The spinal cord is the conduit between the brain and the rest of the body. It sends motor commands from the motor cortex to the muscles of the body, and sensory information from the afferent fibers to the sensory cortex. Additionally, the spinal cord can act without signals from the brain in certain instances. The spinal cord independently coordinates reflexes using reflex arcs. Reflex arcs allow the body to respond to sensory information without waiting for input from the brain.  The reflex arc starts with a signal from a sensory receptor, which is carried to the spinal cord via a sensory nerve fiber, synapsed on an interneuron, carried over to the motor neuron, which stimulates an effector muscle or organ. The spinal cord also has central pattern generators, which are interneurons that form the neural circuits, which control rhythmic movements. Although the existence of central pattern generators in humans is controversial, the lumbar spinal cord produces rhythmic muscle activation without volitional motor control or step-specific sensory feedback, suggesting their role in human movement.[12]

Three connective tissue layers called meninges conceal the spinal cord. Directly lining the spinal cord is the pia mater, which also thickens to form the denticulate ligament, anchoring the spinal cord in the middle of the vertebral canal. The next layer of meninges is the arachnoid mater. Between the pia mater and arachnoid mater is the subarachnoid space, which contains cerebrospinal fluid. On top of the arachnoid mater is the last layer of meninges, the dura mater, then the epidural space separating the meninges from the vertebral column.

The spinal cord extends from the medulla oblongata of the brain stem at the level of the foramen magnum. In an adult human, the spinal cord gives rise to thirty-one pairs of spinal nerves, each of which originates from the adjacent spinal cord segment:

• Cervical nerves (C1-C8): there is an enlargement of the spinal cord here because spinal nerves from this area go to the upper extremities, which has more neural input and output.
• Thoracic nerves (T1-T12)
• Lumbar nerves (L1-L5): there is an enlargement here as well, to account for the lower extremities.
• Sacral nerves (S1-S5)
• Coccygeal nerve (Co1)

Spinal nerves emerge from the spinal cord as rootlets, which conjoin to form two nerve roots. The anterior nerve roots contain motor fibers extending from the anterior horn to peripheral target organs. The motor neurons are multipolar, with at least two dendrites, a single axon, and one or more collateral branches. They control skeletal muscles and the autonomic nervous system. The posterior nerve roots contain sensory fibers and dorsal root ganglia. They contain sensory fibers transmitting sensory information from the periphery towards the central nervous system. The sensory neurons located at the dorsal root ganglia are pseudounipolar. The anterior and posterior nerve roots converge into spinal nerves, which split into dorsal and ventral rami. A dermatome is a skin area innervated by a single spinal nerve root (or spinal cord segment).

There are five spinal plexuses, which include sensory and motor nerves from the anterior rami:

• Cervical plexus (C1-C5): the deep branches innervate neck muscles, and the superficial branches innervate the skin on the neck, head, and chest. The cranial plexus also has an autonomic function, including control of the diaphragm and interactions with the vagus nerve.
• Brachial (C5-T1): controls movement and sensation of the upper extremity.
• Lumbar (L1-L4): controls movement and sensation of the abdominal walls, thigh, and external genitals.
• Sacral (L4, L5, S1-S4): controls movement and sensation of the foot, leg, and thigh.
• Coccygeal (S4, S5, Co): innervates the skin around the tailbone.

The spinal cord tapers to its end, termed the conus medullaris, at the level of the second lumbar vertebra in adults. Past the conus medullaris, a bundle of spinal roots extends termed the cauda equina. The cauda equina and the subarachnoid space continues until S2 and is the target location for a lumbar puncture (AKA the spinal tap).

Electrophysiological testing

Evoked potentials (EPs) measure electrical signals going to the brain and can determine whether there is motor or somatosensory impairment. The signal gets detected by electroencephalography (EEG) or electromyography (EMG). Evoked potentials can be used to assess for spinal cord damage in the setting of spinal cord injury and tumors, as well as to measure the functional impairment and predict disease progression in multiple sclerosis.[13] Somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) are frequently used intra-operatively for monitoring and can be used post-operatively as surrogate endpoints to check muscle strength and sensory status.[14] 

Nerve conduction studies determine whether there has been an injury to a spinal nerve root, peripheral nerve, neuromuscular junction, muscle, cranial nerve, or spinal nerve. They can be used to pinpoint spinal cord lesions. Nerve conduction studies work by stimulating nerves close to the skin or using a needle placed nearby a nerve or nerve root. Neurologists often use them with needle electromyograms.[15]

Lumbar puncture 

A lumbar puncture, or spinal tap, samples the cerebrospinal fluid from the subarachnoid space. The needle to obtain the sample should be inserted between lumbar spinal canal levels L3 and L4 to avoid contact with the spinal cord.[16] The cerebrospinal fluid is then sent to a laboratory to establish whether any insult can be determined. For instance, a lumbar puncture can confirm or exclude bacterial meningitis, which will produce a cloudy fluid suggestive of a high leukocyte count. It is also important to know when not to use a lumbar puncture. Contraindications to lumbar puncture include signs of cerebral herniation, focal neurological signs, uncorrected coagulopathies, or cardiorespiratory compromise.[17]

