Neuro Top 50+ Flashcards
Know this HIGH-YIELD stuff for to be extra smart.
The three components of the blood-brain barrier?
Which organs lack a BBB?
a. endothelial cells
b. basement membrane
c. astrocytic end feet
Circumventricular organs [i.e. area postrema, median eminence of the hypothalamus, neurohypophysis, pineal gland] lack a blood-brain barrier.
Myopathies are associated with what loss patterns?
proximal symmetric weakness, but no sensory loss.
Peripheral neuropathies result in what loss patterns?
distal asymmetric weakness with atrophy, fasciculations, sensory loss and pain.
Most commonly caused by diabetes and alcoholism.
Polyneuropathies result in what pattern?
sensory loss in a stocking/glove pattern.
Guillain-Barre syndrome
The most common motor neuropathy is Guillain-Barre syndrome (aka acute inflammatory demyelinating polyneuropathy [AIDP].
Characterized by ascending symmetric muscle weakness, areflexia and paresthesias in hands and feet 1-3 weeks following a viral respiratory or GI infection. CSF has elevated protein without elevated WBC.
amyotrophic lateral sclerosis loss patterns?
The most common (~2 per 100,000) motor neuron disease is amyotrophic lateral sclerosis which is characterized by both upper AND lower motor neurons signs.
multiple sclerosis
The most common demyelinating disease is multiple sclerosis which is characterized by neurological signs (weakness, spasticity > sensory loss > incontinence > vision loss) that resolve and return progressively worse (relapsing/remitting). The diagnosis of multiple sclerosis requires two separate symptoms at two different times, or lesions separated in time and space.
MRI shows white matter lesions
CSF oligoclonal bands on electrophoresis
Radiculopathies result in what loss patterns?
Radiculopathies result in pain/sensory loss in a dermatomal pattern and weakness in myotomal patterns (i.e. multiple affected nerves and muscle compartments).
Disease at the neuromuscular junction is distinguished by what?
fatigability; patients with myasthenia gravis show fatigue with repetitive stimulation of their muscles.
Upper motor neuron lesions manifestations?
Upper motor neurons are found mainly in the cerebral cortex (some in brainstem – red nucleus, reticular formation, vestibular nuclei) and DO NOT directly innervate skeletal muscle.
Upper motor neuron lesions result in spastic paralysis, hyper-reflexia (muscle stretch reflexes are 3-4/4), Babinski sign, Hoffman sign and clonus. Note that with an acute UMN lesion, there may be hyporeactive reflexes and flaccid paralysis!
Lower facial paralysis
(“can wrinkle their forehead but cannot smile”) is a sign of damage to the corticobulbar tract in the pons or higher (e.g. internal capsule or crus cerebri). This may be accompanied by a tongue that deviates away from the lesion on protrusion (but does demonstrate any signs/symptoms of lower motor neuron injury
Lower motor neuron lesions
Lower motor neurons innervate skeletal muscle and are located in the anterior horn of the spinal cord and motor nuclei of cranial nerves.
Lower motor neuron lesions result in flaccid paralysis, hyporeflexia (muscle stretch reflexes are 0-1/4), fasciculations and atrophy.
Cerebral Palsy
Cerebral Palsy is a disorder in the development of movement and posture which results in activity limitations attributed to non-progressive lesions in the developing fetal or infant brain CNS. Motor signs (present in the first year of life) can be attributed to injury to corticospinal tracts and/or basal nuclei (i.e. they can show signs of spasticity, flaccid paralysis or dystonia/choreoform movements). Motor difficulties are often accompanied by orthopedic complications (contractures, hip dislocation, scoliosis), seizures and/or disturbances of: sensation, cognition, communication, perception.
spinal shock
Sudden trauma to the spinal cord results in spinal shock (temporary flaccid paralysis, hyporeflexia, sensory loss and loss of bladder tone) – hyper-reflexia develops over a period of days to weeks.
anterior spinal artery syndrome
Occlusion of the artery of Adamkiewicz results in anterior spinal artery syndrome = bilateral weakness, loss of pain and temperature and hyper-reflexia below the lesion.
