Has anyone suggested that Reno's health is a negative factor in her holding any kind of serious job? In a BBC article over a year ago, it was reported about Janet Reno that "She also continued to work despite being diagnosed in 1995 with Parkinson's disease, which has caused trembling in both her arms." Hence, this is at least her sixth year with the disease. This is important, as you will see when you read the following.

http://www.parkinson.org/encarta99.htm

Encarta Encyclopedia August 1999

PARKINSON DISEASE

INTRODUCTION

Parkinson disease (PD) is a slowly progressive disease of the nervous system. . . . PD progresses from diagnosis to major disability over 10 - 20 years. Most symptoms are improved by levodopa (given as Atamet or Sinemet).

PD is characterized by four principal symptoms:

(1) Rigidity of the limbs. This is appreciated as stiffness of the joints simulating arthritis.

(2) Tremor of the limbs. This is more prominent in the hands and is asymmetrical. While most people regard PD as synonymous with tremor, 30% of PD patients do not have tremor. . . .

(3) Bradykinesia of the limbs and body. Bradykinesia includes difficulty initiating movement, slowness in movement, and paucity or incompleteness of movement. Bradykinesia is the most prominent and disabling symptom of PD.

Rigidity, tremor, and bradykinesia result, primarily, from a loss of dopamine in two regions of the brain: the substantia nigra and striatum. Dopamine is a chemical, or neurotransmitter, which enhances or facilitates the flow of impulses from nerve cells (neurons) in the substantia nigra to nerve cells in the striatum.

(4) Postural Instability results from impairment of righting or postural reflexes, the reflexes which allow people to adjust to abrupt changes in position. Thus, when someone trips and starts falling, they’re able to rapidly, appropriately, and without thinking adjust their trunk and limbs to stop falling, or, if they fall, ease their fall. In PD postural reflexes are impaired and when patients trip, they are unable to stop falling, or ease their fall–resulting in injury. To the PD patient the impaired postural reflexes may be perceived as unsteadiness or lack-of-balance.

The above four symptoms are considered primary symptoms: symptoms resulting from a specific impairment or imbalance in the nervous system. Difficulty walking is often considered a secondary symptom: a symptom resulting from a combination of bradykinesia and postural instability. The difficulty walking is characterized by short-steps (the heel of the advancing-foot not clearing the toes of the lagging-foot), a tendency to run (festination), be propelled forward (anteropulsion), or backward (retropulsion), a difficulty turning, and a tendency to abruptly and inexplicably stop (freeze). The difficulty walking sometimes resembles a car without steering or brakes.

Although PD is considered a motor disorder, one only affecting those regions of the nervous system that regulate movement, PD is more: when fully developed it affects multiple regions of the nervous system. 40% of PD patients are depressed. In some patients depression is a natural reaction to PD (exogenous depression). In most depression is part of PD (endogenous depression) and in some depression precedes the motor symptoms. 30% of PD develop dementia: a global deterioration in intellect. The dementia develops in older patients: 70+ years and resembles Alzheimer Disease (AD). 30% of PD patients develop symptoms related to impairment of the Autonomic Nervous System, the region of the nervous system that regulates, among other things, blood pressure, gut motility, and bladder function.

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SYMPTOMS AND DIAGNOSIS

Parkinson disease (PD) is diagnosed if a patient has 2 or more of the principal symptoms, one of which is resting tremor or bradykinesia. Resting tremor alone or a combination of it and bradykinesia, or rigidity, or postural instability is sufficient to diagnose PD--and, invariably, within 2-5 years, other PD symptoms appear. Combinations of bradykinesia and rigidity, or postural instability may be sufficient to diagnose PD. The combination of rigidity and postural instability may be sufficient to diagnose PD--but, within 2-5 years, non-PD symptoms may appear and a PD-like disorder, not PD may be diagnosed. . . .

