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Flashcards in Spinal Cord Lesions Deck (22)
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How would a patient present if he suffers from Poliomyelitis and Werdnig-Hoffmann disease?

He will have lower motor neuron lesions only due to destruction of anterior horns; flaccid paralysis.


How would a patient present with MS?

Affects mostly white matter of the cervical region and cause random and asymmetric lesions due to demyelination. Patient will present with scanning speech, intention tremor and nystagmus.


How would a patient present with ALS?

Both upper and lower motor neuron deficits but no sensory deficits.


Describe the pathology of Poliomyelitis

Caused by the polio virus (transmitted fecal-oral). It replicates in the oropharynx and small intestines then virimia into CNS and blood. Destruction of cells in the anterior horn of the spinal cord leading to lower motor neuron destruction.


What are the symptoms of poliomyelitis?

Malaise, headache, fever, nausea, ab pain, sore throat, signs of LMN lesions (muscle weakness and atrophy, fasciculations, fibrillations and hyporeflexia).


What would you find in a patient with poliomyelitis (in the lab)

CSF with lymphocyte increase, slight elevation of protein and no changes in glucose. Cirus can be recovered from stool or throat.


Describe Werdnig-Hoffman disease, aka infantile spinal muscular atrophy?

AR inheritance pattern, presents at birth as a "floppy baby," tongue fasciculations. Death in 7 months generally. Degeneration of anterior horns and LMN involvement only.


What is tabes dorsalis (caused by tertiary syphilis)? What is it caused by and how do patients present?

Degeneration of dorsal roots and dorsal columns, impaired proprioception, locomotor ataxia. It is associated with Charcot's joints, shooting pain, argyll robertson pupils (reactive to accomidation but not light), positive Romberg, absense of DTR, sensory ataxia at night.


What is "Syringomyelia?

Damages anterior white commissure of the ST tract (2nd order neurons). This results in bilateral loss of pain and temperature sensations (usually C8-T1). Seen with Chiari types 1 and 2. Can hit other tracts too eventually.


What will vitamin B12 neuropathy, vit E deficiency and Freidreich's ataxia lead to?

Subacute combined degeneration - demyelination of dorsal columns, LCT and spinocerebellar tracts. Ataxic gait, hyperreflexia, impaired position and vibration sense.


What is a general sign of lower motor neuron damage?

Everything is lowered, less muscle mass, less muscle tone, less reflexes and downgoing toes.


What is the general sign of upper motor neuron damage?

Everything increases, increased tone, deep tendon reflexes, toes. Fasciculations.


Generally describe the pathology of ALS (Amyotrophic Lateral Sclerosis aka Lou Gehrig's disease). What causes it?

Associated with signs of both UMN and LMN damage, however there is no sensory, cognitive or occulomotor deficits. Might be associated with a defect in superoxide dismutase 1 (SOD1).


How do ALS patients present?

Presents with fasciculations and eventual atrophy, it is progressive and fatal.


What is Friedreich's ataxia? How do patients present?

AR trinucleotide disorder in a gene encoding for Frataxin. Leads to impaired mitochondrial functioning. Patients present with stagerring gait, frequent falling, nystagmus, dysarthria, pes cabus, hammer toes, hypertrophic cardiomyopathy (causes death). Presents in childhood with kyphoscoliosis.


If you have a hemisection of the spinal cord, what syndrome is this, and how do they present?

Brown Sequard syndrome: will show ipsilateral UMN signs below the lesion (Lateral corticospinal tract). Also ipsilateral loss of vibration, sensation, tactile discrimination and proprioception (dorsal column).

Contralateral loss of pain and temp sensation 2 dermatones below the lesion (lateral spinothalamic tract).


In Brown Sequard Syndrome, when would the patient lose all sensation and have LMN signs?

Only at the level of the lesions.


When will patients with Brown Sequard syndrome also present with Horner's syndrome (ipsilateral)?

Only if the hemisection is above T1.


What happens if you have a complete lesion of t he spinal cord above C3-5?

Since the phrenic nerve innervates C3-5, lesions above this region may lead to resp insufficiency.


How would a complete lesion of the spinal cord present?

Bilateral spastic paralysis, LMN signs at the level of transaction, no cutaneous sensation below level of lesion.


What is Anterior Spinal Artery Syndrome (ASA)?

Infarction of the anterior 2/3 of the spinal cord. Leads to b/l loss of pain and temperature sensation, (ST tract) b/l weakness (LCT tract), but fine touch, propreception and vibration will be in tact (dorsal column is fine). Leads to occlusion of artery at the level of spine.


What supplies the upper (superior) portions of the ASA? Inferior portion? Where is the watershed area that is prone to infarcts?

Vertebral arteries. Inferior supplied by great anterior medullary artery of Adamkiewicz (coming from perforating arteries of aorta from T8 to L1). T4-T8 is the watershed area.