Spine Health & Spinal Hygiene

"Various problems with the sacrum make up or contribute to a significant portion of lower back problems. Can understanding the anatomy and function help prevent and treat back injuries?"

The Sacrum

The sacrum is a bone shaped like an upside-down triangle located at the base of the spine that helps support the upper body when sitting or standing and provides pelvic girdle flexibility during childbirth. It comprises five vertebrae that fuse during adulthood and connect to the pelvis. This bone takes and endures all of the body's pressure and stress from everyday activities and movements.

Formation

Humans are born with four to six sacral vertebrae. However, fusion does not take place in all sacral vertebrae simultaneously:

• Fusion starts with the S1 and S2.
• As the individual gets older, the overall shape of the sacrum begins to solidify, and the vertebrae fuse into a single structure.
• The process usually starts in the mid-teens and finishes in the early to mid-twenties.
• It is believed to start earlier in females than males.

The timing of the fusion can be used for estimating the age and sex of skeletal remains. (Laura Tobias Gruss, Daniel Schmitt. et al., 2015)

1. The sacrum in a female is wider and shorter and has a more curved top or the pelvic inlet.
2. The male sacrum is longer, narrower, and flatter.

Structure

The sacrum is an irregular bone that makes up the back/posterior third of the pelvic girdle.  There is a ridge across the front/anterior portion of the S1 vertebra known as the sacral promontory. Small holes/foramen on both sides of the sacrum are left over after the vertebrae fuse together. Depending on the number of vertebrae, there can be three to five foramen on each side, though there are usually four. (E. Nastoulis, et al., 2019)

1. Each anterior foramen is typically wider than the posterior or dorsal/backside foramen.
2. Each sacral foramina/plural of foramen provides a channel for the sacral nerves and blood vessels.

• Small ridges develop between each of the fused vertebrae, known as transverse ridges or lines.
• The top of the sacrum is called the base and is connected to the largest and lowest of the lumbar vertebrae - L5.
• The bottom is connected to the tailbone/coccyx, the apex.
• The sacral canal is hollow, runs from the base to the apex, and serves as a channel at the end of the spinal cord.
• The sides of the sacrum connect to the right and left hip/iliac bones. The attachment point is the auricular surface.
• Right behind the auricular surface is the sacral tuberosity, which serves as an attachment area for the ligaments that hold the pelvic girdle together.

Location

The sacrum is at the level of the lower back, just above the intergluteal cleft or where the buttocks split. The cleft starts at around the level of the tailbone or coccyx. The sacrum is curved forward and ends at the coccyx, with the curvature being more pronounced in females than males. It connects to the L5 lumbar vertebra by way of the lumbosacral joint. The disc between these two vertebrae is a common source of low back pain.

1. On either side of the lumbosacral joint are wing-like structures known as the sacral ala, which connect to the iliac bones and form the top of the sacroiliac joint.
2. These wings provide stability and strength for walking and standing.

Anatomical Variations

The most common anatomical variation applies to the number of vertebrae. The most common is five, but anomalies have been documented, including individuals with four or six sacral vertebrae. (E. Nastoulis, et al., 2019)

• Other variations involve the sacrum's surface and curvature, where the curvature differs widely between individuals.
• In some cases, the first and second vertebrae do not fuse and remain separately articulated.
• Failure of the canal to completely close during formation is a condition known as spina bifida.

Function

Studies on the sacrum are ongoing, but some proven functions include:

• It serves as an anchor point for the spinal column to attach to the pelvis.
• It provides stability for the body's core.
• It acts as a platform for the spinal column to rest on when sitting.
• It facilitates childbirth, providing pelvic girdle flexibility.
• It supports upper body weight when sitting or standing.
• It provides extra stability for walking, balance, and mobility.

Conditions

The sacrum can be a main source or focal point for lower back pain. It is estimated that 28% of men and 31.6% of women aged 18 years or older have experienced low back pain in the past three months. (Centers for Disease Control and Prevention. 2020) Conditions that can cause sacrum pain symptoms include.

Sacroiliitis

• This is a common condition of sacroiliac/SI joint inflammation.
• A doctor only makes the diagnosis when all other possible causes of pain have been ruled out, known as a diagnosis of exclusion.
• Sacroiliac joint dysfunction is thought to account for between 15% and 30% of low back pain cases. (Guilherme Barros, Lynn McGrath, Mikhail Gelfenbeyn. 2019)

Chordoma

• This is a type of primary bone cancer.
• About half of all chordomas form in the sacrum, but the tumors can also develop elsewhere in the vertebral column or at the base of the skull. (National Library of Medicine. 2015)

Spina Bifida

• Individuals can be born with conditions that affect the sacrum.
• Spina bifida is a congenital condition that can arise from the malformation of the sacral canal.

