Neuroanatomy Tracts & Paths 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
CN III
Extraocular muscles
Muscle/fun
Superior rectus - intorsion, elevation
Inferior rectus - extorsion, depression
Medial rectus - adduction
Inferior oblique - extorsion, elevation
Levator palpebrae - raise eyelid
Coordinate gaze
Achieved by…
a. Frontal eye fields (area 8)
b. Oculomotor and vestibular nuclei
c. Medial longitudinal fasciculus (MLF)
d. Brainstem gaze centers (PPRF = paramedian pontine reticular formation)
Diplopia
Arises from
Misalignment of eyes, disconjugate gaze
Nystagmus
def
(oscillatory eye movements with quick phases in one direction and slow phases in the other) can arise from oculomotor or vestibular dysfunction
Internuclear ophthalmoplegia
Arise from
Lesion in the MLF
Cranial nerve reflexes
Corneal
Afferent/efferent
A: V1 ophthalmic (nasociliary branch: levator palpebrae)
E: VII (temporal branch: orbicularis oculi)
Cranial nerve reflexes
Lacrimation
Afferent/efferent
A: V1 (loss of reflex does not preclude emotional tears)
E: VII
Cranial nerve reflexes
Jaw Jerk
Afferent/efferent
A: V3 (sensory – muscle spindle from masseter)
E: V3 (motor – masseter)
Cranial nerve reflexes
Pupillary
Afferent/efferent
A: II
E: III
Cranial nerve reflexes
Vestibulo-ocular reflex
Aff/eff
A: CN VIII (vestibular)
E: CN III, IV, VI
Hearing pathway
a. Axons from the auditory apparatus (cochlea) travel via
b. CN VIII to synapses in the
c. Cochlear nucleus, from which there are bilateral projections via
d. The Superior olivary nucleus
e. and the Lateral lemniscus to the
f. Inferior colliculus. From there there are axons to the
g. Medial geniculate nucleus, which projects via the
h. Auditory radiation to the
i. Auditory cortex (areas 41,42)
Ipsilateral hearing loss
(1) Conductive: damping of ossicle movements (2) Sensorineural: damage to CN VIII system
Above the cochlear nucleus the signal is carried bilaterally
Hyperacusis
def
Hyperacusis, excess sensitivity to loud sounds, can be due to impairment of feedback to tensor tympani and stapedial muscles by CN VIII activity
Important localizing syndromes
MCA territory lesion
- Contralateral
a. Hemiparesis, face = arm > leg
b. Horizontal gaze palsy (due to effects on frontal eye fields)
c. Sensory defects
d. Homonymous hemianopia - Language deficits if left/dominant hemisphere
Important localizing syndromes
Internal capsule
- Contralateral hemiparesis
2. “Pure motor” strokes (sensory strokes at this level are thalamic)
Important localizing syndromes
Webers syndrome
Ventral midbrain:
ipsilateral CN III
contralateral hemiparesis
mportant localizing syndromes
Foville’s syndrome
Pons: PPRF, nuclei VI & VII, corticospinal tract, and medial lemniscus:
a. Ipsilateral
(1) Horizontal gaze palsy
(2) Peripheral VII
b. Contralateral
(1) Hemiparesis
(2) Hemisensory loss
(3) Internuclear ophthalmoplegia (INO)
Important localizing syndromes
millard-Gubler Syndrome
- Pons: nuclei/axons of VI & VII, corticospinal tract
a. Ipsilateral
(1) CN VI palsy
(2) Peripheral VII
b. Contralateral
(1) Hemiparesis
Wallenberg syndrome
Medulla: vestibular nuclei, CN V nucleus & tract, CN IX & X, lateral spinothalamic tract, descending sympathetic fibers
a. Ipsilateral
(1) Lateropulsion
(2) Ataxia
(3) Loss of pain & temperature sensation in the face (4) Paralysis of soft palate, posterior pharynx and vocal cord
(5) Horner’s syndrome
b. Contralateral
(1) Loss of pain & temperature sensation in the body
Peripheral nerve lesions
Median neuropathy
The median nerve crosses from the distal forearm to the
hand through the carpal tunnel. The floor of the carpal tunnel is formed by the carpal bones and the roof by the transverse carpal ligament. Compression of the median nerve by the transverse carpal ligament (flexor retinaculum) can occur.
Distal to the carpal tunnel the median nerve innervates the abductor pollicis brevis, flexor pollicis brevis, opponens pollicis and first two lumbrical muscles, and provides sensation to the palmar aspect of the first three digits, and splits to the fourth.
