Visual evoked potential abnormalities in patients with COVID-19.

OBJECTIVE: It has been suggested that diseases that may cause visual evoked potential abnormality, such as optic neuritis, may be associated with the coronavirus disease 2019. This study aimed to find out whether there are visual evoked potential abnormalities in coronavirus disease 2019 patients using pattern reversal visual evoked potential and flash visual evoked potential. METHODS: Patients with a history of coronavirus disease 2019 (coronavirus disease 2019 patients) and controls were included in this prospective case-control study. This study was conducted in the Clinical Neurophysiology Laboratory of Adana City Training and Research Hospital. Individuals without visual impairment were included. Coronavirus disease 2019 patients were required to have clinical features consistent with previous acute infection and a positive nose swab polymerase chain reaction test. Visual evoked potential was applied to coronavirus disease 2019 patients between July 2020 and July 2021. Controls consisted of patients without a history of chronic disease who underwent a visual evoked potential study between June 2017 and June 2018 due to headache or dizziness. Pattern reversal visual evoked potential and flash visual evoked potential were applied to all participants. N75, P100, and N135 waves obtained from pattern reversal visual evoked potential and P1, N1, P2, N2, P3, and N3 waves obtained from flash visual evoked potential were analyzed. RESULTS: A total of 44 coronavirus disease 2019 patients and 40 controls were included in the study. Age and gender were not different between the two groups. Pattern reversal visual evoked potential parameters were not different between the two groups. Right P2 latency was 114.4±21.1 and 105.5±14.7 ms in coronavirus disease 2019 patients and controls, respectively (p=0.031). Patients with P100 and P2 wave abnormalities were 6 (13.6%) and 13 (29.6%), respectively. CONCLUSION: This study showed that there may be visual evoked potential abnormalities in coronavirus disease 2019 patients.

The effect of Jendrassik maneuver on the persistence of the peroneal nerve F-wave.

Objectives: This study investigated whether peroneal nerve F-wave persistence increased when the Jendrassik maneuver (JM) was performed, aiming to obtain information about the physiology of F-waves and JM. Patients and methods: Thirty healthy individuals (HIs; 17 females, 13 males; mean age: 33.6±8.2 years; range, 23-50 years) were included in the prospective experimental study conducted between June 15, 2021, and December 15, 2021. Nerve conduction studies of peroneal, superficial peroneal, posterior tibial, and sural nerves were performed in one extremity of each HI. The peroneal nerve F-wave study was performed at rest (Study 1), during JM (Study 2), and after JM (Study 3). F-wave persistence of the peroneal nerve, maximum F-wave amplitude (ampF-wavemax), mean F-wave amplitude (ampF-wavemean), minimum F-wave latency, and the ratio of ampF-wavemean to maximum M amplitude (F/M ratio) were analyzed. Results: The mean peroneal nerve F-wave persistence in Study 1, Study 2, and Study 3 was 28.7±23.9%, 52.3±32.1%, and 34.7±29.0%, respectively. F-wave persistence in Study 2 was higher compared to Studies 1 and 3 (p<0.001 and p<0.001, respectively). Moreover, ampF-wavemax, ampF-wavemean, and F/M ratio in Study 2 were higher than Studies 1 and 3 (p=0.026 and p=0.021 for ampF-wavemean; p=0.015 and p=0.003 for ampF-wavemax; p=0.033 and p=0.015 for F/M ratio, respectively). F-wave persistence in Study 2 was positively correlated with ampF-wavemax and ampF-wavemean (p<0.001, r= 0.717; p<0.001, r=0.786, respectively). Conclusion: This study demonstrated that JM increased F-wave persistence and amplitude. Jendrassik maneuver may show its effect through motor neuron excitability.

Needle electromyography abnormalities in the upper trapezius muscle in neuromuscular disorders.

