Electrophysiological assessment of visual function in patients with non-arteritic ischaemic optic neuropathy

Background and purpose:  Our study aims to evaluate retinal function and neural conduction in post-retinal visual pathways of patients with non-arteritic ischaemic optic neuropathy (NION).
Methods:  Twenty patients (mean age: 63.7 ± 5.96 year) with NION and 20 age-similar control subjects were enrolled. Simultaneous recording of pattern electroretinograms (PERGs) and visual evoked potentials (VEPs), and Log of minimum angle resolution (MAR) visual acuity (VA) were assessed in NION patients and controls.
Results:  Significantly ( anova , P  < 0.01) abnormal PERG and VEP responses, delayed retinocortical time (RCT, difference between VEP P100 and PERG P50 implicit times), and reduced VA were found in NION patients with respect to control subjects. The delay in RCT was not significantly (Pearson's test, P  > 0.01) correlated with the PERG impairment. The reduction in VA was significantly (Pearson's test, P  < 0.01) correlated to the increase in VEP P100 implicit time and RCT, whereas no correlations ( P  > 0.01) were found with PERG abnormalities.
Conclusions:  Non-arteritic ischaemic optic neuropathy patients with a reduction in VA may present two different, unrelated impairments: a dysfunction of the inner retinal layer (abnormal PERG) and abnormal post-retinal neural conduction (abnormal VEP and RCT). The reduction in VA seems to be related to the post-retinal impairment and seems to be independent from the retinal dysfunction.     

鼻咽癌放疗后视神经病变的临床研究

目的 探讨鼻咽癌放疗后视神经病变(RON)的临床特点及其发病相关的可能危险因素. 方法 回顾性分析中山大学孙逸仙纪念医院自1997年1月至2011年1月收治的22例鼻咽癌放疗后RON患者的病历资料,总结其临床表现、眼科检查及影像学表现. 结果 视力下降甚至失明是RON最常见的表现;18例于首程放疗后出现,2例于首程放疗过程中出现,2例于再程放疗中出现,共8眼失明,27眼视力下降.14例患者眼科检查发现眼底视神经萎缩改变.影像学检查发现视神经增粗30眼,视神经萎缩5眼.照射剂量≥70 Gy时患者RON的发生率高于照射剂量＜70 Gy的患者,差异有统计学意义(P＜0.05). 结论 鼻咽癌放疗可引起视神经损伤,并常伴视力、视野、视觉诱发电位异常及影像学表现.RON的发生与放射野、放射剂量有关.常规进行眼科及影像学检查进行早期诊断具有重要意义.     

Cerebellar ataxia in patients with Leber's hereditary optic neuropathy

We report the cases of a mother and son with Leber's hereditary optic neuropathy (LHON), where a point mutation of mitochondria DNA from guanine to adenine on nucleotide position 11778 was verified. Both also had cerebellar ataxia and dysarthria and in both cases cerebellar atrophies were detected by computed tomography or magnetic resonance imaging. It was not possible to elucidate the relationship between LHON and the cerebellar atrophy, but it should be kept in mind that various neurological complications may occur in LHON.     

Anterior ischemic optic neuropathy in moyamoya disease: a first case report

Neuro-ophthalmological manifestations in moyamoya disease are usually the result of cerebrovascular involvement of the visual pathways. We report a case of ischemic optic neuropathy due to ocular hypoperfusion as a result of moyamoya disease, despite a prior internal to external carotid artery bypass with normal hemisphere perfusion. The blood supply of the optic nerve, a proposed pathogenesis of an anterior ischemic optic neuropathy and complications of the ocular ischemic syndrome are discussed.     

