Dr. Robert M. Eiben, a physician whose own childhood disease never kept him from aiding

CLEVELAND, Ohio – Dr. Robert M. Eiben, a physician whose own childhood disease never kept him from aiding thousands of children during his more than four-decade-long medical career, died Dec. 28 at his home in Lakewood at age 91.
Eiben was born with a congenital heart defect that left him frail, but determined to pursue his dream of becoming a doctor. He struggled with the physical limitations of the defect until he had open heart surgery at age 37.
The award-winning doctor’s life included roles as a treatment specialist for patients with polio and childhood neurological disorders, a teacher of future medical professionals, and a father to six children and 12 stepchildren.
Eiben received his medical degree from the Western Reserve (now Case Western Reserve University) School of Medicine in 1946. That same year he married his first wife, Dorothy, and they raised six children.
He was hired by Dr. John Toomey, director of infectious diseases in the department of pediatrics, at City Hospital (what is now the MetroHealth Medical Center).
After Toomey’s death in 1950, Eiben replaced him as director, and served at the Toomey Pavilion, one of 15 regional respiratory and rehabilitation centers in the country treating polio patients. In a 1959 edition of the facility’s newsletter, one person who had received care at the Pavilion wrote, “Dr. Eiben does not treat only the disease, he treats the patient.”
For his efforts, Eiben became known as "Greater Cleveland's Polio Doc." But with advent of the Salk polio vaccine, the patient load diminished and Eiben accepted a fellowship in pediatric neurology at the University of Washington in 1959.

He returned to MetroHealth in 1963 to lead efforts in children’s neurology, particularly research relating to cognitive and brain-related challenges faced by low-weight babies. He was appointed director of child neurology and worked there until his retirement in 1990.
During that time Eiben served as acting chief of the Clinical Investigations and Therapeutics, Developmental and Metabolic Neurology branch of the National Institute of Neurological Disorders and Strokes from 1976-1977.
In 1981, he married his second wife, Anne, who had 12 children from her first marriage.
Additionally, Eiben served as a professor of pediatric neurology at his alma mater. His honors include the Robert M. Eiben Lectureship in Pediatric neurology established at Case Western Reserve University’s School of Medicine in 2008.
He also was recognized by the Fourth International Congress of Poliomyelitis for his work on respiratory centers, inducted into MetroHealth’s Hall of Honor, and served multiple leadership roles (including president) of the Child Neurology Society.

In 1991, a year into retirement, Eiben reflected on his career in a newspaper story.
“Fate deals so many assists or blocks in your plans that I find it’s a little bit of chance or good fortune that you end up doing what you do,” he said. “I feel I’ve been very, very lucky.
“Honest to goodness, it’s a privilege to be a doctor, because people are entrusting to you and your judgment,” he added. “That’s the reward in medicine.”
Eiben is survived by his sister, Rita E. Broestl, his six children – Daniel, Christopher (Jayne), Thomas (Jan), Mary (George) Balbo, Charles (Leslie) and Lisa – and 12 Balbo stepchildren: Peter (Maria), Marianne (John) Karaffa, Ruth Kahalsa, Janne (Marshall) Bissett, Martha (Patrick) O’Leary, George (Mary), Jack, Susan (Kevin) Kelley, Mark (Zina), Thomas, Joseph (Sheila), and Constance (Larry).
The family will greet visitors from 3-7 p.m. on Jan. 3 at the McGorray-Hanna Funeral Home, 14133 Detroit Avenue, in Lakewood. The funeral will be at 10 a.m. on Jan. 4 in the Cathedral of St. John, 1007 Superior Avenue East, in downtown Cleveland.
Plain Dealer News Researcher Jo Ellen Corrigan contributed to this story.

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Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno




A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.

On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.

Figure 1

The patient's legs, showing massive enlargement of the right calf and wasting on the left


What is that nature of the acute illness in infancy?
What is the nature of the subsequent deterioration?
What investigations should be performed?
What is the differential diagnosis of the cause of the progressive calf hypertrophy?



An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.


A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3


Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.

Figure 2

Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition


The differential diagnosis of the progressive calf hypertrophy is given in the box.

Causes of calf muscle hypertrophy

Chronic partial denervation

  • radiculopathy

  • peripheral neuropathy

  • hereditary motor and sensory neuropathy

  • spinal muscular atrophy

  • following paralytic poliomyelitis

    Neuromyotonia and myokymia

  • Isaac's syndrome

  • generalised myokymia

  • neurotonia

  • continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis

    Muscular dystrophies



  • tumours

  • amyloidosis

  • cysticercosis

    Link here