Anatomy clinical correlates: Spinal cord pathways

Last updated: November 26, 2025

Anatomy clinical correlates: Spinal cord pathways

HDF3 Repro/Neuro

HDF3 Repro/Neuro

Anatomy of the pelvic girdle
Anatomy of the pelvic cavity
Anatomy of the breast
Arteries and veins of the pelvis
Nerves and lymphatics of the pelvis
Anatomy of the female urogenital triangle
Anatomy of the perineum
Anatomy of the female reproductive organs of the pelvis
Anatomy clinical correlates: Breast
Anatomy clinical correlates: Female pelvis and perineum
Development of the reproductive system
Mammary gland histology
Ovary histology
Fallopian tube and uterus histology
Cervix and vagina histology
Anatomy and physiology of the male reproductive system
Puberty and Tanner staging
Testosterone
Anatomy and physiology of the female reproductive system
Estrogen and progesterone
Menstrual cycle
Menopause
Pregnancy
Oxytocin and prolactin
Stages of labor
Breastfeeding
Precocious puberty
Delayed puberty
Klinefelter syndrome
Turner syndrome
Androgen insensitivity syndrome
5-alpha-reductase deficiency
Kallmann syndrome
Amenorrhea
Ovarian cyst
Premature ovarian failure
Polycystic ovary syndrome
Ovarian torsion
Krukenberg tumor
Ovarian sex-cord stromal tumors
Ovarian surface epithelial tumors
Ovarian germ cell tumors
Uterine fibroid
Endometriosis
Endometritis
Endometrial hyperplasia
Endometrial cancer
Choriocarcinoma
Cervical cancer
Pelvic inflammatory disease
Urethritis
Female sexual interest and arousal disorder
Orgasmic dysfunction
Genito-pelvic pain and penetration disorder
Mastitis
Fibrocystic breast changes
Intraductal papilloma
Phyllodes tumor
Paget disease of the breast
Breast cancer
Hyperemesis gravidarum
Gestational hypertension
Preeclampsia & eclampsia
Gestational diabetes
Cervical incompetence
Placenta previa
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Oligohydramnios
Polyhydramnios
Potter sequence
Intrauterine growth restriction
Preterm labor
Postpartum hemorrhage
Chorioamnionitis
Congenital toxoplasmosis
Congenital cytomegalovirus (NORD)
Congenital syphilis
Neonatal conjunctivitis
Neonatal herpes simplex
Congenital rubella syndrome
Neonatal sepsis
Neonatal meningitis
Miscarriage
Gestational trophoblastic disease
Ectopic pregnancy
Fetal hydantoin syndrome
Fetal alcohol syndrome
Disorders of sex chromosomes: Pathology review
Prostate disorders and cancer: Pathology review
Testicular tumors: Pathology review
Uterine disorders: Pathology review
Ovarian cysts and tumors: Pathology review
Cervical cancer: Pathology review
Vaginal and vulvar disorders: Pathology review
Benign breast conditions: Pathology review
Breast cancer: Pathology review
Complications during pregnancy: Pathology review
Congenital TORCH infections: Pathology review
Disorders of sexual development and sex hormones: Pathology review
Amenorrhea: Pathology review
Testicular and scrotal conditions: Pathology review
Sexually transmitted infections: Warts and ulcers: Pathology review
Sexually transmitted infections: Vaginitis and cervicitis: Pathology review
HIV and AIDS: Pathology review
Androgens and antiandrogens
PDE5 inhibitors
Adrenergic antagonists: Alpha blockers
Estrogens and antiestrogens
Progestins and antiprogestins
Aromatase inhibitors
Uterine stimulants and relaxants
Anatomy clinical correlates: Male pelvis and perineum
Bones of the cranium
Anatomy of the cranial base
Anatomy of the cerebral cortex
Anatomy of the cerebellum
Anatomy of the cranial meninges and dural venous sinuses
Anatomy of the brainstem
Anatomy of the basal ganglia
Anatomy of the white matter tracts
Anatomy of the limbic system
Anatomy of the blood supply to the brain
Anatomy of the diencephalon
Anatomy of the ventricular system
Anatomy clinical correlates: Cerebral hemispheres
Anatomy of the vertebral canal
Anatomy of the descending spinal cord pathways
Anatomy of the ascending spinal cord pathways
Anatomy clinical correlates: Vertebral canal
Anatomy clinical correlates: Spinal cord pathways
Memory
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Consciousness
Learning
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Language
Emotion
Attention
Transient ischemic attack
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Shaken baby syndrome
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Normal pressure hydrocephalus
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Pituitary adenoma
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Syringomyelia
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Spinal muscular atrophy
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Congenital neurological disorders: Pathology review
Traumatic brain injury: Pathology review
Dementia: Pathology review
Movement disorders: Pathology review
Demyelinating disorders: Pathology review
Pediatric brain tumors: Pathology review
Adult brain tumors: Pathology review
Central nervous system infections: Pathology review
Cerebral vascular disease: Pathology review
Anti-parkinson medications
Medications for neurodegenerative diseases

Transcript

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The spinal cord is made up of millions of neurons, whose axons and cell bodies are constantly transmitting information between our brain and the rest of our body.

In doing so, the spinal cord acts as an amazing information highway, allowing our brain and body to work together to interact with the world around us!

But what happens when this information highway is disrupted or damaged? Well, injury to the spinal cord leads to a variety of classic clinical conditions with predictable deficits which we will explore in this video, so let’s get to it!

Okay, before we move on to spinal cord injuries, let’s freshen up our knowledge of the spinal cord itself. Zooming in on a cross-section of the spinal cord, it’s made up of both grey and white matter.

Grey matter is found in the centre of the spinal cord and has two dorsal or posterior horns that contain sensory neuron cell bodies, and two ventral or anterior horns that contain motor neuron cell bodies.

