Parkinson's Disease
Parkinson's Disease

Parkinson’s disease is a disease related to the central nervous system characterized by chronic and progressive movement disorders involving bradykinesia and at least one out of tremors, rigidity or postural instability.

Classification of Parkinson’s disease:

The classification of the disease is based on the causes of Parkinson’s disease.

  1. Primary Parkinsonism: This is idiopathic Parkinson’s disease where a clear-cut underlying cause cannot be understood.
  2. Secondary Parkinsonism: It includes a group of disorders whose etiological agents can be identified. Some causes are:
  • Post encephalitic: Post encephalitic lethargica
  • Toxins: Methylphenyltetrahydropyridine, manganese and carbon monoxide
  • Drugs: Certain drugs like reserpine, metoclopramide, phenothiazine and alpha methyldopa are known to increase disease progression
  • Tumors in the basal ganglion of the brain.
  • Brain injury like punches to the skull in boxers
  • Ischemic brain damage: Causes vascular parkinsonism
  • Infections like HIV and influenza can cause Parkinson’s disease.
  1. Parkinsonism plus are a group of degenerative disorders that present with additional neurological features in addition to those of parkinsonism. These need to be ruled out when diagnosing Parkinson’s disease.

 

Pathophysiology underlying Parkinson’s disease

The main mechanism of Parkinson’s disease is a fall in dopamine levels. There is loss of pigmented cells along with deposition of Lewy bodies in locus ceruleus, succeeded by substantia nigra. This degenerates the nigro-striatal pathways whose cells synthesise dopamine. The dopamine levels in the striatum deplete, which is the primary chemical pathology in Parkinson’s. Later on, as the disease progresses, there is loss of non-dopaminergic neurons as well that contribute to non motor features.

Parkinson’s symptoms

Parkinson’s disease affects both sexes equally and usually appears after the sixth decade of life.

  1. Initial symptoms include unilateral tiredness and muscular aches.
  2. Bradykinesia or slowness of movement: It is the slowness of initiation of voluntary movement with progressive speed reduction and amplitude reduction. Arm swing and repetitive supination-pronation of hands is affected, the latter known as dysdiadokinesia. The face takes on a mask-like blank look and the amplitude of writing reduces towards the end of a sentence.
  3. Tremors: A tremor that characteristically appears when at rest. It starts with wrist and fingers and slowly progresses to action or postural tremors. The tremors may also occur at head and upper limbs.
  4. Rigidity: Hypertonia or rigidity is of the cog-wheel variety. It is generally unilateral at the beginning.
  5. Hypokinesia: It is albeit similar to bradykinesia with difficulty in initiating motor acts. This leads to delay or slowness of motor acts after an intention to start.
  6. Postural reflexes are disturbed:
  • Occurs after a few years of disease initiation. It results in a bent or stooped posture. There is an easy tendency to fall repeatedly and there is difficulty in maintaining posture while sitting and standing. Stance of the patient is stooped forward and he walks by shuffling his steps. Turning around is slow and laborious and arm swinging is absent. The arms are fixed by the side.
  • Muscle strength and tendon reflexes are generally unaffected. Speech is monotonous and low in volume.
  • With advancing disease the patient takes on a fixed flexed posture and is unable to get up from the bed.

7. Non-motor features present in advanced stages include autonomic dysfunction affecting bladder and bowel and sensory problems. Neuropsychiatric  symptoms like depression, psychosis and dementia may develop.

Diagnosis is typically made by assessing the clinical features and symptoms of bradykinesia, tremors and rigidity. MRI and CT scan may be required to rule out other disorders with similar features. Apart from medical treatment, a physiotherapist may help the patient to live well with disability. In case medical management is ineffective, surgery of the thalamus may be required. Deep brain stimulation is also successful.

 

 

 

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