Spinal cord lesions Flashcards
Poliomyelitis and Werdnig-Hoffman
LMN lesions only,
Due to destruction of anterior horn
Flaccid paralysis
Multiple sclerosis
Most white matter of cervical region;
random and asymmetric lesions, due to demyelination
Scanning speech,
intention tremor,
nystagmus (MLF)
Amyotrophic lateral sclerosis (Lou Gehrig’s disease)
Combined UMN and LMN deficit with no sensory, cognitive, or oculomotor deficit.
Both UMN and LMN signs
Can be caused by defect in superoxide dismutase I.
Commonly presents as fasciulation with eventual atrophy, progressive and fatal
Riluzole treatment mostly increases survival by decreasing presynaptic glutamate release
Complete occlusion of anterior spinal artery
Spares dorsal columns and Lissauer’s tract (posterolateral tract where posterior nerve roots enter)
Upper thoracic ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below ~ T8.
Tabes dorsalis
3’s syphilis.
Degeneration (demyelination) of dorsal column and roots
Impaired sensation and proprioception and progressive sensory ataxia (inability to sense or feel the legs)
Associated with Charcot’s joint, shooting pain, Argyll Robertson’s pupil (small bilateral pupils that further constricts to accomodation but not to light).
Exam will demonstrate absence of deep tendon reflex and positive romberg
Syringomyelia
Syrinx expands and damages anterior white commissure of spinothalamic tract (2nd order neurons) -> bilateral loss of pain and temp sensation (usually C8-T1)
Seen with Chiari I malformationl
Can expand and affect other tracts
Vitamin B12 or vitamin E deficiency
Subacute combined degeneration
Demyelination of dorsal columns, lateral cortisospinal tract, and spinocerebellar tract; ataxic gait, paresthesia, impaired position and vibration sense.
Poliomyelitis
Caused by poliovirus
Replicates oral pharynx and small intestine before spreading via the bloodstream to the CNS.
Infection causes destruction of cells in anterior horn of spinal cord (LMN death)
Symptoms: LMN signs-weakness, hypotonia, flaccid paralysis, atrophy, fasciculation, hyporeflexia, and muscle atrophy.
Finding: CSF with increase WBC with slight elevation of protein (no change in CSF glucose).
Werdnig-Hoffman disease
Congenital degeneration of anterior horn of spinal cord
Thus LMN lesion
“Flappy baby” with marked hypotonia and tongue fasciculation.
Infantile type has median age of death of 7 months.
AR inheritance
Friedreich’s ataxia
AR, GAA repeat in frataxin gene
Leads to impairment in mitochondrial functioning
Symptoms: staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, hypertrophic cardiomyopathy (cause of death)
Presents in childhood with kyphoscoliosis
“Friedreich is Fratastic; he’s your favorite fat bro, always stumbling, staggering, and falling.”
Brown Sequard
1) Ipsilateral LMN sign below the level of the lesion (due to corticospinal tract damage)
2) Ipsilateral loss of tactile, vibration, proprioception sense below the level of the lesion (due to dorsal column damage)
3) contralateral pain and temp loss below the level of the lesion (due to spinaothalamic tract damage)
4) ipsilateral loss of all sensation at the level of the lesion
5) ipsilateral LMN sign (flaccid paralysis )
If lesion above T1, patient may present with Horner’s syndrome due to damage to sympathetic ganglion.
Horner’s syndrome
Sympathectomy of face
1) ptosis, 2) anhidrosis (and flushing of affected side)
3) miosis
The 3 neuron oculosympathetic pathway projects from the hypothalamus to the intermediolateral column of the spinal cord, and then superior cervical (sympathetic) ganglion, and finally to the pupil, the smooth muscle of the eyelid, and the sweat gland of the forehead and face.
