Ipsilateral vs contralateral side of body

I know that the dorsal columns carry ipsilateral information. Is this fact relative to the dorsal column in question? If I want to talk about the right dorsal column, then the right side of the body would be considered ispilateral. But, if i then go on to talk about the left dorsal column, does this mean that the left side of the body is now considered ipsilateral?

Yes. Ipsilateral and contralateral always have to be relative to something; ipsilateral means "same side" and contralateral means "other side" - you can't really be the same or other side of something unless you have a reference point.

Ipsilateral vs contralateral side of body - Biology

The central nervous system is able to make conscious decisions about how to react to information, such as deciding how to change our behavior if we are cold or in pain. Another option is to use the sensory information to inform a visceral reflex arc, like those involved in the regulation of blood pressure or body temperature. Here we will consider using sensory information to inform somatic reflexes, where automatic motor responses occur as a result of the sensory stimuli.

No matter which type of CNS mediated reflex or response we are referring to, the general model is the same. Sensory information activates a receptor that sends information to the CNS via an afferent neuron, some level of synaptic or higher level processing occurs, and, if a response is necessary or appropriate, the response is initiated through efferent neurons. You might recognize this as the same model used to maintain homeostasis. Reflexes are a unique category of responses because they do not require the higher centers used for conscious or voluntary responses. Instead reflexes are involuntary, stereotyped (they are repeatable under the same stimulus conditions) responses that occur quickly.

Categories of Reflexes

As mentioned, reflexes can either be visceral or somatic. Visceral reflexes involve a glandular or non-skeletal muscular response carried out in internal organs such as the heart, blood vessels, or structures of the GI tract. They utilize neurons of the autonomic nervous system to elicit their actions. Visceral reflexes have been more fully discussed in the section on the autonomic nervous system. In contrast, somatic reflexes involve unconscious skeletal muscle motor responses. In doing so, these reflexes utilize some of the same lower motor neurons (alpha motor neurons) used to control skeletal muscle during conscious movement. Because reflexes are quick, it makes sense that somatic reflexes are often meant to protect us from injury. As examples, reflexes contribute to the maintenance of balance and rapid withdrawal of the hand or foot from damaging stimuli.

Somatic reflexes can either be intrinsic (present at birth) or learned. We will be focusing on intrinsic reflexes, which occur as the result of normal human development. Learned reflexes are much more complicated in their anatomical structure and result from repetitive actions, such as athletic training. Reflexes can also be categorized by the number of synapses they involve (monosynaptic reflex versus polysynaptic reflex) or the relative position of the sensory receptors to the responding muscles (ipsilateral = same side of the body, contralateral = opposite sides of the body).


Brown-Séquard syndrome may be caused by injury to the spinal cord resulting from a spinal cord tumor, trauma [such as a fall or injury from gunshot or puncture to the cervical or thoracic spine], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. [ citation needed ] Decompression sickness may also be a cause of Brown-Séquard syndrome. [2]

The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place. [ citation needed ]

  1. loss of all sensation, hypotonic paralysis
  2. spastic paralysis and loss of vibration and proprioception (position sense) and fine touch
  3. loss of pain and temperature sensation

The hemisection of the cord results in a lesion of each of the three main neural systems: [ citation needed ]

As a result of the injury to these three main brain pathways the patient will present with three lesions:

  • The corticospinal lesion produces spastic paralysis on the same side of the body below the level of the lesion (due to loss of moderation by the UMN). At the level of the lesion, there will be flaccid paralysis of the muscles supplied by the nerve of that level (since lower motor neurons are affected at the level of the lesion).
  • The lesion to fasciculus gracilis or fasciculus cuneatus (dorsal column) results in ipsilateral loss of vibration and proprioception (position sense) as well as loss of all sensation of fine touch.
  • The loss of the spinothalamic tract leads to pain and temperature sensation being lost from the contralateral side beginning one or two segments below the lesion.

In addition, if the lesion occurs above T1 of the spinal cord it will produce ipsilateral Horner's syndrome with involvement of the oculosympathetic pathway.

Magnetic resonance imaging (MRI) is the imaging of choice in spinal cord lesions. [ citation needed ]

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by findings on clinical examination which reflect hemisection of the spinal cord (cutting the spinal cord in half on one or the other side). It is diagnosed by finding motor (muscle) paralysis on the same (ipsilateral) side as the lesion and deficits in pain and temperature sensation on the opposite (contralateral) side. This is called ipsilateral hemiplegia and contralateral pain and temperature sensation deficits. The loss of sensation on the opposite side of the lesion is because the nerve fibers of the spinothalamic tract (which carry information about pain and temperature) crossover once they meet the spinal cord from the peripheries. [ citation needed ]

Classification Edit

Any presentation of spinal injury that is an incomplete lesion (hemisection) can be called a partial Brown-Séquard or incomplete Brown-Séquard syndrome. [ citation needed ]

Brown-Séquard syndrome is characterized by loss of motor function (i.e. hemiparaplegia), loss of vibration sense and fine touch, loss of proprioception (position sense), loss of two-point discrimination, and signs of weakness on the ipsilateral (same side) of the spinal injury. This is a result of a lesion affecting the dorsal column-medial lemniscus tract, well localized (deep) touch, conscious proprioception, vibration, pressure and 2-point discrimination, and the corticospinal tract, which carries motor fibers. On the contralateral (opposite side) of the lesion, there will be a loss of pain and temperature sensation and crude touch 1 or 2 segments below the level of the lesion via the Spinothalamic Tract of the Anterolateral System. Bilateral (both sides) ataxia may also occur if the ventral spinocerebellar tract and dorsal spinocerebellar tract are affected. [ citation needed ]

Crude touch, pain and temperature fibers are carried in the spinothalamic tract. These fibers decussate at the level of the spinal cord. Therefore, a hemi-section lesion to the spinal cord will demonstrate loss of these modalities on the contralateral side of the lesion, while preserving them on the ipsilateral side. Upon touching this side, the patient will not be able to localize where they were touched, only that they were touched. This is because fine touch fibers are carried in the dorsal column-medial lemniscus pathway. The fibers in this pathway decussate at the level of the medulla. Therefore, a hemi-section lesion of the spinal cord will demonstrate loss of fine touch on ipsilateral side (preserved on the contralateral side) and crude touch (destruction of the decussated spinothalamic fibers from the contralateral side) on the contralateral side. [ citation needed ]

Pure Brown-Séquard syndrome is associated with the following:

  • Interruption of the lateral corticospinal tracts:
    • Ipsilateral spastic paralysis below the level of the lesion ipsilateral to lesion
    • Abnormal reflexes and Babinski sign may not be present in acute injury
    • Ipsilateral loss of tactile discrimination, vibratory, and position sensation below the level of the lesion
    • Contralateral loss of pain and temperature sensation. This usually occurs 2–3 segments below the level of the lesion.

