paraplegia - Neurology/IM Flashcards
UMNL VS LMNL
UMNL : SPASTIC PARAPLEGIA
LMNL: FLACCID PARALYSIS
Definition of Spastic paraplegia
Paralysis or weakness of both lower-limbs due to bilateral pyramidal tract lesion, most commonly in the spinal cord (spinal paraplegia), & less commonly in
the brain stem or the cerebral parasagittal region (cerebral paraplegia).
Types of spastic paraplegia ?
1) Focal: paraplegia with a level.
2) Systemic: paraplegia without a level.
3) Disseminated: paraplegia without a level.
Focal causes of spastic paraplegia ?
A. Compression:
1) Vertebral:
-Fracture or fracture-dislocation of the vertebra.
-Disc prolapse and spondylosis.
-Pott’s disease.
-Neoplastic diseases:
1. Primary as osteosarcoma or hemangioma.
2. Metastatic from a 1ry carcinoma (thyroid, breast, lung, stomach and prostate).
-Deformity of the vertebral column as kyphoscoliosis.
2) Meningeal (extramedullary):
-Extradural e.g., leukemic deposits and lymphomas.
-Dural e.g., meningioma, pachymeningitis hypertrophica of syphilis.
-Intradural e.g., neurofibroma, cystic arachnoiditis.
3) Spinal Cord (intramedullary):
- Syringomyelia - Glioma
-Ependymoma of the cord.
B. Inflammatory:
- Transverse myelitis
- Myelomeningitis
- Myeloradiculitis.
C. Vascular: Anterior spinal artery occlusion.
Disseminated causes of spastic paraplegia ?
1) Multiple sclerosis (MS)
2) Acute Disseminated encephalomyelitis (ADEM)
3) Disseminated syphilitic lesions.
Systemic causes of spastic paraplegia ?
1) Heridofamilial:
a) Hereditary spastic paraplegia.
b) Hereditary ataxias e.g., Friedreich’s ataxia & Maries’ataxia..
2) Symptomatic:
a) Pellagra, lateral sclerosis.
b) Subacute combined degeneration (SCD).
3) Idiopathic: motor neuron disease.
Causes of cerebral paraplegia in parasagittal region?
1) Traumatic e.g.
- Depressed fracture of the vault of the skull.
- Subdural hematoma.
2) Vascular e.g., superior sagittal sinus thrombosis.
3) Inflammatory e.g., encephalitis, meningio-encephalitis.
4) Neoplastic e.g., parasagittal meningioma.
5) Degenerative e.g., cerebral palsy (Spastic diplegia).
Causes of cerebral paraplegia in brain stem
1) Syringobulbia.
2) Midline brain stem tumors.
N.B. These lesions arise in the midline & involve the innermost pyramidal fibers which are those of the lower limbs
Clinical picture of focal paraplegia at level of the lesion
- Vertebral manifestations: only present if the cause is vertebral. - Localized pain, tenderness, Localized deformity or swelling.
- Radicular manifestations: only present in extra-medullary causes.
a) Posterior root affection:
-Early pain in the back referred to the distribution of the affected root and described as girdle pain; it is exaggerated by coughing, sneezing & straining.
-Later there is hypoesthesia or anesthesia in the dermatome supplied by the affected root.
b) Anterior root affection: localized LMN weakness in the muscles supplied by the affected root.
Describe the stages of acute paraplegia ? (motor manifestations)
- Stage of flaccidity due to neuronal shock: Immediately following the lesion there is sudden paralysis of the lower limbs, associated with complete loss of tone & absence of reflexes (flaccid paralysis). This stage lasts from 2 to 6 weeks.
- Stage of spasticity due to recovery from the neuronal shock:
- On recovery from the shock stage, the full-blown picture of UMNL will be established including hypertonia, hyperreflexia, positive Babinski sign & maybe clonus.
Describe the gradual onset of paraplegia? (Motor manifestations)
●The shock stage is absent, and there will be gradual progressive weakness of the lower limbs with hypertonia and hyperreflexia:
●The weakness affects the distal group of muscles more than the proximal group and the flexor muscles more than the extensors.
●The hypertonia & hyperreflexia affect the extensor group of muscles (antigravity) more than the flexor group (progravity) the paraplegia in this stage is described as (paraplegia in extension).
●With further progression of the lesion, the extrapyramidal fibers in the cord will be affected. The hypertonia and hyperreflexia will be more in the flexor group of muscles than in the extensors. In this stage the paraplegia is described as (paraplegia in flexion).
●This last stage may be associated with the mass reflex where there is spontaneous urination, defecation and sweating on scratching the skin over the medial side of the thigh associated with reflex erection & ejaculation on squeezing the glans penis.
Sensory manifestations below level of lesion in paraplegia
a) If the cause of the lesion is extramedullary, encroachment on ascending tracts at the site of lesion results in a sensory level below which all types of sensations are diminished. There is early loss of sensation in the saddle area (S 3,4,5), as the sacral fibers lie in the outermost part of the spinothalamic tracts in the cord. Saddle area: proximal medial thigh, inguinoscrotal & anal areas.
b) If the cause of the lesion is intramedullary, there will be a jacket sensory loss (hypothetic area with normal sensations above and below it). The sensory loss is of a dissociated nature i.e., pain & temperature sensations are lost but touch & deep sensations are preserved; this is due to the interruption of the crossing fibers carrying pain & temperature, by the midline lesion, while touch & deep sensation fibers ascend in the posterior column without decussation.
●The sensations over the saddle area are preserved (sacral spare), as the sacral fibers lie far from the midline lesion.
Sphincter manifestations below level of lesion in paraplegia
a) In acute lesions retention of urine in the shock stage, followed by precipitancy of micturition.
b) In gradual lesions: precipitancy of micturition which may terminate in automatic bladder when complete transection of the cord occurs.
●These changes start late in extramedullary lesions & early in intramedullary lesions as pyramidal fibers controlling bladder center lie medially in the cord.
Investigations used in paraplegia
A. Imaging:
1) MRI and CT spine is the most useful diagnostic tool in evaluating cord compression, canal diameter, & most of the other causes of myelopathy.
2) Plain x-ray spine may show
●Destruction of the vertebrae as in Pott’s disease and metastases.
B. CSF Examination:
- Normally the CSF is a clear colorless fluid.
1) CSF pressure: it is measured by tapping the CSF in the lumbar region, using a needle connected to a spinal manometer.
● Normally it is 120 ml of CSF or water.
● In extramedullary compression it is markedly diminished.
● In intramedullary compression it is less markedly diminished.
2) CSF analysis
C. Electrophysiologic studies: EMG and NCS to exclude peripheral neuropathy or widespread AHCs disease; to define level of radiculopathy
Extramedullary VS intramedullary differential diagnosis?
Onset:
● E: Painful (Early) due to posterior root irritation.
● I: Painless
Motor features:
● E: Usually, asymmetrical
● I: Usually, symmetrical
Bladder disturbances
● Late
● Early
UMN
● Prominent paresis and hyperreflexia
● Can be late & less prominent
Spinal subarachnoid block & changes in CSF
● Early and marked
● Late and less marked
Sensory changes
●Sensory level: All types of
sensations are diminished
below the level including pain,
temperature and touch.
Early loss of sensation in
saddle area.
● Jacket sensory loss. Late
loss of sensation in the
saddle area (sacral spare)
Dissociated sensory loss
i.e., loss of pain and temp,
with preservation of touch
