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I. EXTERNAL MOVEMENT PROBLEMS
2. Poverty Of Motion
1. Persistent Tension
2. Blank Expression
3. Stooped Posture
C. SELECTIVE WEAKNESS
1. Swallowing Weakness
2. Limb Weakness
1. Resting Tremor
2. Intention Tremor
3. Action Tremor
4. Dyskinetic Tremor
1. PEAK-DOSE EFFECTS
b. Drug-Induced Tremor
2. END-OF-DOSE EFFECTS
c. Dystonia (Cramp)
a. Chronic Fatigue
b. Quick Exhaustion
1. Toe Dragging
3. Shortened Stride
4. Bilateral Ability
5. Fine Guidance
I. EYE CONTROL
J. SPEECH PROBLEMS
K. FRIGHT REFLEXES
1. Blink Reflex
2. Startle Reflex
II. INTERNAL REGULATION PROBLEMS
B. SEXUAL DYSFUNCTION
1. Abnormal Libido
C. MENSTRUAL EFFECTS
D. URINARY DYSFUNCTION
3. Color In Urine
2. Runny Nose
6. Skin Cysts
F. LOW BLOOD PRESSURE
H. THERMAL CONTROL
III. SENSORY DYSFUNCTION
A. VISION EFFECTS
1. Color Perception
2. Contrast Perception
B. TEMPERATURE SENSATION
C. MECHANICAL SENSATION
D. SMELL AND TASTE
IV. MENTAL SYMPTOMS
A. ATTENTION DEFICIT
1. Short-Term Memory
2. Habit And Rote Learning
3. Pattern Recognition
C. SLEEP DISTURBANCE
2. Vivid Dreams
1. Clinical Depression
2. Mood Swings
I. EXTERNAL MOVEMENT PROBLEMS Return
BRADYKINESIA Return-Greek for "slow movement": In PD, it's not a mere habit that can be overcome by attention, but true inability to move at normal speed. Research has found, it's not due to caution or timidity in the PWP, but a basic deficit in control. Curiously, visual guidance cues do play a part, and sometimes when they are present, bradykinesia momentarily vanishes. It doesn't, however, respond well to the usual PD therapy.
Slowness: Bradykinesia is one of the "classic triad" of prominent motor symptoms in PD. As a rule of thumb, two out of the three justifies a hasty (but tentative) diagnosis of PD. A remarkable feature of the brain is its adaptability in case of trouble. When a normal pathway for neural signals is impaired, the brain automatically seeks out or creates an alternate, or "detour" pathway. This "detour" is likely to be longer, and therefore slower, than the primary path. Any therapy which tends to restore the primary path function will probably reduce the bradykinesia.
Poverty Of Motion: By this is meant the loss of normal animation that continually changes position of body, limbs, or facial expression, conscious or otherwise. The patient may be perfectly attentive and alert, but tends to sit motionless until some purposeful movement is intended. A most common feature is failure or inability to swing the arms when walking. Trying to hide that by conscious effort fails, because the opposing motion is hard to learn.
RIGIDITY Return: Generally results when muscles cannot attain their normal relaxed state. Muscles only pull, not push, and the arrangement for skeletal motion usually involves two or more in opposition. When both directions are tensed, a fixed resistance develops. When only one direction is affected, the result will be something like curled toes, clawed hand, or flexed elbow. Disabling, drug-resistant rigidity and/or dyskinesia may as a last resort be treated by surgery, where a few cubic mm deep in the brain are either destroyed, or stimulated by an implanted electrode. The site of choice is not the substantia nigra, where failure of dopamine production is thought to cause PD, but a part of the globus pallidus, where imbalance of signal feedback is a more immediate cause of PD symptoms.
Persistent Tension: In extreme cases, the patient may become "stiff as a board" and unable to move. More commonly, one or more skeletal muscles remain tensed, due to failure of the "feedback" signal to relax. The biceps muscle, for example, may feel firm to the touch, while the triceps feels loose and floppy. The neurologist will extend or flex the patient's elbow to look for "cogwheel" rigidity, which is the product of muscle tension with a superimposed tremor.
Blank Expression: PWP are noted for blank facial expression and fixed stare. Expression of emotion such as pleasure or anger may require conscious attention.
Stooped Posture: Many illustrations show the PWP leaning forward with stooped shoulders and bent knees. I suspect this is a habit arising from imbalance of calf muscle strength that causes more weight to be borne on the toes. Frequent conscious reminders to straighten knees, force head and shoulders back, may be helpful.