    Treatment is directed at the pathology causing the paralysis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant. [ citation needed ]

    Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord. [3]

    Charles-Édouard Brown-Séquard studied the anatomy and physiology of the spinal cord. He described this injury after observing spinal cord trauma which happened to farmers while cutting sugar cane in Mauritius. French physician, Paul Loye, attempted to confirm Brown-Séquard's observations on the nervous system by experimentation with decapitation of dogs and other animals and recording the extent of each animal's movement after decapitation. [4]

    Ipsilateral versus Contralateral: What Arm & Leg Combination To Use

    These are common things I hear all the time in my training sessions, especially with movements that require split stance or single leg stance and holding a weight with on arm.

    It can seem confusing to put it all together, especially with novel movements where the exact goal may not seem apparent, and where the positioning can take advantage of fascial sling systems and neural drive not readily visible in most anatomy charts.

    Ipsilateral means using the same side arm and leg. For instance, this would me like a boxer throwing a punch with their right hand and driving off their right foot. The benefit to a movement like this is the generation of joint compressive tension throughout the entire system where the impulse from the foot travels fairly efficiently through the entire body and extends through a solid lever system.

    The development of power along this line typically hinges on the ability of the glutes to pull the hip into extension and external rotation. This external rotation of the hip, when the foot is planted, causes the upper body to rotate through and generate some snap.

    Watch how Mike Tyson, one of the most feared hitters of all time generates stupid amounts of hip extension and rotation with his body uppercut combo:

    The slow-motion capture around 2:15 shows it really well.

    The lateral fascial line, shown by Thomas Myers in Anatomy Trains, encapsulates a lot of the anatomical linkages between the driving foot and the arm throwing the blows.

    If you haven’t read Anatomy Trains and you work with anatomy, you’re a step behind.

    When under contraction, the system can produce a great level of rigidity through the entire line, which can make it sort of like a wound up spring. This elasticity and rigidity is not only used to produce power up through the hands, but produce power down through the foot, like in walking or running. The drive back and down from the leg is met with a drive up and forward from the same side arm. The extension and external rotation of the hip is met with an antagonistic movement from the opposing core, involving flexion, rotation and lateral flexion, which produces the upper-lower rotation seen in locomotion.

    This is an incredibly intricate system that this describes in an incredibly simplified manner, and truly doesn’t do it justice, but for the sake of keeping this post under 5000 words, we’ll leave it at that.

    A breakdown in the control of this system is commonly seen when people don’t have the reactive strength through the hips and core to be able to produce the efficient transfer of power through the leg to the reaching arm, and wind up showing something like a trendelenburg gait pattern where their hips flop around like a lava lamp set on high. This is a common issue in runners who get a lot of lateral hip pain, IT band issues, medial knee pain and shin splits, which is pretty much any runner who prides volume over technique. You could also see a coxalgic gait, where the person is leaning hard over the hip to try to reduce the stability requirement of the contralateral stabilizing system.

    The 22 mile mark posture of Every. Marathon. Runner. Ever.

    The continuity seems to break down somewhat when it goes from horizontal force production to vertical force production. This case seems to favour contralateral linkage, as seen in a typical lay up in basketball where the shooting arm extends off the contralateral leg.

    So what does this mean when it comes to training? Essentially, any movement that involves pressing or some level of drive comes into ipsilateral continuation. An example of this would be a cable lunge & press.

    A powerful force in this movement is the extension and rotation of the right hip, as mentioned above.

    Can you stretch the line? Sure, and one of my favorite ways of doing this is to use a lunge with a back rotation of the upper body.

    People with chronically “tight” hip flexors tend to absolutely hate this one, and can’t help but wonder why they can’t get their arm higher than parallel to the ground.

    At a more neurodevelopmental level, rolling patterns take an ipsilateral pattern in a new direction. A lot of people with spinal issues tend to really struggle with rolling, specifically as it relates to the duality of stability and mobility through the system.

    When people get stuck on these, they tend to hold their breath and try to flex harder to get through, not realizing this isn’t the answer. In many ways, it’s one of the harder movements you can get down without cheating, due to how much thoracic mobility and core control is needed. Once it gets easy, there’s no reason to continue using it, but it’s tricky for a lot of people for a long time. I haven’t journied far enough down this specific rabbit hole to offer too much in the way of knowing the why and how, but for more information on that reach out to someone who studies DNS work.

    Where ipsilateral work could be considered the driving movement, contralateral work could be considered pull or reach dominant movements.

    Much of the contralateral work relies on using an interconnected line of tissue known as the posterior functional line. This line connects the gluteus maximus of one hip to the opposite side latissimus dorsi muscle, which essentially crosses the low back in an X-shape, and provides a level of stabilization and also acceleration.

    The main role of this system is to produce force to pull towards the body, such as in a single leg deadlift.

    The glute and lat stretch simultaneously, which happens to get the low back stabilized through the thoracolumbar fascia. These are all fancy words, but they essentially mean this is easier to do with less to no pain compared to a bilateral deadlift or hip hinge movement, and is a cornerstone movement I use with a lot of low back pain clients due to the movement from the hip and pull through this chain.

    A secondary use of this line is as an antagonist for the drive from the ipsilateral line. When running , the one foot drives into the ground while the other knee drives up and forward. This forward knee drive stretches and tenses the functional line, especially when coupled with the arm reach. This stretch provides a brake for the drive side, and allows for an elastic recoil effect to bring the next leg into position to drive into the ground for continued acceleration.

    Combining the ipsilateral drive with the contralateral pull is one of the basic tennets of locomotion, much like a crawling pattern.

