Presidents Kennedy's health history

RAY SUAREZ: According to medical records released this week, former President John F. Kennedy was in far greater pain and taking many more medications during his presidency than previously known. Washington physician Jeffrey Kelman examined the records with historian Robert Dallek, whose excerpts from an upcoming biography appear in this month's Atlantic Monthly. Dr. Kelman joins us now. Well, John F. Kennedy was famously the youngest man elected to the office. But it sounds like he had been sick for a really long time. DR. JEFFREY KELMAN: John Kennedy was sick from age 13 on. In 1930, when he was 13, he developed abdominal pain. By 1934 he was sent to the Mayo Clinic where they diagnosed colitis or it was called colitis. By 1940 his back started hurting him, by 1944 he had his first back operation, by 1947 he was officially diagnosed as having Addison's Disease. And he was basically sick from then on through the rest of his life. He had two back operations, in '54 and '55, which failed. And he needed chronic pain medication from '55 through his White House years, until he died in Dallas. He was never healthy. I mean, the image you get of vigor and progressive health wasn't true. He was playing through pain most of the presidency. RAY SUAREZ: You reviewed his medical records. DR. JEFFREY KELMAN: In aid of this new biography by Robert Dowling, we went to the Kennedy library where they opened the medical archives for the first time and we went back and interviewed all the records, starting from his time in the Mayo Clinic all the way up to his death.
Access to new medical records
RAY SUAREZ: And this was a guy who had to do what just to get through a day? DR. JEFFREY KELMAN: By the time he was president, he was on ten, 12 medications a day. He was on antispasmodics for his bowel, paregoric, lamodal transatine [ph], he was on muscle relaxants, Phenobarbital, Librium, Meprobomate, he was on pain medications, Codeine, Demerol, Methadone, he was on oral cortisone; he was on injected cortisone, he was on testosterone, he was on Nembutal for sleep. And on top of that he was getting injected sometimes six times a day, six places on his back, by the White House physician, with Novocain, Procaine, just to enable him to face the day. RAY SUAREZ: Now, in the late '40s he was diagnosed with Addison's Disease. DR. JEFFREY KELMAN: Right. RAY SUAREZ: Which is what exactly? DR. JEFFREY KELMAN: Addison's Disease is adrenal insufficiency. The adrenal gland makes corticosteroids and other hormones that are used for salt metabolism, response to stress, response to inflammation. In '47 he was officially diagnosed in England, as being adrenally insufficient, and from that point on, at least that point on, he was being treated with daily corticosteroids of some form or another. There is some evidence he was actually being treated earlier, with a form of [inaudible] implanted under his skin. But at, from '47 he had to receive daily steroids to survive. RAY SUAREZ: Now whether this was Addison's or simple adrenal insufficiency, this is still pretty dangerous? DR. JEFFREY KELMAN: It's always dangerous; without being supported, patients die. And the steroids themselves have side effects, including susceptibility to infection. Kennedy needed multiple courses of antibiotics, he had urinary infections, skin infections, he had respiratory infections. RAY SUAREZ: Can you, from the distance of 40 years, from what you were able to look at, his X-rays, his medical records, his prescriptions, talk about whether or how these illnesses affected his performance? DR. JEFFREY KELMAN: We went to a lot of trouble, I mean, you can make a time line at the Kennedy Library looking at day by day, sometimes hour by hour, the history of the Kennedy presidency. And in correlating it as well as you could with the medical records, didn't seem to have affected his presidency at all. His judgment wasn't warped, in spite of the fact that he seemed to be in pain a great deal of the time, it didn't affect his performance as president. In certain ways I came out of it thinking he was a heroic character. RAY SUAREZ: Was his appearance altered by the drugs that he was on? DR. JEFFREY KELMAN: He gained and lost weight, both from the colitis and from the steroids, and from the appetite, that's why he was on testosterone, in order to stimulate muscle growth and stimulate his appetite. So his performance -- his appearance rather did change from time to time.
Possible side effects on his leadership?
RAY SUAREZ: Now, in recent years there's been a lot of controversy over the use of steroids by athletes, by youngsters who are trying body building, people talk about "roid rage" and personality changes from using such medications. How do we know, or can we ever know whether they affected President Kennedy in what was still, I think, a pretty new drug regimen, wasn't it? DR. JEFFREY KELMAN: Right. Steroids became available at all in 1937. And so this is reasonably new. The muscle building steroids are the testosterones, and he didn't appear to be getting doses high enough to cause psychological changes. The maintenance, corticosteroids he was receiving for the Addison's Disease, again, were probably not in high enough doses to cause psychiatric issues. RAY SUAREZ: What can you tell from the X-rays? DR. JEFFREY KELMAN: He had compression fractures in his low back, he had osteoporosis. He had a lot of surgery. In 1954, they put a plate in because the pain was so bad he needed, or they felt he needed to have his spine stabilized. It got infected in '55, they took the plate out. By the late '50s there were periods had he couldn't put his own shoes on because he couldn't bend forward. RAY SUAREZ: And this is a man who also had to walk sideways down the stairs. You never saw this stuff in public apparently, but had trouble walking? DR. JEFFREY KELMAN: He was on crutches. He couldn't bend down. There's one very nice picture of him being lifted up to Air Force One in a cherry picker box with a Secret Service man because he couldn't walk up the stairs. RAY SUAREZ: If you had a patient, if someone been referred to you and you got this box of records, would you be expecting someone sort of tan and fit? DR. JEFFREY KELMAN: No. RAY SUAREZ: The way Kennedy that was presented to us? DR. JEFFREY KELMAN: Never. It was the last thing I expected to find in the medical records. I saw him once, many years ago. And all I can remember is feeling this is a guy who couldn't have a care in the world. And that wasn't the case at all. RAY SUAREZ: Has medicine changed in such a way that these conditions wouldn't be treated this way today?
Living with a disability
DR. JEFFREY KELMAN: Clearly, but it's 40 years later. I mean there's more emphasis on non-steroidal anti-inflammatory agents, there's for emphasis on exercise programs to strengthen backs, less on braces, less on trigger point injection, although it's still used. He'd have been treated differently now, but that's 40 years of hindsight. RAY SUAREZ: One of the reasons it's said that the records were released to you and Bob Dallek was that there was some feeling that this would demonstrate what a heroic thing this was, not that he had deceived the public by giving a false impression of health, but that it was just pretty hard to be John F. Kennedy day after day. After looking at everything that you looked at, which impression did you come away with? DR. JEFFREY KELMAN: That was my impression. It's funny, I mean, the lesson that I got out of it was that this guy had a real disability, I mean, he was living with a disability which probably would get him federal disability or retirement if he was around today, and it was known. He was on enough pain medications to disable him. And he survived through it. He came out of it, and he performed at the highest level RAY SUAREZ: Dr. Jeffrey Kelman, thanks a lot. DR. JEFFREY KELMAN: Thank you.

