All You Should Know about Parkinsonism and Parkinson's Disease (PD)

All You Should Know about Parkinsonism and Parkinson's Disease (PD)

We know by now that we need to eat the right foods, need to work out, and do stuff that is healthy for us. Because maintaining good health does not happen by accident, it requires work and smart lifestyle choices. But sometimes when we wake up at 6 am to hit the gym before work or shunning the donuts in breakfast, it’s easy to lose sight of for what are we doing all these. So here are some top articles choices that can keep you motivated to lead a healthy lifestyle and keep diseases at bay.

All You Should Know about Parkinsonism and Parkinson’s Disease (PD)

Parkinson’s disease (PD) is the one of the commonest form of neurodegenerative disorders characterized by accumulation of presynaptic protein ?-synuclein and a variable degree of Parkinsonism. Parkinsonism is characterized by tremor at rest, rigidity, and bradykinesia (slowness of movements). Parkinsonism may also have symptoms like, shuffling gait and flexed posture. All forms of Parkinsonism are the result of reduction of dopaminergic transmission within the basal ganglion. 25% of all PD are genetically predisposed. Remaining 75% are idiopathic and sporadic. In United States alone more than one million patients of PD are present. Peak age at onset is 60 years (range from 35 to 85 years)., All You Should Know about Parkinsonism and Parkinson’s Disease (PD)

Parkinsonism is of two types; primary and secondary Parkinsonism. Primary Parkinsonism is due to familial, idiopathic, due to other neurodegenerative disorders like Alzheimer’s disease, Shy Drager syndrome etc. Genetically mediated primary Parkinsonism include Wilson’s Disease (hepatolenticular degeneration), Chediak Higashi disease, Fragile X syndrome, Huntington’s disease, Prion disease etc. Secondary Parkinsonism is due to repeated trauma (dementia pugilistica), infectious and post infectious diseases like neurosyphillis, postenchephalitic PD, hypoparathyroidism, non Wilsonian degeneration, drugs like, neuroleptics, antipsychotics, anti emetics, methyldopa, lithium, fluoxetine etc. Toxins like cyanide, manganese, methyl alcohol, carbon monoxide, carbon disulphide can cause secondary Parkinsonism.

Risk factors include a positive family history, male gender, head injury, exposure to pesticide, consumption of well water, and rural living. Incidence is high if there is combination of environmental factors and genetical predisposition. Factors which reduce incidence of PD include, drinking coffee, use of painkillers, estrogen replacement in postmenopausal women, and smoking.

Diagnosis of PD can be made confidently if at least two of the three cardinal signs are present, which are tremor at rest, rigidity, and bradykinesia. Tremor is present in 85% of patient with true PD, so diagnosis is difficult when tremor is absent and other two signs are present. Gradual onset of symptoms and if it is unilateral is also supportive in diagnosis. The most disturbing feature of PD is bradykinesia (slowness of movements) which interfere in day to day activities like walking, dressing, turning in bed, getting up from bed and rising from chair. Handwriting becomes bad or illegible. Speech becomes soft. Tremor starts in periphery first, like tremors of fingers of one hand and spread to the other next, than it spreads to the legs. Later on tremor appear on lips, tongue and jaw, but the head is spared.

Rigidity is uniform resistance to passive movements in a joint throughout the full range of motion, which gives characteristic ‘plastic’ quality. There may be also ‘cogwheel’ sensation, which is due to regular interruption of resistance during passive movement. Gait disturbance with shuffling short steps and a tendency to turn en block is an important sign of PD. Festinating gait is a classical sign of PD, which is due to combination of flexed posture and loss of postural reflexes, which causes the patient to ‘catch up’ with the body’s center of gravity. Other signs of PD include depression, anxiety, sleep disturbance, loss of smell (anosmia), sensory abnormality and pain, change in mood and behavior. Depression is present in almost half of the patients. Daytime drowsiness and frequent napping are common problems.

Studies of monozygotic and dizygotic twins have proved some of the PD as genetically predisposed. Four genes have been clearly linked to familial form of PD, and a number of genes can possibly cause PD. Among these PARK1 and PARK5 lead to an autosomal form of PD and PARK 2 and PARK 7 lead to autosomal recessive form of PD. Other genes which are thought to be a causative factor in development of PD include PARK 3, 4, 6, 9, 10 etc.

In PD dopaminergic cells die due to genetic weakness, environmental factors, protosomal dysfunction, and oxidative stress by free radicals. Pathological examination of brain reveals mild atrophy (shrinkage) with loss of melanin pigment of midbrain. Microscopically, there is degeneration of dopaminergic cells with the presence of Lewy Bodies (LB) in the remaining nerve cells or neurons. Lewy Bodies have high concentration of alpha-synucleinand is the hallmark of the diagnosis of PD.

Treatment of Parkinson’s disease:

The goal of treatment of PD is maintenance of quality of life and avoids complications of drug therapy. In the early course of illness almost all symptoms of PD like rest tremor, rigidity, bradykinesia, and abnormal posture respond well to symptomatic treatment. Other symptoms like soft speech respond poorly. To prevent secondary disability regular physical activity programme is required, so regular physical activity is encouraged. Patient of PD should be mentally very strong to prevent worsening of the condition. Recent studies show that regular physical activity can promote neuroprotection against neurotoxins.

As soon as PD starts interfering with quality of life symptomatic drug therapy should be started. The ideal drug for treatment depends on the age of the patient, and cognitive status of the patient. Studies show that if therapy is initiated early, it reduces side effects in later part of the disease. Treatment can be started with levodopa or carbidopa. Initial dose is 25 to 100 mgs per day in three divided doses. Food increase bioavailability of the drug and it should be taken after food. The tablets should not be split, because it reduces controlled release property. The dose of levodopa/carbodopa should be adjusted according to the response. Other dopamine agonists can be combined with levodopa or carbidopa if monotherapy is not giving desired response. They include, non ergot alkaloids ropinirol, pramipexole, and ergot alkaloids pergolide, bromocriptine etc. Treatment of PD has to continue lifelong.

Treatment of Parkinsonism is also symptomatic like Parkinson’s disease. These two conditions are closely related to each other.


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