Patient with weakness of the legs: history taking and presentation.

This is the way the history was presented.

A 38 year old woman developed weakness of her lower limbs 2 and a 1/2 weeks ago. Two weeks later her upper limbs were affected in that her grip strength became weak too. She could dress herself, feed herself and do her hair without assistance. She developed loss of sensation in her feet because her flip-flop slippers fell off. She needed to be catheterized as she could not pass urine. She is constipated and needs an enema every three or four days. She has no cough, diarrhea, chest pain, breathlessness or fever. She has no coldness of the fingers, rash, joint pains, loss of hair. She has no significant illnesses in the past. She is a housewife with 6 children, does not menstruate because she has had an operation probably hysterectomy though she does not give a reason for this operation. Her condition since the onset of the weakness is static. She had an MRI but does not know the result nor does she have a written report. She has been given some injections in the hospital that she is admitted in but no blood transfusion or other procedure has been done on her.

Examination of the CNS showed normal higher mental functions and no cranial nerve deficits. She has a sensory level at the level of her nipples but can feel some sensation on her lower limbs in patches. the muscle tone in her lower limbs and upper limbs is normal. The power in the lower limbs is 2/4 and no reflexes can be elicited; both planters are upgoing. The initial diagnosis given by the candidate is spinal cord compression syndrome.

The questions asked were:

  1. How did she notice that her legs were weak? Did she fall down? Did she need help getting up from a squatting position or chair? Could she not walk at all and had to be carried to her bed? All these are going to make a difference in her diagnosis.
  2. How long did the weakness take to develop? Hours, minutes, days?
  3. Are her flipflops falling off because she can no longer grip them with her toes because of the weakness of her toes and not because of the loss of sensations? Patients tend to equate weakness with numbness so you need to clarify.
  4. Can she walk? What is her disability? Believe me the candidate who was presenting the case did not know.
  5. Does she have an indwelling catheter and if so why? The patient said she could feel the sensation to pass urine but no one in her house was strong enough to carry her to the toilet so the attending doctor passed a Foley catheter. She did not have retention of urine but simply a nursing problem emptying her bladder.
  6. She had been constipated all her life according to he as she passed hard stools every 2-3 days and now needed an enema as she could not squat on the toilet. She did not have a toilet seat and could not walk to the toilet.
  7. Why was she not menstruating? She had had tubal ligation and early cessation of menstruation need to be looked into as early ovarian failure.
  8. Are the nipples a useful landmark in a 38 year old woman who has breastfed 6 times? No, they will be at a much lower level so use the intercostal spaces instead.
  9. What are her abdominal reflexes like? The candidate had not checked them. Fatal.
  10. Did the patient really have a sensory level? The spurious level “at the level of the nipples”, patchy distribution of sensation which is not coinciding with either a dermatome or sensory nerve distribution and is accompanied by a withdrawal planter reflex show that the patient has an altered perception of her sensations. Fake news as Trump would say and the candidate is ignorant of the pattern of sensory loss in different diseases.
  11. Is this an upper or lower motor neuron loss of function? The candidate could not say.
  12. What is the level of the cord compression? All the way from L1,2,S1-5 to C8? Which disease is likely to fit in?
  13. In the systemic survey what is the significance of cough? A geriatric patient specially in the 80s plus may have a bout if severe coughing and fracture a vertebra but not a previously healthy 38 year old woman. Diarrhea is not connected. Trying to connect it to symptoms of SLE is also an exercise in futility. Fever does not prominently precede transvers myelitis. Fever, with night sweats. an evening rise and loss of weight happens in TB of the spine and may be mentioned.
  14. Are there any local signs or symptoms? The candidate had never once mentioned backache, direct or indirect trauma to the spine, osteoarthritis of the spine or ankylosing arthritis or any other arthritides.
  15. Was she on any drugs which might affect her bones?

You can see how many mistakes were made by a candidate who thought they had taken a comprehensive history and done a complete physical examination. How can this be improved?


A 38 year old woman was standing and washing her clothes when she realised that her legs were not supporting her weight. As she felt she might fall she clutched her washing machine and then the wall and door and dragged herself to a nearby chair. After 15 minutes of rest she called for help. Her daughter came but could not pick her up. Her husband and brother pulled her upright but had to support he as she could not stand by herself, she dragged her feet, her slippers fell off and with the help of the men she reached her bed, By the evening 6 hours later she could not stand even with support. She wanted to empty her bladder but as she could not walk a doctor was called who passed an indwelling catheter. By the next morning she could not hold a glass, cup or spoon and had to be fed. This shows the sudden onset weakness of the lower limbs which took about 12 hours or so to progress to the upper limbs. The need for the catheter is because of the limb weakness which does not allow her to walk to the toilet not because of retention of urine or loss of bladder sensation. It is essential that you understand and mention the difference. She has no backache, history of direct or indirect trauma to the back, has not suffered prominently from osteoarthritis or other arthritides affecting the spine nor does she symptoms suggestive of TB spine like fever, night sweats, weight loss. The need for the operation on her pelvic organs needs to be explored as if she might have had a hysterectomy for a malignancy then secondary deposits in the spine might be a possibility but pain would be expected.

