Motor symptoms are cardinal clinical features of Parkinson’s disease (PD). Progress in drug therapy and rehabilitation has been presenting beneficial effect for motor symptoms. However, non-motor symptoms and signs in PD have been accumulated growing attentions and its amelioration may also give beneficial effect for PD patients’ and their care givers’ quality of life. In this mini-review, I overviewed non-motor symptoms and signs in PD.
James Parkinson described in his historical essay, “Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forwards, and to pass from a walking to a running pace: the senses and intellects being uninjured” [
In this mini-review, I overviewed non-motor symptoms and signs in PD.
Numbers of non-motor symptoms and signs in PD constantly increase with accumulation of information of PD clinical pathogenesis. To investigate non-motor symptoms scale for Parkinson’s disease (NMSSPD), we preliminary investigated overall frequency of non-motor symptoms and signs using questioner sheets [11,12]. We investigate neuropsychological signs (depression, apathy, anxiety, anhedonia, cognitive dysfunction, attention deficit, hallucination, delusion, dementia, delirium, panic disorder), sleep disorders (restless leg syndrome, abnormal behavioral disorders in REM period, insomnia, excessive day time sleep, sleep apnea), dysautonomia (orthostatic hypotension, dysuria, impotent), digestion disorders (drooping, incontinence, dysphagia, dysosmia, visual disorder), behavioral disorder (hypersexuality, compulsive behavior, pathological shopping, pathological gambling), and others (fatigue, weight loss, weight gain) [11-16]. Based on results [
These foregoing investigations indicate that non-motor signs and symptoms in PD have been known to affect their motor syndromes and QOL.
PD patients may develop neuropsychiatry syndromes such as hallucination [17,18] or depression [
Unless hallucination affects ADL, full explanation to patients and their caregivers may lighten their burdens. If hallucination in PD needs immediate integrative treatment with psychosocial interventions, antipsychotic medication and adjustment of anti-PD medication are prescribed, however leaving an adequate L-dopa dose to prevent severe off-states [
For people with PD, depression is quite common. Up to 60 percent of people with PD experience mild or moderate depressive symptoms. Research suggests that PD itself causes chemical changes of dopamine, serotonin, and norepinephrine in the limbic system that may lead to depression. Dopamine and dopamine agonist are used for treatment of depression [20-23]. In addition, depression in PD has close relationship with motor dysfunction. Thus, improvement of motor syndrome is the key factor for improvement of depression in PD.
Anxiety and apathy are dependent syndromes to depression. These signs and symptoms may be found with depression, but may be found without depression unless full drug therapy for motor syndrome conducted [24,25].
James Parkinson firstly described that PD patients never developed dementia. However, we know that PD patients may develop frontal lobe dysfunction such as forgetfulness [26-28]. PD patients have difficulty planning and carrying through tasks. When facing a task or situation on their own, a person with PD may feel overwhelmed by having to make choices. They may also have difficulty remembering information, or have trouble finding the right words when speaking. To some degree, cognitive impairment affects most PD patients. The same chemical changes that lead to motor symptoms can also result in slowness in thinking [
Up to 60% of PD patients have been reported to claim sleep disturbances. PD patients may have difficulty turning over in their sleep due to increased muscle tonus, may be ceased their sleep by pollakisuria, or may have depression [
PD patients frequently show dysautonomia such as orthostatic hypotension [
PD patients may show pollakisuria, dysuria, feeling of residual urine, or incontinence of urine. Even the same man may develop a wide variety of urinary disorders. PD patients may have sleep disorders due to nocturia [9,33]. These urinary signs are improved after adequate dopamine therapy, but anticholinergic agent such as oxybutynin hydrochloride can improve these [39,41].
PD patients frequently develop incontinence without antiparkinsonian agents, but antiparkinsonian agents themselves have some effect on developing incontinence. [42,43] Braak et al. pathologically found Lewy bodies in the Auerbach neural plexus that may be result in incontinence in PD [
PD patients increasingly show drooping with progression of disease, but patients do not have increased amount of saliva sputum but slowing of swallowing may be a cause [
To treat dysphagia in PD, nutrition support team (NST) may be useful in daily clinic [47,48].
James Parkinson described that PD patients never showed sensory disturbances [
Disinhibition including hypersexuality, compulsive behavior, pathological shopping, and pathological gambling are also reported as behavior disturbances in PD [11,12]. In our study in Japan, we less frequently observed these behavior disturbances and considered this is because in Japan relatively small amount of antiparkinsonian drugs are used. Amantadine may be effective for disinhibition [
Fatigue is the most trouble but less familiar syndrome in PD [55-60]. Fatigue can be distinguished from depression. Depressions in PD have some relation with motor syndrome, but fatigue does not. Depression also troubles patients’ caregivers [57-60]. Although pathogenesis of fatigue in PD remains uncertain, we hypothesize that it may have some relation with cognitive dysfunction, especially frontal lobe dysfunction (
PD patients show respiratory dysfunction which results in speech disturbances, dysphagia, and aspiration pneumonia [62,63]. We develop an exercise for PD including respiratory exercise and could improve respiretory dysfunction (
Since PD patients are admitted neurological clinic be-
cause of their motor signs and symptoms such as bradykinesia, tremor, or dystonia, we neurologists mainly pay attention to improve these motor syndrome. However, with advent of PD therapy improve, in some extent, motor syndrome, but nonmotor syndrome has increasingly known to be a crucial factor to improve patients’ and their care givers’ QOL [9,14,57,58]. Pathological examinations mainly by Braak et al. hypothesized that nonmotor syndrome might result from initial pathological changes in PD [