to medication than idiopathic PD. One of the more common forms of secondary parkinsonism is vascular parkinsonism. In contrast to patients with idiopathic PD, patients with vascular parkinsonism are older with a shorter duration of illness; present with symmetrical gait difficulties; are less responsive to levodopa; and are more prone to postural instability, falls, and dementia (Benítez-Rivero et al., 2014). Pyramidal signs (spasticity, hyperreflexia, and difficulty moving); pseudobulbar palsy (difficulty with speech and swallowing); and incontinence are also more common in vascular parkinsonism. Additionally, tremor is typically not a main feature of vascular PD. Parkinson-plus syndromes Parkinson-plus syndromes are a group of neurodegenerative diseases displaying the typical features of idiopathic PD (akinesia/bradykinesia, tremor, rigidity, postural instability) with additional symptoms that distinguish them from idiopathic PD, such as early onset of dementia, early and severe balance problems, or inability to perform certain eye movements. Progressive supranuclear palsy: Is the most common of the Parkinson-plus syndromes. This condition results from degeneration of neurons in the basal ganglia, brain stem, thalamus, and frontal cortex. The underlying cause of this degeneration is unknown. Symptoms include postural instability leading to falls within the first year of disease onset and supranuclear ophthalmoplegia, a weakening of the vertical gaze, especially in the downward direction. Individuals with progressive supranuclear palsy have a median survival rate of 7 to 9 years from onset of symptoms (Fabbrini et al., 2019). Multiple system atrophy: Is a progressive, idiopathic, degenerative process, beginning in adulthood and presenting with varying degrees of parkinsonism, autonomic failure, cerebellar dysfunction, and pyramidal signs. It is poorly responsive to levodopa or dopamine agonists and has a median survival of 6.2 years, with a range of 0.5 to 24 years. It is characterized by symptoms of autonomic nervous system failure such as fainting spells and bladder control problems, along with cerebellar symptoms and early speech problems (Fabbrini et al., 2019). Striatonigral degeneration: Is a progressive degenerative disorder that is one type of multiple system atrophy. The major
finding is parkinsonism with autonomic and cerebellar signs. It is not responsive to levodopa. Olivopontocerebellar atrophy: Involves the degeneration of the cerebellum, pons, and inferior olivary nucleus, resulting in ataxia, balance difficulty, abnormal eye movements, bowel or bladder problems, lightheadedness when standing, rigidity, and tremor. It is present in multiple system atrophy and prion disorders (rare neurodegenerative diseases such as Creutzfeldt-Jakob Disease). Corticobasal ganglionic degeneration: Involves cortical atrophy of the frontal and parietal lobes and loss of dopamine in the substantia nigra. Typical symptoms are bradykinesia, tremor, focal rigidity, and marked dystonia, usually in one arm; limb apraxia is also common. The prognosis is for severe disability and death within 10 years (Fabbrini et al., 2019). Lewy body dementia: Involves the typical signs and symptoms of parkinsonism (bradykinesia, tremor, rigidity, and postural instability) and early onset of dementia. It is very difficult to differentially diagnose LBD, and individuals with this disease are usually first diagnosed with PD or AD. Hallucinations are more common in LBD, and their manifestation may lead the clinician to a differential diagnosis. As a result of the hallucinations, these individuals are sometimes hospitalized and given antipsychotic medication. Individuals with LBD have extreme sensitivity to antipsychotics, and this heightened sensitivity may be the clue that leads to a differential diagnosis (Walker et al., 2015). Individuals with LBD also tend to have earlier onset of more significant sleep disturbances (Scharre et al., 2016). A study comparing and contrasting motor and cognitive features of AD, PD, and LBD found that AD had more amnesia and orientation impairments but less executive and visuospatial deficits than LBD subjects. The LBD group had more sleepiness, cognitive/ behavioral fluctuations, hallucinations, and sleep apnea than the AD or PD groups. Axial motor, gait, and balance disturbances correlated with executive, visuospatial, and global cognition deficits and the Tinetti Mobility Test (TMT), Berg Balance Scale (BBS), and 9-Hole Peg Tests differentiated LBD from both AD and PD (Fritz et al., 2016; Scharre et al., 2016). Table 1 differentiates PD from other disorders of the basal ganglia based on commonly observed symptoms.
Table 1: Parkinson-Like Syndromes and Their Symptoms
Identified disorder*
PD Yes
PSP Yes
MSA
SND
OPCA CBGD
LBD
Symptom
Bradykinesia
Yes
Yes
Yes/no
Yes
Yes
Rigidity
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Gait disturbance
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Tremor
Yes
No
Yes/no
No
Yes/no
Yes/no
Yes
Ataxia
No
No
Yes
No
Yes
No
No
Dysautonomia
Yes/no
Yes/no
Yes
Yes/no
Yes/no
No
Yes
Dementia
Yes/no
Yes
Yes/no
No
No
Yes/no
Yes/early
Dysarthria or dysphagia
Yes/no
Yes
Yes
Yes
Yes
Yes
Yes
Dystonia
Yes/no
Yes/no
Yes
Yes/no
No
Yes
Yes/no
Limb apraxia
No
No
No
No
No
Yes
No
Myoclonus
Yes/no
No
No
No
No
Yes
Yes
Neuropathy
No
No
Yes/no
No
Yes/no
No
No
Oculomotility disturbance
No
Yes
Yes
No
Yes
Yes
No
Orthostatic hypotension
Yes/no
Yes/no
Yes
Yes/no
Yes/no
No
Yes
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