Numbness is the most common term used by patients with PD to describe unwanted somatic sensations. Other patients describe tingling, others burning, yet others itching or crawling. Some experience focal coldness as though the limb were going to sleep. The extent to which all these different descriptions reflect differing pathophysiology or semantics is uncertain. When asked what they think is the origin or depth of these types of sensations, most patients chose skin rather than muscle or bone. This class of symptoms will be referred to as parasthesias for the remainder of the chapter. These superficial parasthesias are common in the more parkinsonian arm or leg as compared with the contralateral side. They can last for hours at a time or can be continuous.
Another dysesthesia, fairly specific to PD, is the unpleasant restless sensation in muscle or skin that impels the patient to contract the muscle. The sensation mimics in character the experience of patients with restless legs syndrome, though the heredity, age of onset, and associated features are not identical.1 When patients develop restless sensations in the years after PD onset and treatment with dopaminergic drugs, then the symptom usually occurs as an end of dose or off-state phenomenon.
Internal tremors, the subjective experience of rhythmic truncal vibrations in the absence of visible tremor, occur in PD patients only some of whom also have visible limb tremors.2 Internal tremors appear to be distinct from palpitations, and while anxiety is common in these patients, the symptom is not likely a somatic manifestation of anxiety; anxious people who do not have PD do not describe it in terms of a tremor inside the trunk.
Occasionally, a patient will describe a brief shooting sensation, usually from the spine into an extremity. While these dysesthesias are not unique to PD, PD patients may be predisposed. In one case report, there was lancinating facial pain of trigeminal neuralgia, which was secondary to PD as indicated by its response to levodopa.3
Muscle aches, sometimes described as fatigue or heaviness, are not unusual. In some cases, the experience reaches a threshold for pain (although, in my clinic, when a patient with PD complains of an ache that I later call a pain, quite commonly I am pulled up: "It's not a pain, it's an ache."). Discomfort that sounds rheumatologic in nature was described in PD by Parkinson and by Charcot. Lumbar, cervical, and shoulder aches seem to be more common in people with PD than in others. Perhaps the chronic rigidity and paucity of spontaneous movements precipitate or worsen arthropathies.
Sensory symptoms generally follow, within a few years, the onset of motor impairment, although in about 20% of patients, dysesthesias come first.4 The various sensory complaints described above are often fairly mild in severity. Motor and cognitive symptoms are usually of greater concern to the patient. However the shooting pains, the restlessness, and (less frequently) the heaviness and the parasthesias are very distressing to a significant minority of patients.5
Surveys of PD patients regarding dysesthesias find that roughly half of patients are affected. Snider et al. surveyed 101 consecutive patients in their clinic who had PD and who lacked an identifiable predisposition to neuropathy. Forty-three reported sensory complaints, compared with 8% of controls.4 Koller surveyed 50 consecutive patients with PD and found that 9 had intermittent sensory complaints, and in 10 such symptoms were continuous. The most common dysesthesia in this cohort was parasthesia.6 Shulman et al. asked 99 patients who had had PD for, on average, seven years and who were, for the most part, taking levodopa, "Do you notice any of the following sensations (pain, numbness, tingling or burning) related to your PD?" Sixty-three percent responded in the affirmative.7 Gunal et al. surveyed 85 sequential PD patients, 72 of whom had motor fluctuations. Fifty-nine had sensory complaints, and, for many, these were parasthesias occurring specifically during the off period.8
Recognizing that dysesthesias can appear as one of a number of nonmotor fluctuations, a number of studies have addressed the prevalence of sensory symptoms specifically during the off state. Witjas et al. asked 50 patients with motor fluctuations a series of 54 yes/no questions about various sensory, autonomic, and neurop-sychiatric symptoms occurring at specific stages of the dose cycle.5 About 40% of the subjects described tightness or parasthesias, while others described sensations that the authors listed as autonomic phenomena (feeling warm all over, feeling cold distally, feeling hungry). Five patients felt the off-state parasthesias or pains were more disabling than the motor component of the off state. However, less directed surveys provide lower estimates of prevalence and severity. Hillen et al. asked patients to volunteer those symptoms they associated with the "off" state. Of 130 consecutive patients with PD and motor fluctuations, only 3 described dysesthesias.3
Surveys about restlessness (or akathisia, used synonymously with restlessness by some authors) in PD produce a wide range of prevalence estimates, the variability probably due to the wording of the survey questions. The low estimates are 15 to 20%,1,9 while other studies report prevalence of 45 to 54%.5,10 Sixty-eight of 100 patients interviewed by Lang et al. described the frequent need to move, which was felt to be secondary to an uncomfortable sensation in most cases, though in a minority it was proactive (i.e., akathisia) rather than reactive.11
The surveys referenced in these past few paragraphs were performed at tertiary referral centers. None of the population studies of PD has systematically quantified the burden of sensory complaints.
It is easy to explain radiculopathies and musculoskeletal pains as secondary to motor disruption without invoking direct parkinsonian involvement of the sensory system. The pathophysiology of parasthesias and restlessness in PD on the other hand is unknown. Clinical risk factors such as early age of PD onset and long duration of treatment and higher doses of levodopa8 provide ambiguous clues at best. Despite the high prevalence of parasthesias, clinical exam signs and objective findings are uncommon. Deep tendon reflexes are usually intact. Exam of touch, vibration, temperature, and other sensory modalities typically do not uncover abnormalities. While challenging tests of proprioception and kinesthesia can reveal deficits as described later in the chapter, joint position sensation is generally intact as determined by bedside testing. There was a report of mildly impaired two-point discrimination in PD,12 but this finding has not been replicated.
