“Proprioceptive feedback from extensor muscles during the stance phase ensures that the leg does not go into swing when loaded and that the magnitude of extensor activity is adequate for support. Proprioceptive feedback from flexor muscles towards the end of the stance phase facilitates the initiation of the swing phase of walking. Evidence that muscle afferent feedback also contributes to the magnitude and duration of flexor activity during the swing phase has been demonstrated recently. The regulation of the magnitude and duration of extensor and flexor activity during locomotion is mediated by monosynaptic, disynaptic, and polysynaptic muscle afferent pathways in the spinal cord. In addition to allowing for rapid adaptation in motor output during walking, afferent feedback from muscle proprioceptors is also involved in longer-term adaptations in response to changes in the biomechanical or neuromuscular properties of the walking system.” (2)
Neuromechanics? This early in the morning?
It has been a while since we have done a neuromechanics post. While doing some research for one of our PODcasts, We ran across this paper: http://www.ajronline.org/content/184/3/953.full
Midbrain Ataxia: An Introduction to the Mesencephalic Locomotor Region and the Pedunculopontine Nucleus
Yikes! What a mouthful!
What’s the bottom line?
The paper review a condition called “gait ataxia”. In plain English this means “aberrant or unsteady” gait. Things which usually cause gait ataxia originate in an area of the brain called the cerebellum, which coordinates all muscle activity. If you drink to much alcohol, it affects your cerebellum and you have a “wobbly” gait : ).
This paper looks at another area of the brain called the midbrain. It is the top part of the brainstem and contains an important gait integration and initiation center called the “midbrain locomotor nucleus”. The paper looks at 3 different cases and has some cool MRI images to see, along with alot of fancy neurological words and pathways.
There are many factors to consider when evaluating ataxic (or wobbly) gait, and this just gives us all one more place to look.
The Gait Guys. Making you smarter every day!
Why do we have difficulty with our gait when we drink too much alcohol ? It is not unlike the disturbed sense of balance we experience when we have an inner ear problem such as an infection.
Alcohol affects one’s balance by changing the viscosity of the endolymph within the otolithic membrane, the fluid inside the semicircular canals inside the ear. The endolymph surrounds the cupula which contains hair cells within the semicircular canals. When the head is tilted, the endolymph flows and moves the cupula. The hair cells then bend and send signals to the brain indicating the direction in which the head is tilted. By changing the viscosity of the endolymph to become less dense when alcohol enters the system, the hair cells can move more easily within the ear, which sends the signal to the brain and results in exaggerated and overcompensated movements of body. This can also result in vertigo, or “the spins.” Many of us have experienced this event in one shape or another and we know what it feels like. The unsteadiness of our gait is disturbing and uncorrectable until the problem is solved or the alcohol’s effect wear off. In chronic alcoholism however, the problem is different and more lasting.
Disturbed gait and balance are among the most consistent sequelae of chronic alcoholism. Research studies have shown evidence that partial recovery of gait and balance functions in alcoholics may be achieved with abstinence. This study ( http://www.ncbi.nlm.nih.gov/pubmed/21919921) showed that alcoholics’ gait and balance can continue to recover with long abstinence from alcohol, but that deficits persist, especially in eyes-closed standing balance.
Chronic alcohol abuse consistently damages the cerebellum. The cerebellum has multiple functions, including control of balance and coordination and even motor pattern generation. Alcohol also damages subcortical white matter, the myelinated fiber tracts that connect different parts of the cortex, and other central nervous systems. Long-term alcohol dependence also results in impaired dopamine transmission in the striatum, an important area for motor control.
The next time you are the designated driver, spend some time appreciating the subtle nuances and changes in people’s gait. Not only is it amusing, but fascinating as well.
Studies quoted in this blog post.
Gait and Balance Deficits in Chronic Alcoholics: No Improvement from 10 Weeks Through 1 Year Abstinence
Gait Issues: When Proprioception is Lost … What we lose when we wear “the wrong” shoes …
You have heard us use this word proprioception a million times (OK, some, maybe not a million). Proprioception is our ability to be aware of and orient our body or a body part in space. Poor proprioception can result in balance and coordination difficulties as well as being a risk factor for injury (Like this poor pooch). *Note: there is no such thing as a “proprioceptor”. All receptors have a more specific name but there are no receptors in the body actually called a proprioceptor, it is a rough classification if that.