    This brings us back to the original questions: “which arm/leg combo?” Essentially, the way I use it is if it’s a driving movement, ipsilateral produces the greatest power production and stability, meaning the right hand has the right leg back. Contralateral work provides the greatest reach potential for pulling, which means the right hand has the left leg forward or standing on. Funny enough, they both wind up being kind of the same position, which makes it that much easier. This isn’t the only way to do things, but it’s a way I’ve used successfully with a lot of clients and it seems to work well.

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    The Effect of Ipsilateral and Contralateral Loading on Muscle Activity During the Lunge

    A recent study was published in the Journal of Strength and Conditioning Research that investigated the effect of holding a dumbbell in either the contralateral or ipsilateral hand during a split squat and forward lunge. (Note: they called it a “walking lunge” but I am 99% certain it was a forward lunge, so I’m just going to say forward lunger in this article… probably just semantics.)

    • Holding the dumbbell on the ipsilateral side had no effect on glute med activity.
    • Holding the dumbbell on the contralateral side resulted in a significant increase in glute med activity, but only during the forward lunge, not the split squat.

    I was a bit surprised that glute med activity was not impacted during the split squat, but perhaps the static nature of the position inherently requires less transverse and frontal plane stability.

    There was one other finding from this study that I thought was interesting. Kinematic differences during the forward lunge were found between a group of trained individuals in comparison to a group without training experience.

    This makes sense as the forward lunge is a complex movement pattern that requires an understanding of how to control the pattern. It requires both mobility and stability, but also the ability to control the eccentric deceleration phase.

    However, there were no kinematic differences between training age during the split squat, meaning that both novice and experienced trainees performed the split squat in a similar fashion. This make split squats a great exercise to incorporate in the early phases of training for those with limited training experience, eventually progressing to forward lunge as they get better at moving and stabilizing the pattern.

    This helps solidify the use of split squats in our lunge regression system.


    I like simple studies like this. Having the rationale to make small tweaks to your program is what sets you apart. It’s the small things that may not be obvious at first but will produce better results over time.

    Based on these results, I would recommend using the split squat with bilateral dumbbells to maximize strength gains since a unilateral load did not alter glute med activity. The split squat is more of a basic exercise, so why not just use it to work on strength gains in the novice trainee. As the person progresses, you can add the forward lunge variation with a contralateral load to enhance triplanar stability.


    Several lines of research demonstrate that primary motor cortex (M1) is principally involved in controlling movements of the contralateral side of the body. Anatomically, greater than 90% of corticospinal projections project to the contralateral spinal cord (Dum and Strick, 1996 Brösamle and Schwab, 1997 Lacroix et al., 2004 Rosenzweig et al., 2009). Most of the 10% that project ipsilaterally bifurcate and synapse bilaterally, with few thought to synapse purely onto ipsilateral targets (Rosenzweig et al., 2009). While there are many monosynaptic projections from M1 to contralateral limb motoneurons (Bennett and Lemon, 1996 Bennett and Lemon, 1996 McKiernan et al., 1998 Smith and Fetz, 2009), there are no monosynaptic projections from M1 to ipsilateral motoneurons (Soteropoulos et al., 2011). Stimulation in M1 largely produces contralateral movements and occasionally bilateral movements (Montgomery et al., 2013). Lastly, inactivation of ipsilateral motor cortex has minimal effects on ipsilateral hand movements (Nishimura et al., 2007).

    An early study suggested M1 was largely insensitive to ipsilateral movement (Tanji et al., 1988). However, several subsequent studies highlight substantial M1 activity during ipsilateral movements (Donchin et al., 1998 Kermadi et al., 1998 Cisek et al., 2003 Bundy and Leuthardt, 2019 Willett et al., 2019). Donchin et al. (2002) examined macaque M1 activity in relation to ipsilateral and contralateral reaching movements. They found 46% of neurons responded to both hand movements, whereas 34% of neurons responded to only contralateral movements and 19% responded to only ipsilateral movements. As well, functional magnetic resonance imaging (fMRI) revealed considerable motor cortical activity related to ipsilateral movements (Cramer et al., 1999 Kobayashi et al., 2003 Gallivan et al., 2011). In particular, Diedrichsen et al. (2013) found areas in motor cortex associated with an ipsilateral digit overlapped with its representation for the corresponding contralateral digit.

    An obvious question arises as to why ipsilateral activity in M1 does not cause contralateral limb movement. One hypothesis is that this M1 activity cancels out at spinal circuits (Druckmann and Chklovskii, 2012 Kaufman et al., 2014). For example, consider two neurons that have equal, excitatory synapses onto an alpha-motoneuron (Figure 1A). If both neurons increase their firing rate, the result will lead to excitation in the alpha-motoneuron and thus an increase in motor output (potent pattern, Figure 1B top row). Conversely, if one neuron increases and the other neuron decreases its firing rate equally, the net effect on the alpha-motoneuron will be zero leading to no change in motor output (null pattern, bottom row). Examination of the potent and null patterns in state space, where each axis represents the firing rate of a neuron, reveals that these two patterns are in dimensions that are at 90° (orthogonal) to each other (Figure 1C). This strategy can allow motor cortex to perform computations necessary for planning an upcoming movement without causing movement (Churchland et al., 2012 Kaufman et al., 2014 Elsayed et al., 2016). Similarly, rapid visual feedback of the hand may be isolated in subspaces orthogonal to the subspaces used for the subsequent motor correction (Stavisky et al., 2017). Thus, this hypothesis predicts that ipsilateral activity occupies subspaces that are orthogonal to contralateral activity.

    Example of orthogonal subspaces.

    (A) Simple example of two neurons that synapse onto an alpha-motoneuron with equal, positive weights. (B) Top row, when both neurons increase their firing rate to an event (shaded area), their total activity is summed by the alpha-motoneuron leading to an increase in motor output (potent activity). Bottom row, when neuron one increases and neuron two decreases their firing rate, their net effect cancels at the alpha-motoneuron, thus preventing changes in motor output (null activity). (C) State space plots of the firing rates of neurons 1 and 2. Plotting the potent (blue axis) and null (red axis) activity reveals that these patterns are orthogonal with respect to each other (i.e. 90 degrees). Thus, the one-dimensional potent axis represents an orthogonal dimension to the one-dimensional null dimension.

