The development of the neurocritical care specialty in China based on the analysis of neurocritical care unit volume and quality.

PURPOSE: Through three neurocritical care unit (NCCU) surveys in China, we tried to understand the development status of neurocritical care and clarify its future development. METHODS: Using a cross-sectional survey method and self-report questionnaires, the number and quality of NCCUs were investigated through three steps: administering the questionnaire, sorting the survey data, and analyzing the survey data. RESULTS: At the second and third surveys, the number of NCCUs (76/112/206) increased by 47% and 84%, respectively. The NCCUs were located in tertiary grade A hospitals or teaching hospitals (65/100/181) in most provinces (24/28/29). The numbers of full-time doctors (359/668/1337) and full-time nurses (904/1623/207) in the NCCUs increased, but the doctor-bed ratio and nurse-bed ratio were still insufficient (0.4:1 and 1.3:1). CONCLUSION: In the past 20 years, the growth rate of NCCUs in China has accelerated, while the allocation of medical staff has been insufficient. Although most NCCU hospital bed facilities and instruments and equipment tend to be adequate, there are obvious defects in some aspects of NCCUs.

Brain abscess from oral microbiota approached by metagenomic next-generation sequencing: A case report and review of literature.

BACKGROUND: Brain abscess is a serious and potentially fatal disease caused primarily by microbial infection. Although progress has been made in the diagnosis and treatment of brain abscesses, the diagnostic timeliness of pathogens needs to be improved. CASE SUMMARY: We report the case of a 54-year-old male with a brain abscess caused by oral bacteria. The patient recovered well after receiving a combination of metagenomic next-generation sequencing (mNGS)-assisted guided medication and surgery. CONCLUSION: Therefore, mNGS may be widely applied to identify the pathogenic microorganisms of brain abscesses and guide precision medicine.

Immune-mediated necrotizing myopathy: Report of two cases.

BACKGROUND: Immune-mediated necrotizing myopathy is a rare autoimmune myopathy characterized by muscle weakness and elevated serum creatine kinase, with unique skeletal muscle pathology and magnetic resonance imaging features. CASE SUMMARY: In this paper, two patients are reported: One was positive for anti-signal recognition particle antibody, and the other was positive for anti-3-hydroxy-3-methylglutaryl coenzyme A reductase antibody. CONCLUSION: The clinical characteristics and treatment of the two patients were analysed, and the literature was reviewed to improve the recognition, diagnosis, and treatment of this disease.

Postoperative cerebral hemorrhage death in a patient with secondary hyperparathyroidism: a report of one case and literature review.

Secondary Hyperparathyroidism (SHPT) is a common complication of end-stage renal disease (ESRD), and parathyroid surgery (PTX) is an effective way to treat patients with severe SHPT. ESRD has multiple associations with cerebrovascular diseases. For example, the incidence of stroke in patients with ESRD is 10 times higher than that in the general population, the risk of death after acute stroke is three times higher, and the risk of hemorrhagic stroke is significantly higher. High/low serum calcium, high PTH, low serum sodium, high white blood cell count, previous occurrences of cerebrovascular events, polycystic kidney disease (as a primary disease), and the use of anticoagulants are independent risk factors for hemorrhagic stroke in hemodialysis patients with uremia. The risk of stroke in patients who undergo PTX decreases significantly in the second year of follow-up and persist thereafter. However, studies on the risk of perioperative stroke in SHPT patients are limited. After undergoing PTX, the PTH levels in SHPT patients drop suddenly, they undergo physiological changes, bone mineralization increases, and calcium in the blood gets redistributed, often accompanied by severe hypocalcemia. Serum calcium might influence the occurrence and development of hemorrhagic stroke at various stages. To prevent bleeding from the operated area, the use of anticoagulants after surgery is reduced in some cases, which often decreases the frequency of dialysis and increases the quantity of fluid in the body. An increase in the variation in blood pressure, instability of cerebral perfusion, and extensive intracranial calcification during dialysis promote hemorrhagic stroke, but these clinical problems have not received enough attention. In this study, we reported the death of an SHPT patient who suffered a perioperative intracerebral hemorrhage. Based on this case, we discussed the high-risk factors for perioperative hemorrhagic stroke in patients who undergo PTX. Our findings might help in the identification and early prevention of the risk of profuse bleeding in patients and provide reference for the safe performance of such operations.