SELECTIVE WEAKNESS Return: The PWP will notice as the disease progresses that habitual acts requiring some strength, such as climbing a stair, opening a jar, etc. become difficult. This is due not to loss of muscle itself but to a deficit in its control system, and is little affected by therapy. Doctors always advise more exercise, to maintain strength as long as possiblle. Semi-autonomous functions such as breathing are affected as well as voluntary ones, and a common cause of mortality that follows late-stage PD is either suffocation or pneumonia from inhaled food or liquid.
Swallowing Weakness: The swallowing act requires coordination of several muscles that are partly under reflex (autonomous) control. PWP must be more careful than others to avoid trying to swallow while talking, and to pause between mouthfuls, despite inability to eat as fast as table companions. Late-stage PWP may lose ability to swallow altogether.
Limb Weakness: The arm, wrist, hand, or leg opposite to the side with most pronounced tremor may become weaker, making it harder, for example, to open twist-tops.
TREMOR Return: A rhythmic reciprocating motion which may or may not be noticed, or voluntarily suppressed, by the PWP. All tremors result from failure of the feedback loop, that is, imbalance or mis-timing between a signal that tells a muscle to act and the corresponding signal that tells it when to stop. In engineering terms, the system oscillates. Some PWP report internal tremors in various parts of the body. Tremor is one of the 3 cardinal symptoms of PD, evidently arising from a defect in supply or employment of dopamine. It often abates or disappears under therapy, either medicinal or surgical. Tremor of a different kind also appears in dyskinesia, to be discussed later, resulting from an excess of dopamine. When disabling tremor is of primary concern and does not respond to drug therapy, surgery is a last resort. Since tremor seems to originate in the thalamus, or more precisely the subthalamic nucleus, that is the site of choice for the electrode, either for ablation (destruction) or for chronic deep-brain stimulation.
Resting Tremor: Of the 3 named kinds, resting tremor was once considered exclusive to PD. It appears most often as a 5-7 hz torsional vibration of a hand when hanging loosely, or of a foot when relaxed, and is easily suppressed when it is noticed by the patient. The tremor of dyskinesia, discussed elsewhere, is not subject to such voluntary control. Resting tremor usually appears as the current dose of levodopa or other medicine wears off, and disappears as the new dose takes effect.
Intention Tremor: This is the tremor of muscle under load, as when holding a parcel or when the neurologist tells you to "make a fist". It once was thought to distinguish PD from the less-well-understood Essential Tremor, because it is suppressed (briefly) by alcohol or the antitremor drugs primidone and propranolol, while resting tremor is not.
Action Tremor: This is the tremor that occurs during movement, as when drawing or writing. A common and easy test of tremor prominence at a given moment is to draw, with either hand, a circular closely-spaced spiral. Tremor prominence is affected by stress, fatigue, or the status of medication.
Dyskinesic Tremor: This kind of tremor may be forcible, and is akin to other involuntary motion caused by too much free dopamine following immediately after a medication dose. Likewise, it is unaffected by alcohol, but susbsides as the medication wears off.
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FLUCTUATIONS Return: Motor fluctuations are drastic, sometimes sudden, changes in mobility, rigidity, tremor, energy, and symptoms such as dyskinesia. They are all related to the level or the availability in the brain of dopamine, one of numerous so-called neurotransmitter chemicals that are made and used by nerve cells to transmit signals between themselves. Dopamine is the dominant neurotransmitter whose deficiency results in PD, and all drugs for PD are designed to increase either the supply or the efficient use of dopamine. In the simplest terms, insufficient dopamine leads to the immobilizing symptoms of PD, and an excess leads to unwanted, involuntary movement. In a healthy system, the level of dopamine is regulated by several elegant mechanisms. When dopamine is deficient, as in PD, the problem of drug medication is to keep between the bounds of too much or too little.
