For voice to be classified as "dysphonic", abnormalities must be present in one or more vocal parameters: pitch, loudness, quality, or variability. Perceptually, dysphonia can be characterised by hoarse, breathy, harsh, or rough vocal qualities, but some kind of phonation remains.Dysphonia can be categorized into two broad main types: organic and functional, and classification is based on the underlying pathology. While the causes of dysphonia can be divided into five basic categories, all of them result in an interruption of the ability of the vocal folds to vibrate normally during exhalation, which affects the voice. The assessment and diagnosis of dysphonia is done by a multidisciplinary team, and involves the use of a variety of subjective and objective measures, which look at both the quality of the voice as well as the physical state of the larynx. Multiple treatments have been developed to address organic and functional causes of dysphonia. Dysphonia can be targeted through direct therapy, indirect therapy, medical treatments, and surgery. Functional dysphonias may be treated through direct and indirect voice therapies, whereas surgeries are recommended for chronic, organic dysphonias. Types
Voice disorders can be divided into 2 broad categories: organic and functional. The distinction between these broad classes stems from their cause, whereby organic dysphonia results from some sort of physiological change in one of the subsystems of speech (for voice, usually respiration, laryngeal anatomy, and/or other parts of the vocal tract are affected). Conversely, functional dysphonia refers to hoarseness resulting from vocal use (i.e. overuse/abuse).
MRIs help identify the iron deposits in the cerebellum, basal ganglia, and motor cortex common to neuroferritinopathy. MRIs of affected individuals also show mild cerebellar and cerebral atrophy, or tissue breakdown, and gas cavity formation in the putamen. Most importantly, the MRIs show misfolded ferritin proteins and iron deposits in the glial cells of the caudate, putamen, globus pallidus, cerebral cortex, thalamus, and purkinje cells, causing neuronal death in these areas. Physiological testing
Blood tests usually come back normal in affected individuals, so they do not serve as a reliable means of diagnosis. Blood tests can show low serum ferritin levels. However, this is unreliable as method of diagnosis, as some patients show typical serum ferritin levels even at the latest stages of neuroferritinopathy. Cerebral spinal fluid tests also are typically normal. Ferritin aggregates found in the skin, liver, kidney, and muscle tissues may help in diagnosing neuroferritinopathy. More cytochrome c oxidase-negative fibers are also often found in the muscle biopsies of affected individuals. Genetic testing
Genetic testing can confirm a neuroferritinopathy diagnosis. A diagnosis can be made by analyzing the protein sequences of affected individuals  and comparing them to known neuroferritinopathy sequences. Treatment
Due to neuroferritinopathys genetic etiology, the disorder is not currently curable. Furthermore, progression of the disorder is unable to be effectively halted. Therefore, current treatment focuses on managing symptoms of the disorder. No medication is available to treat all symptoms. Botox has been shown to help with focal dystonia. The dopamine depleter Tetrabenazine shown to help with involuntary movements.