The development of neurocritical care in China from the perspective of evaluation and treatment of critical neurological diseases.

Objective: To understand the varieties, evaluation, treatment, and prognosis of severe neurological diseases using the third NCU survey in China. Design: A cross-sectional questionnaire study. The study was completed in three main steps: filling in the questionnaire, sorting out the survey data, and analyzing the survey data. Results: Of 206 NCUs, 165 (80%) provided relatively complete information. It was estimated that 96,201 patients with severe neurological diseases were diagnosed and treated throughout the year, with an average fatality rate of 4.1%. The most prevalent severe neurological disease was cerebrovascular disease (55.2%). The most prevalent comorbidity was hypertension (56.7%). The most prevalent complication was hypoproteinemia (24.2%). The most common nosocomial infection was hospital-acquired pneumonia (10.6%). The GCS, APACHE II, EEG, and TCD were the most commonly used (62.4-95.2%). The implementation rate of the five nursing evaluation techniques reached 55.8-90.9%. Routinely raising the head of the bed by 30°, endotracheal intubation and central venous catheterization were the mostprevalent treatment strategies (97.6, 94.5, and 90.3%, respectively). Traditional tracheotomy, invasive mechanical ventilation and nasogastric tube feeding (75.8, 95.8, and 95.8%, respectively) were more common than percutaneous tracheotomy, non-invasive mechanical ventilation and nasogastric tube insertion (57.6, 57.6, and 66.7%, respectively). Body surface hypothermia brain protection technology was more commonly used than intravascular hypothermia technology (67.3 > 6.1%). The rates of minimally invasive hematoma removal and ventricular puncture were only 40.0 and 45.5%, respectively. Conclusion: In addition to traditional recognized basic life assessment and support technology, it is necessary to the use of promote specialized technology for neurological diseases, according to the characteristics of critical neurological diseases.

Correlative increasing expressions of KIF5b and Nav1.7 in DRG neurons of rats under neuropathic pain conditions.

Nav1.7, one of tetrodotoxin-sensitive voltage-gated sodium channels, mainly expressed in the small diameter dorsal root ganglion (DRG) neurons. The expression and accumulation on neuronal membrane of Nav1.7 increased following peripheral tissue inflammation or nerve injury. However, the mechanisms for membrane accumulation of Nav1.7 remained unclear. We report that KIF5b, a highly expressed member of the kinesin-1 family in DRGs, promoted the translocation of Nav1.7 to the plasma membrane in DRG neurons of the rat. Following nociceptive behaviors in rats induced by peripheral spared nerve injury (SNI), synchronously increased KIF5b and Nav1.7 expressions were observed in DRGs. Immunohistochemistry staining demonstrated the co-expressions of KIF5b and Nav1.7 in the same DRG neurons. Immunoprecipitation experiments further confirmed the interactions between KIF5b and Nav1.7. Moreover, intrathecal injections of KIF5b shRNA moderated the SNI-induced both mechanical and thermal hyperalgesia. The rescued analgesic effects also alleviated SNI-induced anxiety-like behaviors. In sum, KIF5b was required for the membrane localizations of Nav1.7, which suggests a novel mechanism for the trafficking of Nav1.7 involved in neuropathic pain.

Morphological investigations of endomorphin-2 and spinoparabrachial projection neurons in the spinal dorsal horn of the rat.

It has been proved that endomorphin-2 (EM2) produced obvious analgesic effects in the spinal dorsal horn (SDH), which existed in our human bodies with remarkable affinity and selectivity for the µ-opioid receptor (MOR). Our previous study has demonstrated that EM2 made synapses with the spinoparabrachial projection neurons (PNs) in the SDH and inhibited their activities by reducing presynaptic glutamate release. However, the morphological features of EM2 and the spinoparabrachial PNs in the SDH have not been completely investigated. Here, we examined the morphological features of EM2 and the spinoparabrachial PNs by using triple fluorescence and electron microscopic immunohistochemistry. EM2-immunoreactive (-ir) afferents directly contacted with the spinoparabrachial PNs in lamina I of the SDH. Immunoelectron microscopy (IEM) were used to confirm that these contacts were synaptic connections. It was also observed that EM2-ir axon terminals contacting with spinoparabrachial PNs in lamina I contained MOR, substance P (SP) and vesicular glutamate transporter 2 (VGLUT2). In lamina II, MOR-ir neurons were observed to receive direct contacts from EM2-ir varicosities. The synaptic connections among EM2, MOR, SP, VGLUT2, and the spinoparabrachial PNs were also confirmed by IEM. In sum, our results supply morphological evidences for the analgesic effects of EM2 on the spinoparabrachial PNs in the SDH.

