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Balance Disorders in Children
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Louisa Murdin, Gavin A.J. Morrison
Acute cerebellar ataxia occurs, usually in the first 3 years of life, in a child who was previously normal. It follows a viral febrile illness a few weeks beforehand. There is sudden ataxia, and the condition may take a number of months to resolve or leave some permanent sequelae. Neuroimaging should be considered in all children with new-onset ataxia.42
The Problems
Published in John Greene, Ian Bone, Understanding Neurology a problem-orientated approach, 2007
The preferred neuroimaging for acute cerebellar ataxia is: MRI.CT.CT followed by MRI.Plain X-ray of the skull base.
Toxicity of Antineoplastic Chemotherapy in Children
Published in Sam Kacew, Drug Toxicity and Metabolism in Pediatrics, 1990
Theodore Zwerdling, Steven K. Bergstrom, Stephen D. Smith
As the systemic dose of Ara-C has been increased, CNS toxicity has been seen more frequently.37 Signs of CNS toxicity include seizure, fever, headache, vomiting, and paraparesis. Dunton et al. reported two patients with leukemia who developed ascending paralysis after receiving high doses of systemic Ara-C and low-dose intrathecal Ara-C.38 At autopsy, spinal demyelination was seen. The development of dyskinesia, motor difficulties, and acute cerebellar ataxia has been reported.39 With intrathecal administration in combination with other drugs, arachnoiditis may occur. This is characterized by fever, headache, vomiting, and meningismus. At times, chemical arachnoiditis may be difficult to differentiate from infectious meningitis.
Neurological manifestations of COVID-19: a systematic review and detailed comprehension
Published in International Journal of Neuroscience, 2023
Zeina Hassan Ousseiran, Youssef Fares, Wafaa Takash Chamoun
Cerebellar ataxia, myoclonus and opsoclonus-myoclonus-ataxia (OMA) syndrome were reported among COVID-19 population in several case reports/series. In fact, acute cerebellar ataxia was reported in a 30 year- COVID-19 patient that was diagnosed with cerebellitis and characterized by incoordination, imbalance and trouble reaching for objects [89]. Acute cerebellar ataxia and myoclonus (ACAM) were also reported in a single 44 year-COVID-19 patient without opsoclonus and presented with prominent limb ataxia, severe myoclonic jerks, speech impairment and neuropsychiatric symptoms [34]. In addition, ACAM was also reported in two patients between 10 days and six weeks after the first symptoms of viral infection [90]. The first case had confusion with myoclonic jerks, ataxic dysarthria and opsoclonus. The second case was characterized by progressive cerebellar syndrome with stimulus-sensitive action myoclonus. Their cerebral MRI and CSF analyses were normal.
Turkish version of Brief Ataxia Rating Scale
Published in Disability and Rehabilitation, 2021
Elif Acar Arslan, Arzu Erden, Beril Dilber, Gülnur Esenülkü, Sevim Şahin, Tülay Kamaşak, Pınar Özkan Kart, Erhan Arslan, Murat Topbaş, Ali Cansu
Ataxia is a disorder of balance and coordination. Conditions accompanying ataxia include coordination weakness, imbalance, dysarthric speech, nystagmus, and swallowing disorder. The reported incidence of acute cerebellar ataxia in children is 1/100 000–1/500 000 [1,2]. Acute ataxia is the most common type, representing 40% of all cases as acute post-infectious cerebellar ataxia. Toxic causes are another very common source of acute childhood ataxias, accounting for approximately a further 30–32% [2–4]. The most common causes of childhood acute ataxia are acute post-infectious cerebellar ataxia, intoxications and acute disseminated encephalomyelitis. Other causes include cerebellar neoplasms, acute hydrocephalus, acute cerebellitis, traumatic or vascular causes, paraneoplastic causes and autoimmune diseases [3]. Congenital abnormalities, degenerative diseases, and hereditary ataxias are involved in the etiology of chronic and progressive ataxia. The estimated prevalence of acquired, hereditary and mixed childhood ataxia is 26/100 000 among children in Europe [5].
Acute cerebellar ataxia: a rare Toscana Virus (TOSV) meningoencephalitis complication
Published in International Journal of Neuroscience, 2020
Lorenzo Roberto Suardi, Nicoletta Di Lauria, Marco Pozzi, Pier Giorgio Rogasi, Alessandro Barilaro, Federica Azzolini, Elio Prestipino, Maria Grazia Colao, Gian Maria Rossolini, Alessandro Bartoloni
TOSV central nervous system involvement is characterized by typical meningeal signs with severe headache and high fever. Consequently, evaluating this clinical presentation, hospital admission is often required in order to perform blood cultures and a lumbar puncture to exclude especially bacterial or other viral meningitis/meningoencephalitis. When TOSV infection diagnosis is performed, physicians usually face a mild clinical course self-extinguishing in 7-10 days without need of treatments other than antypiretics and analgesia. Nevertheless, rare complicated TOSV infection cases are reported in literature. In this regard, Baldelli et al. [4] described, in a 19-year-old girl and her 16-year-old brother living in Tuscany, a TOSV infection with atypical clinical presentations with severe meningoencephalitis and systemic involvement (hepatic, renal, lymphoglandular and testicular). Both of the patients suffered then from hydrocephalus but had a full, even if slow, recovery lasting almost 4 months. Likewise, some years after, Serata et al. [5] reported a possible permanent personality changes after probable TOSV encephalitis in a 49-year-old Italian man. Before the hospital admission, the patient had a four-month history of agitation, irritability, confusion and depression. Pharmacological control was required due to seizure episodes and antidepressant drugs with psychiatric support somehow improved the aggressiveness and the sexual disinhibition. To the best of our knowledge, a TOSV-related acute cerebellitis has never been reported before. Analyzing the time (9–10 days) between the “classical” TOSV infection symptoms onset and the occurrence of ataxia symptoms, it seems plausible to exclude a delayed neurological manifestation as post-infectious complication [6]. The differential diagnosis of acute cerebellar ataxia, during a central nervous system viral infection, should include ischemic or hemorrhagic cerebellar stroke, hydrocephalus and medication toxicity (e.g. neurotropic drugs). The presented case, in addition to confirming TOSV neurotropism, adds another atypical manifestation to the so far reported spectrum of neurological manifestation.