Unlocking the Secrets of Inflammation

General Disclaimer *

The information herein is not intended to replace a one-on-one relationship with a qualified healthcare professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional. Our information scope is limited to chiropractic, musculoskeletal, physical medicines, wellness, sensitive health issues, functional medicine articles, topics, and discussions. We provide and present clinical collaboration with specialists from various disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system. Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and directly or indirectly support our clinical scope of practice.* Our office has reasonably attempted to provide supportive citations and identified the relevant research studies or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.

We understand that we cover matters that require an additional explanation of how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, don't hesitate to get in touch with Dr. Alex Jimenez or contact us at 915-850-0900.

Dr. Alex Jimenez DC, MSACP, CCST, IFMCP*, CIFM*, ATN*

email: coach@elpasofunctionalmedicine.com

Licensed in: Texas & New Mexico*

References

Neurophysiology: There are two ways that nociceptive information reaches the central nervous system. One is the neospinothalamic tract for quick pain and two is the paleospinothalamic tract for slow pain that increases.

Neurophysiology Of Pain Part II

Intensity, Location & Quality of Pain...

... involve Spinothalamic and Trigeminal Pathways

• The trigeminal pathway brings information from the face area.
• The spinothalamic pathway brings information from the rest of the body.
• Both these pathways project to the sensory cortex, which also receives information on innocuous stimuli such as touch, pressure and warmth via a separate pathway.

2 Pain Transmission Pathways For Location Intensity Quality

Neuroscience Purves et al.

• Spinothalamic pathway
• (Anterolateral Pathway)
• Trigeminal pathway

Unpleasant Quality & Autonomic Affective Motivational Pathway For Pain

Brain Areas Involved In Processing Of Nociceptive Signals

The Anterior Cingulate & Insula Cortex Are Activated In Human Subjects

... in connection with an intense burning sensation following hand contact with the thermal grill.

Adapted from Craig et al. 1994, 1996. From Principles of Neural Science, Kandell et al.

Control Of Pain Perception

• There is difference between the objective and subjective aspects of injury and pain.
• Despite similar injury, people can differ in how much pain they feel.
• Depending on the context, pain may not be felt despite injury, e.g. battlefield injury, during intense sports.
• This suggests that there is a physiological mechanism that controls the transmission of nociceptive signals to the brain or modifies the interpretation of pain.
• The pain control system can also explain the placebo effect.

Pain Modulation Pathway

• Nerve signals are sent form the somatic sensory cortex and hypothalamus to the periaqueductal gray matter (PAG).
• PAG sends signals to the parabrachial nucleus, medullary reticular formation, locus coeruleus, and Raphe neulei.
• These in turn can control the in the transmission of nociceptive signals from the spinal cord to the brain.
• This involves different involves different neurotransmitters.

Endogenous Opioids

Internally produced molecules with opioid-like action which regulate transmission of nociceptive signals.

Three classes of these molecules have been identified. All are peptide molecules

1. Enkephalins
2. Endorphins
3. Dynorphins

Despite these being powerful, endogenous modifiers of nociceptive signals, it has been difficult to produce and administer them in a way than can used in clinical practice.

Location Of Nerve Cells With Endogenous Opioid Receptors

• Spinal cord, Medulla, Periaqueductal gray matter (PAG)
• In the spinal cord, endogenous opioids can prevent transmission between 1st order nerve cells (bringing signals from the periphery) and 2nd order spinal nerve cells that transmit the signals to the brain.
• Also can prevent the increased synaptic efficiency, which plays a role in hyperalgesia.

(Center for Brain Research, Uni Vienna)

Modulation Of Pain Signal Transmission In The Spinal Cord

Connections in the spinal cord where opiates act.

Neurotransmitters – serotonin (5- HT) and norephinephrine (noradrenaline) – in the spinal cord can block transmission of pain signals to the brain.

Inflammatory Soup - Hyperalgesia

• Tissue damage results in the release of a number of chemicals.
• These increase nociceptors’ response to a stimulus (=hyperalgesia) & produce inflammation.
• Hyperalgesia = when the magnitude of the response to a nociceptive stimulus is higher than normal.