Herpes simplex virus type 2 encephalitis in a child with chronic progressive white matter lesions: A case report.

RATIONALE: This case is a rare manifestation of central nervous system infection of Herpes simplex virus (HSV)-2. Due to few studies in China, it provides a pathological basis for further diagnosis and treatment of HSV-2. PATIENT CONCERNS: We describe a patient with HSV-2 virus infection who was diagnosed with HSV-2 encephalitis in a Chinese patient. DIAGNOSIS: Based on brain biopsy and pathological findings, the patient was diagnosed with HSV-2 encephalitis. INTERVENTIONS: Hormone and antiviral therapy were given. OUTCOME: The patient eventually died. LESSONS: The diagnosis and differential diagnosis of the disease is very difficult. Its differential diagnosis include cerebrovascular disease, bacteria or fungi and other viral infection of the brain.

Various BDNF administrations attenuate SPS-induced anxiety-like behaviors.

Post-traumatic stress disorder (PTSD) has become epidemic following severely stressful incidents. Previous studies have shown that brain-derived neurotrophic factor (BDNF) has anxiolytic effects on various anxiety or depression disorders including PTSD. However, the detailed mechanisms of BDNF for treating PTSD were rarely investigated. In the current study, single-prolonged stress (SPS) was used as an animal model recapitulating specific aspects for a PTSD-like phenotype. The effects of BDNF on SPS-induced anxiety-like behaviors were investigated. We showed that the levels of BDNF in the cerebro-spinal fluid (CSF) were significantly reduced after the rats experienced SPS. The SPS-induced reductions of percentages of time spent in the central area to total time in the open field test, were dose-dependently mitigated after BDNF intracerebroventricular (i.c.v.) injections. BDNF i.c.v. administration also dose-dependently increased the preference of the light box in the light-dark box test. Both expressions of tyrosine kinase receptor B (TrkB) protein and mRNA in the prefrontal cortex (PFC) and amygdala were significantly increased after SPS challenges. BDNF i.c.v. administration attenuated these compensatory increases of TrkB. At last, the anxiolytic effects of BDNF on SPS model were also observed by using other two injection methods. These results inspired us to study that different administrations of BDNF were used in patients with PTSD in the future, in-depthly.

Cerebral hemodynamic changes assessment by transcranial doppler ultrasound in patients with acute cerebral infarction before and after treatment with butylphthalide.

To assess cerebral hemodynamic changes by transcranial doppler ultrasound in patients with acute cerebral infarction before and after treatment with butylphthalide, A total of 90 patients with acute cerebral infarction admitted to our hospital from January 2019 to January 2020 were selected and equally divided into the control group and the experimental group according to the order of admission. The control group was treated with conventional treatment, while the experimental group was additionally given butylphthalide drug treatment. The experimental group obtained better hemodynamic indexes as compared with the control group (P<0.05). The experimental group yielded a notably higher total clinical effective rate after treatment in contrast with the control group (P<0.05). After treatment, the serum indexes of the experimental group were evidently lower than those of the control group (P<0.05). After treatment, a remarkably lower NIHSS score of the experimental group than the control group was observed (P<0.05). The BI index score of the experimental group after treatment was considerably higher than that of the control group (P<0.05). After treatment, the MMSE score in the experimental group was significantly higher than it was in the control group (P<0.05). The treatment of butylphthalide in patients with acute cerebral infarction can effectively improve the clinical symptoms of the patients and the cerebral hemodynamics of the patients tested by TCD found that this treatment yields an excellent therapeutic effect and is worthy of promotion and application.

Case Report: Stress-Induced Childhood-Onset Neurodegeneration With Ataxia-Seizures Syndrome Caused by a Novel Compound Heterozygous Mutation in ADPRHL2.

