Recent reports indicate that besides respiratory and systemic symptoms among coronavirus disease (COVID-19) patients, the disease has a wide spectrum of neurological manifestations (encephalitis, meningitis, myelitis, acute disseminated encephalomyelitis, metabolic and acute hemorrhagic necrotizing encephalopathy, cerebrovascular diseases, Guillain-Barré syndrome, polyneuritis cranialis, dysautonomia, and myopathies). The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can spread from the respiratory system to the central nervous system, using transneuronal and hematogenous mechanisms. Although not every COVID-19 patient will test positive for the virus in the cerebrospinal fluid exam, the appearance of neurological symptoms associated with SARS-CoV-2 infection reveals the importance of understanding the neurologic manifestations and capacity for neural invasion associated with the pathogen. These aspects are relevant for correct diagnosis and treatment, and for the potential development of vaccines. This review highlights the latest evidence of SARS-CoV-2 infection with a focus on neurological involvement and potential neuropathogenesis mechanisms.

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Introduction: The association of depressive and apathetic symptoms after lesions in the frontal region in the territory of the anterior cerebral artery is described, presumably due to interruption of complex subcortical frontal circuits. Objectives: Illustrate and discuss a bilateral frontal syndrome resulting from stroke in the territory of the anterior cerebral artery, as well as, the possible confusion between functional and organic conditions presenting the same symptoms. Results: 61-year-old man complaining of falls and left lower limb weakness. Moreover, had been interned due to suicide attempt recently. He is hypertensive and was addicted to alcohol and illicit drugs. Two years before, he had a left anterior cerebral artery ischemic that led to right lower limb paresis. At admission, he had poor interaction and presented hyperreflexia and Babinski sign at the right lower limb while normoreflexia at left. Computed tomography (CT) of the skull showed left frontal encephalomalacia. It was discarded metabolic and infectious disturbance as well as no signs of trauma from reported falls or high-risk lesions for new stroke. Psychiatric evaluations identified depression related to social, and economic factors. Pharmacological and behavioral measures were instituted. However, the condition worsened with the onset of mutism, akinesia, and abulia, which was attributed to the wors ening of depression. Antidepressant regimen was adjusted again and new brain CT was performed. It disclosed a new stroke of the right anterior cerebral artery. Initially, the symptoms were attributed to a functional condition and no organic justification was found. Nevertheless, the worsening of the basal status evolved to a catatonic manifestation, in parallel to a new frontal stroke. Previous contralateral frontal stroke might have turned the patient vulnerable to this condition. Nonetheless, the course of time eased by pharmacological strategy used (lithium, amitriptyline, and risperidone), was able to reverse the condition, except for left leg monoplegia evidenced after the restoration of spontaneous motricity. Conclusion: The case illustrates the clinical-anatomical correlations of anterior cerebral artery stroke, but also highlights the interface between neurology and psychiatry.

Diabetic amyotrophy is a rare condition in diabetic patients, usually associated with important weight loss. In the present case, we show a rare presentation of diabetic amyotrophy phenotype in the context of treatment induced neuropathy of diabetes neuropathy (TIND) after a strict glycemic control in a patient with long-standing poor controlled diabetes and without related weight loss. Even though it’s an uncommon presentation, because of diabetes high prevalence worldwide the knowledge of its complications is important to the adequate treatment and follow-up to improve patients’ quality of life.