**2. Definition and classification of Parkinsonism and PD**

PD is a progressive parkinsonism of undetermined cause without features suggestive of an alternative diagnosis. It responds to dopaminergic treatment and is associated with depletion of dopaminergic neurons and the presence of Lewy body inclusions in some of the remaining nerve cells [13-15].

The diagnosis of PD is based on clinical criteria as there is no definitive laboratory test to diagnose the disorder. Pathological confirmation of Lewy bodies on autopsy, a hallmark of PD, has historically been considered the standard criterion for diagnosis [13]. In clinical practice, diagnosis is usually based on the presence of a number of cardinal motor features, response to levodopa, associated symptoms, and the exclusion of other disorders [15]. When patients have a classical presentation, diagnosis of PD is relatively simple. However, differ‐ entiating PD from other forms of parkinsonism in the early stages of the disease, when signs and symptoms overlap with other syndromes, can be difficult [16]. Criteria for diagnosis of PD were developed by the UK Parkinson's Disease Society Brain Bank (Table 1) and the National Institute of Neurological Disorders and Stroke (NINDS) [7,14]. When standard clinical criteria such as the UK Parkinson's disease brain bank criteria are used, significantly more accurate clinical diagnosis of the disease is possible; however, as many as 10% of patients diagnosed with the disease in life will still need to be reclassified at post-mortem examination [17]. These criteria have been estimated to have a diagnostic specificity and sensitivity of 98.6% and 91.1%, respectively [18].

Parkinsonian disorders can be classified into four categories: primary (idiopathic) parkinson‐ ism, secondary (acquired, symptomatic) parkinsonism, heredodegenerative parkinsonism, and multiple system degeneration (parkinsonism plus syndromes). A number of features, including tremor, early gait abnormality (e.g., freezing), postural instability, pyramidal tract signs, and response to levodopa, can be used to distinguish PD from other parkinsonian disorders. While differences in the density of postsynaptic dopamine receptors in PD patients or patients with atypical parkinsonian disorders have been used to account for the poor response to levodopa therapy in the latter group, other explanations may also be possible [19].


**Table 1.** Diagnostic criteria for Parkinson's disease (PD) [7,14]

five patients being affected. The prevalence of dysphagia in four studies was between 72% and 87%, with a pooled prevalence estimate of 82% (95% CI 77%–87%), suggesting that while the condition is common in PD, patients do not always report swallowing difficulties unless asked. This under-reporting calls for a proactive clinical approach to dysphagia, particularly in light

The aim of this chapter is to show dysphagia as a symptom/sign and an important cause of

PD is a progressive parkinsonism of undetermined cause without features suggestive of an alternative diagnosis. It responds to dopaminergic treatment and is associated with depletion of dopaminergic neurons and the presence of Lewy body inclusions in some of the remaining

The diagnosis of PD is based on clinical criteria as there is no definitive laboratory test to diagnose the disorder. Pathological confirmation of Lewy bodies on autopsy, a hallmark of PD, has historically been considered the standard criterion for diagnosis [13]. In clinical practice, diagnosis is usually based on the presence of a number of cardinal motor features, response to levodopa, associated symptoms, and the exclusion of other disorders [15]. When patients have a classical presentation, diagnosis of PD is relatively simple. However, differ‐ entiating PD from other forms of parkinsonism in the early stages of the disease, when signs and symptoms overlap with other syndromes, can be difficult [16]. Criteria for diagnosis of PD were developed by the UK Parkinson's Disease Society Brain Bank (Table 1) and the National Institute of Neurological Disorders and Stroke (NINDS) [7,14]. When standard clinical criteria such as the UK Parkinson's disease brain bank criteria are used, significantly more accurate clinical diagnosis of the disease is possible; however, as many as 10% of patients diagnosed with the disease in life will still need to be reclassified at post-mortem examination [17]. These criteria have been estimated to have a diagnostic specificity and sensitivity of 98.6%

Parkinsonian disorders can be classified into four categories: primary (idiopathic) parkinson‐ ism, secondary (acquired, symptomatic) parkinsonism, heredodegenerative parkinsonism, and multiple system degeneration (parkinsonism plus syndromes). A number of features, including tremor, early gait abnormality (e.g., freezing), postural instability, pyramidal tract signs, and response to levodopa, can be used to distinguish PD from other parkinsonian disorders. While differences in the density of postsynaptic dopamine receptors in PD patients or patients with atypical parkinsonian disorders have been used to account for the poor response to levodopa therapy in the latter group, other explanations may also be possible [19].

of the serious clinical consequences of the condition [12].

**2. Definition and classification of Parkinsonism and PD**

disability in patients with PD.

180 Seminars in Dysphagia

nerve cells [13-15].

and 91.1%, respectively [18].

### **3. Non-motor symptoms in Parkinson's disease**

In his "Essay on the Shaking Palsy," James Parkinson did not consider PD to be just a motor disorder, and in 1817 he described the presence of sleep disturbance, constipation, dysarthria, dysphonia, dysphagia, sialorrhea, urinary incontinence, and constant sleepiness with slight delirium [20]. What has been well established is that in PD patients, non-motor symptoms (NMS) occur in more than 90% of individuals in all stages of the disorder and include a variety of symptoms from neuropsychiatric and autonomic dysfunction to sleep disturbances and little-understood and little-reported sensory symptoms such as pain and impaired vision [21]. These NMS frequently occur throughout the course of PD and may occur concurrently with motor symptoms or precede their onset by several years [22]. In advanced PD, NMS have been recognized as important factors associated with impaired quality of life [23] and impose a considerable economic burden on patients' families and society [24].

In contrast to the motor symptoms of PD, NMS are often under-recognized during routine clinical visits and poorly managed in clinical practice [21,25]. Indeed, they have only recently been considered sufficiently important to warrant study by clinicians and researchers. In a prospective study of 101 PD patients, neurologists failed to identify the presence of depression, anxiety, and fatigue in over 50% of patients and the presence of sleep disturbance in 40% [26].