Sex in autoimmune disease

Reduce weight

Drug reaction prevention

Prevent Osteoporosis

Some rheumatic disorders

Skin repair Clinic

Neck Pain

Rabinder N Tagore

Breast Lymph Drainage

Osteoporosis

Electronic Treatment

Breast Size & Disease

Female Sex Disease

PARKINSON

Memory problems

Breast Lymph Drainage

Kidney stone Buster

Bras & breast cancer

Lahore Clinic

Lahore skin Clinic

Pandas

Backpain

Fibromyalgia

Personality

Electrical Stimulation Therapy

Quranic Shifa

Vitamin D Deficency

Cupping

Microwaves

Radiowaves

Infrared

Visible Light

UltraViolet

Gamma

Osteoporosis

Iodine Deficiency

X-Rays

attack on self tissue

the poet

Inflammatory neuropathy

Carbohydrate supplements

Learn about the neuron

Avoid headaches with IVIg

Cholesterol drugs & Bleeding

Learn about Self

Myofacial Pain

Chronic Pain Management

Subcutaneous IVIg Page

Apple juice fights for you

Best Fat Lowering diet.

911 CIDP story

Tetanus Vaccine Story

Stem Cell Story

Surgery CIDP

Cranial nerve CIDP

Farmer CIDP

Story 7

Story 8

Story 9

Recurrent attack CIDP

Charcot

Story 12

Story 13

Pain Med. 2002 Jun;3(2):119-27.

