Type 2 Diabetes

Unlike Alzheimer’s disease, which involves a buildup of tau proteins in the brain, people with Parkinson’s disease have a buildup of alpha-synuclein in the brain. The dementia doesn’t develop until the patient is severely affected and memory is not always the first sign of the dementia. PD is more closely linked to Lewy body dementia, which has a similar buildup of alpha-synuclein in the brain.

The patient may have a history and physical that is suggestive of the disease. Imaging will rule out other causes of the problem but will not rule in Parkinson’s disease, except for an MRI, which may or may not show abnormalities in the substantia nigra. Substantia nigra Lewy bodies are seen at autopsy but cannot be used to diagnose the disease in life. Parkinsonism unrelated to true PD is less helped with antiParkinson’s drugs. There are both autosomal dominant and autosomal recessive patterns of Parkinson’s disease.

There is no known cure for PD; however, there are many treatments. The main treatment is exogenous L-dopa and other dopamine agonists (used secondary to L-dopa). The medications gradually lose effectiveness over time so that involuntary movements are prevalent. Severe cases are treated with deep brain stimulation.

The disease affects males more than females and tends to affect people older than sixty years of age. The life expectancy of the patient with PD is about 7-14 years after initial diagnosis. The most common form of parkinsonian symptoms is PD, which is completely idiopathic. Other causes include strokes, multiple head trauma, infections, metabolic disease, and drug toxicity. Atypical parkinsonism is evident in diseases that are related to PD but have other symptoms, such as progressive supranuclear palsy, Lewy body dementia, cortico-basilar degeneration, and multiple system atrophy.

When giving L-dopa or levodopa for PD, the treatment is always given with a dopa decarboxylase inhibitor and sometimes with a catechol-O-methyl transferase (COMT) inhibitor. MAO-B inhibitors can be used as well as dopamine agonist drugs (if L-dopa fails to work). L-dopa is the most effective treatment but there are side effects related to its use and it does not work forever. L-dopa is used instead of dopamine because dopamine doesn’t cross the blood-brain barrier. Carbidopa and benserazide are dopa carboxylase inhibitors that “deactivate” levodopa outside of the brain.

COMT Inhibitors like tolcapone will block the enzyme that degrades dopamine and is used as a complement to L-dopa. Several dopamine agonists can be used that will help patients to delay the onset of disease including apomorphine, cabergoline, piribedil, ropinirole, pramipexole, pergolide, and bromocriptine. MAO-B inhibitors include selegiline, safinamide, and rasagiline. These block MAO-B (an enzyme that breaks down dopamine).

Type 2 diabetes is the most common endocrine disorder in humans, resulting in insulin resistance, high blood pressure, and later, a lack of insulin. Typical symptoms include increased frequency of urination, weight loss that cannot be explained, and increased thirst/hunger. Patients have open sores that don’t heal after an injury and fatigue. The symptoms of diabetes happen only when it is severe. Some patients will have itching, peripheral neuropathy, blurry vision, and recurrent fungal infections. Fatigue is a common symptom, although most patients are not symptomatic at the time of their diagnosis.