Early midline interactions are important in mouse optic chiasm formation but are not critical in man: a significant distinction between man and mouse

The optic chiasm is one of the most popular models for studying axon guidance. Here axons make a key binary decision either to cross the midline to innervate the contralateral hemisphere or to remain uncrossed. In rodents, midline interactions between axons from the two eyes are critical for normal development, as early removal of one eye systematically disrupts hemispheric projections from the remaining eye, increasing the crossed projection at the expense of the uncrossed. This is similar to the abnormal decussation pattern seen in albinos. This pattern is markedly different in marsupials where early eye removal has no impact on projections from the remaining eye. These differences are related to the location of the uncrossed projection through the chiasm. In rodents these axons approach the midline whereas in marsupials they remain segregated laterally. We provide anatomical evidence in man suggesting that, unlike in rodents, uncrossed axons are confined laterally and do not mix in each hemi-chiasm, which is a pattern similar to that found in marsupials. Further, we demonstrate electrophysiologically, using visual cortical evoked potentials, that the failure of one eye to develop in man has no impact on the hemispheric projections from the remaining eye. These data demonstrate that the mechanisms regulating chiasmal development in man differ from those in rodents but may be similar to those in marsupials. We suggest that mouse models of the organization and development of the optic chiasm are not common to placental mammals in general.     

Change of retinal nerve fiber layer thickness in patients with nonarteritic inflammatory anterior ischemic optic neuropathy

In this study, 16 patients (19 eyes) with nonarteritic anterior ischemic optic neuropathy in the acute stage (within 4 weeks) and resolving stage (after 12 weeks) were diagnosed by a series of complete ophthalmic examinations, including fundus examination, optical coherence tomography and fluorescein fundus angiography, and visual field defects were measured with standard automated perimetry. The contralateral uninvolved eyes were used as controls. The retinal nerve fiber layer thickness was determined by optical coherence tomography which showed that the mean retinal nerve fiber layer thickness and the retinal nerve fiber layer thickness from temporal, superior, nasal and inferior quadrants were significantly higher for all measurements in the acute stage than the corresponding normal values. In comparison, the retinal nerve fiber layer thickness from each optic disc quadrant was found to be significantly lower when measured at the resolving stages, than in the control group. Statistical analysis on the correlation between optic disc nerve fiber layer thickness and visual defects demonstrated a positive correlation in the acute stage and a negative correlation in the resolving stage. Our experimental findings indicate that optical coherence tomography is a useful diagnostic method for nonarteritic anterior ischemic optic neuropathy and can be used to evaluate the effect of treatment.     

Pathogenetic aspects of the glaucomatous optic neuropathy: fluorescein angiographic findings in patients with primary open angle glaucoma

PURPOSE: To identify and quantify the role of retinal circulation, capillary leakage and/or nonperfusion of the optic nerve head in digital fluorescein angiography in normal subjects and patients with open angle glaucoma. METHODS: Eighteen patients with primary open angle glaucoma (POAG) and 18 healthy age matched subjects were included. Fluorescein angiograms were performed using the scanning laser ophthalmoscope. The arteriovenous passage time (AVP) was assessed by dye dilution technique and describes the shortest passage through a retinal vascular segment. Optic nerve head nonperfusion was marked manually in early angiographic images and is given as percentage of the optic disk area. The fluorescence of the optic nerve head (as measure of the disruption of the blood-brain barrier) and the surrounding retina (ratio of leakage) was measured using digital imaging analysis in the late phases of the angiogram (9-10min). RESULTS: The AVP time was significantly prolonged ( P=0.001) in patients with open angle glaucoma (AVP 2.29+/-0.32 s) compared to healthy subjects (AVP 1.37+/-0.42 s). The mean percentage of the optic nerve head nonperfusion was 16%. The ratio of optic nerve head fluorescence compared to retinal reference loci was significantly increased (P = 0.02) in patients with glaucoma (1.32+/-0.25) compared with normal subjects (1.32+/-0.19). CONCLUSIONS: Fluorescein angiography revealed altered retinal perfusion along with optic nerve head nonperfusion and increased vascular leakage in open angle glaucoma patients. These factors appear to influence each other, with ultrastructural changes of the lamina cribrosa accompanying changes in the vasculature and nerve fibers. Longitudinal and interventive studies should help better elucidate the relationship between circulatory and neural loss, adding vasoprotective therapeutic approaches to interfere with the glaucomatous neurodegenerative chain of events.     

