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Movement Disorder

  1. Parkinson’s Disease
Definition – It is a chronic, progressive disorder in which idiopathic parkinsonism (i.e. variable combination of tremor, rigidity brady kinesia, gait disturbance)

Pathogenesis – It is due to loss of nerve cells in the pigmented substantia nigra pars compacta, symptoms occur when there is loss of at least 80% cell loss. There is an imbalance between dopamine and acetyl choline neurotransmitters (either an increase in acetylcholine or a decrease in dopamine level)

Clinical Features – 

  1. General - (Ref. Hari. 18th ed., Pg- 3317)
    1. Expressionless face with straight look with infrequent blinking.
    2. Rapid, monotonous speech.
    3. Flexed posture (universal flexion)
  2. Gait -
    1. Festinating gait

Gait/Postural reflexes (disturbed)

  1. Difficulty in maintaining balance
  2. Slow to start walking
  3. Shortened stride
  4. Rapid small steps (tendency to run) : festination gait
  5. Reduced arm swing
  6. Difficulty in stopping suddenly
  7. Impaired balance on turning.
  1. Tremor -
    1. Resting tremors – 4 – 8/Sec                       
    2. Usually first in fingers/ thumb
    3. Pill rolling movements
  2. Rigidity -
    1. Cogwheel type – mostly appreciated in upper limbs especially in wrist joint
    2. Plastic (lead pipe) – mostly appreciated in the legs and trunk.
    3. In the trunk rigidity manifests itself by the presence of a flexed and stooped posture.
  3. Hypokinesis - 
    1. Handwriting – micrographia
  4. Eye Signs in Parkinsonism –
    1. Decrease Blink rate     
    2. Impaired smooth pursuit
    3. Hypometri saccades
    4. Myerson’s sign (Glabellar tap sign)
    5. Blepharospasm
    6. Reversed Argyll Robertson pupils (post encephalitic parkinsonism)

Extra Edge:

  1. Glabellar reflex (also known as the "glabellar tap sign")
    1. It is a primitive reflex.                         
    2. It is elicited by repetitive tapping on the forehead.
    3. Subjects blink in response to the first several taps.       
    4. If the blinking persists
  2. Myerson's sign and is abnormal
  3. The afferent trigeminal nerve, and the efferent the facial nerve

Myerson's sign is often seen in patients with Parkinson's disease.

Causes –


   Mechanism                                               Example

1. Impaired release of dopamine               Idiopathic Parkinson’s disease

2. Drugs depleting dopamine stores          Reserpine, tetrabenazine

3. Trauma                                                   Repeated head injury (Punch Drunk Syndrome)

4. Blockage of striatal dopamine receptor       Phenothiazine, Butyrophenones

5. Copper deposition (LQ 2012)               Wilson’s disease


Important Points: Parkinsonism: Quick Revision:
  1. Parkinsonism is caused by a disturbance in substantia nigra. 
  2. Resting Tremor with frequency 4 - 6 Hz. 
  3. Tendon reflexes are Normal
  4. Plantar reflex is typically flexor
  5. Festinating Gait
  6. Small handwriting
  7. Normal intelligence
  8. Emotional liability
  9. Masked expressionless facies
  10. Slurred indistinct speech

Treatment of Parkinsonism
 (Ref. Hari. 18th ed., Pg- 3321)

  1. MAO-B inhibitor
    1. Selegiline             
    2. Rasagiline      
    3. Lazabemide
  2. Central Anticholinergic:  Benztropine, Biperiden, Orphenadrine, Procyclidine, Trihexyphenidyl.
    [Trihexyphenidyl: Most commonly used drug, benztropine is the DOC for drug induced parkinsonism]
  3. Dopamine agonist
    1. Levodopa
    2. Amantadine
    3. Non ergot alkaloid: Pramipaxol, Ropinirol, Rotigotine
    4. Ergot alkaloid: Pergolide, Cabergoline, Bromocriptine
  4. COMT inhibitor: Tolcapone, Entacapone
  5. Atypical antipsychotic, clozapine, olanzapine, risperidone, quetiapine
  6. Continuous infusion by levodopa.
  7. Recent Advances:
    High frequency stimulation of selected area - Subthalamus nuclei or globus pallidus improve symptoms.
  8. Surgery
    1. Stereotactic thalamotomy and pallidotomy
    2. Transplantation of fetal midbrain dopaminergic cells into putamen of pt.
    3. Transplantation of autologous adrenal medullary tissue.

Recent Advances:


Newer Drugs in the treatment of parkinson: Lazabemide, Pramipaxol, Ropinirol, Rotigotine, Pergolide, Cabergoline, Tolcapone, Entacapone, clozapine, olanzapine, risperidone, quetiapine.