    Several studies have shown M1 responds to proprioceptive feedback (Evarts and Tanji, 1976 Wolpaw, 1980 Chapman et al., 1984 Pruszynski et al., 2011 Takei et al., 2018) and represents loads applied to the contralateral limb (Cabel et al., 2001 Herter et al., 2009 Omrani et al., 2014 Pruszynski et al., 2014). Here, we used a postural perturbation task to explore M1 responses to ipsilateral and contralateral motor function. We found

    55% of neurons were active when loads were applied to the contralateral and ipsilateral limbs. However, contralateral loads tended to evoke neural responses that were twice as large as responses for ipsilateral loads. Furthermore, contralateral loads evoked changes in neural activity

    10 ms earlier than ipsilateral loads. Lastly, we found contralateral activity occupied subspaces that were orthogonal to the ipsilateral activity suggesting a mechanism on how motor cortex can sequester the ipsilateral activity without causing contralateral movement.

    Vestibular Rehabilitation and Stroke

    Lateral Medullary Syndrome

    The most common stroke of the vestibular system, first reported in the late 19th century, 31 is lateral medullary syndrome , also known as Wallenberg syndrome. 3 This syndrome is caused by a stroke of either the PICA or AICA. Therefore, it is a lateral brainstem stroke. Because both arteries that supply the vestibular nuclei also supply other areas, lateral medullary syndrome is manifested by mixed sensory and motor loss, including vertigo, lateropulsion, disequilibrium, ataxia, contralateral loss of pain and temperature sensation in the trunk and limbs, and the following ipsilateral signs: facial numbness, Horner syndrome (drooping of the upper eyelid, constriction of the pupil, and decreased sweating), and dysphagia. Involvement of the PICA also includes hoarseness and skew deviation of the eyes. Involvement of the AICA also includes ipsilateral tinnitus, hearing loss, facial weakness, and reduced peripheral vestibular responses on objective diagnostic tests. These patients have vertigo, difficulty standing and walking, sensory loss on the ipsilateral side of the face and on the contralateral side of the body, difficulty speaking and swallowing, abnormal eye movements, and hearing impairments. In addition to thrombosis and ischemia, dissection of the vertebral artery caused by sports injuries or by chiropractic manipulation of the neck can cause this syndrome. 34

    Lateral medullary syndrome is relatively common. These patients may be referred for rehabilitation, although many of them recover spontaneously. No studies have evaluated the effectiveness of rehabilitation in this population, but these patients usually respond well to therapy. Therapy should involve functional skills, balance therapy, and habituation exercises to reduce vertigo, which are the kinds of exercises used to reduce vertigo in patients with peripheral vestibular disorders. 23,29

    Ipsilateral vs contralateral side of body - Biology

    The sensory nuclei of the thalamus, such as the ventral posterolateral (VPL) nucleus, which receives incoming tactile and pain signals, are often referred to as precortical relays. This term seems to imply that the sensory information is simply transferred unchanged to the cortex, where the true work of sensory integration takes place .

    But in reality, electrophysiological studies have shown that this is not the case: the signals undergo numerous transformations at each of the connections in the chain of neurons leading from the point where the initial stimulus is received to the cortex. The descending control of pain , which is applied to the various connections in this chain, is a good example of these changes.

    What pathways do pain signals follow to perform their protective function? How do these messages reach your brain to tell you which part of your body is hurt? As you might expect for a function as essential as the sensing of pain, the pathways for these signals are numerous, complex, and mutually redundant.

    But before we can trace these pain pathways (also known as nociceptive pathways), we must distinguish them from the sensory pathways for non-painful temperature, touch, and proprioception.

    These various sensory signals take two different paths to reach the brain, both of which start in a given part of the body and end in the brain&rsquos somatosensory cortex. Each of these paths consists of a chain of three neurons that pass the nerve impulses from one to the next. Where these two paths differ is in the location where they cross the midline in the spinal cord.

    Remember that in the human body, the nerves responsible for sensory inputs, as well as those responsible for motor control, are crossed. In other words, the neural pathways from the left side of the body terminate in the right hemisphere of the brain, and vice versa. Hence, at some point in the body, these pathways must cross the body&rsquos midline (in scientific terminology, they must &ldquodecussate&rdquo).

    Now let&rsquos follow the path that any incoming sensory impulse—whether for touch, pain, heat, or proprioception—follows from the spinal cord to the brain. Regardless of the sensory modality, the three neurons in question form a chain running from one side of the spinal cord to the other, and the cell body of the first neuron in this chain is always located in a spinal (dorsal root) ganglion. This neuron is said to be T-shaped, because its axon emerges as a short extension from its cell body and then soon divides into two branches going in opposite directions: one goes to the part of the body that is innervated by this spinal nerve, while the other immediately enters the dorsal root of the spinal cord (an essentially sensory part of the spinal cord, as opposed to the ventral root, which is a motor area). It is from this point on that the two pathways differ.

    Adapted from Neuroscience: Exploring the Brain, M.F. Bear, B.W. Connors, and M.A. Paradiso, 2007

    The pathway responsible for touch and proprioception is called the lemniscal pathway. The first axon in this pathway runs along the dorsal root of the spinal nerve and up the dorsal column of the spinal cord. (Along the way, this axon also sends out collaterals: branches in the dorsal root that play a valuable role in the local inhibition of pain, among other functions.)

    The primary axon, however, remains on the same side of the spinal cord as the side of the body that it innervates (the &ldquoipsilateral&rdquo side) until it connects with the second neuron in the chain, which in the case of the lemniscal pathway is located in the medulla. The axon of this second neuron crosses the midline immediately. It then travels up through the medial lemniscus to the ventral posterolateral (VPL) nucleus of the thalamus, where it connects with the third neuron in the chain.

    The pathway that carries information about pain and non-painful temperatures is called the neospinothalamic pathway (or often simply the spinothalamic pathway). The first neuron in this pathway connects to the second neuron not in the medulla, but in the dorsal horn of the spinal cord, on the same side that the nerve impulse comes from. This second neuron has a single axon, which immediately crosses the midline to the other (contralateral) side of the spinal cord and goes up to the brain along with the other axons forming the lateral spinothalamic tract. This part of the pathway is described as contralateral, meaning that it runs along the side of the body opposite to the area that its axons innervate.

