Intentional movement is an internally driven process that requires the integration of motivational and sensory cues with motor preparedness. In addition to the motor cortical-basal ganglia circuits, the limbic circuits are also involved in the integration of these cues. Individuals with Parkinson’s disease (PD) have a particular difficulty with internally generating intentional movements and maintaining the speed, size, and vigor of movements. This difficulty improves when they are provided with external cues suggesting that there is a problem with the internal motivation of movement in PD. The prevailing view attributes this difficulty in PD to the dysfunction of motor cortical-basal ganglia circuits. First, we argue that the standard cortical-basal ganglia circuit model of motor dysfunction in PD needs to be expanded to include the insula which is a major hub within the limbic circuits. We propose a neural circuit model highlighting the interaction between the insula and dorsomedial frontal cortex which is involved in generating intentional movements. The insula processes a wide range of sensory signals arising from the body and integrates them with the emotional and motivational context. In doing so, it provides the impetus to the dorsomedial frontal cortex to initiate and sustain movement. Second, we present the results of our proof-of-concept experiment demonstrating that the functional connectivity of the insula-dorsomedial frontal cortex circuit can be enhanced with neurofeedback-guided kinesthetic motor imagery using functional magnetic resonance imaging in subjects with PD. Specifically, we found that the intensity and quality of body sensations evoked during motor imagery and the emotional and motivational context of motor imagery determined the direction (i.e., negative or positive) of the insula-dorsomedial frontal cortex functional connectivity. After 10–12 neurofeedback sessions and “off-line” practice of the successful motor imagery strategies all subjects showed a significant increase in the insula-dorsomedial frontal cortex functional connectivity. Finally, we discuss the implications of these results regarding motor function in patients with PD and propose suggestions for future studies.

INTRODUCTION: Botulism is a rare, but potentially life-threatening neuroparalytic syndrome that can be caused by accidental (Foodborne or wound infection) or Iatrogenic exposure to botulinum toxins. Iatrogenic causes of botulism have been reported rarely in patients who have received botulinum toxin for cosmetic indications. Botulinum toxins work by blocking Acetylcholine release causing muscle relaxation. Serotypes A to G has been identified with type A causing the most severe syndrome. Botox (onabotulinum toxin A), used for cosmetic purposes, including but not limited to cervical dystonia, hyperhidrosis, upper and lower limb spasticity, and urinary incontinence. If botulinum neurotoxin enters the vascular system and is transported to peripheral cholinergic nerve terminals, including neuromuscular junctions, postganglionic parasympathetic nerve endings, and peripheral ganglia, it can lead to loss of strength, double vision, drooping eyelids, hoarseness, loss of bladder control, trouble breathing.

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Coronavirus disease 2019 (COVID-19) grew to pandemic proportions in 2020. Research has shown that the causative virus, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), uses the angiotensinconverting enzyme II (ACE-II) receptor to attack host cells. These ACE-II receptors are present essentially in all organs, acting as a route of entry for SARS-CoV-2 to cause a wide variety of manifestations. There is growing research showing the neurologic effects of COVID-19. There have been several cases of encephalopathy, stroke, and encephalitis associated with COVID-19, however, intraventricular hemorrhages (IVH) have rarely been reported. Here we present a case of an IVH in the setting of COVID-19. A 32-year-old male with no past medical history, and not taking any medications, presented to the emergency room after acute onset loss of consciousness. Inflammatory markers were elevated, and computerized tomographic (CT) of the head and chest showed an intraventricular hemorrhage and bilateral interstitial infiltrates, respectively. Although possibly coincidental, this may represent a rare extrapulmonary fatal manifestation of COVID-19. With the growing evidence of neurologic presentations in patients with COVID-19, clinicians should maintain a high index of suspicion for COVID-19 to cause fatal extrapulmonary manifestations.

SARS-CoV-2 is a respiratory virus causing mostly pulmonary manifestations. It has been associated with intracerebral pathology including stroke encephalitis and encephalopathy. Intraventricular hemorrhage may be an unknown fatal extrapulmonary presentation in patients with COVID-19 or a coincidental finding. CASE PRESENTATION: We report a case of a 32-year-old man with asthma not on any home medications particularly antiplatelet and anti-coagulation medications who presented to the hospital after cardiac arrest at home. He reported blurry vision that morning and collapsed soon after. As per family patient is not on any medications or drug abuse. He was resuscitated and mechanically ventilated in the field and arrived in the emergency department in an irreversible coma. On arrival, his vitals are recorded as tachycardia to 120, and blood pressure is 136/80. Initial labs showed anion gap metabolic acidosis with lactic acidosis and respiratory acidosis, leukocytosis, elevated ferritin, elevated AST, and ALT and in acute kidney injury, urine toxicology is negative. Computed tomographic imaging of the brain revealed diffuse intraventricular hemorrhage with associated hydrocephalus with no obvious parenchymal source of bleeding. Computed tomographic imaging of the chest showed bilateral pneumonia highly suspicious of COVID-19.