PEAK-DOSE EFFECTS Return: A few decades ago, dopamine and another neurotransmitter, acetylcholine, were thought normally to be in a kind of balance, where dopamine enabled movement and acetylcholine inhibited it. Since dopamine cannot pass from the blood into the brain directly, therapists tried to restore balance the other way, by limiting acetylcholine via so-called anticholinergic drugs. Anticholinergics are still used, but since the discovery that levodopa can enter the brain and then convert to dopamine, not so popular anymore. The main problem with dopamine and levodopa is that they both dissipate, or convert to non-useful forms, rather quickly. I think of the dopamine supply in the brain as having two parts: A long-term "baseline" level which in PD declines gradually, until it is insufficient to prevent the motor symptoms, and a "therapeutic" amount added by any of several means, that declines according to an exponential law. The latter is just a mathematical way of stating that the rate of decline is proportional to the level at any moment. So the time to sink from 100% to 50% is the same as from 50% to 25%, and so on. This "half-life" for the therapeutic dopamine is only from a half-hour to an hour or so. Therefore, maintaining the desired level between an upper limit, where dyskinesia appears, and the lower limit, where symptoms of under-medicated PD appear, requires frequent dosage in small amounts, just enough to raise the total level from the lower limit to the upper one. Those limits are unchanged by progress of the disease, but as the "baseline" level diminishes, an increasing proportion of "supplemental" medication is needed. Since the "supplemental" portion, in my theory, declines faster when it is greater, it must be taken at ever shorter intervals to keep the total available dopamine level within the desired range. PWP cope with this problem by dividing the daily medication into small doses taken every 4, 3, or even 2 hours. At some point it becomes more convenient to mix the Sinemet with a liquid such as orange juice, that can be sipped continually as needed. Beyond that, it is possible to implant a tube through the abdominal wall into the stomach, with a timed electric pump to ensure continual infusion. Much work is done at present to develop agonist drugs that prolong the half-life of dopamine, or a skin patch that avoids the peaks and valleys of intermittent supply.
Dyskinesia: Greek for "false motion" which appears when the most recent dose of levodopa begins to take effect, and the resulting concentration of dopamine is at a maximum. It usually is an involuntary writhing motion of the arms, head, neck and shoulders, and gradually subsides as the medication wears off. Not necessarily disabling, it must still be disconcerting to the patient and to onlookers. Dyskinesia may be caused by a dopamine agonist alone, but the general term is still "levodopa-induced dyskinesia". In theory, dyskinesia and inherent PD symptoms such as dystonia don't occur together.
Drug-Induced Tremor: This is another form of dyskinesia, quite different from the gentle tremor of untreated PD. The dyskinetic tremor may be quite forcible pounding of a hand or foot, possibly hard enough to be injurious.
END-OF-DOSE EFFECTS Return: Dopamine that appears in the brain as a product of levodopa medication somehow substitutes for the dopamine emitted by individual nerve cells as they pass their signals along. But free dopamine quickly breaks down to other compounds, so it needs continual replenishment. Before the discovery of levodopa therapy, PD patients generally became completely catatonic and helpless, even while wide awake. As the therapeutic dopamine declines, the patient approaches that state. Needless to say, the clearest indication of an end-of- dose effect is that it vanishes quickly after the next dose.
Wearing-Off: The popular term for signs telling the PWP or caregiver that time for another dose is approaching. Besides a general loss of "ambition" or energy, the resting tremor reappears, and (usually in bed) painful muscle cramps announce that the autonomous feedback control is gone.
On-Off: In more advanced PD, a troubling feature of levodopa medication it that its effect doesn't wear off slowly, but disappears suddenly and unpredictably, seeming to some PWP like switching off a lamp. Those patients develop a clear sense of "off" and "on" periods, which is used in clinical research to evaluate various forms of therapy.
Dystonia (Cramp): When a muscle gets an unlimited signal to contract, not balanced by a corresponding signal to stop or relax, it may become very painful. People without PD may develop a "charley horse" in a leg muscle whose control has been degraded by unaccustomed exertion, or disabling low back pain caused by a "pinched nerve". In PD, one or more such cramps may appear without warning anywhere, regardless of any recent strain or abuse. Massage is ineffective, since the muscle is getting an improper or unbalanced signal from the brain. Dystonia of PD responds quickly (within minutes) to levodopa medication, and there is a clinically recognized condition of levodopa-responsive dystonia in the absence of PD.
Lethargy: An insidious feature of wearing-off, especially if a schedule for medication at night is not strictly followed. It may be tempting at those times to go back to sleep, ignoring the future penalty for skipping or delaying a dose. During daytime, however, many PWP find an afternoon nap to be pleasant and beneficial.
STRESS Return: I haven't heard of professional agreement, but I believe that the need for dopamine replenishment increases with any kind of stress or strenuous activity, either physical or mental. Certainly, PWP find that motor symptoms become more pronounced during periods of stress, such as an argument or in preparation for any kind of trial. I think PWP are subject to a special sort of fatigue, that responds to dopamine.
