BACKGROUND: Conus medullaris infarction (CMI) is a rare vascular phenomenon that has been scarcely reported in the literature. While previous studies have described the clinical and radiological features of CMI, little attention has been paid to its associated neurophysiological findings.
METHODS: We present a case of idiopathic CMI and its neurophysiological findings, then present our findings from a systematic review of other reports of CMI with neurophysiological features found via PubMed search.
RESULTS: Nine articles describing ten cases of CMI with associated neurophysiological data were found, in addition to our case. Out of all 11 cases, 7 cases (64%) had absent F-waves on the first nerve conduction study (NCS) performed as early as 4 h after onset, 5 of whom demonstrated reappearance of F-waves on subsequent follow-up NCS. Seven patients (64%) had diminished compound muscle action potentials (CMAPs), which was usually detectable on NCS performed between day 8 and day 18 of onset. None of them showed recovery of CMAPs in follow-up studies. Four patients (36%) had absent H-reflexes and two patients (18%) had sensory abnormalities. Electromyography (EMG) was reported in seven patients (64%), showing reduced recruitment as early as day 1 of onset, and denervation potentials as early as 4 weeks after onset.
CONCLUSIONS: Absent F-waves and diminished CMAPs are the most common NCS abnormalities in CMI. Absent F-waves are detectable very early but tend to recover on subsequent NCS, while diminished CMAPs are detectable later but do not seem to resolve. Further research to determine the utility of neurophysiological studies in CMI diagnosis and prognostication is needed.

BACKGROUND: Generalized joint hypermobility (GJH) can be the result of several hereditary connective tissue disorders, especially Ehlers-Danlos syndrome. Cerebrovascular manifestations are among the most common complications in this disorder, and understanding their extent can help better diagnosis and prevention of hazardous events. We investigated visual evoked potential (VEP) changes in patients with GJH and compared them with healthy individuals.
METHODS: Our case-control study included 90 patients who fulfilled the Beighton score (B score) for joint hypermobility and other 90 healthy participants. All of them went under VEP study, and the amplitude and latency of the evoked potential (P100) were compared to each other.
RESULTS: The Case group had significantly higher B score (7.18 ± 0.967 vs. 1.18 ± 0.712), P100 latency (110.23 ± 6.64 ms vs. 100.18 ± 4.273 ms), and amplitude (6.54 ± 1.26 mv vs. 6.50 ± 1.29 mv) compared with the Control group, but the difference was only significant regarding B score, and P100 latency (p-value <.0001). Moreover, both latency and amplitude of P100 had significantly positive correlations with the B score in the Case group (p-value <.0001), but such correlations were not found in the Control group (p-value = .059).
CONCLUSIONS: Our study could reveal VEP changes, especially significant P100 latency in GJH patients without previous neurologic or musculoskeletal disorders. Whether these changes are due to GJH itself or are predictive of inevitable neurologic disease or visual pathway involvement, particularly Multiple Sclerosis needs further investigation with longer follow-up periods.

Sjogren\'s syndrome is an inflammatory disease affecting many systems. We report a Sjogren case with the presenting feature of an acute motor-predominant polyneuropathy resembling Guillain-Barre syndrome. Upon further investigation, it was found that the patient had sicca symptoms for months. Scrupulous history should be taken to prevent a missed diagnosis.

SARS-CoV2 virus could be potentially myopathic. Serum creatinine phosphokinase (CPK) is frequently found elevated in severe SARS-CoV2 infection, which indicates skeletal muscle damage precipitating limb weakness or even ventilatory failure.
We addressed such a patient in his forties presented with features of severe SARS-CoV2 pneumonia and high serum CPK. He developed severe sepsis and acute respiratory distress syndrome (ARDS) and received intravenous high dose corticosteroid and tocilizumab to counter SARS-CoV2 associated cytokine surge. After 10 days of mechanical ventilation (MV), weaning was unsuccessful albeit apparently clear lung fields, having additionally severe and symmetric limb muscle weakness. Ancillary investigations in addition with serum CPK, including electromyogram, muscle biopsy, and muscle magnetic resonance imaging (MRI) suggested acute myopathy possibly due to skeletal myositis.
We wish to stress that myopathogenic medication in SARS-CoV2 pneumonia should be used with caution. Additionally, serum CPK could be a potential marker to predict respiratory failure in SARS-CoV2 pneumonia as skeletal myopathy affecting chest muscles may contribute ventilatory failure on top of oxygenation failure due to SARS-CoV2 pneumonia.

The obturator nerve lies deep within the pelvis, and it can be damaged by direct injury during surgery. In this study, nerve conduction was used to confirm an obturator nerve injury in a patient who presented with hip adductor weakness following gynecological surgery for endometrial cancer. A 56-year-old woman complained of weakness in the right adductor muscles after a laparoscopic hysterectomy due to endometrial cancer. Seven days after surgery, the degree of weakness of the right hip adductor was Medical Research Council (MRC) Scale 1; thus, a nerve conduction velocity test was conducted. To obtain the compound muscle action potentials of the obturator nerve, stimulation was performed (1.5 cm inferior and 1.5 cm lateral to the pubic tubercle) with a surface electrical simulator and recording (midpoint of the right medial thigh) of the adductor muscles. The compound muscle action potentials of the right obturator nerve showed lower amplitude (left side: 2.7 mV vs. right side: 0.3 mV) and delayed onset latency (left side: 3.2 ms vs. right side: 2.2 ms). These results indicate a partial right obturator neuropathy. Therefore, nerve conduction could be useful to diagnose an early-stage obturator nerve injury and provide information on the degree of damage.

