ABSTRACT
Intro: Coronavirus disease (COVID-19) is currently a global health crisis and is caused by a new strain of coronavirus. However, emerging literature of case reports noted possible extrapulmonary manifestations of the disease. Because COVID 19 is a relatively new disease, at present, little existing literature tackles the diagnosis and therapeutic management of COVID-19-related conditions outside the pulmonary system. Method(s): This is a case of a 24-year-old male presented with the chief complaint of sudden stiffening of all extremities. Non-contrast computed tomography (CT) scan was unremarkable. Chest X-ray revealed interstitial pneumonia and SARS-CoV-2 RT-PCR (OPS/NPS) was positive. Electrocardiogram (ECG) findings showed supraventricular tachycardia and had elevated Troponin I levels. Pertinent physical findings noted were slurring of speech, dysmetria, and vertical nystagmus. Finding(s): The patient was initially treated as a case of Bacterial Abscess versus Viral encephalitis. Pericardial ultrasound revealed small pericardial effusion and was started on Colchicine. Repeat cranial CT scan noted unremarkable results but due to persistence of symptoms, the patient was started with Dexamethasone. On Day 16 of illness, the patient was noted to have full resolution of symptoms. Rapid antibody testing was done which revealed positive for both IgG and IgM hence the patient was discharged with the final diagnosis of Viral Myopericarditis resolved, Viral encephalitis resolved, COVID-19 pneumonia recovered. Conclusion(s): Extrapulmonary manifestations have been reported increasingly as an atypical presentation of COVID 19 infection. Early recognition of viral myopericarditis and viral encephalitis as a manifestation of COVID 19 can lead to the initiation of proper treatment and management. More reports on these cases can aid future studies on diagnostics and therapeutic approaches during the COVID-19 pandemic.Copyright © 2023
ABSTRACT
A 27- year-old previously healthy man presented to the emergency department with a 3-day history of confusion, urinary retention, cough, slurred speech, intermittent vertigo, and unsteady gait after being started on outpatient abx for diagnosis of community acquired pneumonia at an outside facility. On presentation, his vital signs were significant for a Temp. of 102.4 F, a HR of 118 bpm, a RR of 22 bpm, a BP of 135/75 mmHg, O2 sats down to the 80s% with a new oxygen requirement of 3 L/min. His neurological exam was remarkable for dysarthria, a wide based and unsteady gait, forward drift on standing, bilateral dysmetria and was otherwise non-focal. Bilateral basilar rales were noted on lung exam. Initial workup was significant for a sodium level of 129, potassium 3.1, AST 178, ALT 31. His urine legionella antigen test was positive and COVID-19 PCR test was negative. CT of the chest demonstrated multifocal pneumonia. The predominant neurological picture on presentation warranted a lumbar puncture as well as an MRI of the brain, both of which came back negative. HIV test was negative as well. The spectrum of neurological manifestations of legionnaire's disease is quite wide ranging from simple headaches to acute disseminated encephalomyelitis (ADEM). While up to 40% of patients may present with headaches and some confusion, the specific cerebellar presentation is quite rare and has been described in case reports. According to Shelburne(1), there has been instances where the neurological manifestations have lasted up to 3 years after resolution of the pulmonary disease. In a review article detailing 29 cases of cerebellar dysfunction in Legionnaire's disease, a lumbar puncture performed in 16 of the cases showed that the majority had no abnormalities in CSF studies. The propensity for Legionella to specifically manifest as cerebellar Sx remains to be studied. Interestingly, another case report of two patients with neurological symptoms, showed hypoperfusion of the cerebellar and frontal lobes on single photon emission while CT and MRI imaging of the brain were normal. We add to the literature another 'cerebellar' presentation of Legionnaire's disease.
