Spine Health & Spinal Hygiene

Cauda equina syndrome is an emergency that needs to be treated as soon as possible. It is a form of spinal nerve compression, but if left untreated, it can lead to permanent paralysis of one or both legs and permanent loss of bowel/bladder control. Lower back pain after sitting for too long or improperly lifting something heavy happens to most if not all of us.

However, sometimes pain in the lower back can be an indicator of something more serious. Especially, for individuals that are dealing with or managing back pain. One condition is cauda equina syndrome. It’s not like sciatica or arthritis, but it does have specific symptoms that individuals should be aware of.

Cauda Equina Syndrome

The term comes from Latin that means horse’s tail. The cauda equina forms the group of nerves that run through the lumbar spinal canal. Generally, the condition means two things:

• There is nerve compression of most of the lumbar spinal canal
• Compression symptoms like numbness or weakness in the leg/s

How cauda equina syndrome differs from typical compression of the lumbar spinal canal is that it can be caused by different issues, from fractures, tumors, and infections. More commonly, it is disc herniations that cause the problems. The key difference is the degree of nerve compression, and the number of nerves compressed.

For example, compression of a single nerve will not cause loss of bladder function. But compression of multiple nerves, especially the sacral nerves can cause loss of function. Nerve compression that leads to pain or numbness can be treated differently. Surgery is reserved for severe cases and for individuals that are not improving with non-invasive treatment.

Sneaky Presentation

One of the major factors is long-term compression that individuals do not realize they have. Individuals are more likely to be aware of symptoms from another spinal condition before cauda equina syndrome presents. However, the condition presents quickly but often other overlapping back problems mask cauda equina syndrome.

Causes

The syndrome can be brought on from anything that compresses the nerves. Most commonly, it is a root compression from degenerative processes, specifically lumbar disc herniations. Other causes include:

• Bleeding like an epidural hematoma
• Trauma like fractures or penetrating trauma
• Tumors growing in the canal or the collapse of a tumor-affected bone
• Disc herniations can progressively grow in size, which leads to a slowly-evolving cauda equina syndrome.
• An enlarging disc herniation or synovial cyst can further compromise the already compressed nerves.
• Overgrowth of arthritic joints or bone spurs into the spinal canal can lead to long-term compression.

Symptoms

The symptoms vary based on the degree that the spinal canal has been affected:

• Back pain
• Leg pain
• Sciatica
• Saddle numbness that extends into other areas of the legs
• Neurogenic bladder dysfunction. This can range from difficulty starting to urinate or limited and/or non-voluntary control urinating.
• Bowel dysfunction
• Sexual dysfunction

Diagnosis

A doctor will examine any significant changes in bladder, bowel, or leg function that are considered red flags prompting an early and complete assessment. A physician will ask for a complete/detailed history of the onset and progression of symptoms.

The second is a close physical examination which includes testing sensation and strength along with a rectal exam to assess voluntary contraction. Also checking the body's reflexes, assess walking gait and alignment. If most or all of the symptoms are presenting this will set in motion spinal imaging or an MRI. If the symptoms, exam, and imaging match, it will lead to an emergency admission to the hospital.

Body Composition Spotlight

Obesity and Osteoarthritis Connection

A variety of factors contribute to the development of osteoarthritis, including genetic factors and lifestyle choices. Research supports obesity is a significant risk factor in the development of osteoarthritis. It is pretty straightforward as body weight increases this equals increased load on the spine, and joints, especially the weight-bearing ones like the hips and knees. Increased pressure leads to early wearing, tearing, and eventual development of osteoarthritis. Added weight affects the body's biomechanics and gait patterns.

However, obesity has also been shown to be a risk factor even on the non-weight-bearing joints. This is based on adipose tissue, which is more than just insulation. Adipose tissue is metabolically active and is involved in the secreting adipokines and cytokines which promote an inflammatory response. Pro-inflammatory adipokines and cytokines can have detrimental effects on joint tissue including damage to cartilage, synovial joints, and subchondral bone. The effect of inflammation on the joints in the body can contribute to the development of osteoarthritis.