Julius-D & Basbaum-AI, Nature 2001;413:203

Clinical Application

• Knowing the molecules involved in the “inflammatory soup” and how they are synthesized provides possible targets for pain reduction.
• e.g. prostaglandins are produced by the COX enzyme. The activity of this enzyme is blocked by non-steroidal anti- inflammatory drugs (NSAIDs) such as ibuprofen, diclofenac.

Allodynia

• A condition when normally non- painful stimuli cause pain, e.g., touch, light pressure, cold.
• Involves changes in the synaptic sensitivity of the nociceptive neurons in the spinal cord (central sensitization).
• Drugs such as ketamine, block NMDA receptors and so reduce transmisison of the nociceptive stimuli.

Gate Control Theory of Pain

• Mother says to child, “Come I will rub the area which is painful and this will make it feel better.”
• After stubbing a toe, we instinctively rub the area; this reduces the sensation of pain.
• Ronald Melzack and Patrick Wall in 1962 provided an possible explanation for this effect.

Ascending Tracts | Pain Modulation: Gate Control Theory

Gate Theory

Rubbing the area that hurts stimulates receptors of innocuous stimuli like touch, pressure and vibration.

These mechano-receptors send signals along the Aβ nerve fibers that:

(1) stimulate spinal nerves (inhibitory inter-neurons) that in turn inhibit signaling in the 2nd order neurons (projection neuron) and (2) directly inhibit the 2nd order neuron to reduce or stop pain signal from being sent to the brain

http://wikidoc.org/images/f/fe/Gate_control_A_firing.png

Clinical Application

Transcutaneous Nerve Stimulation (TENS) is based on the Gate Control Theory. Nerves of the innocuous sensory system are stimulated and they in turn, inhibit transmission of nociceptive stimuli in the spinal cord.

Abnormalities Of Pain System

Phantom Pain

• Patients with amputation often have burning or tingling pain in the body part removed.
• One possible cause is that nerve fibers at the stump are stimulated and the brain interprets the signals as originating in the amputated portion.
• The other is the rearrangement within the cortical areas so that area say for the hand now responds to signals from other parts of the body but still interprets them as coming for the amputated hand.

Peripheral Sensitization

• Peripheral sensitization represents a reduction in the threshold and/or an increase in magnitude of responsiveness at the peripheral ends of sensory nerve fibers.
• This occurs in response to chemical mediators released by nociceptors and non-neuronal cells (e.g. mast cells, basophils, platelets, macrophages, neutrophils, endothelial cells, keratinocytes and fibroblasts) at the site of tissue injury or inflammation.
• Basically, it is an increased sensitivity to an afferent nerve stimuli.

Central Sensitization

Peripheral & Central Sensitisation

• A condition of the nervous sytem that is associated with the development and maintenance of chronic pain.
• Known as “wind-up” or persistent high reactivity.
• “Plastiticity in pain pathways” or the persistence of pain even after an injury has healed.
• Is this negative or positive plasticity?

Central Sensitization & C Fibers

Two Main Characteristics Of Central Sensitization:

– Allodynia – occurs when a person experiences pain with things that are normally not painful, ie, soft touch causes pain.

– Hyperalgesia – occurs when a stimulus that is typically painful is perceived as more painful that it should be, ie, a simple bump.

Both are due to hyperreactivity of the nervous system.

Somatosensory Cortex Organization

Cortical Reorganization

Neuroscience. 2nd edition. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Fig 25.14

Referred Pain

• Often originates from a visceral organ.
• May be felt in a part of the body remote from the site of the pathology.
• The mechanisms may be spinal convergence of visceral and somatic afferent fibers on spinothalamic neurons.
• Common manifestations: cutaneous and deep hyperalgesia, tenderness, muscular contractions.

Pain Sensation Referred From Visceral Organs ...

... to another part of the body surface 

Pain Hypersensitivity Mechanisms At A Glance

Physicians, neurologists, and other healthcare professionals may often run a cranial nerve examination as part of a neurological evaluation to analyze the operation of the cranial nerves. This involves a highly formalized series of tests that evaluate the status of each cranial nerve. A cranial nerve test begins with observation of the patient partly due to the fact that cranial nerve lesions may ultimately affect the symmetry of the face or eyes, among other signs and symptoms.

