Physiology Flashcards
What is the somatosensory pathways?
The somatosensory pathway is the neural pathway that transmits sensory information from the skin, muscles, joints, and viscera to the central nervous system. It is responsible for processing touch, pressure, vibration, proprioception, pain, and temperature. The pathway consists of three-order neurons:
- First-order neurons: Detect stimuli and transmit signals from peripheral receptors to the spinal cord or brainstem.
- Second-order neurons: Relay signals from the spinal cord or brainstem to the thalamus, where they cross the midline (decussation).
- Third-order neurons: Project from the thalamus to the somatosensory cortex (postcentral gyrus) for perception.
The receptors, which are specialized for each sensory function, connect to ganglion cells responsible for transducing the stimuli into electrical signals.
What are ganglion cells? Why are some myelinated and others aren’t?
In the nervous system, ganglion cells are neurons located in ganglia, which are clusters of nerve cell bodies found outside the central nervous system—typically in the peripheral nervous system.
There are different types based on location and function : sensory ganglion cells, autonomic ganglion cells, retinal ganglion cells.
Some fibers are highly myelinated like the A-alpha and A-beta others aren’t myelinated like C fibers.
The high velocity of the conduction depends on the myelin sheath : more myelin means faster the conduction.
What are some different receptors involved in the sensory system?
Mechanoreceptors—> mechanical stress causes the opening of sodium channels which depolarized the cells. The change in the membrane potential is proportional to intensity of the stimulus.
Chemoreceptors—> selective binding of a specific molecule with a portion of the receptor causes sodium channels to open and triggering of an action potential.
Photoreceptors—> photons will trigger downstream signaling pathway that ultimately result in an action potential.
During a neurological evaluation, how can you evaluate the somatosensory pathways of the patient?
- Cutaneous :
- mechanoreception—> non painful mechanical stimuli
- thermoreception—> cold induces an increase firing rate while warmth decreases. But as temperature drops below 0 or over 45/50 a painful stimulus is conveyed.
- Deep
- position and movement of muscles, tendons and joints—> the patient can be actively or passively moved in order to test if he or she can receive information.
How do we asses proprioception of a patient?
To assess the ability of the patient to identify the position of a limb, a wrist is passively moved and he/she, with eyes closed, is asked to describe its spatial orientation.
To assess the ability of the patient to comprehend movement of joints, muscles and tendons, a finger (or a wrist, if testing with the finger fails) is moved and the patient is asked whether he can perceive the movement or not. Patient answer yes and often lie therefore sometimes the question is asked when the physician isn’t moving anything or the physician can ask a different question, like is the limb moving up or down.
Moreover, a test for proprioception is also the finger-to-nose, performed with eyes closed
What are some superficial and deep receptors?
Superficial :
Meissner’s corpuscles—> rapid, found in superficial layers of skin and most abundant in non hairy areas like palms, maximal response to local skin pressure.
Merkel disks—> slow, located in superficial layers of skin and most abundant in non hairy areas like fingertips, involved shape and material perception.
Deep :
Pacini corpuscles—> rapid, deep in the skin, maximal response to vibration, especially at 200 Hz.
Ruffini receptors—> slow, deep in the skin, unidirectional skin tension and unconscious hand and finger movement.
Muscle spindle fibers 1A —> proprioception.
Golgi tendon organs 1B —> tendon stretch.
How is vibration perception assessed during neurological examination?
It is assessed using a tuning fork, specifically a Rydel-Seiffer tuning fork. It uses an arbitrary scale of 0 to 8 which indicates the vibration amplitude, 0 being very fast vibration.
What is a long refractory period of the visual system responsible for?
It causes afterimages, where retinal photochemical activity continues briefly even after the stimulus ends.
What is the two point discrimination test?
It is a test used to discriminate the minimal distance at which two stimuli are perceived as separate is measured. Patients with a loss of peripheral nerve receptors will have a reduced 2 point discrimination and will perceive 2 close points as one single one.
3 receptors are needed to discriminate two close points: two firing and one non firing in the middle. The neurons compete with one another sending inhibitory signals through interneurons. Eventually the higher firing neurons will suppress the lower firing neuron, enhancing spatial resolution. This is called center surrounding inhibition.
What is somatotopy?
Somatotopy refers to the organization of the body’s sensory and motor functions in specific areas of the brain or spinal cord, corresponding to specific parts of the body.
From an upright image it may seem that the lumbar roots innervate structures located lower than those from the sacral roots. If you change the perspective as if we were a quadruple animal, the sacral roots actually innervate the furthers part of the body.
It is important to remember the somatotopic arrangement of the ascending tract. The sensory signals arriving from the lower portion of the body are more medial while the more superior parts are more lateral.
What are afferent fibers and how are they classified?