She has a lower motor neuron paralysis i.e. marked weakness of the limbs with an ascending pattern, no increase in her muscle tone, loss of tendon reflexes and withdrawal planter reflexes. I would put my money on Guillain Barre syndrome.

Sensory Loss.

Higher cortical sensation can be examined if touch sensation remains relatively preserved and the patient is suspected of having a cortical lesion. Examination of cortical sensation includes two-point discrimination, graphesthesia, stereognosis, and extinction

Sensory loss that is confined to a part of a limb suggests injury to a peripheral nerve, nerve plexus, or spinal root (eg, mononeuropathy or radiculopathy).

Involvement of both sides of the body is consistent with a polyneuropathy or spinal cord disease, while involvement of one side is consistent with contralateral disease of the brainstem, thalamus, or cerebral cortex.

“Stocking-glove” sensory loss is most commonly seen with length-dependent axonal neuropathies, although other disorders may also present with this pattern. Diabetes mellitus for example and alcohol, vitamin B12 deficiency, syphilis, human immunodeficiency virus, Lyme disease, uremia, chemotherapy, vasculitis.

Disproportionate loss of vibration sense and proprioception, compared with pain and temperature sensation, tends to occur with diseases of the dorsal columns of the spinal cord (eg, tabes dorsalis, vitamin B12 deficiency, multiple sclerosis) and demyelinating polyneuropathy

Sensory loss of the face can result from lesions in the upper cervical spine, brainstem, thalamus, or cerebral hemispheres. With lower brainstem disease (eg, lateral medullary syndrome), the sensory loss on the face is typically opposite that of the body, although ipsilateral sensory loss has also been reported; sensory loss is on the same side of the face and body with upper brainstem, thalamic, or hemispheric disease.

Sensory neuronopathies are often idiopathic in etiology. However, they may be associated with paraneoplastic phenomenon. The latter is most commonly associated with small cell lung cancer and the presence of anti-Hu antibodies. Can occur in Sjogren’s syndrome, Guillain-Barré syndrome variant, chemotherapy-induced, especially the platinum drugs, Friedreich’s ataxia and vitamin B 6 deficiency. 

Spinal cord lesions.

Cape distribution sensory loss is an uncommon but well-described pattern of sensory loss resulting from lesions of the central cervical cord. Sensory loss occurs over the upper back, shoulders and upper limbs.

Central lesions affecting the cervical spinal cord can also present with a stocking-glove pattern of sensory loss.

Brown-Sequard syndrome — The Brown-Sequard syndrome results from a lesion involving only one side of the spinal cord. In this situation, the patient presents with diminished proprioception, diminished vibration sensation, and weakness on the side ipsilateral to the lesion, and decreased pinprick and temperature sensation on the contralateral side.

Wallenberg syndrome is probably the most well-known brainstem abnormality leading to sensory loss. It results from a lesion of the lateral medulla and was originally described as involving pain and temperature loss on the ipsilateral face and contralateral limbs and trunk. However, several other patterns of pain and temperature loss have been described in association with this syndrome, including contralateral face and bilateral face involvement.

Thalamic lesions may cause a contralateral sensory deficit that involves all sensory modalities to varying degrees. Although tumors and abscesses can involve the thalamus, typically the onset of sensory loss in thalamic lesions is acute or subacute and is the result of a lacunar infarct

Spinal cord compression syndrome/ Epidural spinal cord compression syndrome (ESCC).

The spinal cord is enclosed by a protective ring of bones comprised of the vertebral body anteriorly, the pedicles laterally, and the lamina and spinous process posteriorly. Within this ring is the thecal sac, the outermost layer of which is comprised of dura. Between the bone and dura lies the epidural space, which normally contains fat and the venous plexus.

Approximately 85 to 90 percent of cases of ESCC are due to metastatic tumor in the vertebral bones.

The cardinal clinical features of ESCC are symptomatic spinal cord or nerve root compression and mechanical instability of the spinal column. Early diagnosis of spinal metastases prevents the development of neurologic deficits and severe structural instability.

Clinical presentation — The majority of patients with ESCC have pain as the initial symptom, prior to the onset of motor or bladder dysfunction. Delayed recognition and therapy of ESCC may result in the development or progression of neurologic deficits.

ESCC most commonly arises in the thoracic spine. Approximately 60 to 70 percent of cases occur in the thoracic spine, 20 to 30 percent in the lumbosacral spine, and 10 percent in the cervical spine. These percentages are in rough proportion to the combined volumes of the vertebral bodies in each region.