BACKGROUND: : Needle electromyography (EMG) abnormalities in the trapezius muscle (TM) can be seen in neuromuscular disorders. The aim was to determine the characteristics of needle EMG abnormalities observed in the TM in neuromuscular disorders. METHODS: The data of patients who applied to the Clinical Neurophysiology Laboratory of University of Health Sciences Adana City Training and Research Hospital between December 2018 and October 2021 were reviewed. Polio survivors, amyotrophic lateral sclerosis (ALS) patients, patients with sensorimotor polyneuropathy, patients with spinal cord lesions involving C2/C3/C4 segments, patients with spinal accessory nerve (SAN) lesions, neuralgic amyotrophy (NA) patients, and patients with myopathy were included. Needle EMG findings of the upper TM of the patients were analyzed. Positive sharp waves, fibrillation potentials, fasciculation potentials, myotonic discharges, and motor unit action potential (MUAP) changes were considered needle EMG abnormalities. RESULTS: Eighty-one polio survivors, 23 ALS patients, 39 patients with sensorimotor polyneuropathy, 10 patients with cervical spinal lesions, eight NA patients, seven patients with SAN lesions, and three patients with myopathy were included in the study. Fifteen (65.2%) ALS patients, 18 (22.2%) polio survivors, three (30%) patients with cervical spinal lesions, two (5.1%) patients with sensorimotor neuropathy, one (12.5%) NA patient, seven (100%) patients with SAN lesions, and two (66.7%) patients with myopathies had at least one needle EMG abnormality in the TM. Fasciculation potentials in the TM were seen in 10 (43.5%) ALS patients. In four patients with SAN lesions and one polio survivor, MUAP could not be obtained from the TM. DISCUSSION: There may be more frequent needle EMG abnormalities, particularly in ALS patients and patients with SAN lesions. Since the number of patients with myopathy included in this study was low, it is difficult to comment on the needle EMG features of the TM for these patients. In addition, this study indicated that fasciculation potentials in the TM are typical in ALS patients and that MUAP may not be obtained from the TM in patients with SAN lesions.

Neuropathic pain in peroneal nerve entrapment at the fibular head.

BACKGROUND: Peroneal neuropathy at the fibular head (PNFH) is a mononeuropathy that typically presents with drop foot and sensory abnormalities over the skin area innervated by the peroneal nerve. OBJECTIVE: The aim of the present study was to evaluate neuropathic pain in patients with PNFH. METHODS: Patients with clinical and electrodiagnostic features consistent with PNFH associated with weight loss, leg postures, or prolonged sleep were included in the present retrospective cohort study. Nerve conduction studies were performed in the bilateral lower extremities of all patients. The Leeds assessment of neuropathic symptoms and signs scale (LANSS) was applied to all patients. RESULTS: Thirty-two PNFH patients (78% males) were included in the study. The LANSS score in the majority of patients was lower than 12. There was 1 patient with a LANSS score of 12. The electrodiagnostic features of 16 patients were compatible with axonal degeneration. The mean LANSS scores of PNFH patients with and without axonal degeneration were 4.3 ± 3.7 and 5.2 ± 2.9, respectively (p = 0.255). CONCLUSION: The present study showed that neuropathic pain is a rare symptom in patients with PNFH associated with weight loss, leg postures, or prolonged sleep.

ANTECEDENTES: A neuropatia fibular na cabeça da fíbula (PNFH) é uma mononeuropatia que normalmente se apresenta com pé caído e anormalidades sensoriais sobre a área da pele inervada pelo nervo fibular. OBJETIVO: O objetivo do presente estudo foi avaliar a dor neuropática em pacientes com PNFH. MéTODOS: Pacientes com características clínicas e eletrodiagnósticas consistentes com PNFH associada a perda de peso, postura das pernas ou sono prolongado foram incluídos neste estudo de coorte retrospectivo. Estudos de condução nervosa foram realizados nas extremidades inferiores bilaterais de todos os pacientes. A escala de avaliação de sintomas e sinais neuropáticos de Leeds (LANSS) foi aplicada a todos os pacientes. RESULTADOS: Trinta e dois pacientes com PNFH (78%) foram incluídos no estudo. A pontuação LANSS em outros pacientes foi menor que 12. Houve 1 paciente com pontuação LANSS de 12. As características eletrodiagnósticas de 16 pacientes foram compatíveis com degeneração axonal. Os escores médios do LANSS de pacientes com PNFH com e sem degeneração axonal foram 4,3 ± 3,7 e 5,2 ± 2,9, respectivamente (p = 0,255). CONCLUSãO: O presente estudo mostrou que a dor neuropática é um sintoma raro em pacientes com PNFH associada à perda de peso, postura das pernas ou sono prolongado.

Neuropathic pain in peroneal nerve entrapment at the fibular head / Dor neuropática no aprisionamento do nervo fibular na cabeça da fíbula

Abstract Background Peroneal neuropathy at the fibular head (PNFH) is a mononeuropathy that typically presents with drop foot and sensory abnormalities over the skin area innervated by the peroneal nerve. Objective The aim of the present study was to evaluate neuropathic pain in patients with PNFH. Methods Patients with clinical and electrodiagnostic features consistent with PNFH associated with weight loss, leg postures, or prolonged sleep were included in the present retrospective cohort study. Nerve conduction studies were performed in the bilateral lower extremities of all patients. The Leeds assessment of neuropathic symptoms and signs scale (LANSS) was applied to all patients. Results Thirty-two PNFH patients (78% males) were included in the study. The LANSS score in the majority of patients was lower than 12. There was 1 patient with a LANSS score of 12. The electrodiagnostic features of 16 patients were compatible with axonal degeneration. The mean LANSS scores of PNFH patients with and without axonal degeneration were 4.3 ± 3.7 and 5.2 ± 2.9, respectively (p = 0.255). Conclusion The present study showed that neuropathic pain is a rare symptom in patients with PNFH associated with weight loss, leg postures, or prolonged sleep.