Vestibular dysfunction in patients with auditory neuropathy detected by vestibular evoked myogenic potentials

ObjectivesThis study aimed to determine vestibular involvement in patients with auditory neuropathy (AN) using ocular vestibular evoked myogenic potential (oVEMP), cervical vestibular evoked myogenic potential (cVEMP), caloric tests, video Head Impulse Tests (vHIT), and Suppression Head Impulse Paradigm (SHIMP) tests.MethodsTwenty-two patients with AN (study group) and 50 age-and-gender-matched healthy subjects (control group) were enrolled. All patients underwent air-conducted sound oVEMP and cVEMP tests. In the study group, 20 patients underwent a caloric test, 10 patients underwent a video Head Impulse Test (vHIT), and nine patients underwent the Suppression Head Impulse Paradigm (SHIMP) test.ResultsSignificant differences in VEMP abnormalities were found between the two groups. Most AN patients showed no VEMP response, while only a few patients showed VEMP responses with normal parameters. Some AN patients presented abnormal VEMP parameters, including thresholds, latencies, and amplitudes. The abnormal rate (including no response and abnormal parameters) was 91% in the cVEMP test and 86% in the oVEMP test. No significant difference was found between oVEMP and cVEMP abnormalities. AN patients exhibited a 70% abnormal rate in the caloric test. Most AN patients showed normal VOR gains. Most patients showed no overt corrective saccades in vHIT, and exhibited normal anticompensatory saccades in the SHIMP test.ConclusionMany AN patients experience vestibular dysfunction, which may be detected by using a vestibular functional test battery.SignificanceVEMP abnormalities might reflect the status and degree of vestibular involvement in AN.     

Peripheral neuropathy in patients with benign monoclonal gammopathy — A pilot study

Summary It is well known that peripheral neuropathy ocurs in patients with myeloma or macroglobulinaemia, but its pathogenesis is still obscure. In recent years, neuropathy has also been reported in association with benign monoclonal or oligoclonal gammopathy. Modern histo-immunological methods have revealed evidence of antibody production to peripheral nerve tissue, probably the myelin sheath.The present study included 21 unselected, consecutive patients with benign monoclonal gammopathy observed in the Division of Haematology. Clinical and laboratory investigations included electrophysiological examination and analyses of the M components. Of the 21 patients 11 had noticed slight neuropathic symptoms in their extremities; in 5 both clinical and electrophysiological findings were compatible with neuropathy; 6 showed positive clinical signs of neuropathy; 4 had either positive electromyographic or electroneurographic findings. In summary, 15 of 21 patients had some signs of peripheral neuropathy. In spite of the screening design of the study, this strikingly high frequency is comparable with other recent reports. Haematological studies did not reveal any significant differences between the patient groups with positive or negative neurological findings. The findings indicate that even benign gammopathies may be associated with peripheral neuropathy.

