The physician must first determine if the hypotonia is due to muscle, neuromuscular junction, nerve, or central cause. This will narrow the possible causes. If the cause of the hypotonia is found to lie in the brain, then it can be classified as a cerebral palsy. If the cause is localized to the muscles, it can be classified as a muscular dystrophy. If the cause is thought to be in the nerves, it is called hypotonia due to polyneuropathy. Many cases cannot be definitively diagnosed.Diagnosing a patient includes obtaining family medical history and a physical examination, and may include such additional tests as computerized tomography (CT) scans, magnetic resonance imaging (MRI) scans, electroencephalogram (EEG), blood tests, genetic testing (such as chromosome karyotyping and tests for specific gene abnormalities), spinal taps, electromyography muscle tests, or muscle and nerve biopsy.Mild or benign hypotonia is often diagnosed by physical and occupational therapists through a series of exercises designed to assess developmental progress, or observation of physical interactions. Since a hypotonic child has difficulty deciphering his spatial location, he may have some recognizable coping mechanisms, such as locking the knees while attempting to walk. A common sign of low-tone infants is a tendency to observe the physical activity of those around them for a long time before attempting to imitate, due to frustration over early failures. Developmental delay can indicate hypotonia.MRI Brain is used to rule out structural malformations in the brain or metabolic disorders. Magnetic resonance spectroscopic imaging is used to detect metabolic disorders.
The changes are indistinguishable from those observed in IgA nephropathy. HSP can develop after infections with streptococci (β-haemolytic, Lancefield group A), hepatitis B, herpes simplex virus, parvovirus B19, Coxsackievirus, adenovirus, Helicobacter pylori, measles, mumps, rubella, Mycoplasma and numerous others. Drugs linked to HSP, usually as an idiosyncratic reaction, include the antibiotics vancomycin and cefuroxime, ACE inhibitors enalapril and captopril, anti-inflammatory agent diclofenac, as well as ranitidine and streptokinase. Several diseases have been reported to be associated with HSP, often without a causative link. Only in about 35% of cases can HSP be traced to any of these causes.The exact cause of HSP is unknown, but most of its features are due to the deposition of abnormal antibodies in the wall of blood vessels, leading to vasculitis. These antibodies are of the subclass IgA1 in polymers; it is uncertain whether the main cause is overproduction (in the digestive tract or the bone marrow) or decreased removal of abnormal IgA from the circulation. It is suspected that abnormalities in the IgA1 molecule may provide an explanation for its abnormal behaviour in both HSP and the related condition IgA nephropathy. One of the characteristics of IgA1 (and IgD) is the presence of an 18 amino acid-long "hinge region" between complement-fixating regions 1 and 2. Of the amino acids, half is proline, while the others are mainly serine and threonine. The majority of the serines and the threonines have elaborate sugar chains, connected through oxygen atoms (O-glycosylation).