spinal cord diseases

Where does the spinal cord extend, and what lies below its termination?

From the foramen magnum to approximately L1–L2; below this lies the cauda equina, consisting of nerve roots.

Where are spinal grey and white matter located, and what do they contain?

Grey matter is internal and butterfly-shaped, containing neuronal cell bodies; white matter is external and contains long nerve tracts.

What functions do the corticospinal, dorsal column, and spinothalamic tracts carry?

Corticospinal: motor movement; dorsal columns: vibration and position sense; spinothalamic: pain and temperature.

Which territories are supplied by the anterior and posterior spinal arteries?

The anterior spinal artery supplies the anterior two-thirds of the cord; the two posterior spinal arteries supply posterior regions, including the dorsal columns.

What is the artery of Adamkiewicz, and where is it usually found in this file?

A major feeder of the lower thoracic cord and conus, usually arising on the left at T9–T12.

What is a complete transverse spinal cord lesion, and what causes are listed?

Complete interruption of cord function below a level; causes include trauma, acute transverse myelitis, ischemia, and hemorrhage.

What motor and reflex findings characterize acute spinal shock?

Flaccid paralysis, areflexia, and absent plantar responses below the lesion during the first days to weeks.

What bladder and sensory findings accompany acute complete cord interruption?

Urinary retention that may lead to overflow incontinence, with a clear sensory level.

What findings characterize the chronic spastic stage after a complete cord lesion?

After approximately 4–6 weeks: spastic paraplegia/quadriplegia, hyperreflexia, positive Babinski, reflex bladder emptying, and a persistent sensory level.

Can slowly developing spinal cord lesions occur without an obvious spinal-shock phase?

Yes. Slowly progressive lesions may skip spinal shock.

What are the late flexor-withdrawal and mass reflexes described in the file?

Flexor withdrawal: stimulation can cause both legs to flex; mass reflex: sweating, bladder emptying, and ejaculation may occur together.

What is Brown–Séquard syndrome?

A spinal cord hemisection syndrome, although complete hemisection is rare and partial patterns are more common.

Which deficits occur ipsilateral to a Brown–Séquard lesion?

Upper motor neuron weakness below the lesion and loss of vibration and position sense.

Which deficits occur contralateral to a Brown–Séquard lesion, and where do they begin?

Pain and temperature loss, typically starting 1–2 segments below the lesion.

What causes of Brown–Séquard syndrome are listed?

Trauma, especially stab wounds; tumors/metastases; radiation myelopathy; MS; and disc herniation.

What is syringomyelia, and where is the cavity commonly located?

A fluid-filled cavity in the central spinal cord, commonly in the mid-to-lower cervical region.

What is the classic sensory pattern of syringomyelia?

Cape-like loss of pain and temperature over shoulders and arms, with preserved touch, vibration, and position sense: dissociated sensory loss.

Why does syringomyelia cause dissociated sensory loss?

The cavity damages crossing spinothalamic fibers anterior to the central canal while initially sparing dorsal-column modalities.

How do motor findings in syringomyelia evolve?

Early lower motor neuron wasting in the hands may be followed by upper motor neuron signs in the legs.

Which additional clues support syringomyelia?

Painless burns or cuts on the hands and associated Chiari I malformation on MRI.

How do typical onset and pain differ between conus medullaris and cauda equina syndromes in the file?

Conus: sudden onset with relatively little pain; cauda equina: more gradual onset with severe radicular leg pain. These are typical patterns.

How do sensory loss and weakness differ between conus and cauda equina syndromes?

Conus: symmetric saddle anesthesia with mild or absent leg weakness; cauda equina: asymmetric root-pattern sensory loss and asymmetric LMN weakness.

How do reflex and sphincter findings differ between conus and cauda equina syndromes?

Conus: knee reflexes preserved, ankle reflexes may be lost, and early severe sphincter dysfunction; cauda equina: knee/ankle reflexes may be lost and sphincter dysfunction is typically later.

Which new symptoms require urgent MRI for possible conus or cauda equina involvement?

New saddle anesthesia or urinary retention.

What is the classic pattern of anterior spinal artery syndrome?

Sudden weakness/paraplegia, pain-temperature loss, and bladder/bowel dysfunction, with vibration and position sense relatively preserved.

Why are vibration and position sense preserved in anterior spinal artery syndrome?

The dorsal columns retain their posterior spinal arterial blood supply.

What settings commonly precede spinal cord infarction?

Aortic surgery, aortic dissection, atherosclerosis, and hypotension; onset is usually over minutes to hours.

