Animals affected by laryngeal paralysis have reduced tolerance for exercise and heat and an increased risk of aspiration pneumonia. The condition is not generally regarded as causing pain, other than physical distress and anxiety caused by any difficulty in breathing or emotional distress from any difficulty with physical movement. Where laryngeal paralysis is related to a general progressive polyneuropathy, as in GOLPP, the nervous system will gradually degenerate causing increasing difficulty in management of the limbs (especially rear limbs), swallowing and breathing, and eventually in most cases euthanasia. Laryngeal paralysis is fairly common in large breed and geriatric dogs, particularly in the Labrador retriever, is rarely found in cats, and can also occur in horses where it is referred to as roaring, roarers syndrome, or medically as laryngeal hemiplegia or  recurrent laryngeal neuropathy (RLN). Laryngeal paralysis can be unilateral or bilateral depending upon dysfunction of one or both arytenoid cartilages. Causes
In most cases, the cause of laryngeal paralysis is unknown or idiopathic. However, the disorder may arise secondary to general neuropathies, generalized neuromuscular diseases, muscular diseases, neoplasia either in the cervical (neck) region or the cranial mediastinum, or trauma. This acquired form occurs predominantly in middle-aged to old large breed or giant breed dogs such as the Labrador Retriever, golden retriever, Siberian Husky, Newfoundland, and St. Bernard. Usually these dogs are born with a normal larynx, but over time the nerves and muscles that control the laryngeal cartilages lose function.Laryngeal paralysis may also be congenital in some breeds (e.g.
They cross the blood–brain barrier and enter the brain, where they most concentrated at the thalamus, basal ganglia, midbrain, and cingulate gyrus.Selegiline is mostly metabolized in the intestines and liver; it and its metabolites are excreted in the urine.Buccal administration of selegiline results in 5-fold higher bioavailability, more reproducible blood concentration, and produces less amphetamine metabolites than the oral tablet form. Metabolism
Selegiline is metabolized by cytochrome P450 to L-desmethylselegiline and levomethamphetamine. Desmethylselegiline has some activity against MAO-B, but much less than that of selegiline. It is thought to be further metabolized by CYP2C19. Levomethamphetamine (the less potent of the two enantiomers of methamphetamine) is converted to levoamphetamine (the less potent of the two enantiomers of amphetamine, with regards to psychological effects). Due to the presence of these metabolites, people taking selegiline may test positive for "amphetamine" or "methamphetamine" on drug screening tests. While the amphetamine metabolites may contribute to selegilines ability to inhibit reuptake of the neurotransmitters dopamine and norepinephrine, they have also been associated with orthostatic hypotension and hallucinations. The amphetamine metabolites are hydroxylated and, in phase II, conjugated by glucuronyltransferase. A newer anti-Parkinson MAO-B inhibitor, rasagiline, metabolizes into 1(R)-aminoindan, which has no amphetamine-like characteristics. Patch
Following application of the patch to humans, an average of 25% to 30% of the selegiline content is delivered systemically over 24 hours.