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Zusammenfassung Das Vorkommen peripherer Neuropathien bei Myelomen und Makroglobulinämien ist wohl bekannt. Die Pathogenese allerdings ist noch unklar. In den letzten Jahren wurde über einen möglichen kausalen Zusammenhang zwischen Polyneuropathien und den gutartigen Formen von monoklonalen oder oligoklonalen Gammopathien berichtet. Moderne immunologische Methoden ergaben Anhaltspunkte für eine Antikörperproduktion gegen peripheres Nervengewebe, wahrscheinlich gegen Myelinstrukturen.Der vorliegende Bericht bezieht sich auf 21 nicht selektionierte Patienten mit gutartiger monoklonaler Gammopathie, die wir in der hämatologischen Abteilung beobachten konnten. Die Patienten wurden klinisch und labormäßig untersucht, wobei auch elektrophysiologische Untersuchungen und eine Analyse der M-Komponenten durchgeführt wurde. Von den 21 Patienten hatten fünf leichte polyneuropathische Symptome ihrer Extremitäten bemerkt. Bei fünf waren sowohl die klinischen wie elektrophysiologischen Befunde mit einer Neuropathie vereinbar; sechs hatten lediglich positive klinische Zeichen einer Neuropathie, und vier weitere hatten entweder ein positives Elektromyogramm oder eine positive Elektroneurographie. Zusammenfassend hatten also 15 von 21 Patienten mindestens einen Hinweis auf eine periphere Neuropathie. Trotz der begrenzten Zahl von Patienten ist diese erstaunlich große Häufigkeit neuropathischer Syndrome durchaus vergleichbar mit anderen kürzlichen Untersuchungen. Hämatologische Untersuchungen ergaben keine signifikanten Unterschiede zwischen der Patientengruppe mit und jener ohne neurologische Befunde.Unsere Untersuchungsergebnisse sprechen dafür, daß auch gutartige Gammopathien mit einer peripheren Neuropathie einhergehen können.

     

Leber's hereditary optic neuropathy associated with a disorder indistinguishable from multiple sclerosis in a male harbouring the mitochondrial DNA 11778 mutation

This report describes a multiple sclerosis (MS)-like disorder in a male patient with Leber's hereditary optic neuropathy (LHON) harbouring the mitochondrial DNA 11778 base pair mutation. Given the population frequencies of MS and LHON, coincidental occurrence is unlikely. Hypothetically the mitochondrial mutation underlying LHON may contribute to presumably immunologically mediated involvement of other myelinated axons in the central nervous system in susceptible individuals, producing a disorder indistinguishable from MS. We recommend that investigation for oligoclonal bands in CSF, evoked potentials and MR brain scan in these patients be supplemented with mitochondrial DNA analysis.     

Macular thickness as a predictor of loss of visual sensitivity in ethambutol-induced optic neuropathy

Ethambutol is a common cause of drug-related optic neuropathy. Prediction of the onset of ethambutol-induced optic neuropathy and consequent drug withdrawal may be an effective method to stop visual loss. Previous studies have shown that structural injury to the optic nerve occurred earlier than the damage to visual function. Therefore, we decided to detect structural biomarkers marking visual ifeld loss in early stage ethambutol-induced optic neuropathy. The thickness of peripapillary retinal nerve ifber layer, macular thickness and visual sensitivity loss would be observed in 11 ethambutol-induced optic neuropathy patients (22 eyes) using optical coherence tomography. Twenty-four healthy age- and sex-matched participants (48 eyes) were used as controls. Results demonstrated that the temporal peripapil-lary retinal nerve ifber layer thickness and average macular thickness were thinner in patients with ethambutol-induced optic neuropathy compared with healthy controls. The average macular thickness was strongly positively correlated with central visual sensitivity loss (r2=0.878,P=0.000). These ifndings suggest that optical coherence tomography can be used to efifciently screen patients. Macular thickness loss could be a potential factor for predicting the onset of ethambutol-induced optic neuropathy.     

Phenotyping animal models of diabetic neuropathy: a consensus statement of the diabetic neuropathy study group of the EASD (Neurodiab)

