ANXIETY DISORDERS
IN PARKINSON’S DISEASE: INSIGHTS
INTO THE NEUROBIOLOGY OF NEUROSIS
It is within living professional memory that mental states in clinical medicine were understood as radically demarcated from their underlying neuroanatomy, neurochemistry, and neuropsychology.
The behavioral disorders were relegated to the realm of the “functional,” whereas all the rest of clinical medicine was navigated to the “organic” subcontinents of neurology, cardiology, and general medicine. The bridging insights of neuropsychiatry over the past 20 years have greatly improved our insights about the interactive nature of neurology and psychiatry [1]. First in the aphasias, then in the dementias, and later in the affective disorders, neuropsychiatry has helped us to understand how thought, feeling, and action can be directly influenced by the neurobiology of certain neurologic diseases.
The anxiety disorders may be the most common of the psychiatric disorders [2].
Lifetime prevalence rates for DSM-III-R-diagnosable anxiety disorders are as high as 30.5% for women and 19.2% for men [3]. These disorders occur across the lifespan, from childhood to later years. They include a variety of distressing symptoms including nervousness, sleeplessness, hypochondrias is, and many somatic symptoms.
They tend to persist, and they are difficult to diagnose and treat. One might wonder whether these disorders will become the mood disorders of the next century.
The observation that persons suffering from certain neurological diseases develop certain behavioral syndromes at incidence rates greater than expected has been a most useful insight for neuropsychiatry. Such observations have substantially shaped our theoretical understanding of the affective disorders [4], obsessive–compulsive disorder [5], and the psychoses [6].
The anxiety disorders, however, have not received analogous clinical neuropsychiatric investigation. We do have certain neurobiological insights concerning the neuroanatomy and neurochemistry which is of importance to the clinical expression of generalized or episodic anxiety [7]; however, these insights derive primarily from animal experiments, or from functional imaging in humans. Disease-based neuropsychiatry has yet to make its contributions to our understanding of the anxiety disorders.
Clinical reports are now becoming available which indicate that there might be an association between the anxiety disorders and idiopathic Parkinson’s disease (PD), or its treatments [8]. Both episodic and generalized anxiety syndromes have been reported to occur in PD populations at elevated rates compared with normal and disease controls [9–11]. Some of these patients clearly seem to have onset of the anxiety symptomatology prior to first motor symptoms of PD, suggesting some underlying, shared neurobiologic vulnerability to PD and anxiety [12]. It has been difficult to specify a relationship between episodic or generalized anxiety in PD patients and dopamine agonist pharmacotherapy. Some investigators have reported an association between the timing of levodopa dosing and panic attacks [13], but others have not [9]. In one study of levodopa infusions under controlled conditions anxiety was reduced in patients with advanced PD and motor fluctuations [14]. It is certainly the case, however, that older neurologists recall remarkable anxiety symptoms in PD patients prior to the advent of levodopa therapy, and that many PD patients demonstrate their anxiety symptoms prior to the initiation of levodopa [15].
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ANXIETY,
cardiology,
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DISEASE,
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Lifetime,
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NEUROBIOLOGY,
neurology,
neuropsychiatry,
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02 22nd, 2008| 