Cauda equina syndrome
weakness and sensory loss in the lower extremities, radicular pain, saddle anesthesia and urinary incontinence.
The most important spinal cord sensory levels are:
C6 C7 C8 T4 T6 T10 L4 L5 S1
C6 = thumb C7 = middle finger C8 = little finger T4 = nipple T6 = xiphoid T10 = umbilicus L4 = medial knee L5=big toe S1 = little toe
The most important muscle stretch reflexes are: C5 C6 C7 L4 S1
The most important muscle stretch reflexes are: C5 = biceps C6 = brachioradialis C7 = triceps L4 = quadriceps S1 = Achilles
Explain the muscle stretch reflex scale
0 = absent 1 = trace or only with reinforcement 2 = normal 3 = brisk 4 = clonus
Cutaneous Reflexes:
Babinski sign Bing sign Abdominal reflex Cremaster reflex Hoffman sign Anal wink
Babinski sign (aka plantar reflex) – scrap sole of the foot, flexion of toes is normal; upper motor neuron lesion = extension of big toe (“upgoing” big toe) and fanning of digits 2-5.
Bing sign – stab dorsum of foot with pin, normal = plantar flexion; upper motor neuron lesion = dorsiflexion
Abdominal reflex – scratch abdominal skin, absent in UM neuron lesion
Cremaster reflex – absent in UM neuron lesion
Hoffman sign – scrape tip of 3rd digit, thumb and 2nd digit flex in UM neuron lesion
Anal wink – scratch perineum to elicit contraction of external anal sphincter
Syringomyelia/Hyromelia
cavitation of the central spinal cord, impinges the anterior white commissure producing bilateral loss of pain and temperature in a dermatome distribution
Brown-Sequard syndrome
hemisection of the spinal cord producing ipsilateral UMN paralysis and loss of discriminative touch and contralateral loss of pain and temperature
Anterior cord syndrome
results from compression of anterior spinal artery, affects the neurons of the anterior horn, spinothalamic tract and lateral corticospinal tract
Tabes dorsalis (spine)
loss of posterior columns (discriminative touch, proprioception and vibration)
Subacute combined degeneration (spinal cord lesion)
B12 deficiency, peripheral neuropathy that can progress to cord (posterior columns and lateral corticospinal tracts)
Medial medullary syndrome
contralateral [spastic] hemiparesis (corticospinal tract)
ipsilateral deviation of tongue on protrusion (hypoglossal nucleus or nerve)
contralateral loss of discriminative touch, proprioception and vibration (medial lemniscus)
From blockage of anterior spinal artery!
Lateral medullary syndrome
ipsilateral loss of pain and temperature on face (spinal trigeminal tract)
contralateral loss of pain and temperature on body (spinothalamic tract)
nystagmus, dizziness, nausea (vestibular nuclei)
hoarseness, ipsilateral sagging palate, dysphagia (nucleus ambiguous)
loss of taste (solitary nucleus)
ataxia (restiform body, inferior cerebellar peduncle)
Horner syndrome (hypothalamospinal fibers);
From posterior inferior cerebellar artery!
Tonsillar Herniation
central apnea, hypertension, hyperventilation, loss of consciousness
Foville Syndrome (pons)
contralateral [spastic] hemiparesis (corticospinal tract)
diplopia, paralysis of abduction (CN VI; maybe also intranuclear ophthalmoplegia)
ataxia (middle cerebellar peduncle)
contralateral loss of discriminative touch, proprioception and vibration
paramedian branches of basilar
Gubler Syndrome (pons)
contralateral [spastic] hemiparesis (corticospinal tract)
ipsilateral facial paralysis (facial nerve or nucleus)
ipsilateral loss of pain and temperature on face (CN V)
contralateral loss of pain and temperature on body (spinothalamic tract)
paramedian branches of basilar