NIDDK, JDRF, and the Diabetic Neuropathy Study Group of EASD sponsored a meeting to explore the current status of animal models of diabetic peripheral neuropathy. The goal of the workshop was to develop a set of consensus criteria for the phenotyping of rodent models of diabetic neuropathy. The discussion was divided into five areas: (1) status of commonly used rodent models of diabetes, (2) nerve structure, (3) electrophysiological assessments of nerve function, (4) behavioral assessments of nerve function, and (5) the role of biomarkers in disease phenotyping. Participants discussed the current understanding of each area, gold standards (if applicable) for assessments of function, improvements of existing techniques, and utility of known and exploratory biomarkers. The research opportunities in each area were outlined, providing a possible roadmap for future studies. The meeting concluded with a discussion on the merits and limitations of a unified approach to phenotyping rodent models of diabetic neuropathy and a consensus formed on the definition of the minimum criteria required for establishing the presence of the disease. A neuropathy phenotype in rodents was defined as the presence of statistically different values between diabetic and control animals in 2 of 3 assessments (nocifensive behavior, nerve conduction velocities, or nerve structure). The participants propose that this framework would allow different research groups to compare and share data, with an emphasis on data targeted toward the therapeutic efficacy of drug interventions.     

Computed tomography in patients with transient ischaemic attacks: when is a transient ischaemic attack not a transient ischaemic attack but a stroke?

Summary In a prospective community-based study, 184 patients with transient ischaemic attacks (TIAs) were identified from a study population of about 105,000 between 1981 and 1986. Computed tomography (CT) was attempted in all those with cerebral ischaemic attacks (n=152, 83%); patients with amaurosis fugax only (n=32, 27%) were not scanned routinely. Scans were obtained in 120 (79%) of those with cerebral attacks and 12 (38%) of those with amaurosis fugax. The scans were reported by a neuroradiologist who was blinded to the patients' clinical features. Of 120 (27% :95% confidence interval 19–35) scans in patients with cerebral attacks, 32 showed a focal area of hypodensity or cortical loss, but in only 14 (12% :95% confidence interval 6–18) was this in an area of the brain appropriate to the patients' symptoms. There were no significant differences in the clinical features, the duration of attacks or the prognosis (i.e, risk of death, stroke or myocardial infarction) of patients with and without ischaemic lesions on CT. It is concluded that patients with clinically definite TIAs who have a presumed ischaemic and appropriately sited lesion on CT should not be re-classified as having had a stroke.     

Abnormal visual processing in migraine with aura: a study of steady-state visual evoked potentials

BACKGROUND: Although a number of studies reported different interictal findings between migraine with aura (MA) and migraine without aura (MO), the pathophysiology of the visual aura in migraine remains unclear. OBJECTIVE: To investigate the visual processing in patients who experience MA between attacks using steady-state visual evoked potentials (SSVEPs). METHODS: SSVEPs to high (98%) and low (29%) contrast black and white checkerboard gratings with two spatial frequencies (0.5 and 2.0 cpd) at 5 and 10 Hz (10 and 20 reversal/s) were recorded binocularly from 10 patients with MA, 10 patients with MO between attacks and 20 healthy controls (HC). The SSVEPs were Fourier analyzed to obtain the amplitude and phase of the second (2F) and fourth (4F) harmonic response. RESULTS: In the amplitude of 2F, at 0.5 cpd, there was significant increased amplitude in both MA and MO in comparison to HC at 5 Hz in high and low contrast. However, no significant differences were detected at 2.0 cpd in both 5 and 10 Hz in high and low contrast. In the amplitude of 4F, at 2.0 cpd, there was significant increased amplitude in MA in comparison to MO and HC at 10 Hz in high contrast. However, there were no significant differences at 0.5 cpd at both 5 and 10 Hz in high and low contrast. There were no significant phase differences between MA, MO, and HC. CONCLUSION: The high amplitude of the SSVEPs suggests that interictally migraine patients have abnormal excitability in the primary visual cortex, and this change in excitability may exist, at least partially, in the visual association cortex in MA.     

