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There is a reduction in corneal nerve fiber density and length in type 2 diabetes mellitus with chronic kidney disease compared with type 2 diabetes mellitus alone; however, this difference does not result in worse ocular surface discomfort or dry eye disease.This study aimed to determine the clinical impact of corneal nerve loss on ocular surface discomfort and markers of ocular surface homeostasis in people with type 2 diabetes mellitus without chronic kidney disease (T2DM-no CKD) and those with type 2 diabetes mellitus with concurrent chronic kidney disease (T2DM-CKD).Participants were classified based on estimated glomerular filtration rates into two groups: T2DM-CKD (n = 27) and T2DM-no CKD (n = 28).There was a significant difference between the T2DM-CKD and T2DM-no CKD groups in corneal nerve fiber density (14.9 ± 8.6 and 21.1 ± 7.1 no./mm 2 , respectively; P = .005) and corneal nerve fiber length (10.0 ± 4.6 and 12.3 ± 3.7 mm/mm 2 , respectively; P = .04). Fluorescein tear breakup time was significantly reduced in T2DM-CKD compared with T2DM-no CKD (8.1 ± 4.4 and 10.7 ± 3.8 seconds, respectively; P = .01), whereas ocular surface staining was not significantly different (3.5 ± 1.7 and 2.7 ± 2.3 scores, respectively; P = .12). In terms of ocular surface discomfort, there were no significant differences in the ocular discomfort score scores (12.5 ± 11.1 and 13.6 ± 12.1, respectively; P = .81) and Ocular Pain Assessment Survey scores (3.3 ± 5.4 and 4.3 ± 6.1, respectively; P = .37) between the T2DM-CKD and T2DM-no CKD.The current study demonstrated that corneal nerve loss is greater in T2DM-CKD than in T2DM-no CKD. However, these changes do not impact ocular surface discomfort or markers of ocular surface homeostasis.

Aim: To determine the impact of chronic kidney disease on corneal nerve measures and dendritic cell counts in type 2 diabetes. Methods: In vivo corneal confocal microscopy images were used to estimate corneal nerve parameters and compared in people with type 2 diabetes with chronic kidney disease (T2DM-CKD) (n = 29) and those with type 2 diabetes without chronic kidney disease (T2DM-no CKD) (n = 29), along with 30 healthy controls. Corneal dendritic cell densities were compared between people with T2DM-CKD and those with T2DM-no CKD. The groups were matched for neuropathy status. Results: There was a significant difference in corneal nerve fiber density (p < 0.01) and corneal nerve fiber length (p = 0.04) between T2DM-CKD and T2DM-no CKD groups. The two diabetes groups had reduced corneal nerve parameters compared to healthy controls (all parameters: p < 0.01). Immature central dendritic cell density was significantly higher in the T2DM-CKD group compared to the T2DM-no CKD group ((7.0 (3.8–12.8) and 3.5 (1.4–13.4) cells/mm2, respectively, p < 0.05). Likewise, central mature dendritic cell density was significantly higher in the T2DM-CKD group compared to the T2DM-no CKD group (0.8 (0.4–2.2) and 0.4 (0.6–1.1) cells/mm2, respectively, p = 0.02). Additionally, total central dendritic cell density was increased in the T2DM-CKD group compared to T2DM-no CKD group (10.4 (4.3–16.1) and 3.9 (2.1–21.0) cells/mm2, respectively, p = 0.03). Conclusion: The study showed that central corneal dendritic cell density is increased in T2DM-CKD compared to T2DM-no CKD, with groups matched for peripheral neuropathy severity. This is accompanied by a loss of central corneal nerve fibers. The findings raise the possibility of additional local factors exacerbating central corneal nerve injury in people with diabetic chronic kidney disease.