    The axon of the second neuron connects to the third and final neuron of this ascending pathway in the ventral posterolateral (VPL) nucleus of the thalamus.

    In both of these pathways, the third neuron sends its axon to the somatosensory cortex, the part of the brain that determines exactly where the original stimulus occurred in the body.

    The difference between the routes of the lemniscal pathway (for touch and proprioception) and the spinothalamic pathway (for pain) have special clinical significance, because some injuries that affect only one side of the spinal cord will disrupt only the sense of touch, while others will affect only the sensation of pain.

    For example, suppose that the woman in the figure to the right has been injured on the left side of her spinal cord, at the 10th thoracic vertebra. She will experience a reduced sense of touch on the left side of her body below the level of the injury, because the lemniscal pathway runs up the same (ipsilateral) side. She will also experience a reduced sense of pain below the injury, but on the right side of her body, because the spinothalamic pathway runs up the opposite (contralateral) side. As a result of this sensory dissociation, she will be able to feel it when a mosquito lands on her right leg, but not if the mosquito then bites it.


    The perception of pain results not simply from the activation of the ascending nociceptive pathways, but from an actual dialogue between these pathways and the various descending pathways that control this pain. The control mechanism involved is often described as a system of filters or a set of gates whose closing is controlled by the cortex, the midbrain, and the medulla.

    But the incoming nociceptive impulse encounters its very first gate as soon as it enters the dorsal root of the spinal cord. This first relay point in the ascending pathway is thus not just an area through which the nociceptive impulse passes, but rather the first place where it is filtered and integrated with other information.

    This first level of integration is referred to as segmental controls of non-pain peripheral origin . The word &ldquosegmental&rdquo refers to the fact that this process occurs in each of the segments of the spinal cord corresponding to each vertebra. This segmental control results from the interaction between the nociceptive sensory fibres (A delta and C) and the non-nociceptive ones (A alpha and A beta).

    This interaction was modelled in an article, first published in 1962 and then amplified in 1965, that many regard as the most important one ever written on the subject of pain. In this article the authors, Canadian Ronald Melzack and Englishman Patrick Wall , proposed the first model for the endogenous control of pain: the now-famous gate control theory of pain. This theory posits a special form of connectivity involving not only the sensory input fibres for pain and for light touch, as mentioned above, but also a set of inhibitory interneurons that are the key element in the authors&rsquo explanation.

    As the diagram to the right shows, the nociceptive and non-nociceptive impulses from the body converge at non-specific neurons in the dorsal horn, which project their axons into the contralateral spinothalamic tract. These two types of nerve fibres also communicate with the non-specific neurons through inhibitory interneurons that they contact via collateral fibres. The important difference is the nature of the connection with these interneurons: for the large, non-nociceptive fibres, it is excitatory, but for the nociceptive fibres, it is inhibitory.

    It is this particular circuit that forms the virtual gate whose opening and closing will modulate the passage of pain. Under normal conditions, the inhibitory interneurons spontaneously produce action potentials at their own specific frequency. But when the nociceptive fibres are activated by a pain stimulus, in addition to stimulating the non-specific neuron that projects to the spinothalamic pathway (also known as the &ldquoprojection neuron&rdquo), they also inhibit the spontaneous inhibitory activity of the interneurons, thus depolarizing the projection neuron and increasing the likelihood that it will trigger action potentials.

    Another aspect of this circuit&rsquos operation is illustrated by what happens when you hurt yourself and start to rub the injured part of your body vigorously. This instinctive reaction reduces the sensation of pain by &ldquoclosing the gate&rdquo. The animation below shows how: rubbing your skin activates the sensory fibres for touch, which in turn excite the projection neuron. But these fibres also make numerous excitatory connections to the inhibitory interneurons. As a result, if you keep rubbing your skin, these interneurons will produce a strong hyperpolarization of the projection neuron, thus greatly reducing the probability that it will emit nerve impulses.

    Thus we see how it is the relative frequencies of the action potentials in the nociceptive and non-nociceptive fibres that determine how open the &ldquogate&rdquo in the spinal cord will be and hence how much pain information will pass through. In addition, there are projections of central origin that can also activate these inhibitory interneurons in the spinal cord and further close the gate at the segmental level.

    Data gathered since 1965 have led to some changes in Melzack and Wall&rsquos original model, but the idea that the perception of pain is modulated from the moment that the pain messages enter the spinal cord remains fundamental to the clinical treatment of pain. For example, it is the origin of clinical applications such as transcutaneous electrical nerve stimulation (TENS), which produces local analgesia by stimulating the non-nociceptive fibres in the skin.

    Scientists have long known about the phenomenon of stress-induced analgesia (SIA), best exemplified by the many reported cases of wounded soldiers and injured athletes who feel no pain while the battle or the game is on , but do feel it afterward, as soon as they are back in conditions of safety and calm.

    From an evolutionary standpoint, stress-induced analgesia can be regarded as a component of the fight-or-flight response . It would not be highly adaptive if pain from injuries could prevent us from fighting or fleeing even when our lives depended on it. But once the threat of death has passed, our normal pain-sensing mechanisms have to do their work in order to immobilize the injured part of the body and prevent the injury from getting worse.

    Research done on the mechanisms of the descending control pathways for pain since the early 1980s has now given us a better understanding of stress-induced analgesia. We now know that the tendency to experience this phenomenon varies from one individual to another and is influenced by variables such as age, sex, degree of sensitivity to opiates , and past stressful experiences.

    The mechanisms by which stress-induced analgesia inhibits pain seem to involve the descending systems of the midbrain, applying both opioid and non-opioid mechanisms. Research is also tending to show that neurotransmitters associated with stress, such as norepinephrine, and brain structures associated with fear reactions, such as the amygdala , are also involved. Many other endogenous substances, such as anandamide and its cannabinoid receptors , also seem to play a role, in this case in the non-opioid effect in the periaqueductal grey matter.