Chronic Fatigue: PWP often complain of constant tiredness or lack of energy, even in the morning after a restful night. "Chronic Fatigue Syndrome" is a recognized clinical condition, but I think it is unrelated to PD because it affects others as well. Ordinary fatigue or exhaustion follows prolonged strenuous exertion, such as an athletic contest or a difficult mountain climb, as muscles are depleted of chemicals that enable them to function, for example blood sugars and oxygen. Ordinary fatigue abates upon prolonged rest, which permits weary muscles to recover their normal chemical state.
Quick Exhaustion: What some PWP call "Chronic Fatigue", I prefer to call "Quick Exhaustion". It is not due to running out of blood sugar or oxygen, but mimics the real thing with labored breath and rapid pulse, even in moderate exertion such as climbing a flight of stairs, or doing a tedious manual task. Ignoring this kind of fatigue may trigger pain in an unrelated area, such as the upper back. Its sudden onset and equally quick recovery, after a brief rest or an extra dose of levodopa, shows the connection with PD. In a treadmill test, the technician may notice the unusually quick "cooling off" of pulse and breathing rates.
BALANCE Return: Balance in a normal individual is maintained by many sources: There is the system of the inner ear to detect acceleration and angular position, complex visual cues to sense rotary or linear speed, direction, and position, and there is the internal sense of how weight is distributed between different parts of the feet. Ordinary acts of standing erect or walking involve autonomous coordination of many different muscles, which is lost in PD. The brain's marvelous ability to compensate preserves some aspects of balance, and the PWP's unconscious development of new habits also helps.
Posture: The PWP's typical standing posture is easily recognizable. Without doubt it arises from the unaccustomed weakness or tension of certain muscles, and impairment of the many continual reflexes needed to keep standing. In a simple test, the neurologist gives the PWP a gentle push backward, which produces a distinctive reaction.
Falling: Falls are frequent in PD, sometimes anticipated and sometimes not. The PWP feels and is much more vulnerable when the footing is unfamiliar or uncertain, for example an icy pavement. As the disease progresses, the patient usually begins to depend on a cane or staff to help keep his balance; later on turns to use of a walker, and still later a wheelchair.
GAIT Return: The various forms of the PD gait are also easy to recognize. Failure to swing arms has already been mentioned, but action of the legs and feet also is quite different from normal. Poor balance is partly to blame, and PWP have trouble with the common sobriety test of heel-to-toe walking along a line, and compensate by exaggerating the lateral component of each step. Another compensation is that PWP replace lost autonomous reflexes by habitual attention to each step.
Toe Dragging: This annoying gait impairment results in continual stumbling over small obstacles such as doorsills or doormats. The ankle flexor muscle (front of the calf) gets weaker than the extensor (back of the calf). To compensate, one may put more weight on the ball (toe) of each foot.
Shuffling: Instead of stepping normally from toe of one foot to the heel of the other, PWP neglect to transfer weight from heel to toe, walking mainly on their heels.
Shortened Stride: Seems to be caused mainly by too much weight on heels. Conscious kicking each foot forward in a reduced version of the "goose step" helps to increase stride length, but still not to the normal distance.
Festination: The peculiar phenomenon of very short rapid steps while leaning forward, due to combined impairment of lower leg action and balance. Walking faster and faster, the PWP will fall unless he reaches support.
Freezing: The PWP cannot start, or suddenly stops, often at a partial obstruction such as a narrow doorway, as though one or both feet were glued to the floor. Hard for others to understand, but the subject is unable to move, and the incidence is very common among PWP. A visual cue such as a pattern on the floor, or an object to step over, "unfreezes" the walking, for reasons that are equally hard to understand. One PWP has invented a visual aid that seems miraculous; a small brightly colored wand extending at a right angle from the lower end of a cane provides something to step over, and eliminates the freezing. The most common form of subliminal compensation for loss of internal guidance is a growing habitual dependence on external stimuli.
COORDINATION Return: The PWP tends to lose coordination of voluntary movement such as speech, swallowing, or tasks done with the hands. The loss affects accuracy, speed, and doing more than one thing at a time.
Mis-position: Another routine neurologist's test is to have the PWP, with eyes closed and arms extended, touch the tips of forefingers together. The miss distance depends on status of medication dosage as well as progress of the disease.
Mis-direction: The PWP, with eyes open, is asked to touch alternately the tip of his nose and the neurologist's index fingertip, as fast as he can. Accuracy is usually poor, and worse with one eye closed. In everyday living activity, the common kitchen task of breaking an egg with a fork (hit the center, not too weak or too strong) becomes a challenge.