Human pooled immunoglobulin in the treatment of chronic pain syndromes.

Goebel A, Netal S, Schedel R, Sprotte G.

Klinik fur Anaesthesiologie, University Wurzburg, Wurzburg, Germany.

Objective. To examine the use of intravenous immunoglobulin (IVIG) in chronic pain. Design. A prospective multiple-dose, open-label cohort study in 130 consecutive patients who suffered from 12 chronic pain syndromes. The largest symptom groups were (number of patients): Fibromyalgia (48); Spinal pain (20); Complex regional pain syndrome (CRPS, 11); Peripheral neuropathic pain (12); and Atypical odontalgia or atypical facial pain (11). All patients had insufficient pain relief with established treatments. Pain relief was recorded using average pain intensity values as documented in standardized diaries. A specific treatment protocol was developed, and patients were enrolled over a 36-month period. Results. Overall, 20% of patients had>70% pain relief and 27.7% of patients reported relief between 25% and 70%. Six patients (4.6%) had moderately increased pain levels for a duration of up to 9 weeks. Good relief, of more than 70%, was found in all major symptom groups. Patients with pain of short duration (<2 years) reported high relief rates (33.8% of patients in this group reported relief openface>70%). No serious adverse events were reported. Conclusions. IVIG may be effective in patients suffering from chronic pain. Controlled studies are needed to evaluate the efficacy of IVIG in these patients. Patients with a good response to IVIG may be models for the study of neuroimmune interactions in chronic pain.

PMID: 15102158 [PubMed - in process]

: Drugs. 2003;63(3):275-87.

Management of chronic inflammatory demyelinating polyradiculoneuropathy.

Hughes RA.

Department of Clinical Neurosciences, Guy's, King's and St Thomas' School of Medicine, London, UK. richard.a.hughes@kcl.ac.uk

This review briefly describes current concepts concerning the nosological status, pathogenesis and management of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). CIDP is an uncommon variable disorder of unknown but probably autoimmune aetiology. The commonest form of CIDP causes more or less symmetrical progressive or relapsing weakness affecting proximal and distal muscles. Against this background the review describes the short-term responses to corticosteroids, intravenous immunoglobulin (IVIg) and plasma exchange that have been confirmed in randomised trials. In the absence of better evidence about long-term efficacy, corticosteroids or IVIg are usually favoured because of convenience. Benefit following introduction of azathioprine, cyclophosphamide, cyclosporin, other immunosuppressive agents, and interferon-beta and -alpha has been reported but randomised trials are needed to confirm these benefits. In patients with pure motor CIDP and multifocal motor neuropathy, corticosteroids may cause worsening and IVIg is more likely to be effective. General measures to rehabilitate patients and manage symptoms, including foot drop, weak hands, fatigue and pain, are important.

PMID: 12534332 [PubMed - indexed for MEDLINE]

Neurology. 1997 Feb;48(2):321-8.

Chronic inflammatory demyelinating polyneuropathy: clinical features and response to treatment in 67 consecutive patients with and without a monoclonal gammopathy.

Gorson KC, Allam G, Ropper AH.

Neurology Service, St. Elizabeth's Medical Center, Boston, MA 02135, USA.

We report the clinical and EMG details of 67 consecutive patients with strictly defined chronic inflammatory demyelinating polyneuropathy (CIDP) during a 4-year period and compare responses to treatment in patients with idiopathic CIDP (CIDP-I) and CIDP with monoclonal gammopathy of uncertain significance (CIDP-MGUS). Patients were examined an average of 28 months after first symptoms. There were several variant presentations that still conformed to the clinical and electrophysiologic definitions of CIDP, including a pure motor syndrome (10%), sensory ataxic variant (12%), mononeuritis multiplex pattern (9%), paraparetic pattern (4%), and relapsing acute Guillain-Barre syndrome (16%). Pain was more frequent than in previous studies (42%). Conduction block was the commonest EMG abnormality (detected in at least one nerve in 73% of patients), but only 31% had a pure demyelinating neuropathy and the majority had some degree of axonal change. Patients with CIDP-MGUS had less severe weakness, greater imbalance, leg ataxia, vibration loss in the hands, and absent median and ulnar sensory potentials, but were as likely as CIDP-I patients to respond to plasma exchange. Seventeen of 44 patients (39%) with idiopathic CIDP improved for at least 2 months with an initial therapy. Although the response rates among plasma exchange, IVIG, and steroids were similar, functional improvement (Rankin score) was greatest with plasma exchange. Of 26 patients who failed to respond to an initial therapy, 9 (35%) benefited from an alternative treatment, and of the 11 who required a third modality 3 (27%) improved. Overall, 66% responded to one of the three main therapies for CIDP.