Think about people with syphilis, who lose all afferent (sensory) information coming in through the dorsal root ganglia at the spine level. This ultimately leads to a wide based ataxic gait (due to a loss of position and tactile sense) and joint destruction (due to loss of position sense and lack of pain perception). The same consequences can occur, albeit on a smaller scale, when we have diminished proprioception from a joint or its associated muscle spindles. Just like when we put shoes on our feet, proprioception is lost. Just as it would be lost if we wore oven mitts on our hands all day long; there is a cost to optimal functioning of those muted joints.
To review, proprioception is subserved by both cutaneous receptors in the skin (pacinian coprpuscles, Ruffini endings, etc.), joint mechanoreceptors (types I,II,III and IV) and from muscle spindles (nuclear bag and nuclear chain fibers) . It is both conscious and unconscious and travels in two main pathways in the nervous system.
Conscious proprioception arises from the peripheral mechanoreceptors in the skin and joints and travels in the dorsal column system to ultimately end in the thalamus, where the information is relayed to the cortex. Unconscious proprioception arises from joint mechanoreceptors and muscle spindles and travels in the spino-cerebellr pathways to end in the midline vermis and flocculonodular lobe of the cerebellum.
Conscious proprioceptive information is relayed to other areas of the cortex and the cerebellum. Unconscious proprioceptive information is relayed from the cerebellum to the red nucleus to the thalamus and back to the cortex, to get integrated with the conscious proprioceptive information. This information is then sent down the spinal cord to effect some response in the periphery. There is a constant feed back loop between the proprioceptors, the cerebellum and the cerebral cortex. This is what allows us to be balanced and coordinated in out movements and actions.
Thankfully a fashion trend of wearing oven mitts on our hands has never hit the runways, but in a way we continue to do a similar disservice to our feet wearing shoes. Watch the video again and think about this next time you are contemplating, at the very least, a motion control shoe for yourself or a client. If we all walked like this when we put shoes on we would never have done this disservice of footwear to ourselves long ago.
Ivo and Shawn….Good Looking and Proprioceptively different.
We hope you have begun the new year in a NON ATAXIC manner. Lets look at the origin of the word:
Ataxia: Greek, from a or without + tassein to put in order or “without order”. Ataxia is truly gait without order, and we will see why momentarily. The term was coined in 1670. Every September 25th is International Ataxia Awareness Day. Mark THAT ONE on your calendars!
Ataxia an inability to coordinate voluntary muscular movements that is symptomatic of some nervous system disorders and injuries and not due to muscle weakness.
It is a lack of afferent information either GETTING TO the CNS, BEING PROCESSED BY the CNS, or OUTPUT FROM the CNS. We can still hear Dr Carrick saying “where is the longitudinal level of the lesion? Is it at the receptor, the effector, the peripheral nerve, the spinal cord, the brain stem, the thalamus, the cerebellum or cerebrum?” This mantra, still rings true many years later, as it gives us the afferent pathway to the brain and higher centers of the CNS.
Ataxic gait, not to be considered synonymous with Fredreich’s Ataxia (the genetic disorder described in the 1860’s, related to spinal cord and cerebellar degeneration), can be due to any number of causes which affect processing of afferent information. One too many Tequila’s (100% agave of course), barbituates, joint pathomechanics, diseases affecting receptors (like syphilis or leprosy), diabetes and other forms of peripheral neuropathy, spinal cord injury or disease are only a few of the causes. Virtually anything that can affect the afferent processing or efferent arc of the processing of proprioceptive information.
The large amplitude corrective movements are clues to the CNS that something is awry and are a necessary component of the compensation. Here , you truly are seeing the result of the compensation.
The video offers a simplified explanation and nice clinical example of an ataxic gait. If you don’t believe it, try some field research (or perhaps you already have) with the ethanol of your choice and see for yourself. Of course, some of THAT ataxia comes from changes in specific gravity of the endolymph in your inner year, but that is the subject of another post.
Ivo and Shawn. The Gait Guys…New and Improved for 2012