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Background The association of tuberculosis and motor neuron disease-like illness has not been described previously. We present a case of co-existent pulmonary and extra-pulmonary tuberculosis in a young man whose clinical presentation was suggestive of a motor neuron disease-like illness and was subsequently diagnosed with tubercular infection. This case provokes our thought as to whether the association between tuberculosis and motor neuron dysfunction was just a co-incidence, given the high prevalence of tuberculosis in our set-up, or does it point towards a possible causative role of infection in motor neuron disease. Case presentation A 31-year-old man presented with progressive thinning of bilateral upper and lower limbs with associated pain and twitching sensation in upper and lower limb muscles. He had a history of loss of appetite and unintentional weight loss. On clinical examination, there was evidence of fasciculations in bilateral quadriceps, bilateral biceps, and paraspinal muscles which was further confirmed with electrophysiology. The work-up for underlying autoimmune, toxic and metabolic aetiology, and paraneoplastic aetiology was found to be negative. CT scan of the chest was suggestive of consolidations in bilateral upper lobes with multiple tree-in-bud nodules in both the lungs. Hybrid 18-Flourine-flourodeoxyglucose positron emission tomography and magnetic resonance imaging (F-18-FDG PET/MRI) imaging was also suggestive of pulmonary and extra-pulmonary tuberculosis. Imaging of the brain revealed atrophy along bilateral motor cortices with reduced tracer uptake. Diagnosis of tubercular infection was confirmed with nucleic acid amplification test and the patient was put on anti-tubercular therapy. On follow-up after 6 months, the patient reported improvement in the symptoms and the muscle power in bilateral upper and lower limbs. Conclusion We have described a very rare association of pulmonary and extra-pulmonary tuberculosis with motor neuron-like illness. It may be debated that such an association may just be co-incidental; however, given the improvement in the symptoms and signs of the motor neuron disease-like illness on follow-up while the patient was on anti-tubercular therapy, it may point towards a causative relationship between tubercular infection and motor neuron dysfunction. Further epidemiological studies should be sought for in order to reach a conclusive answer.
Background The association of tuberculosis and motor neuron disease-like illness has not been described previously. We present a case of co-existent pulmonary and extra-pulmonary tuberculosis in a young man whose clinical presentation was suggestive of a motor neuron disease-like illness and was subsequently diagnosed with tubercular infection. This case provokes our thought as to whether the association between tuberculosis and motor neuron dysfunction was just a co-incidence, given the high prevalence of tuberculosis in our set-up, or does it point towards a possible causative role of infection in motor neuron disease. Case presentation A 31-year-old man presented with progressive thinning of bilateral upper and lower limbs with associated pain and twitching sensation in upper and lower limb muscles. He had a history of loss of appetite and unintentional weight loss. On clinical examination, there was evidence of fasciculations in bilateral quadriceps, bilateral biceps, and paraspinal muscles which was further confirmed with electrophysiology. The work-up for underlying autoimmune, toxic and metabolic aetiology, and paraneoplastic aetiology was found to be negative. CT scan of the chest was suggestive of consolidations in bilateral upper lobes with multiple tree-in-bud nodules in both the lungs. Hybrid 18-Flourine-flourodeoxyglucose positron emission tomography and magnetic resonance imaging (F-18-FDG PET/MRI) imaging was also suggestive of pulmonary and extra-pulmonary tuberculosis. Imaging of the brain revealed atrophy along bilateral motor cortices with reduced tracer uptake. Diagnosis of tubercular infection was confirmed with nucleic acid amplification test and the patient was put on anti-tubercular therapy. On follow-up after 6 months, the patient reported improvement in the symptoms and the muscle power in bilateral upper and lower limbs. Conclusion We have described a very rare association of pulmonary and extra-pulmonary tuberculosis with motor neuron-like illness. It may be debated that such an association may just be co-incidental; however, given the improvement in the symptoms and signs of the motor neuron disease-like illness on follow-up while the patient was on anti-tubercular therapy, it may point towards a causative relationship between tubercular infection and motor neuron dysfunction. Further epidemiological studies should be sought for in order to reach a conclusive answer.
This study aimed at analyzing the corneal neural regeneration in ankylosing spondylitis patients using in vivo corneal confocal microscopy in correlation with Langerhans cell density, morphology, and dry eye parameters. Approximately 24 ankylosing spondylitis subjects and 35 age- and gender-matched control subjects were enrolled. Data analysis showed that all corneal nerve-fiber descriptives were lower in the ankylosing spondylitis group, implicating disrupted neural regeneration. Peripheral Langerhans cell density showed a negative correlation with nerve fiber descriptions. A negative correlation between tear film break-up time and corneal nerve fiber total branch density was detected. The potential role of somatosensory terminal Piezo2 channelopathy in the pathogenesis of dry eye disease and ankylosing spondylitis is highlighted in our study, exposing the neuroimmunological link between these diseases. We hypothesized earlier that spinal neuroimmune-induced sensitization due to this somatosensory terminal primary damage could lead to Langerhans cell activation in the cornea, in association with downregulated Piezo1 channels on these cells. This activation could lead to a Th17/Treg imbalance in dry eye secondary to ankylosing spondylitis. Hence, the corneal Piezo2 channelopathy-induced impaired Piezo2-Piezo1 crosstalk could explain the disrupted neural regeneration. Moreover, the translation of our findings highlights the link between Piezo2 channelopathy-induced gateway to pathophysiology and the gateway reflex, not to mention the potential role of spinal wide dynamic range neurons in the evolution of neuropathic pain and the flare-ups in ankylosing spondylitis and dry eye disease.
This case report describes an uncommon overlap syndrome between ankylosing spondylitis (AS) and amyotrophic lateral sclerosis (ALS). Initially, the patient was diagnosed with AS, for which he received various specific treatments, including TNF-α inhibitors. After five years of treatment with TNF-α inhibitor etanercept, the patient was referred for a full neurological assessment after he reported balance disturbances, postural instability, muscle weakness, and other neurological symptoms that indicated the presence of a neurological disorder. After a thorough investigation, the patient was diagnosed with ALS. This case report aims to contribute to the limited literature by providing a detailed case study regarding the crosstalk between AS and ALS while also exploring the potential underlying mechanisms and the possible link between TNF-α inhibitors therapy and ALS.
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