Neurological manifestations of coronavirus disease 2019: exploring past to understand present.

SARS-CoV-2 infection, resulting in Coronavirus disease 2019 (COVID-19), has significantly affected the entire world. It was labelled a pandemic by World Health Organization. Although it commonly produces respiratory symptoms, neurological features have been described. Neurological manifestations may vary from non-specific symptoms such as headache, dizziness, myalgia and/or fatigue, olfactory or taste dysfunction to specific syndromes including meningitis, stroke, acute transverse myelitis and Guillain-Barre syndrome. This review describes potential pathogenetic mechanisms and neurological manifestations of COVID-19 along with its management. Considering structural and pathogenetic similarity of SARS-CoV-2 with SARS-CoV and MERS viruses, we compared their neurological manifestations and mentioned few features expected in COVID-19 in future. Interestingly, many COVID-19 cases may present with pure neurological manifestations at onset with non-neurological features manifesting few days later and we propose the term "Neuro-COVID syndrome" for such cases. Awareness of neurological manifestations may facilitate its management and improve outcome in such patients.

Connecting the Dots: Exploring the Relationship between Optical Coherence Tomography and 99mTc-TRODAT-1 SPECT Parameters in Parkinson's Disease.

Background and Objective: While optical coherence tomography (OCT) is explored as a potential biomarker in Parkinson's disease (PD), technetium-99m-labeled tropane derivative (99mTc-TRODAT-1) single-photon emission computed tomography (SPECT) imaging has a proven role in diagnosing PD. Our objective was to compare the OCT parameters in PD patients and healthy controls (HCs) and correlate them with 99mTc-TRODAT-1 parameters in PD patients. Materials and Methods: This cross-sectional study included 30 PD patients and 30 age- and gender-matched HCs. Demographic data, PD details including Movement Disorders Society Unified Parkinson's Disease Rating Scale-III (MDS-UPDRS-III) and Hoehn-Yahr (HY) staging, and OCT parameters including macular and peripapillary retinal nerve fiber layer (RNFL) thickness in bilateral eyes were recorded. PD patients underwent 99mTc-TRODAT-1 SPECT imaging. The terms "ipsilateral" and "contralateral" were used with reference to more severely affected body side in PD patients and compared with corresponding sides in HCs. Results: PD patients showed significant ipsilateral superior parafoveal quadrant (mean ± standard deviation [SD] = 311.10 ± 15.90 vs. 297.57 ± 26.55, P = 0.02) and contralateral average perifoveal (mean ± SD = 278.75 ± 18.97 vs. 269.08 ± 16.91, P = 0.04) thinning compared to HCs. Peripapillary RNFL parameters were comparable between PD patients and HCs. MDS-UPDRS-III score and HY stage were inversely correlated to both ipsilateral (Spearman rho = -0.52, P = 0.003; Spearman rho = -0.47, P = 0.008) and contralateral (Spearman rho = -0.53, P = 0.002; Spearman rho = -0.58, P < 0.001) macular volumes, respectively. PD duration was inversely correlated with ipsilateral temporal parafoveal thickness (ρ = -0.41, P = 0.02). No correlation was observed between OCT and 99mTc-TRODAT-1 SPECT parameters in PD patients. Conclusion: Compared to HCs, a significant thinning was observed in the ipsilateral superior parafoveal quadrant and the contralateral average perifoveal region in PD patients. Macular volume and ipsilateral temporal parafoveal thickness were inversely correlated with disease severity and duration, respectively. OCT and 99mTc-TRODAT-1 SPECT parameters failed to correlate in PD patients.

Phenomenological patterns and aetiological spectrum in patients visiting a tertiary care Movement disorders service in India: An observational study.

OBJECTIVE: Although previous studies have described phenomenological diagnoses, they lacked description of aetiological spectrum in patients visiting movement disorders (MD) service. Herein, we classify the MD phenomenology and describe aetiology wise distribution of each phenomenology in patients visiting a tertiary care movement disorders service. METHODS: Collected information included demographic profile (age of onset, age at presentation, gender, duration of illness before presentation), predominant MD phenomenology [such as parkinsonism, dystonia, ataxia, tremor, chorea, ballism, myoclonus, tics, stereotypy, restless legs syndrome (RLS) and others], diagnostic evaluations and detected aetiology. RESULTS: This observational study included 1140 MD patients over a span of 5 years. The median (IQR) age of onset was 49 (35-60) years and age at presentation was 54 (40-65) years, with median duration of illness being 36 (18-72) months. Nearly two-third of patients were males (M:F=731:409). Parkinsonism (n=494, 43.3 %) was the most common MD phenomenology observed, followed by dystonia (n=219, 19.2 %), ataxia (n=125, 11 %), tremor (n=118, 10.4 %), myoclonus (n=73, 6.4 %), chorea (n=40, 3.5 %), spasticity (n=22, 1.9 %), tics (n=8, 0.7 %), and RLS (n=8, 0.7 %). Thirty-three (2.9 %) patients were grouped under miscellaneous MDs. Overall, neurodegenerative disorders (57.4 %) were the most common cause of MDs. Parkinson's disease, genetic dystonia, essential tremor, genetic ataxias, hemifacial spasm, and Huntington's disease were the most common aetiologies for parkinsonism, dystonia, tremor, ataxia, myoclonus, and chorea, respectively. CONCLUSION: Parkinsonism was the most common phenomenology observed in MD patients, and was followed by dystonia, ataxia and tremor. Neurodegenerative disorders were the most common aetiology detected.

Spinal Muscular Atrophy and Progressive Myoclonic Epilepsy: A Rare Association.

The association of spinal muscular atrophy (SMA) with progressive myoclonic epilepsy, also known as "SMA plus," is a unique syndrome linked to non-survival motor neuron (non-SMN) genes. The disease starts in childhood with progressive weakness and atrophy of muscles; myoclonic epilepsy develops during later childhood, after the onset of motor symptoms. In this report, we describe a case of SMN gene unrelated SMA and myoclonic epilepsy, supported by electrophysiological and neuropathological evidences.