Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia (slowed movements), rigidity, and postural instability. These are the four motor symptoms found in Parkinsons disease (PD), after which it is named, dementia with Lewy bodies (DLB), Parkinsons disease dementia (PDD), and many other conditions. This set of symptoms occurs in a wide range of conditions and may have many causes, including neurodegenerative conditions, drugs, toxins, metabolic diseases, and neurological conditions other than PD. Signs and symptoms
Parkinsonism is a clinical syndrome characterized by the four motor symptoms found in Parkinsons disease: tremor, bradykinesia (slowed movements), rigidity, and postural instability.Parkinsonism gait problems can lead to falls and serious physical injuries. Other common symptoms include:

Tremors when resting (mostly in the hands)
Short, shuffling gait
Slow movements (bradykinesia)
Loss of sound perception leading to low, soft speech
Difficulty sleeping
Dry skin
Apathy
Lack of facial expressions
Balance problems
Frequent falls
Very small handwriting
Rigid, stiff muscles
Cogwheeling (jerky feeling in arm or leg)

Conditions
Parkinsonism occurs in many conditions. Neurological
Neurodegenerative conditions and Parkinson plus syndrome that can cause parkinsonism include:
Corticobasal degeneration
Dementia with Lewy bodies
The relationship (if any) with essential tremor is not clear.
However, an Israeli study found no increased risk of miscarriage in the group of mothers using NSAIDs. Pharmacology
NSAIDs such as ibuprofen work by inhibiting the cyclooxygenase (COX) enzymes, which convert arachidonic acid to prostaglandin H2 (PGH2). PGH2, in turn, is converted by other enzymes to several other prostaglandins (which are mediators of pain, inflammation, and fever) and to thromboxane A2 (which stimulates platelet aggregation, leading to the formation of blood clots). Like aspirin and indomethacin, ibuprofen is a nonselective COX inhibitor, in that it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to operate mainly through inhibition of COX-2, which decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Inhibition of COX-1 instead would be responsible for unwanted effects on the gastrointestinal tract. However, the role of the individual COX isoforms in the analgesic, anti-inflammatory, and gastric damage effects of NSAIDs is uncertain, and different compounds cause different degrees of analgesia and gastric damage.Ibuprofen is administered as a racemic mixture. The R-enantiomer undergoes extensive interconversion to the S-enantiomer in vivo. The S-enantiomer is believed to be the more pharmacologically active enantiomer. The R-enantiomer is converted through a series of three main enzymes. These enzymes include acyl-CoA-synthetase, which converts the R-enantiomer to (−)-R-ibuprofen I-CoA; 2-arylpropionyl-CoA epimerase, which converts (−)-R-ibuprofen I-CoA to (+)-S-ibuprofen I-CoA; and hydrolase, which converts (+)-S-ibuprofen I-CoA to the S-enantiomer.