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.

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.

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.

[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.

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.

Herpes zoster-induced trunk muscle paresis presenting with abdominal wall pseudohernia, scoliosis, and gait disturbance and its rehabilitation: a case report.

Herpes zoster (HZ)-induced abdominal wall pseudohernia has been frequently reported, but there has been no report describing HZ-induced trunk muscle paresis leading to functional problems. We describe a 73-year-old man with T12 and L1 segmental paresis caused by HZ presenting with abdominal wall pseudohernia, scoliosis, and standing and gait disturbance who responded well to a systematic rehabilitation approach. He first noticed a right abdominal bulge in the 6th postherpetic week, which was gradually accompanied by right convex thoracolumbar scoliosis, pain, and standing and gait disturbance in the 12th week. Needle electromyography revealed abnormal spontaneous activities at rest in the right T12 myotomal muscles, and motor unit recruitment was markedly decreased. We arranged an outpatient rehabilitation program consisting of using a soft thoracolumbosacral orthosis for pain relief and trunk stability, muscle reeducation of the paretic abdominal muscles, strengthening of the disused trunk and extremity muscles, and gait exercise. Based on electromyographic findings, we instructed him in an effective method of muscle reeducation. After 4 months of rehabilitation, he showed marked improvement and became an outdoor ambulator. We suggest that electromyography is a useful tool to evaluate clinical status and devise an effective rehabilitation program in patients with HZ trunk paresis.

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.

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.

[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.

[Severe course of tick-borne encephalitis (Encephalomeningomyelitis): a case report]. / Ciezki przebieg kleszczowego zapalenia mózgu, rdzenia i opon mózgowo-rdzeniowych--opis przypadku.

A 19-year-old male student was admitted to the Department of Infectious Diseases and Neuroinfections with suspected encephalomeningitis. Three weeks before admission the patient was bitten by a tick. The first symptoms were manifested by mild consciousness disorders, headache, vomiting, and fever with the presence of meningeal syndrome. In the course of the disease, the signs of focal lesions in the central nervous system developed: horizontal nystagmus, bilateral ptosis, paresis of cranial nerves: peripheral damage to nerve VII on the right and nerve XI, weakness of proximal muscles of upper and lower extremities. Examination of the cerebrospinal fluid showed lymphocytic pleocytosis with the presence of antibodies against TBE virus. CT and MRI scans did not show any pathology. The applied treatment reduced neurological abnormalities. In the course of the disease, generalized convulsions were twice observed. On the day of discharge, slight nystagmus, bilateral ptosis with normal movement of eyeballs, slight peripheral paresis of nerve VII on the right and nerve XI, massive paresis of the shoulder girdle muscles as a result of their atrophy were found. Mental status was normal. Residual signs of peripheral paresis of peripheral nerve VII, slight nystagmus as well as paresis and atrophy of the shoulder girdle muscles are still present.

[Complications of tick-borne encephalitis in 15-year long experience of the Department of Infectious Diseases and Neuroinfections]. / Powiklania kleszczowego zapalenia mózgu w 15-letniej obserwacji Kliniki Chorób Zakaznychi Neuroinfekcji AMB.

The clinical features of tick-borne encephalitis (tbe) were analyzed in the group of 477 patients hospitalized in the Department of the Infectious Disease and Neuroinfections of the Medical Academy in Bialystok. The group included 31.4% women and 68.6% men, aged from 15 to 76 years. Persistent neurological sequelae were noted in 10.9% of patients: paresis or plegia in 5.66%, spinal dysfunction with lower limbs paraparesis in 1.68%, significant paresis of upper extremities in 0.63%, brachial plexus paresis in 2.31%. Cranial nerves involvement was present in 2.93%, including uni- or bilateral facial nerve palsy in 2.73% and trigeminal nerve involvement in 0.21%. Cerebellar dysfunction was present in 2,09% of patients. No fatal cases of tbe occured.

