History

Fact Explanation
Features of Parkinsonism Blockage of postsynaptic dopaminergic receptors in the basal ganglia motor circuit manifest the clinical symptoms of parkinsonism. Symptoms begin after the use of the offending drug and usually resolve after the drug is being withdrawn.
Bradykinesia Patients often experience bradykinesia, which is one of the cardinal feature of parkinsonism. Bradykinesia develops due to the involvement of basal ganglia. Fine motor tasks like buttoning and writing are impaired initially. [1,2]
Finger tremor Tremor is usually absent in drug induced parkinsonism (DIP), however 30-50% of patients may present with asymmetrical resting tremor. Those patients usually shows postural tremor as well. However patients with DIP usually present with symmetrical tremor. [2,3]
Recurrent falls PD causes postural instability and recurrent falls. [1,3]
Freezing Patients with PD often develop "freezing", so called motor block. Suddenly the patient stops what he or she was doing for some time and restart. [1]
Expressionless face Patients develop expressionless face due to bradykinesia. [1]
Abnormal gait PD causes reduced arm swinging while walking. [1,3]
Joint pain Patients with PD can develop joint pain due to muscle rigidity. [1]
Postural deformities As the disease progresses patients develop postural deformities. These are due to rigidity of the muscles. Neck and the truck is flexed so as the elbows and the knees. [1,3]
Drug history Typical antipsychotics (Chlorpromazine, phenothiazine, prochloroperazine, perphenazine, fluphenazine, promethazine, pimozide) is the commonest cause of DIP. Atypical antipsychotics (risperidone, olanzapine), gastrointestinal prokinetics (metoclopramide, levosulpiride, clebopride, itopride, domperidone), antidepressants, calcium channel blockers (flunarizine and cinnarizine) and antiepileptic drugs can also cause DIP. [2,4]
Past medical history Antipsychotics are usually prescribed for psychotic disorders (schizophrenia, bipolar effective disorders). So patients may have delusions, hallucinations, or disordered thought. Headache, dizziness, diarrhea and anxiety are other side effects of antipsychotics. Gastrointestinal prokinetics are prescribed for abdominal discomfort, bloating, constipation, heart burn, nausea, and vomiting. Calcium channel blockers are prescribed for hypertension, angina and arrhythmia.
References
  1. JANKOVIC J. Parkinson's disease: clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry [online] 2008 April, 79(4):368-376 [viewed 10 September 2014] Available from: doi:10.1136/jnnp.2007.131045
  2. SHIN HW, CHUNG SJ. Drug-Induced Parkinsonism J Clin Neurol [online] 2012 Mar, 8(1):15-21 [viewed 10 September 2014] Available from: doi:10.3988/jcn.2012.8.1.15
  3. FEMI OL, IBRAHIM A, ALIYU S. Clinical profile of parkinsonian disorders in the tropics: Experience at Kano, northwestern Nigeria J Neurosci Rural Pract [online] 2012, 3(3):237-241 [viewed 10 September 2014] Available from: doi:10.4103/0976-3147.102589
  4. OLIVARES ROMERO J., ARJONA PADILLO A.. Diagnostic accuracy of 123I-FP-CIT SPECT in diagnosing drug-induced parkinsonism: A prospective study. Neurología (English Edition) [online] 2013 June, 28(5):276-282 [viewed 10 September 2014] Available from: doi:10.1016/j.nrleng.2012.05.007

Examination

Fact Explanation
Features of Parkinsonism Most of the examination findings of DIP are similar to Parkinson's disease. Bilateral and symmetrical parkinsonism without resting tremor is the differentiating feature of DIP and primary Parkinson's disease. [2]
Rigidity Rigidity is a cardinal feature of PD. “Cogwheel” rigidity is commonly elicited. As rigidity worsens patient adopt a posture where the neck, truck, elbows and the knees are flexed. [1]
Tremor Absence of resting tremor enables the differentiation of DIP from Parkinson's disease. However around 50% of the affected patients may have resting tremor. [2]
Bradykinesia Patients with PD demonstrate difficulties in planning, initiating and executing motor tasks. When the patient is asked to do repetitive finger taps, hand grips, hand pronation–supination and heel taps the amplitude of the movements reduces and they become progressively slow. However if the patient is excited he will be able to do quick tasks which is called "kinesia paradoxica". [1]
Expressionless face (hypomimia) Patients with PD have "mask face" and reduced or absent eye blinking as bradykinesia progresses. [1]
Reduced arm swinging Reduced arm swinging is another manifestation of bradykinesia. This is also asymmetrical. [1]
References
  1. JANKOVIC J. Parkinson's disease: clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry [online] 2008 April, 79(4):368-376 [viewed 10 September 2014] Available from: doi:10.1136/jnnp.2007.131045
  2. SHIN HW, CHUNG SJ. Drug-Induced Parkinsonism J Clin Neurol [online] 2012 Mar, 8(1):15-21 [viewed 10 September 2014] Available from: doi:10.3988/jcn.2012.8.1.15