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Objective: NA Background: Creutzfeldt-Jakob disease (CJD) is an extremely rare but fatal neurodegenerative disease with incidence of one in a million worldwide, and few than 1000 cases per year in the United States per year. Design/Methods: NA Case Summary: We present two probable CJD cases seen in the same hospital within one month. Case one was a 67-year-old white female, former psychology practice manager, presenting with worsening cognition, vertigo, behavioral changes and 15 lb weight loss over 6 months. Exam findings significant for MoCA of 17/30 (decreased to 15/30 after one week), constant right eye shut, mild dysmetria in both lower extremities, a wide based gait with small strides. Blood work and initial Spinal fluid studies were negative. Continuous EEG showing occasional right temporal slow, frequent generalized rhythmic theta and delta slowing. MRI brain findings were suggestive of CJD with hyperintensities in bilateral caudate nucleus and putamen. Patient did not respond to high dose steroid. Case two was a 78-year-old white male, admitted for deterioration in cognition, gait, speech, fatigue and intermittent body jerking. Progression of his symptoms was so rapid, from a highly functional retired funeral director, he became minimal speech, loss of ADL within 3 months. Exam was significant for orientation to self only, global aphasia, muscle weakness and startle myoclonus. Blood work and initial spinal fluid studies were negative. MRI brain showed asymmetric cortically based diffuse restriction within cingulate, caudate nucleus also left temporoparietal. EEG showed generalized rhythmic delta activity. CSF from both cases eventually showed positive RT-QuIC, 14-3-3 protein and highly elevated T-Tau protein. Conclusions: CJD is a transmittable, reportable disease. Two cases seen in the same hospital within one month skews from the previously known CJD prevalence. Surveillance and investigation on the reason of regional CJD arise during COVID-19 pandemic may prove to be important and urgent.
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Objective: To describe the occurrence of acute cerebellar ataxia after COVID-19 infection in a 5- year-old boy. Background: Neurologic manifestations can occur in many adult patients with COVID-19 but are less frequently described in the literature than the respiratory or inflammatory effects of the disease. There are even fewer reports of the neurologic manifestations of the disease in children. Design/Methods: A 5-year-old boy with type I diabetes mellitus was exposed to a COVID-19 positive classmate in school. He tested positive for the SARS-CoV-2 virus and developed mild symptoms including rhinorrhea and decreased energy. Eight days later he developed acute ataxia, double vision, tremor and dysmetria. He was admitted to the hospital for further evaluation. Results: He had hyperglycemia at presentation, however labs were not consistent with diabetic ketoacidosis. Nasopharyngeal swab for SARS-CoV-2 was positive by polymerase chain reaction, and SARS-CoV-2 IgG nucleocapsid antibody testing was positive in serum. Cerebrospinal fluid showed white blood cells 8 cells/uL, red blood cells 0 cells/uL, protein 20 mg/dL and glucose 110 mg/dL. Other infectious testing in the CSF was negative including CSF testing for SARS-CoV-2. Brain magnetic resonance imaging with and without contrast was normal. The patient was treated with supportive care and discharged home after 4 days. Symptoms gradually improved and resolved at 2 month follow up. Conclusions: Acute cerebellar ataxia can be seen in children, often following a viral infection. Rare reports have described acute ataxia in adults recovering from COVID-19. Only one case report has previously described acute cerebellar ataxia in a pediatric patient of 13 years (Tomar et al 2021). Providers should be aware of acute cerebellar ataxia as a possible sequela in pediatric patients recovering from COVID-19.
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Objective: To understand that COVID-19 can cause epochs of sneezing. Background: While Coronavirus 19 has been reported to inhibit sternutation (Mattu, 2021), Coronavirus-induced epochs of sternutation has not henceforth been described. Case Study: 38-year-old right-handed nasute woman, seven months prior to presentation, experienced an acute onset of loss of smell and taste, with a positive nasopharyngeal swab for SARS COV-2. Since then there has been no improvement in her chemosensory complaints and has developed periods of sternutation, whereby she sneezes 18 times in a row every morning. Results: Abnormalities of physical examination: Neurological Examination: Motor Examination: Drift testing: Left pronator drift with left abductor digiti minimi sign. Cerebellar examination: dysmetria in both upper extremities, left more than right. High frequency low amplitude tremor on extension of both upper extremities. Reflexes: 3+ biceps and brachioradialis and absent ankle jerks bilaterally. Bilateral Hoffman reflexes. Chemosensory testing: Alcohol Sniff Test: 0 (anosmia). Olfactory Retronasal Smell Test Index: 0 (anosmia). Gustatory testing: Propylthioruacil Disk Taste Test: 0 (ageusia). Conclusions: The neuroanatomy of the sneeze reflex suggests that it occurs through the afferent pathway from the trigeminal nerve to the rostral dorsolateral medullary sneezing center where the efferent discharge of the autonomic nervous system occurs through the nervous intermedius to the greater superficial petrosal nerve and to the sphenopalatine ganglion. In any of these afferent or efferent pathways or in the central nervous system itself, COVID may have acted to cause intermittent irritation and thus epochs of sneezing (Songu, 2009;Herman, 1983). The common experience of sneezing occurring in threes may be centrally mediated and this occurred with eighteen sneezes may just be a prolonged variant of such a chronobiological reflex. In those who present with COVID-19, query as to epochs of sternutation may be revealing.