Dr. Alex Jimenez’s Blog Post Disclaimer

The scope of our information is limited to chiropractic, musculoskeletal, physical medicines, wellness, and sensitive health issues and/or functional medicine articles, topics, and discussions. We use functional health & wellness protocols to treat and support care for injuries or disorders of the musculoskeletal system. Our posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate and support directly or indirectly our clinical scope of practice.*

Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. We understand that we cover matters that require an additional explanation as to how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900. The provider(s) Licensed in Texas& New Mexico*

References

Causes of Cauda Equina: Neurosurgical Focus. (June 2004) “Spinal epidural hematoma causing acute cauda equina syndrome” https://pubmed.ncbi.nlm.nih.gov/15202871/

Arriving at a Diagnosis: British Journal of Neurosurgery. (August 2010) “Reliability of clinical assessment in diagnosing cauda equina syndrome” https://www.tandfonline.com/doi/abs/10.3109/02688697.2010.505987

After a neurological exam, physical exam, patient history, x-rays and any previous screening tests, a doctor may order one or more of the following diagnostic tests to determine the root of a possible/suspected neurological disorder or injury. These diagnostics generally involve neuroradiology, which uses small amounts of radioactive material to study organ function and structure and ordiagnostic imaging, which use magnets and electrical charges to study organ function.

Neurological Studies

Neuroradiology

• MRI
• MRA
• MRS
• fMRI
• CT scans
• Myelograms
• PET scans
• Many others

Magnetic Resonance Imaging (MRI)

Shows organs or soft tissue well

• No ionizing radiation

Variations on MRI

• Magnetic resonance angiography (MRA)
• Evaluate blood flow through arteries
• Detect intracranial aneurysms and vascular malformations

Magnetic resonance spectroscopy (MRS)

• Assess chemical abnormalities in HIV, stroke, head injury, coma, Alzheimer's disease, tumors, and multiple sclerosis

Functional magnetic resonance imaging (fMRI)

• Determine the specific location of the brain where activity occurs

Computed Tomography (CT or CAT Scan)

• Uses a combination of X-rays and computer technology to produce horizontal, or axial, images
• Shows bones especially well
• Used when assessment of the brain needed quickly such as in suspected bleeds and fractures

Myelogram

Contrast dye combined with CT or Xray

Most useful in assessing spinal cord

• Stenosis
• Tumors
• Nerve root injury

Positron Emission Tomography (PET Scan)

Radiotracer is used to evaluate the metabolism of tissue to detect biochemical changes earlier than other study types

Used to assess

• Alzheimer's disease
• Parkinson's disease
• Huntington's disease
• Epilepsy
• Cerebrovascular accident

Electrodiagnostic Studies

• Electromyography (EMG)
• Nerve Conduction Velocity (NCV) Studies
• Evoked Potential Studies

Electromyography (EMG)

Detection of signals arising from the depolarization of skeletal muscle

May be measured via:

• Skin surface electrodes
• Not used for diagnostic purposes, more for rehab and biofeedback

Needles placed directly within the muscle

• Common for clinical/diagnostic EMG

Diagnostic Needle EMG

Recorded depolarizations may be:

• Spontaneous
• Insertional activity
• Result of voluntary muscle contraction

Muscles should be electrically silent at rest, except at the motor end-plate

• Practitioner must avoid insertion in motor end-plate

At least 10 different points in the muscle are measured for proper interpretation

Procedure

Needle is inserted into the muscle

• Insertional activity recorded
• Electrical silence recorded
• Voluntary muscle contraction recorded
• Electrical silence recorded
• Maximal contraction effort recorded

Samples Collected

Muscles

• Innervated by the same nerve but different nerve roots
• Innervated by the same nerve root but different nerves
• Different locations along the course of the nerves

Helps to distinguish the level of the lesion

Motor Unit Potential (MUP)

Amplitude

• Density of the muscle fibers attached to that one motor neuron
• Proximity of the MUP

Recruitment pattern can also be assessed

• Delayed recruitment can indicated loss of motor units within the muscle
• Early recruitment is seen in myopathy, where the MUPs tend to be of low amplitude short duration

Polyphasic MUPS

• Increased amplitude and duration can be the result of reinnervation after chronic denervation

Complete Potential Blocks

• Demyelination of multiple segments in a row can result in a complete block of nerve conduction and therefore no resulting MUP reading, however generally changes in MUPs are only seen with damage to the axons, not the myelin
• Damage to the central nervous system above the level of the motor neuron (such as by cervical spinal cord trauma or stroke) can result in complete paralysis little abnormality on needle EMG

Denervated Muscle Fibers

Detected as abnormal electrical signals

• Increased insertional activity will be read in the first couple of weeks, as it becomes more mechanically irritable

As muscle fibers become more chemically sensitive they will begin to produce spontaneous depolarization activity