Resumo Antecedentes A neuropatia fibular na cabeça da fíbula (PNFH) é uma mononeuropatia que normalmente se apresenta com pé caído e anormalidades sensoriais sobre a área da pele inervada pelo nervo fibular. Objetivo O objetivo do presente estudo foi avaliar a dor neuropática em pacientes com PNFH. Métodos Pacientes com características clínicas e eletrodiagnósticas consistentes com PNFH associada a perda de peso, postura das pernas ou sono prolongado foram incluídos neste estudo de coorte retrospectivo. Estudos de condução nervosa foram realizados nas extremidades inferiores bilaterais de todos os pacientes. A escala de avaliação de sintomas e sinais neuropáticos de Leeds (LANSS) foi aplicada a todos os pacientes. Resultados Trinta e dois pacientes com PNFH (78%) foram incluídos no estudo. A pontuação LANSS em outros pacientes foi menor que 12. Houve 1 paciente com pontuação LANSS de 12. As características eletrodiagnósticas de 16 pacientes foram compatíveis com degeneração axonal. Os escores médios do LANSS de pacientes com PNFH com e sem degeneração axonal foram 4,3 ± 3,7 e 5,2 ± 2,9, respectivamente (p = 0,255). Conclusão O presente estudo mostrou que a dor neuropática é um sintoma raro em pacientes com PNFH associada à perda de peso, postura das pernas ou sono prolongado.

COVID-19 can cause blink reflex abnormalities.

Background and purpose: Neurological symptoms and complications associated with coronavirus 2019 (COVID-19) are well known. It was aimed to evaluate the brainstem and trigeminal/facial nerves and the pathways between these structures in COVID-19 using the blink reflex test. Methods: Thirty patients with post COVID-19 (16 males, 14 females) and 30 healthy individuals (17 males, 13 females) were included in this prospective study. Individuals who previously had a positive nose swap polymerase chain reaction test for severe acute respiratory syndrome coronavirus 2 and whose previously clinical features were compatible with COVID-19 were included in the post COVID-19 patient group. Neurological examination of the participants should be normal. Blink reflex test was performed on all participants. R1, ipsilateral R2 (IR2), and contralateral R2 (CR2) waves obtained from the test were analyzed. Results: The mean ages of healthy individuals and post COVID-19 patients were 34.0±6.4 and 38.4±10.6 years, respectively. Both age and gender were matched between the groups. R1, IR2, and CR2 latencies/amplitudes were not different between the two groups. The side-to-side R1 latency difference was 0.5±0.3 and 1.0±0.8 ms in healthy individuals and post COVID-19 patients, respectively (p=0.011). One healthy individual and 12 patients with post COVID-19 had at least one abnormal blink reflex parameter (p=0.001). Conclusion: This study showed that COVID-19 may cause subclinical abnormalities in the blink reflex, which includes the trigeminal nerve, the seventh nerve, the brainstem, and pathways between these structures.

Reduced Occipital Cortex Excitability in Amyotrophic Lateral Sclerosis.

PURPOSE: In addition to motor cortex involvement, sensory abnormalities have been demonstrated in amyotrophic lateral sclerosis (ALS), including structural and metabolic alterations in the occipital cortex. The aim of this study was to examine occipital excitability changes in ALS. METHODS: Twenty-one patients with ALS and 16 healthy subjects were enrolled into the study. Phosphene experience and phosphene threshold were studied to assess occipital excitability. Cognitive function was evaluated in both groups by means of Montreal Cognitive Assessment and Addenbrooke's Cognitive Examination-Revised visuospatial score tests. RESULTS: Phosphene was experienced in 13 (81.3%) healthy subjects and 9 (42.9%) patients with ALS ( P = 0.04). The mean phosphene threshold was not significantly different between the two groups. No correlation existed between phosphene threshold and motor cortical excitability parameters, ALS Functional Rating Scale Revised, Montreal Cognitive Assessment, and Addenbrooke's Cognitive Examination-Revised scores. CONCLUSIONS: Visual cortex is affected, and the occipital excitability is reduced in ALS, without any relation to motor cortical excitability changes, providing another clue suggestive of sensory involvement in ALS.

The relationship between nerve conduction studies and neuropathic pain in sciatic nerve injury due to intramuscular injection.