The visual fields for neural lesions or nystagmus are tested via an evaluation of particular eye movements. The sensation of the face is tested by asking patients to execute different facial movements, like puffing out their cheeks. Hearing is tested through voice and tuning forks. The position of the individual’s uvula is also examined because asymmetry in its placement could indicate a lesion of the glossopharyngeal nerve. After the capability of the individual to use their shoulder to test the accessory nerve (XI), the patient’s tongue operation is generally assessed by detecting various tongue movements.

Ankylosing spondylitis, or AS, is a type of inflammatory arthritis that usually impacts the spine, causing back stiffness and pain, pain in the hips, and decreased range of motion. Brain fog can also be a symptom of AS and other chronic inflammatory conditions. Brain fog can affect memory, concentration, decision-making, learning, and problem-solving. Injury Medical Chiropractic and Functional Medicine Clinic can educate on the causes of ankylosing spondylitis brain fog and how to reduce its effects.

Brain Fog

Experts do not fully understand how conditions like AS cause brain fog and how it affects the brain and central nervous system. However, they believe brain fog is linked to chronic inflammation and pain associated with the condition, along with certain factors.

Chronic Inflammation

• Inflammation occurs when the body's immune system attacks healthy cells.
• This triggers the release of inflammation-causing cytokines.
• Cytokines can interfere with normal brain function.

Ankylosing Spondylitis Chronic Pain 

• Chronic pain can cause fatigue and unhealthy sleep quality.
• Fatigue and poor sleep can worsen chronic pain, leading to intense fatigue and extreme sleep issues, becoming a vicious cycle.

Corticosteroids

• Doctors typically treat ankylosing spondylitis with corticosteroids.
• Individuals with cardiovascular risk factors have an increased risk of brain fog from the medications.

Depression

• Individuals with AS can present symptoms of depression, which has been linked to cognitive impairment.
• Depression can contribute to the development of brain fog.

Other Medical Conditions

• Thyroid Imbalances
• Fibromyalgia
• Lupus
• Sjogren's
• Chronic Fatigue Syndrome
• Anemia
• Encephalitis
• Multiple sclerosis

Other Possible Causes

• Stress
• Sleep problems
• Little to no physical activity or exercise.
• Pregnancy
• Menopause
• Antidepressants
• Chemotherapy

Effects

The effects of brain fog.

• Thoughts are blurry and difficult to recall.
• There are major lapses in concentration.
• Thinking is harder.
• There is constant confusion.
• More effort is required to maintain thoughts in short-term memory.
• Constantly forgetting what to do.

Chiropractic Care

Doctors recommend a multidisciplinary approach to manage AS brain fog. This includes:

• An anti-inflammatory nutrition plan.
• Ergonomic adjustments
• Regular physical activity and exercise.
• Mental exercises
• Concurrent treatment with a rheumatologist in combination with chiropractic care.
• Chiropractic care focuses on improving joint mobility and the function of the musculoskeletal system.
• Manual and instrument-assisted adjustments are paired with the following:
• Soft-tissue therapies
• Non-surgical spinal decompression
• Health Coaching
• Fitness Coaching
• Nutritional recommendations

Brain Cognition

General Disclaimer *

The information herein is not intended to replace a one-on-one relationship with a qualified healthcare professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional. Our information scope is limited to chiropractic, musculoskeletal, physical medicines, wellness, sensitive health issues, functional medicine articles, topics, and discussions. We provide and present clinical collaboration with specialists from a wide array of disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system. Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and directly or indirectly support our clinical scope of practice.* Our office has reasonably attempted to provide supportive citations and identified the relevant research study or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.

We understand that we cover matters that require an additional explanation of 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.

Dr. Alex Jimenez DC, MSACP, CCST, IFMCP*, CIFM*, ATN*

email: coach@elpasofunctionalmedicine.com

Licensed in: Texas & New Mexico*

References

Chiropractic. (2019). nccih.nih.gov/health/chiropractic

Cornelson, Stacey M et al. “Chiropractic Care in the Management of Inactive Ankylosing Spondylitis: A Case Series.” Journal of chiropractic medicine vol. 16,4 (2017): 300-307. doi:10.1016/j.jcm.2017.10.002

Creaky Joints. (September 17, 2018) “You can ease inflammatory arthritis brain fog with these 12 tips for a sharper mind.” https://creakyjoints.org/living-with-arthritis/arthritis-brain-fog/

Vitturi, Bruno Kusznir, et al. “Cognitive Impairment in Patients with Ankylosing Spondylitis.” The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques vol. 47,2 (2020): 219-225. doi:10.1017/cjn.2020.14

Zhang, Jun-Ming, and Jianxiong An. “Cytokines, inflammation, and pain.” International anesthesiology clinics vol. 45,2 (2007): 27-37. doi:10.1097/AIA.0b013e318034194e

Neurophysiology of pain: Pain defined is the unpleasant sensation that accompanies injury or near injury to tissues, though it can also occur in the absence of such damage if the nociception system is not functioning. Nociception means the system that carries pain signals of injury from the tissues. This is the physiological incident that comes with pain.

