Localization of Motor Diseases Flashcards
Lateral Corticospinal Tract (LCST):
- Function:
- Lesion:
-
Function:
- movement of contralateral body
-
Lesion:
- contralateral weakness
It takes at least _ neurons to transmit impulse from cortex to muscle
2 neurons:
- **UMN: **originating from primary motor cortex that synapses onto LMN
- **LMN: **in the ventral horn of the spinal cord
- α-motor neuron
To localize lesions further along LCST look for:
- Contralateral weakness & aphasia, apraxia, neglect or other cortical sign ⇒ lesion in cortex
- Contralateral weakness & ipsilateral CN deficits ⇒ lesion in brainstem
-
Bilateral weakness below a certain spinal level ⇒ complete spinal cord lesion at that level
- Ipsilateral hemibody weakness & **contralateral hemisensory deficit below a spinal level **⇒ lesion of hemicord (Brown-Sequard syndrome)
Corticobulbar tract:
- Function:
- Lesion:
-
Function:
- **Controls contralateral facial movement **
-
Lesion:
- contralateral weakness
UMN pattern of facial weakness:
lesion of corticobulbar tract
-
contralateral weakness of lower face
- facial droop, drooling, weak smile
- intact forehead wrinkle
- forehead spared due to bilateral cortical input to upper face
LMN pattern of facial weakness:
lesion of facial nucleus or facial nerve
-
ipsilateral weakness of upper & lower face
- facial droop, inability to close eye
- no forehead movement
Reticulospinal tract:
Function
- Unconscious motor control & for giving your muscles ‘tone’
- LMNs are tonically active ⇒ INHIBITED by the reticulospinal tract
- ↑UMN (specifically the reticulospinal tract) activity ⇒ inhibits LMN ⇒ muscle relaxes
- ↓UMN activity ⇒ loss of inhibition of LMN ⇒ muscle contracts
- Antigravity muscles are more tonically active than muscles that move in the plane of gravity
Lesion of reticulospinal tract:
-
Acute lesion ⇒ contralateral hypotonia
- acute stroke
-
Chronic lesion⇒contralateral hypertonia
- chronic stroke
-
UMN pattern of weakness (chronic):
- due to increased tone in antigravity muscles
- see flexion at elbow/fingers/wrists, knee extension, ankle plantarflexion, ankle inversion, hip adduction

Reflexes:
- Hyperreflexia:
- Hyporeflexia:
- Hyperreflexia ⇒ UMN lesion
- Hyporeflexia ⇒ LMN lesion or lesion of afferent or efferent limb
Anterior horn cell lesion:
- Signs: flaccid paralysis, severe muscle atrophy, fasciculations, cramping, loss of reflexes
-
fasciculation (α-motor neuron lesion)
- spontaneous firing of motor neuron
- can see ‘twitching’ of muscle under skin
- not painful
-
cramping
- firing of mutiple motor neurons or entire muscle
- usually causes entire muscle to contract
- painful
- Ex: ALS, polio
Root lesion:
shooting pain in a root dermatomal distribution
- loss of reflexes that corresponds to root
- little or no weakness & atrophy
- in order to have muscle atrophy due to root lesion ⇒ all roots to that muscle need to be lesioned
- Ex: disc herniation
Plexus lesion:
lesion of lumbosacral or brachial plexus
- multiple muscles in an arm or leg are weak
-
sensory loss & loss of reflexes usually well defined
- depends on location of lesion
- usually painful
Plexus Lesion:
Erb’s palsy

due to lesion of upper trunk of brachial plexus
- arm is held internally rotated, extended at elbow, flexed at wrist at side of body
- characteristic “waiter’s tip” pose
Signs & Symptoms:
- loss of arm abduction ⇒ axillary nerve; C5 & suprascapular nerve; C5/6
- loss of elbow flexion ⇒ musculocutaneous nerve; C5/6
- loss of external rotation of humerus ⇒ suprascapular nerve; C5
- loss of wrist extensors ⇒ radial nerve; C6
- Can have sensory loss, as well as loss of biceps & brachioradialis reflexes
- NOTE: Movements of fingers are spared because they are innrvated by the lower brachial plexus
Plexus Lesion:
Klumpke’s palsy
lesion of lower trunk of brachial plexus
- Opposite symptoms of Erb’s palsy
- Weakness in fingers but no difficulty moving across shoulder & elbow
- Weakness of all ulnar innervated muscles, median innervated hand muscles, radially innervated extensor digitorum communis (extends fingers)
- May have an ipsilateral Horner’s syndrome due to sympathetic fibers traveling from T1 cord ascending to superior cervical gangion
- Can be caused by birth trauma or any other trauma
Plexus Lesion:
Pancoast tumor
lesion of lower trunk of brachial plexus due to tumor infiltration
- usually by apical lung tumor
- symptoms depend on extent of infiltration
- affects lower trunk first (like Klumpke’s)
Peripheral nerve lesion:
muscles innevated by that nerve are affected
- can be associated with profound atrophy
- dense sensory loss in the distribution of peripheral nerve
- reflexes may be lost if muscle being tested is innervated by lesioned nerve
Peripheral nerve lesion:
Carpal Tunnel Syndrome