Slowness: In laboratory tests, researchers have found that the slowness of coordinated movement, such as tapping, is not due entirely to hesitation or caution to improve aim, but largely to a genuine deficit in the speed that is commanded by the brain. In a recent trial curiously, the speed to reach and grasp a stationary object was impaired, but when the object was moving, PWP responded much faster than they thought possible.
Bilateral Ability: Psychology researchers have used many ingenious mechanical tests to explore the effect of PD on coordination. For example, in turning a crank with each hand at a preset speed, PWP were about normal. But when the required motions were out of phase, or otherwise different, PWP did much worse than normal control subjects.
Fine Guidance: PWP are familiar with decreased dexterity in fine tasks, such as threading a needle or adjusting a watch. The loss is probably due as much to visual defects as to mechanical control. More trouble comes from apparent loss of touch sensitivity in the fingertips, like that experienced when working in cold weather.
EYE CONTROL Return: PWP often of difficulty or loss of interest in reading, which they blame on inability to concentrate. The true cause may be in muscles that control eye direction, so that the PWP literally "can't see straight".
Jitter: The PD tremor that appears near the time for the next medication dose, or when you are tired, extends also to muscles that direct the eyes. PWP may notice that visual objects, such as printed words, are doing a little dance, that makes reading difficult, especially if the type is small or the lighting dim.
Convergence: For both eyes to be aimed at the same point in an object, their position must vary slightly as the object distance changes. This feature is what permits autonomous judgement of distance by humans and other animals (mostly predators) with eyes at the front, rather than sides, of the head. But it also helps greatly in interpretation of detail, to have two similar images that can be merged in the brain. In PD, the control that keeps both eyes focused on a close object such as a printed page is impaired, and the eyes tend to drift into the "distance" position, resulting in a double image. The PWP notices, sometimes every few seconds, that he is using only one eye, and needs to make a conscious effort to pull the images together.
SPEECH PROBLEMS Return: Listeners have trouble understanding PWP because they may speak in a low, slurred monotone, made worse by occasional stuttering.
Voice: PWP often need a microphone to be heard, even in a small group, and especially in a noisy place. Training and exercise, such as singing, can help. I have heard of a specialized course called Lee Silverman Voice Training, which is highly recommended. One cause of voice weakness may be failure of the vocal cords in the pharynx to close completely during vocalization. This condition has been treated by injection of collagen into the vocal cords to strengthen them.
Slurring: The slurring comes from poor coordination of lips, cheeks and tongue when enunciating certain consonant combinations, as in "rural railroads", etc. For uncertain reasons, some PWP tend to speak very rapidly, adding to the difficulty.
Stuttering: Researchers differentiate between loss of verbal fluency, which probably originates in the mental process of speech, and of phonemic fluency, more likely due to poor control of speech muscles. Researchers find that the latter type predominates in PWP.
FRIGHT REFLEXES Return: PWP seem generally to be more "jumpy" than others, whether from a constant personality trait, stress associated with the disease, medicines, or from a basic change in neural circuitry.
Blink Reflex: In this interesting phenomenon, first described by the philosopher Descartes, everyone blinks involuntarily when an object, apparent or real, seems to be rapidly approaching the face. Researchers find that in PD, the blink reflex is hyperactive.
Startle Reflex: Just as normal people jump visibly on hearing a loud unexpected noise, PWP seem to be more sensitive, and may jump even when the noise is a familiar one, such as a telephone ring. The jump is similar to one of internal origin, called myoclonus.
II. INTERNAL REGULATION PROBLEMS Return
CONSTIPATION Return: Seldom discussed but often experienced in PD, constipation can be very troublesome. Doctors may blandly dismiss the complaint with advice to eat more bulk and fibrous foods, drink more water, exercise more, and so forth. But the problem arises from weakening or paralysis in PD of the colon (lower or large intestine). Dopamine figures in neural control elsewhere than in the brain, and the autonomous control of muscles in the intestines seems to be impaired by PD. Neglected constipation may result in a hard impacted mass called megacolon, that becomes a surgical emergency. Even when controlled, the transit time of food waste through the colon may be increased in PD from a few hours to a day or more. I think for most PWP the alternative is a chemical laxative every few days, plus a precautionary stool softener. My doctor advises that the least harmful chemical is bisacodyl (Dulcolax or other tradenames) which stimulates nerve action in the colon. A suitable stool softener is docusate (various tradenames), which inhibits the colon's normal function of water extraction.