Other PD symptoms include difficulty speaking (a low or hoarse voice), lack of facial expression (hypo-mimia, Poker-face), drooling (sialorrhea), difficulty swallowing (dysphagia), oily skin (seborrhea), cramped handwriting (micrographia), stooped-posture (kyphoscoliosis), hand and foot contractures (dystonic posture), shortness of breath, light-headiness on standing, increased sweating, difficulty urinating including frequency, hesitancy, and urgency, sexual dysfunction including impotence and loss of libido, leg cramps, dementia, cognitive impairment without dementia, depression, anxiety, sleep disturbances. These are called secondary symptoms, not because they’re unimportant or untroubling but because:

(1) They’re not essential for the diagnosis e.g. seborrhea, drooling

(2) Appear after the principal symptoms e.g. difficulty swallowing

(3) Are present in a smaller number of patients e.g. hand and foot deformities, leg cramps

(4) Are a specific manifestation of a principal symptoms e.g. lack of facial expression results from rigidity of the facial muscles, cramped handwriting: results from finger bradykinesia, shortness of breath results from bradykinesia and rigidity of the chest-wall muscles.

(5) Represent involvement of the nervous system outside the basal ganglia e.g. light headiness on standing, difficulty urinating result from dysfunction of the Autonomic Nervous System, while dementia results from dysfunction of the cortex.

In some patients secondary symptom such as difficulty swallowing and dementia are more troubling than the principal symptoms.

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NEURO-PSYCHIATRIC DISORDERS

PD is regarded as a motor disorder but neuropsychiatric disorders including dementia, cognitive impairment without dementia, depression, and anxiety may be prominent. These symptoms are usually appreciated after the motor symptoms appear. When these symptoms precede the motor symptoms, as they sometimes do, other diagnoses such as Alzheimer disease (AD), Diffuse Lewy Body disease (DLBD), or depression may be made. Usually, only after the motor symptoms are prominent are the neuropsychiatric symptoms appreciated as PD.

1. Parkinson Disease with Dementia

Approximately 30% of PD patients, usually age 70+, develop a dementia, a global deterioration in intellect: PD-dementia. In 90% of these patients there are changes in the cortex of the brain as well as the basal ganglia. In 76% of the patients the changes in the cortex are similar to Alzheimer Disease. In 24% of the changes consist of the presence of Lewy bodies in nerve cells throughout the cortex: Diffuse Lewy Body Disease. However, there’s an overlap: In many patients with Alzheimer changes there are diffuse Lewy bodies and in many patients with diffuse Lewy bodies there are Alzheimer changes. Diffuse Lewy Body Disease may begin earlier, in the 50s and 60s. Most of the neuropsychiatric symptoms of PD-dementia are aggravated by anti-parkinson drugs.

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3. Cognitive Impairment Without Dementia

Symptoms include slowness of information processing: bradyphrenia analogous to slowness of moment, bradykinesia. Symptoms also include impaired executive function such as difficulty in planning, sequencing, organizing, and innovating. Cognitive impairment may present as a loss of drive or initiative, as a declining job performance, or as difficulty in performing previously learned tasks such as balancing a checkbook or doing a crossword puzzle. However, unlike dementia, cognitive impairment may go unrecognized by the patient’s family, friends, or associates. Cognitive impairment occurs in approximately 20% of PD patients and may be a fore-runner of dementia.

4. Depression.

An endogenous depression accompanied by feelings of guilt, remorse, hopelessness, and pessimism occurs in approximately 40% of PD patients. The endogenous depression is part of PD and is independent of age, disease duration, or disease severity. In approximately 20% of PD patients, depression precedes the motor symptoms. The endogenous depression is often accompanied by an exogenous, reactive depression–reactive to external events. The exogenous depression may be related to job loss, retirement, impotence , or fear of having PD--a chronic and debilitating illness. The depression responds to anti-depressant drugs. The depression may be severe.