    The cerebellum is the largest structure in the posterior fossa (see figures 15.1, 15.2, & 15.3). It is attached to the dorsal aspect of the pons and rostral medulla by three white matter peduncles and forms the roof of the fourth ventricle. It consists of:

    • Vermis – the midline structure, named for its “wormlike” appearance
    • Cerebellar Hemispheres

    Cerebellar Tonsils

    • Important landmark on the inferior surface, which may be herniated secondary to mass lesions of the cerebrum or cerebellum, or brain swelling and associated severely elevated intracranial pressure
    • With severe herniation, the tonsils may herniate through the foramen magnum, compress the medulla, and cause death through impingement on the medullary respiratory centers

    Cerebellar Peduncles

    • Superior Cerebellar Peduncle Carries mainly output from the cerebellum
    • Middle and Inferior Cerebellar Peduncles Carry mainly input to the cerebellum

    Cerebellar Functions

    • Serves to integrate sensory and other inputs from many regions of the brain and spinal cord (SC)
    • Coordinates and “smoothes” ongoing movements and participates in motor planning
    • Has no direct connections to lower motor neurons, but exerts its influence through connections to motor systems of the cortex and brainstem

    Different regions of the cerebellum have specialized functions

    • Inferior Vermis and Flocculonodular Lobes Regulate balance and eye movement through interactions with the vestibular circuitry
      • Act with other parts of the vermis to control medial motor systems (i.e., proximal trunk and limb muscles)

      Additional Functions of the Cerebellar Pathways

      • Articulation of speech
      • Respiratory movements
      • Motor learning
      • Higher-order cognitive functions

      Functional Regions of the Cerebellum – Table

      Region Functions Motor Pathways Influenced
      Lateral Hemispheres (largest part of the cerebellum) Motor planning for extremities Lateral Corticospinal tract
      Intermediate Hemispheres Distal limb coordination (especially the appendicular muscles in the legs and arms) Lateral Corticospinal tract and Rubrospinal tract
      Vermis Proximal limb and trunk coordination Anterior Corticospinal tract, Retibulospinal tract, Vestibulospinal tract and Tectospinal tract
      Flocculonodular Lobe Balance and vestibulo-ocular reflexes Medial Longitudinal fasciculus

      Of Interest: Cerebellar lesions typically result in a characteristic type of irregular uncoordinated movement – Ataxia.

      Cerebellar Output Pathways

      Output pathways are organized around the three functional regions of the cerebellum:

      • Lateral Hemispheres
      • Intermediate Hemispheres
      • Vermis plus Flocculonodular Lobe

      Pathways from the cerebellum to the lateral motor systems and then to the periphery are “double crossed”

      • 1st crossing occurs as the cerebellar output pathways exit in the decussation of the superior cerebellar peduncle
      • 2nd crossing occurs as the corticospinal and rubrospinal tracts descend to the spinal cord. Inputs also follow this pattern, so each cerebellar hemisphere receives information about the ipsilateral limbs

      Cerebellar Input Pathways

      Input to the Cerebellum Arises From

      • All areas within the CNS
      • Multiple sensory modalities (e.g., vestibular, visual, auditory & somatosensory systems)
      • Brainstem nuclei
      • Spinal cord

      Input is somatotopically organized, with the ipsilateral body represented in both the anterior and posterior lobes Major source of input consists of corticopontine fibers (i.e., from frontal, temporal, parietal & occipital lobes) that travel in the internal capsule and cerebral peduncles

      • Derive from primary sensory and motor cortices and part of the visual cortex
      • Travel to the ipsilateral pons and synapse in the pontine nuclei
      • Pontocerebellar fibers cross the midline to enter the contralateral middle cerebellar peduncle and give rise to mossy fibers that innervate much of the cerebellar cortex

      Spinocerebellar fibers comprise another major source of cerebellar input and provide afferent information to the cerebellum

      • Information about limb movements conveyed by the dorsal spinocerebellar tract and the cuneocerebellar tract
      • Of Interest: Spinocerebellar input is either ipsilateral or “double-crossed” —> ipsilateral limb ataxia when lesioned

      Vascular Supply to the Cerebellum

      Blood Supply to the Cerebellum

      Provided by three branches of the vertebral and basilar arteries:

      Posterior Inferior Cerebellar Artery (PICA)

      Anterior Inferior Cerebellar Artery (AICA)

      Superior Cerebellar Artery (SCA)

      In addition to supplying the cerebellum, these arteries course through the brainstem, providing blood to portions of the lateral medulla and pons.

      Of Interest: Infarcts are more common in the PICA and SCA than in the AICA territory.

      Principles for Localizing Cerebellar Lesions

      • Ataxia is ipsilateral to the side of the cerebellar lesion
      • Midline lesions of the cerebellar vermis or flocculonodular lobes mainly cause unsteady gait (i.e., truncal ataxia) and eye movement abnormalities, which often are accompanied by intense vertigo, nausea and vomiting
        • Affect the medial motor systems
        • Do not typically cause unilateral deficits because the medial motor systems influence the proximal trunk muscles bilaterally

        Of Interest: The cerebellum has multiple reciprocal connections with the brainstem and other regions therefore ataxia may be seen with lesions in those areas as well

        Lesion Location Functional Impact
        Lateral cerebellum Distal limb coordination
        Medial cerebellum Trunk control, posture, balance and gait

        Of Interest: Deficits in coordination occur ipsilateral to the lesion

        Cerebellar Infarcts – Key Clinical Concepts

        Characteristic Symptom Presentation

        • Vertigo
        • Nausea and vomiting
        • Horizontal nystagmus
        • Limb ataxia
        • Unsteady gait
        • Headache (localized to occipital, frontal, or upper cervical regions)

        Of Interest: Many of the signs and symptoms of cerebellar artery infarct result from infarction of the lateral medulla or pons, rather than the cerebellum – Infarcts of these areas may cause trigeminal and spinothalamic sensory loss, and Horner’s syndrome.

        *Conversely, infarcts of the lateral medulla or pons can cause ataxia because of involvement with cerebellar peduncles, even if the cerebellum is spared.