ADPRHL2 gene mutations have been demonstrated as the cause of stress-induced childhood-onset neurodegeneration with variable ataxia and seizures (CONDSIAS), an autosomal recessive genetic disorder characterized by an abnormal gait, intellectual disability, seizures, ataxia, other nervous system degenerative diseases, and axonal sensorimotor neuropathy. Since first reported in 2018, ADP-ribosylhydrolase like 2 (ADPRHL2) gene mutations in previous cases were all diallelic homozygous. Here, we report a case of CONDSIAS with a novel compound heterozygous mutation in the ADPRHL2 gene. This patient is presented with autonomic nervous dysfunction manifested as polyuria, gastrointestinal disturbance, and sinus arrhythmia, which may be considered as new clinical manifestations in addition to the above classical manifestations. Muscle biopsy revealed myogenic lesions, which is a previously unreported feature.

Anti-neuron antibody syndrome: clinical features, cytokines/chemokines and predictors.

BACKGROUND: Neuroimmunology is a rapidly expanding field, and there have been recent discoveries of new antibodies and neurological syndromes. Most of the current clinical studies have focused on disorders involving one specific antibody. We have summarized a class of antibodies that target common neuronal epitopes, and we have proposed the term "anti-neuron antibody syndrome" (ANAS). In this study, we aimed to clarify the clinical range and analyse the clinical features, cytokines/chemokines and predictors in ANAS. METHODS: This was a retrospective cohort study investigating patients with neurological manifestations that were positive for anti-neuron antibodies. RESULTS: A total of 110 patients were identified, of which 43 patients were classified as having autoimmune encephalitis (AE) and the other 67 were classified as having paraneoplastic neurological syndrome (PNS). With regards to anti-neuron antibodies, 42 patients tested positive for anti-N-methyl-D-aspartate receptor (NMDAR) antibody, 19 for anti-Hu, 14 for anti-Yo and 12 for anti-PNMA2 (Ma2). There were significant differences between the ANAS and control groups in serum B cell-activating factor (BAFF) levels and in cerebrospinal fluid (CSF) C-X-C motif chemokine10 (CXCL10), CXCL13, interleukin10 (IL10), BAFF and transforming growth factor ß1 (TGFß1) levels. Predictors of poor outcomes included having tumours (P = 0.0193) and having a chronic onset (P = 0.0306), and predictors of relapses included having lower levels of CSF BAFF (P = 0.0491) and having a larger ratio of serum TGFß1/serum CXCL13 (P = 0.0182). CONCLUSIONS: Most patients with ANAS had a relatively good prognosis. Having tumours and a chronic onset were both associated with poor outcomes. CSF BAFF and the ratio of serum TGFß1/serum CXCL13 were associated with relapses.

Selenium modulated gut flora and promoted decomposition of methylmercury in methylmercury-poisoned rats.

INTRODUCTION: Selenium plays important roles in antagonizing the toxicity of methylmercury. The underlying mechanism for the antagonism between Se and MeHg is still not fully understood. OBJECTIVE: The role of gut flora against the toxicity of environmental contaminants is receiving more and more attention. The objective of this study was to investigate the role of Se against MeHg-poisoning in the modulation of gut flora and the decomposition of MeHg. METHODS: MeHg-poisoned rats were treated with sodium selenite every other day for 90 days. Fecal samples were collected on Day 8, 30, 60 and 90. Gut flora in feces was determined using 16S rRNA gene profiling, and the concentrations of Se and total mercury (THg) were measured by ICP-MS, and the concentration of MeHg was measured by CVAFS. RESULTS: Gut flora at both the ranks of phylum and genus in the MeHg-poisoned rats after Se treatment was modulated towards that in the control group, suggesting the restoration of the profile of gut flora. Increased THg was found in fecal samples after Se treatment on day 30. The percentage of MeHg (of total mercury) in the MeHg-poisoned group was in the range of 81-105% while it was 65-84% in the Se treatment group on different days, suggesting the increased decomposition of MeHg in MeHg-poisoned rats after Se treatment. CONCLUSIONS: This study suggests that MeHg poisoning damaged the abundance of gut flora and decreased their capacity for the decomposition of MeHg. After Se treatment, the abundance of gut flora was partially restored and the decomposition and excretion of MeHg was enhanced. These findings suggest that the modulation of gut flora may be one way to promote the health status in MeHg-poisoned rats and possibly in human beings.

Vascular endothelial growth factor improves the cognitive decline of Alzheimer's disease via concurrently inducing the expression of ADAM10 and reducing the expression of ß-site APP cleaving enzyme 1 in Tg2576 mice.

