Neuroanatomy Review II Flashcards
Primary motor cortex
Receives input from…
The primary motor cortex (Brodmann area 4, the precentral gyrus), receives programming inputs from the secondary motor area (area 6, premotor) and the frontal eye fields (area 8), and sends axons from pyramidal cells to the corticobulbar and →
corticospinal tracts
Path of axons from primary motor cortex
Axons descend via the corona radiata to the internal capsules, then through the Cerebral peduncles, basis pontis, pyramids & pyramidal decussation to become the Corticospinal tracts: lateral (crossed), anterior (uncrossed). They terminate in the Ventral horns in the spinal cord, or the cranial nerve motor nuclei in the brainstem. Here the alpha-motor neuron sends axons out of the CNS
Peripheral nerve path from ventral horn
Axons emerge through the ventral nerve root, possibly the brachial or lumbosacral plexus and travel through peripheral nerves to synapse on the Skeletal muscle
LMN sx
Damage to neuromuscular unit
list
i) Radiculopathy (damage to spinal root)
ii) Plexopathy (damage to a nerve plexus)
iii) Mononeuropathy (damage to a single nerve)
LMN lesion
sx
(a) Weakness/paralysis
(b) Decreased muscle tone (hypotonia)
(c) Decreased reflexes (hyporeflexia)
(d) Atrophy of muscle
(e) Fasciculations
UMN lesion
site
(a) Descending corticobulbar/spinal pathways at any level
(b) Symptoms are contralateral if lesion is above the pyramidal decussation, ipsilateral if below.
UMN lesion
sx
a) Weakness/paralysis
(b) Increased muscle tone (hypertonia)
(c) Increased reflexes (hyperreflexia)
(d) Abnormal reflexes (e.g., Babinski)
Cerebellar system
Major divisions
a. Archicerebellum, vestibular cerebellum, flocculonodular lobe (balance, eye movements)
b. Paleocerebellum, spinal cerebellum (muscle tone, adjusts ongoing movements)
c. Neocerebellum, corticopontine cerebellum (coordination of skilled movements)
Signs of cerebellar dysfunction
list
a. Ataxia: uncoordinated movements
b. Dysmetria: inaccurate measurement of distance, difficulty reaching a target
c. Cerebellar tremor: rhythmic oscillation during movements
d. Dysdiadochokinesia: inability to make rapid alternating movements
Signs of cerebellar dysfunction
Vestibulocerebellum/spinocerebellum/ cerebellar hemispheres
Vestibulocerebellum
a. Nystagmus (rhythmic eye movements)
b. Truncal ataxia
c. Dysarthria
Spinocerebellum (anterior lobe of vermis)
a. Truncal and lower extremity ataxia (ipsilateral to lesion)
Cerebellar hemispheres
a. Cerebellar tremor
b. Decomposition of coordinated movements
Extrapyramidal motor system
components
Basal ganglia:
(1) Caudate nucleus
(2) Globus pallidus
(3) Putamen
Substantia nigra
Subthalamic nucleus
Red nucleus
Signs of basal ganglia lesions
list (9)
Dyskinesias Athetosis Chorea Ballism Dystonia Resting tremor Hypokinesia Bradykinesia Rigidity
Brainstem systems regulating posture
Important pathways
list
a. Vestibulospinal
b. Brainstem reticulospinal
c. Rubrospinal
d. Tectospinal
Brainstem systems regulating posture
Decerebrate/Decorticate
Decerebrate state:
(1) Lesion between red nucleus and vestibular nucleus
(2) Upper and lower extremity extension and internal rotation
(3) Probably due to release of inhibition of vestibulospinal and reticulospinal systems or loss of flexor (e.g., rubrospinal) tone
Decorticate rigidity:
(1) Supratentorial lesion
(2) Upper extremity flexion/adduction
(3) Lower extremity extension
Dorsal column-medial lemniscus pathway
(discriminative touch, vibration/position)
(1) Dorsal root ganglion cells send axons to the periphery and to the spinal column, where they ascend ipsilaterally in the
(2) Dorsal columns (fasciculus gracilis for the lower extremities and fasciculus cuneatus for the upper extremities) and