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Objective: NA Background: The etiology of MOGAD post-COVID-19 infection is not well understood and there are limited publications describing cases in pediatric patients. Here we report a case of a 14-year-old male with MOG antibody positive ADEM (Acute Disseminated Encephalomyelitis) and positive COVID-19 PCR. Design/Methods: NA Results: The patient presented to our hospital in December of 2020 with acute onset of ataxia and lower extremity weakness. His exam was pertinent for mild and symmetric weakness in bilateral hip flexors, dysmetria with ataxic gait, as well as bilateral patellar and ankle hyporeflexia. MRI brain showed symmetric areas of T2 signal hyperintensity, predominantly adjacent to the fourth ventricle as well as the peri-insular and frontal regions. MRI of the lumbosacral spine demonstrated T2 signal hyperintensity within the conus medullaris without enhancement. CSF studies revealed an increased white blood cell count of 74 (90% lymphocyte), elevated protein of 51, elevated kappa free light chain (0.12) and positive oligoclonal bands (3). He was also found to be serum anti-MOG antibody positive (1:100) and COVID-19 positive (PCR). He received 1000 mg of intravenous methylprednisolone daily for 5 days and 2 g/kg IVIG. He was subsequently placed on a 6 week taper of oral prednisone. 2 months after his initial presentation, his neurologic symptoms have completely resolved, and he has been asymptomatic since. Repeat MRI brain 4 months later showed improvement in his multifocal supratentorial FLAIR signal abnormalities. Conclusions: Here we describe a case of a 14-year-old male with MOGAD post-COVID-19, with complete resolution of his symptoms after high dose corticosteroid and IVIG treatment.
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We report a 15-year-old boy presenting at our emergency department with acute onset of dysarthria and prior headache, rotary vertigo, nausea, vomiting and gait disturbance for 2 days. 18 days earlier he was tested positive for SARS CoV-19. Physical examination showed pronounced dys-arthria, nystagmus, absent reflexes, dysmetria and ataxia. Laboratory findings showed relative lymphocytosis with a negative C-reactive pro-tein, normal coagulation and elevated liver enzymes (AST, ALT, GGT). Drug screening was negative. First suspicion was postinfectious cerebellitis and he was admitted to IMC for observation. Subsequently, vomiting fre-quency rose, hence cMRI was performed, but showed no abnormalities. Miller-Fisher syndrome was suspected, however CSF examination showed no cytoalbumin dissociation, but discrete mononuclear cell count eleva-tion. Ceftriaxone and acyclovir were administered empirically. In addition, intravenous immunoglobulin and corticosteroids were given to treat viral cerebellitis/encephalitis. Due to suggestive atypical lymphocytes in the blood count, EBV testing was performed and serologies were positive. Multiple CSF viral/bacterial testings (Borrelia burgdorferi, Enterovirus, VZV, HSV 1/2) showed slightly positive EBV (PCR), congruent with blood results. Additionally, SARS-CoV-19 IgG were positive. The patient's condi-tion barely improved, a follow up cMRI showed no changes. Mobilization was fostered with a wheel chair and physical therapy. After two and a half weeks, he was discharged to pediatric neurorehabilitation in order to im-prove dysarthria, ataxia and address neuropsychological abnormalities. Two months after the diagnosis he is walking without aids but still shows trunk ataxia and dysarthria. He is still making constant progress and will hopefully recover completely. Neurological manifestation of EBV infection is extremely rare with the ma-jority of cases described in children. Nevertheless, some neurological manifestations have already been described including encephalitis, cere-bellitis, meningitis, transverse myelitis, and Guillain-Barré syndrome. These manifestations can occur alone or in the setting of infectious mon-onucleosis. In our case a co-infection of SARS-Cov-19 and EBV or a reactivation of EBV due to SARS-Cov-19 is possible as cause of the cerebellitis. Treatment op-tions were fully employed, but the recovery presented a slow course.