Alzheimer's disease (AD) is primarily characterized by the production and deposit of ß-amyloid protein (Aß) in ß-amyloid plaques (APs). On this basis, we investigated whether vascular endothelial growth factor (VEGF), a growth factor with important neuroprotective activity, may provide a therapeutic opportunity for treating AD. We initially found that the expression and production of VEGF was downregulated in the brains of Tg2576 mice during the course of AD development and progression. Restoring VEGF in the brains of Tg2576 mice antagonized the production and deposit of Aß in Tg2576 mice. The addition of VEGF concurrently increased the expression of disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) and decreased the expression of ß-site APP cleaving enzyme 1 (BACE1), which contributes to the enhanced clearance of Aß in vivo. By decreasing the production and deposit of Aß, VEGF improved the cognitive decline of Tg2576 mice. These observations provide a novel implication for VEGF as a therapeutic approach for the treatment of AD.

Corrigendum: Clinical Characteristics and Predictors of Outcome for Onconeural Antibody-Associated Disorders: A Retrospective Analysis.

[This corrects the article DOI: 10.3389/fneur.2017.00584.].

Retrospective study of paraneoplastic neurological syndromes in a Chinese Han population from Shandong, East China.

OBJECTIVE: To analyze the clinical features, diagnostic strategies and therapeutic methods associated with paraneoplastic neurological syndromes. METHODS: A retrospective study of paraneoplastic neurological syndromes was performed at a single center in Shandong, East China. The medical records and follow-up data of 28 patients were intensively reviewed between February 2011 and December 2014. RESULTS: Twenty-four (85.7%) patients experienced subacute or chronic onset of disease, and the most common symptoms reported were mild myasthenia and paresthesias. Twenty-five (89.3%) patients presented nervous system lesions prior to occult tumors, and the median time frame between paraneoplastic neurological syndromes onset and the diagnosis of a tumor was 15 weeks. Sensorimotor neuropathy, Lambert-Eaton myasthenic syndrome and limbic encephalitis were the three most common neurological syndromes reported. Elevated serum tumor markers were observed in 44.0% of patients, while 40.7% of patients were positive for onconeural antibodies. Tumors were detected in 21 (75.0%) patients after repeated whole-body screening, and lung carcinomas were the most common primary tumor detected. Seventeen patients received anti-tumor or immunological therapy, and clinical symptoms were relieved in 13 (76.5%) of these patients. CONCLUSIONS: In the majority of paraneoplastic neurological syndromes patients, the onset of disease is subacute or chronic with mild clinical symptoms. Nervous system lesions usually occur prior to occult tumors with complicated and various clinical manifestations. Neither tumor markers nor onconeural antibodies exhibit a high rate of occurrence, while repeated whole-body screening is helpful in identifying occult tumors. Early diagnosis and treatment are crucial to these patients.

Clinical Characteristics and Predictors of Outcome for Onconeural Antibody-Associated Disorders: A Retrospective Analysis.

Objective: To describe and analyze the clinical characteristics, laboratory data, management, and outcome of patients with onconeural antibody-associated disorders (OAAD) and identify predictors for poor outcome. Methods: This was a retrospective review of all patients with potential OAAD, who were hospitalized in Jinan General Hospital between September 2009 and July 2017. We clarified the diagnosis, collected comprehensive information and categorized patients into three groups: paraneoplastic neurological disorders (PNDs), autoimmune encephalitis (AE), and possible OAAD. Within the three groups, we analyzed a range of clinical and laboratory parameters and used univariate and multivariate regression analysis to identify predictors for poor outcome [modified Rankin Scale (mRS) = 3-6]. Results: From 158 patients, we identified 70 who fulfilled the criteria for OAAD, including 44 men (62.9%) and 26 women (37.1%). There were 38 patients (54.3%) in the PNDs group, 14 patients (20%) in the AE group, and 18 patients (25.7%) in the possible OAAD group. After the last follow-up, 14 (36.8%), 9 (64.2%), and 12 (66.7%) had a good outcome (mRS = 0-2). However, 6 (15.8%), 2 (14.3%), and 3 (16.7%) died, respectively. Univariate analysis showed that duration prior to the hospital (p = 0.0224) and urinary incontinence/retention (p = 0.0043) were associated with poor outcome (mRS = 3-6). After multivariate regression analysis, urinary incontinence/retention (p = 0.0388) and an immunocompromised state (p = 0.0247) remained as significant factors for poor outcome. Conclusion: Urinary incontinence/retention and an immunocompromised state represent significant predictors of a worse prognosis for patients with OAAD. By contrast, the results showed that [corrected] cerebrospinal fluid analysis, serum autoantibodies and tumor markers, [corrected] the function of crucial organs, electrophysiology, and radiological findings were not associated with a poor outcome.

