COVID-19 and spinal cord injuries: The viewpoint from an emergency department resident with quadriplegia.

Spinal cord injuries (SCIs) present distinct physiological and social considerations for the emergency physician. During the COVID-19 pandemic, these considerations may generate unique challenges for emergency physicians managing patients with SCIs. Physiological disruptions may alter the way SCI patients present with COVID-19. The same disruptions can affect management of this vulnerable patient group, perhaps warranting early aggressive treatment. The medical picture will often be complicated by unique social characteristics. The reliance on caregivers for activities of daily living can, as an example, increase the human resource requirement of an ED. Considering the vulnerabilities and complexities of patients with SCI, the community should prioritise prevention of COVID-19 infections in this group. In the event that they do present to an ED, planning for and understanding their complexities will facilitate optimal management.

Dengue fever presenting as quadriparesis due to hypokalaemia: a rare presentation.

Dengue is one of the leading causes of arthropod borne viral haemorrhagic fever. Majority of the times, it clinically manifests as fever, arthralgia and rash; however, we present a case of a young man who presented with progressively increasing weakness of all four limbs. Initial investigations showed low potassium, hence he was managed as hypokalaemic periodic paralysis. With initial history of fever and low platelets, dengue was suspected. Dengue antibody was checked which came out to be positive. Potassium was replaced which led to improvement in power of his limbs. He was discharged in a stable condition with a diagnosis of dengue with hypokalaemic quadriparesis.

Dengue Fever Presenting with Cervicodorsal Acute Spinal Spontaneous Subdural Hematoma-Case Report and Review of Literature.

BACKGROUND: Neurologic complications are increasingly being reported in dengue epidemics. Intraspinal hematomas are rare, and those associated with dengue fever are still rarer with only 1 being reported in the literature. CASE DESCRIPTION: We report a case of dengue fever presenting with acute-onset quadriparesis (upper limbs Medical Research Council [MRC] 4/5 and lower limbs 0/5) and urinary incontinence. The patient was radiologically diagnosed with cervicodorsal acute to subacute anterior epidural hematoma. On the basis of clinical and radiologic evaluations, the patient underwent an anterior cervical approach via a split-manubriotomy, C6-D4 right anterolateral partial oblique corpectomies for evacuation of the hematoma. Intraoperatively, however, there was no evidence of anterior epidural collection and the dura revealed a bluish hue. A durotomy revealed a subdural hematoma. After evacuation of the hematoma, the patient remained paraplegic and her upper limb power worsened by MRC 1 grade. Postoperative magnetic resonance imaging revealed good evacuation and no new bleed; however, the intramedullary T2-weighted signal hyperintensities extending up to C2 persisted. She was on ventilatory support for almost 5 months. For diaphragmatic incapacity she underwent bilateral cervical phrenic nerve stimulation (diaphragmatic pacing). Despite initial improvement, she succumbed to multiple underlying comorbidities. CONCLUSIONS: Acute spontaneous spinal subdural hematoma (SSDH) is extremely rare but should be kept in mind in patients with dengue hemorrhagic fever. The radiologic findings could be deceptive and plain computed tomography and magnetic resonance imaging should be used as complementary studies to establish the diagnosis of acute spontaneous SSDH. The outcomes of SSDH are guarded, and elaborate patient counseling should be done preoperatively, keeping these in perspective.

Case report: subacute tetraplegia in an immunocompromised patient.

BACKGROUND: Clinical reasoning in Neurology is based on general associations which help to deduce the site of the lesion. However, even "golden principles" may occasionally be deceptive. Here, we describe the case of subacute flaccid tetraparesis due to motor cortical lesions. To our knowledge, this is the first report to include an impressive illustration of nearly symmetric motor cortical involvement of encephalitis on brain MRI. CASE PRESENTATION: A 51 year old immunocompromized man developed a high-grade pure motor flaccid tetraparesis over few days. Based on clinical presentation, critical illness polyneuromyopathy was suspected. However, brain MRI revealed symmetrical hyperintensities strictly limited to the subcortical precentral gyrus. An encephalitis, possibly due to CMV infection, turned out to be the most likely cause. CONCLUSION: While recognition of basic clinical patterns is indispensable in neurological reasoning, awareness of central conditions mimicking peripheral nervous disease may be crucial to detect unsuspected, potentially treatable conditions.

Rare natural type 3/type 2 intertypic capsid recombinant vaccine-related poliovirus isolated from a case of acute flaccid paralysis in Brazil, 2015.