They are the nerve fibers that send the information from the PNS to the CNS. They vary based on axon diameter and myelinization, which both affect conduction velocity of the signal.
They can be classified based on the Erlanger and Gasser classification which divides them in three classes, A being largest and fastest, B and C being smallest and slowest.
They can also be classified based on specific sensation conveyed of fibers : Ia, Ib, II, III, IV.
What is the lemniscal pathway?
Also known as the dorsal column pathway, is responsible for transmitting tactile (2 point), proprioceptive, pressure and vibratory sensory information from the body to the brain.
Pathway—> sensory information is received by specialized receptors, signals transmitted via afferent nerve fibers to the dorsal root ganglion where the sensory neurons are located. From the dorsal root ganglion (1st order neuron) the signal travels along the dorsal columns of the spinal cord composed of the fasciculus gracilis (belowT6) and cuneatus (above T6), they then ascend through the spinal cord and synapse in the medulla oblongata at specific nuclei called nucleus cuneatus and gracilis (2nd order neuron) depending on whether the information is coming from the upper or lower body respectively. Then the information crosses over through the internal arcuate fibers and becomes contralateral to the original stimulus. It then ascends the medial leminiscus tract through the brain stem, finally it reaches the thalamus, specifically the ventral posterior nucleus (3rd order neuron). They then pass through the posterior 1/3 of the internal capsule, and than relayed to the primary and secondary somatosensory cortex in the parietal lobe through the corona radiata.
Which nerves does diabetic neuropathy affect first and why?
They first lose the ability to coordinate lower limbs. This is because the pathway is longer for the legs. Therefore a longer cell has more chance to undergo a degenerative process.
How can we test coordination in patient with diabetic neuropathy?
Heel to knee, which is performed first with eyes open and then with eyes closed.
Romberg test, asking the patient to stand up with heels tight together, performed first eyes open then eyes closed.
Moreover patients will also have visual deficits, and will have problems orienting themselves in the dark.
How can you distinguish the lack of coordination because of afferent deficits from cerebellar lesion?
If you have a cerebellar involvement, the performance will be bad equally with eyes closed or open, while if the problem is in the afferent, the performance will get worst.
Also patients with central conditions affecting the long pathway will have more problems in the lower limbs that the upper limbs.
What are some deficits caused by afferent fibers lesions of the dorsal column of the spinal cord?
- 2-point discrimination comes when patients have to recognize very small objects, like buttons, that they do not feel properly.
- Vibration is lost as well. This can be tested by the tuning fork.
- Conscious proprioception (limb position, passive movement) is tested by asking the patient to tell whether the examiner is moving the finger up and down or not.
- Astereognosia (object recognition).
- Agraphestesia (impossibility to recognize “words written on the skin”).
- Ataxia, loss of coordination worsening with eyes closed.
- Parasthesia, patient feels something that is not there aka Lheermitte’s sign.
What is Lhermitte’s sign? Why is it important?
It refers to demyelinating lesions in the cervical dorsal columns where the axons are still capable of conducting but they are more sensitive to mechanical stress.
E.g if the patient is flexing the neck anteriorly and leads to a sort of electrical current running through arms or legs.
It is important because it could be the first sing of someone having a demyelinating disease without actually having any symptoms.
Thalamus divisions?
The thalamus has many subdivisions but we are going to focus on the motor and somatosensory thalamus. The somatosensory thalamus is the ventral posterior portion, of which the medial portion receives and processes afferent from then head and face while the lateral from limbs and trunk.
Then 3 neurons, ganglion cell, medial longitudinal fasciculus and thalamocortical projection, send the signal to the contra lateral somatosensory cortex.
What is the somatosensory homunculus?
It is the visual representation of the body sensory cortex.
The lower limbs in the medial portion of the cortex and shoulder/trunk at the vertex. Laterally, there are different parts of upper limbs, with the most distal parts that are more lateral.
Somatotopy is important for recognizing lesions. If we have a lesion medially, somatosensory processing to the lower limb is lost.
What if a person has a loss of somatosensory processing of only one lower limb?
It could be caused by a lesion in the medial portion of the contralateral cortex or a lesion on the ipsilateral spine.
What is the top down mechanism?
The cortex is able to inhibit all central neurons that are participating to the afferent pathway, so that only the strongest signals will pass the inhibition. Works like a filter.
What is the spinocerebellar tract?
All of these tracts mainly respond unconscious proprioception.
Dorsal spinocerebellar tract —>
Origin: Clarke’s nucleus (T1–L2 spinal segments)
Pathway:
• Ascends ipsilaterally in the spinal cord.
• Enters the inferior cerebellar peduncle and projects to the vermis of the cerebellum.
Function:
• Carries unconscious proprioceptive information from lower limb muscles and joints.