Neurophysiology Of Pain

Objectives

• Basics of the nervous system
• Synaptic function
• Nerve impulses
• Transduction of peripheral painful stimuli
• Central pathways
• Central Sensitization
• PeripheralSensitization
• Control or modulation of pain signals
• Pathophysiology of pain signaling pathway

Definition Of Pain

"Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage".

(The International Association for the Study of Pain)

The Nervous System

• It is important to know the basic structure of the nervous system.
• This will help in:
  – Understanding the mechanism by which nociceptive signals are produced.
  – Know the different regions of the nervous system involved in processing these signals.
  – Learn how the different medications and treatment for pain management work.

Nervous System

Central nervous system (CNS)

• Brain and Spinal Cord

Peripheral Nervous System (PNS)

• Nerve fibers go to all parts of the body.
• Send signals to the different tissues and send signals back to the CNS. 

Nerve Cells

• The nervous system is made up of nerve cells which send long processes (axons) to make contact with other cells.

Nerve Cell-To-Nerve Cell Communication

Nerve cells communicate with other cells by releasing a chemical from the nerve endings – Neurotransmitters

Basic Steps In Synaptic Transmission

Synaptic Transmission

Steps in the passage of signal from one nerve cell to other.

• Drugs are used to block the transmission of signals from one nerve cell to other.

These drugs can effect:

1. Ca2+ ion channel to prevent Ca2+ inflow which is essential for neurotransmitter (NT) release, e.g., the action of gabapentin.
2. Release of NT.
3. Prevent NT from binding to its receptor so stop further transmission of the signal.

Electrical Impulse

• Signals move along a nerve process (axon) as a wave of membrane depolarization called the Action Potential.
• The inside of all nerve cells has a negative electrical potential of around – 60 mV.
• When stimulated this negative electrical potential becomes positive and then negative again in milliseconds.
• The action potential moves along the nerve process (axon) to the nerve ending where it cause release of NT.

Action Potential

• When there is no stimulation the membrane potential is at its Resting Potential.
• When stimulated, channels in the nerve membrane open allowing the flow of sodium ions (Na+) or calcium ions (Ca2+) into the nerve or cell. This makes the inside less negative and in fact positive -the peak of the action potential (+40 mV).
• These channels than close and by the opening of K+ channels the membrane potential returns to its resting level.

Stopping Action Potentials To Stop Nociceptive Stimuli

• Nociceptive stimuli are those that will create a sensation of pain after they are processed in the CNS.
• Nociceptive signals can be prevented from reaching the CNS by blocking the action of the channels that control the movement of ions across the nerve membrane.
• A number of anesthetic agents stop Na+ channel from working and hence stop the generation of actions potentials and transmission of signals to the CNS.

Sensory Systems

The sensory system that can be divided into two divisions:

• A Sensory System that transmits innocuous stimuli such as touch, pressure, warmth.
• A System that transmits stimuli that indicate that tissues have been damaged = nociceptive .

These two systems have different receptors and pathways in the PNS & CNS

Skin Receptors 

Neuroscience. 2nd edition. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001.

Nociceptors

• Nociceptors are free nerve endings that respond to stimuli that can cause tissue damage or when tissue damage has taken place.
• Present in membrane of free nerve endings are receptors (protein molecules) whose activity changes in the presence of painful stimuli.
• (Note the use of the same term receptor is used for cell or organs or molecules that involved in transduction of a stimuli.)

Transduction

• Transduction is the process of converting the stimuli into a nerve impulse.
• For this to occur the flow of ions across the nerve membrane has to change to allow entry of either Na+ or Ca2+ ions to cause depolarization of the membrane potential.
• This involves a receptor molecule that either directly or indirectly opens the ion channels.

Chemical Agents...

... which can cause the membrane potential at the free nerve ending (nociceptor) to produce an action potential.

