Adult-Onset Tics After Being Crushed by an Air Conditioner: A Case Report.

Tics are sudden, repetitive, non-rhythmic movements and/or vocalizations. Generally, tics begin during childhood as a part of Tourette syndrome (TS) and rarely have an onset during adulthood. We describe a 30-year-old male who presented with multiple motor and vocal tics two weeks following a closed head injury with alteration of consciousness as a result of being crushed against the wall by a 4,100-pound air-conditioning unit. He started having motor tics that developed in a rostrocaudal distribution, followed by simple and complex vocal tics. His tics increased in severity over several months following the injury until presentation. He was started on pimozide and received hyperbaric oxygen treatment which improved both motor and vocal tics.

New-Onset Chorea Post-COVID-19 Infection: A Case Report.

Although the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily involves the cardiovascular and respiratory systems, neurological manifestations, including movement disorders such as myoclonus and cerebellar ataxia, have also been reported. However, the occurrence of post-SARS-CoV-2 chorea is rare. Herein, we describe a 91-year-old female with a past medical history of hypothyroidism who developed chorea after two weeks of contracting a mild coronavirus disease (COVID-19).

Abdominal Compartment Syndrome with Super-K (Ketamine) for Super-R(efractory) Status Epilepticus: A Case Report.

Refractory status epilepticus is commonly defined as status epilepticus that fails to respond to two or more appropriately dosed intravenous anti-seizure medications including at least one non-benzodiazepine drug. Super-refractory status epilepticus (SRSE) is when status epilepticus continues for ≥24 h despite anesthetic treatment or recurs on an attempted wean of the anesthetic drugs. There is little evidence to guide the management of SRSE. Of late, unconventional therapies have been described in the literature regarding the management of SRSE, with ketamine leading the pack. Studies have noted ketamine's therapeutic efficacy up to 91% in SRSE cessation. Common side effects of ketamine include nausea, vomiting, headache, and hallucinations; but to our knowledge, ketamine has not been implicated in the pathogenesis of abdominal compartment syndrome. We describe a 74-year-old male who developed severe abdominal compartment syndrome in the setting of ketamine infusion for new-onset SRSE to increase awareness about this potential complication.

Predictors of Seizure Recurrence after Acute Symptomatic Seizures in Ischemic Stroke Patients.

PURPOSE: Seizure is a well-recognized complication of both remote and acute ischemic strokes. Predictors of seizure recurrence and epilepsy in patients with ischemic stroke who develop acute symptomatic seizures (ASyS) on continuous electroencephalography (cEEG) have not been well studied. METHODS: We present a five-year retrospective study of acute and remote ischemic stroke patients who developed ASyS on cEEG. We then identified risk factors for the development of seizure recurrence. RESULTS: Sixty-five patients with ischemic stroke and ASyS were identified and reviewed. All ASyS were noted to be nonconvulsive seizures. Clinical recurrence of seizures was identified in 19 of these patients (29.2%) at follow-up. Rate of seizure recurrence was higher in remote ischemic stroke patients (84.2%), compared to acute ischemic stroke patients (15.8%, p = 0.0116, OR 0.17, 95% CI 0.049-0.65). Sharp waves/spikes on follow-up EEG significantly correlated with seizure recurrence (p = 0.006, OR 0, 95% CI 0-0.3926). Patients discharged on ≥3 antiepileptic drugs (AEDs) were at a higher risk of having seizure recurrence (p = 0.0015, OR 0.05, 95% CI 0.0089-0.37). CONCLUSION: We identified risk factors of seizure recurrence in patients with ASyS as remote ischemic stroke, requiring multiple AEDs, and the presence of sharp waves on follow-up EEG. This study highlights the usefulness of cEEG in evaluating patients with acute or remote strokes.

Brain and Peripheral Atypical Inflammatory Mediators Potentiate Neuroinflammation and Neurodegeneration.

Neuroinflammatory response is primarily a protective mechanism in the brain. However, excessive and chronic inflammatory responses can lead to deleterious effects involving immune cells, brain cells and signaling molecules. Neuroinflammation induces and accelerates pathogenesis of Parkinson's disease (PD), Alzheimer's disease (AD) and Multiple sclerosis (MS). Neuroinflammatory pathways are indicated as novel therapeutic targets for these diseases. Mast cells are immune cells of hematopoietic origin that regulate inflammation and upon activation release many proinflammatory mediators in systemic and central nervous system (CNS) inflammatory conditions. In addition, inflammatory mediators released from activated glial cells induce neurodegeneration in the brain. Systemic inflammation-derived proinflammatory cytokines/chemokines and other factors cause a breach in the blood brain-barrier (BBB) thereby allowing for the entry of immune/inflammatory cells including mast cell progenitors, mast cells and proinflammatory cytokines and chemokines into the brain. These peripheral-derived factors and intrinsically generated cytokines/chemokines, α-synuclein, corticotropin-releasing hormone (CRH), substance P (SP), beta amyloid 1-42 (Aß1-42) peptide and amyloid precursor proteins can activate glial cells, T-cells and mast cells in the brain can induce additional release of inflammatory and neurotoxic molecules contributing to chronic neuroinflammation and neuronal death. The glia maturation factor (GMF), a proinflammatory protein discovered in our laboratory released from glia, activates mast cells to release inflammatory cytokines and chemokines. Chronic increase in the proinflammatory mediators induces neurotoxic Aß and plaque formation in AD brains and neurodegeneration in PD brains. Glial cells, mast cells and T-cells can reactivate each other in neuroinflammatory conditions in the brain and augment neuroinflammation. Further, inflammatory mediators from the brain can also enter into the peripheral system through defective BBB, recruit immune cells into the brain, and exacerbate neuroinflammation. We suggest that mast cell-associated inflammatory mediators from systemic inflammation and brain could augment neuroinflammation and neurodegeneration in the brain. This review article addresses the role of some atypical inflammatory mediators that are associated with mast cell inflammation and their activation of glial cells to induce neurodegeneration.