Nerve conduction studies are generally normal in uncomplicated PD even in the presence of parasthesias.6 A single study reported electrophysiologic evidence of radiculopathies in 53% (cervical) and 73% (lumbar) of 26 patients with PD.13 Electrophysiologic abnormalities can be found in approximately one-third of cases of juvenile and young-onset PD,14 although it is suspected that this subpopulation differs from the general population of PD patients in the mix of etiologies and pathologies, including some which involve the peripheral in addition to the central nervous system.
Somatosensory evoked responses up to and including the parietal N20-P25 are generally normal in idiopathic PD15-17. Some but not all studies reported the frontal peaks N30-P45 are low in amplitude and can be boosted with dopaminergic medication.1819 Central aspects of the somatosensory evoked potentials can be delayed.20
While systematic histologic study of the sensory system in PD has not been undertaken as far as I am aware, the preceding observations imply integrity in the peripheral nerves and the primary somatosensory pathways extending from the spine to the thalamus and the primary sensory cortex. Logically, then, dysesthesias in PD are the result of either a central sensory distortion or the activation of sensory nerves secondary to motor or autonomic dysfunction. As outlined below, central mechanism seems plausible, although this has not been established, nor has peripheral activation of nerves been excluded.
We know that stimulation of the skin produces responses in the basal ganglia21 and that the substantia nigra modulates sensory processing in thalamic nuclei.22 It is reasonable to suspect that disruption of this extrapyramidal circuitry in PD will sometimes produce parasthe-sias and other sensory complaints.
Levodopa can relieve parasthesias in PD, and the fact that large neutral amino acids can interfere with the relief suggests that this is not a local action of dopamine at the extremity.23 However, it is likely that more than simple dopamine deficiency is responsible; dopamine antagonists can produce uncomfortable sensations or a restless need to move but at a lower frequency than seen in PD, and chronic superficial parasthesias are not reported to occur widely in patients using neuroleptics.
Notwithstanding the tentative assumption that the parasthesias of PD are for the most part central in origin, some parkinsonian patients with dysesthesias have identifiable peripheral sources. Focal compression neuropathies and plexopathies can occur in patients frozen in abnormal positions for extended periods.24 Iatrogenic neuropathy has been described as a result of amantadine toxicity.25 There are uncommon neurodegenerations affecting the peripheral nervous system in combination with the extrapyramidal system. Some of these are genetic.26 27 Parkinsonism developing at a young age probably has a different mix of genetic and biochemical etiologies as compared with PD arising later in life and, as noted in the previous section, extension of neuropathology into the peripheral nervous system seems more common. Polyglu-cosan body disease can affect both systems.28 Some toxins29-31 and Guamanian neurodegeneration,32 which may be toxic, can cause neuropathy in combination with parkinsonism. Finally, sensory complaints are sometimes independent of the PD. Absent data to the contrary, it is assumed that PD patients have sensory and sensorimotor neuropathies to the same extent as age-matched non-PD controls. Thus, if symmetric sensory complaints and signs such as hyporeflexia and loss of vibration sensation are found in PD, they likely reflect a coincidental and independent neuropathy rather than a PD complication.
There is no randomized controlled trial of treatment of sensory complaints in PD. That said, when patients with PD desire relief from dysesthesias, empiric treatment with dopaminergic drugs is generally practical and often rewarding. I usually adjust times and doses of dopaminergic drugs as a first step in addressing sensory complaints in PD. If the symptom tends to be better when drug levels tend to be higher, then no further investigation is needed for either cause or solution. Rarely, parasthesias, particularly burning sensations, are worsened by dopaminergic drugs.4 There is little data on the relative efficacy of dopamine agonists as compared with levodopa for treating sensory symptoms, and each can be tried initially at low dose and then slowly increased as needed and tolerated. Post hoc analysis of the CALM-PD data revealed that, while those randomized to levodopa had more improvement in a number of motor and ADL items of the UPDRS, there was a trend toward better improvement of sensory item in the pramipexole arm.33 As regards the time course of symptom relief, parasthesias and restlessness can improve as soon as a therapeutic dose of the dopaminergic drug is reached. By contrast, rheumatologic aches secondary to prolonged excessive rigidity and immobility often do not resolve for many weeks after hypertonicity is pharmacologically reduced. Musculoskeletal complaints can also be helped by physical therapies, including passive and active exercises, massage, and ultrasound.
Deep brain stimulation of the globus pallidus tends to improve sensory complaints; half of the 16 patients operated on by Loher et al. had dysesthesias, and in each case the dysesthesia essentially disappeared postoperatively.34 The effect on sensory symptoms of subthalamic stimulation, now a more common intervention for PD, has not been systematically studied. High-frequency thalamic stimulation, sometimes used to alleviate parkinsonian tremor, in many patients will cause parasthesias at high settings. This iatrogenic sensory symptom is easily and instantly cured by reducing the stimulation. Alternatively, the stimulation can be delivered via adjacent lead contacts to reduce the field. In this way, side effects can be restricted without sacrificing tremor control. Parenthetically, thalamic (ventrocaudal) stimulation was found not to worsen somatosensory acuity.35
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