Pain is usually the first symptom of ESCC, present in 80 to 95 percent of patients at the time of diagnosis. On average, pain precedes other neurologic symptoms of ESCC by seven weeks.

Affected patients usually notice a severe local back pain, at the level of the lesion, which progressively increases in intensity. Over time, the pain may develop a radicular quality. It may, for example, radiate into a limb with movement of the spine or Valsalva maneuver. Radicular pain is more common in lumbosacral lesions than in thoracic lesions.

The severity of weakness tends to be greatest in patients with compressive thoracic metastases. Unless there is profound weakness or severe pain with movement, the motor examination must include standing and walking to be complete.

When the site of compression is at or above the conus medullaris, weakness is from corticospinal tract dysfunction and has the typical pyramidal pattern, preferentially affecting the flexors in the lower extremities (ie, weakness of hip flexion, knee flexion, and ankle dorsiflexion with relative preservation of hip extension, knee extension, and plantar flexion strength). If compression is above the thoracic spine, the extensors of the upper extremities may also be affected (ie, more pronounced weakness in the triceps and wrist extensors than in the deltoid and biceps). Hyperreflexia below the level of the compression and extensor plantar responses may be seen.

Patients frequently report a pattern of ascending numbness and paresthesias if questioned and examined carefully.

When a spinal sensory level is present, it is typically one to five levels below the actual level of cord compression. Saddle sensory loss is commonly present in cauda equina lesions, while lesions above the cauda equina frequently result in sparing of sacral dermatomes to pinprick.

Bladder and bowel dysfunction due to ESCC is generally a late finding that was present in as many as one-half of patients in older series. Urinary retention as a manifestation of autonomic dysfunction is the most common finding and is rarely the sole symptom of ESCC.

New gait ataxia in the setting of back pain in a cancer patient should raise suspicion of ESCC.

Bilateral lower extremity pain is the classic presentation that raises concern for cauda equina syndrome. Bowel and bladder dysfunction may occur with compression of the lower sacral nerve roots. Elevated post-void residual volume on bladder scan may be a particularly sensitive marker of urinary retention in this setting.

Other causes of cord compression.

Degenerative spine disease – Intervertebral disc herniation, synovial cysts, and cervical or lumbar spondylosis can cause acute or subacute myelopathy and radiculopathy, along with pain. Spondylotic myelopathy is the most common cause of myelopathy in older adults. MRI of the spine in the appropriate clinical context is diagnostic. 

Vertebral compression fracture with retropulsed bone – Osteoporotic vertebral compression fractures, which most commonly occur in the thoracolumbar spine, occasionally present with spinal cord compression due to retropulsed bone fragments in the spinal canal. Symptoms vary depending on the level of the fracture and degree of compression and may include cauda equina syndrome for lumbar fractures.

Spinal epidural abscess is an important condition to recognize and distinguish from ESCC. Predisposing factors include intravenous drug use, vertebral osteomyelitis, and hematogenous infection. Tuberculosis and fungal infections in particular can mimic tumor. The leading bacterial pathogen causing spinal epidural abscess is Staphylococcus aureus, which accounts for approximately two-thirds of cases of bacterial etiology. Other infectious causes include Mycobacterium tuberculosis, which is responsible for up to 25 percent of cases.

Vascular malformations of the spinal cord, such as dural arteriovenous fistulas, can cause an acute or chronic progressive spinal cord syndrome with local back pain or radiculopathy. Spinal epidural hematoma. Nontraumatic, spontaneous spinal epidural hematomas occurring in the presence of anticoagulant therapy, arteriovenous malformations, or inherited or acquired bleeding disorders are a rare cause of spinal compression.

Intradural extramedullary tumor – Meningiomas and nerve sheath tumors can compress the spinal cord and produce radicular and myelopathic syndromes.

Extramedullary hematopoiesis – Spinal cord compression can rarely be induced by extramedullary hematopoiesis due to thalassemia or chronic myeloproliferative or myelodysplastic disorders.

Systemic inflammatory diseases – Rare cases of epidural involvement by rheumatoid arthritis, sarcoidosis, and tophaceous gout have been described

While you refresh your knowledge about cord compression (I have not included traumatic cord compression as physicians do not deal with those) and get prepared for the FCPS 2 exam I will read up and write important points of the GB Syndrome soon.

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I am a Professor of Medicine and a Nephrologist. Having served in the Army Medical College, Pakistan Army for 27 years I eventually became the Dean and Principal of the Bahria University Medical and Dental College Karachi from where I retired in 2016. My passion is teaching and mentoring young doctors. I am associated with the College of Physicians and Surgeons Pakistan as a Fellow and an examiner. I find that many young doctors make mistakes because they do not understand how they should answer questions; basically they do not understand why a question is being asked. My aim is to help them process the information they acquire as part of their education to answer questions, pass examinations and to best take care of patients without supervision of a consultant. Read my blog, interact and ask questions so that I can help you more.

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