Neurological features and outcome in COVID-19: dementia can predict severe disease.

The COVID-19 pandemic has infected more than 22 million people worldwide. Although much has been learned about COVID-19, we do not know much about its neurological features and their outcome. This observational study was conducted on the patients of Imam Hossein Hospital, and 361 adult patients (214 males) with confirmed diagnosis of COVID-19 from March 5, 2020 to April 3, 2020, were enrolled. Data was gathered on age, sex, comorbidities, initial symptoms, symptoms during the disease course, neurological symptoms, and outcome. The mean age of the patients was 61.90 ± 16.76 years. The most common initial symptoms were cough, fever, and dyspnea. In 21 patients (5.8%), the initial symptom was neurological. History of dementia was associated with severe COVID-19 disease (odds ratio = 1.28). During the course of the disease, 186 patients (51.52%) had at least one neurological symptom, the most common being headache (109 [30.2%]), followed by anosmia/ageusia (69, [19.1%]), and dizziness (54, [15%]). Also, 31 patients had neurological complications (8.58%). Anosmia, ageusia, dizziness, and headache were associated with favorable outcome (P < 0.001), while altered mental status and hemiparesis were associated with poor outcome. The mortality rate of patients who had neurological complications was more than twice than that of patients without neurological complication (P = 0.008). Almost half of the patients experienced at least one neurological symptom, which may be the initial presentation of COVID-19. Dementia appears to be associated with severe COVID-19. Mortality was higher in patients with neurological complications, and these patients needed more intensive care.

Neurological Development, Epilepsy, and the Pharmacotherapy Approach in Children with Congenital Zika Syndrome: Results from a Two-Year Follow-up Study.

Clinical outcomes related to congenital Zika syndrome (CZS) include microcephaly accompanied by specific brain injuries. Among several CZS outcomes that have been described, epilepsy and motor impairments are present in most cases. Pharmacological treatment for seizures resulting from epilepsy is performed with anticonvulsant drugs, which in the long term are related to impairments in the child's neuropsychomotor development. Here, we describe the results from a two-year follow-up of a cohort of children diagnosed with CZS related to the growth of the head circumference and some neurological and motor outcomes, including the pharmacological approach, and its results in the treatment of epileptic seizures. This paper is part of a prospective cohort study carried out in the state of Mato Grosso Sul, Brazil, based on a Zika virus (ZIKV)-exposed child population. Our data were focused on the assessment of head circumference growth and some neurological and motor findings, including the description of seizure conditions and pharmacological management in two periods. Among the 11 children evaluated, 8 had severe microcephaly associated with motor impairment and/or epilepsy. Seven children were diagnosed with epilepsy. Of these, 3 had West syndrome. In four children with other forms of epilepsy, there was no pharmacological control.

Acute viral encephalitis associated with human parvovirus B19 infection: unexpectedly diagnosed by metagenomic next-generation sequencing.

We report here a case of a 17-year-old boy with viral encephalitis associated with human parvovirus B19 who presented consciousness disturbance, left hemiparesis, and focal neurologic signs. The diagnosis was based on the specific sequence reads corresponding to human parvovirus B19 (PVB19) in a CSF sample as analyzed by metagenomic next-generation sequencing (mNGS). Thus, PVB19 should be considered in the differential diagnosis of encephalitis and encephalopathy of unknown etiology. The introduction of mNGS into the diagnostic protocol of neuropathies, especially for those undiagnosed, could interrogate all genetic information in a biologic sample and facilitate the identification of the etiological agent.

Segmental zoster paresis of unilateral upper extremity: A case report and literature review.

