Neuroanatomy Tracts & Paths

Question 1

Primary motor cortex

Receives input from…

Answer 1

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

Question 2

Path of axons from primary motor cortex

Answer 2

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

Question 3

Peripheral nerve path from ventral horn

Answer 3

Axons emerge through the ventral nerve root, possibly the brachial or lumbosacral plexus and travel through peripheral nerves to synapse on the Skeletal muscle

Question 4

LMN sx

Damage to neuromuscular unit

list

Answer 4

i) Radiculopathy (damage to spinal root)
ii) Plexopathy (damage to a nerve plexus)
iii) Mononeuropathy (damage to a single nerve)

Question 5

LMN lesion

sx

Answer 5

(a) Weakness/paralysis
(b) Decreased muscle tone (hypotonia)
(c) Decreased reflexes (hyporeflexia)
(d) Atrophy of muscle
(e) Fasciculations

Question 6

UMN lesion

site

Answer 6

(a) Descending corticobulbar/spinal pathways at any level

(b) Symptoms are contralateral if lesion is above the pyramidal decussation, ipsilateral if below.

Question 7

UMN lesion

sx

Answer 7

a) Weakness/paralysis
(b) Increased muscle tone (hypertonia)
(c) Increased reflexes (hyperreflexia)
(d) Abnormal reflexes (e.g., Babinski)

Question 8

Cerebellar system

Major divisions

Answer 8

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)

Question 9

Signs of cerebellar dysfunction

list

Answer 9

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

Question 10

Signs of cerebellar dysfunction

Vestibulocerebellum/spinocerebellum/ cerebellar hemispheres

Answer 10

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

Question 11

Extrapyramidal motor system

components

Answer 11

Basal ganglia:

(1) Caudate nucleus
(2) Globus pallidus
(3) Putamen

Substantia nigra
Subthalamic nucleus
Red nucleus

Question 12

Signs of basal ganglia lesions

list (9)

Answer 12

Dyskinesias
Athetosis
Chorea
Ballism
Dystonia
Resting tremor
Hypokinesia
Bradykinesia
Rigidity

Question 13

Brainstem systems regulating posture

Important pathways

list

Answer 13

a. Vestibulospinal
b. Brainstem reticulospinal
c. Rubrospinal
d. Tectospinal

Question 14

Brainstem systems regulating posture

Decerebrate/Decorticate

Answer 14

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

Question 15

Dorsal column-medial lemniscus pathway

discriminative touch, vibration/position

Answer 15

(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)

Question 16

Lateral spinothalamic pathway

pain and temperature

Answer 16

(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)

Question 17

Anterolateral pathway

light touch

Answer 17

(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)

Question 18

Look up the head and neck sensory pathways

Answer 18

Mediated by trigeminal nerve (CN V)

Question 19

Sensory abnormalities

def

Answer 19

a. Anesthesia(absence of sensation)/hypesthesia (increased threshold for sensation)
b. Causalgia: burning pain

Question 20

Spinal cord syndromes

Acute vs chronic

Answer 20

Acute (“spinal shock”):
(a) Complete paralysis & anesthesia below lesion (b) Areflexia

Chronic:
(a) Complete paralysis & anesthesia below lesion (b) Hyperreflexia (upper motor neuron)

Question 21

Brown sequard syndrome

spinal cord hemisection

Answer 21

(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

Question 22

Anterior Cord syndrome

Answer 22

(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

Question 23

Central cord syndrome

Answer 23

(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

Question 24

Cauda Equina Syndrome

Answer 24

(1) Saddle distribution sensory distribution

(2) LMN paralysis below the level of lesion

Question 25

Visual pathway

Answer 25

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)

Question 26

Visual field defects Anopia def

Answer 26

Complete blindness

Question 27

Visual field defects Cortical blindness

Answer 27

Causes asymmetric vision loss without an afferent pupillary defect

Question 28

Visual field defects Chiasm lesions

Answer 28

Cause bitemporal vision loss

Question 29

Visual field defects hemianopia

Answer 29

(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

Question 30

Visual field defect quadrantopia

Answer 30

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

Question 31

Visual field defects Scotoma def

Answer 31

Focal defect in the visual field

Question 32

CN Location of nuclei

Answer 32

1,2=abovebrainstem 3,4=midbrain 5,6,7,(8)= pons (8),9,10,11,12 = medulla (bulbar)

Question 33

CN VI Extraocular muscles Muscle/fun

Answer 33

Lateral rectus abduction

Question 34

CN IV Extraocular muscles Muscle/fun

Answer 34

Superior oblique Intorsion, depression

Question 35

CN III Extraocular muscles Muscle/fun

Answer 35

Superior rectus - intorsion, elevation Inferior rectus - extorsion, depression Medial rectus - adduction Inferior oblique - extorsion, elevation Levator palpebrae - raise eyelid

Question 36

Coordinate gaze Achieved by…

Answer 36

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)

Question 37

Diplopia Arises from

Answer 37

Misalignment of eyes, disconjugate gaze

Question 38

Nystagmus def

Answer 38

(oscillatory eye movements with quick phases in one direction and slow phases in the other) can arise from oculomotor or vestibular dysfunction

Question 39

Internuclear ophthalmoplegia Arise from

Answer 39

Lesion in the MLF

Question 40

Cranial nerve reflexes Corneal Afferent/efferent

Answer 40

A: V1 ophthalmic (nasociliary branch: levator palpebrae) E: VII (temporal branch: orbicularis oculi)

