Jacquelin Perry

Geoff Watts

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Orthopaedic surgeon and leading authority on gait analysis. She was born in Denver, CO, USA, on May 31, 1918, and died in Downey, CA, USA, on March 11, 2013, aged 94 years.
When orthopaedic surgeon Jacquelin Perry found herself obliged for health reasons to stop operating she followed the advice she was accustomed to give her patients: accommodate to your new reality. With a prior qualification in physical therapy and already interested in human movement, her own accommodation with reality was to set up a gait laboratory at Rancho Los Amigos National Rehabilitation Center in California. Perry established first a national and then an international reputation as one of the leading authorities on the biomechanics of walking and other forms of movement. In 1992 she wrote what is still a highly regarded textbook on gait analysis, and she continued working until the end of her life. Despite living with Parkinson's disease for 20 years and eventually requiring a wheelchair, she never gave in to her own loss of mobility. Neurologist Professor Helena Chui of the Keck School of Medicine at the University of Southern California worked with Perry for 10 years and knew her well for more than 30. “She was in the lab until the week before she passed away”, she says. “Jacquelin was a giant in her field.”
Although Perry had known from the age of 10 years that she wanted to be a doctor, this is not how her career began. With a degree in physical education she joined the US Army and trained as a physical therapist at the Walter Reed Hospital in Washington DC. It was another 5 years before she had the opportunity to study medicine. In 1950, with a medical degree from University of California, San Francisco, she moved into orthopaedics, becoming one of the first ten women to be certified by the American Board of Orthopaedic Surgery. In 1955, Perry joined Rancho Los Amigos, the rehabilitation hospital where she was to spend the rest of her career. In collaboration with a colleague, orthopaedic surgeon Dr Vernon Nickel, she designed a device known as the halo, a metal ring attached by four screws into the skull and used in conjunction with metal rods to immobilise the spine and neck of patients with polio who had recovered sufficiently to leave the iron lung used to maintain their respiration, and who needed support in an upright position.
It was in the late 1960s that Perry was forced to abandon surgery says Professor Mary Ann Keenan of the Department of Orthopaedic Surgery at the University of Pennsylvania. “She had a vascular abnormality at the base of her brain, and when she turned her head she would get severe vertigo. She coped well with this change. But then she was always very practical.” By focusing on gait analysis Perry was able to continue in orthopaedics, and also use her skills as a physical therapist. “She looked at everything from a functional perspective”, says Keenan. “It could be someone with very severe physical limitations or a high-performing professional athlete. She worked from one end of the spectrum to the other.” As Chui adds, “She made herself the supreme expert on what was wrong with someone's gait. She took it apart to understand it, and then set out to fix it.” Perry's thinking is still influential, notes Chui: “It's the gold standard for gait analysis.”
During the 1980s Perry was among the first to make a close study of what became known as the post-polio syndrome. This condition affects polio survivors years after their recovery from infection with the virus and is characterised by progressive muscle weakness and atrophy, fatigue, pain from joint degeneration, and skeletal deformities such as scoliosis. She guided their rehabilitation, all the time advising them, “Listen to your body and adopt a programme that avoids strain.”
“Most people who worked with her would tell you she was intimidating, and that's how I felt on first meeting her”, says Keenan. “She would challenge you with difficult questions. She could see the essence of problems and wanted to hear your reasoning.” Chui agrees, commenting that “She was tough love. People were afraid of her because she held them to such a high standard. But they loved her because they knew she had the same standard for herself.” And although Perry was not a golfer, Keenan adds, she could criticise your play: “She'd tell you what was wrong with your swing even though she'd never hit a golf ball. She understood movement. And if you did what she said you played better!”Post Polio Litaff, Association A.C _APPLAC Mexico

The Polio Crusade

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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