RATIONALE: Segmental zoster paresis (SZP) is a relatively rare neurologic complication of herpes zoster (HZ), and is characterized by focal asymmetric motor weakness in the myotome that corresponds to skin lesions of the dermatome. The upper extremities are the second most commonly involved regions after the face, and predominantly involve proximal muscles. The pathogenesis of SZP remains unclear; however, most of the reports indicate that it is the inflammation because of the spread of the herpes virus. PATIENT CONCERNS: A 72-year-old man without trauma history of the left shoulder joint developed weakness of the left proximal upper extremity 10 days after vesicular eruption of HZ. DIAGNOSES: His left shoulder girdle paresis was diagnosed with the upper truncus of the brachial plexus as a HZ complication according to a series of tests, including cervical magnetic resonance imaging (MRI), cerebral fluid analysis, sonography, and electrophysiological studies. INTERVENTIONS: Acyclovir and prednisolone were administered during hospitalization to treat SZP. Meanwhile, analgesics and gabapentin were administered to control the patient's neuralgic pain. He also received inpatient (daily) and outpatient (3 times per week) physical therapy along with range of motion and strengthening exercises. OUTCOMES: Partial improvement of the strength of the left shoulder girdle, and no improvement of the left deltoid muscle was observed 2 months after the interventions. LESSONS: This case emphasizes that HZ infections may be complicated by segmental paresis and they should be considered in the differential diagnosis of acute paresis in the upper limb. Awareness of this disorder is important because it avoids unnecessary invasive investigations and interventions, leading to suitable treatments with favorable prognosis.

Axillary mononeuropathy after herpes zoster infection misdiagnosed as neuropathic pain

Zoster-associated extremity paresis is a rare complication of herpes zoster (HZ) and is usually due to zoster-associated mononeuropathy. Complaints of a 77-year-old man started with pain in his right arm and 4 days later he developed itchy red HZ lesions in the same area. One week later, the patient developed weakness in his right arm. The patient was diagnosed with isolated axillary mononeuropathy by physical examination and electromyography. Here, we present a case of axillary mononeuropathy which is a rare complication of HZ infection and needs particular attention.

[Abdominal wall paresis as a complication of herpes zoster]. / Buikwandparese als complicatie van herpes zoster.

BACKGROUND: Herpes zoster is an illness which is especially common amongst the elderly in the Netherlands and which can express itself in various ways. Besides affecting sensory nerves, which leads to postherpetic pain, the varicella zoster virus may also invade motor nerves. CASE DESCRIPTION: A 73-year-old female went to the surgeon with symptoms of a painful swelling in the left lower abdomen. She had experienced herpes zoster at the site of the swelling a few months earlier. A CT scan revealed asymmetry of the abdominal wall musculature, which led us to suspect a link between motor involvement of herpes zoster and the abdominal swelling. EMG revealed denervation of the affected abdominal wall muscle, which confirmed the link with herpes zoster in that dermatome. CONCLUSION: Abdominal wall paresis caused by herpes zoster is a rare condition. It can be diagnosed on the basis of clinical findings and may be confirmed by EMG investigation of the affected muscle. In view of the temporary nature of the paresis, it is possible to opt for conservative management of the condition.

Brainstem encephalitis and acute polyneuropathy associated with hepatitis E infection.

A 59-year-old man presented with feverish illness. His Glasgow Coma Scale was 15, had reduced visual acuity in the left eye with partial left ptosis and mild left hemiparesis with an extensor left plantar. Over 48 hours, he accrued multiple cranial nerves palsies and progressed to a flaccid paralysis necessitating admission to an intensive care unit.Cerebrospinal fluid (CSF) study showed 20 lymphocytes and raised protein. Viral and bacterial PCRs were negative. Samples for Lyme, blood-borne viruses, syphilis and autoantibodies were also negative. MRI brain showed T2 abnormalities within the brainstem. Nerve conduction studies revealed an acute motor and sensory axonal neuropathy pattern of Guillian Barre Syndrome (GBS). The patient was treated for both infective and inflammatory causes of brainstem encephalitis and GBS.Retrospective studies confirmed the presence of hepatitis E virus (HEV) RNA in CSF and serum studies showed positive HEV IgG and IgM prior to intravenous infusion. After 3 months of intensive rehabilitation, the patient was discharged home walking with a frame.

[A 4-year-old girl with diarrhoea, paresis and mutism]. / En fire år gammel jente med diaré, kraftsvikt og mutisme.