Differential Diagnoses

Fact Explanation
Parkinson's disease (PD) Tremor, rigidity, bradykinesia and postural instability are the cardinal features of PD.The clinical features of both PD and DIP are more or less similar, but neurological symptoms are more severe in DIP. Absent resting tremor and symmetrical parkinsonism are characteristic of DIP. However about 50% of the patients with DIP can present with asymmetrical parkinsonism and resting tremor, making the clinical diagnosis of PD difficult. [2,3]
Essential tremor Essential tremor can also involve the distal extremities. [1]
Tardive dyskinesia (TD) TD is the painful muscle spasms that occurs commonly secondary to use of typical antipsychotics. [4,5]
Myoclonus Myoclonus is the sudden brief jerks that are caused by involuntary muscle activity. [6]
Senile chorea Although rare senile chorea can present with late onset, generalised chorea. Dementia is usually absent in senile chorea. [7]
Dementia with lewy bodies Dementia with lewy bodies is the second most common cause of dementia. It is one of the neurodegenerative dementia. Patient can present with functional disability. [8]
Wilson disease Wilson disease is an inherited disease. Affected individuals lack the enzymes needed for the copper metabolism, leading to accumulation of copper mainly in the liver and in the brain. Hepatic accumulation of copper finally leads to cirrhosis whereas copper depositions in the brain leads to neuropsychiatric symptoms. Dystonia of the bulbar muscles cause speech and swallowing difficulties and drooling of saliva. Limb dystonia leads to abnormal posturing. Unsteady gait, incoordination of speech and tremor are other neuropsychiatric manifestations of the disease. Clinical manifestations usually develop in their twenties and forties, so Wilson disease should be considered a possible differential diagnosis in young patients. [9]
References
  1. JANKOVIC J. Parkinson's disease: clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry [online] 2008 April, 79(4):368-376 [viewed 10 September 2014] Available from: doi:10.1136/jnnp.2007.131045
  2. SHIN HW, CHUNG SJ. Drug-Induced Parkinsonism J Clin Neurol [online] 2012 Mar, 8(1):15-21 [viewed 10 September 2014] Available from: doi:10.3988/jcn.2012.8.1.15
  3. FEMI OL, IBRAHIM A, ALIYU S. Clinical profile of parkinsonian disorders in the tropics: Experience at Kano, northwestern Nigeria J Neurosci Rural Pract [online] 2012, 3(3):237-241 [viewed 10 September 2014] Available from: doi:10.4103/0976-3147.102589
  4. BELLA V. L., PICCOLI F.. Olanzepine-induced tardive dyskinesia. The British Journal of Psychiatry [online] 2003 January, 182(1):81-82 [viewed 10 September 2014] Available from: doi:10.1192/bjp.182.1.81-b
  5. MüLLER D J, SHINKAI T, DE LUCA V, KENNEDY J L. Clinical implications of pharmacogenomics for tardive dyskinesia. Pharmacogenomics J [online] 2004 December, 4(2):77-87 [viewed 10 September 2014] Available from: doi:10.1038/sj.tpj.6500233
  6. CAVINESS JOHN N, BROWN PETER. Myoclonus: current concepts and recent advances. The Lancet Neurology [online] 2004 October, 3(10):598-607 [viewed 10 September 2014] Available from: doi:10.1016/S1474-4422(04)00880-4
  7. GRIMES D A. Late adult onset chorea with typical pathology of Hallervorden-Spatz syndrome. [online] 2000 September, 69(3):392-395 [viewed 11 September 2014] Available from: doi:10.1136/jnnp.69.3.392
  8. MCKEITH IAN, MINTZER JACOBO, AARSLAND DAG, BURN DAVID, CHIU HELEN, COHEN-MANSFIELD JISKA, DICKSON DENNIS, DUBOIS BRUNO, DUDA JOHN E, FELDMAN HOWARD, GAUTHIER SERGE, HALLIDAY GLENDA, LAWLOR BRIAN, LIPPA CAROL, LOPEZ OSCAR L, MACHADO JOãO CARLOS, O'BRIEN JOHN, PLAYFER JEREMY. Dementia with Lewy bodies. The Lancet Neurology [online] 2004 January, 3(1):19-28 [viewed 11 September 2014] Available from: doi:10.1016/S1474-4422(03)00619-7
  9. DAS SHYAMAL K, RAY KUNAL. Wilson's disease: an update. Nat Clin Pract Neurol [online] 2006 September, 2(9):482-493 [viewed 12 September 2014] Available from: doi:10.1038/ncpneuro0291