median nerve compression at wrist (neuropathy)
- overuse of finger flexors from repetitive tasks cause these muscles to hypertrophy
- hypertrophied muscles & median nerve pass through a tunnel (called carpal tunnel)
- bound by a thick ligament called transverse carpal ligament
- muscles compress the nerve as they grow
Signs & Symptoms
- pain and tingling in median region of hand (thumb to lateral half of ring finger)
- especially bothersome at night
- hand gets accidently hyperflexed at wrist & pt wakes up and shakes out hand
- if chronic, cause cause atrophy of median innervated hand muscles causing loss of bulk of thenar eminence
Neuromuscular junction defect:
fatigable weakness
- worse later in the day & after repetitive movement
- improved strength after rest
- no sensory loss
- reflexes usually normal
- no muscle atrophy
What muscles do NMJ defects affect?
Affects muscles that are constantly working:
- Levator palpebrae (raises eyelid) ⇒ ptosis
- Extraocular muscles ⇒ diplopia
- Neck extensors ⇒ dropped head
- Core muscles ⇒ difficulty rising from chair, stairs
- Swallowing muscles ⇒ dysphagia
- Intercostals/diaphragm ⇒ difficulty breathing
- Eg. myasthenia, Lambert-Eaton myasthenic syndrome, botulism
Muscle lesion:
weakness confined to certain muscle groups
- sensation preserved
- slowly progressive weakness (not fatigable)
- reflexes are normal (profound muscle atrophy can result in areflexia or hyporeflexia)
-
Muscle can degenerate due to:
- inflammation (myositis)
- genetic defect
- muscular dystrophy like Duchenne muscular dystrophy
CASE: 31 yo F developed sudden R f/a/l weakness 2 weeks ago. She has mild slurred speech & has been falling. She denies numbness & headache.
Exam:
- Normal language; no neglect ⇒ no cortical signs & leg involved (so 2 vascular territories involved)
- ↓R nasolabial fold ⇒ L corticobulbar tract (before pons)
- ↑tone in R arm; R finger taps slow & 4+/5 strength in R arm/leg ⇒ LCST on L lesioned
- Reflexes 3+ on R arm/leg ⇒ L LCST lesioned
- Spastic gait ⇒ indicative of corticospinal injury
-
Lesion: L LCST & L corticobulbar tract at internal capsule or L pons
- i.e. L posterior limb of internal capsule
- Cause(s): stroke or multiple sclerosis
CASE: 62 yo F with DM, HTN develops sudden aphasia and R face/arm weakness.
Exam:
- Speech is halting, effortful, agrammatic, few words ⇒ Broca’s aphasia ⇒ L frontal cortex (a cortical sign & hence lesion in cortex)
- L gaze preference ⇒ R frontal eye fields are working & L FEF are NOT ⇒ another cortical sign
- R lower facial weakness & R arm drift; leg normal ⇒ L LCST in face & arm ⇒ L frontal lobe (leg is medial frontal lobe, which is not in MCA territory)
- Reflexes: absent in RUE; normal elsewhere; Babinski absent on L and mute on R ⇒ reflexes are low immediately after stroke & Babinski has not evolved yet; it takes at least 1-2 weeks for hyperreflexia & spasticity to develop after a lesion to UMN
- R face/arm sensory deficit ⇒ L parietal somatosensory cortex
- Lesion: L frontal & parietal cortices (MCA distribution)
- Causes: stroke
CASE: 22 yo F develops neck pain, vertigo, ataxia, L sided facial numbness after chiropractic manipulation.
Exam:
- • R beating horizontal nystagmus on R gaze, N/VL cerebellar pathways or vestibular nuclei
- • L V1-V3 ↓ PP sensationL trigeminal nucleus & tract
- • Hoarse voice & ↓palate elevation L, ↓gag on LL nucleus ambiguus &/or CN 10lesion in medulla
- • No weakness
- • L FTN ataxia on hands/feetL inferior cerebellar peduncle
- • R ↓PP on bodyL spinothalamic tract
- • L Horner’s syndrome (ipsilateral ptosis, miosis, anhidrosis)L descending hypothalamic fibers
- Notice absence of cortical signs
- Notice **crossed signs: **L face & R body reduced sensation ⇒ places lesion in brainstem
o
- Since cranial nerves on L are affected ⇒ should be L brainstem involved
-
Lesion: left lateral medulla (supplied by L vertebral artery)
- Wallenberg syndrome
- Cause: vertebral dissection secondary to chiropractic manipulation (rapid rotation of neck ⇒ layers of artery to separate ⇒ ‘dissection’) ⇒ causes blood in lumen to enter b/w the layers & causes a clot to form ⇒ no blood flows through that vessel ⇒ stroke
CASE: 62 yo M with HTN has 2 days of R f/a/l numbness.
Exam:
- Normal language
- R face↓ PP/temp
- Normal body/facial strength
- Reflexes normal
- R body ↓PP/vibration/temp
- No neglect
-
Lesion: L thalamus
- receives STT and dorsal column/medial lemniscus afferent information from both body & face
- Cause: stroke