Ventral spinocerebellar tract —>
Origin: Spinal border cells (lumbar and sacral spinal cord)
Pathway:
• Crosses to the contralateral side in the spinal cord.
• Ascends to the superior cerebellar peduncle.
• Crosses again within the cerebellum to terminate in the ipsilateral cerebellar cortex.
Function:
• Transmits whole limb movements and proprioception from lower limbs.
•Important for detecting motor efference copy (predicting movements).
Cuneocerebellar tract —>
Origin: DRG
Pathway:
• Carries upper limb proprioceptive input via the fasciculus cuneatus.
• Synapses in the external cuneate nucleus in the medulla.
• Ascends ipsilaterally through the inferior cerebellar peduncle to the cerebellum.
Function:
• Analogous to DSCT but for upper limbs.
Spino-olivary tract —>
Origin: Spinal cord neurons.
Pathway:
• Crosses in the spinal cord and ascends to the inferior olivary nucleus in the medulla.
• Then, projects to the contralateral cerebellum via the inferior cerebellar peduncle.
Function:
• Integrates proprioceptive information with motor learning and coordination.
• Important for error correction in movement.
What is the spinothalamic tract?
The spinothalamic tract is responsible for transmitting pain and temperature sensations to the brain. This pathway consists of two main types of fibers:
• A-Delta fibers: These are fast-conducting fibers that respond primarily to mechanical and cold temperature stimuli.
• C fibers: These are slow-conducting fibers that mainly transmit chemical pain stimuli, often associated with tissue damage or inflammation.
Both fiber types enter the spinal cord dorsally but synapse in different laminae of the dorsal horn before crossing to the contralateral side via the anterior commissure:
• C fibers synapse mainly in Rexed lamina II and III, ascend two spinal levels, and then cross contralaterally.
• Aδ fibers synapse primarily in Rexed lamina I and V, ascend two spinal levels, and then cross to the opposite side.
A lesion in the spinothalamic tract will result in loss of pain and temperature sensation on the contralateral side of the body, starting two dermatomes below the level of the lesion. This occurs because each neuron enters the spinal cord, ascends two levels before synapsing, and then crosses the midline.
For example, if a person is stabbed at the T5 level of the spinothalamic tract, they will experience loss of pain and temperature sensation on the contralateral side starting from T7 downward.
What happens if there is a lesion at the level of the crossing fibers in the spinothalamic tract?
If the lesion is at the level of the crossing of fibers, it will involve both sides of the fibers and result in bilateral damage.
How is pain and absence of pain classified?
- Negative somatosensory symptom : sensory reduction (deficit), absence of pain.
- Positive somatosensory symptoms : sensory increase/ alteration, presence in the absence of stimuli.
Positive symptoms include :
- Spontaneous—> no external stimulus but we feel like there is one.
- Paresthesia—> not painful, Lhermittes phenomenon. We feel stimulus which is not really there.
- Dysesthesia—> painful.
- Evoked—> Exaggerated pain sensation evoked by an actual stimulus.
- Hyperalgesia—> becomes severe from mild pain.
- Allodynia—> painful from non painful stimulus.
Touch sensory pathway for the face?
The pathway conveys touch information from the face. The pathway consists of—> sensory input which travels from the face via CN V, with the cell bodies located in the semilunar ganglion (Gasserian ganglion), then the afferent fibers enter the pons where they synapses with the main sensory nucleus of the trigeminal nerve. From there the neurons decussate and join the medial leminiscus which carries the fibers up to the thalamus, specifically the ventral posterior medial nucleus. From there it it relayed to the somatosensory cortex.
If lesion occurs at level of the nucleus—> loss of ipsilateral touch sensation of the ipsilateral face. If lesion occurs after the crossing (i.e. in the midbrain)—> loss of contralateral touch in the hemiface.
What is the corneal reflex pathway? Clinical relevance?
It is a protective reflex where touching the cornea of the eye triggers a blink response in both eyes. This reflex involves the trigeminal nerve as the afferent nerve and the facial nerve as the efferent nerve.
Pathway—>
Afferent pathway : the cornea sends sensory information through the ophthalmic branch of the trigeminal nerve, the signal travels to the main sensory nucleus and the spinal trigeminal nucleus in the pons.
Efferent pathway : the signal from the trigeminal nucleus is relaye to the facial nerve nuclei in the pons. Then they send motor signal via CN VII to the orbicularis oculi muscles, causing both eyes to blink.
Lesion in R main trigeminal nucleus :
- Touch right eye—> no eye movement bc loss of afferent ipsilateral.
- Touch left eye—> both eyes blink because left afferent and left efferent are not damaged.
Lesion in R facial nerve :
- Touch right eye—> only left closes, as right efferent is damaged.
- Touch left eye—> only left closes, same as before.
Pathway of pain and temperature sensation in the face?