Investigations - for Diagnosis

Fact Explanation
Clinical diagnosis DIP is mainly a clinical diagnosis. Diagnostic criteria include presence of parkinsonism, absence of history of parkinsonism before the use of the offending drug, and onset of parkinsonian symptoms during use of the offending drug. Imaging is indicated to exclude possible organic etiology. [1]
PET scan or Single-photon-emission computed tomography (SPECT)[1] Brain imaging is indicated to exclude possible degenerative causes for parkinsonism.
MRI [2] MRI of the brain is useful to detect the presence of degenerative changes.
CT scan [2] Similarly CT scan of the head is useful to exclude degenerative changes.
References
  1. SHIN HW, CHUNG SJ. Drug-Induced Parkinsonism J Clin Neurol [online] 2012 Mar, 8(1):15-21 [viewed 10 September 2014] Available from: doi:10.3988/jcn.2012.8.1.15
  2. FEMI OL, IBRAHIM A, ALIYU S. Clinical profile of parkinsonian disorders in the tropics: Experience at Kano, northwestern Nigeria J Neurosci Rural Pract [online] 2012, 3(3):237-241 [viewed 10 September 2014] Available from: doi:10.4103/0976-3147.102589

Management - General Measures

Fact Explanation
Health education Patients should be reassured about the fact that DIP usually reverses with the cessation of the offending drug. If the patient should be prescribed a drug which is known to cause DIP patient should be educated about the possibility of DIP and they should also be educated about the possible alternative treatment options which have lower risk of DIP (prescription of atypical antipsychotics instead of typical antipsychotics).
References

Management - Specific Treatments

Fact Explanation
Cessation of the offending drug Once the offending drug is withdrawn, the symptoms usually reverse within few weeks to months. If the typical antipsychotics can not be stopped it is indicated to use an atypical antipsychotic instead of typical antipsychotic, because it has less risk of DIP. About 10 to 50% of patients may worsen or may continue to have symptoms even after cessation of the offending drug. [1,2]
Levodopa Levodopa is prescribed for a short period of time till the resolution of symptoms. [3]
Anticholinergic agents Similarly anticholinergic agents can be used for symptom relief. Anticholinergic drugs are effective in relieving motor symptoms. [3,5]
Dopamine agonists Dopamine agonists are indicated for symptom relief. Dopamine agonists act directly on dopamine receptors and mimick the endogenous neurotransmitter. [3,4]
References
  1. SHIN HW, CHUNG SJ. Drug-Induced Parkinsonism J Clin Neurol [online] 2012 Mar, 8(1):15-21 [viewed 10 September 2014] Available from: doi:10.3988/jcn.2012.8.1.15
  2. OLIVARES ROMERO J., ARJONA PADILLO A.. Diagnostic accuracy of 123I-FP-CIT SPECT in diagnosing drug-induced parkinsonism: A prospective study. Neurología (English Edition) [online] 2013 June, 28(5):276-282 [viewed 10 September 2014] Available from: doi:10.1016/j.nrleng.2012.05.007
  3. ALVAREZ M. V. G., EVIDENTE V. G. H.. Understanding drug-induced parkinsonism: Separating pearls from oy-sters. Neurology [online] 2008 February, 70(8):e32-e34 [viewed 10 September 2014] Available from: doi:10.1212/01.wnl.0000302255.49113.51
  4. BROOKS D J. Dopamine agonists: their role in the treatment of Parkinson's disease. [online] 2000 June, 68(6):685-689 [viewed 10 September 2014] Available from: doi:10.1136/jnnp.68.6.685
  5. KATZENSCHLAGER R, SAMPAIO C, COSTA J, LEES A. Anticholinergics for symptomatic management of Parkinson's disease. Cochrane Database Syst Rev [online] 2003:CD003735 [viewed 10 September 2014] Available from: doi:10.1002/14651858.CD003735