UNASSIGNED: Vitamin B12 deficiency is common in adult and elderly patients and is often underdiagnosed because of its polymorphous manifestations. Neurological symptoms of this condition include subacute combined degeneration and polyneuropathy, with possible affection of thin-myelinated A-delta fibers. Cutaneous silent periods (CSPs) may serve to test small-diameter fiber function non-invasively, using routine electrodiagnostic equipment, but to the best of our knowledge have not been studied so far in vitamin B12 deficiency.
UNASSIGNED: We report a 49-year-old male patient suffering from B12 hypovitaminosis due to autoantibodies against gastric parietal cells, who underwent neurophysiological investigation to confirm clinically suspected polyneuropathy during the first month of intramuscular vitamin B12 supplementation. We performed standard electroneurography, needle electromyography in tibialis anterior muscle, quantitative sensory testing, and cutaneous silent periods six months after symptom onset and repeated the electrodiagnostic study 21 months later, after intramuscular vitamin B12 supplementation.
UNASSIGNED: Standard electroneurography demonstrated axonal sensory polyneuropathy. Needle electromyography (EMG) in tibialis anterior muscle was unremarkable. Cutaneous silent periods in tibialis anterior muscle after noxious electrical sural nerve stimulation were delayed, with incomplete EMG suppression concurring with dysfunction of thin-myelinated A-delta fibers. Quantitative sensory testing revealed altered cold and warm perception thresholds in both upper limbs, but normal values in both lower limbs. A follow-up electrodiagnostic study after 21 months intramuscular vitamin B12 supplementation revealed improvement of all neurophysiological findings, including normalization of cutaneous silent periods.
UNASSIGNED: Thin-myelinated A-delta fibers may be affected in B12 hypovitaminosis and may show recovery after intramuscular vitamin B12 supplementation. CSP may serve to diagnose small fiber affection in this medical condition and to monitor their recovery after vitamin supplementation.
UNASSIGNED: CSP testing represents a useful, non-invasive, rapidly available diagnostic and follow-up tool in vitamin B12 deficiency.

BACKGROUND: Segmental zoster paresis (SZP) of limbs, characterized by focal weakness of extremity, is recognized as a rare complication of herpes zoster (HZ). The following study analyzes the clinical characteristics and data from electromyography and MRI scans in patients with motor weakness after zoster infection.
METHODS: One thousand three hundred ninety-three patients from our database (Shandong Provincial Qianfoshan Hospital) suffering from HZ were retrospectively reviewed from June 2015 to July 2017. Patients who fulfilled the diagnostic criteria for SZP were included in the analysis. The clinical characteristics, as well as electromyography findings and MRI scans were analyzed.
RESULTS: SZP was present in 0.57% of patients with HZ (8/1393). The average age of symptom onset in 8 SZP patients was 69 years old (SD: 13, range 47-87). The severity of muscle weakness ranged from mild to severe. The electrophysiological testing revealed the characteristics of axonopathy. Radiculopathy (2/8), plexopathy (2/8), radiculoplexopathy (3/8) and combined radiculopathy and mononeuropathy (1/8) were also identified. MRI revealed hyperintensity of the affected spinal dorsal horns, nerve roots or peripheral nerves.
CONCLUSIONS: SZP is associated with obvious limb weakness, nerve axons lesions and localization to nerve roots, plexus or peripheral nerves.

OBJECTIVE: We report the case of a patient who presented with right dorsal scapular neuropathy after a trigger point injection into the right rhomboid major muscle. Through a nerve conduction study and electromyography, we demonstrated dorsal scapular nerve injury in this patient.
METHODS: A 38-year-old man complained that his right shoulder functioned less optimally during push-up exercises after a trigger point injection 4 weeks prior. Physical examination revealed mildly reduced right shoulder retractor muscle strength compared with the left side. We performed a nerve conduction velocity test and electromyography 5 weeks after the injection. The compound muscle action potential of the right dorsal scapular nerve showed low amplitude (left vs. right side: 5.2 vs. 1.6 mV) and delayed latency (left vs. right side: 4.9 vs. 6.8 ms). Positive sharp wave (1+) and mildly reduced recruitment were seen on electromyography of the rhomboid major muscle. The findings of the nerve conduction velocity test and electromyography indicated partial right dorsal scapular neuropathy. The nerve injury seemed to have been caused by the needle inserted during trigger point injection.
CONCLUSIONS: Clinicians should pay attention to the occurrence of dorsal scapular nerve injury when performing trigger point injection into the rhomboid muscle.

The 1.4Mb tandem-duplication in the PMP22 gene at 17p11.2 usually manifests as hereditary sensorimotor polyneuropathy with foot deformity, sensorineural hearing-loss, moderate developmental delay, and gait disturbance. Hypertelorism and marked phenotypic variability within a single family has not been reported. In a single family, the PMP22 tandem-duplication manifested as short stature, sensorimotor polyneuropathy, tremor, ataxia, sensorineural hearing-loss, and hypothyroidism in the 27 years-old index case, as mild facial dysmorphism, muscle cramps, tinnitus, intention tremor, bradydiadochokinesia, and sensorimotor polyneuropathy in the 31 year-old half-brother of the index-patient, and as sensorimotor polyneuropathy and foot-deformity in the father of the two. The half-brother additionally presented with hypertelorism, not previously reported in PMP22 tandem-duplication carriers. The presented cases show that the tandem-duplication 17p11.2 may present with marked intra-familial phenotype variability and that mild facial dysmorphism with stuck-out ears and hypertelorism may be a rare phenotypic feature of this mutation. The causal relation between facial dysmorphism and the PMP22 tandem-duplication, however, remains speculative.