BACKGROUND Rotavirus is a common cause of gastroenteritis in children. Neurological manifestations associated with rotavirus infections are well described and range from benign afebrile convulsions to lethal encephalopathy or encephalitis.CASE PRESENTATION We present an uncommon neurological manifestation in a Caucasian child in the course of a rotavirus infection. A 4-year old girl presented with mutism, hypotonia and reduced consciousness. Magnetic resonance imaging revealed diffusion abnormalities in the splenium corpus callosum and bilaterally in the nuclei dentate in the cerebellum. She was diagnosed with rotavirus cerebellitis.INTERPRETATION Her clinical symptoms and the magnetic resonance imaging abnormalities were uncommon and previously described in only a few Caucasian children. The outcome has varied, and some children have shown long term neurological sequela. Treatment with immunoglobulins and corticosteroids has been used in similar cases, but there is no established treatment for this condition.

Tumefactive multiple sclerosis and hepatitis C virus 2a/2C infection: Dual benefit of long-term interferon beta-1a therapy?

Hepatitis C virus (HCV) infection has been implicated in triggering acute disseminated encephalomyelitis but not tumefactive multiple sclerosis. We report the case of a 17-year-old female who presented with a 5-day history of left hemiparesis and hemisensory loss followed by a right third nerve palsy. Tumefactive multiple sclerosis was diagnosed based on the absence of encephalopathic signs, the presence of tumefactive brain lesions, the exclusion of neoplastic and infectious causes of the lesions by biopsy, and the occurrence of relapse after a period of remission. The patient was at risk for HCV infection due to parenteral drug abuse and multiple sexual partners. Serial HCV antibody tests and RNA polymerase chain reaction assays revealed acute HCV infection and genotyping showed HCV genotype 2a/2c. She was treated with high-dose methylprednisolone and discharged with only mild left hand weakness. Interferon beta-1a 30mcg was administered intramuscularly once a week. Remission from HCV infection was achieved in three years without standard anti-HCV therapy. This case suggests that CNS myelin is a potential target of the immune response to HCV 2a/2c infection, the HCV 2a/2c virus may be involved in triggering autoimmune tumefactive brain lesions, and interferon beta-1a is effective against HCV 2a/2c infection. We recommend serial HCV antibody testing and HCV RNA PCR assay, preferably with HCV genotyping, in all patients with acute inflammatory demyelinating diseases of the CNS.

Clinical, electrophysiologic, and imaging features of zoster-associated limb paresis.

INTRODUCTION: Paresis is a long-recognized complication of herpes zoster, but there has been comparatively little study of zoster-associated limb paresis (ZALP). METHODS: In this study we reviewed 49 Mayo Clinic patients with ZALP. RESULTS: The mean age of onset was 71 years, 67% were men, and the lower limb was affected in 55%. The mean weakness score was 2.0 (0 = normal strength, 4 = plegia). Most patients developed postherpetic neuralgia (PHN, 92% at 1 month and 65% at 3 months), and the average minimum duration of weakness was 193 days. ZALP was caused by radiculopathy (37%), plexopathy (41%), mononeuropathy (14%), and radiculoplexus neuropathy (8%). MRI demonstrated nerve enlargement, T2 signal prolongation, or enhancement in a majority (64%) of affected plexi and peripheral nerves. CONCLUSIONS: ZALP is associated with considerable weakness. It typically lasts at least several months, localizes to plexus or peripheral nerve in 63%, and is associated with high rates of PHN.

Hernia pulmonar secundaria a la paresia del músculo intercostal tras un episodio de herpes zóster torácico / Lung hernia secondary to intercostal muscle paresis after epidode of thoracic heres zoster

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Zoster-associated segmental paresis in a patient with cervical spinal stenosis.

Segmental zoster paresis is a rare complication of herpes zoster, characterized by focal motor weakness that does not always present simultaneously with skin lesions. Zoster paresis can be easily confused with other neuromuscular or spinal diseases. This case report describes the case of a 72-year-old woman with herpes zoster and cervical spinal stenosis at the same spinal level, where it was difficult to distinguish segmental zoster paresis from cervical radiculopathy combined with motor neuropathy. Although segmental zoster paresis in the upper extremity is rare, it should be included in the differential diagnosis of segmental pain and weakness in the extremities, especially in older or immunocompromised patients. Correct diagnosis is required, to avoid unnecessary surgery and allow timely antiviral treatment.