For convenience, care-focused publications classify patients into "non-sitters", "sitters" and "walkers" based on their actual functional status. Motor development and disease progression in people with SMA is usually assessed using validated functional scales – CHOP-INTEND (The Childrens Hospital of Philadelphia Infant Test of Neuromuscular Disorders) or HINE (Hammersmith Infant Neurological Examination) in infants; and either the MFM (Motor Function Measure) or one of several variants of the HFMS (Hammersmith Functional Motor Scale) in older patients. The eponymous label Werdnig–Hoffmann disease (sometimes misspelled with a single n) refers to the earliest clinical descriptions of childhood SMA by Johann Hoffmann and Guido Werdnig. The eponymous term Kugelberg–Welander disease named after Erik Klas Hendrik Kugelberg (1913–1983) and Lisa Welander (1909–2001), who first documented the late-onset form and distinguished it from muscular dystrophy. Very rarely used Dubowitz disease (not to be confused with Dubowitz syndrome) is named after Victor Dubowitz, an English neurologist who authored several studies on the intermediate SMA phenotype. Signs and symptoms
The symptoms vary depending on the SMA type, the stage of the disease as well as individual factors.
Similarly, selective serotonin reuptake inhibitors can cause mydriasis. Dissociatives such as dextromethorphan (an SSRI and sigma-1 agonist). Certain GABAergic drugs, such as phenibut and GHB. Adrenergic agonists, such as phenylephrine and cyclomydril. Adrenergic agonists may be used if strong mydriasis is needed in surgery. Norepinephrine is a hormone and neurotransmitter that regulates the involuntary muscles of the autonomic nervous system, including dilation of the pupil aperture via the muscles of the iris. Hence adrenergic agonists mimic the activity of norepinephrine, which is how they induce mydriasis.Natural release of the hormone oxytocin can cause mild to moderate mydriasis.Long term effects of drugs can also cause mydriasis, for example opioid withdrawal. Autonomic neuropathy
Parasympathetic fibers travel with cranial nerve III, the oculomotor nerve, to innervate the circular layer of muscle of the eye (sphincter pupillae). Damage to this nerve typically manifests itself as mydriasis, because the sympathetic supply to the pupil, which causes mydriasis, remains unaffected, and therefore unopposed. Multiple central nervous system disorders e.g. epilepsy, stroke, and impending brain herniation are known to lead to temporal mydriasis as well. A brain catastrophe, or a rapidly increasing brain mass, can cause compression of the oculomotor nerve. Trauma
In cases of head injury or orbit trauma (eye injury), the iris sphincter (the muscle responsible for closing the pupil) or the nerves controlling it can be damaged, reducing or eliminating the normal pupillary light reflex. References


== External links ==