A natural type 3/type 2 intertypic capsid recombinant vaccine-related poliovirus was isolated from an acute flaccid paralytic case in Brazil. Genome sequencing revealed the uncommon location of the crossover site in the VP1 coding region (nucleotides 3251-3258 of Sabin 3 genome). The Sabin 2 donor sequence replaced the last 118 nt of VP1, resulting in the substitution of the complete antigenic site IIIa by PV2-specific amino acids. The low overall number of nucleotide substitutions in P1 region indicated that the predicted replication time of the isolate was about 8-9 weeks. Two of the principal determinants of attenuation in Sabin 3 genomes were mutated (U472C and C2493U), but the temperature-sensitive phenotype of the isolate was preserved. Our results support the theory that there exists a PV3/PV2 recombination hotspot site in the tail region of the VP1 capsid protein and that the recombination may occur soon after oral poliovirus vaccine administration.

Longitudinal extensive transverse myelitis with cervical epidural haematoma following dengue virus infection.

BACKGROUND: Longitudinal extensive transverse myelitis associated with dengue infection is rare with no reported paediatric cases. METHODS: We report a 12-year-old girl who presented with flaccid quadriplegia 8 days after onset of acute dengue fever. MRI spine showed T2 hyperintensity associated with epidural hematoma at C3-C6 level of the spinal cord. Transcranial magnetic brain stimulation revealed absent motor evoked potentials bilaterally. We also summarise and compare the reported cases of transverse myelitis associated with dengue infection. RESULTS: Immunomodulatory treatment was given which included pulse methylprednisolone, intravenous immunoglobulin and plasmapharesis. Six months post-admission, there was a good (near-complete) clinical recovery with the repeat MRI showing mild residual hyperintensity at C4 level and complete resolution of epidural haematoma. CONCLUSION: This is the first reported paediatric case of longitudinal extensive transverse myelitis following dengue infection. It is also the first to illustrate that in patients with concomitant epidural haematoma a good outcome is possible despite not having surgical decompression. Clinicians should be aware of parainfectious dengue-related longitudinal extensive transverse myelitis in children and consider prompt immunomodulatory treatment.

Acute longitudinal and hemorrhagic myelitis caused by varicella-zoster virus in an immunocompetent adolescent.

OBJECTIVES: In immunocompetent person, varicella-zoster virus (VZV)-induced myelitis is rare and the lesion usually comprise focal spinal cord segment. VZV-induced hemorrhagic myelitis with lesions comprising longitudinal spinal cord has never been reported. METHODS: We report a 15-year-old male patient who developed acute flaccid quadriplegia, days after a common cold. One week after the quadriplegia developed, he presented a typical herpes zoster on the lateral side of his left waist. RESULTS: IgG antibody for VZV was detected in cerebrospinal fluid and the spinal cord magnetic resonance imaging findings were consistent with that of small vessel vasculitis. Treatment with acyclovir and corticosteroids resulted in no significant clinical improvement. CONCLUSIONS: In this report, we wanted to emphasize the hemorrhage, the extensiveness of inflammatory changes induced by VZV in spinal cord. It is suggested that VZV should be considered as a possible cause of a severe hemorrhagic myelitis even in immunocompetent adolescent.

Dengue infection presenting as acute hypokalemic quadriparesis.

Dengue infection is one of the most common viral hemorrhagic fevers seen in the tropical countries, including India. Its presentation varies from an acute self-resolving febrile illness to life-threatening hemorrhagic shock and multiorgan dysfunction leading to death. Neurological presentations are uncommon and limited to case reports only. Most common neurological manifestations being encephalitis, acute inflammatory demyelinating polyradiculoneuropathy, transverse myelitis, and acute disseminated encephalomyelitis.Hypokalemic quadriparesis as a presenting feature of dengue is extremely rare. Here, we report this case of a 33-year-old female, who presented with hypokalemic quadriparesis and was subsequently diagnosed as dengue infection.

Dengue infection causing acute hypokalemic quadriparesis.

Dengue infection is endemic to India and an important public health problem. We report three confirmed cases of dengue infection with acute, pure motor, reversible quadriparesis due to hypokalemia. Clinicians should be aware of such an association and consider the clinical possibility in the differential diagnosis while evaluating acute quadriparesis in patients with dengue fever, especially in endemic areas.

Central hypoventilation syndrome after Haemophilus influenzae type b meningitis and herpes infection.

A case of central hypoventilation syndrome was identified in a child with brainstem and cervical cord injury following Haemophilus influenzae type b meningitis and extensive herpes simplex infection. This process resulted in a spastic tetraplegia, and the child continues to require respiratory support. Possible mechanisms of causation are discussed including an evolving, progressive inflammatory or vasculitic process in the setting of transient immunosuppression.

A 41-year-old HIV-positive man with acute onset of quadriplegia after West Nile virus infection.