Tolcapone: COMT is an enzyme responsible for the peripheral metabolism of levodopa. Peripheral dopa decarboxylase is another such enzyme. Block of latter enzyme may not be able to block the total peripheral degradation. Tolcapone is more potent and longer acting than entacapone.


Recent Advances:


Neuroprotection: Several promising agents such as rasagiline, selegiline, coenzyme Q10, pramipexole, and ropinirole may delay or prevent the onset for PD. (Ref. Hari. 18th ed., Pg- 3324)

In 17th edition of Harrison, maintained HRT, NSAIDS as neuro protective drugs but has been removed in 18th edition. !!!

  1. Multisystem atrophy (Shy dragger syndrome)

The features are as follows:

  1. Parkinsonism
  2. Autonomic neuropathy
  3. Cerebellar ataxia (due to olivo ponto cerebellar atrophy)

Additional feature which may be there are – Dystonia, Myoclonus, Emotional incontinence, Sleep deprivation.   

Pathology: There is presence of alpha Synuclein positive inclusion located in the various part of the brain.


Recent Advances
New Drug:
Droxidopa is a synthetic amino acid precursor which acts as a prodrug to the neurotransmitters norepinephrine and epinephrine. Unlike norepinephrine and epinephrine themselves, droxidopa is capable of crossing the protective blood–brain barrier (BBB)

Indications of uses of Droxidopa

  1. Neurogenic orthostatic hypotension (NOH), as well as NOH associated with multiple system atrophy (MSA), familial amyloid polyneuropathy (FAP), pure autonomic failure (PAF), and Parkinson's disease (PD).
  2. Intradialytic hypotension (IDH) or hemodialysis-induced hypotension.
  3. Hypotension associated with fibromyalgia syndrome (FMS) and chronic fatigue syndrome (CFS)

  1. Progressive Supranuclear Palsy – (AIPG 2006) (Ref. Hari. 18th ed., Pg- 3310)
    1. Also known as Steel- Richardson –Syndrome.
    2. Degenerative disorder characterised by neuronal loss, gliosis and neurofibrillary tangles in part of CNS which are involved with maintenance of posture & equilibrium namely in mid brain, pons, basal ganglia and dentate nuclei of cerebellum.
    3. Age b/w 45 – 75 years. Males > females.
    4. Vertical supranuclear gaze paresis, with difficulty in down gaze.
    5. Failure of voluntary saccadic gaze in a vertical plane.
    6. Later smooth pursuit movements are also affected.
    7. Axial dystonia in extension esp of neck Frequent falls.
    8. Limb rigidity and brady kinesia
    9. Tremors unusual.
    10. Pseudobulbar palsy – Facial weakness, dysarthria, dysphagia and exaggerated jaw Jerk and gag reflexes.
    11. Pseudobulbar effect – Exaggerated and in appropriate emotional responses.
    12. DTR – Brisk. Plantar ↑↑.
    13. Cerebellar signs positive.
    14. Intellectual functions are impaired.
Important Points:

The clinical features are characteristic
"Progressive supranuclear palsy should be considered whenever a middle aged or elderly person presents with history of repeated falls and has an extrapyramidal syndrome accompanied by nuchal dystonia and paralysis of voluntary down gaze"

Factors which distinguish this from Parkinson's

  1. Marked impairment of voluntary downward gaze and horizontal gaze
  2. Extended rather than flexed dystonic posturing
  3. Absence of tremor
  4. Poor response to antiparkinsonian medication

Protein Aggregations in major dementias and related cognitive disorders:




Alzheimer’s disease

A-beta, Tau

Fronto temporal dementia, Pick's disease


Progressive supranuclear palsy


Corticobasal degeneration


Parkinson's disease

Alpha-synuclein (LQ 2012)

Multiple system atrophy


Facts to Remember:


Pick’s Bodies contain Tau protein


Lewy bodies contain a synuclein

  1. Hyperkinetic disorders (Ref. Hari. 18th ed., Pg- 3327)

Abnormal movement

Site of lesion

1. Chorea

2. Athetosis

3. Hemiballismus

4. Parkinsonism

Caudate nucleus and putamen (striatum)

Lentiform nucleus (Globus pallidus)