Nerve conduction studies (NCS) are the current objective measure for diagnosis of peripheral neuropathy in type 2 diabetes but do not assess nerve structure. This study investigated the utility of peripheral nerve ultrasound as a marker of the presence and severity of peripheral neuropathy in type 2 diabetes.A total of 156 patients were recruited, and nerve ultrasound was undertaken on distal tibial and distal median nerves. Neuropathy severity was graded using the modified Toronto Clinical Neuropathy Scale (mTCNS) and Total Neuropathy Score (TNS). Studies were undertaken by a single ultrasonographer blinded to nerve conduction results.A stepwise increase in tibial nerve cross-sectional area (CSA) was noted with increasing TNS grade (p lt; 0.001) and each mTCNS quartile (p lt; 0.001). Regression analysis demonstrated a correlation between tibial nerve CSA and neuropathy severity (p lt; 0.001). Using receiver operator curve analysis, tibial nerve CSA ofgt;12.88 mm yielded a sensitivity of 70.5% and specificity of 85.7% for neuropathy detection. Binary logistic regression revealed that tibial nerve CSA was a predictor of abnormal sural sensory nerve action potential amplitude (odds ratio = 1.239, 95% confidence interval [CI] = 1.142-1.345) and abnormal neuropathy score (odds ratio = 1.537, 95% confidence interval [CI] = 1.286-1.838).Tibial nerve ultrasound has good specificity and sensitivity for neuropathy diagnosis in type 2 diabetes. The study demonstrates that tibial nerve CSA correlates with neuropathy severity. Future serial studies using both ultrasound and NCS may be useful in determining whether changes in ultrasound occur prior to development of nerve conduction abnormalities and neuropathic symptoms.

Multiple sclerosis (MS) is a neurological inflammatory disorder known to attack the heavily myelinated regions of the nervous system including the optic nerves, cerebellum, brainstem and spinal cord. This review will discuss the clinical manifestations and investigations for MS and other similar neurological inflammatory disorders affecting vision, as well as the effects of MS treatments on vision. Assessment of visual pathways is critical, considering MS can involve multiple components of the visual pathway, including optic nerves, uvea, retina and occipital cortex. Optical coherence tomography is increasingly being recognised as a highly sensitive tool in detecting subclinical optic nerve changes. Magnetic resonance imaging (MRI) is critical in MS diagnosis and in predicting long-term disability. Optic neuritis in MS involves unilateral vision loss, with characteristic pain on eye movement. The visual loss in neuromyelitis optica spectrum disorder tends to be more severe with preferential altitudinal field loss, chiasmal and tract lesions are also more common. Other differential diagnoses include chronic relapsing inflammatory optic neuropathy and giant cell arteritis. Leber's hereditary optic neuropathy affects young males and visual loss tends to be painless and subacute, typically involving both optic nerves. MS lesions in the vestibulocerebellum, brainstem, thalamus and basal ganglia may lead to abnormalities of gaze, saccades, pursuit and nystagmus which can be identified on eye examination. Medial longitudinal fasciculus lesions can cause another frequent presentation of MS, internuclear ophthalmoplegia, with failure of ipsilateral eye adduction and contralateral eye abduction nystagmus. Treatments for MS include high-dose corticosteroids for acute relapses and disease-modifying medications for relapse prevention. These therapies may also have adverse effects on vision, including central serous retinopathy with corticosteroid therapy and macular oedema with fingolimod.

A 72-year-old woman with a history of asthma and bronchiectasis presented with a 7-year history of bilateral hand cramps, initially affecting the right, frequently resulting in clenched fists. Examination revealed clenched fists bilaterally in the resting state and pseudomyotonia with incomplete relaxation following active finger extension (figure 1, A–C; video 1). Myokymia and percussion myotonia were not observed. No weakness was elicited in the muscles. Needle EMG of the forearm flexors demonstrated bursts of spontaneous high-frequency waning discharges typical of neuromyotonia (figure 2; video 2). Significant clinical improvement was observed following treatment with botulinum toxin injections and oxcarbazepine (figure 1, D–F).