Surrounding the grey matter is white matter, which consists of the axons of various neurons. They are organized into tracts that carry information to and from the brain.

There are four main sensory pathways ascending the spinal column. First, there’s the spinothalamic tract which is divided into two parts.

The lateral tract carries sensory information for pain and temperature, while the anterior tract carries information for crude touch and pressure.

Next, there are two dorsal column tracts: the fasciculus gracilis which carries sensory information from the lower trunk and legs, and the fasciculus cuneatus which carries sensory information from the upper trunk and arms.

These tracts both carry sensations such as two point discrimination, vibration, fine touch and proprioception. Then, there’ s the spinocerebellar tract which has an anterior and posterior part.

These are ascending pathways from the spinal cord to the cerebellum, and carry proprioceptive information from the body.

Finally, the major motor pathways descending down the spinal column are the anterior and lateral corticospinal tracts, which are descending tracts that allow us voluntary movement of the limbs. Spinal cord injuries can happen because of a number of different causes.

First, the spinal cord can undergo compression or increased pressure such as from a protruding intervertebral disk or osteophytes, and this can produce sensory and motor symptoms in the area innervated by that particular spinal segment.

In more severe cases, the spinal cord may undergo transection, leading to the loss of all sensation and voluntary movement inferior to the site of lesion.

Let's take a closer look at the effects of spinal cord transection. The higher the level the transection occurs at, the more function is lost.

If transection happens between C1 and C3, then there’s no function below the level of the head and a ventilator is needed to maintain respiration.

If transection happens between C4 and C5 then the individual will suffer quadriplegia, meaning they have no function of their upper and lower limbs or trunk, however they can still breath on their own since the phrenic nerve is spared.

If transection happens between C6 and C8, then there’s still a complete loss of trunk and lower limb function, however some movements of the upper limb will be intact, allowing for functions such as feeding or using a wheelchair.

If transection happens between T1 and T9, the individual becomes paraplegic, so there’s paralysis of both lower limbs, while upper limb function remains intact.

In this case, the amount of trunk control varies with the height of the lesion, meaning the higher the lesion, the more severe the deficits are.

If transection happens anywhere between T10 and L3, then there will be some level of dysfunction of the lower limbs resulting in difficulties with walking and ambulation.

Now, unlike a complete lesion of the spinal cord, which causes bilateral loss of function of the structures below the lesion, a hemilesion, which is a lesion to only one side of the spinal cord, also known as Brown Sequard syndrome, will spare certain functions on each side of the body depending on the side of the lesion.

The most common cause is a penetrating trauma like a gunshot injury or stab wound in the back, but a large spinal cord tumor can lead to this syndrome. A complete hemisection would result in damage to multiple neural tracts, while sparing others.

When we consider each tract, we have to think about what happens to that motor or sensory modality at the level of the lesion, and below the level of the lesion.

We also need to think about which side of the body will be affected since the tracts crossover at different locations! For example, a complete hemisection on the right hand side would result in the following.

First, there’d be damage to the dorsal column on the right side, which will lead to loss of fine touch, two point discrimination, vibration, and proprioception in the right side of the body, which is ipsilateral to the side of the lesion. The loss of these sensory modalities would occur at the level of the injury and below it.

Second, the anterior horn will be damaged, resulting in a lower motor neuron lesion at that particular level.

Remember, the lower motor neurons synapse with upper motor neurons of the descending tracts such as the corticospinal tract.

Damage to the anterior horn cells will lead to lower motor neuron signs such as ipsilateral flaccid paralysis and hypoactive deep tendon reflexes at the specific spinal level of the lesion.

Third, damage to the lateral corticospinal tract passing through that spinal level, results in upper motor neuron signs on the ipsilateral side of the lesion, below the level of the lesion.

These signs include things such as spastic paralysis, hyperactive deep tendon reflexes and a positive Babinski reflex. Finally, there’s damage to the spinothalamic tract.

The spinothalamic tract is a bit different though because fibers of the anterior tract, which carries crude touch and pressure, will actually ascends 1 or 2 spinal segments above the level where the 1st order neurons enter, and then cross over to the opposite side of the spinal cord.

In contrast, the fibers of the lateral tract, which carry pain and temperature, typically cross over right away.

So, since these fibres all cross over within the spinal cord, a hemilesion on the right side of the spinal cord will cause loss of these sensory modalities on the left side The level that’s affected though will change a bit!

This means on the contralateral side 1-2 levels starting below the lesion there is a loss of crude touch and pressure due to anterior tract damage, and at the level of the lesion and below there is loss of pain and temperature due to lateral tract damage.

Furthermore, on the ipsilateral side of the lesion, the lateral spinothalamic tract which synapse at that level and the anterior spinothalamic tract fibers that have not crossed yet will both be damaged.

So at the level of the lesion on the ipsilateral side, there will be complete loss of all sensory sensation.

But starting 1-2 levels below the lesion there is a complete sparing of crude touch, pressure, pain and temperature.

To sum up, during a hemi-section, on the ipsilateral side of the lesion, there will be 1) at the level of the lesion there is loss of all sensory sensation 2) Below the lesion complete loss of fine touch, two point discrimination, vibration, and proprioception, where 1-2 levels starting below the lesion there is complete sparing of crude touch, pressure, pain and temperature 3) there will be lower motor neuron signs such as flaccid paralysis at the level of the lesion 4) upper motor neuron signs below the level of the lesion, and 5) on the contralateral side, at the level of the lesion and below there is loss of pain and temperature where 1-2 levels starting below the lesion there is loss of crude touch and pressure.

Of note, hemisection at T1 may result in ipsilateral horner syndrome. Alternatively, damage to the spinal cord can also be a result of ischemia.

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