Fields HL. 1987. Pain. New York: McGraw-Hill.

Summary Of Transduction Process At The Periphery

TRP Channels

• Many stimuli – mechanical, chemical and thermal – give rise to painful sensation making transduction a complex process.
• Recently receptor molecules have been identified – Transient Receptor Potential (TRP) channels – that respond to a number of strong stimuli.
• TRP receptors are also involved in transmitting the burning sensation of chili pepper.
• In time, drugs that act on these receptors will be developed to control pain.

Different TRP Channels 

• Capsasin, the active ingredient in chili pepper, is used in patches for relief of pain.
• Menthol and peppermint gels are used to relieve muscle pain.

Motor Output & Sensory Input To Spinal Cord 

• Sensory nerves have their cell body outside the spinal cord in the dorsal root ganglia ( = 1st order neurons).
• One process goes to the periphery, the other goes to the spinal cord where it makes synaptic contact with nerve cells in the spinal cord ( = 2nd order neurons).
• The 2nd order neuron sends processes to other nerve cells in the spinal cord and to the brain.

2nd Order Nerve Cells Send Nerve Fibers In The Spinal Cord White Matter

Transmission Of Nociceptive Signals From The Periphery To The Brain

A Delta (δ) & C Nerve Fibers

Nerve fibers are classified according to the:

– (1) diameter of the nerve fiber and
– (2) whether myelinated or not.

• Aδ and C nerve fiber endings respond to strong stimuli.
• Aδ are myelinated and C are not.
• Action potentials are transmitted 10 times faster in the Aδ
  (20 m/sec) fibers than in C fibers (2 m/sec).

Aδ & C fibers

• Aδ fibers respond mainly to mechanical and mechno-thermal stimuli.
• C fibers are polymodal, i.e. the nerve ending responds to several modalities – thermal, mechanical and chemical
• This polymodal ability is due to the presence of different receptor molecules in a single nerve ending.

Fast & Slow Pain 

• Most people when they are hit by an object or scrape their skin, feel a sharp first pain (epicritic) followed by a second dull, aching, longer lasting pain (protopathic).
• The first fast pain is transmitted by the myelinated Aδ fibers and the second pain by the unmyelinated C fibers.

Central Pain Pathways

Nociceptive signals are sent to the spinal cord and then to different parts of the brain where sensation of pain is processed.

There are a pathways/regions for assessing the:

1. Location, intensity, and quality of the noxious stimuli
2. Unpleasantness and autonomic activation (fight-or-flight response, depression, anxiety).

Dr. Sletten Discussing Central Sensitization Syndrome (CSS)

Ataxia is a degenerative disease of the nervous system. Symptoms can mimic those of being inebriated/intoxicated, with  slurred speech, stumbling, falling, and unable to maintain coordination. This comes from degeneration of the cerebellum, which is the part of the brain responsible for coordinating movement. It is a disease that affects people of all ages. However, age of symptom onset can vary, from childhood to late adulthood. Complications from the disease can be serious, even debilitating and life shortening.

Symptoms can vary from person to person, as well as, the type of Ataxia. Symptom onset and progression can vary as well. Symptoms can worsen slowly, over decades or quickly, over a few months. The common symptoms are lack of coordination, slurred speech, trouble eating, swallowing, eye movement abnormalities, motor skill deterioration, difficulty walking, gait abnormalities, tremors, and heart problems. People with Ataxia usually require wheelchairs, walkers, and/or scooters to aid in mobility.

Ataxia

The Loss Of Full Control Of Bodily Movements, Especially Gait

History Of Ataxia

• How long has it been present?
• Slow onset ➔ Degenerative disease?
• Acute onset ➔ Stroke?
• When does it occur?
• If worsened by walking on uneven surfaces, or with limited vision ➔ Sensory ataxia?
• Are there any coexisting symptoms?
• Vertigo, weakness, stiffness, cognitive changes, etc.
• Have others noticed this gait disturbance?
• If no, consider psychogenic cause
• Is the gait change explainable by physical problems such as pain or weakness?
• Antalgic gait, limp, etc.

• Weakness

• Proximal muscle weakness ➔ Myopathy?
• Distal muscle weakness ➔ Neuropathy?
• UMN signs?
• LMN signs?
• Has the patient fallen? Or at risk for fall?
• Is ataxia limiting ADLs?