More than half of patients with neurosarcoidosis present primarily with neurological symptoms, often with delayed diagnosis given the heterogeneous presentation of this granulomatous multisystem inflammatory disorder.1 We report two cases of neurosarcoidosis that illustrate the under-recognised dissociation between clinical and radiological features in patients with sarcoid myelopathy. An otherwise well 70-year-old man presented with acute left ocular pain following an insidious 12-month history of mild paraesthesia in his distal extremities. Ophthalmological assessment demonstrated anterior uveitis. Neurological examination revealed reduction to sensation in a glove-and-stocking distribution to the wrists and ankles and absent ankle jerks. There was no weakness or upper motor neuron features. Electrophysiological assessment demonstrated markedly reduced sensory responses in the upper and lower limbs with preserved motor responses consistent with a generalised axonal sensory neuropathy. MRI of the brain and spinal cord revealed significant T2-hyperintensity and enhancement of the central canal of the cord at C4–5 (figure 1A,B), without concurrent intracranial lesions. The patient’s neurological presentation was deemed to be secondary to the generalised peripheral sensory neuropathy rather than the cord abnormalities given the absence of myelopathic features clinically. Figure 1 T2 sagittal (A) and axial (B) MRI sequence of the …

IntroductionSporadic Creuzfeldt-Jakob disease (sCJD) is a rare disease caused by prion proteins and usually presents in the 7th decade of life. sCJD classically presents with a rapidly progressive dementing illness, associated myoclonus and a median time to death of 6 months. Less commonly younger patients are described with a neuropsychiatric presentation and a prolonged disease course. We report two young sCJD patients with neuropsychiatric presentations and slow disease progression admitted to Liverpool Hospital, Sydney (2016–2017).Case 1 A 48 year old Chinese man presented with a 12 month history of depressive symptoms and insomnia. Over the next 5 months, he developed progressive cognitive impairment, disinhibited behaviour, aggression, paranoia and ataxia of gait. Serial EEG and MRI brain scans, cerebrospinal fluid (CSF) testing for 14–3–3 protein and PRNP gene testing were negative or non-contributory. He progressively became mute, bedbound and died at 24 months from symptom onset. Diagnosis was only confirmed with a limited brain autopsy at post-mortem that revealed severe microvacuolar change, gliosis, neuronal loss and status spongiosus. Anti-prion antibody 12 F10 staining showed a diffuse fine synaptic pattern in the frontal cortex and striatum consistent with sCJD.Case 2 A 42 year old Afghani man presented with a 36 month history of emotional lability and progressive social withdrawal followed by auditory and visual hallucinations, cognitive impairment and gait ataxia. Screening for vasculitis, infective (including HIV/syphilis) and autoimmune encephalopathies were negative. EEG demonstrated non-specific slowing, without characteristic periodic sharp-wave complexes. MRI brain was initially normal but progress imaging showed bilateral cortical ribboning, caudate nucleus T2-hyperintensity and associated diffusion restriction consistent with sCJD. CSF 14–3–3 protein analysis was positive. The patient died 38 months from symptom onset. Post-mortem examination was not performed.ConclusionsCJD in younger patients may present as a slowly progressive neuropsychiatric disorder and ante-mortem investigations may remain negative. Post-mortem remains the gold standard for CJD diagnosis.

This article aims to explore the factors contributing to sustained or nonsustained behaviour change following a lifestyle intervention in general practice.Twenty patients who had participated in a general practice health check and group lifestyle support program were interviewed by telephone after 12 months. The interviews were transcribed and analysed thematically.Patients reported positive effects of the intervention on their behaviour change, especially the group peer support. However, their maintenance of these changes varied. Factors that contributed to sustained behaviour change included social support and self efficacy. Factors contributing to relapse included competing demands on time, comorbidity and stress.Greater attention needs to be given to maintenance of behaviour change in lifestyle management programs. Following completion of the program, there needs to be greater support for relapse prevention and management and effective integration back into general practice.