        Infarct Patterns

        • Infarcts that spare the brainstem and involve predominantly the cerebellum are more common with SCA infarcts than with PICA or AICA, therefore infarcts causing unilateral ataxia with little or no brainstem signs are most commonly in the SCA territory
        • Infarcts of the PICA and AICA more often involve both the lateral brainstem and cerebellum
        • Infarcts of the lateral pons or medulla that spare the cerebellum typically occur with PICA or AICA rather than SCA
        • Large cerebellar infarcts that involve the territories of the PICA or SCA can cause swelling of the cerebellum
          • Subsequent compression of the fourth ventricle can cause hydrocephalus
          • Compression in the posterior fossa may be life threatening because the respiratory centers and other vital brainstem structures may be affected
          • Surgical decompression and resection of portions of the infracted cerebellum
          • Hemorrhage into the cerebellar white matter also can cause brainstem compression

          Cerebellar Hemorrhage – Key Clinical Concepts

          Characteristics Symptom Presentation

          Large Cerebellar Hemorrhages May Cause

          • Hydrocephalus [treated with ventriculostomy]
          • 6th nerve palsies
          • Impaired consciousness
          • Brainstem compression
          • Death

          Can Occur Secondary To

          • Chronic hypertension
          • Arteriovenous malformation
          • Hemorrhagic conversion of an ischemic infarct
          • Metastases
          • May include surgical evacuation of the hemorrhage and decompression of the posterior fossa.
          • Hydrocephalus treated by ventriculostomy carries with it the risk of upward transtentorial herniation.

          Signs and Symptoms of Cerebellar Disorders

          • Nausea
          • Vomiting
          • Vertigo
          • Slurred speech
          • Unsteadiness
          • Uncoordinated limb movements
          • Headache Occurs in the frontal, occipital, or upper cervical regions, and usually occurs on the side of the lesion

          Most Abnormalities a Combination Of


          Incipient Tonsilar Herniation Lesions May Cause

          • Depressed consciousness
          • Brainstem findings
          • Hydrocephalus
          • Head tilt [also seen with lesions to the anterior medullary velum]

          Additional Cerebellar Disorders


          • (aka adiadochokinesia) Abnormalities of rapid alternating movements, such as tapping one hand with the palm and dorsum of the other hand

          Eye Movement Abnormalities

          • Ocular Dysmetria Saccades overshoot or undershoot their target
          • Slow Saccades Present in some degenerative disorders involving the cerebellum
          • Nystagmus Typically of the gaze paretic type in which the patient looking toward a target in the periphery exhibits slow phases toward the primary position and fast phases occur back toward the target. May change directions depending upon the direction of gaze (unlike peripheral vertigo).
          • Vertical Nystagmus may occur.

          Speech Abnormalities

          • Scanning or Explosive Speech Individual’s speech may have an ataxic quality in cerebellar disorders with irregular fluctuations in both rate and volume
          • Cerebellar dysfunction also may cause slurring or articulatory problems

          Cerebellar Disease

          Abnormalities That Can Confound the Cerebellar Exam

          Upper Motor Neuron Signs

          Lower Motor Neuron Signs

          • With severe upper or lower motor weakness, cerebellar testing may not be possible
          • Precision finger tapping may be helpful, as cerebellar involvement typically causes the tip of the finger to hit a different spot on the thumb each time [See Video 63]

          Sensory Loss

          • Loss of joint position sense can cause sensory ataxia
          • Loss of position sense must be severe and sensory ataxia usually improves with visual feedback

          Basal Ganglia Dysfunction

          • Movement disorders (e.g., parkinsonism) associated with basal ganglia involvement can cause slow, clumsy movements or gait unsteadiness
          • Tremor and dyskinesia also may confound the cerebellar examination

          Clinical Findings and Localization of Cerebellar Ataxia

          • Means literally “lack of order”
          • Refers to the disordered contractions of the agonist and antagonist muscles and lack of normal coordination between movements at different joints
          • Characterized by movements that have an irregular, wavering course that seems to consist of continuous overshooting, overcorrecting and then overshooting again around the intended trajectory

          Characteristics of Ataxic Movements

          Ipsilateral Localization of Ataxia

          • Cerebellar connections involved in the lateral motor system are either ipsilateral or cross twice (i.e., “double crossed’) between the cerebellum and spinal cord
          • Lesions of the cerebellar hemispheres cause ataxia in the extremities ipsilateral to the side of the lesion
          • Lesions of the cerebellar peduncles lead to ipsilateral ataxia

          In contrast: cerebellar lesions affecting the medial motor system cause truncal ataxia, which is a bilateral disorder, but patients with truncal ataxia often fall or sway toward side of lesion

          False Localization of Ataxia

          • Ataxia may be caused by lesions to the cerebellar input or output pathways located outside the cerebellum
          • Lesions in the cerebellar peduncles or pons (without damage to the cerebellar hemisphere) —> severe ataxia
          • Hydrocephalus [which may damage frontopontine pathways] and lesions within the prefrontal cortex —> gait abnormalities similar to truncal ataxia
          • Disorders of the spinal cord —> gait abnormalities

          Truncal Ataxia versus Appendicular Ataxia

          Truncal Ataxia

          • Caused by lesions confined to the cerebellar vermis
          • Affect primarily the medial motor systems
          • Lead to wide-based, unsteady, or “drunk like” gait or truncal ataxia
          • In severe cases, patients may even have difficulties sitting up without support

          Appendicular Ataxia

          • Caused by lesions of the intermediate and lateral portions of the cerebellum
          • Affect the lateral motor systems
          • Cause ataxia on movement of the extremities

          Of Interest: Lesions often extend to include both the vermis & cerebellar hemispheres and truncal and appendicular symptoms may coexist. More severe and longer-lasting deficits may occur with lesions of the intermediate hemisphere, vermis, deep nuclei, and cerebellar peduncles.

          • Unilateral lesions in the medial portion of the cerebellar hemisphere may produce no appreciable deficit.