PMID: 9040714 [PubMed - indexed for MEDLINE]

Diabetes Metab. 2001 Apr;27(2 Pt 1):155-8.

An unusual neuropathy in a diabetic patient: evidence for intravenous immunoglobin-induced effective therapy.

Romedenne P, Mukendi R, Stasse P, Indekeu P, Buysschaert M, Colin IM.

Department of Internal Medicine, CHR-St Joseph Medical Center, Mons, Belgium.

We report the case of a 68-year old type-2 diabetic male patient who was admitted to hospital for progressive weakness in the right lower limb. Although his metabolic control was good, he lost more than 20 kg of weight. Despite intensive physio- and vitaminotherapy, his neurological condition kept on degrading with a severe amyotrophy and pain of the right thigh. He was unable to walk and to stand alone. Besides a yet known sensitive polyneuropathy, the electrophysiological study revealed an obvious motor involvement with signs of demyelination and axonal degeneration. Combined with the albuminocytologic dissociation observed in the cerebrospinal fluid, these specific clinical and electrophysiological features led us to postulate a diagnosis of inflammatory neuropathy. The patient underwent a treatment by methylprednisolone and immunoglobins that rapidly induced a striking improvement of his neurological condition. This case report illustrates that rare forms of neuropathy such as inflammatory neuropathies close to chronic inflammatory demyelinating polyneuropathy (CIDP) can occur in diabetic patients and superimpose on the more commonly described forms of neuropathies. It recalls the importance of recognizing CIDP-like neuropathies because unlike other forms of neuropathy, inflammatory neuropathies are perfectly curable.

Publication Types:

Case Reports

PMID: 11353882 [PubMed - indexed for MEDLINE]

: The spectrum of chronic inflammatory demyelinating polyneuropathy.

Rotta FT, Sussman AT, Bradley WG, Ram Ayyar D, Sharma KR, Shebert RT.

Department of Neurology, University of Miami School of Medicine, PO Box 016960, Miami, FL, USA.

Research criteria for the diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) were proposed by an Ad Hoc Subcommittee of the American Academy of Neurology (AAN) in 1991, and since then these criteria have been widely used in clinical studies. We have been impressed by the frequent finding of electrophysiological changes of a demyelinating neuropathy in patients whose clinical presentation does not conform to the usually accepted clinical phenotype of CIDP. To determine the clinical spectrum of CIDP, we conducted a retrospective review of patients of the peripheral electrophysiology laboratory of the University of Miami-Jackson Memorial Medical Center. Diagnostic criteria for acquired demyelination of an individual nerve were adapted from the AAN research criteria for the diagnosis of CIDP (1991). Patients were accepted for inclusion when such evidence was demonstrated in at least one motor nerve or at least two sensory nerves. We then reviewed the clinical phenotype and the underlying etiology of the neuropathy in these cases. Eighty-seven patients, 63 male and 24 female, age of onset 4-84 (mean 49.3) years, met these inclusion criteria. Forty-seven patients (54%) had distinct features outside the usual clinical presentation of CIDP. Of these, 15 (17%) had predominantly distal features, 13 (15%) had exclusively sensory polyneuropathy; seven (8%) had markedly asymmetric disease, seven (8%) had associated CNS demyelination, four (5%) had predominant cranial nerve involvement, and one (1%) had only the restless legs syndrome. An associated medical condition that may have been responsible for the acquired demyelinating neuropathy was present in 60% of the patients. We conclude that spectrum of CIDP is broader than would be indicated by the strict application of the AAN research criteria, and that many of the cases meeting more liberal criteria frequently respond to immunosuppressive therapy.