Pain and temperature receptors (1st order neuron), afferent fibers then enter the pons and descend through the descending trigeminal tract to synapse the spinal nucleus in the medulla(2nd order neuron). After synapsing they decussate and ascend along the ventral trigeminothalamic tract. They finally end up in the ventral posterior medial nucleus of the thalamus.
What is the mesencephalic nucleus?
It is part of the trigeminal nerve, located in the rostral midbrain and plays a role in processing proprioceptive information of the face, particularly the masticatory muscles, temporomandibular joint and oculomotor muscles.
A key features include : it uses electrical coupling instead of chemical synapses for faster transmission, and that it acts as a 1st order neuron for the masticatory muscles.
The proprioceptive receptors, which for the ocolumotor muscles have their cell bodies in the gasserian ganglion while the masticatory muscles and temporomandibular joint have them directly into the mesencephalic nucleus, are 1st order neurons.
The first order neurons from the mesencephalic nucleus project directly to the ventral posteromedial nucleus of the thalamus.
What is the masticatory nucleus?
It is the motor nucleus of the trigeminal nerve and it is responsible for sending motor signals to muscles involved in mastication.
It is located in the pons, specifically medial to the sensory nucleus of the trigeminal nerve.
The efferent fibers travel from the motor nucleus to innervate the muscles via the mandibular branch of the trigeminal nerve.
These fibers innervate :
- muscles of mastication—> temporalis, masseter, medial and lateral pterygoids.
- orla floor muscles—> mylohyoid and anterior belly of digastric muscles.
- middle ear muscles—> tensor tympani.
- pharyngeal muscles—> tensor veli palatini (swallowing).
The masticatory reflex is clinically tested to assess the integrity of the trigeminal nerve.
What is somatosensory evoked potentials?
SEP is a neurological test used to assess the integrity of the sensory pathways in the nervous system. It involves the stimulation of a sensory or motor nerve using a mild, non painful electrical stimulus. The test records the brains electrical response to the sensory stimulus, measuring how quickly and effectively information travels from a peripheral nerve to the somatosensory cortex.
SEP is a very poor localizing exam but very sensitive to demyelination and indicate problem if we have differences between limbs caused by demyelination in dorsal column or spino-thalamic pathway.
What is referred pain?
It occurs when pain from an internal organ (visceral pain), is perceived as originating from a different, typically cutaneous, region of the body. This occurs as both visceral and cutaneous pain fibers may converge on the same neurons in the spinal cord.
E.g MI can cause pain sends afferent to same spino thalamic neurons as the cutaneous area of chest and/or arm.
What is the gate control theory?
It suggests that non painful stimuli can inhibit the transmission of pain signals to the CNS by closing the gate at the spinal cord level. Large, non painful sensory fibers can activate interneurons in the spinal cord which in turn inhibit smaller pain fibers.
What causes the sensation of a phantom limb after amputation?
Phantom limb sensation occurs due to cortical plasticity, where the somatosensory cortex region that previously represented the amputated limb is activated by neighboring body parts. When surrounding areas, such as adjacent fingers or the shoulder, are stimulated, the brain mistakenly interprets the sensation as coming from the missing limb. This is due to the cortex not reorganizing properly, leading to a mismatch in sensory perception. This is known as maladaptive plasticity.
Functional anatomy of the motor system?
Primary motor cortex—> M1, area 4. Located in the pre central gyrus of the frontal lobe. It directly controls voluntary movements by sending signals to the muscles via the corticospinal tract.
Premotor cortex—> area 6, anterior lateral portion. It is located anterior to M1 and it is involved in planning and coordinating movements in response to external stimuli. This region is also where mirror neurons are found. It is also largely connected to the parietal lobe.
Supplementary motor area—> medial portion of area 6, Important for planning and executing self initiated movements. It is connected to the basal ganglia.
What are descending motor pathways? Which are they?
Descending motor pathways are neural pathways that carry motor commands from the brain to the spinal cord and ultimately to the muscles, facilitating voluntary and involuntary movements. They can be divided based on their origin.
Pyramidal pathway—> originates from the frontal cortex-
- Corticospinal
- Corticobulbar
Extrapyramidal pathways—> originate from the brainstem.
- Rubrospinal (magnocellular red nucleus),midbrain.
- Tecto-spinal (superior colliculus), midbrain.
- Vestibulo-spinal (medial and lateral), Pons.
- Reticulo-spinal, pons and medulla.
- Projections from locus coeruleus (noradrenaline) and raphe (serotonin).
What is the pyramidal tract?
The pyramidal tract is a major pathway responsible for conveying high-skilled, voluntary movements from the brain to the contralateral side of the body.
It is composed of 94% myelinated fibers and it originates from the lateral aspect of the PMC, specifically the 5th layer.