5. Relationship of Cognitive Impairment Without Dementia and Depression

Cognitive impairment without dementia and depression may overlap and it may be difficult to separate them. This is especially so when cognitive impairment is associated with depression-like symptoms such as anergy, apathy, and passivity. These patients usually don’t respond to anti-depressant drugs. Cognitive impairment without dementia and the endogenous depression of PD may both arise because of a loss of dopamine cells adjacent to the nigra, a loss of noradrenaline cells in the locus ceruleus (a region of the brainstem), a loss of serotonin cells in the raphe nucleus (a region of the brainstem), and loss of acetyl-choline cells in the nucleus basalis of Meynert (a region of the brain near the striatum). The loss of non-nigral dopamine, noradrenaline, serotonin, and acetyl-choline nerve cells may release one or more non-motor cortical-subcortical loops triggering cognitive impairment without dementia or depression.

6. Anxiety

This is a prominent feature in 40% of PD patients. Whether it’s part of the disease or a reaction to the disease in unknown. The anxiety may or may not be associated with depression. In addition, many PD patients have panic attacks: episodic outbursts of anxiety. The attacks are characterized by a variety of symptoms including: fear of dying, fear of going insane, breathlessness, sweating, chest pain, choking, and dizziness. Panic attack may simulate a heart attack, and occasionally, a panic attack must be distinguished from a heart attack. In many PD patients the panic attacks are situationally cued and are linked to sudden immobility.

7. Sleep Disturbance

This may present as inability to sleep at night and daytime drowsiness. The sleep disturbance may be related to anxiety, depression, or the anti-parkinson drugs. The sleep disturbance maybe related to an inability to turn in bed: a manifestation of PD. Or, the sleep disturbance may be unrelated to any of the above. The sleep centers are in the brainstem near the substantia nigra and may be altered in PD. It must be remembered that von Economo’s encephalitis which between 1918-1926 resulted in 6 million cases of parkinsonism was called "sleeping sickness" because sleep disturbances were so prevalent.

MEDICAL TREATMENT

Most PD symptoms arise from a deficiency of dopamine and most anti-parkinson drugs restore dopamine or mimic dopamine’s actions. However, the drugs don’t permanently restore dopamine or exactly mimic dopamine’s actions. While a loss of dopamine cells in the nigra is the main feature of PD, non-dopamine nerve cells are also lost. This explains why anti-parkinson drugs don’t help all symptoms. Moreover, dopamine cells are present not only in the nigra but in other brain regions. Thus drugs that are effective in PD can, by stimulating non-nigral dopamine cells, cause side-effects such as nausea, hallucinations, and confusion.

[There follows a discussion of the various drugs used to treat the disease. There is also a section on surgical treatment for Parkinson's. One wonders if Ms. Reno has undergone some surgery, given that the very obvious tremors observed in her last days as Attorney General are no longer evident. Or is she being maintained on drug cocktails?]

-- Anonymous, September 04, 2001

Answers

Response to WHAT IS PARKINSON'S - I'm glad you asked. . .

Please feel free to cut and paste the above to any other forum or e-mail you choose--but please don't attach my name to it.

-- Anonymous, September 04, 2001

It has been reported that instead of holding a press conference for her announcement, Reno invited reporters to her home, where she sat in a chair on the back porch and gave five-minute, one-on-one interviews. This approach would conceal or minimize the symptoms affecting limbs described above--rigidity, tremor and bradykinesia. Answering a group of reporters from a dais would necessitate much swiveling and pointing; apparently, Reno is now incapable of such freedom of movement. One wonders what other symptoms are being concealed and just how far the disease has progressed. One of her doctors has said her disease "should" not affect her candidacy. "Should not" and not "would not." Hmm.

It is also interesting to note that Reno was hospitalized overnight twice for "nausea and fainting" attacks in November 1997 and September 1998. The dizziness and unsteadiness described in the list of symptoms above?

-- Anonymous, September 05, 2001

I printed out the original.

Ever since PA Engineer's commentary a week or so ago, I've wondered more if this is mother's basic problem. In particular, the depression and cognitive impairment as described in the article (very bizarre sequencing misqueues of the most basic tasks). I have been rather unsympathetic to her condition, resenting, I suppose, that my own mother can't function any more. It's time for her to see her doctor again, so I should have him focus on it.

-- Anonymous, September 05, 2001