Deep tendon testing 

Part of the neurological exam is a test of the deep tendon reflexes, which are involuntary motor responses to various stimuli that function via reflex arcs within the spinal cord. They can be used to test the function of the motor and sensory nerves at specific spinal cord levels. Reflex grading is on a scale of 0 (absent reflex) to 5+ (sustained clonus).[18] Some commonly tested reflexes are as follows: 

• Biceps reflex: C5/C6
• Brachioradialis reflex: C6
• Triceps reflex: C7
• Patellar reflex: L2/L3/L4
• Achilles reflex: S1 

Additionally, the Babinski reflex, or the extensor plantar reflex, can be seen in newborns but is an abnormal response after between six to twelve months of age, and indicative of an abnormality in the corticospinal system.[19]

Spinal cord injury

Primary spinal cord injury occurs due to local deformation of the spine, for instance, direct compression.  Secondary spinal cord injury occurs following primary damage and involves cascades of biochemical and cellular processes, including electrolyte disturbances, free radical damage, edema, ischemia, and inflammation.[20]  Secondary spinal cord injury has several phases: acute, subacute, and chronic.  During the acute phase (up to 48 hours after the primary injury), there is hemorrhage and ischemia, which leads to ion balance disruption, excitotoxicity, and inflammation.  During the subacute phase (up to two weeks following primary injury), there is a phagocytic response and a reactive proliferation of astrocytes, which leads to a glial scar in the chronic phase. The thinking is that the scarification is the critical component to permanent disability because it prevents axonal regeneration; axons otherwise could regenerate, but their growth is blocked. However, that notion has been subject to challenge and there are even suggestions that astrocyte scar formation could aid regeneration.[21] In the chronic phase (over six months after the primary injury), the scarification process is complete.[22]

Developmental

Open neural tube defects occur when there is a failure of the neural tube to close. If it fails to close at the cranial end, the fetus can result in anencephaly. If the failure is at the caudal end, the fetus can have myelomeningocele or open spina bifida. Craniorachischisis can also occur if the entire neural tube remains open. Closed neural tube defects are spinal cord development problems that are skin-covered, such as occult spina bifida. Folic acid supplements lower the risk of neural tube defects, although severe folate deficiency in mouse models does not lead to neural tube defects unless there is already a genetic predisposition. Suggestions are that folate can overcome the adverse effects of a genetic predisposition, which might lead to neural tube defects.[23]

A spinal cord injury can be “complete” or “incomplete.” A complete injury, based on the “International Standard Neurological Classification of Spinal Cord Injury” (ISNCSCI) examination developed by American Spinal Cord Injury Association (ASIA), implies that there is no sensation at the inferior segments of the spinal cord (S4-S5), and no deep anal pressure (DAP) or voluntary anal contraction (VAC) are present. If no perianal sensation is present and DAP and VAC are absent, the present function below the level of injury is a zone of partial preservation.[24][25]

An injury in the cervical region often results in quadriplegia if both sides of the spinal cord are affected, and hemiplegia if only one side is affected. Nerves from C3, C4, and C5 stimulate the phrenic nerve, which controls the diaphragm so injury to C4 and above may result in a permanent need for a ventilator. An injury to the thoracic region often limits the function of nerves related to the lower torso and lower extremities and usually does not affect the upper torso and upper extremities, except in rare cases such as, for example, subacute posttraumatic ascending myelopathy (SPAM).[26][27] Injury to the spinal cord often causes loss of bowel and bladder control, loss of sexual function, and blood pressure dysregulation, as spinal cord relays autonomic and somatic information.

Syndromes

Several syndromes correlate with spinal cord injury. Central cord syndrome usually occurs with individuals who suffer a hyperextension injury, and it often leads to incomplete injury with weakness predominantly affecting the upper limbs. The reason for this phenomenon is the organization of the fibers in the spinal cord: the fibers running to the lower extremities are longer than those running to the upper extremities; the longer fibers are located more laterally in the spinal cord (“L-L rule”). As the central portion of the spinal cord is injured, there is a sparing of the fibers running to the lower extremities. Brown-Sequard syndrome is due to a spinal cord hemisection, and it leads to a complete loss of sensation at the level of the lesion, as well as deficits below the lesion – loss of proprioception, vibration, and motor control, ipsilaterally and a loss of pain and temperature sensation, contralaterally. Anterior cord syndrome is due to a compromised blood supply to the anterior two-thirds of the spinal cord, damaging the corticospinal and spinothalamic tracts. This syndrome is associated with several deficits at and below the lesion, including motor loss and a loss of pain and temperature sensation. However, light touch and joint position sense, from the dorsal columns, are left intact.[28] Injury to T12-L2 segments might result in conus medullaris syndrome, while injury to L3-L5 segments might lead to cauda equina syndrome. Usually, these syndromes present as incomplete injuries, and result in neurogenic bladder and/or bowel, loss of sexual function, and perianal loss of sensation.[29]