What treatment priorities for spinal cord infarction are stated in the file?

Maintain spinal cord perfusion and avoid hypotension; lumbar CSF drainage may help in the setting of aortic surgery.

Which spinal region is affected in posterior spinal artery syndrome and tabes dorsalis?

The dorsal columns.

Which viruses are associated with anterior horn injury, and what signs result?

Enteroviruses such as polio, EV-D68, and EV-A71; they cause lower motor neuron signs and flaccid weakness.

Which other viral spinal cord disorders are listed?

HSV/VZV myelitis, HIV-associated vacuolar myelopathy, and HTLV-1-associated myelopathy.

What findings suggest tabes dorsalis?

Late syphilis with lightning pains, Argyll Robertson pupils, dorsal-column sensory loss, sensory ataxia, and a positive Romberg sign.

How can spinal tuberculosis produce neurologic deficits?

Pott disease may cause an abscess or vertebral collapse, compressing the cord and producing motor and sensory deficits.

What is transverse myelitis, and what is its typical clinical course?

Inflammation of one or more cord segments, predominantly involving white matter; weakness, a sensory level, and bladder dysfunction develop over hours to days and peak within about 3 weeks.

What causes of transverse myelitis are listed?

MS, NMOSD, MOG antibody disease, postinfectious/postvaccination myelitis, sarcoidosis, SLE, and Sjögren syndrome.

What must be excluded first in suspected transverse myelitis, and how?

Cord compression, using urgent contrast-enhanced spinal MRI; compressive lesions may be surgical emergencies.

What CSF findings may occur in transverse myelitis?

Normal CSF or mild pleocytosis around 10–100 cells/mm3, mildly elevated protein, and normal glucose.

What targeted investigations are listed for transverse myelitis?

Serology, CSF cultures, IgG index/oligoclonal bands, AQP4/MOG antibodies, brain MRI, B12, and copper.

How do spinal MRI lesions in MS and NMOSD typically differ?

MS: short, usually under 2 segments, peripheral dorsal/lateral partial lesions; NMOSD: long lesions spanning at least 3 segments, centrally located, often with cord swelling.

Which laboratory and associated clinical findings distinguish MS from NMOSD in the file?

MS: CSF-restricted oligoclonal bands and periventricular brain lesions; NMOSD: AQP4-IgG in most, usually absent oligoclonal bands, severe optic neuritis, or area postrema syndrome.

What symptoms define area postrema syndrome in the file?

Hiccups and vomiting.

Which tracts are affected in B12-related subacute combined degeneration, and what deficits follow?

Dorsal columns: impaired vibration/position and sensory ataxia; lateral corticospinal tracts: spastic weakness and UMN signs.

What causes or risk factors for B12 deficiency are listed?

Pernicious anemia, Crohn/celiac disease, gastric or ileal surgery, long-term metformin/PPI use, an unsupplemented vegan diet, and nitrous oxide exposure.

What clinical findings suggest subacute combined degeneration?

Tingling feet, spastic-ataxic gait, vibration/position loss, positive Romberg, spasticity/brisk knee reflexes, sometimes absent ankle reflexes, and possible bladder/cognitive changes.

What laboratory and MRI findings support B12-related myelopathy?

Low or low-normal B12, elevated methylmalonic acid and homocysteine, and dorsal-column T2 hyperintensity with an inverted-V appearance; anemia may be absent.

How is B12-related myelopathy treated, and why is timing important?

Intramuscular or high-dose oral B12; do not treat with folate alone. Early deficits may be largely reversible, whereas late deficits may persist.

What causes copper-deficiency myelopathy, and what treatment is listed?

Gastric surgery, malabsorption, or excess zinc can produce a B12-like syndrome; treatment is copper replacement and stopping excess zinc.

Which other nutritional/toxic/metabolic myelopathies are listed?

Vitamin E deficiency: spinocerebellar syndrome; hepatic myelopathy: slowly progressive pure spastic paraparesis; nitrous oxide: B12 inactivation; organophosphates: delayed neuropathy/myelopathy.

What are the typical presentation and common genetic form of hereditary spastic paraplegia?

Very slowly progressive symmetric leg stiffness/weakness with brisk reflexes and extensor plantar responses; the most common form is autosomal dominant SPG4 due to SPAST.

How do pure and complicated hereditary spastic paraplegia differ, and how is diagnosis supported?

Pure: predominantly leg symptoms, sometimes mild bladder/vibration changes; complicated: additional neurologic features. Use family history/genetic testing and exclude treatable compression, B12/copper deficiency, and MS.