Balance

• Utilizes
• Vestibular system
• Cerebellar system
• Conscious proprioceptive information (joint position sense)
• Visual information
• Motor strength and coordination

Vestibular System

• Generally, if the problem lies in the vestibular system the patient will experience dizziness, possibly having vertigo or nystagmus
• Unable to walk a straight line
• When walking, will tend to veer to one side

Testing The Vestibular System

• Fukuda Stepping Test

• Patient marches in place with eyes closed and arms raised to 90 degrees in front of them
• If they rotate more than 30 degrees = positive
• Patient will rotate toward the side of vestibular dysfunction

• Rhomberg Test

• If patient sways a different direction every time their eyes are closed, this may indicate vestibular dysfunction

Cerebellar System

• Cerebellar gaits present with a wide-base and generally involve staggering and titubation
• Patient will have difficulty doing Rhomberg’s test with eyes open or closed, because they cannot stand with their feet together
• Afferent information helps make assessments about where the body is in space
• Ventral spinocerebellar tract
• Dorsal spinocerebellar tract
• Cuneocerebellar tract
• Olivocerebellar tract
• Efferent tracts carry responsive information to make adjustments to muscle tone and position to maintain balance

Testing The Cerebellar System

• Piano-playing test & hand-patting test

• Both assess for dysdiadochokinesia
• Both tests, patient will have more difficulty moving the limb on the side of cerebellar dysfunction

• Finger-to-nose test

• Patient may be hyper/hypo metric in movement
• Intention tremor may be reveled

Joint Position Sense

• Conscious proprioception may be diminished, especially in elderly patients and patients with neuropathy

Visual Information

• Patients with joint position sense losses often rely on visual information to help compensate.
• When visual input is removed or diminished these patient’s have exaggerated ataxia.

Motor Strength & Coordination

• If patient has reduced frontal lobe control they may end up with an apraxia of gait, where they have difficult with the volitional control of movement
• Extrapyramidal disorders such as Parkinson disease result in inability to control motor coordination
• Pelvic girdle muscle weakness due to a myopathy will produce an abnormal gait pattern

Commonly Seen Abnormal Gait Patterns

• Circumduction gait

• Hemiplegia
• Often due to stroke
• Bilaterally (Diplegic gait), causes toe walking
• Typical gait of cerebral palsy patients

• Festinating gait

• Small steps due to spasticity
• Often seen in Parkinson Disease

• Myopathicgait(waddling)

• Seen in disorders of proximal muscle weakness

• Steppage gait/Neuropathic gait

• Leg is lifted from the hip, without dorsiflexion at the ankle
• Often seen in patients with foot-drop due to a LMN lesion
• Wide-BasedCerebellargait

Gait Deviation/Examination Videos

Gait Deviations 2012

Gait Examination (Stanford Medicine 25) 

Dizziness

The Sensation Of Loss Of Balance

• 4 Main Types

• Vertigo
• Peripheral
• Central
• Pre-Syncope/Light-headedness
• Disequilibrium
• Other/Floating type

Peripheral Vertigo

• More common than central vertigo
• Due to damage to the inner ear or CN VIII
• Usually produces abnormal eye movements
• Nystagmus – May be horizontal or rotary
• Usually jerky in nature, with a fast and slow phase
• Named for the direction of the fast phase
• Vertigo usually worsens when patient looks to the side of the fast phase of nystagmus
• Severity of nystagmus usually correlates with severity of vertigo
• No other symptoms/signs of CNS dysfunction
• Patient may have nausea or difficulty walking, but only because of vestibular dysfunction
• Patient may also have hearing loss or tinnitus due if CN VIII or auditory mechanism function is damaged
• Typically the causes are benign, including
• Benign paroxysmal positional vertigo (BPPV)
• Cervicogenic vertigo
• Acute labyrinthitis/Vestibular neuronitis
• Meniere’s Disease
• Perilymph fistula
• Acoustic Neuroma

Narrowing It Down

• If movement, particularly of the head/neck exacerbate vertigo, consider:
• BPPV
• Vertebrobasilar artery insufficiency
• Cervicogenic vertigo
• If noise brings on episodes, consider:
• Meniere’s disease
• Perilymph fistula

Vertigo Hx Questions

• Does your dizziness feel like you’re on an amusement park ride?
• Do you get nauseous when you’re dizzy?
• Are you spinning?
• Or is the world spinning?