SEXUAL DYSFUNCTION Return: PWP have various kinds of sexual dysfunction, but it is difficult to separate the effects of the disease from those of drug medication, indirect reflection of mental state, and normal aging. Men can experience painful dystonia in muscle surrounding the prostate gland, which may or may not be related to PD.
Abnormal Libido: Sexual desire, pleasure, or energy may be either weakened by PD or enhanced by drugs taken for PD. A small controlled study showed that women with PD experienced and enjoyed sex less than the normal controls. In anecdotal reports, a few men getting apomorphine for PD had psychotic increase of libido, leading to psychological dependence and need for restraint.
Impotence: I have heard remarks about this effect, but have no specific data.
MENSTRUAL EFFECTS Return: Motor symptoms and fluctuations are much worsened during the peak of the ovulation cycle. In one report, acetazolamide (Diamox) dramatically relieved the effect.
URINARY DYSFUNCTION Return: Normal discharge of urine requires coordination of muscles at several points along the urinary tract. Both incontinence and retention (at different times) may occur, I believe more often in men. An urologist unaware of a male patient's PD may diagnose a common obstruction due to precancerous growth in the prostate gland, and strongly urge a popular surgery called Trans-Urethral Resection of Prostate (TURP), which not only fails to remedy the problem if due to PD, but needlessly destroys the sexual function of the prostate.
Incontinence: As the effect of PD medication declines after each dose, the PWP may have an uncontrollable urge to urinate. Urination therefore tends to synchronize with the medication schedule.
Retention: Due to lost coordination of various muscles under autonomous control, intentional voiding just prior to the scheduled dose of PD medication may be incomplete. Levodopa in particular seems to have some effect within a minute or less, and immediately after a dose the need to urinate returns.
Color In Urine: Some PD drugs, including Sinemet, may as a harmless side effect cause deeper color in urine.
EXUDATIONS Return: Among the more annoying symptoms of autonomous system failure in PD are changes in the body's normal secretions of the skin and elsewhere. Drooling, runny nose, excessive or abnormally dark perspiration, oily skin, sebaceous cysts, and eyelid irritation are all well known in PD.
Drooling: This is simply excess salivation, which may occur either when awake or asleep. It is more noticable when the patient with reduced autonomous function forgets to swallow.
Runny Nose: At times the subject's nose may suddenly "drip like a faucet" a clear watery discharge, with no sign of a cold or allergic insult, and just as suddenly stop. I think it might be a peak-dose effect of levodopa.
Sweating: This sometimes frightening effect has been noted in scientific literature as due specifically to levodopa therapy which has reached the fluctuation stage. It occurs within a narrow range of plasma dopamine level, and is said to be abolished by addition of a dopamine agonist to therapy. Unusual dark-colored perspiration has also been blamed on levodopa. A possibly interesting sidelight is that the Sinemet formulation of levodopa in tap water, which usually contains chlorine as a disinfectant, will leave a black evaporation residue, but not in distilled water.
Seborrhea: Excessive oiliness of the scalp, face, and neck is common enough to be mentioned in patient handbooks, although the recommended remedy of an astringent shampoo offers only short-lived relief.
Dandruff: Usually a harmless byproduct of oily scalp, in people with or without PD. You probably can forget the usual anti-dandruff preparations, and concentrate on the oiliness. I use Boraxo, a powdered hand soap, instead of shampoo.
Skin Cysts: The sebaceous glands become clogged by overactivity, and develop pores containing waxy matter that may be gently squeezed out. When the outlet is clogged, a solid benign cyst may form, that may require surgical removal to avoid possible infection or further growth. More often such cysts on the hairless part of the scalp are tiny and can be removed by liquid nitrogen.
Blepharitis: When related to seborrhea, called "seborrheic blepharitis" (irritation of eyelids). With no pain or sign of infection, eyelids are continually red and swollen, often accompanied by copious tears and/or solid deposit that interferes with vision unless frequently removed. Books (and doctors who read them) advise "no tears" baby shampoo, but plsin water will do just as well. Note, this condition is just the opposite of the "dry eye" complaint that results from inadequate blinking by PD patients.
LOW BLOOD PRESSURE Return: Low blood pressure has been cited in scientific literature as a symptom of PD, and I have heard it mentioned often by other PWP. In related diseases such as multiple system atrophy (MSA), orthostatic hypotension (failure to compensate upon arising from seated or supine position) is an important diagnostic sign.
