Welding Rods Side Effects: Parkinson's Disease Information

Parkinson's disease (PD; paralysis agitans) is a neurodegenerative disease of the substantia nigra (an area in the basal ganglia of the brain). The disease was first discovered and its symptoms documented in 1817 (Essay on the Shaking Palsy) by the British physician Dr. James Parkinson; the associated biochemical changes in the brain of patients were identified in the 1960s. Some genes were identified only recently; others remain unknown.

The disease involves a progressive movement disorder of the extrapyramidal system, which controls and adjusts communication between neurons in the brain and muscles in the human body. It also commonly involves depression and disturbances of sensory systems.

In the United States, the prevalence of Parkinson's disease is 1 per 625 people, though this increases with age, as indicated by the mean onset of 55 years of age. Symptoms usually begin in the upper extremity, and are usually unilateral (one-sided) or asymmetrical at onset.

The cause of Parkinson's disease is not known. Geneticists have since 1997 found nine different specific genetic defects, each of which causes the disease in one or a few families with extraordinarily high incidences of the disease, but such families are rare. While a strong inheritance pattern occurs in only a very small percentage of cases, an affected individual is three to four times more likely than an unaffected individual to have a close relative with Parkinson's. Having a parent with Parkinson's raises one's lifetime risk of developing the disorder threefold, from the general population's figure of 2% to about 6%. Genes that have been identified include SNCA (protein alpha-synuclein), UCHL1 (protein ubiquitin carboxy-terminal hydrolase L1), PARK2 (protein parkin), and PARK7 (protein DJ-1). Indeed, recent linkage studies excluded most of the above gene defects from consideration in the causation of sporadic (i.e. non-familial) Parkinson's disease, which constitutes more than 95% of cases. Most recently, a new gene was identified, ND5, mutation in which is thought to account for a vast majority of sporadic PD cases.

Symptoms may vary among patients, and additionally may vary greatly over time in a single patient. However, the cardinal symptoms are:

• tremor (while this is the best known symptom, it is not displayed by an estimated 30% of patients)
• rigidity (increased tone or stiffness in the muscles)
• bradykinesia (slowness of movement) and akinesia (lack of spontaneous movement)
• failing balance
• walking problems

Additionally, the following signs and symptoms are commonly associated with Parkinson's Disease:

• Psychological
  • depression (occurs in 50% of cases)
  • anxiety or panic attacks
  • dementia, in approximately 20% of all patients, typically starting with slowing of thought and progressing to difficulty organizing thoughts
  • memory loss
  • altered sexual function
  • sleep disturbances
• Sensory
  • impaired visual contrast sensitivity, colour discrimination, and oculomotor control
  • dizziness
  • loss of sense of smell (anosmia)
  • pain
• Physical
  • speech problems (hypophonia; vocal cords can also be affected, causing monotonous, soft speech qualities)
  • stooped or flexed posture
  • constipation
  • fatigue (up to 50% of cases)
  • oily skin
  • difficulty in swallowing
  • masked facies (a mask-like face, with infrequent blinking)
  • drooling
  • micrographia (small handwriting)
  • decreased arm swing
  • difficulty rolling in bed
  • slowness of gait

Symptoms usually only begin to appear after about 80% of the dopamine in the brain has been lost. More recent data based on PET scans suggests that symptoms may occur when 50-60% of dopaminergic neurons are lost. The level of dopamine will continue to fall slowly over time, with an attendant worsening of symptoms.

The treatment of Parkinson's disease mainly relies on replacing dopamine with levodopa (L-DOPA) or mimicking its action with dopamine agonists such as pramipexole, ropinirole, pergolide or bromocriptine. Discovered as a Parkinson's treatment by Arvid Carlsson, levodopa is a dopamine precursor that is transfomed into dopamine by the brain. Levodopa is almost always supplemented with carbidopa, a drug which prevents levodopa from being metabolized in the gut, liver and other tissues, thus allowing more levodopa to reach the brain and allowing for a reduced dosage, thus reducing some of the side effects. The most frequent side effects of these dopaminergic drugs are nausea, sleepiness, dizziness, involuntary writhing movements and visual hallucinations. Often times, the treatment of the Parkinson's patient with these two drugs can result in them very much "coming back to life" in the eyes of their family and doctors, to the point of them appearing to not have any disease at all. However, the drugs are not effective forever. Sometimes a point is reached where the drugs only work for a few hours, or become completely ineffective ("off periods").

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