Endothelial Progenitor Cells for Ischemic Stroke: Update on Basic Research and Application.

Ischemic stroke is one of the leading causes of human death and disability worldwide. So far, ultra-early thrombolytic therapy is the most effective treatment. However, most patients still live with varying degrees of neurological dysfunction due to its narrow therapeutic time window. It has been confirmed in many studies that endothelial progenitor cells (EPCs), as a kind of adult stem cells, can protect the neurovascular unit by repairing the vascular endothelium and its secretory function, which contribute to the recovery of neurological function after an ischemic stroke. This paper reviews the basic researches and clinical trials of EPCs especially in the field of ischemic stroke and addresses the combination of EPC application with new technologies, including neurovascular intervention, synthetic particles, cytokines, and EPC modification, with the aim of shedding some light on the application of EPCs in treating ischemic stroke in the future.

Transcriptome Sequencing Reveals Astrocytes as a Therapeutic Target in Heat-Stroke.

Heat-stroke is a serious form of hyperthermia with high mortality, and can induce severe central nervous system disorders. The neurovascular unit (NVU), which consists of vascular cells, glial cells, and neurons, controls blood-brain barrier (BBB) permeability and cerebral blood flow, and maintains the proper functioning of neuronal circuits. However, the detailed function of each BBB component in heat-stroke remains unknown. In order to interpret alterations caused by heat stress, we performed transcriptome comparison of neuron and astrocyte primary cultures after heat treatment. Differentially-expressed genes were then selected and underwent Gene Ontology annotation and Kyoto Encyclopedia of Genes and Genomes pathway analysis. Gene-act networks were also constructed, and the expression of pivotal genes was validated by quantitative PCR, as well as single-cell qPCR in heat-stroke rats. Our work provides valuable information on the transcriptional changes in NVU cells after heat stress, reveals the diverse regulatory mechanisms of two of these cellular components, and shows that a cell-type-specific approach may be a promising therapeutic strategy for heat-stroke treatments.

A case report of hereditary neuropathy with liability to pressure palsies accompanied by type 2 diabetes mellitus and psoriasis.

RATIONALE: Hereditary neuropathy with liability to pressure palsy (HNPP) is an episodic, multifocal neuropathy, with a typical clinical presentation of recurrent transient pressure palsies, which is induced by a PMP22 deletion. Another neuropathy caused by a PMP22 duplication is Charcot-Marie-Tooth disease type 1A (CMT1A). PMP22 is a gene coding a protein called peripheral myelin protein 22 (PMP22), which plays an essential role in the formation and maintenance of compact myelin. Coexistence of type 2 diabetes mellitus (T2DM) and CMT1A has been reported in many work, however HNPP patients with T2DM are rare, and comorbidity of HNPP and psoriasis has not been reported previously. Electrophysiological features of HNPP has been found progressing with aging. Patient concerns: Here we present a 20-year-old man who exhibited lower extremity weakness and foot drop as the initial manifestation. DIAGNOSES: HNPP was diagnosed on the basis of clinical features, positive sural nerve biopsy findings, and genetic testing results. Moreover, physical examination, blood/urine glucose test, and diabetes-related autoantibodies investigations demonstrated that he had psoriasis and T2DM. The electrophysiological manifestations revealed profound demyelinating injuries and axonal injuries in distal peripheral nerves and facial nerves, which were more severe than general HNPP cases. INTERVENTIONS: The young patient was treated with continuous subcutaneous insulin infusion and blood glucose monitoring, and then transferred to oral acarbose therapy. The psoriatic lesions were treated with calcipotriol ointment. OUTCOMES: In the follow-up, the right leg weakness was alleviated, and his gait was improved. LESSONS: The findings indicate that diabetes mellitus may have an impact on the severity of HNPP. Physicians should consider that worsening of symptoms might result from newly diagnosed diabetes mellitus while treating patients with HNPP.