PROLACTINEMIA Return: The bean-size pituitary gland, situated at the base of the brain and connected by a stalk of neurons to the hypothalamus, secretes several important hormones including prolactin, which stimulates lactation in nursing mothers but also is present to a degree in men. Prolactin is inhibited in a feedback loop by dopamine, so one might expect an elevated prolactin level to accompany the dopamine shortage of PD. The accepted treatment for prolactinemia is a dopamine agonist such as bromocriptine (Parlodel). An increased level may also be due to a pituitary tumor, therefore an MRI scan to rule out that possibility may be a good idea.
THERMAL CONTROL Return: PD affects the perception of ambient temperature, causing the subject to feel colder or warmer than warranted by actual conditions, but not the internal body temperature. However at times one hand or foot may be colder or warmer than the other.
NAUSEA Return: I don't know of nausea caused directly by PD, but it is a common side effect of numerous PD medications. Levodopa in particular causes nausea, that may be avoided by addition of carbidopa. The combination is named Sinemet, after the Latin "sine emesis", for "no vomiting".
III. SENSORY DYSFUNCTION Return
SENSORY DYSFUNCTION: Although the effects may be overshadowed by the more urgent motor symptoms of PD, Virtually all the senses are impaired. Sensory impairment is very common, if not universal, among PWP but tends to be ignored, not only by attending neurologists but also in research projects. Its importance lies in the evidence that PD definitely affects parts of the brain other than the basal ganglia.
VISION EFFECTS Return: Aside from the motor effects already discussed above, PD affects the optical function of the eyes, sometimes long before appearance of the skeletal movement symptoms.
Color Perception: There are several known kinds of color blindness, distinguishable by ingenious neuropsychological tests. In PD the sensitivity to color is only partly lost, but it appears early enough for use as a preclinical indicator.
Contrast Perception: In tests involving a grid with two different shades of alternating gray bars, PWP definitely are less sensitive to contrast. This loss may affect driving ability, where poorly maintained lane-marking stripes or other visual aids may require a bigger share of the driver's attention.
TEMPERATURE SENSATION Return: PWP may feel colder or warmer than called for by actual temperature of surroundings. The effect seems to be more pronounced as the levodopa dosage interval draws to an end.
MECHANICAL SENSATION Return: Numerous common manual tasks that may need a fine sense of touch in the fingertips, reliable control of applied force, or kinesthetic sense of position (as in sewing on a button) are harder for PWP.
SMELL AND TASTE Return: These closely related senses are very commonly impaired in PD. Insensitivity to smell (anosmia) may be nearly complete, so that even strong odors, such as that of gasoline, are barely noticed. The PWP may also develop a preference for strong flavors in food.
TINNITUS Return: Neurologists claim there is no connection with PD, but I'm not sure. In my own case, tinnitus in the form of a loud, very high-pitched whistle has persisted 24 hours a day since about the time I was diagnosed with PD. Hearing sensitivity is about normal for my age, 76: high-frequency (in the range of the tinnitus) loss is pronounced.
IV. MENTAL SYMPTOMS Return
MENTAL SYMPTOMS: It is becoming clear that PD affects many parts of the brain other than centers of motor control. Specific aspects such as memory, sleep disturbance, hallucinations and psychoses have been thoroughly studied, but since PD is age- related, it's hard to know whether such symptoms are due to the disease or merely to normal aging deterioration.
ATTENTION DEFICIT Return: Many patients (and caregivers) report difficulty concentrating on a mental task. To be sure it's a cognitive effect, one must rule out such causes as reading and eye problems. Tests do confirm that PWP are less able than normal controls to handle multiple simultaneous tasks.
MEMORY Return: It was recently discovered that there are at least two distinct kinds of memory, which occupy different locations in the brain. That supports the idea that loss of one or another comes from localized degeneration that is typical of PD. Long-term memory of facts, such as dates, places, and events, seems to be spared in PD, but other kinds are not.
Short-Term Memory: In my own lexicon, there is a sort of scratch-pad memory, which we depend on after deciding to go to the next room for some article, or for avoiding some obstacle that appears in view while walking. PWP seem more likely than usual to forget the object of a very short errand, or to bump into something which they had seen was in the way.
