Parkinson’s Disease is a chronic, slow progressive, degenerative disease of central nervous system affecting the motor neurons.

There is gradually increasing cell death in subsrantia nigra resulting in reduced dopamine secretion with accumulation of abnormal alpha-synuclien (lewy bodies) in remaining neurons due to which its classified under Synucleopathies.

It is characterised with parkinsonism, where in, patient has tremors, bradykinesia, rigidity and postural instability. Patients with parkinson’s disease also presents with neuropsychiatric disorder(mood, cognition, thought, behavioural). Parkinson’s Disease is also called Idiopathic Parkinsonism.


Causes of Parkinson’s Disease are not known but it is believed to be due to environmental and genetic factors and has familial predesposition towards the condition. Those who has history of head injury, psychological stress, frequently exposed to certain toxins, have increased risk of developing Parkinson’s Disease. It is found that those addicted to stimulants like tobacco smoking tea and coffee are less prone to this condition.

There are certain genes identified, mutations in which are believed to increase the risk of developing Parkinson’s Disease viz.

  • SNCA – responsible for production of normal Alpha-Synuclein, an essential protein.
  • PARK7 – Encodes Protein Deglycase DJ-1 also called parkinson disease protein 7, inhibits aggregation of alpha-synuclein and protects neurons from oxidative stress and cell death
  • LRRK2 – responsible for production of Dardarin(Lucine-Rich Repeat Kinase 2) an essential cytoplasmic protein.
  • GBA – responsible for production of Beta – Glucocerebrosidase an essential enzyme localised in lysosome which has essential intermediate role in metabolism glycolipid (abundantly present in cell membrane)
  • PRKN – responsible for production of Parkin a ligase responsible for labelling molecules covallently with ubiquitin (ubiquitination) for degradation in proteosome or lysosome.
  • PINK1 – responsible for production of PTEN Induced Kinase 1 is a mitochondrial serine which is involved in process of quality control check on mitochondria where in damaged mitochondria are identified and recruited for degradation this its believed to protect cells from stress induced mitochondrial damage.
  • VPS35 – Encodes Vacoular Protein Sorting-associated protein 35 is component of retromer complex responsible for retrograde transportation of proteins from endosomes to trans-Golgi network.
  • EIF4G1 – encodes Eukaryotic Translation Initiation Factor 4 Gamma 1 involved in process of mRNAcap recognition, ATP dependent unwinding 5′-terminal secondary structure and recruits mRNA to ribosome
  • DNAJC13 – encodes “DnaJ(Hsp40), homolog, subfamilyC, member13”, involved on endosome organisation.
  • CHCHD2 – Encodes protein called “Coiled coil Helix Coiled coil Helix Domain containing 2”, it acts as negative regulator of mitochondrial apoptosis


Although Parkinson’s Disease is classically recognised by 4 cardinal symptoms of parkinsonism viz tremor, bradykinesia, rigidity, postural instability which belong to sphere of motor neurons, Parkinson’s Disease also presents non motor symptoms of autonomic nerves and neuropsychiatric symptoms(cognitive, behavioural, mood, thoughts) of which neuropsychiatric cognitive deficits tends to appear in very early stage of disease even before classical cardinal motor symptoms are perceptible but its often not properly evaluated or linked to PD by physicians and diagnosis is delayed. Also sleep disorder starts appearing in patients years before motor or other neuropsychiatric symptom appear like somnolence, insomnia, REM sleep behavioural disorder(RBD) where in dreamy sleep patient starts acting and may inflict injury to self or others in bed.



  • Comes during rest and subsides on active voluntary motion and in deeper stages of sleep.
  • Usually tremors ranges 4-6Hz per second
  • Classically many patients presents with a common pill-rolling pattern of tremor, where in, thumb and index finger are set in circular motion as if making pill manually.


  • Slowness of movement throughout its course right from planning the course of movement to execution of movement.
  • Slughishness and difficulty in day to day routine activity
  • Impaired sequential and simultaneous movements.


  • Increased muscle tone causes rigidity in limbs.
  • Initially rigidity may be due to pain in joints and typically starts asymetrically from neck and shoulder and in later stages of disease whole body is involved.
  • Rigidity may be Uniform (Lead-Pipe Rigidity) or Retchety(Cogwheel rigidity)

Postural Instability

  • Appears in later stages of disease
  • Festination
  • Forward flexed posture
  • Freezing of gait as if feet were made of wood and were stucked to ground especially while turning or changing direction.
  • Toneless flat and sluggish voice
  • Mask-Like facial expressions or hang-dog appearance
  • Postural Instability also causes lack of balance and falls causing various injuries.



Cognitive Disorders causing dificulty in Executive Functions due to cognitive difficulty in.

  • Planning Action
  • Flexibility
  • Abstract thinking
  • Rule Acquisition
  • Inhibiting inappropriate action
  • Initiating appropriate action
  • Memory
  • Attention
  • Processing speed
  • Recall – needs cues
  • Perception and estimation of time
  • Visuospatial – face recognition and geometric Orientation

Behaviour, Thoughts and Mood

  • Depression
  • Apathy
  • Anxiety
  • Hallucinations
  • Illusion
  • Delusion
  • Dementia
  • Psychosis with delusion and associated delirium
  • Paranoid ideation


These symptoms in most appears years before the disease is classically diagnosed

  • Orthostatic Hypotension
  • Oily Skin
  • Copious perspiration
  • Incontinence of Urine
  • Sexual Dysfunctions
  • Fatal Gastric Dismolity
  • Fatal Constipation
  • Altered olfaction
  • Visual disturbances
  • Paraesthesia limbs


  • NAJA

4 thoughts on “PARKINSON’s DISEASE”

  1. I was diagnosed with Parkinson’s disease nearly 4 years ago, at age 51. I had a stooped posture, tremors, muscle stiffness, sleeplessness, and slow movement. I was placed on Sinemet for 7 months and then Sifrol and rotigotine were introduced which replaced the Sinemet but I had to stop due to side effects. I was in denial for a while as there is no history of PD in my family. I also used amantadine, and physical therapy to strengthen muscles all failed. I decided to adopt a more natural approach.

  2. After my Parkinsons Disease diagnosis, i was on Carbidopa and Pramipexole for two years, as the disease progressed my symptoms worsened, with my neurologist guidance i started on natural PARKINSONS DISEASE TREATMENT. The treatment worked very effectively for my Parkinson’s, most of my severe symptoms simply vanished within the first 3 months on the treatment, i feel better now than I have felt in years and i can feel my strength again. My neurologist was very open when looking at alternative medicines and procedures, this alternative parkinson disease treatment is indeed a breakthrough.

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