• Fibrillation potentials

Fibrillation Potentials

• DO NOT occur in normal muscle fibers
• Fibrillations cannot be seen with the naked eye but are detectable on EMG
• Often caused by nerve disease, but can be produced by severe muscle diseases if there is damage to the motor axons

Positive Sharp Waves

• DO NOT occur in normally functioning fibers
• Spontaneous depolarization due to increased resting membrane potential

Abnormal Findings

• Findings of fibrillations and positive sharp waves are the most reliable indicator of damage to motor axons to the muscle after one week up to 12 months after the damage
• Often termed “acute” in reports, despite possibly being visible months after onset
• Will disappear if there is complete degeneration or denervation of nerve fibers

Nerve Conduction Velocity (NCV) Studies

Motor

• Measures compound muscle action potentials (CMAP)

Sensory

• Measures sensory nerve action potentials (SNAP)

Nerve Conduction Studies

• Velocity (Speed)
• Terminal latency
• Amplitude
• Tables of normal, adjusted for age, height and other factors are available for practitioners to make comparison

Terminal Latency

• Time between stimulus and the appearance of a response
• Distal entrapment neuropathies
• Increased terminal latency along a specific nerve pathway

Velocity

Calculated based on latency and variables such as distance

Dependent on diameter of axon

Also dependent on thickness of myelin sheath

• Focal neuropathies thin myelin sheaths, slowing conduction velocity
• Conditions such as Charcot Marie Tooth Disease or Guillian Barre Syndrome damage myelin in large diameter, fast conducting fibers

Amplitude

• Axonal health
• Toxic neuropathies
• CMAP and SNAP amplitude affected

Diabetic Neuropathy

Most common neuropathy

• Distal, symmetric
• Demyelination and axonal damage therefore speed and amplitude of conduction are both affected

Evoked Potential Studies

Somatosensory evoked potentials (SSEPs)

• Used to test sensory nerves in the limbs

Visual evoked potentials (VEPs)

• Used to test sensory nerves of the visual system

Brainstem auditory evoked potentials (AEPs)

• Used to test sensory nerves of the auditory system

Potentials recorded via low-impedance surface electrodes

Recordings averaged after repeated exposure to sensory stimulus

• Eliminates background “noise”
• Refines results since potentials are small and difficult to detect apart from normal activity
• According to Dr. Swenson, in the case of SSEPs, at least 256 stimuli are usually needed in order to obtain reliable, reproducible responses

Somatosensory Evoked Potentials (SSEPs)

Sensation from muscles

• Touch and pressure receptors in the skin and deeper tissues

Little if any pain contribution

• Limits ability to use testing for pain disorders

Velocity and/or amplitude changes can indicate pathology

• Only large changes are significant since SSEPs are normally highly variable

Useful for intraoperative monitoring and to assess the prognosis of patients suffering severe anoxic brain injury

• Not useful in assessing radiculopathy as individual nerve roots cannot be easily identified

Late Potentials

Occur more than 10-20 milliseconds after stimulation of motor nerves

Two types

• H-Reflex
• F-Response

H-Reflex

Named for Dr. Hoffman

• First described this reflex in 1918

Electrodiagnostic manifestation of myotatic stretch reflex

• Motor response recorded after electrical or physical stretch stimulation of the associated muscle

Only clinically useful in assessing S1 radiculopathy, as the reflex from the tibial nerve to triceps surae can be assessed for velocity and amplitude

• More quantifiable that Achilles reflex testing
• Fails to return with after damage and therefore not as clinically useful in recurrent radiculopathy cases

F-Response

So named because it was first recorded in the foot

Occurs 25 -55 milliseconds after initial stimulus

Due to antidromic depolarization of the motor nerve, resulting in a orthodromic electrical signal

• Not a true reflex
• Results in a small muscle contraction
• Amplitude can be highly variable, so not as important as velocity
• Reduced velocity indicates slowed conduction

Useful in assessing proximal nerve pathology

• Radiculopathy
• Guillian Barre Syndrome
• Chronic Inflammatory Demyelinating Polyradiculopathy (CIDP)

Useful in assessing demyelinative peripheral neuropathies

Sources

1. Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
2. Day, Jo Ann. “Neuroradiology | Johns Hopkins Radiology.” Johns Hopkins Medicine Health Library, 13 Oct. 2016, www.hopkinsmedicine.org/radiology/specialties/ne uroradiology/index.html.
3. Swenson, Rand. Electrodiagnosis.

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