Frequency of Fabry disease in patients with small‐fibre neuropathy of unknown aetiology: a pilot study

Background: Early occurrence of small‐fibre neuropathy (SFN) is a common feature of Fabry disease (FD) – an X‐linked storage disorder caused by reduced activity of the α‐galactosidase A (α‐GAL). Although SFN may result from different disorders, the cause is often unclear. Therefore, we investigated the frequency of FD in patients with SFN of unknown aetiology. Methods: Patients with idiopathic SFN, established by sensory quantitative testing and/or skin biopsy, were examined for mutations in the α‐GAL gene. Where mutations in the α‐GAL gene were identified, levels of globotriaosylceramide (Gb₃) were measured in urine and blood and the α‐GAL activity was evaluated. When new mutations were detected, a diagnostic work‐up was performed as well as a Gb₃ accumulation in the skin, lyso‐Gb₃ in blood and Gb₃_24 in urine were proved. Results: Twenty‐four of 29 eligible patients were enrolled in the study. Mutations in the α‐GAL gene were observed in five patients. A typical mutation for FD (c.424T>C, [C142R]) was detected in one patient. In four patients, a complex intronic haplotype within the α‐GAL gene (IVS0‐10C>T [rs2071225], IVS4‐16A>G [rs2071397], IVS6‐22C>T [rs2071228]) was identified. The relevance of this haplotype in the pathogenesis of FD remains unclear until now. However, these patients showed increased concentrations of Gb₃ and/or lyso‐Gb₃, while no further manifestations for FD could be proved. Conclusions: Fabry disease should be considered in patients with SFN of unknown aetiology, and screening for FD should be included in the diagnostic guidelines for SFN. The significance of the intronic haplotype regarding SFN needs further evaluation.     

Median nerve ultrasonography in distinguishing neuropathy sub-types: a pilot study

Rajabally YA, Morlese J, Kathuria D, Khan A. Median nerve ultrasonography in distinguishing neuropathy sub‐types: a pilot study.
Acta Neurol Scand: 2012: 125: 254–259.
© 2011 John Wiley & Sons A/S. Background – The diagnostic potential of ultrasonography (US) in polyneuropathy has been studied rarely, with complex measurement/correction techniques. Whether US may be useful in clinical practice remains uncertain. Materials and Methods – We aimed to ascertain the value of US, as performed routinely at our institution, in differentiating neuropathy sub‐types. We prospectively studied 14 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and 14 patients with sensory axonal neuropathy (SAN). Median nerves were studied bilaterally at wrist and forearm by a radiologist blinded to the neuropathy sub‐type. Nerve width (medial to lateral diameter), thickness (anterior to posterior diameter) and cross‐sectional area were compared in between patient groups and anatomical sites. Optimal cut‐off values were determined using receiver operating characteristic (ROC) curves. Results – Largest measured median nerve thickness was significantly greater in patients with CIDP (P = 0.014), and ROC curve analysis indicated a cut‐off offering a sensitivity of 57.1% for CIDP and specificity of 92.9% vs SAN. Nerves were wider and had larger cross‐sectional areas, but were not thicker, at wrist compared to forearm in both patient groups. There was an equal prevalence in both patients with CIDP and SAN, of increased median nerve wrist‐to‐forearm area ratio, compatible with sub‐clinical carpal tunnel syndrome. Conclusion – This prospective, blinded, pilot study is the first to indicate the diagnostic potential of US, as performed routinely, in distinguishing between acquired demyelinating and axonal neuropathy. These findings now require confirmation in larger, adequately designed studies, evaluating other nerves/nerve sites, assessing healthy controls and taking into account interrater and equipment variabilities.     