The descending fibers travel through the internal capsule, where fibers for motor control of the facial nerves pass through the through the genu and those for the limbs pass through the anterior 2/3 of the posterior limb.
Corticospinal tract—> The fibers continue to descend through the midbrain, pons, medulla. In the medulla 80/90% of the fibers decussate and form the lateral corticospinal tract which then synapse with the lower motor neurons in the anterior horn, the remaining fibers do not decussate and form the anterior corticospinal tract which continue to descended to the cervical and higher thoracic levels where they will synapse with their motor neurons.
Corticobulbar tract—> Responsible for the voluntary control of head, face and neck. Similarly the the corticospinal tract they originate in the cerebral cortex and pass through the internal capsule. However rather then descending these neurons have their axons synapsing to the lower motor neurons in the brainstem, specifically cranial nerve nuclei. The main difference is that these neurons innervate bilaterally.(exceptions include CNVII, CNXII, CNXI)
Concepts of muscle tone, spasticity and rigidity?
Muscle tone : refers to the continuous and passive partial contraction of muscles which helps maintain posture and readiness for action. Abnormal tone is referred to as : hypotonia, decreased muscle tone resulting in loose floppy muscles, or hypertonia, increased muscle time kadiung to rigidity and stiffness.
Spasticity : is a type of hypertonia that occurs due to upper motor neuron lesions, commonly seen in conditions like cerebral palsy, multiple sclerosis or stroke. It is characterized by increased muscle tone due to exaggerated stretch reflex. It is velocity dependent.
Rigidity : is a type of hypertonia but characterized by a more constant movement, regardless of speed or stretch. Can be referred to as an increase in resistance to passive movement throughout its range of motion.
Facial nerve, projections, lesions and diagnostic importance?
Projections —>
- the inferior part of the facial nerve nucleus receives fully crossed projections from the contralateral side. This part controls the muscles in the lower half of the face.
- the superior part of the facial nerve nucleus receives partially crossed projections from both hemispheres and controls the muscles in the the upper half of the face.
Due to this it is IMPOSSIBLE to voluntarily contact one side of the upper face while keeping the homologous muscle on the other side fully relaxed. It is POSSIBLE to voluntarily smile on one side of the mouth due to the fully crossed nature of the projections.
A lesion affecting the motor cortex (stroke), would cause contralateral motor deficit in the lower part of the face. This is because the upper part of the face is innervated partially bilaterally, so the unaffected hemisphere can still provide input.
A peripheral lesion (Bell’s palsy) instead causes motor deficit on the ipsilateral side, affecting both upper and lower parts. This is because it affects the nerve after it has left the brainstem, so that both upper and lowers parts lose input.
Which cranial nerves are involved in in eye movements?
Oculomotor nerve CN III —> controls the superior rectus which move the eye upward, the medial rectus which move the eye inward (toward the nose), the inferior oblique which moves the eye upward and outward. The nerve also controls other eye movements such as constriction of the pupil.
Trochlear nerve CN IV —> controls the superior oblique which moves the eye downward and inwards, especially when the eye is already looking medially.
Abducens nerve CN VI —> controls the lateral rectus which moves the eye outward.
How are horizontal eye movements carried out?
Horizontal eye movements are controlled by 1 pair of muscle for each eye.
- Lateral Rectus (CN VI in the pons): abduction the eye (away from nose).
- Medial Rectus (CN III, in the midbrain): adduction of the eye (towards the nose).
When looking horizontally the eyes are coupled and there must be a coordination of excitation and inhibitor of the two muscles. As one eye needs to be abducted and the other adducted.
Pathway : the frontal eye field in the cerebral cortex initiate the command, the signal travels down through the internal capsule to the pontine paramedian reticular formation (the brainstem center for horizontal glaze). The PPRF send the signal to the abducens nucleus (CN VI) to move the lateral rectus of the ipsilateral eye (if you want to look right, the right lateral rectus contracts to move the eye outwards). To ensure that both eyes move together the medial longitudinal fasciculus connects the abducens nucleus to the oculomotor nucleus on the opposite side which allows the medial recutus of the opposite eye to adduct, ensuring both eyes move in the same direction.
What is internuclear opthalmoplegia?
It occurs due to a lesion in the medial longitudinal fasciculus. The hallmark symptom is impaired adduction of one eye while the abduction of the other remains intact. This is due to the impairment of the connection between the abducens nerve and the oculomotor nerve.
It could be unilateral leading to deficit only when looking in one direction.
Convergence testing is used to distinguish INO from medial rectus weakness. It consists in moving the eyes towards the nose, in other words focusing on a close object. Convergence is controlled solely by the midbrain, so if the test is normal it suggest the medial rectus is intact and the problem lies in the MLF.
What is the vestibulo-ocular reflex?
The VOR is a reflex that stabilizes vision during head movement by coordinating the eye movements in the opposite direction of the head movement.