Question 41

Cranial nerve reflexes Lacrimation Afferent/efferent

Answer 41

A: V1 (loss of reflex does not preclude emotional tears) E: VII

Question 42

Cranial nerve reflexes Jaw Jerk Afferent/efferent

Answer 42

A: V3 (sensory – muscle spindle from masseter) E: V3 (motor – masseter)

Question 43

Cranial nerve reflexes Pupillary Afferent/efferent

Answer 43

A: II E: III

Question 44

Cranial nerve reflexes Vestibulo-ocular reflex Aff/eff

Answer 44

A: CN VIII (vestibular) E: CN III, IV, VI

Question 45

Hearing pathway

Answer 45

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)

Question 46

Ipsilateral hearing loss

Answer 46

(1) Conductive: damping of ossicle movements (2) Sensorineural: damage to CN VIII system Above the cochlear nucleus the signal is carried bilaterally

Question 47

Hyperacusis def

Answer 47

Hyperacusis, excess sensitivity to loud sounds, can be due to impairment of feedback to tensor tympani and stapedial muscles by CN VIII activity

Question 48

Important localizing syndromes MCA territory lesion

Answer 48

1. Contralateral a. Hemiparesis, face = arm > leg b. Horizontal gaze palsy (due to effects on frontal eye fields) c. Sensory defects d. Homonymous hemianopia 2. Language deficits if left/dominant hemisphere

Question 49

Important localizing syndromes Internal capsule

Answer 49

1. Contralateral hemiparesis | 2. “Pure motor” strokes (sensory strokes at this level are thalamic)

Question 50

Important localizing syndromes Webers syndrome

Answer 50

Ventral midbrain: ipsilateral CN III contralateral hemiparesis

Question 51

mportant localizing syndromes Foville’s syndrome

Answer 51

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)

Question 52

Important localizing syndromes millard-Gubler Syndrome

Answer 52

1. Pons: nuclei/axons of VI & VII, corticospinal tract a. Ipsilateral (1) CN VI palsy (2) Peripheral VII b. Contralateral (1) Hemiparesis

Question 53

Wallenberg syndrome

Answer 53

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

Question 54

Peripheral nerve lesions Median neuropathy

Answer 54

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.

Question 55

Peripheral nerve lesions Median neuropathy dx

Answer 55

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.

Question 56

Peripheral nerve lesions Ulnar neuropathy Most common site

Answer 56

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.

Question 57

Ulnar nerve function

Answer 57

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.

Question 58

Second most common site of nerve entrapment in upper extremity

Answer 58

elbow

Question 59

Radial nerve injury Caused by…

Answer 59

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.

Question 60

Radial nerve path

Answer 60

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.

Question 61

Radial neuropathy How common

Answer 61

Fourth most common mononeuropathy

Question 62

Sciatic nerve neuropathy

Answer 62

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.

Question 63

Peroneal Neuropathy How does it occur

Answer 63

Injury to the common peroneal nerve often occurs with compression where the nerve wraps around the head of the fibula below the knee.

Question 64

Peroneal Neuropathy sx

Answer 64

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.

Question 65

Consciousness/coma def

Answer 65

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.

Question 66

Consciousness Composed of which two elements

Answer 66

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.

Question 67

RAS Receives input from…/fun

Answer 67

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.

Question 68

Causes of coma focal

Answer 68

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.)

Question 69

Causes of coma diffuse

Answer 69

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.

Question 70

Clinical signs to localize lesions causing coma Respiratory patterns list

Answer 70

``` Cheyne-stokes respiration Central neurogenic hyperventilation Apneustic breathing Cluster breathing Ataxic respiration. ```

Question 71

Cheyne-stokes respiration

Answer 71

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.

Question 72

Clinical signs to localize lesions causing coma Pupil size and reaction to light

Answer 72

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.

Question 73

Clinical signs to localize lesions causing coma Pupil size and reaction to light Large fixed pupils

Answer 73

Large fixed pupils: lesion is in the tectum (dorsal midbrain).

Question 74

Clinical signs to localize lesions causing coma Pupil size and reaction to light Unilateral dilated pupil

Answer 74

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.

Question 75

Clinical signs to localize lesions causing coma Pupil size and reaction to light mid-position fixed pupils

Answer 75

The lesion is in the midbrain

Question 76

Clinical signs to localize lesions causing coma Pupil size and reaction to light Pinpoint pupils

Answer 76

Pinpoint pupils (may respond to light if examined with magnifying glass): lesion is in the pons.

Question 77

Clinical signs to localize lesions causing coma Pupil size and reaction to light Small pupils with ptosis and anhidrosis

Answer 77

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.

Question 78

Vestibular reflexes oculocephalics

Answer 78

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).

Question 79

Vestibular Reflexes Calorics

Answer 79

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.

Question 80

Glasgow coma scale Based on/score

Answer 80

Based on responses in 3 areas, total score is 3-15

Question 81

Glasgow coma scale How does is it scored

Answer 81

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

Question 82

Glasgow coma scale Used for…

Answer 82

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.

Question 83

States of pseudocoma psychogenic Psychogenic unresponsiveness

Answer 83

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.

Question 84

States of pseudocoma Locked in syndrome

Answer 84

Locked-in syndrome – the patient is completely paralyzed (quadriplegic and paralysis of the facial muscles and horizontal eye movements) but the patient is awake.

Question 85

States of pseudocoma Abulia, akinetic mutism

Answer 85

The patient is completely apathetic. There is lack of initiative. The lesion is in the premotor cortex or borders the third ventricle.

Question 86

States of pseudocoma Persistent vegetative state

Answer 86

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.