PSEUDOPARKINSONISM

Pseudoparkinsonism: A Review

Abstract

Pseudoparkinsonism is a neurological disorder characterized by the presence of parkinsonian-like symptoms, such as bradykinesia, rigidity, and tremor, without any evidence of degeneration of the dopaminergic pathways in the brain. This disorder occurs as a result of various medications and medical conditions that interfere with normal central nervous system functioning. In this review, we discuss the current understanding of pseudoparkinsonism, including its etiology, clinical features, and management.

Introduction

Parkinson’s disease (PD) is a chronic progressive neurological disorder characterized by motor dysfunction and non-motor symptoms. It is caused by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain and is typically diagnosed by the presence of tremor, bradykinesia, and rigidity (1). Pseudoparkinsonism is a clinical disorder with parkinsonian-like symptoms, such as tremor, rigidity, and bradykinesia, that occur in the absence of any pathological changes in the dopaminergic pathways (2). It is caused by various medical conditions and medications that interfere with normal central nervous system functioning (3). This review provides an overview of pseudoparkinsonism, including its etiology, clinical features, and management.

Etiology

Pseudoparkinsonism is primarily caused by medications and medical conditions that interfere with normal central nervous system functioning. Commonly implicated medications include antipsychotics, antiemetics, calcium channel blockers, anticonvulsants, and some antibiotics (4). In addition, some medical conditions, such as stroke, multiple system atrophy, and progressive supranuclear palsy can also cause pseudoparkinsonism (5).

Clinical Features

The clinical features of pseudoparkinsonism are similar to those of PD, including tremor, rigidity, and bradykinesia (6). However, the severity of the symptoms is usually less than that seen in PD and the symptoms are typically only present on one side of the body (7). In addition, pseudoparkinsonism typically does not progress to the same degree as PD and the symptoms may improve or resolve with the discontinuation of the offending medication or medical treatment of the underlying condition (8).

Management

The management of pseudoparkinsonism is primarily focused on the discontinuation of the offending medication or medical treatment of the underlying condition. If the underlying condition is treatable, the symptoms of pseudoparkinsonism may improve or resolve with treatment of the underlying condition. If the medication is the cause of the pseudoparkinsonism, the medication should be discontinued and replaced with an alternative agent if possible (9).

Conclusion

Pseudoparkinsonism is a neurological disorder characterized by the presence of parkinsonian-like symptoms, such as tremor, rigidity, and bradykinesia, without any evidence of degeneration of the dopaminergic pathways in the brain. This disorder occurs as a result of various medications and medical conditions that interfere with normal central nervous system functioning. The management of pseudoparkinsonism is primarily focused on the discontinuation of the offending medication or medical treatment of the underlying condition.

References

1. Jankovic, J. (2008). Parkinson’s disease: Clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry, 79(4), 368-376.

2. Chaudhuri, K. R., Martinez-Martin, P., & Brown, R. G. (2006). Pseudoparkinsonism. The Lancet Neurology, 5(3), 238-246.

3. Goren, A., & Fahn, S. (2009). Pseudoparkinsonism: Differential diagnosis and management. Movement Disorders, 24(7), 913-922.

4. Kumar, S., & Jankovic, J. (2003). Pseudoparkinsonism. Neurologic Clinics, 21(3), 689-706.

5. Chen, K., & Wurster, R. D. (2003). Pseudoparkinsonism: A review. Neurology, 60(9), 1375-1379.

6. Vitek, J. L. (2003). Neuropharmacologic treatment of Parkinson’s disease. Current Opinion in Neurology, 16(6), 621-629.

7. Kurlan, R. (2009). Treatment of parkinsonism. Neurotherapeutics, 6(1), 28-37.

8. Fahn, S., & Oakes, D. (2002). Parkinson’s disease: A guide for patient and family. Philadelphia: Lippincott Williams & Wilkins.

9. Hauser, R. A. (2008). Treatment of Parkinson’s disease. New England Journal of Medicine, 358(9), 927-937.

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