VOR is important in assessing brainstem integrity, as moving a patients head side to side should cause the eyes to remain fixed in a position indicating the reflex pathways are working.
What is the reflex arc?
The simplest is the monosynaptic reflex which involves a direct connection between a sensory and motor neuron, without any interneurons in between. The only true monosynaptic reflex is the stretch reflex, such as the patellar reflex.
While in polysynaptic reflex, one or more interneurons are involved, allowing more complex processing. The corticospinal tract plays a critical role in modulating reflexes by influencing interneurons, such as strong excitatory effect on interneurons that inhibit the reflex—> presynaptic inhibition.
In case of a stroke this can result in less inhibition of interneurons, so in turn a stronger reflex due to reduced inhibition.
What are the effects of a stroke on reflexes?
If the corticospinal tract is damaged (e.g., in a stroke), its ability to inhibit reflexes can be lost. Initially, this may lead to areflexia (loss of reflexes) and reduced muscle tone, but over time, this inhibition loss leads to hyperreflexia (exaggerated reflexes) in the chronic phase.
This is because without corticospinal modulation, there is excessive excitatory input to the motor neurons, causing the reflex to be abnormally strong.
What is the stretch reflex?
It is a monosynaptic reflex consisting in the muscle contraction that occurs in response to the stretching of a muscle.
Pathway —> it involves Ia sensory fibers in muscle spindle fibers which detect stretch and send a signal directly to motor neurons in the anterior horn of the spinal cord. These motor neurons stimulate the same muscle to contract, counteracting this stretch.
What is deep tendon reflex?
It involves complex interplay between alpha motor neurons, gamma motor neurons and muscle spindles.
The gamma motor neurons innervate intrafusal fibers within muscle spindles and adjusts the sensitivity of them to stretch.
Alpha motor neurons if activated cause extrafusal muscle fibers to contract.
The deep tendon reflex involves a quick stretch of the muscle (taping the patellar tendon), leading to immediate contraction of the muscle due to the activation of the Ia fibers that synapse the alpha motor neurons.
What is the inverse myotatic reflex?
It is a simple reflex that guarantees a protective (negative) feedback mechanism preventing to much tension on the muscle and tendon. The only way to inhibit motor neurons that are firing excessively is to act on inhibitory interneurons.
What is the flexor reflex?
It is a polysynaptic reflex arc aimed at protecting out body from painful stimuli. The reflex rapidly coordinates the contraction of all the flexor muscles and the relaxation of the extensor in that limb causing sudden withdrawal from the potentially damaging stimulus.
It is like a voluntary movement but occurs to quickly for it to be voluntary.
What is the plantar reflex?
The reflex is tested by stroking the lateral aspect of the sole of the foot, from heel to toes, using a blunt instrument. The response in a normal adult is flexion of the toes. This indicated normal function of the corticospinal tract.
The babinski sign —> if the same stimuli causes the big toe to extend and the other types to fan out, it is known as the babinski sign. It is normal in infants up to about 12 months due to immature development of the corticospinal tract. In adults it can indicate neurological damage.
The reflex is primarily mediated by the lumbosacral spinal cord, specifically L5 to S1.
Unilateral hemispheric corticospinal lesions?
Cause: Stroke, tumors, trauma, or demyelinating diseases affecting one cerebral hemisphere.
• Motor Deficits: Contralateral hemiparesis or hemiplegia due to the corticospinal tract crossing at the medullary pyramids.
Distribution:
• Medial cortical lesions: Affect the lower limb more (scapulo-crural region).
• Lateral cortical lesions: Affect the face and upper limb (facio-brachial region).
Associated Features:
• Dysarthria/dysphagia (if the corticobulbar tract is involved).
• Gaze deviation (eyes deviate toward the lesion due to frontal eye field damage).
• Pathologic reflexes, including Babinski sign on the contralateral side.
• Unilateral spasticity and hyperreflexia due to upper motor neuron involvement.
Prognosis: May improve with neuroplasticity and rehabilitation, especially if one hemisphere is intact.
What is clonus?
Clonus —> caused by Corticospinal tract dysfunction. Is a form of hyperreflexia and is characterized by rhythmic, involuntary muscle contraction triggered by a sudden stretch. Often appears when there is damage to the descending motor pathways. A common location. To observe clonus is in the ankle and calf muscles.
Bilateral hemispheric corticospinal lesions?
Cause: Severe brain injuries, large strokes (e.g., bilateral anterior cerebral artery infarcts), diffuse axonal injury, anoxic brain injury, or neurodegenerative diseases like primary lateral sclerosis.
Motor Deficits:
• Bilateral paresis or paralysis (paraplegia if lower limbs affected, quadriplegia if both upper and lower limbs affected).
• Severe spasticity and hyperreflexia due to loss of descending inhibition from both hemispheres.
