“I guess it’s my time,” the 50-year-old man said quietly as his wife drove him home from his doctor’s office in southwest Houston. “No,” his wife responded sharply. “I won’t accept that. We’re going to get a second opinion.” To the patient, a software engineer and father of two teenage girls, it seemed as if this was the end of his 14 months of rapid decline from a robust man to this skeleton who needed a walker to get from car to door.

Just two summers before, he was healthy. By fall, he noticed that his morning walks with his golden retriever were getting shorter. His 30-minute route became 20, then 10, then even less. His feet felt like bricks: cold, unfeeling, heavy. A simple trip to the park or upstairs to their bedroom felt like a workout.

First, he went to see his primary-care doctor. He had no fevers or chills. His appetite was good, though he’d lost weight. He was sleeping fine. His exam seemed normal until the doctor tapped the front of his knee with his little rubber hammer. Nothing happened. There was no kick reflex. He tried again; still nothing. He tapped the tendons behind his ankles and the ligaments in his forearms, but he couldn’t elicit the normal jerks of an intact reflex.

In Search of Missing Reflexes

His doctor wasn’t sure what was wrong, but he was worried. He referred his patient to a neurologist for further evaluation. When that doctor examined him, he noticed significant weakness in the man’s hip and leg muscles. His shoulders and arms were not as strong as they should have been. And he had no reflexes anywhere. The neurologist reviewed the blood test obtained by the primary-care doctor. It wasn’t his muscles. It wasn’t his thyroid. There was no sign of anemia, infection or inflammation.

The loss of reflexes indicated that the man’s weakness was probably caused by his nerves rather than his muscles. The neurologist performed a nerve-conduction study, during which a tiny electrode, inserted into the muscle, measures the electrical impulses the nerve fibers send to the brain when the muscle is working. In areas of the patient’s weakness, the test showed that the fine strands of nerve tissue were damaged and transmission was slowed. A spinal tap revealed high levels of protein in the cerebral spinal fluid, suggesting that the patient might have some type of autoimmune neuropathy, nerve damage caused by rogue antibodies. The neurologist thought the patient most likely had either Guillain-Barré syndrome (G.B.S.) or its longer-lasting cousin, chronic inflammatory demyelinating polyneuropathy (C.I.D.P.).

Feeling Better, Then Worse

The doctor first treated him with plasmapheresis — a technique that removes antibodies from the circulation. This process can be used to treat both G.B.S. and C.I.D.P. It worked. In the weeks following that first series of treatments, the man felt stronger. He was excited to be back to about 70 percent of normal. But it didn’t last. Two months after his last treatment, he started losing ground. His balance went, and after a couple of falls, he had to start relying on a cane. The doctor changed his treatment to IVIG — intravenous gamma globulin, flooding his system with other people’s antibodies. Maybe it helped a little, but he continued to weaken. The cane stopped being enough, and he had to use a wheelchair outside the house.

Because the patient was not responding to treatment as expected, the neurologist looked for other possible causes of the severe weakness. Was it H.I.V.? Could it be lupus? Or a rare cancer of white blood cells called POEMS? He sent out more blood and scanned his bones, but those results revealed nothing new. Imaging showed no pathology in his brain or spine to account for the weakness. He put the patient back on plasmapheresis and sent him to physical therapy. He continued to worsen. His hands became clumsy, and eating was difficult. He also kept losing weight. He started out at just over 210 pounds. After that year of treatment, he was down to 150.

Could It Be a Zebra?

Throughout this devastating illness, the man’s wife had taken the research and problem-solving skills she’d developed as a lawyer and tried to apply them to his case. She recalled that the neurologist had mentioned the possibility that he had POEMS — an acronym of the symptoms caused by an overproduction of antibodies, including polyneuropathy (pain and weakness and a loss of sensation in different parts of the body), organomegaly (enlarged organs), endocrinopathy (hormonal abnormalities), monoclonal plasma cell proliferation (too many antibody-producing cells) and skin changes. But he had ruled out that diagnosis.

Reading up on it, she found case reports of patients who sounded remarkably like her husband. He had at least two of the symptoms (polyneuropathy and monoclonal plasma cell proliferation). Maybe it is POEMS, she suggested to the neurologist. Not likely, he said. It’s quite rare, and her husband didn’t fully fit the diagnostic criteria. Besides, the proliferation of antibodies that made him think of POEMS in the first place is seen in up to 10 percent of patients with C.I.D.P. He cited the aphorism leveled at all who suspect “zebras”: An unusual manifestation of a common disease is much more likely than even a classic presentation of a rare disease.

That’s when the patient’s wife decided they needed a second opinion and made an appointment with Dr. Kazim Sheikh, a neurologist at the University of Texas at Houston. The first neurologist had encouraged them to seek a new neurologist, because if the patient didn’t have C.I.D.P., he wasn’t sure what he had.

An Important Clue

She took her husband to see Dr. Sheikh a few weeks later. He listened to the patient and his wife describe their hellish year, and even before he examined the patient, he made his first diagnosis: “I think you have a cancer. I’m not sure what kind, but I think you should be seen at MD Anderson Cancer Center.” She shared her thoughts about POEMS syndrome. It might fit, he agreed. But there were also other possibilities. He ordered a PET scan to look for lesions on the bone. In POEMS, patients often develop tumors made up of cells that produce antibodies. A PET scan looks for cell activity, and because malignant tumors are constantly producing abnormal cells, they light up on this kind of scan. There, on his pelvic bone, was a tiny hot spot, a tumor, too small to be seen on the earlier scan.

Harsh Treatment

The patient was referred to MD Anderson, where he was finally given the diagnosis of POEMS. Initial treatments were ineffective. His last chance was a stem-cell transplant. This is a brutal therapy in which after collecting a sample of stem cells that can grow into both red and white blood cells, the patient is blasted with chemotherapies designed to kill everything left behind. Only then can the harvested cells be reintroduced to their newly cleaned bone marrow to repopulate. Cure is nearly 100 percent — for those who survive.

At this point, though, the patient’s doctors were concerned that he was too sick to survive this terrible treatment. His wife insisted that the doctors should let him take the risk of dying from the treatment rather than be certain of death without it. Seeing the patient, Dr. Muzaffar Qazilbash, the transplant oncologist, was reminded of Stephen Hawking, with his six foot frame folded into a wheelchair, shrunk down to just over 100 pounds. He re-evaluated the man — could he survive the procedure? — and agreed.

The patient made it through the transplant and then the many complications afterward. Slowly, slowly, he recovered. His transplant was just over four years ago. He no longer needs a cane and is back to walking. He’s once again driving his daughters to their after-school events. And he’s back to work, full time.

He knows that he is one lucky man. He was lucky to have the insurance he had, lucky to have survived both the disease and the cure and really lucky to have a wife who wasn’t going to let him go.