Benign Paroxysmal Positional Vertigo (BPPV/BPV)

• May develop spontaneously, especially in the elderly
• May arise due to head trauma
• Vertiginous episodes associated with specific movements:
• Looking at a high shelf (“top-shelf vertigo”)
• Bending over
• Rolling over in bed
• Onset of vertigo begins a few seconds after the movement, and resolves within about a minute
• Diagnostic test
• Dix-Hallpike Maneuver
• Treatment procedure
• Epley Maneuver
• Brandt-Daroff Exercises
• Can self resolve as crystals dissolve, but it may take months and new otoliths can become displaced

Cervicogenic Vertigo

• Occurs after head/neck injuries, but is not very common
• Usually accompanied by pain and/or joint restriction
• Usually vertigo and nystagmus will be less severe than in BPPV
• Vertigo begins with change in head position but does not subside as quickly as it does in BPPV

Vertebrobasilar Artery Insufficiency

• Occurs if the vertebral artery is compressed during head rotation/extension
• Onset of vertigo is delayed more than in BPPV or cervigogenic vertigo, because ischemia will take up to 15 seconds to occur
• Orthopedic test may help in evaluation
• Barré-Liéou Sign
• DeKlyn Test/Hallpike Maneuver
• Hautant test
• Underberg Test
• Vertebrobasilar After Functional Maneuver

Acute Labyrinthitis/ Vestibular Neuronitis

• Not well understood, but believed to be inflammatory in origin
• Follows viral infection or arise seemingly without cause
• Single, monophasic attack of vertigo
• Resolves in days to a few weeks and generally does not reoccur

Meniere’s Disease

• Increased pressure in the endolymph causes membrane ruptures and sudden mixture of endolymph and perilymph
• Episodes last 30 minutes to several hours, until equilibrium between the fluids is reached
• Over time, episodes damage vestibular and cochlear hair cells
• Low-pitch buzzing tinnitus
• Loss of hearing of low tones

Meniere’s Disease vs. Syndrome

• Meniere’s syndrome is when then symptoms of Meniere’s disease are found to be secondary to another condition, such as:
• Hypothyroidism
• Acoustic neuroma
• Superior semicircular canal dehiscence (SCDS)
• Perilymph fistula
• True Meniere’s disease is idiopathic

Perilymph Fistula

• Small leak due to trauma, especially barotrauma
• Can look very similar symptomatically to Meniere’s disease/syndrome
• Exacerbated by changes in pressure
• Airplane rides
• Driving uphill
• Hennebert’s sign
• Vertigo or nystagmus episode brought on by sealing pressure of the ear (such as by inserting an otoscope)

Central Vertigo

• Less common than peripheral vertigo
• Caused by damage to the processing centers of vestibular information in the brain stem and the cerebral cortex
• Typically “dizziness” is less severe than with peripheral vertigo
• Nystagmus
• Usually more severe than the description/patient’s complaint
• May go in multiple directions, including vertical
• May or may not have other CNS findings on examination
• No change in hearing expected

Causes Include:

• Cerebrovascular disease (such as transient ischemic attacks)
• Multiple Sclerosis
• Arnold-Chiari Malformation
• Damage to caudal brainstem or vestibulocerebellum
• Migraine condition

Pre-Syncope Hx Qustions

• Does it feel like you’re going to pass out?
• Does the dizziness feel similar to when you stand up too fast?

Pre-Syncope

• “Light-headedness”
• CardiacOrigin
• Output disorders
• Arrhythmias
• Holter monitor testing
• Postural/Orthostatic hypotension
• May be secondary to other problems (diabetic neuropathy, adrenal hypofunction, Parkinsons, certain medications, etc.)
• Vasovagal episodes
• Slow heart rate with low blood pressure
• Often brought on by stress, anxiety or hyperventilation
• Migraine
• Due to cerebrovascular instability
• Blood sugar dysregulation

Disequilibrium Hx Questions

• Does the dizziness only occur when you’re on your feet?
• Does it get better if you touch/hold onto something?

Disequilibrium

• Common in the elderly
• Due to sensory deficits
• Gradual onset
• Worsened by reduced vision
• Dark
• Eyes closed
• Visual acuity losses
• Improved by touching a stationary object
• Subjective of dizziness often improves with a gait assistive device (cane, walker, etc.)

Other Causes

• Psychological stress
• Often patient will describe dizziness as “floating”
• Rule out hyperventilation and other types of dizziness

Sources

Blumenfeld, Hal. Neuroanatomy through Clinical Cases. Sinauer, 2002.
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.