Localization of Motor Diseases Flashcards

1
Q

Lateral Corticospinal Tract (LCST):

  • Function:
  • Lesion:
A
  • Function:
    • movement of contralateral body
  • Lesion:
    • contralateral weakness
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2
Q

It takes at least _ neurons to transmit impulse from cortex to muscle

A

2 neurons:

  1. **UMN: **originating from primary motor cortex that synapses onto LMN
  2. **LMN: **in the ventral horn of the spinal cord
    • α-motor neuron
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3
Q

To localize lesions further along LCST look for:

A
  1. Contralateral weakness & aphasia, apraxia, neglect or other cortical sign ⇒ lesion in cortex
  2. Contralateral weakness & ipsilateral CN deficits ⇒ lesion in brainstem
  3. 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)
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4
Q

Corticobulbar tract:

  • Function:
  • Lesion:
A
  • Function:
    • **Controls contralateral facial movement **
  • Lesion:
    • ​contralateral weakness
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5
Q

UMN pattern of facial weakness:

A

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
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6
Q

LMN pattern of facial weakness:

A

lesion of facial nucleus or facial nerve

  • ipsilateral weakness of upper & lower face
    • facial droop, inability to close eye
    • no forehead movement
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7
Q

Reticulospinal tract:

Function

A
  • Unconscious motor control & for giving your muscles ‘tone’
  • LMNs are tonically activeINHIBITED by the reticulospinal tract
  • ↑UMN (specifically the reticulospinal tract) activityinhibits LMNmuscle relaxes
  • ↓UMN activityloss of inhibition of LMNmuscle contracts
  • Antigravity muscles are more tonically active than muscles that move in the plane of gravity
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8
Q

Lesion of reticulospinal tract:

A
  • Acute lesioncontralateral hypotonia
    • acute stroke
  • Chronic lesioncontralateral 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
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9
Q

Reflexes:

  • Hyperreflexia:
  • Hyporeflexia:
A
  • HyperreflexiaUMN lesion
  • HyporeflexiaLMN lesion or lesion of afferent or efferent limb
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10
Q

Anterior horn cell lesion:

A
  • 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
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11
Q

Root lesion:

A

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
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12
Q

Plexus lesion:

A

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
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13
Q

Plexus Lesion:

Erb’s palsy

A

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:

  1. loss of arm abduction ⇒ axillary nerve; C5 & suprascapular nerve; C5/6
  2. loss of elbow flexion ⇒ musculocutaneous nerve; C5/6
  3. loss of external rotation of humerus ⇒ suprascapular nerve; C5
  4. loss of wrist extensors ⇒ radial nerve; C6
  5. Can have sensory loss, as well as loss of biceps & brachioradialis reflexes
  6. NOTE: Movements of fingers are spared because they are innrvated by the lower brachial plexus
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14
Q

Plexus Lesion:

Klumpke’s palsy

A

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
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15
Q

Plexus Lesion:

Pancoast tumor

A

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)
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16
Q

Peripheral nerve lesion:

A

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
17
Q

Peripheral nerve lesion:

Carpal Tunnel Syndrome

A

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

  1. pain and tingling in median region of hand (thumb to lateral half of ring finger)
  2. especially bothersome at night
    • hand gets accidently hyperflexed at wrist & pt wakes up and shakes out hand
  3. if chronic, cause cause atrophy of median innervated hand muscles causing loss of bulk of thenar eminence
18
Q

Neuromuscular junction defect:

A

fatigable weakness

  • worse later in the day & after repetitive movement
    • improved strength after rest
  • no sensory loss
  • reflexes usually normal
  • no muscle atrophy
19
Q

What muscles do NMJ defects affect?

A

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
20
Q

Muscle lesion:

A

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
21
Q

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
A
  • 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
22
Q

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
A
  • R face/arm sensory deficit ⇒ L parietal somatosensory cortex
  • Lesion: L frontal & parietal cortices (MCA distribution)
  • Causes: stroke
23
Q

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/VL cerebellar pathways or vestibular nuclei
  • • L V1-V3 ↓ PP sensationL trigeminal nucleus & tract
  • • Hoarse voice & ↓palate elevation L, ↓gag on LL nucleus ambiguus &/or CN 10lesion in medulla
  • • No weakness
  • • L FTN ataxia on hands/feetL inferior cerebellar peduncle
  • • R ↓PP on bodyL spinothalamic tract
  • • L Horner’s syndrome (ipsilateral ptosis, miosis, anhidrosis)L descending hypothalamic fibers
A
  • 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
24
Q

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
A
  • Lesion: L thalamus
    • receives STT and dorsal column/medial lemniscus afferent information from both body & face
  • Cause: stroke
25
Q

CASE: 38 yo M working in a Cola factory has R thumb, index & middle finger pain & tingling x 2 month, especially at night.

Exam:

  • Decreased PP in R index, middle, thumb ⇒ region too localized to be cortex or thalamus; so, most likely a peripheral lesion
  • Weakness in R opponens pollicis & reduced bulk in thenar eminence ⇒ these muscles are done by median nerve
  • Reflexes normal
A
  • Localize: right median nerve
  • Cause: median neuropathy at the wrist
    • Carpal Tunnel syndrome
26
Q

CASE: A patient falls from a tree and develops L sided weakness.
Exam:
• No weakness in hand
• L lateral forearm ↓PP
• Reflexes: L biceps, brachioradialis 1+

A
  • Localize: L upper trunk of brachial plexus
  • Cause: usually related to trauma in which angle between shoulder & neck is rapidly increased, causing tearing of upper portion of brachial plexus
    • lesion could be in the trunk or roots
    • if lesion was at level of roots, there may be shooting pain down arm
    • additional studies (like EMG) need to be done to confirm clinical suspicion