Subthalamic nucleus

Substantia nigra

  1. Tremor
    1. Resting tremor = Parkinson,
    2. Intention tremor = cerebellar disease,
    3. Positional tremor =  hyperthyroidism,
    4. Flapping tremors = Renal failure, Hepatic failure, Respiratory failure, Phenytoin toxicity, acute parietal lobe or thalamic lesion.
    5. Benign essential tremor is characterized by a posture-related 5-9- Hz oscillation of the hands and forearms that impairs performance of fine motor tasks.
      1. This type of tremor is often familial and may be accompanied by titubation (head tremor).
      2. Consumption of alcohol may temporarily suppress the tremor; stress, caffeine, or sleep deprivation may  exacerbate the condition.
      3. β-Adrenergic blocking agents and primidone are effective treatments.
  2. Chorea describes rapid, "dance-like" distal limb and facial movements.
    Causes (Ref. Hari. 18th ed., Pg- 3330)
    1. Hyperthyroidism,                        
    2. Drugs (e.g., birth control pills and levodopa),
    3. Sydenham's chorea,            
    4. Pregnancy,
    5. SLE,                           
    6. Antiphospholipid syndrome,
    7. Stroke,                               
    8. Porphyria,
    9. Lyme disease,                     
    10. Huntington's disease,           
    11. Neuroacanthocytosis.

Milkmaid’s Grip (LQ 2012)

  1. A sign of generalised muscle weakness and inability to maintain tetanic muscle contraction;
  2. the subjects, when asked to squeeze the examiner’s fingers, do so by a ‘milking’ motion of contraction and relaxation,
  3. A finding typical of Sydenham’s chorea, one of the Jones’ major criteria for diagnosing rheumatic fever

  1. Athetosis - Involuntary, slow, writhing, "snake-like" limb movements.
    1. Wilson's disease,          
    2. Huntington's disease,           
    3. Anoxic encephalopathy,  
    4. Trauma,                      
    5. Birth control pills,         
    6. Several rare hereditary disorders.
  2. Dystonia
    1. Slow, writhing, sustained and involuntary contractions of the proximal limb, trunk, and neck musculature.
    2. Dystonia is associated
      1. Wilson's disease,                   
      2. Parkinson's disease,             
      3. Huntington's disease,
      4. Trauma,                              
      5. Neuronal storage disorders,  
      6. Encephalitis,
      7. Drugs (e.g., neuroleptics, levodopa),  
      8. Other rare hereditary conditions.
    3. Focal dystonias such as writer's cramp, blepharospasm, spastic dysphonia, and torticollis can occur. Treatment with local botulinum toxin infiltration can be beneficial.

Extra Edge: Movement disorders in Wilson disease.

  1. Dystonia
  2. In coordination
  3. Tremors.
  1. Hemiballismus describes wild, flinging, principally proximal movements of the arms or legs. It is often caused by an infarct in the subthalamic nucleus. Haloperidol can decrease the involuntary movements.     
  2. Blepharospasm can occur in isolation or as part of a more widespread disorder such as Parkinson's disease, stroke, or Meige's syndrome (orofacial dystonia). Blepharospasm can be of such severity as to cause functional blindness.
    1. Many drugs have been tried in an attempt to control the problem with modest effect.
    2. Infiltration of botulinum toxin about the eyes can provide relief by decreasing neuromuscular transmissions.
  3. Neuroleptic malignant syndrome (NMS) (Ref. Hari. 18th ed., Pg- 3333) is an idiosyncratic reaction to on starting neuroleptic agents. It can also occur in Parkinson's disease patients after the abrupt discontinuation of anti parkinsonian medications. Dopamine receptor blockade is thought to be the cause of NMS.
    1. Clinical signs include altered mentation, high fever, rigidity, autonomic instability, high creatine kinase (CK) levels, and myoglobinuria.
    2. Therapy for this potentially lethal condition includes hydration, cooling blankets, antipyretics, dantrolene, and levodopa/carbidopa preparations or bromocriptine, although the use of antiparkinsonian drugs is controversial.
  4. Tardive dyskinesia is an almost constant writhing movement of the tongue and oromandibular area, which may be accompanied by blepharospasm, respiratory grunts, choreoathetosis, and truncal hyperactivity. 
    1. Tardive dyskinesia is usually an adverse side effect of long- term use of neuroleptic agents; occasionally other drugs such as amphetamines, antihistamines, and carbamazepine are .' causally implicated.
    2. Clonazepam, reserpine, tetrabenazine, and other drugs have been used to treat tardive dyskinesia with variable success.
  5. Spasmodic torticollis
    1. Dystonia of neck movements. Head turns to one side for prolonged periods
  6. Tics
    1. Simple: Repeated stereotyped brief face and limb co-ordinate movements
    2. Complex: Multiple often obscene (coprolalia) an rude gestures (Giles de la Tourette syndrome)

Uses of Botulinum toxin type A

(Inhibits Ach release)

Glabellar lines (cosmetic use) in adult men and women. Also used in Strabismus, (Blepharospasm, Cervical dystonia hemifacial spasms)

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