Given the assumption that the neuropsychiatric profile of a neurological disorder reflects the underlying neuropathology, the neuropsychiatric assessment may also provide important information per taining to the diagnosis. The differential neuropsychiatry profile may be most pronounced at early stages because of the disappearance during later stages of the relatively distinct anatomical involvement observed initially.
During the last decade an increasing number of studies describing the neuropsychiatric characteristics of patients with neurodegenerative disorders have been published. Among the group of movement disorders, however, the majority of studies have focused on patients with PD, and only few studies with a low number of participants have explored the pattern of neuropsychiatry symptoms in atypical parkinsonian disorders, and thus the knowledge of the neuropsychiatric characteristics of these disorders is still limited. In addition, there are several other methodological caveats to consider when comparing different studies of the neuropsychiatric profile of patients with parkinsonism. First, patients can be selected from different sources. Clinical and demographic characteristics of patients attending a specialized movement disorder clinic may differ from patients referred to a neuropsychi-atric unit or residing in the community with regard to age, education, duration of disease, cognitive functioning, and social and economic status. Such differences may influence the frequency of neu-ropsychiatric symptoms. Second, the clinical diagnostic accuracy of movement disorders is not optimal as (43-46) clinico-pathologic studies have shown significant false-positive and false-negative rates for diagnosing parkinsonian disorders (47). Studies using patients with autopsy confirmed diagnoses are rare, and the clinical diagnostic criteria employed may vary. Third, the assessment of neu-ropsychiatric symptoms varies. Some studies are retrospective chart reviews using unstructured clinical notes, whereas others have prospectively assessed patients using standardized instruments with established reliability and validity. In addition, different instruments may yield different results. For instance, highly different frequencies of depression may occur depending on whether a diagnosis of major depression according to the DSM (Diagnostic and Statistical manual of Mental Disorders) system IV is used, or whether rating scales such as NPI, HAM-D, or BDI, with different possible cutoff scores are used (13,14). In addition, the time frame is of importance since the prevalence may differ depending on whether a point-prevalence, a 1-wk, 1-mo, or even lifetime diagnosis of depression is recorded. Finally, the neuropsychiatric profile may vary with disease duration. For example, psychosis is more common in later stages rather than in earlier stages of PD (42,48,49), and thus comparative studies should control for disease duration or disease stage.
With these caveats in mind, some information with potential diagnostic value can nevertheless be drawn from the literature of neuropsychiatric symptoms in parkinsonian disorders. The interpretation of existing studies benefits from the fact that several studies have used the NPI to assess neuropsy-chiatric symptoms, and thus it is possible to compare the NPI profile of the different parkinsonian disorders.
NEUROPSYCHIATRIC SYMPTOMS IN PARKINSON'S DISEASE
The cardinal pathological feature of PD is Lewy body degeneration of the substantia nigra, causing loss of dopaminergic innervation of the striatum. In addition, other pigmented brainstem and cholinergic nuclei are involved, and Lewy bodies are found in the neocortex of most patients. The cardinal clinical features are resting tremor, bradykinesia, and rigidity.
Neuropsychiatric symptoms are common, and their prevalence, phenomenology, and clinical implications have been extensively studied during the last decade. The majority of PD patients develop dementia with cortical and subcortical features when disease duration exceeds 10 yr (41). Depression is the most common psychiatric symptom in PD (12,50), and may occur in up to 40% of patients (51). Different studies report wide variations in prevalence rates, however, and population-based studies suggest that major depression according to the DSM system is uncommon, occurring in less than 10% of cases (52,53).
The etiology of depression in PD is not yet determined. Although psychosocial factors, i.e., social support, psychological reaction to the disease, and coping strategies, certainly play a role (54), bio logical factors are also thought to contribute. Serotonergic, dopaminergic, and noradrenergic deficits, cortical and subcortical neurodegeneration, and genetic factors may contribute to depression in PD (55). Stefurak and Mayberg proposed a model for depression in PD based on clinical, imaging, treatment, and behavioral challenge studies, which involves cortical-limbic and frontostriatal pathways. According to this model, a dorsal-cortical compartment (prefrontal, premotor, and parietal cortices and dorsal and posterior cingulate) is postulated to mediate the cognitive aspects of depression (including apathy, attentional, and executive dysfunction), whereas a ventral-limbic compartment (ventral cingulate, hippocampus, and hypothalamus) mediates circadian, somatic, and vegetative aspects of depression (sleep, appetite, libidinal, and endocrine disturbances). Finally, the rostral cingulate, with reciprocal connections to both compartments, is suggested to serve a regulatory role, including a major role in determining the response to treatment (19). Key neurotransmitters involved in these structures include dopamine and serotonin.
Is depression more prevalent in PD compared to other conditions with comparable functional impairment? If not, there is little reason to assume a disease-specific association between PD and depression. Studies of this question have usually included small samples subject to selection and participation biases. Nilsson et al. used the Danish registers of somatic and psychiatric in-patients to address this question. Data from more than 200,000 persons were analyzed, and more than 12,000 subjects with PD were identified. A significant increased risk for hospitalization owing to depression in patients with PD compared to subjects with osteoarthritis or diabetes mellitus was found, and the authors suggest that the increased risk was not a mere psychological reaction to the disease, but rather because of disease-specific brain changes in PD patients (56).
Visual hallucinations are also common in PD, and typically involve people of normal size and configuration who do not communicate with the patient. A substantial proportion of patients report vague feelings of a presence (57). The patients may or may not be aware of the abnormality of the experience, and the visions usually do not cause emotional disturbance. However, more severe psychotic symptoms with delusions and behavioral disturbances may occur as well, particularly in patients with dementia (48). Although these symptoms have previously been considered secondary to dopaminergic treatment, there is evidence suggesting that other factors may be even more important. First, psychotic symptoms were described in PD before levodopa was introduced and in untreated patients. Second, most studies find that psychotic symptoms are not related to the dose, duration of treatment, or number of dopaminergic agents (57). Third, hallucinations do not relate to levodopa plasma level or to sudden changes in plasma level (58). Fourth, although dopaminergic agents may induce psychotic symptoms in non-PD patients, PSP patients treated with dopaminergic agents do not develop hallucinations (49). Similarly, the phenomenology of well-formed images of people, usually not threatening to the patients and sometimes with insight retained, as well as the content of delusions, is very similar to the symptoms in DLB, which usually occur without dopaminergic treatment (59). Thus, dopaminergic agents may provide a neurochemical milieu with a high risk for psychosis in PD, but are not necessary or sufficient to cause psychosis. The association between duration and severity of disease, dementia, depression, sleep disturbance, visual disturbances, and psychotic symptoms suggests a multifactorial etiology, including brain changes associated with the disease itself. Neurochemical changes potentially contributing to hallucinations in PD include limbic dopam-inergic hypersensitivity and cholinergic and serotonergic changes. Sensory deprivation may also contribute, and patients with PD may process retinal images abnormally. In fact, there is evidence that visual hallucinations in PD and DLB arise as a result of abnormal activation of higher order. This would fit well with the finding that visual hallucinations are associated with Lewy bodies in the temporal lobe (60).
The NPI profile of a community-based sample of 139 patients with PD was characterized by relatively high levels of depression (38%), hallucinations (27%), and anxiety (20%), whereas euphoria and disinhibition were uncommon (12) (Table 1). A positive score on at least one NPI item was
Frequency of Neuropsychiatrie Symptoms in Parkinsonian Disorders Using the NPI
Frequency of Neuropsychiatrie Symptoms in Parkinsonian Disorders Using the NPI
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