(3) Synapse in nucleus gracilis and nucleus cuneatus
(4) The secondary axon decussates in the lower medulla and then ascends in the
(5) Medial lemniscus to the
(6) Thalamus and synapses in the VPL nucleus, from which axons project to the
(7) Somatosensory cortex (postcentral gyrus, areas 3,1,2)
Lateral spinothalamic pathway
(pain and temperature)
(1) Dorsal root ganglion cells send axons to the periphery and to synapses in the substantia gelatinosa
(2) Decussates at the spinal level of entry, and ascends in the
(3) Lateral spinothalamic tract to the
(4) Thalamus and synapses in the VPL nucleus, from which axons project to the
(5) Somatosensory cortex (postcentral gyrus, areas 3,1,2)
Anterolateral pathway
(light touch)
(1) Dorsal root ganglion cells send axons to the periphery and to synapses in the substantia gelatinosa (2) Decussates at the spinal level of entry, and ascends in the
(3) Anterior spinothalamic tract to the
(4) Thalamus and synapses in the VPL nucleus, from which axons project to the
(5) Somatosensory cortex (postcentral gyrus, areas 3,1,2)
Look up the head and neck sensory pathways
Mediated by trigeminal nerve (CN V)
Sensory abnormalities
def
a. Anesthesia(absence of sensation)/hypesthesia (increased threshold for sensation)
b. Causalgia: burning pain
Spinal cord syndromes
Acute vs chronic
Acute (“spinal shock”):
(a) Complete paralysis & anesthesia below lesion (b) Areflexia
Chronic:
(a) Complete paralysis & anesthesia below lesion (b) Hyperreflexia (upper motor neuron)
Brown sequard syndrome
(spinal cord hemisection)
(1) Possible ipsilateral LMN paralysis at the level of lesion
(2) Possible ipsilateral cutaneous anesthesia at the level of lesion
(3) Ipsilateral UMN paralysis below the level of lesion
(4) Ipsilateral proprioceptive loss below the level of lesion
(5) Contralateral pain/temp loss below the level of lesion
Anterior Cord syndrome
(1) UMN paralysis below the level of lesion
(2) Pain/temp loss below the level of lesion
(3) Relative sparing of proprioception below the level of lesion
Central cord syndrome
(1) Bilateral spinothalamic loss below the level of lesion
(2) UMN paralysis affecting upper extremities more than lower extremities
(3) Associated with cervical injury, frequently involves bladder dysfunction
Cauda Equina Syndrome
(1) Saddle distribution sensory distribution
(2) LMN paralysis below the level of lesion
Visual pathway
a. Axons from the retina project through the
b. Optic nerve (CN II) to the
c. Optic chiasm, where axons from the medial half of each retina cross to the other side, and continue with the uncrossed fibers as the
d. Optic tract to synapses in the
e. Lateral geniculate nucleus. From there axons project in the
f. Opticradiationstothe
g. Calcarine cortex (area 17)
Visual field defects
Anopia
def
Complete blindness
Visual field defects
Cortical blindness
Causes asymmetric vision loss without an afferent pupillary defect
Visual field defects
Chiasm lesions
Cause bitemporal vision loss
Visual field defects
hemianopia
(1) Homonymous deficits are the same in each eye
(2) Heteronymous deficits are the different in each eye
(3) Bitemporal deficits affect lateral vision in each eye
Visual field defect
quadrantopia
Quadrantanopia is a visual defect in on quadrant of the visual field
(1) Superior quadrantanopia results from lesions affecting Meyer’s loop of the optic radiations
(2) Inferior quadrantanopia results from lesions affecting the remainder of the optic radiations and is rare
Visual field defects
Scotoma
def
Focal defect in the visual field
CN
Location of nuclei
1,2=abovebrainstem
3,4=midbrain
5,6,7,(8)= pons
(8),9,10,11,12 = medulla (bulbar)
CN VI
Extraocular muscles
Muscle/fun
Lateral rectus
abduction
CN IV
Extraocular muscles
Muscle/fun
Superior oblique
Intorsion, depression