Double function of noninvasive intracranial pressure monitoring based on flash visual evoked potentials in unconscious patients with traumatic brain injury

Intracranial pressure (ICP) monitoring based on flash visual evoked potentials (F-VEP) is a noninvasive method of monitoring ICP. The early diagnosis of traumatic optic neuropathy (TON) in unconscious patients with traumatic brain injury (TBI) is a challenge. The aim of this study was to evaluate the function of F-VEP ICP monitoring in predicting TON and detecting contusion enlargement (CE) in unconscious TBI patients using a modified approach. A series of F-VEP ICP-monitored unconscious TBI patients were included in the study. The interocular differences in N2 wave latency (DL) and amplitude (DA) were obtained through monocular flash stimulation. The increases in ICP (dxP) and interchannel difference (dxDC) across various time points were obtained through binocular flash stimulation. The predictive power of DL and DA on TON, as well as of dxP and dxDC on CE, was assessed by logistic regression and receiver operating characteristic (ROC) curve analysis. Patients with TON had a longer DL and a higher DA than those without TON. The dxP and dxDC of patients with CE were both higher than those of patients without CE. The differences were statistically significant. The logistic regression showed that both DL and DA were predictors of TON, whereas only dxDC was a predictor of CE. However, the ROC curve analysis showed that DL had greater predictive power for TON, and dxDC had greater predictive power for CE. An F-VEP ICP monitoring system with a modified approach is beneficial for early diagnosis of TON and prediction of CE in unconscious TBI patients.     

Injection with corticosteroids (ultrasound guided) in patients with an ulnar neuropathy at the elbow,feasibility study

Introduction and purpose: Unlike carpal tunnel syndrome, little is known about injection with corticosteroids in patients with an ulnar neuropathy at the elbow (UNE). The purpose of this feasibility study is to see whether injection with corticosteroids is safe in patients with UNE and whether there are grounds to launch a prospective placebo‐controlled study on the effects of corticosteroids. Methods: Patients with clinical symptoms of UNE and a nerve conduction study compatible with UNE or thickened ulnar nerve at the elbow (> 10 mm²) by ultrasonography were included. All included patients received an ultrasound‐guided injection of 1 ml containing 40 mg methylprednisoloneacetate and 10 mg lidocainhydrochloride (Depo‐Medrol^®). Complications of the injection were monitored. After 3 months, nerve conduction studies and ultrasonography were repeated and a clinical outcome determined. Results: Eight patients with nine UNE were included. None of the patients mentioned increase in the symptoms directly after the injection nor had an infection on the injection site or haematoma. After 3 months, there was improvement of the symptoms in five patients. One patient deteriorated and three had no change of the symptoms at all. Overall, there was no significant change of the thickness of the ulnar nerve with mean difference ?0.056 mm² (95% CI ?2.56 to 2.45 mm²). Conclusion: We showed that injection with corticosteroids in patients with UNE is easy and safe, and based on this result, we found enough arguments to launch a prospective, placebo‐controlled trial to explore the effectiveness of corticosteroids in patients with UNE.     

Regional homogeneity abnormalities in patients with transient ischaemic attack: A resting-state fMRI study

ObjectiveTo investigate regional activity abnormalities in the resting state in patients with transient ischaemic attack (TIA) using a regional homogeneity (ReHo) method combined with functional magnetic resonance imaging (fMRI) and to examine the relationship between regional activity abnormalities and clinical variables.MethodsResting-state fMRI was conducted in 21 patients with right-sided TIA and in 21 healthy volunteers. The ReHo was calculated to assess the strength of the local signal synchrony and was compared between the two groups.ResultsCompared with the controls, the TIA patients exhibited a decreased ReHo in the right dorsolateral prefrontal cortex (dlPFC), the right inferior prefrontal cortex (iPFC), the right ventral anterior cingulate cortex (vACC) and the right dorsal posterior cingulate cortex (dPCC). In addition, the mean ReHo values in the right dlPFC and the right iPFC were significantly correlated with the Montreal Cognitive Assessment (MoCA) in TIA patients.ConclusionsNeural activities in the resting state are changed in TIA patients even without visible ischaemic lesions on conventional MRI. The positive correlation between the ReHo of resting-state fMRI and cognition suggests that ReHo could be a promising tool to observe the neurobiological consequences of TIA.SignificanceThe present study revealed abnormal local synchronisation of spontaneous neural activities in patients with TIA.