[Paresis of the vagus and accessory nerve in the course of the herpes zoster]. / Porazenie nerwów X i XI w przebiegu pólpasca.

INTRODUCTION: The cephalic zoster is a cranial neuritis, with great tendency to diffusion along the nerves. The objective of this article is both to report a case of cranial polineuritis due to herpes zoster infection with laryngeal involvement and review of the relevant literature. MATERIAL AND METHODS: The case of 57-years-old man with unilateral laryngeal mucosal eruptions and complete left vocal paralysis is reported. Laryngeal symptoms, diagnostic criteria and therapeutic result are described. CONCLUSION: 1. In cases of head and neck herpes zoster, the investigations of all cranial nerves should be carried out, and the larynx must always be examinated; 2. Co-occurrence of the neuralgic pain (radiating especially to the ear or the occipital region) with unilateral laryngeal palsy should raise a suspicion that herpes zoster infection may by the causative factor; 3. The explanation of the etiologic cause of a vocal fold paralysis in idiopathic cases, may yield not only diagnostic, but also therapeutic value.

Herpetic shoulder paresis in a Chinese elderly patient.

A patient with left shoulder girdle weakness secondary to herpetic myotomal paresis is reported. Needle electromyography revealed denervational discharge from the left supraspinatus, deltoid, and brachioradialis muscles, compatible with a radiculopathy that was relevant to his myotomes affected by zoster infection. The patient was managed with range-of-movement and strengthening exercises as well as pain relief for post-herpetic neuralgia. Further studies are required to determine whether antiviral treatment can limit the extent of motor deficit and hasten recovery. Zoster paresis should be one of the differential diagnoses of girdle muscle weakness.

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.

Chronic active VZV infection manifesting as zoster sine herpete, zoster paresis and myelopathy.

After lumbar-distribution zoster, an HTLV-1-seropositive woman developed chronic radicular sacral-distribution pain (zoster sine herpete), cervical-distribution zoster paresis and thoracic-distribution myelopathy. Detection of anti-varicella zoster virus (VZV) IgM and VZV IgG antibody in cerebrospinal fluid (CSF), with reduced serum/CSF ratios of anti-VZV IgG compared to normal serum/CSF ratios for albumin and total IgG, proved that VZV caused the protracted neurological complications. Diagnosis by antibody testing led to aggressive antiviral treatment and a favorable outcome.

Herpes zoster sciatica with paresis preceding the skin lesions. Three case-reports.

We report three cases of herpes zoster sciatica with motor loss preceding the typical skin lesions. Serological tests and cerebrospinal fluid examination established the diagnosis. Two patients had residual motor loss after 1 and 3 months, respectively. Immunodepression and other risk factors should be looked for routinely. Early diagnosis and treatment may improve the prognosis. Tests for antibodies or viral DNA in cerebrospinal fluid can be helpful, although negative results do not rule out the diagnosis.

Causes of losses including a Borna disease paralytic syndrome affecting young ostriches of one breeding organization over a five-year period (1989-1993).

Necropsy records and causes of mortality of ostriches up to 3 months old over a 5-year period (1989-1993) are presented. The data relate to one ostrich enterprise that comprises 10 breeding flocks, five rearing farms, and one hatchery. Causes of mortality are classified into nine major categories. The annual mortality percentages of all hatched ostriches over the 5-year period were 61%, 58%, 30%, 29%, and 16.6%, and the most significant cause of death was a paresis syndrome that accounted for 20%, 11%, 16%, 10.1%, and 2% mortality, respectively. Limb deformities and gastroenteritis were the other principal specific causes of mortality. The paresis syndrome was caused by an agent serologically related to Borna disease virus. Brain extracts from paralyzed ostriches, when given orally or intramuscularly to 5-week-old birds, reproduced the clinical signs and microscopic lesions. The mean time to death was less than 3 weeks for the intramuscularly infected group and was almost twice as long for the orally infected group.