Most cases of West Nile encephalitis virus (WNV) infection are asymptomatic. In cases where WNV is symptomatic, patients usually experience high fever of sudden onset, myalgia, headache, and gastrointestinal symptoms, accompanied by a macular erythematous rash in a quarter to half of cases. More severe infections manifest as a poliomyelitis. Immunocompromise and immune senescence confer an increased risk of severe central nervous system (CNS) infection. Patients with human immunodeficiency virus (HIV) infection are therefore more susceptible, but, because the symptoms of WNV infection may be attributed to other CNS syndromes common in HIV patients, it is likely that the presence of WNV infection is underdiagnosed and underreported. We present a patient with severe WNV infection who was found to be HIV positive, who also suffered hearing loss. Several key differences in the presentation of WNV infection and Guillain-Barré syndrome that have treatment implications are discussed.

Infantile spasms and cytomegalovirus infection: antiviral and antiepileptic treatment.

From 1 January 1995 to 31 December 2004, 22 patients (13 males, nine females; age range 2-12mo) with infantile spasms and cytomegalovirus (CMV) infection were treated with intravenous ganciclovir (GCV) and antiepileptic drugs. GCV was given for 3 to 12 weeks with a 1-month interval (one, two, or three courses). Epileptic spasms occurred before (group A: eight patients), simultaneously (group B: eight patients), and after (group C: six patients) a diagnosis of human CMV (HCMV) infection and antiviral treatment. In 11 patients, DNA CMV [corrected] was found in cerebrospinal fluid by nested-polymerase chain reaction method (neuroinfection). All infants excreted CMV in urine. DNA CMV [corrected] and specific immunoglobulin M and immunoglobulin G antibodies were present in blood. Ten patients, including four with neuroinfection, have been seizure-free for at least the past 18 months. In two patients with neuroinfection, vigabatrin monotherapy was withdrawn after a 2 year 6 month seizure-free period. Eighteen patients required antiepileptic drugs polytherapy, four of whom required additional adrenocorticotropic hormone (ACTH). Six patients on polytherapy were seizure-free on follow-up, two of whom were treated with ACTH, but one patient [corrected] who required ACTH [corrected] was seizure-free on follow-up. In five patients, psychomotor development was normal, 16 had tetraplegia (Gross Motor Function Classification System [GMFCS] Level V), and one had diplegia (GMFCS Level III). Early antiviral and antiepileptic therapy could result in the long-term cessation of seizures.

Hepatitis C virus acute quadriparetic vasculitic neuropathy responsive to cyclophosphamide.

PURPOSE: Hepatitis C viral [HCV] infection is a chronic multisystem disorder that may have an indolent course initially. Peripheral neuropathy associated with cryoglobulinemia and a systemic vasculitis is a well-described complication of HCV infection. But this neuropathy is not known to have a late-onset acute fulminant phase. This acute fulminant phase is characterized by quadriparesis associated with pulmonary and/or renal insufficiency, and it may occur despite adequate treatment for HCV infection. The purpose of this study is to report that patients treated for chronic HCV infection may manifest a secondary progressive acute fulminant neuropathy associated with respiratory and/or renal insufficiency that is responsive to cyclophosphamide. METHODS: Case series retrospective data analysis. RESULTS: Three patients with biopsy-proven HCV associated vasculitic neuropathy manifested a secondary progressive acute fulminant course resulting in quadriparesis within 5 years of the initial diagnosis. Complete remission was achieved with cyclophosphamide therapy such that all patients became ambulatory. CONCLUSIONS: HCV-associated vasculitic neuropathy may manifest a secondary phase, which is acute, fulminant and progressive that is superimposed on an otherwise slowly progressive disorder. Cyclophosphamide therapy may abort progression and induce remission of this acute fulminant phase.

Acute pure motor quadriplegia: is it dengue myositis?

BACKGROUND AND AIM: In view of paucity of comprehensive evaluation about dengue infection producing quadriplegia, we report the clinical, laboratory and neurophysiological studies in these patients. SUBJECTS AND METHODS: Seven out of 16 patients with dengue infection presented with quadriplegia and they were subjected to a detailed clinical history and examination. Diagnosis of dengue was based on characteristic clinical and positive serum IgM ELISA. Blood counts, serum chemistry, CSF analysis and nerve conduction and electromyographic (EMG) studies were performed in all. Outcome was defined at the end of 1 month into complete, partial and poor on the basis of activities of daily living RESULTS: The age of the patients ranged between 9 and 42 years and 2 were females. Fever was present in all and myalgia in 5 patients. Weakness developed within 3-5 days of illness, which was severe in 4 and moderate in 3 patients. Hypotonia and hyporeflexia were present in 5 patients. Nerve conduction and EMG studies were normal in all except one whose EMG was myopathic. Serum CPK and SGPT were raised in all and serum bilirubin in 3 patients. All the patients had coagulopathy and 6 had thrombocytopenia. Muscle biopsy in 1 patient was suggestive of myositis. Six patients improved completely and one had poor recovery who needed ventilatory support. CONCLUSION: Dengue virus infection may result in acute pure motor quadriplegia due to myositis. In an endemic area it should be considered in the differential diagnosis of acute flaccid paralysis.