BACKGROUND: Sciatic nerve injury due to intramuscular injection (SNIII) is still a health problem. This study aimed to determine whether there is a correlation between neuropathic pain and electrodiagnostic findings in SNIII. METHODS: Patients whose clinical and electrodiagnostic findings were compatible with SNIII participated in this retrospective cohort study. Compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes of the sural, superficial peroneal, peroneal, and tibial nerves were graded from 1 to 4. Leeds assessment of neuropathic symptoms and signs scale (LANSS) was applied to all patients. RESULTS: Forty-eight patients were included in the study, 67% of whom had a LANSS score ≥ 12. Sural SNAP amplitude abnormalities were present in 8 (50%) out of 16 patients with a LANSS score < 12, and 28 (87.5%) out of 32 patients with a LANSS score ≥ 12, with significant differences between the groups (P = 0.011). There was a positive correlation between the LANSS score and the sural SNAP amplitude grading (P = 0.001, r = 0.476). A similar positive correlation was also found in the LANSS score and the tibial nerve CMAP amplitude grading (P = 0.004, r = 0.410). CONCLUSIONS: This study showed a positive correlation between the severity of tibial nerve CMAP/sural SNAP amplitude abnormality and LANSS score in SNIII. Neuropathic pain may be more common in SNIII patients with sural nerve SNAP amplitude abnormality.

The needle electromyography findings in the neurophysiological classification of ulnar neuropathy at the elbow

Background/aim: Although ulnar neuropathy at the elbow (UNE) is the second most common entrapment mononeuropathy, there are few reports on its neurophysiological classification. In this study, we tried to find out the role of needle electromyography (EMG) in the neurophysiological classification of UNE. Materials and methods: UNE patients who met the clinical and neurophysiological diagnostic criteria and healthy individuals were included in this study. Reference values of nerve conduction studies were obtained from healthy individuals. Needle EMG was performed to all UNE patients. According to the neurophysiological classification proposed by Padua, UNE patients were classified as mild, moderate, and severe. Results: Thirty-one controls and thirty-five UNE patients were included in the study. There was mild UNE in 23 patients, moderate UNE in 8, and severe UNE in 4. Abnormal needle EMG findings were present in all patients with moderate and severe UNE and in 12 patients with mild UNE. Conclusion: Abnormal needle EMG findings are seen in most of the UNE patients. Therefore, it is not practical to use needle EMG findings in the neurophysiological classification. Needle EMG abnormalities may also be present in patients with mild UNE due to axonal degeneration or motor conduction block.

Impaired short- and long-latency afferent inhibition in amyotrophic lateral sclerosis.

INTRODUCTION: To test the hypothesis of impaired cholinergic activity in amyotrophic lateral sclerosis (ALS), we studied short- and long-latency afferent inhibition (SAI and LAI). METHODS: The ulnar nerve was stimulated at the wrist preceding transcranial magnetic stimulation (TMS), 21 ms for SAI and 200 ms for LAI, in 21 patients and 17 control subjects. Short-interval intracortical inhibition (SICI) and cognitive function was assessed in ALS patients using automatic threshold tracking and the Montreal Cognitive Assessment (MoCA). RESULTS: The SAI paradigm resulted in inhibition in all control subjects, whereas inhibition was observed in 13 of 21 (62%) patients. Mean SAI and LAI values were significantly reduced in ALS. No significant correlation existed between afferent inhibition and other neurophysiological data. The MoCA was normal in all but 1 patient. DISCUSSION: LAI and SAI are both impaired in ALS, probably unrelated to increased cortical excitability or cognitive dysfunction. Muscle Nerve 59:699-704, 2019.

Sleep bruxism possibly triggered by multiple sclerosis attacks and treated successfully with botulinum toxin: Report of three cases.

Sleep bruxism refers to a nocturnal parafunctional activity including the clenching, grinding or gnashing of teeth. While most of the nocturnal bruxism cases seen in the general population are apparently idiopathic, it has been reported to be associated with a range of neurological diseases such as Huntington's disease, cranio-cervical dystonia and post-anoxic brain damage, but not multiple sclerosis (MS). We describe three cases of MS patients who have had moderate to severe complaints of bruxism in the two weeks following their relevant MS attacks. None of the three patients had a diagnosis of bruxism prior to her attack. The diagnosis was confirmed in one out of three by a polysomnography. One patient did not have any complaints related to bruxism previous to her attack, whereas two had mild and infrequent complaints. The symptoms of the relevant attacks were left hemihypesthesia in all and hemiparesis in two. None of the patients had spasticity that could result in severe teeth clenching. All three patients presented with morning headaches and jaw pain or tightness and were treated successfully with botulinum toxin (Btx) injections applied to their masseter and temporalis muscles. The cause of bruxism is controversial but lesions of the cortico-basalganglia-thalamo-cotrical loops are thought to be most likely. However, acute or chronic lesions in those pathways were not demonstrated in the 3 patients. It is feasible that they had normal appearing white matter interruptions in their cortico-basalganglia-thalamocortical loops along with their relevant attack.