(From Dr. Glasser’s Lecture, 26-28 July 2000, by Brian Buschman)
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Syringomyelia is an enlargement of the central canal which will hit the ventral white commisure. It will cause bilateral loss of pain/temperature at the level of the legion by taking out the anterior white commisure. Syringomyelia is most common at the cervical level. It may grow to include ventral horn cells which cause flaccid paralysis.
Tabes dorsalis is associated with late stage (tertiary) syphilis and is a bilateral demyelination of the dorsal columns causing bilateral loss of epicritics (fine touch and such).
Polio is a loss of the LMN function causing flaccid paralysis, atrophy and fasciculations.
A legion of one half of the spinal cord causing loss of UMNs which leads to spastic paralysis, clonus and Babinski sign below the legion. It also has ipsilateral epicritic loss (fine touch) due to dorsal column legions and contralateral protopathic loss (temp and pain).
ALS is a bilateral loss of both UMNs and LMNs.
It may be due to B12 deficiency or from AIDS. It includes demyelination of anything, especially dorsal columns (epicritic), spinocerebellar (ataxia) and corticospinal (UMN).
Loss of the dorsal column will cause a sensory ataxia associated with a wide based gate. The patient puts with heals down before their toes and they tend to look down while they walk because they are unable to sense their feel hitting the ground.
Open eyes with III
Close eyes with VII
Look down and out with VI
Pupilary light reflex: In on II out on III bilaterally.
Accommodation is in on II and out on III. With Argyle-Robertson the pupils will still constrict with accommodation but not reflexly.
Optokinetic (visual reflex) is in on II out on III, IV, VI via the MLF.
Vestibulocular (auditory reflex) is in on VIII and out on III, IV, VI via the MLF.
Jaw Jerk reflex is in and out on V.
Corneal reflex (direct and consensual) is in on V (ophthalmic) and out on VII.
Gag reflex (direct and consensual) is in on IX out on X.
The spinal cord is supplied by three arteries. One anterior spinal artery and two posterior spinal arteries. The anterior spinal artery supplies the anterior 2/3 of the spinal cord which includes just about all of the tracts except for the dorsal column. Blockage of the anterior spinal artery will cause bilateral loss of everything except the epicritics in the dorsal column.
The posterior spinal arteries each supply the posterior 1/3 of the spinal cord on their respective side. Spinal arteries supply the dorsal columns so their occlusion will cause ipsilateral loss of epicritics.
The spinal arteries are branches off of the vertebral arteries. They also get some input from the redicular arteries which are small branches off of segmental arteries that go to supply the nerve roots. There are 6-10 larger ones that function as collaterals called rediculomedullary arteries to supply the spinal arteries. It would also be hard for such a small artery (anterior spinal artery) so supply all the way down to the conus medularis. There is a large artery that branches off of a left lumbar intersegmental artery, called the Artery of Adam Krevicz, which is a large collateral to the spinal arteries. It is the primary source of blood to supply the spinal cord from about T8 to the conus. If it’s clamped during surgery then it will cause paralysis from around T8 down.
If a neural legion is due to a blood supply problem then it will probably have a very rapid onset of symptoms. If it’s due to a tumor the symptoms will slowly appear as the tumor grows.
With these legions just think about the name and what part is missing. They all really make sense if you know your brainstem anatomy.
It is due to a brainstem legion that will cause an ipsilateral CN loss and a contralateral hemiplegia (since the corticospinal tract has not yet crossed).
Lateral medullary syndrome can be caused by a blockage of the PCIA (post. inferior cerebellar artery) and will cause the loss of CN V, VII-XI as well as loss of the spinothalamic tract. It would cause a clinical presentation of contralateral loss of protopathics (pain/temp) as well as ataxias and vertigo from the CN loss. The part of V at this level will cause ipsilateral loss of touch to the lower face. Remember that sensory to the upper face is bilateral.
Medial medullary syndrome can be caused by occlusion of the medullary branches of the vertebral arteries. It knocks out the pyramids, medial lemniscus and CN XII. The patient presents with tongue deviation to the injured side, contralateral spastic hemiplegia and contralateral protopathic loss (proprioception and vibratory sense).
Medial pontine syndrome is usually a result of occlusion of the paramedian pontine branches of the basilar artery. You loose the corticospinal tract, medial lemniscus and fibers of CN VI. The patient presents with loss of protopathics and spastic paralysis contralaterally but it can be differentiated from medial medullary syndrome in that you have a medial strabismus (eyes point medially) from loss of the nucleus of VI rather then tongue deviation.
Lateral pontine syndrome is often a result of loss of the AICA (anterior inferior cerebral artery) and is related to a loss of V, VII, VIII, ICP, descending hypothalamics and spinothalamics. The presentation includes vertigo, hearing loss, limb ataxia, loss of facial protopathics and facial paralysis ipsilaterally. It also shows contralateral protopathic (pain/temp) loss.
Ventral midbrain syndrome is usually a result of occlusion of the posterior cerebral artery (PCA). It causes loss of the corticospinal tract, corticobulbar tract and CN III. You will see contralateral spastic paralysis of the lower half of the face and body but mostly of the upper limb. You also get lateral strabismus (down and out of eyes), ptosis and a dilated pupil.
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