Peripheral nerve lesions
Median neuropathy
dx
Tinel sign: Paresthesias are provoked by tapping over the median nerve at the wrist in 26-73% of patients with carpal tunnel syndrome and 6-45% of controls.
Phalen test: While holding the wrist flexed, paresthesia occurs within 1-2 minutes in 74% of patients with carpal tunnel syndrome and 25% of controls.
Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy in the upper extremity.
Peripheral nerve lesions
Ulnar neuropathy
Most common site
The most common site of entrapment is at or near the elbow region, especially in either the cubital tunnel or the ulnar groove. The second most likely location of entrapment is at or near the wrist, especially in Guyon’s canal.
Ulnar nerve
function
In the hand the ulnar nerve innervates the adductor pollicis, flexor pollicis brevis, the abductor digiti minimi, opponents digiti minimi, flexor digiti minimi, the interossei and the third and fourth lumbricals. The nerve provides sensation over the medial half of the fourth and the entire fifth digit of the hand, and branches from above the wrist got to the ulnar part of the palm, and the ulnar portion of the posterior aspect of the hand.
Second most common site of nerve entrapment in upper extremity
elbow
Radial nerve injury
Caused by…
Often Called “Saturday Night Palsy” as it is easily caused
by sleeping with an arm hooked over a chair back or other
hard object, can also occur with a fracture of the humerus.
Radial nerve
path
In the upper arm, the radial nerve gives off a branch to the
triceps muscle before it wraps around the humerus at the spiral groove. Here, its proximity to the humerus makes it susceptible to compression and/or trauma.
After exiting the spiral groove, the radial nerve supplies the brachioradialis muscle before dividing into the posterior interosseous branch and a sensory branch. The posterior interosseous branch is a pure motor nerve that supplies the supinator. It then dives into the supinator through the fascia to supply the muscles of the wrist and finger extension. The sensory branch that arises approximately at the elbow travels down the forearm and supplies the lateral aspect of the dorsum of the hand.
Radial neuropathy
How common
Fourth most common mononeuropathy
Sciatic nerve neuropathy
Injury to the sciatic nerve in the mid-to-lower thigh will affect all of the muscles below the knee which are innervated by the two distal branches, the tibial nerve and the common peroneal nerve. The sensory disturbance will include the lateral leg below the knee and the entire foot.
Peroneal Neuropathy
How does it occur
Injury to the common peroneal nerve often occurs with compression where the nerve wraps around the head of the fibula below the knee.
Peroneal Neuropathy
sx
Weakness occurs in all the dorsiflexors of the foot, causing a foot drop. Inversion of the ankle is spared, as those muscles receive innervation via the tibial nerve (helps to distinguish from a L5 root palsy). The sensory disturbance will include the lateral leg below the knee and the dorsum of the foot.
Consciousness/coma
def
Consciousness can be defined as the state of awareness of one’s self and one’s environment. Coma is the total absence of this awareness. Gradations of impaired consciousness have different terminologies such as confusional state, drowsiness or lethargy, and stupor.
Consciousness
Composed of which two elements
a. Arousal: the state of alertness. Anatomic substrate for arousal is the reticular activating system (RAS) and the posterior hypothalamus.
b. Content of consciousness: higher cortical functions.
RAS
Receives input from…/fun
The reticular activating system is the central core of the brainstem, extending from the rostral midbrain to the caudal medulla.
a. It receives collaterals from and is stimulated by every major somatic and special sensory pathway.
b. involved in functioning of the RAS include acetylcholine, norepinephrine, serotonin, GABA, glutamate, hypocretins, and histamine.
Causes of coma
focal
Focal structural abnormalities include any pathologic process that damages the RAS.
a. Primary damage is usually vascular in nature, such as
hemorrhage or infarction, but may also be caused by
trauma, tumor, infection, or inflammation.
b. Secondary damage is due to herniation, defined as the
forced protrusion (due to increased intracranial pressure) of brain tissue from one compartment to another (eg. herniation of the uncus through the tentorial notch to the posterior fossa.)
Causes of coma
diffuse
Diffuse abnormalities include metabolic or toxic disorders such as:
a. global ischemia (normal cerebral blood flow is 55 cc/100 gm/min. - brain function is critically reduced when flow is <20 cc/100 gm/min;
b. hypoxia
c. Hypoglycemia
d. Enzyme cofactor deficiency (thiamine, niacin,pyridoxine, cyanocobalamin, folate)
e. Hepatic encephalopathy due to toxins including
ammonia, abnormal fatty acids, metabolic products, false neurotransmitters
f. Uremic encephalopathy due to retention of urea, phosphates, proteins, amines
g. Toxins such exogenous poisons and anesthetics.
