Segmental syndrome

Pathologies that affect all functions of the spinal cord at one or more levels produce a segmental syndrome. Loss of function may be total or incomplete. A total cord transection syndrome results from the cessation of function in all ascending and descending spinal cord pathways and results in the loss of all types of sensation and loss of movement below the level of the lesion. Less profound injuries produce a similar pattern of deficits, which are less severe： ie, weakness rather than paralysis and decreased sensation rather than anesthesia(麻木).

Acute transection can cause spinal shock, with a flaccid paralysis, urinary retention, and diminished tendon reflexes(hyporeflexia or areflexia). This is usually temporary, and increased tone, spasticity, and hyperreflexia will usually supervene(接著發生) in days or weeks after the event.

Transverse injuries above C3 involve cessation of respiration and are often fatal if acute. Cervical cord lesions that spare the phrenic nerve but impair intercostal nerve function can produce respiratory insufficiency. Lesions above the L2 cord level will cause impotence(陽痿) and spastic paralysis of bladder. There is loss of voluntary control of the bladder, which will empty automatically by reflex action.

Causes of a cord segmental syndrome include acute myelopathies, such as traumatic injury and spinal cord hemorrhage. Epidural or intramedullary abscess, tumors, and transverse myelitis may have a more subacute presentation.

Dorsal cord syndrome

Dorsal cord syndrome results from the bilateral involvement of the dorsal columns, the corticospinal tracts, and descending central autonomic tracts to bladder control centers in the sacral cord. Dorsal column symptoms include gait ataxia and paresthesias(尤其是proprioception及vibration). Corticospinal tract dysfunction produces weakness that, if acute, is accompanied by muscle flaccidity and hyporeflexia and, if chronic, by muscle hypertonia and hyperreflexia. Extensor plantar responses(腳蹠部的伸張反應) and urinary incontinence may be present.

Causes of a dorsal cord syndrome include multiple sclerosis(more typically the primary progressive form), tabes dorsalis(脊髓癆；由neurosyphilis造成), Friedreich ataxia, subacute combined degeneration(常因維他命B12缺乏所引起), vascular malformations, epidural and intradural extramedullary tumors, cervical spondylotic myelopathy, and atlanto-axial subluxation(寰椎樞椎半脫位).

Ventral cord syndrome

Ventral cord or anterior spinal artery syndrome usually includes tracts in the anterior two-thirds of the spinal cord, which include the corticospinal tracts, the spinothalamic tracts, and descending autonomic tracts to the sacral centers for bladder control. Corticospinal tract involvements produce weakness and reflex changes. A spinothalamic tract deficit produces the bilateral loss of pain and temperature sensation(雙測溫痛覺喪失). Discriminative tactile, position(proprioception), and vibratory sensation are normal(∵intact dorsal funiculus). Urinary incontinence is usually present. The causes of a ventral cord syndrome include spinal cord infarction, intervertebral disc herniation, and radiation myelopathy.

Brown–Sequard syndrome

A lateral hemisection syndrome, also known as the Brown–Sequard syndrome, involves the dorsal column, corticospinal tract, and spinothalamic tract unilaterally. This produces weakness, loss of vibration, and proprioception ipsilateral to the lesion and loss of pain and temperature on the opposite side. The unilateral involvement of descending autonomic fibers does not produce bladder symptoms. While there are many causes of this syndrome, knife or bullet injuries(單側脊髓槍傷、刀傷) and demyelination are the most common. Rarer causes include spinal cord tumors, disc herniation, infarction, and infections.

Central cord syndromes

The central cord syndrome is characterized by loss of pain and temperature sensation in the distribution of one or several adjacent dermatomes at the site of the spinal cord lesion caused by the disruption of crossing spinothalamic fibers in the ventral commissure. Dermatomes above and below the level of the lesion have normal pain and temperature sensation, creating the so-called "suspended sensory level." Vibration and proprioception are often spared.

As a central lesion enlarges, it may encroach on(侵入) the medial aspect or the corticospinal tracts or on the anterior horn gray matter, producing weakness in the analgesic areas. Fibers mediating the deep tendon reflexes are interrupted as they pass from the dorsal to the ventral horn, thus causing tendon reflex loss(areflexia) in the analgesic areas. There are usually no bladder symptoms.

The classic causes of a central cord syndrome are slow-growing lesions such as syringomyelia(脊髓空洞症) or intramedullary tumor. However, central cord syndrome is most frequently the result of a hyper-extension injury in individuals with long-standing cervical spondylosis. This form of central cord syndrome is characterized by disproportionately greater motor impairment in upper compared with lower extremities(上肢比下肢嚴重!!!), bladder dysfunction, and a variable degree of sensory loss below the level of injury.

Pure motor syndrome

A pure motor syndrome produces weakness without sensory loss or bladder involvement. This may involve only the upper motor neurons(UMN), producing hyperreflexia and extensor plantar responses, or only the lower motor neuron(LMN) bilaterally, producing muscle atrophy and fasciculations. Other disorders involve both the upper and lower motor neurons and produce mixed signs.

The causes of a pure motor syndrome include chronic myelopathies such as HTLV-I myelopathy, hereditary spastic paraplegia, primary lateral sclerosis, amyotrophic lateral sclerosis(ALS), progressive muscular atrophy, post-polio syndrome, and electric shock-induced myelopathy.

Conus medullaris syndrome

Lesions at vertebral level L2 often affect the conus medullaris. There is early and prominent sphincter dysfunction with flaccid paralysis of the bladder and rectum, impotence, and saddle (S3-S5) anesthesia. Leg muscle weakness may be mild if the lesion is very restricted and spares both the lumbar cord and the adjacent spinal and lumbar nerve roots.

Causes include disc herniation, spinal fracture, and tumors.

Cauda equina syndrome

Though not a spinal cord syndrome, cauda equina syndrome is considered here because its location within the spinal canal subjects it to many of the same disease processes that cause myelopathy. The syndrome is caused by the loss of functions of two or more of the 18 nerve roots constituting the cauda equina. Deficits usually affect both legs but are often asymmetric. Symptoms include：

1.       Low back pain accompanied by pain radiating into one or both legs. Radicular pain reflects involvement of dorsal nerve roots and may have localizing value.

2.       Weakness of plantar flexion(S1) of the feet with loss of ankle jerks(Achilles reflex) occurs with mid cauda equina lesions, involving S1/S2 roots. Involvement of progressively higher levels leads to corresponding weakness in other muscles.

3.       Bladder and rectal sphincter paralysis usually reflect involvement of S3~S5 nerve roots.

4.       Sensory loss of all sensory modalities occurs in the dermatomal distribution of the affected nerve roots.

Many etiologies can cause a cauda equina syndrome, including intervertebral disc herniation, epidural abscess, epidural tumor, intradural extramedullary tumor, lumbar spine spondylosis, and a number of inflammatory conditions including spinal arachnoiditis, chronic inflammatory demyelinating polyneuropathy, and sarcoidosis(類肉瘤). The cauda equina can also be the primary site of involvement in carcinomatous meningitis and a number of infections, e.g, cytomegalovirus(CMV), herpes simplex virus(HSV), herpes zoster virus, Epstein Barr virus(EBV), Lyme disease(Borrelia burgdorferi), mycoplasma, and tuberculosis.