Some of the most consistent abnormalities observed in patients with ataxia dysarthria are alterations of the normal timing pattern, with prolongation of certain segments and a tendency to equalize the duration of syllables when speaking. As the severity of the dysarthria increases, the patient may also lengthen more segments as well as increase the degree of lengthening of each individual segment.Common clinical features of ataxic dysarthria include abnormalities in speech modulation, rate of speech, explosive or scanning speech, slurred speech, irregular stress patterns, and vocalic and consonantal misarticulations.Ataxic dysarthria is associated with damage to the left cerebellar hemisphere in right-handed patients.Dysarthria may affect a single system; however, it is more commonly reflected in multiple motor–speech systems. The etiology, degree of neuropathy, existence of co-morbidities, and the individuals response all play a role in the effect the disorder has on the individuals quality of life. Severity ranges from occasional articulation difficulties to verbal speech that is completely unintelligible.Individuals with dysarthria may experience challenges in the following:

Timing
Vocal quality
Pitch
Volume
Breath control
Speed
Strength
Steadiness
Range
ToneExamples of specific observations include a continuous breathy voice, irregular breakdown of articulation, monopitch, distorted vowels, word flow without pauses, and hypernasality. Treatment
Articulation problems resulting from dysarthria are treated by speech language pathologists, using a variety of techniques. Techniques used depend on the effect the dysarthria has on control of the articulators. Traditional treatments target the correction of deficits in rate (of articulation), prosody (appropriate emphasis and inflection, affected e.g. by apraxia of speech, right hemisphere brain damage, etc. ), intensity (loudness of the voice, affected e.g.
The onset of symptoms can range from weeks up to tens of years from the initial exposure. In some individuals, a single exposure to beryllium can cause berylliosis. Pathogenesis
In susceptible persons, beryllium exposure can lead to a cell-mediated immune response. The T-cells become sensitized to beryllium. Each subsequent exposure leads to an immune response involving CD4+ helper T-lymphocytes and macrophages accumulating in the lungs. As this response continues macrophages, CD+4 T-lymphocytes and plasma cells aggregate together to form the noncaseating granulomas. When beryllium is phagocytized by macrophages, the beryllium triggers macrophage apoptosis, thereby reducing beryllium clearance from the lungs and eventually resulting in secondary necrosis and lysis. Eventually, the outcome is fibrosis of the lung.Several studies have shown that there is a genetic component to beryllium sensitivity. Specifically, those beryllium exposed workers with a mutation at the HLA-DPB1 Glu69 position have increased prevalence of beryllium sensitization and CBD. The HLA-DPB1 gene is important for MHC class II molecule function on antigen presenting cells.According to the International Agency for Research on Cancer (IARC), beryllium and beryllium compounds are Category 1 carcinogens; they are carcinogenic to both animals and humans. Diagnosis
The differential diagnosis for berylliosis includes:
Sarcoidosis
Granulomatous lung diseases
Tuberculosis
Fungal infections (e.g., histoplasmosis)
Granulomatosis with polyangiitis
Idiopathic pulmonary fibrosis
Hypersensitivity pneumonitis
AsthmaOf these possibilities, berylliosis presents most similarly to sarcoidosis. Some studies suggest that up to 6% of all cases of sarcoidosis are actually berylliosis.Definitive diagnosis of berylliosis is based on history of beryllium exposures, documented beryllium sensitivity and granulomatous inflammation on lung biopsy.