Acute cerebellar ataxia of childhood is a childhood condition characterized by an unsteady gait, most likely secondary to an autoimmune response to infection, drug induced or paraneoplastic. Most common virus causing acute cerebellar ataxia are chickenpox virus and Epstein–Barr virus, leading to a childhood form of post viral cerebellar ataxia. It is a diagnosis of exclusion. Signs and symptoms
Acute cerebellar ataxia usually follows 2–3 weeks after an infection. Onset is abrupt. Vomiting may be present at the onset but fever and nuchal rigidity characteristically are absent. Horizontal nystagmus is present in approximately 50% of cases. Truncal ataxia with deterioration of gait
Slurred speech and nystagmus
Afebrile

Cause
Possible causes of acute cerebellar ataxia include varicella infection, as well as infection with influenza, Epstein–Barr virus, Coxsackie virus, Echo virus or mycoplasma. Diagnosis
Acute Cerebellar ataxia is a diagnosis of exclusion. Urgent CT scan is necessary to rule out cerebellar tumor or hemorrhage as cause of the ataxia; however in acute cerebellar ataxia, the CT will be normal. CSF studies are normal earlier in the course of disease. Later on CSF shows moderate elevation of proteins. Differential diagnosis
Brain tumors, including cerebellar astrocytoma, medulloblastoma, neuroblastoma
Cerebellar contusion
Subdural hematoma
Toxins, including ethanol or anticonvulsants
Cerebellar infarction or hemorrhage
Meningitis
Encephalitis
Acute disseminated encephalomyelitis
Multiple sclerosis

Management
Supportive treatment is the only intervention for acute cerebellar ataxia of childhood. Symptoms may last as long as 2 or 3 months. Epidemiology
Acute cerebellar ataxia is the most common cause of unsteady gait in children. The condition is rare in children older than ten years of age.
Acute erythrocyte leukemia is a rare form of acute myeloid leukemia (less than 5% of AML cases) where the myeloproliferation is of erythrocytic precursors. It is defined as type "M6" under the FAB classification. Signs and symptoms
The most common symptoms of AEL are related to pancytopenia (a shortage of all types of blood cells), including fatigue, infections, and mucocutaneous bleeding. Almost half of people with AEL exhibit weight loss, fever and night sweats at the time of diagnosis. Almost all people with AEL are anemic, and 77% have a hemoglobin level under 10.0 g/dl. Signs of thrombocytopenia are found in about half of people with AEL. Causes
The causes of AEL are unknown. Prior to a 2008 reclassification by the World Health Organization, cases that evolved from myelodysplastic syndromes, myeloproliferative neoplasms, chemotherapy for other cancers or exposure to toxins were defined as secondary AEL. These cases are now likely to instead be classified as acute myeloid leukemia with myelodysplasia-related changes or therapy-related AML. +

Diagnosis
Acute erythroid leukemias can be classified as follows:

M6a (Erythroleukemia)
50% or more of all nucleated bone marrow cells are erythroblasts, dyserythropoiesis is prominent and 20% or more of the remaining cells (non- erythroid) are myeloblasts. M6b (Pure erythroid leukemia)
In rare cases the erythroid lineage is the only obvious component of an acute leukemia; a myeloblast component is not apparent. The erythroid component consists predominantly or exclusively of proerythroblasts and early basophilic erythroblasts. These cells may constitute 90% or more of the marrow elements.