• Babinski sign bilaterally.
Associated Features:
• Dysphagia, dysarthria, and pseudobulbar palsy (difficulty controlling facial and swallowing muscles due to corticobulbar tract damage).
• Loss of voluntary motor control with preserved reflexive movements (e.g., primitive reflexes).
• Cognitive impairment if widespread cortical damage is present.
• Emotional lability (pseudobulbar affect) – inappropriate laughing or crying due to loss of frontal inhibition.
Prognosis: Generally worse than unilateral lesions, as bilateral damage limits compensatory function from the unaffected hemisphere.
Peripheral motor neuron lesions?
These lesions differ from central corticospinal lesion in how they affect the motor function. While central lesions lead to exaggerated reflexes and spasticity, peripheral lesions cause a loss of muscle activity due to direct impairment of the motor neurons that innervate the muscles.
Symptoms include :
- Hyposthenia
- Severe hypotrophy
- Reduction or absence of tendons stretch reflex
- Muscle hypotonia.
- Fasciculations
What are fasciculations?
They are visible, involuntary muscle twitches that result from spontaneous discharges of motor units. They often occur in diseases like Amyotrophic Lateral Sclerosis before motor neurons degenerate.
They are caused by hyper excitability of remaining motor neurons. As neurons begin to degenerate, the surviving ones try to adopt orphaned muscle fibers leading to larger than normal motor units.
Why do lesions in the upper and lower limbs show different patterns of spasticity?
In the upper limbs spasticity mainly affects the flexors due to the activity of the rubrospinal tract. In the lower limbs, spasticity mainly affects the extensors due to the activity of the vestibulospinal tract.
What role does the red nucleus play in upper limb spasticity following a corticospinal lesion?
The red nucleus, located in the midbrain, gives rise to descending fibers that terminate in the cervical region of the spinal cord. These fibers, part of the Rubrospinal tract, facilitate flexor motor neurons of the upper limbs. When a corticospinal lesion occurs the Rubrospinal tract becomes disinhibited, leading to exaggerated flexor activity in the upper limbs, resulting in spasticity.
How can reflex responses in coma patients help assess the level of a lesion in the brain or brainstem?
Extension of all four limbs indicate decerebration which is indicative of a bad prognosis as it suggests a deficit of the rubrospinal tract due to a lesion in the brainstem.
Combined flexion of upper limbs and extension of lower limbs indicates decortication which has a better prognosis as the rubrospinal tract seems intact and the lesion found be in the cortex or non existent. The condition can be transient due to drug intoxication or hypoxia.
What are motor evoked potentials?
MEPs are a way to test whether the corticospinal tract is intact and if it has a delay in conduction as in demyelinating lesions.
The test consists in a brain stimulation with a magnetic coil. We activate motor neurons and record the muscle response. We measure the total motor conduction time, that is the span from the brain stimulation to the beginning of muscle contraction. We also measure a total peripheral conduction time, done by putting the coil to the neck or vertebrae.
Then the difference between the two times is the central motor conduction time, if there is a difference of more that 2 or 3 ms there may be demyelination.
What are the components of basal ganglia?
It is composed by the striatum, formed by the caudate and putamen nuclei, the global pallidus which is divided in external and internal, the substantial nigra and the subthalamic nucleus.
The motor thalamus is not part of the basal ganglia but it is considered to be part of their circuitry. It is formed by the ventral anterior and ventral lateral nuclei.
Direct and indirect pathways of basal ganglia?
Direct Pathway: The overall function is to facilitate movement by promoting cortical activation. The striatum receives excitatory (glutamate) input from the cortex, which then inhibits the internal segment of the globus pallidus (GPi). Since the GPi normally inhibits the thalamus, its inhibition results in a disinhibited thalamus, which sends excitatory signals back to the cortex, promoting movement.
Indirect Pathway: The overall function is to suppress unwanted movement and regulate motor activity. The striatum receives excitatory (glutamate) input from the cortex, which then inhibits the external segment of the globus pallidus (GPe). Since the GPe normally inhibits the subthalamic nucleus (STN), its inhibition leads to disinhibition of the STN, allowing it to excite the GPi. The GPi then inhibits (GABA) the thalamus, thereby limiting excitatory signals to the cortex, reducing movement.
What is deep brain stimulation?
It consists in an electrode that is implanted in the STN which gives continuous inputs. Disorders like tremors and dystopia can be treated this way.
What are the hypokinetic disorders of Parkinson’s disease?
Parkinson’s disease is a reduction of dopaminergic projections on striatal neurons participating to both direct and indirect pathways. This results in increased activity of the internal pallidum (GPi), reduced activity of the thalamic motor nuclei VA & VL and reduced thalamic facilitation on SMA & M1.