Habit And Rote Learning: Everyone has to learn how to deal with stochastic situations without memorizing specific facts; for instance how to navigate on foot through a crowd, how to play a game of chance, habits of hygiene, and so forth. In a fascinating study, PWP were found deficient in ability to learn what amounted to new habits. Some PWP, and a group of people with confirmed amnesia, were given a short training course in a simple guessing game of chance, where the sequence of clues gave not the precise outcome but only a statistical hint. The amnesiacs forgot taking the training but did learn to play as well as normal subjects. The PWP recalled taking the training but they didn't learn from it how to play.
Pattern Recognition: Learning a set of numbers or other parameters is different from learning a pattern, such as a face. In one study, PWP were not only less able to assume specified emotional expressions, but also less able to recognize such expressions on the faces of others.
SLEEP DISTURBANCE Return
Interruption: Sleep of PWP may be interrupted in many ways. Some of the drugs commonly taken, such as Sinemet, cause insomnia because of their stimulating effect. Also, the dosage schedule may require waking up two or three times each night. Because of the brief "lift" from dopaminergic drugs, patients may report that they stay up for a half hour or so after a dose, to read or otherwise occupy themselves before returning to bed. If the dopaminergic regimen is frugal, the sleeper may be awakened by painful dystonia, usually in the leg or foot, as a reminder that the time for the next dose has arrived.
Vivid Dreams: Neither PD itself nor its drugs seem to interfere with the soundness of sleep, as shown by frequent reports of vivid dreams, often with a complex plot. The dreams may result from some psychological state, but I suspect that medication drugs are the root.
Violence: Researchers have collected many reports that PWP punch, kick, or shove their bed partners while in deep sleep. It may come from the medications, as do the dreams.
HALLUCINATIONS Return: These are a mild form of delusions, reminding that some PD drugs may cause genuine psychosis in certain patients. It is also noted that dementia of many forms may occur in advanced stages of PD, particularly in elderly patients who are more susceptible.
Visual: Visual hallucinations are a common side effect of some PD medications, and can be troublesome enough to force discontinuance of a drug. The effect seems to vary widely, with patients having different susceptibility to different drugs. Therefore the recourse is to try various drugs until one having similar therapeutic benefit is found to be tolerable.
Auditory: Not all hallucinations are visual; auditory hallucinations are often reported, but seldom by patients who don't also have visual hallucinations. At one time during the course of my own loss of smell sensitivity, I had olfactory hallucinations- unfamiliar odors that I could not identify and no one else could detect.
DEPRESSION Return: When a patient has PD, there is no guarantee of immunity from any other neurological dysfunction. Depression is very often diagnosed along with PD, and when found is considered to place the subject in a different category, for such purposes as a research program. I perceive two basic kinds of depression: so-called clinical depression, which is even more common in absence of PD, and the short-term mood swings that are exclusively related to PD.
Clinical Depression: This illness is beyond the scope of the present discussion, except to say that it is now treatable very effectively in many cases by drugs alone. Unfortunately for PWP who also suffer clinical depression, some of those drugs have serious, potentially fatal, interaction with certain drugs used to treat PD. Clinical depression may be distinguished from the mood swings of PD by its very long development time, and of course by its lack of response to drugs used for PD. Mood swings, in contrast, are brief and sudden, and response to the usual antidepressant drugs may be disappointing.
Mood Swings: The reason why cocaine, nicotine, and chocolate evoke psychological dependence is that they all contain elements that bind to dopamine receptors related to the sensation of pleasure. No surprise then, that dopamine itself has a similar effect. I'm not clear how the effect can be virtually instantaneous, since dopamine by mouth has to go a long way to enter the brain, but it's true. PWP in the fluctuation stage very often feel depressed as their levodopa dose nears exhaustion, and get a quick lift immediately on taking the next dose. This is so common that the onset of gloomy thoughts may serve as an indicator of the best dosage interval. It seems that many patients and doctors don't recognize the difference between this short-lived depression and true "clinical" depression, and therefore choose antidepressants such as Prozac or Zoloft, which may not be really needed. In contrast to clinical depression, the mood swings from fluctuating dopamine supply are not nearly so severe, and are quick to come and go. The depression may arrive within seconds, like a big wave on the seashore, and recede within a few more seconds, after taking the next scheduled dopamine-enhancing medication.
BRADYPHRENIA Return (Slow Or Impaired Reasoning): Another phenomenon that has generated much research and debate, on whether it is a true symptom of PD, or (since most PWP are middle-aged or older) merely the result of "normal" aging. Scientific opinion presently is about evenly divided. It's easy to test thinking speed, the hard part is to prove where any such effect originates.
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