia, and numbness over the anterolateral thigh may mimic hip, lumbar, or pelvic disorders, contributing to diagnostic delay. Imaging has gained increasing relevance in the evaluation of meralgia paresthetica, both for confirming neuropathy and for identifying contributory anatomical factors. High-resolution ultrasound enables direct visualization of the lateral femoral cutaneous nerve, characterization of its anatomical variants, and detection of focal changes at typical entrapment sites. Quantitative ultrasound parameters, particularly cross-sectional area, provide additional objective information and may help distinguish symptomatic nerves from normal variants, while elastography offers preliminary insight into chronic stiffness alterations. Magnetic resonance imaging complements ultrasound by allowing assessment of deeper nerve segments and by differentiating intrinsic signal abnormalities from extrinsic compression. Advanced techniques such as diffusion tensor imaging, although still investigational for this small sensory nerve, may eventually provide microstructural information beyond the capabilities of conventional sequences. This review summarizes current knowledge on the anatomy of the lateral femoral cutaneous nerve, outlines qualitative and quantitative ultrasound approaches, and discusses how multimodal imaging can support a more comprehensive and confident evaluation of patients with meralgia paresthetica.

A 68-year-old woman with cervical cancer and pulmonary metastases presented with limb paresthesia and pain one week after chemotherapy. Whole-body bone scintigraphy performed to evaluate for bone metastases revealed rib metastases, along with poor visualization of the right distal lower extremity, raising suspicion for possible arterial flow obstruction in the right lower limb. Further imaging confirmed extensive thrombosis in the right common iliac artery and its distal branches. This case suggests that decreased uptake in the skeletal structures and surrounding soft tissues on whole-body bone scintigraphy may indicate a risk of arterial thrombosis.

A 71-year-old woman presented with acute muscle weakness and paresthesia in her left lower limb with the preceding back pain and impaired deep sensation. Although initial brain and spinal MRI were normal, follow-up spinal MRI confirmed the left-sided posterior lesion at T10 to T12 vertebral level, leading to the diagnosis of posterior spinal artery (PSA) infarction. PSA infarction with unilateral lumbar spinal cord lesion is rare and can mimic cerebral stroke. Clinicians should check for back pain and deep sensation in cases with symptoms of acute unilateral lower limb on suspicion of PSA infarction, even when initial MRI is normal.

Background: Achondroplasia, the most common genetic dwarfism caused by the FGFR3 mutation (autosomal dominant, 80% de novo), results in a disproportionately short stature. Thoracolumbar kyphosis (TLK), combined with characteristic spinal canal stenosis, increases the risk of symptomatic compression, yet the literature lacks clear thresholds for symptom onset or progressive deformity angles. Methods: A 16-year-old female with achondroplasia presented with rapidly progressive kyphosis despite conservative management (bracing and therapy). Over six months, she developed neurogenic claudication; bilateral leg pain; weakness; and paresthesia that worsened with standing/walking, which was relieved by flexion/sitting. Imaging demonstrated surgical-threshold kyphosis with progressive spinal misalignment. Her symptoms indicated compressive myeloradiculopathy from lumbar stenosis, critical given achondroplasia's congenitally narrowed canal and heightened neurologic vulnerability. Results: Staged surgery planned: Posterior fusion T6-L4 with pedicle screws and then extensive decompression (laminectomy/foraminotomy T11-L3), L1 corpectomy with expandable titanium cage, and Ponte osteotomies. Intraoperative complications included a malpositioned left T10 screw breaching the anterior/lateral cortex near the aorta, requiring urgent revision. Postoperatively: Neurogenic bladder, wound leakage, and E. coli urinary tract infection (UTI) with fever (treated with IV antibiotics). After infection resolution, definitive surgery removed the malpositioned screw and completed decompression, corpectomy, cage placement, bone grafting, and osteotomies, successfully resolving neurological symptoms. However, 13 cm trunk lengthening caused severe functional impairment-disproportionately short arms prevented independent toileting and dressing. Left arm lengthening via external fixation restored partial function. At 2.5-year follow-up, there was solid fusion, no neurological deficits, and improved quality of life. Conclusions: Surgery addresses severe TLK, vertebral wedging, and neurogenic claudication in achondroplasia. Vertebral column resection effectively corrects TLK and neurological deficits but carries a high complication risk. This should be reserved for severe TLK with hypoplastic vertebrae, performed by experienced surgeons. Critically, correction magnitude must preserve limb-trunk proportions to prevent functional disability, as excessive lengthening may necessitate additional limb procedures for independence restoration.

(1) Background: Creutzfeldt-Jakob disease (CJD) is a progressive neurodegenerative disorder, characterized by cognitive decline, and motor and psychiatric symptoms; it primarily affects the central nervous system; however, peripheral nervous system involvement has rarely been described, particularly as an atypical presentation. (2) Methods: A 78-year-old Caucasian man, a retired farmer with no family history of neurological disease, presented with diarrhea followed by progressive lower limb weakness, which eventually evolved into encephalopathy and generalized areflexia. An initial diagnosis of inflammatory neuropathy was considered; the diagnostic assessment included blood and cerebrospinal fluid testing, a CT whole body scan, brain MRI, neuropsychological testing, electroencephalography, a nerve conduction study and electromyography. (3) Results: Neurophysiological studies demonstrated an acute asymmetrical sensorimotor, predominantly axonal polyneuropathy, initially suggestive of an axonal form of inflammatory polyradiculoneuritis. This pattern was confirmed on follow-up neurophysiological assessment performed three weeks later. Unexpectedly, the diagnostic course ultimately led to a diagnosis of sporadic Creutzfeldt-Jakob disease, confirmed by post-mortem neuropathological examination. Based on these findings, we conducted a literature review to summarize the current evidence on CJD-related neuropathy. (4) Conclusions: Our case emphasizes the importance of maintaining clinical suspicion for CJD even in patients presenting with progressive lower limb weakness and suggests that peripheral neuropathy may be concomitant or even precede the CNS manifestations. Careful consideration is required to avoid misdiagnosis of inflammatory neuropathy in the context of neurodegenerative diseases such as CJD.