Characterized by :
Akinesia—> reduced number fo voluntary movements.
Bradykinesia—> slower voluntary movements.
Hypokinesia—> reduced amplitude of voluntary movements (small handwriting.)
Rigidity—> increased resistance to passive movements.
Tremors—> alteration of agonist and antagonist muscle activity.
Anatomy of the cerebellum?
The cerebellum is located inferior to the occipital and temporal lobes within the posterior cranial fossa, at the same level as and posterior to the pons. It is anatomically divided into three lobes and three functional zones:
Lobes of the Cerebellum:
1. Anterior lobe
2. Posterior lobe
3. Flocculonodular lobe
Zones of the Cerebellum:
1. Vermis (Midline Zone) – Located centrally.
2. Intermediate Zone – On either side of the vermis.
3. Lateral Zone – Outermost part of the cerebellum.
Functional Divisions:
1. Archicerebellum / Medial Zone (Vermis + Flocculonodular Lobe)
• Oldest part of the cerebellum.
• Connected to vestibular nuclei (for balance) and eye movement control.
• Ensures smooth movements and postural stability.
2. Paleocerebellum / Intermediate Zone
• Controls lower limb coordination and balance.
• Plays a role in postural adjustments during movement.
3. Neocerebellum / Lateral Zone
• Newest part of the cerebellum.
• Controls fine motor coordination, particularly hand movements and complex voluntary motor planning.
Role of the cerebellar peduncles?
- Inferior Cerebellar Peduncle
Function: Brings proprioceptive information to the cerebellum.
Afferent fibers:
• From spinal cord (dorsal spinocerebellar tract, cuneocerebellar tract).
• From vestibular nuclei (vestibulocerebellar pathway).
• From inferior olive (olivocerebellar fibers).
Efferent fibers:
• Sends output to vestibular nuclei (important for balance). - Middle Cerebellar Peduncle
Function: Conveys a copy of the motor plan from the cerebral cortex to the cerebellum.
Afferent fibers (ONLY):
• From the contralateral pontine nuclei (corticopontocerebellar tract). - Superior Cerebellar Peduncle
Function: Sends corrective motor output from the cerebellum to the motor cortex to refine movement.
Efferent fibers:
• To red nucleus (rubrospinal tract).
• To thalamus (ventral lateral nucleus), which relays corrections to the motor cortex.
Afferent fibers (fewer):
• From the ventral spinocerebellar tract (carries proprioceptive input from the lower limbs).
What is an intentional tremor?
It is a particular tremor typical of cerebellar lesions. It arises only when there is a voluntary movement to distinguish it from postural parkinsonian and physiological tremors. Cerebellar lesions cause abnormalities in motor control, but do not initiate any tremor. Can use the arm pulling test.
What are the optic radiations?
They are the axons of neuronal cells found in the lateral geniculate nucleus, which reach the occipital cortex.
Lower optic radiation (Meyer’s loop) —> runs in the temporal lobe carrying information from the lower part of the retina (so the upper visual field).
Upper optic radiations —> run in the parietal lobe carrying information from the upper part of the retina (so the lower part of the visual field.
The mechanism is an X. What is up and right in the visual field will run below and left in the brain.
Visual pathway lesions?
- Central scotoma (right eye).
- Eye blindness (right eye) —> pre-chiasmatic lesion such as in the optic nerve or eye/retina
- Heteronymous hemianopia —> central chiasmatic lesion such as the case of a pituitary tumor beneath the chiasm.
- Lateral homonymous hemianopia (left hemifield)—> retro-chiasmatic lesion (right) such as in the optic tract, lateral geniculate or upper/lower optic radiations.
- Superior quadrantanopia (upper left) —> right lower optic radiations (Meyer’s loop-temporal lobe).
- Lower quadrantanopia (left lower) —> right upper optic radiations (parietal lobe).
- Lateral homonymous hemianopia with spared foveal vision —> primary visual cortex(large occipital foveal representation).
What is amblyopia?
Amblyopia consists in a phenomenon of ocular dominance (OD) and the effects of monocular deprivation in the mammalian visual cortex.
In early life the thalamic inputs innervate the entire visual cortex. In adult life visual inputs from each eye segregate into alternating eye specific regions in the primary visual cortex, such that each column becomes predominantly innervated by one eye only. Vision of amblyopic eye can be restored in adulthood e.g. combining eye patching with a
treatment that induces Plasticity.
What are visual evoked potentials?
Bioelectrical signals recorded over the occipital cortex after retinal stimulation (oneeye at the time). Usually, we use a checkerboard with black/white alternating squares that are reversing (the white becomes black and vice-versa) 3 times/sec.
In order to see the checks reversing (hence the visual stimulus), we need good visual acuity, so if we cannot see the squares there will be no response recorded.
We can measure the time from the retina to the occipital cortex.