Clinical signs to localize lesions causing coma
Respiratory patterns
list
Cheyne-stokes respiration Central neurogenic hyperventilation Apneustic breathing Cluster breathing Ataxic respiration.
Cheyne-stokes respiration
due to dysfunction of cortical and/or deep subcortical structures. Typical causes are congestive heart failure, cerebral hemisphere strokes (50%), hypertensive encephalopathy, metabolic encephalopathy, and hypoxia.
The breathing is crescendo-decrescendo.
Clinical signs to localize lesions causing coma
Pupil size and reaction to light
The pupillary pathways are relatively resistant to metabolic dysfunction. The presence or absence of the light reflex is the single most important physical sign distinguishing structural from metabolic causes of coma.
Clinical signs to localize lesions causing coma
Pupil size and reaction to light
Large fixed pupils
Large fixed pupils: lesion is in the tectum (dorsal midbrain).
Clinical signs to localize lesions causing coma
Pupil size and reaction to light
Unilateral dilated pupil
Unilateral dilated pupil with third nerve paralysis (ptosis and paralysis of medial rectus, superior rectus, inferior rectus, and inferior oblique): lesion often is supratentorial with herniation compressing oculomotor nerve and brainstem.
Clinical signs to localize lesions causing coma
Pupil size and reaction to light
mid-position fixed pupils
The lesion is in the midbrain
Clinical signs to localize lesions causing coma
Pupil size and reaction to light
Pinpoint pupils
Pinpoint pupils (may respond to light if examined with magnifying glass): lesion is in the pons.
Clinical signs to localize lesions causing coma
Pupil size and reaction to light
Small pupils with ptosis and anhidrosis
Small pupils with ptosis and anhidrosis (lack of sweating), ie Horner’s syndrome: lesion of sympathetic pathways (hypothalamus, brainstem, spinal cord [C8-T1], or peripheral paths to orbit.
Vestibular reflexes
oculocephalics
passive rotation of head to one side is associated with movement of eyes in opposite direction (eyes tend to remain in same direction of gaze).
Vestibular Reflexes
Calorics
COWS (cold opposite, warm same). The acronym refers to the fast component. Thus, if cold water is introduced into the left ear, the eyes will deviate tonically to the left and the fast component of the nystagmus will be to the right. Loss of voluntary gaze (as in coma from cortical dysfunction) will result in elimination of the fast component of the nystagmus; the tonic component will remain. Both the tonic and fast components will disappear with a brainstem lesion (destroying the medial longitudinal fasciculus [MLF] bilaterally.
Glasgow coma scale
Based on/score
Based on responses in 3 areas, total score is 3-15
Glasgow coma scale
How does is it scored
a. Eyes open: Spontaneously=4, To verbal command=3, To pain=2, Don’t open=1
b. Best motor response: Obeys verbal command=6, Localizes pain=5, Flexion- withdrawal=4, Flexion- abnormal (decorticate)=3, Extension- decerebrate=2, None=1
c. Best verbal response: Oriented and converses=5, Disoriented and converses=4, Inappropriate words=3, Incomprehensible sounds=2, None=1
Glasgow coma scale
Used for…
a. After trauma, a Glasgow Coma Scale score of 3 to 5 may indicate fatal brain damage, especially if pupils are fixed or oculovestibular reflexes are absent.
b. If pupils are unreactive or the motor response to noxious stimuli is absent or is only a reflex response 3 days after cardiac arrest, patients have virtually no chance of a good neurologic recovery.
c. After coma, the early return of speech (even if incomprehensible), spontaneous eye movements, or ability to follow commands is a favorable prognostic sign.
d. If the cause is a reversible condition (eg, sedative overdose, some metabolic disorders such as uremia), patients may lose all brain stem reflexes and all motor response and yet recover fully.
States of pseudocoma
psychogenic
Psychogenic unresponsiveness
a. When the passively raised arm is released, the patient avoids hitting the face.
b. With the patient on the side, the eyes will always point to the floor or bed.
c. There is resistance to an attempt to open the closed lids.
States of pseudocoma
Locked in syndrome
Locked-in syndrome – the patient is completely paralyzed (quadriplegic and paralysis of the facial muscles and horizontal eye movements) but the patient is awake.
States of pseudocoma
Abulia, akinetic mutism
The patient is completely apathetic. There is lack of initiative.
The lesion is in the premotor cortex or borders the third ventricle.
States of pseudocoma
Persistent vegetative state
a. No conscious awareness; no interaction.
b. No purposeful response to stimuli.
c. No language function.
d. Sleep-wake cycles present.
e. Brainstem function more or less intact.
f. Bowel and bladder incontinence.