          • Syndrome caused by lacunar infarcts
          • Presentation includes a combination of unilateral motor neuron signs and ataxia, usually affecting the same side
          • Both the ataxia and hemiparesis are contralateral to the lesion side
          • Most often caused by lesions in the:
            • Corona radiata
            • Internal capsule
            • Pons that involve both corticospinal and corticopontine fibers
            • Frontal lobes
            • Parietal lobes
            • Sensorimotor cortex
            • Midbrain lesions that involve fibers of the superior cerebellar peduncle or red nucleus

            Sensory Ataxia

            • Occurs when the posterior column – medial lemniscal pathway is disrupted
            • Causes impaired or loss of joint position sense [not typically observed in cerebellar patients]
            • Characterized by ataxic-appearing overshooting movements of the limbs and a wide-based, unsteady gait [similar to cerebellar involvement]
            • May improve significantly with visual feedback
            • Worsens with eyes closed or in the dark
            • Typically involves lesions of the peripheral nerves or posterior columns —> ipsilateral ataxia
            • May occur secondary to lesions in the thalamus, thalamic radiations or somatosensory cortex —> contralateral ataxia

            Tests for Ataxia

            Finger-Nose-Finger Test

            (see Figure 15.14 and Video 64)

            • Patient alternately touches her nose and then the examiner’s finger
            • Sensitivity of the test may be increased by holding the target finger at the limit of the patient’s reach or by moving the target finger to a different position each time the patient touches her nose

            Heel-Shin Test

            (see Video 65)

            • Patient rubs his heel up and down the length of his shin in as straight a line as possible
            • Performed in the supine position to decrease contribution of gravity
            • Variations include tapping the heel repeatedly on the same spot just below the knee or having the patient alternately touch his knee and the examiner’s finger

            Of Interest: Rapid tapping of the fingers together, hand on the thigh, or foot on the floor are good tests for dysrhythmia (see Videos 52 & 53).

            Testing for Overshoot or Loss of Check

            • Have patient raise both arms suddenly from their lap or lower them suddenly to the level of the examiner’s hand [see Video 66] or
            • Apply pressure to the patient’s outstretched arms and suddenly release it

            Testing for Truncal Ataxia

            Wide-based, unsteady gait that resembles the drunk or a toddler may be observed with cerebellar involvement. Alcohol impairs cerebellar function and the cerebellar pathways of toddlers is not fully myelinated.

            Tandem Gait Testing

            • The patient is instructed to touch the heel with the toe of the other foot on each step, which forces the patient to assume a narrow stance
            • Patients will fall or deviate toward the side of the lesion (see Video 68)

            Romberg or Romberg’s Test

            • Patient is asked to stand with feet together for half a minute, then asked to close eyes
            • A positive Romberg’s test occurs if the patient can stand with eyes open, but falls when they are closed.
            • The Romberg test indicates a proprioceptive lesion and is NOT a test of cerebellar function
            • With midline cerebellar lesions, the patient has difficulty standing with eyes open as well as closed [with these lesions, a peculiar tremor of the trunk or head, titubation, also can occur]
            • May help differentiate cerebellar lesions from lesions of the vestibular or proprioceptive systems

            (see Video 67)

            Differential Diagnosis and Common Causes of Ataxia

            Differential Diagnosis (depends on)

            Common Causes

            Acute Ataxia in Adults

            Chronic Ataxia in Adults

            • Brain metastases
            • Chronic toxin exposure (especially to alcohol)
            • Multiple sclerosis
            • Degenerative disorders of the cerebellum or cerebellar pathways

            Acute Ataxia in Pediatric Patients

            Chronic or Progressive Ataxia in Pediatric Patients

            • Cerebellar astrocytoma
            • Medulloblastoma
            • Friedreich’s ataxia
            • Ataxia-telangiectasia

            Brief Anatomical Study Guide

            • Located in the posterior fossa
            • Consists of:
              • midline vermis
              • intermediate part of the cerebellar hemisphere
              • lateral part of the cerebellar hemisphere
              • superior cerebellar peduncle
              • middle cerebellar peduncle
              • inferior cerebellar peduncle

              Outputs of the Cerebellum

              All are carried by the deep cerebellar nuclei and the vestibular nuclei. The cerebellar cortex and the deep nuclei can be divided into three functional zones:

              • Vermis (via fastigial nuclei) and flocculonodular lobes (via vestibular nuclei)
                • Function in the control of proximal and trunk muscles and vestibulo-ocular control, respectively
                • Functions in the control of more distal appendicular muscles mainly in the arms and legs
                • Largest part of the cerebellum
                • Involved in planning the motor program for the extremities

                Cerebellar input and output pathways

                • Form a complex system
                • Follow a medial-lateral organization and all pathways to the lateral motor systems are either ipsilateral or double crossed so that cerebellar lesions cause ipsilateral deficits

                Local Cerebellar Neurons

                • Granule cells
                • Inhibitory cells
                • Golgi cells
                • Basket cells
                • Stellate cells

                Principles of Localizing Cerebellar Lesions

                (based on anatomical organization of the cerebellar pathways)

                • Ataxia is ipsilateral to the side of the cerebellar lesion
                • Midline lesions of the cerebellar vermis or flocculonodular lobes cause mainly unsteady gait (i.e., truncal ataxia) and eye movement abnormalities
                • Lesions of the intermediate part of the cerebellar hemisphere cause mainly ataxia of the limbs (i.e., appendicular ataxia)
                • Ataxia is often caused by lesions of the cerebellar circuitry in the brainstem or other locations rather than in the cerebellum itself, which can lead to false localization
                • Because of the strong reciprocal connection between the cerebellum and vestibular system, cerebellar lesions often are associated with:
                  • Vertigo
                  • Nausea
                  • Vomiting
                  • Nystagmus

                  Characteristic irregular movement abnormalities seen in cerebellar disorders

                  Functional Neurologic Disorders

                  D.M. Baguley , . D.J. McFerran , in Handbook of Clinical Neurology , 2016

                  Is it functional?

                  Hyperacusis is occasionally associated with facial nerve palsies which cause loss of the ear's protective stapedial reflex. In such cases, because the symptom is associated with a demonstrable lesion, it cannot be regarded as functional. The vast majority of cases of hyperacusis, however, are not associated with structural pathology. Although various pathophysiological mechanisms have been suggested, the cause remains unknown. Some theories are directed at the auditory periphery but many focus on the central auditory system, proposing similar mechanisms to those seen in tinnitus (see above). It therefore seems likely that impaired loudness tolerance has a functional basis in at least a proportion of cases.

                  Watch the video: Ipsilateral vs Contralateral (January 2022).